FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Sato, S Sato, N Kudej, RK Uechi, M Asai, K Shen, YT Ishikawa, Y Vatner, SF Vatner, DE AF Sato, S Sato, N Kudej, RK Uechi, M Asai, K Shen, YT Ishikawa, Y Vatner, SF Vatner, DE TI beta-adrenergic receptor signalling in stunned myocardium of conscious pigs SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE adenylyl cyclase; forskolin; regional myocardial function; myocardial ischemia; porcine; beta-adrenergic receptors; G-proteins ID ADENYLYL CYCLASE SYSTEM; PROTEIN-KINASE-C; CORONARY-ARTERY; INOTROPIC STIMULATION; METABOLIC RESERVE; ISCHEMIA; SENSITIZATION; DYSFUNCTION; REPERFUSION; HEARTS AB The primary goal of this study was to compare the effects of isoproterenol which stimulates beta-adrenergic receptors and forskolin, and NKH 477, a water soluble derivative of forskolin, which stimulate adenylyl cyclase in stunned myocardium of conscious pigs, previously instrumented for measurements of left ventricular pressure and dP/dt, arterial pressure, and wall thickening, Ten min of coronary artery occlusion induced transmural reductions in blood now (radioactive microspheres) in subepicardium (-98 +/- 2%) and subendocardium (-99 +/- 1%). Wall thickening (piezoelectric crystals) fell from 2.50 +/- 0.26 mm to -0.26 +/- 0.26 mm and remained depressed at 1.37 +/- 0.19 mm after 20-30 min coronary artery reperfusion, reflecting myocardial stunning. At that time, isoproterenol (0.2 mu g/kg) increased wall thickening in stunned myocardium (+1.40 +/- 0.16 mm, P < 0.05) more than in control (+ 0.71 +/- 0.22 mm), while forskolin elicited the opposite effects. NKH 477 (30 mu g/kg), which does not penetrate the blood-brain barrier, increased systolic wall thickening similarly before (+ 0.95 +/- 0.25 mm) and during (+ 1.01 +/- 0.24 mm) myocardial stunning, The reflex inotropic responses to inferior vena caval occlusion on wall thickening were diminished, P < 0.05, in the stunned myocardium (+ 0.53 +/- 0.05 mm) compared with control (+ 0.95 +/- 0.07 mm). beta-adrenergic receptor density, which was quantitated with I-125-cyanopindolol binding, was increased transmurally in stunned myocardium compared with non-ischemic myocardium (subepicardium: + 23 +/- 5%, subendocardium: + 34 +/- 13%, P < 0.05). Basal and forskolin-stimulated adenylyl cyclase activities were decreased slightly, but significantly, in the stunned subendocardium but not in the subepicardium, while isoproterenol stimulation of adenylyl cyclase activity showed no differences. In summary, paradoxical responses to beta-adrenergic receptor stimulation were observed in stunned myocardium, with pharmacological stimulation with isoproterenol evoking enhanced responses, and neural stimulation with inferior vena caval occlusion eliciting depressed responses, The diminished responses to forskolin in vivo, in stunned myocardium were out of proportion to the biochemical measurements, and may be attributed to neurally mediated cardiac effects of forskolin, since the responses to direct stimulation of adenylyl cyclase by NKH 477 were preserved. (C) 1997 Academic Press Limited. 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, SERV PEDIAT, BOSTON, MA 02114 USA. NR 53 TC 20 Z9 20 U1 0 U2 3 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD MAY PY 1997 VL 29 IS 5 BP 1387 EP 1400 DI 10.1006/jmcc.1997.0377 PG 14 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA XD296 UT WOS:A1997XD29600010 PM 9201624 ER PT J AU Sweet, WH AF Sweet, WH TI Early history of development of boron neutron capture therapy of tumors SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE history; neutron capture treatment; boron; lithium; glioma; melanoma ID CHEMISTRY AB The stable isotope B-10 has a peculiarly marked avidity to capture slow neutrons whereupon it disintegrates into a lithium and a helium atom. These give up the 2.4 MeV of disintegration energy which they share within 5 and 9 mu m of the B-10 atom respectively. This means that the cell closest to the B-10 atom bears the brunt of its atomic explosion. The objective of the tumor therapist is to find a carrier molecule for the boron atom which will concentrate in the tumor. Although a number of investigators saw the peculiar advantage of this selective tactic to achieve destruction of a species of unwanted cells, no success in animal studies was achieved until 1950. Sweet and colleagues found that the capillary blood-brain barrier keeps many substances out of the normal brain but that the gliomas had much less of such a barrier. He, Brownell, Soloway and Hatanaka in Boston together with Farr, Godwin, Robertson, Stickley, Konikowski and others at the Brookhaven National Laboratory worked partially in collaboration and partly independently. We irradiated at 3 nuclear reactors several series of glioma patients with no long-term remission, much less a cure being achieved. Hatanaka on his return to Japan kept BNCT alive by treating a total of 140 patients with various brain tumors. Beginning in 1972, Mishima and colleagues have achieved useful concentrations of B-10-borono-phenylalanine, an analogue of the melanin precursor tyrosine, for BNCT of melanomas. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 42 TC 45 Z9 50 U1 0 U2 5 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD MAY PY 1997 VL 33 IS 1-2 BP 19 EP 26 DI 10.1023/A:1005752827194 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA WX655 UT WOS:A1997WX65500003 PM 9151220 ER PT J AU Delalle, I Bhide, PG Caviness, VS Tsai, LH AF Delalle, I Bhide, PG Caviness, VS Tsai, LH TI Temporal and spatial patterns of expression of p35, a regulatory subunit of cyclin-dependent kinase 5, in the nervous system of the mouse SO JOURNAL OF NEUROCYTOLOGY LA English DT Article ID DIRECTED PROTEIN-KINASE; BOVINE BRAIN; TAU-PROTEIN; CELL-CYCLE; CDC2-LIKE KINASE; KDA SUBUNIT; CDK5; ACTIVATOR AB The protein p35 is a regulatory subunit of cyclin-dependent kinase 5. It has no recognized homology to cyclins but binds to and activates cyclin-dependent kinase 5 directly in the absence of other protein molecules. Cyclin-dependent kinase 5 was initially isolated by homology to the key cell cycle regulator cdc2 kinase and later identified as a neuronal kinase that phosphorylates histone H1, tau or neurofilaments. This kinase is localized in axons of the developing and mature nervous system. To understand the role of p35 as a regulator of cyclin-dependent kinase 5 activity in the CNS, we examined the pattern of expression of p35 mRNA in the nervous system of embryonic, early postnatal and adult mice. In separate experiments, we also examined the spatial distribution of cyclin-dependent kinase 5 mRNA and the activity of cyclin-dependent kinase 5/p35 kinase complex. Postmitotic cells express p35 mRNA immediately after they leave the zones of cell proliferation. It is also expressed in developing axonal tracts in the brain. Cyclin-dependent kinase 5 mRNA is present in postmitotic and in proliferative cells throughout the embryonic central nervous system. During early postnatal period signal for p35 mRNA declines while that for cyclin-dependent kinase 5 mRNA increases throughout the brain. In the adult brain although both p35 and cyclin-dependent kinase 5 mRNAs are expressed at relatively high levels in certain structures associated with the limbic system, considerable differences exist in the patterns of their distribution in other parts of the brain. These data suggest that the p35/cyclin-dependent kinase 5 complex may be associated with early events of neuronal development such as neuronal migration and axonal growth while in the limbic system of the mature brain it may be associated with the maintenance of neuronal plasticity. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA. RP Delalle, I (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 12005, NS 32657] NR 33 TC 60 Z9 65 U1 0 U2 1 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0300-4864 J9 J NEUROCYTOL JI J. Neurocytol. PD MAY PY 1997 VL 26 IS 5 BP 283 EP 296 DI 10.1023/A:1018500617374 PG 14 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA XD489 UT WOS:A1997XD48900002 PM 9192293 ER PT J AU Frosch, MP Collins, T Zhang, J Ahn, P Berezovskaja, O Xia, M Hyman, BT Koo, EH AF Frosch, MP Collins, T Zhang, J Ahn, P Berezovskaja, O Xia, M Hyman, BT Koo, EH TI Transgenic mice expressing mutant and wild type human presenilin-1 (PS-1) SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 1 EP 1 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300013 ER PT J AU GomezIsla, T Nochlin, D Bird, TD Sumi, SM Hyman, BT AF GomezIsla, T Nochlin, D Bird, TD Sumi, SM Hyman, BT TI Phenotypic characterization of PS1 and PS2 related Alzheimer's disease. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 6 EP 6 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300018 ER PT J AU Knowles, RB Christie, RH Hyman, BT AF Knowles, RB Christie, RH Hyman, BT TI Heparan sulfate labeling in neocortex of Alzheimer's Disease patients. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 17 EP 17 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300029 ER PT J AU Burns, KL Ueki, K Louis, DN AF Burns, KL Ueki, K Louis, DN TI Molecular genetic and immunohistochemical analysis of the p16-cdk4-pRb pathway in glioblastomas. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 40 EP 40 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300052 ER PT J AU StemmerRachamimov, AO GonzalezAgosti, C Xu, L Ramesh, V Louis, DN AF StemmerRachamimov, AO GonzalezAgosti, C Xu, L Ramesh, V Louis, DN TI Expression of NF2-encoded merlin and related ERM family proteins in the human central nervous system. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 43 EP 43 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300055 ER PT J AU Ferrante, RJ Beal, MF Kowall, NW AF Ferrante, RJ Beal, MF Kowall, NW TI Immunohistochemical localization of markers for oxidative injury in Parkinson's disease. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BEDFORD VA MED CTR,BOSTON,MA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 71 EP 71 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300083 ER PT J AU Richfield, EK Vonsattel, JP AF Richfield, EK Vonsattel, JP TI Selective loss of preprotachykinin neurons in a phenocopy of Huntington's disease. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 UNIV ROCHESTER,ROCHESTER,NY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 74 EP 74 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300086 ER PT J AU Newell, K Hyman, B Growdon, J HedleyWhyte, ET AF Newell, K Hyman, B Growdon, J HedleyWhyte, ET TI Evaluation of NIA-Reagan Institute criteria for the neuropathological diagnosis of Alzheimer disease. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 87 EP 87 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300099 ER PT J AU Young, K Russell, JA Ma, JM HedleyWhyte, TE Dlouhy, SR Piccardo, P Ghetti, B AF Young, K Russell, JA Ma, JM HedleyWhyte, TE Dlouhy, SR Piccardo, P Ghetti, B TI Gerstmann-Straussler-Scheinker (GSS) disease with the prion protein gene (PRNP) P102L mutation and lower motor neuron degeneration. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 LAHEY HITCHCOCK CLIN,BURLINGTON,MA. INDIANA UNIV,INDIANAPOLIS,IN 46204. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 100 EP 100 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300112 ER PT J AU Kowall, NW Shinobu, LA Beal, MF Ferrante, RJ AF Kowall, NW Shinobu, LA Beal, MF Ferrante, RJ TI Injury in the spinal cords of transgenic mice expressing mutant human superoxide dismutase. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 BEDFORD VA MED CTR,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 159 EP 159 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300170 ER PT J AU delaMonte, SM Iulian, M Wands, JR Cudkovicz, M Brown, RH AF delaMonte, SM Iulian, M Wands, JR Cudkovicz, M Brown, RH TI Molecular neuropathology of SOD-1 mutant transgenic mice: Evidence for neuritic sprouting and apoptosis SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 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 ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 160 EP 160 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300171 ER PT J AU Vonsattel, JPG Zhao, Y Lenzi, S GomezIsla, T Hyman, BT Myers, R DiFiglia, M Gusella, J MacDonald, M Ma, MJ HedleyWhyte, ET AF Vonsattel, JPG Zhao, Y Lenzi, S GomezIsla, T Hyman, BT Myers, R DiFiglia, M Gusella, J MacDonald, M Ma, MJ HedleyWhyte, ET TI Alzheimer disease does not protect the neostriatum in combined cases of Huntington (HD) and Alzheimer disease (AD). SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 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 ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 185 EP 185 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300196 ER PT J AU Etiene, D Kraft, J Wands, JR GomezIsla, T Hyman, BT HedleyWhyte, ET delaMonte, SM AF Etiene, D Kraft, J Wands, JR GomezIsla, T Hyman, BT HedleyWhyte, ET delaMonte, SM TI Cerebral infarction contributes to the heterogeneity of Alzheimer's disease (AD). SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 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 ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 186 EP 186 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300197 ER PT J AU Selcuki, D delaMonte, SM AF Selcuki, D delaMonte, SM TI Spinal cord and neuromuscular pathology in AIDS. SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 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 ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 196 EP 196 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300207 ER PT J AU StemmerRachamimov, AO Horgan, MA Taratuto, AL Munoz, DG Smith, TW Frosch, MP Louis, DN AF StemmerRachamimov, AO Horgan, MA Taratuto, AL Munoz, DG Smith, TW Frosch, MP Louis, DN TI Meningioangiomatosis is associated with neurofibromatosis 2 but not with somatic alterations of the NF2 gene SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE meningioangiomatosis; neurofibromatosis 2; NF2 gene ID VON RECKLINGHAUSENS DISEASE; VONRECKLINGHAUSENS DISEASE; MENINGIO-ANGIOMATOSIS; TUMOR; MUTATION AB Meningioangiomatosis occurs sporadically and in patients with neurofibromatosis. The literature, however, is unclear concerning the type of neurofibromatosis associated with meningioangiomatosis. Because determining which form of neurofibromatosis predisposes to meningioangiomatosis would clarify the genetic alterations of this lesion, we reviewed all reported cases of meningioangiomatosis associated with neurofibromatosis in light of current diagnostic criteria for neurofibromatosis 1 (NF1) and neurofibromatosis 2 (NF2). All well-documented cases of meningioangiomatosis occurred in the setting of NF2, implying that germline alterations of the NF2 gene predispose to meningioangiomatosis. To determine whether sporadic (non-NF) cases of meningioangiomatosis arise from somatic alterations of the same gene, we screened the NF2 gene for mutations in 12 sporadic cases of meningioangiomatosis and in constitutional DNA from 6 of these 12 patients. No mutations were found in either the lesional or constitutional DNA, which suggests that sporadic meningioangiomatosis is not a forme fruste of NF2 and that somatic alterations of the NF2 gene do not play a major role in sporadic meningioangiomatosis. For some tumor suppressor genes, germline mutations may predispose to specific tumors, while similar sporadic lesions only rarely suffer somatic mutations in these genes. The present findings suggest a similar dichotomy for the NF2 gene in meningioangiomatosis. C1 MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOL NEUROONCOL LAB,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. OREGON HLTH SCI UNIV,DIV NEUROSURG,PORTLAND,OR 97201. HOSP NACL PEDIAT JUAN P GARRAHAN,DEPT NEUROPATHOL,BUENOS AIRES,DF,ARGENTINA. UNIV WESTERN ONTARIO,UNIV HOSP,DEPT NEUROPATHOL,LONDON,ON N6A 5A5,CANADA. UNIV MASSACHUSETTS,MED CTR,DEPT PATHOL,WORCESTER,MA. CHILDRENS HOSP,DIV NEUROPATHOL,BOSTON,MA 02115. OI Munoz, David/0000-0003-0957-6244 FU NINDS NIH HHS [NS24279] NR 43 TC 27 Z9 28 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1997 VL 56 IS 5 BP 485 EP 489 DI 10.1097/00005072-199705000-00004 PG 5 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WY073 UT WOS:A1997WY07300004 PM 9143261 ER PT J AU Ferrante, RJ Gutekunst, CA Persichetti, F McNeil, SM Kowall, NW Gusella, JF MacDonald, ME Beal, MF Hersch, SM AF Ferrante, RJ Gutekunst, CA Persichetti, F McNeil, SM Kowall, NW Gusella, JF MacDonald, ME Beal, MF Hersch, SM TI Heterogeneous topographic and cellular distribution of Huntington expression in the normal human neostriatum SO JOURNAL OF NEUROSCIENCE LA English DT Article DE Huntington's disease; Huntington; neostriatum; immunofluorescence; NADPH-diaphorase; nitric oxide synthase; calbindin D28k ID CALCIUM-BINDING PROTEIN; DISEASE GENE HOMOLOG; STRIATAL NEURONS; BASAL GANGLIA; WIDESPREAD EXPRESSION; NADPH-DIAPHORASE; SPINY NEURONS; SUBSTANCE-P; BRAIN; RAT AB A striking heterogeneous distribution of topographic and cellular huntingtin immunoreactivity was observed within the human neostriatum using three distinct huntingtin antibodies. Patchy areas of low huntingtin immunoreactivity were present in both the caudate nucleus and putamen, surrounded by an intervening area of greater immunoreactivity. Comparison of huntingtin immunoreactivity with contiguous serial sections stained for enkephalin and calbindin D28k immunoreactivities showed that the topographic heterogeneity of huntingtin immunostaining corresponded to the patch (striosome) and matrix compartments within the striatum. Huntingtin immunoreactivity was confined primarily to neurons and neuropil within the matrix compartment, whereas little or no neuronal or neuropil huntingtin immunostaining was observed within the patch compartment. There was marked variability in the intensity of huntingtin immunolabel among medium-sized striatal neurons, whereas a majority of large striatal neurons were only faintly positive or without any immunoreactivity. Combined techniques for NADPH-diaphorase enzyme histochemistry and huntingtin immunocytochemistry, as well as double immunofluorescence for either nitric oxide synthase or calbindin D28k in comparison with huntingtin expression, revealed a striking correspondence between calbindin D28k and huntingtin immunoreactivities, with little or no colocalization between NADPH-diaphorase or nitric oxide synthase neurons and huntingtin expression. These observations suggest that the selective vulnerability of spiny striatal neurons and the matrix compartment observed in Huntington's disease is associated with higher levels of huntingtin expression, whereas the relative resistance of large and medium-sized aspiry neurons and the patch compartments to degeneration is associated with low levels of huntingtin expression. C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. EMORY UNIV,SCH MED,DEPT NEUROL,ATLANTA,GA 30322. MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Ferrante, RJ (reprint author), BEDFORD VA MED CTR,GERIATR RES EDUC CLIN CTR,UNIT 182B,200 SPRINGS RD,BEDFORD,MA 01730, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [1P30AG13846, AG12922]; NINDS NIH HHS [NS16367] NR 55 TC 102 Z9 103 U1 0 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD MAY 1 PY 1997 VL 17 IS 9 BP 3052 EP 3063 PG 12 WC Neurosciences SC Neurosciences & Neurology GA WU675 UT WOS:A1997WU67500013 PM 9096140 ER PT J AU Narula, J Petrov, A Ditlow, C Pak, KY Chen, FW Khaw, BA AF Narula, J Petrov, A Ditlow, C Pak, KY Chen, FW Khaw, BA TI Maximizing radiotracer delivery to experimental atherosclerotic lesions with high-dose, negative charge-modified Z2D3 antibody for immunoscintigraphic targeting SO JOURNAL OF NUCLEAR CARDIOLOGY LA English DT Article DE angioplasty; hyperlipidemia; smooth muscle cells; antibody; gamma imaging; atherosclerosis ID LOCALIZATION AB Background. Two factors that directly affect target/background ratio in immunoscintigraphy are the concentration of the antibody bound to the target and the concentration of the antibody in the circulation, High dosages of monoclonal antibody have been reported to be more efficacious in visualization of tumors. Although administration of a higher dosage of antibody increases the absolute target accumulation of the radiotracer, it also increases the background activity, which may offset this advantage, Negative charge-modified antibodies carry high specific radioactivity to the target sites without significantly increasing the background activity, Therefore we investigated whether higher dosages of negative charge-modified antibody can be used to improve imaging of experimental atherosclerotic lesions. Methods and Results, Experimental atherosclerotic lesions were produced in 16 New Zealand White rabbits by balloon deendothelialization of the infradiaphragmatic aorta and hyperlipidemic diet for 12 weeks, Negative charge-modified Z2D3 antibody F(ab')(2) specific for an antigen on proliferating smooth muscle cells of human atheroma labeled with In-111 was used for imaging experimental atherosclerotic lesions either at high (100 to 125 mu g) or low (25 to 50 mu g) dosages. A lower dosage of Z2D3 was labeled with 507 +/- 29.5 mu Ci (25 to 50 mu g) In-111 label, compared with 2.9 +/- 0.24 mCi (100 to 125 mu g) for the higher dosage. Although noninvasive visualization of atherosclerotic lesions was possible in all animals at 33 hours, high antibody dose allowed unequivocal visualization of the lesion as early as 3 hours after intravenous administration of the antibody, Eight animals were killed at 23 hours and the remaining eight animals at 48 hours, Mean radioactivity dose delivered per gram of lesion with the low-dose protocol at 24 hours was 0.46 +/- 0.09 mu Ci, which remained essentially unchanged at 48 hours (0.37 +/- 0.09 mu Ci; p = 0.51). With the high-dosage protocol, the total radioactivity idose) per gram uptake in the lesion increased by about eightfold (3.39 +/- 0.58 mu Ci; p = 0.002) at 24 hours and was sixfold higher at 48 hours (2.21 +/- 0.45 mu Ci; p < 0.02). Conclusions. The study demonstrated that the increase in the dosage of negatively charge-modified antibody allows a very high delivery of specific radioactivity to the target, which in turn enables early visualization of experimental atherosclerotic lesions. C1 NORTHEASTERN UNIV,CTR DRUG TARGETING & ANAL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SCOTGEN BIOPHARMACEUT INC,MENLO PK,CA. NR 16 TC 17 Z9 17 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1071-3581 J9 J NUCL CARDIOL JI J. Nucl. Cardiol. PD MAY-JUN PY 1997 VL 4 IS 3 BP 226 EP 233 DI 10.1016/S1071-3581(97)90083-0 PG 8 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA XF067 UT WOS:A1997XF06700007 PM 9199260 ER PT J AU Narula, J Kolodgie, F Virmani, R Petrov, A Khaw, BA AF Narula, J Kolodgie, F Virmani, R Petrov, A Khaw, BA TI Should assessment of the rate of smooth muscle cell proliferation by In-111-Z2D3 antibody imaging allow for predicting post-angioplastic restenosis? SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NORTHEASTERN UNIV,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1 EP 1 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000001 ER PT J AU Dong, Q Babich, JW Graham, W Barzana, M Ferrill, K Fischman, AJ AF Dong, Q Babich, JW Graham, W Barzana, M Ferrill, K Fischman, AJ TI HYNIC-maleimide, a thiol-specific linker for labeling peptides with Tc-99m: Conjugation, labeling and in vivo evaluation. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 60 EP 60 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000060 ER PT J AU Correia, JA Burnham, CA Kaufman, D Chester, DA Fischman, AJ AF Correia, JA Burnham, CA Kaufman, D Chester, DA Fischman, AJ TI Small animal PET imaging device - Preliminary design study SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 158 EP 158 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000158 ER PT J AU Dragotakes, SC Werner, J FernandezdelCastillo, C Rivera, JA Ou, J Rattner, D Fischman, AJ Warshaw, AL AF Dragotakes, SC Werner, J FernandezdelCastillo, C Rivera, JA Ou, J Rattner, D Fischman, AJ Warshaw, AL TI Characterization of 99mTc white blood cells: Localization in an experimental pancreatitis model. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 186 EP 186 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000186 ER PT J AU Fischman, AJ Babich, JW Bonab, AA Alpert, NM Elmaleh, DR Barrow, SA Graham, WA Meltzer, PC Madras, BK AF Fischman, AJ Babich, JW Bonab, AA Alpert, NM Elmaleh, DR Barrow, SA Graham, WA Meltzer, PC Madras, BK TI Rapid detection of Parkinson's disease by SPECT with altropane: A selective ligand for dopamine transporters. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 219 EP 219 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000219 ER PT J AU Madras, BK Babich, JW Elmaleh, DE Meltzer, PC Fischman, AJ AF Madras, BK Babich, JW Elmaleh, DE Meltzer, PC Fischman, AJ TI The SPECT ligand altropane effectively detects Parkinson's disease in human putamen. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ORGANIX INC,WOBURN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 220 EP 220 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000220 ER PT J AU Hashimoto, A Abraham, S Fischman, AJ Force, T Gewirtz, H Palmer, E Rabito, C Scott, J Zervos, G Yasuda, T AF Hashimoto, A Abraham, S Fischman, AJ Force, T Gewirtz, H Palmer, E Rabito, C Scott, J Zervos, G Yasuda, T TI Comparison of various imaging stress tests; Complications and accuracy in 2097 patients. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 270 EP 270 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000270 ER PT J AU Elmaleh, DR Narula, J Babich, JW Petrov, A Rapoport, E Zamecnik, PC Fischman, AJ Khaw, BA AF Elmaleh, DR Narula, J Babich, JW Petrov, A Rapoport, E Zamecnik, PC Fischman, AJ Khaw, BA TI Tc-99m-labeled nucleotides as tumor imaging agents in a SCID mouse breast tumor model. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NORTHEASTERN UNIV,BOSTON,MA 02115. WORCESTER FDN EXPT BIOL INC,SHREWSBURY,MA 01545. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 324 EP 324 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000324 ER PT J AU Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Fischman, AJ AF Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Fischman, AJ TI 6-mercaptomethylpyridine-3-carboxylic acid (MEMNIC): A new reagent for peptide labeling with Tc-99m. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 372 EP 372 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000372 ER PT J AU VandenAbbeele, AD Shulkin, BL Neuberg, DS Kehoe, KM AF VandenAbbeele, AD Shulkin, BL Neuberg, DS Kehoe, KM TI The role of SPECT in the evaluation of the abdomen on Gallium-67 scintigraphy. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV MICHIGAN,MED CTR,ANN ARBOR,MI. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 429 EP 429 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000429 ER PT J AU Rajendran, JG Jacobson, AF AF Rajendran, JG Jacobson, AF TI Long-term outcome in patients with low probability lung scans: Effect of the modified PIOPED criteria. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 458 EP 458 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000458 ER PT J AU Moroi, M Fischman, AJ Gold, HK Yasuda, T AF Moroi, M Fischman, AJ Gold, HK Yasuda, T TI Prompt improvement in myocardial perfusion and glucose metabolism by percutaneous coronary revascularization in patients with unstable angina: Assessment with F-18 FDG/Tc-99m MIBI spect. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 632 EP 632 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000586 ER PT J AU Zhu, H Baxter, LT Jain, RK AF Zhu, H Baxter, LT Jain, RK TI Potential and limitations of radioimmunodetection and radioimmunotherapy with monoclonal antibodies SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE radioimmunodetection; radioimmunotherapy; antibody pharmacokinetics; mathematical modeling; radiation dosimetry ID BINDING-SITE BARRIER; SINGLE-CHAIN FV; F(AB')2 FRAGMENTS; NUDE-MICE; PHARMACOKINETIC MODEL; TUMOR-LOCALIZATION; COLORECTAL-CANCER; XENOGRAFT MODEL; CELL CARCINOMA; SOLID TUMORS AB Recently, we developed a physiologically based pharmacokinetic model capable of predicting antibody biodistribution in humans by scaling up from mice. By applying this model to anticarcinoembryonic antigen murine antibody ZCE025, we address several critical issues in radioimmunodetection and radioimmunotherapy, including the optimal antibody doses, the desirable antibody form for cancer detection, the optimal combinations of antibody forms and radionuclides for cancer treatment and the effectiveness of the modality, Methods: Under the baseline conditions of a standard 70-kg man with a 20-g tumor embedded in the liver, the model was used to: (a) estimate absorbed doses in tumor and normal tissues, (b) determine dose-dependent antibody uptake in the tumor, (c) simulate tumor-to-background antibody concentration ratio and (d) calculate therapeutic ratios for different antibody forms and radionuclides, Sensitivity analysis further enabled us to determine antibody delivery barriers and to assess the modality under average and favorable tumor physiological conditions, Results: By using ZCE025 under the baseline conditions, the model found that Fab was the most suitable form for cancer diagnosis, while I-131 combined with F(ab')(2) provided the highest tumor-to-bone marrow therapeutic ratio for cancer treatment. Sensitivity analysis showed that antibody permeability was the major barrier for antibody accretion in tumors, It also demonstrated that normal tissue antigen expression at a level lower than in the tumor had little effect on the therapeutic ratio. Conclusion: The model demonstrates that: (a) for radioimmunodetection, the most effective antibody form (Fab for ZCE025) was the lower mol weight form, yet not sensitive enough for hepatic metastasis detection; and (b) for radioimmunotherapy, a relatively fast-clearing antibody form (F(ab')(2) for ZCE025) in combination with long half-life beta(-)-emitiers was optimal, yet inadequate as the sole therapeutic modality for solid tumors. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,RADIOL SCI PROGRAM,CAMBRIDGE,MA 02139. FU NCI NIH HHS [R35-CA-56591] NR 58 TC 38 Z9 38 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 BP 731 EP 741 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WX896 UT WOS:A1997WX89600024 PM 9170438 ER PT J AU Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Zubieta, J Fischman, AJ AF Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Zubieta, J Fischman, AJ TI N,N-bis(2-mercaptoethyl)methylamine (NS2): A new co-ligand for Tc-99m labeling of hydrazino-nicotinamide (HYNIC) peptides. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SYRACUSE UNIV,SYRACUSE,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 805 EP 805 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000711 ER PT J AU Brownell, AL Livni, E Madras, BK AF Brownell, AL Livni, E Madras, BK TI Global approach in modeling of [N-(C-11)-methyl]-(-)-cocaine pharmacokinetics in nonhuman primate brain. SO JOURNAL OF NUCLEAR MEDICINE 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 SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 857 EP 857 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000763 ER PT J AU Bonab, AA Alpert, NM Fischman, AJ AF Bonab, AA Alpert, NM Fischman, AJ TI Binding potential estimation for the 5-HT2 receptor ligand, 18F-setoperone using reference region graphical analysis method. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 860 EP 860 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000766 ER PT J AU Hsu, H Alpert, HM Christian, BT Bonab, AA Morris, E Fischman, AJ AF Hsu, H Alpert, HM Christian, BT Bonab, AA Morris, E Fischman, AJ TI Noise properties of a graphical assay of receptor binding SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 871 EP 871 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000777 ER PT J AU Bonab, AA Babich, JW Alpert, NM Madras, BK Fischman, AJ AF Bonab, AA Babich, JW Alpert, NM Madras, BK Fischman, AJ TI Comparison of 3 methods for quantification of dopamine transporters by SPECT with I-123 altropane SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 949 EP 949 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000855 ER PT J AU VandenAbbeele, AD Rybicki, FJ Cowart, DM Kehoe, KM AF VandenAbbeele, AD Rybicki, FJ Cowart, DM Kehoe, KM TI Quantification of Gallium-67 avidity as a function of the histology in patients with non-Hodgkin's lymphoma. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1007 EP 1007 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000913 ER PT J AU Carter, EA Tompkins, RG Babich, JW Graham, W Fischman, AJ AF Carter, EA Tompkins, RG Babich, JW Graham, W Fischman, AJ TI Accumulation of Tc-99m chemotactic peptides in eosinophilic infiltrates. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1080 EP 1080 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98000986 ER PT J AU Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Pike, M Fischman, AJ AF Babich, JW Dong, Q Graham, W Barzana, M Ferrill, K Pike, M Fischman, AJ TI A novel high affinity chemotactic peptide antagonist for infection imaging. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 3 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1129 EP 1129 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001035 ER PT J AU Hsu, H Carter, EA Christian, B Alpert, NM Tompkins, RG Fischman, AJ AF Hsu, H Carter, EA Christian, B Alpert, NM Tompkins, RG Fischman, AJ TI PET studies of the effect of thermal injury on skeletal muscle energy metabolism in rabbits. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1131 EP 1131 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001037 ER PT J AU Fischman, AJ Babich, JW Bonab, AA Alpert, NM Vincent, J Callahan, RJ Correia, JA Rubin, RH AF Fischman, AJ Babich, JW Bonab, AA Alpert, NM Vincent, J Callahan, RJ Correia, JA Rubin, RH TI Pharmacokinetics of F-18 trovafloxacin in healthy human subjects studied with PET. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. PFIZER INC,GROTON,CT 06340. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1134 EP 1134 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001040 ER PT J AU Silverman, DHS Munakata, JA Mandelkern, MA Hoh, CK Mayer, EA AF Silverman, DHS Munakata, JA Mandelkern, MA Hoh, CK Mayer, EA TI Comparing regional cerebral activity associated with visceral stimuli in male and female patients. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1150 EP 1150 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001056 ER PT J AU Kosslyn, SM Alpert, NM Thompson, WL AF Kosslyn, SM Alpert, NM Thompson, WL TI Neural systems that underlie visual imagery and visual perception: A PET study. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 HARVARD UNIV,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1205 EP 1205 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001111 ER PT J AU Madras, BK Elmaleh, DR Brownell, AL AF Madras, BK Elmaleh, DR Brownell, AL TI PET imaging with (C-11) SCH 39166 reveals D1 dopamine receptor occupancy by a D1 agonist SO JOURNAL OF NUCLEAR MEDICINE 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 SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1210 EP 1210 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001116 ER PT J AU Jacobson, AF Hammersmith, SM AF Jacobson, AF Hammersmith, SM TI Value of the baseline bone scan in patients with newly diagnosed prostate cancer and low prostate specific antigen level. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1262 EP 1262 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001167 ER PT J AU Huggins, GS Bishop, TA Fischman, AJ Pasternak, RC Gewirtz, H AF Huggins, GS Bishop, TA Fischman, AJ Pasternak, RC Gewirtz, H TI Correction of hyperlipidemia improves endothelium independent microvascular function in patients with ischemic heart disease. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1997 VL 38 IS 5 SU S BP 1316 EP 1316 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY980 UT WOS:A1997WY98001200 ER PT J AU Clinton, SK AF Clinton, SK TI Diet, anthropometry and breast cancer: Integration of experimental and epidemiologic approaches SO JOURNAL OF NUTRITION LA English DT Article; Proceedings Paper CT Symposium on Diet, Anthropometry and Breast Cancer: Integration of Experimental and Epidemiologic Approaches given at Experimental Biology 96 CY APR 15, 1996 CL WASHINGTON, DC SP Amer Soc Nutr Sci DE breast cancer; nutrition; anthropometry; dietary fat ID MAMMARY-TUMORS; FISH OIL; FAT; RATS; GROWTH; MICE; CARCINOMAS; RISK AB The interrelationships of dietary fat and energy, growth rates and anthropometry, and breast carcinogenesis have been examined by a diverse array of approaches throughout the last 50 y as new investigative tools have been developed by laboratory scientists and epidemiologists. A consensus among investigators has not emerged, however, and dietary recommendations for breast cancer prevention have not been clearly formulated or effectively communicated to the public. Indeed, the gap between those investigators utilizing laboratory-based approaches and those using epidemiologic models has expanded in recent years. Cancer epidemiologists have become increasingly skeptical that results derived form laboratory animal models of breast carcinogenesis and in vitro systems are directly applicable to human breast cancer risk. Concurrently, laboratory scientists have questioned the ability of epidemiological tools to accurately measure dietary intake and relevant biomarkers and to account for a diverse array of potentially confounding environmental and genetic factors characteristic of human populations under study. These polarized views are reinforced by a failure of investigators using diverse approaches to interact, integrate their skills and resources, develop novel hypotheses, and propose solutions using both laboratory and epidemiologic techniques. Therefor, the objectives of this symposium are to summarize experimental and epidemiologic knowledge, foster communication and collaboration, and attempt to identify appropriate studies to bridge the gaps in our knowledge concerning dietary lipid and energy, anthropometrics, and breast cancer risk. C1 DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115. NR 26 TC 9 Z9 9 U1 0 U2 1 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD MAY PY 1997 VL 127 SU 5 BP S916 EP S920 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA WZ923 UT WOS:A1997WZ92300029 PM 9164263 ER PT J AU Kharrazi, FD Rodgers, WB Kennedy, JG Lhowe, DW AF Kharrazi, FD Rodgers, WB Kennedy, JG Lhowe, DW TI Parturition-induced pelvic dislocation: A report of four cases SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE pelvic dislocation; parturition ID PUBIC SYMPHYSIS; VAGINAL DELIVERY; SEPARATION AB Objective: To describe our experience with four cases of severe pelvic dislocation associated with difficult parturition. Design: Retrospective case series. Patients: Four patients, each with rupture of the symphysis pubis and sacroiliac joints during labor. All injuries were associated with significant initial pain and disability. All developed persistent symptoms related to the sacroiliac disruption. Interventions: The three patients who had presented acutely were treated with closed reduction and application of a pelvic binder. Two underwent closed reduction of their pelvic dislocation while anesthetized with a general anesthetic. One patient (N.A.), who presented late, had not been treated with a binder. Results: All four patients had persistent posterior pelvic (sacroiliac) pain. In two patients a postpartum neuropathy persisted. Conclusions: Severe pelvic dislocations are rare during labor, with conservative treatment reported to be successful in most cases. The persistence of symptoms in our patients emphasizes the need for careful examination and follow-up of these rare injuries. Because the outcome in our patients was poor and results in the literature are equivocal, we suggest the consideration of an operative approach to treatment in patients with symphyseal diastasis of >4.0 cm. C1 Massachusetts Gen Hosp, Orthopaed Trauma Serv, Boston, MA 02114 USA. Childrens Hosp, Dept Orthopaed Surg, Boston, MA 02115 USA. Capital Reg Orthopaed & Sports Med, Jefferson, MO USA. Mater Mesicordia Hosp, Dept Orthopaed Surg, Dublin, Ireland. RP Kharrazi, FD (reprint author), Massachusetts Gen Hosp, Orthopaed Trauma Serv, 15 Parkman St, Boston, MA 02114 USA. NR 22 TC 22 Z9 25 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PD MAY PY 1997 VL 11 IS 4 BP 277 EP 281 DI 10.1097/00005131-199705000-00009 PG 5 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA YQ617 UT WOS:000071405800009 PM 9258826 ER PT J AU Klein, S Kinney, J Jeejeebhoy, K Alpers, D Hellerstein, M Murray, M Twomey, P Bistrian, B Bothe, A Heitkemper, M Hubbard, V Schnackenberg, D Bernstein, E Hambidge, M Heymsfield, S IretonJones, C Wolfson, M Jacobs, D Keithley, J Meguid, M Pingleton, S Kopple, J Koretz, R Shulman, R Wilmore, D Driscoll, D Fleming, CR Greene, H Sitrin, M Herrmann, V Lipman, T Mock, D Borum, P Shronts, E AF Klein, S Kinney, J Jeejeebhoy, K Alpers, D Hellerstein, M Murray, M Twomey, P Bistrian, B Bothe, A Heitkemper, M Hubbard, V Schnackenberg, D Bernstein, E Hambidge, M Heymsfield, S IretonJones, C Wolfson, M Jacobs, D Keithley, J Meguid, M Pingleton, S Kopple, J Koretz, R Shulman, R Wilmore, D Driscoll, D Fleming, CR Greene, H Sitrin, M Herrmann, V Lipman, T Mock, D Borum, P Shronts, E TI Nutrition support in clinical practice: Review of published data and recommendations for future research directions SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Review ID TOTAL PARENTERAL-NUTRITION; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; SHORT BOWEL SYNDROME; CHAIN AMINO-ACIDS; BONE-MARROW TRANSPLANTATION; SEVERE ACUTE-PANCREATITIS; ACUTE-RENAL-FAILURE; DOUBLE-BLIND TRIAL; PERCUTANEOUS ENDOSCOPIC GASTROSTOMY; SUBJECTIVE GLOBAL ASSESSMENT AB In the last 30 years, marked advances in enteral feeding techniques, venous access, and enteral and parenteral nutrient formulations have made it possible to provide nutrition support to almost all patients. Despite the abundant medical Literature and widespread use of nutritional therapy, many areas of nutrition support remain controversial. Therefore, the leadership at the National Institutes of Health, The American Society for Parenteral and Enteral Nutrition, and The American Society for Clinical Nutrition convened an advisory committee to perform a critical review of the current medical literature evaluating the clinical use of nutrition support; the goal was to assess our current body of knowledge and to identify the issues that deserve further investigation. The panel was divided into five groups to evaluate the following areas: nutrition assessment, nutrition support in patients with gastrointestinal diseases, nutrition support in wasting diseases, nutrition support in critically ill patients, and perioperative nutrition support. The findings from each group are summarized in this report. This document is not meant to establish practice guidelines for nutrition support. The use of nutritional therapy requires a careful integration of data from pertinent clinical trials, clinical expertise in the illness or injury being treated, clinical expertise in nutritional therapy, and input from the patient and his/her family. C1 HARVARD UNIV,MED CTR,BETH ISRAEL DEACONESS MED CTR,BOSTON,MA 02115. UNIV CHICAGO,MED CTR,CHICAGO,IL 60637. UNIV WASHINGTON,SEATTLE,WA 98195. NIDDKD,BETHESDA,MD 20892. ASCN,BETHESDA,MD. ASPEN,SILVER SPRING,MD. ROCKEFELLER UNIV,NEW YORK,NY 10021. ST MICHAELS HOSP,TORONTO,ON M5B 1W8,CANADA. UNIV COLORADO,MED CTR,DENVER,CO 80202. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. CORAM HEALTHCARE,CARROLLTON,TX. BAXTER HEALTHCARE CORP,MCGAW PK,IL. SAN FRANCISCO VET ADM MED CTR,SAN FRANCISCO,CA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. MAYO CLIN,ROCHESTER,MN. HARBOR UCLA MED CTR,TORRANCE,CA 90509. OLIVE VIEW UCLA MED CTR,SYLMAR,CA 91342. BAYLOR COLL MED,HOUSTON,TX 77030. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. MAYO CLIN,JACKSONVILLE,FL 32224. SLIM FAST FOOD CO,W PALM BEACH,FL. UNIV CHICAGO,CHICAGO,IL 60637. UNIV CALIF BERKELEY,BERKELEY,CA 94720. ST LOUIS UNIV,SCH MED,ST LOUIS,MO. DEPT VET AFFAIRS MED CTR,WASHINGTON,DC. UNIV ARKANSAS MED SCI HOSP,LITTLE ROCK,AR 72205. UNIV FLORIDA,GAINESVILLE,FL. UNIV MINNESOTA,MINNEAPOLIS,MN. RP Klein, S (reprint author), WASHINGTON UNIV,SCH MED,660 S EUCLID AVE,BOX 8127,ST LOUIS,MO 63110, USA. NR 256 TC 224 Z9 245 U1 2 U2 5 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD MAY-JUN PY 1997 VL 21 IS 3 BP 133 EP 156 DI 10.1177/0148607197021003133 PG 24 WC Nutrition & Dietetics SC Nutrition & Dietetics GA XA043 UT WOS:A1997XA04300002 PM 9168367 ER PT J AU Heimburger, DC Geels, WJ Bilbrey, J Redden, DT Keeney, C AF Heimburger, DC Geels, WJ Bilbrey, J Redden, DT Keeney, C TI Effects of small-peptide and whole-protein enteral feedings on serum proteins and diarrhea in critically ill patients: A randomized trial SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID PLASMA FIBRONECTIN; CLINICAL-TRIAL; HYPOALBUMINEMIC PATIENTS; NUTRITION; DIET; FORMULA; ABSORPTION; STARVATION; TOLERANCE; NEED AB Background: It has been proposed that enteral feeding formulas containing small peptides are more efficacious and better tolerated than whole-protein formulas in critically ill patients. Methods: Intensive care unit patients were stratified with regard to treatment with antibiotics and serum albumin and randomized to treatment with a small-peptide enteral diet or. an isoenergetic, isonitrogenous whole-protein diet for 10 days. To assess efficacy, we measured serum prealbumin and fibronectin, and to assess tolerance, we monitored the incidence of diarrhea. A protocol was followed to ascertain all causes of diarrhea (defined as >200 g stool or greater than or equal to 3 liquid stools on 2 consecutive days). Results: Fifty subjects completed the trial. Serum prealbumin and fibronectin increased between 21% and 36% in both groups, but the increase was significant only in the small-peptide group. The change in fibronectin between days 5 and 10 was significantly greater in the small-peptide group (p = .02). Diarrhea occurred in 10 subjects (17.8% of days) receiving small-peptide feeding and 4 subjects (7.5% of days) receiving whole-protein feeding (p = .07 for incidence and 0.03 for prevalence), but the difference was explained by the coincidental use of more diarrhea-causing medications in the former Only one case of diarrhea could be attributed to tube feeding. Conclusions: During 10 days of feeding, the small-peptide diet produced slightly greater increases in serum rapid-synthesis proteins than did the whole-protein diet, especially between days 5 and 10. The clinical implications of this difference between the diets are unknown. Both small-peptide and whale-protein diets were well tolerated. C1 UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT NURSING,BIRMINGHAM,AL 35294. UNIV ALABAMA,BIOSTAT UNIT,CTR COMPREHENS CANC,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,DEPT DIETET,BIRMINGHAM,AL. UNIV ALABAMA HOSP & CLIN,DEPT FOOD & NUTR SERV,BIRMINGHAM,AL. RP Heimburger, DC (reprint author), UNIV ALABAMA,DEPT NUTR SCI,UAB STN,BIRMINGHAM,AL 35294, USA. FU NCI NIH HHS [CA-28103, CA-47888] NR 30 TC 17 Z9 17 U1 0 U2 5 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD MAY-JUN PY 1997 VL 21 IS 3 BP 162 EP 167 DI 10.1177/0148607197021003162 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA XA043 UT WOS:A1997XA04300004 PM 9168369 ER PT J AU Chang, E Boyd, A Nelson, CC Crowley, D Law, T Keough, KM Folkman, J Ezekowitz, RAB Castle, VP AF Chang, E Boyd, A Nelson, CC Crowley, D Law, T Keough, KM Folkman, J Ezekowitz, RAB Castle, VP TI Successful treatment of infantile hemangiomas with interferon-alpha-2b SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article DE hemangioma; therapy; interferon; alpha-2b; basic fibroblast growth factor; idiopathic hypertrophic subaortic stenosis ID KASABACH-MERRITT SYNDROME; LIFE-THREATENING HEMANGIOMAS; ALFA-2A THERAPY; HYPERTROPHIC CARDIOMYOPATHY; NEONATAL HEMANGIOMATOSIS; COMPLEX HEMANGIOMAS; ALPHA-INTERFERON; MANAGEMENT; INFANCY; GROWTH AB Purpose: Hemangiomas are benign tumors occurring in 10% of infants. A small percentage are complicated by blockage of vital structures, consumptive coagulopathy, or heart failure, resulting in a mortality of -20% of patients with complications. Here, we describe four infants with complicated hemangiomas responding to interferon-alpha-2b therapy. Patients and Methods: Four children with hemangiomas were treated with interferon-alpha-2b for complicating heart failure (1), visual impairment (2), or coagulopathy (1). Patients received interfron-alpha-2b alone or in conjunction with corticosteroid therapy over 2 to 9 months. Imaging studies and urinary basic fibroblast growth factor (bFGF) levers were used to monitor treatment response. Results: Three of four patients demonstrated involution of the hemangiomas with improvement in their coagulopathy or visual impairment. The fourth patient expired due to cardiac complications despite radiologic evidence of hemangioma involution. Side effects associated with interferon-alpha-2b treatment included elevated transaminases (2) and leukocytosis (2), which resolved upon completion of therapy. One patient developed mild gross motor delay (1), which improved after cessation of therapy. Decreased urinary bFGF levels correlated with hemangioma involution. Conclusion: Interferon-alpha-2b therapy is an effective, well-tolerated treatment for complicated hemangiomas. Measurement of urinary bFGF levels may provide an objective method for monitoring treatment response. C1 UNIV MICHIGAN,CTR MED,DEPT PEDIAT,ANN ARBOR,MI 48109. UNIV MICHIGAN,CTR MED,DEPT OPHTHALMOL,ANN ARBOR,MI 48109. CHILDRENS HOSP,DEPT PEDIAT SURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. NR 41 TC 116 Z9 124 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-4114 J9 J PEDIAT HEMATOL ONC JI J. Pediatr. Hematol. Oncol. PD MAY-JUN PY 1997 VL 19 IS 3 BP 237 EP 244 DI 10.1097/00043426-199705000-00011 PG 8 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA XF157 UT WOS:A1997XF15700011 PM 9201147 ER PT J AU Pellegrini, M Royo, M Chorev, M Mierke, DF AF Pellegrini, M Royo, M Chorev, M Mierke, DF TI Conformational consequences of i,i+3 cystine linkages: Nucleation for alpha-helicity? SO JOURNAL OF PEPTIDE RESEARCH LA English DT Article DE alpha-helices; cystine linkage; distance geometry calculations; helix nucleation; parathyroid hormone; peptide conformation in SDS micelles ID MOLECULAR-DYNAMICS; DISTANCE CONSTRAINTS; MAGNETIC-RESONANCE; 2-DIMENSIONAL NMR; CROSS-RELAXATION; HELIX FORMATION; ROTATING-FRAME; ANALOGS; SPECTROSCOPY; PEPTIDE AB Methods to introduce specific secondary structural elements into peptides and proteins are vital fur the rational design of peptide and non-peptide drug, candidates as well as in the Lie novo design of proteins, Here the incorporation of a disulfide linkage between cysteine residues spaced three amino acids apart (i, i+3) as a method to induce helicity is examined. Two dodecamer peptides, A-V-S-E-C-Q-L-C-H-D-K-G-NH2, differing in the chirality of the cysteine at the fifth position (the i position. have been synthesized and conformationally studied both in the linear and cyclized form. This peptide sequence, derived from the N-terminal sequence of parathyroid hormone related protein, does not form helices, even as part of the 1-34 fully active domain of the protein. The four analogs (two cyclic and two linear) were analyzed both in aqueous solution and in the presence of sodium dodecyl sulfate micelles. In aqueous solution the linear peptides display no evidence for secondary structure, while the cyclization induces a turn centered about the cysteine residues, In the presence of micelles the linear form of the peptides adopts bent conformations, containing turns, but results from both NMR and CD provide no evidence of helices. The oxidized L,L-peptide in the micellar solution does not present a well defined conformation. although the presence of one helical turn is evident. The cyclic D,L analog adopts a helical structure (not an alpha-helix) extending from residue 2 to 9, with non-standard phi, psi values caused by the presence of the D-amino acid. These results clearly illustrate that the ability of D-Cys(i), Cys(i+3) cyclization to initiate helix formation depends greatly on the solvent used. Therefore, ally drug-design principle utilizing this modification for helix nucleation must keep the environment in which the peptide is biologically active in mind. (C) Munksgaard 1997. C1 CLARK UNIV,GUSTAF H CARLSON SCH CHEM,WORCESTER,MA 01610. HARVARD UNIV,SCH MED,DEACONESS MED CTR,DEPT MED,DIV BONE & MINERAL METAB,HARVARD THORNDIKE LAB,BOSTON,MA. HARVARD UNIV,SCH MED,DEACONESS MED CTR,DEPT MED,CHARLES A DANA LAB,BOSTON,MA. UNIV MASSACHUSETTS,MED CTR,DEPT PHARMACOL & TOXICOL,WORCESTER,MA. RI Royo, Miriam/B-1665-2013; OI Royo, Miriam/0000-0001-5292-0819; Pellegrini, Maria/0000-0003-3817-4412 NR 43 TC 28 Z9 28 U1 0 U2 7 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1397-002X J9 J PEPT RES JI J. Pept. Res. PD MAY PY 1997 VL 49 IS 5 BP 404 EP 414 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XC664 UT WOS:A1997XC66400005 PM 9211221 ER PT J AU Chapman, PF Irizarri, MC Nilsen, S Hyman, BT Hsiao, KK AF Chapman, PF Irizarri, MC Nilsen, S Hyman, BT Hsiao, KK TI Abnormal synaptic transmission in aged APP transgenic mice SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract C1 UNIV WALES COLL CARDIFF,PHYSIOL UNIT,SCH MOL & MED BIOSCI,CARDIFF CF1 3NS,S GLAM,WALES. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,CAMBRIDGE,MA 02138. UNIV MINNESOTA,SCH MED,DEPT NEUROL,MINNEAPOLIS,MN 55455. NR 2 TC 3 Z9 3 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 MAY PY 1997 VL 501P SI SI BP P95 EP P95 PG 1 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA XD091 UT WOS:A1997XD09100134 ER PT J AU Fischer, CP Bode, BP Hurley, BP Souba, WW AF Fischer, CP Bode, BP Hurley, BP Souba, WW TI Alterations in oxidative metabolism and glutamine transport support glucose production in the tumor-influenced hepatocyte SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Academic-Surgery CY NOV 13-16, 1996 CL CHICAGO, IL SP Assoc Acad Surg ID AMINO-ACID-TRANSPORT; BEARING RATS; NECROSIS-FACTOR; LIVER; ANTIBODY AB Glutamine is the primary substrate whose hepatic transport is upregulated in the tumor-bearing host; however, the subsequent metabolism of transported glutamine is currently unknown. The purpose of this study was to determine if glutamine is an important oxidative fuel source for hepatocytes in cancer. Specifically we compare rates of glutamine transport and oxidation in hepatocytes from control and tumor-bearing animals. We also compare rates of glucose oxidation and rates of glucose production from glutamine in control hepatocytes versus those from tumor-bearing animals. Hepatocytes from rats bearing the MCA fibrosarcoma were isolated when tumors comprised 5 and 15% of total body weight and compared to sham-implanted and pair-fed control animals. [H-3]GLN transport, GLN and glucose oxidation to CO2, and glucose production from glutamine were assayed. Tumor burden of 5% stimulated a 2.52-fold increase in hepatocyte glutamine transport and a a-fold increase when tumor burden reached 15%, Rates of oxidation of glutamine were suppressed by 1.5-fold when tumors comprised 5% of body weight compared to sham animals and were equivalent to sham animals when tumors comprised 15% of body weight, Significant alterations in glucose oxidation were observed when tumors were both small and large-glucose oxidation was suppressed by 3.6- and 3.7-fold when tumors comprised 5 and 15% of body weight respectively compared to sham-implanted rats. Incubation of hepatocytes from tumor-bearing animals with glutamine as a gluconeogenic substrate induced a 1.84-fold increase in glucose production compared to sham hepatocytes. In conclusion, (i) despite a doubling of GLN transport by the tumor-influenced hepatocyte, GLN oxidation by hepatocytes was not increased, (ii) Glucose oxidation by hepatocytes from tumor-bearing animals was decreased compared to sham hepatocytes and, simultaneously, glucose production by tumor-influenced hepatocytes from glutamine was increased. The augmentation of hepatic glutamine transport and decreased glutamine oxidation seen in tumor-influenced hepatocytes appear to support hepatocyte gluconeogenesis from glutamine. (C) 1997 Academic Press. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NCI NIH HHS [CA57690]; NIDDK NIH HHS [DK40561] NR 21 TC 5 Z9 6 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD MAY PY 1997 VL 69 IS 2 BP 379 EP 384 DI 10.1006/jsre.1997.5100 PG 6 WC Surgery SC Surgery GA XL453 UT WOS:A1997XL45300024 PM 9224411 ER PT J AU Carroll, NM Chase, M Chiocca, EA Tanabe, KK AF Carroll, NM Chase, M Chiocca, EA Tanabe, KK TI The effect of ganciclovir on herpes simplex virus-mediated oncolysis SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Academic-Surgery CY NOV 13-16, 1996 CL CHICAGO, IL SP Assoc Acad Surg ID GENE-THERAPY; RIBONUCLEOTIDE REDUCTASE; THYMIDINE KINASE; COLORECTAL-CARCINOMA; CYTOSINE DEAMINASE; BRAIN-TUMORS; IN-VITRO; CELLS; VECTORS; GROWTH AB Entry of herpes simplex virus (HSV) into tumor cells results in viral gene expression followed by cellular lysis. Attenuated HSVs selectively destroy tumors with sparing of surrounding normal tissue. HSV encodes a thymidine kinase (TK) that converts ganciclovir to a toxic metabolite. This metabolite may be transferred between cells and lead to the death of neighboring uninfected cells, termed bystanders, We sought to determine if HSV-mediated oncolysis is enhanced by ganciclovir treatment. In addition, we examined bystander killing in cocultures of TK transfectants and parental cells. hrR3, an attenuated HSV, expresses TK. The 50% lethal dose of hrR3 for a rat gliosarcoma (9L) and three human colorectal carcinomas (HT29, KM12C6, and KM12L4) was determined. Cells were infected with a 50% lethal dose of hrR3, followed by treatment with ganciclovir, and then cell survival was quantitated. In separate experiments 9L and HT29 cells were transfected with TK, Parental cells and TK transfectants were cocultured in various ratios, in the presence of ganciclovir, and cell survival was quantitated. hrR3-mediated oncolysis was enhanced by ganciclovir in the gliosarcoma but not in the three colorectal carcinomas. Cocultures of both 9L and HT29 parental cells with their corresponding TK transfectants demonstrated bystander killing. The mortality of 9L cocultures was 54% greater than that predicted for exclusive killing of transfectants. HT29 mortality was 8% greater than predicted. The ability of ganciclovir to augment hrR3-mediated oncolysis varies significantly between tumor cells lines. The extent of ganciclovir-mediated killing of neighboring nontransduced parental cells similarly varies. Consideration should be given to these factors in the design of gene therapy strategies using HSV vectors as oncolytic agents. (C) 1997 Academic Press. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NCI NIH HHS [CA 64454]; NIDDK NIH HHS [DK43351] NR 29 TC 41 Z9 42 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD MAY PY 1997 VL 69 IS 2 BP 413 EP 417 DI 10.1006/jsre.1997.5089 PG 5 WC Surgery SC Surgery GA XL453 UT WOS:A1997XL45300029 PM 9224416 ER PT J AU Pan, M Fischer, CP Wasa, M Bode, BP Souba, WW AF Pan, M Fischer, CP Wasa, M Bode, BP Souba, WW TI Characterization of glutamine and glutamate transport in rat lung plasma membrane vesicles SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Academic-Surgery CY NOV 13-16, 1996 CL CHICAGO, IL SP Assoc Acad Surg ID ENDOTHELIAL-CELLS; OXIDANT INJURY; GLUTATHIONE; EXPRESSION; SEPSIS AB Insufficient glutamine for the lungs during sepsis may contribute to an impairment in lung function. Lung glutamine metabolism is supported by both blood glutamine uptake and de novo biosynthesis using circulating glutamate as a precursor. Information regarding the specific plasma membrane carriers involved in this uptake is lacking. Furthermore, the effect of sepsis on amino acid transport in whole lung has not been studied. We isolated lung plasma membrane vesicles (LPMVs) from control and LPS-treated rats and assayed glutamine and glutamate transport activity in LPMVs. Vesicle purity and functionality were confirmed by time-dependent concentrative amino acid uptake in the presence of Na+, impoverishment of microsomal enzymes, and a 25-fold enrichment in the plasma membrane marker 5'-nucleotidase. Eighty percent of glutamine uptake in lung vesicles was mediated via the high affinity Na+-dependent carrier System ASC (V-max = 80 +/- 10 pmole/mg protein/15 sec; K-m = 224 +/- 30 mu M) while 19% occurred via the Na+-independent System ASC (V-max = 11 +/- 2 pmole/mg/15 sec; K-m = 141 +/- 23 mu M). Ninety percent of glutamate transport was mediated by the Na+-independent System X-AG(-). Treatment of rats with LPS resulted in a decrease in both glutamine and glutamate transport in LPMVs. LPMVs offer a novel method for characterizing lung amino acid transport and studying the effects of catabolic states on this activity. The effects of endotoxin on System ASC and X-AG(-) activity may contribute to reduced lung glutamine availability during septic states which may impair cellular metabolism and function. (C) 1997 Academic Press. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. FU NHLBI NIH HHS [HL44986] NR 26 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD MAY PY 1997 VL 69 IS 2 BP 418 EP 424 DI 10.1006/jsre.1997.5102 PG 7 WC Surgery SC Surgery GA XL453 UT WOS:A1997XL45300030 PM 9224417 ER PT J AU Puria, S Peake, WT Rosowski, JJ AF Puria, S Peake, WT Rosowski, JJ TI Sound-pressure measurements in the cochlear vestibule of human-cadaver ears SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID HUMAN MIDDLE-EAR; INPUT IMPEDANCE; HEARING; MODEL; CAT AB The middle-ear pressure gain for the 50-Hz to 12-kHz range was determined from the ratio of sound pressures measured in the vestibule and the ear canal of four human-cadaver ears. The magnitude of the middle-ear pressure gain is 20 dB for frequencies between 500 Hz and 2 kHz. Above 4 kHz, the gain changes as a function of frequency at a rate of approximately -8 dB/octave and below 400 Hz at 4 dB/octave. The standard error of the mean magnitude across the four ears is typically less than 3 dB. The phase angle of the pressure gain also changes with frequency. interruption of the ossicular chain decreases the vestibule pressure by at least 20 dB. It is shown that air bubbles in the inner ear can diminish the vestibule pressure; procedures are used to remove bubbles. From these pressure measurements and previous measurements of stapes motion, the frequency dependence of behavioral thresholds for tones was tested to discover whether it corresponds to the constancy of a physiological variable at the cochlear input. Among pressure, power, or stapes-motion measures, the vestibule pressure is most nearly constant with frequency at the behavioral ''minimum audible pressure.'' (C) 1997 Acoustical Society of America. C1 HARVARD UNIV, SCH MED, DEPT OTOL & LARYNGOL, CAMBRIDGE, MA 02139 USA. MIT, ELECT RES LAB, CAMBRIDGE, MA 02139 USA. RP MASSACHUSETTS EYE & EAR INFIRM, EATON PEABODY LAB AUDITORY PHYSIOL, 243 CHARLES ST, BOSTON, MA 02114 USA. FU NIDCD NIH HHS [F32 DC00073, P01 DC00119, R03 DC02677-01] NR 57 TC 118 Z9 123 U1 1 U2 9 PU ACOUSTICAL SOC AMER AMER INST PHYSICS PI MELVILLE PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA SN 0001-4966 EI 1520-8524 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD MAY PY 1997 VL 101 IS 5 BP 2754 EP 2770 DI 10.1121/1.418563 PN 1 PG 17 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA WZ041 UT WOS:A1997WZ04100038 PM 9165730 ER PT J AU Vibhagool, C Byers, HR Grevelink, JM AF Vibhagool, C Byers, HR Grevelink, JM TI Treatment of small nevomelanocytic nevi with a Q-switched ruby laser SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID TATTOOS; LESIONS AB Background: Small nevomelanocytic nevi are common and some are of cosmetic concern. Conventional therapy may cause a scar or permanent hypopigmentation, Objective: Our purpose was to determine whether selective photothermolysis of pigmented cells by Q-switched ruby laser treatment removes small nevomelanocytic nevi in a nonscarring fashion. Methods: Twelve patients with 18 small nevomelanocytic nevi were treated with a Q-switched ruby laser (694 nm, 28 nsec) at fluences of 8 J/cm(2). Biopsy specimens were obtained after treatment at varying time intervals. Results: Twelve lesions (67%) showed a complete response and six lesions (33%) had a partial response. The only adverse sequela observed was mild fibrosis of the papillary dermis, without loss of papillary architecture. Conclusion: The Q-switched ruby laser is effective in removing small melanocytic nevi. However, some might recur depending on the depth of the nevomelanocytic nests. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DERMATOL LASER CTR,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT DERMATOPATHOL,BOSTON,MA 02215. NR 12 TC 31 Z9 31 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD MAY PY 1997 VL 36 IS 5 BP 738 EP 741 DI 10.1016/S0190-9622(97)80327-1 PN 1 PG 4 WC Dermatology SC Dermatology GA WX860 UT WOS:A1997WX86000011 PM 9146536 ER PT J AU Isaacson, K Nardella, P AF Isaacson, K Nardella, P TI Development and use of a bipolar resectoscope in endometrial electrosurgery SO JOURNAL OF THE AMERICAN ASSOCIATION OF GYNECOLOGIC LAPAROSCOPISTS LA English DT Article; Proceedings Paper CT 25th Annual Meeting of the American-Association-of-Gynecologic-Laparoscopists CY SEP 24-29, 1996 CL CHICAGO, IL SP Amer Assoc Gynecol Laparoscopists ID HYSTEROSCOPY; ABLATION AB We conducted a prospective, blinded study to compare the tissue response and mechanical properties of a bipolar resectoscope with standard monopolar cutting and coagulation instruments. At the animal care facility of Tufts Medical School (Medford, MA), four surgeons blinded to instrumentation and distention media cut segments out of a rabbit uterine horn and desiccated the abdominal wall using either the bipolar device in 0.9% saline or the monopolar system in 1.5% glycine. Both systems used a Force 2 Valleylab radiofrequency generator at identical power settings. Cut and desiccated sections were fixed and stained with hematoxylin and eosin as well as Masson's trichrome to evaluate thermal damage, The pathologist was blinded to the system used to make the cut or desiccation. Both systems cut and coagulated tissue with similar properties. Most surgeons noted a longer delay from radiofrequency activation to actual cutting with the bipolar system. The depth of thermal damage when cutting or desiccating tissue was similar for the two systems. This disposable, inexpensive device allows for standard resectoscopic hardware to be transformed into a bipolar device. All current techniques of intrauterine cutting and coagulation may soon be performed in the presence of physiologic uterine distention media. Human clinical data remain to be gathered. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA. MED SCI INC,TAUNTON,MA. NR 9 TC 14 Z9 14 U1 0 U2 0 PU JOURNAL AMER ASSOC GYNECOLOGIC LAPAROSCOPISTS PI SANTA FE SPRINGS PA 13021 EAST FLORENCE AVE, SANTA FE SPRINGS, CA 90670-4505 SN 1074-3804 J9 J AM ASSOC GYN LAP JI J. Am. Assoc. Gynecol. Laparoscopists PD MAY PY 1997 VL 4 IS 3 BP 385 EP 391 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA XB817 UT WOS:A1997XB81700016 PM 9154791 ER PT J AU Prelack, K Dwyer, J Yu, YM Sheridan, RL Tompkins, RG AF Prelack, K Dwyer, J Yu, YM Sheridan, RL Tompkins, RG TI Urinary urea nitrogen is imprecise as a predictor of protein balance in burned children SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID PARENTERAL-NUTRITION; LEUCINE KINETICS; REQUIREMENTS; METABOLISM; INFANTS; INJURY AB Objective To compare estimates of protein balance using the urinary urea nitrogen method to predict total urinary nitrogen with isotopically derived estimates of metabolic protein balance as defined by the difference between rates of protein synthesis and breakdown. Design Prospective, descriptive, repeated measures analysis. Urinary urea nitrogen collections were obtained for 8 to 24 hours before infusion of L-[1-C-13] leucine during fed and fasted states. Subjects/setting Eight acutely burned pediatric patients consecutively admitted to Shriners Burns Institute, Boston Unit, for medical and surgical care of their injuries. Main outcome measures The difference between isotopically measured rates of protein synthesis and breakdown was used as an index of protein balance and compared with estimates of protein balance determined using the urinary urea nitrogen method. Statistical analysis Least squares regression analysis was used to assess the value of urinary urea nitrogen as a predictor of metabolic protein balance. Limits of agreements were used to determine bias and precision between the two methods. Results Urinary urea nitrogen was a significant predictor of metabolic protein balance (r(2)=.77; P<.001). The direction of protein balance was the same in 14 of 16 measurements; however, there was a significant lack of agreement between the two methods as demonstrated by large quantitative differences in protein balance. Conclusion Although the urinary-urea-nitrogen-based estimates of protein balance correlate well with isotopically derived protein balance, they are not precise in determining protein balance in seriously burned children. C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,TRAUMA SERV,BOSTON,MA 02114. TUFTS UNIV,SCH MED,BOSTON,MA 02111. TUFTS UNIV,SCH NUTR,BOSTON,MA 02111. TUFTS UNIV,NEW ENGLAND MED CTR HOSP,FRANCES STERN NUTR CTR,BOSTON,MA 02111. RP Prelack, K (reprint author), SHRINERS BURN INST,BOSTON UNIT,51 BLOSSOM ST,BOSTON,MA 02114, USA. OI Dwyer, Johanna/0000-0002-0783-1769 NR 34 TC 9 Z9 9 U1 1 U2 3 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD MAY PY 1997 VL 97 IS 5 BP 489 EP 495 DI 10.1016/S0002-8223(97)00127-2 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA WX316 UT WOS:A1997WX31600009 PM 9145086 ER PT J AU Cherrier, MM Mendez, MF Perryman, KM Pachana, NA Miller, BL Cummings, JL AF Cherrier, MM Mendez, MF Perryman, KM Pachana, NA Miller, BL Cummings, JL TI Frontotemporal dementia versus vascular dementia: Differential features on mental status examination SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Geriatrics-Society CY MAY 01-05, 1996 CL CHICAGO, IL SP Amer Geriatr Soc ID FRONTAL-LOBE DEGENERATION; ALZHEIMERS-DISEASE CERAD; COGNITIVE STATUS EXAMINATION; PICKS-DISEASE; NEUROPSYCHOLOGICAL FINDINGS; MULTIINFARCT DEMENTIA; PRESENILE-DEMENTIA; CONSORTIUM; ESTABLISH; REGISTRY AB OBJECTIVE: After Alzheimer's disease, vascular dementia (VaD) and frontotemporal dementia (FTD) are among the most common dementing illnesses. FTD may have a neuropsychological profile similar to that of VaD, and patients with these dementias may be difficult to distinguish on clinical examination. The purpose of this study was to elucidate distinct cognitive profiles of a large group of FTD and VaD patients on a brief, clinical mental status examination. DESIGN: A comparison of 39 FTD patients and 39 VaD patients on a brief, clinical mental status examination. SETTING: A Dementia Research Center and affiliated, university hospitals. METHODS: The FTD patients were diagnosed by noncognitive clinical and neuroimaging criteria, and the VaD patients met NINDS-AIREN criteria for vascular dementia. The two dementia groups were comparable on three dementia assessment scales. MEASUREMENTS: The mental status measures included the neuropsychological battery from the Consortium to Establish a Registry for Alzheimer's Disease (CERAD), plus supplementation from the Neurobehavioral Cognitive Status Examination (NCSE) for cognitive areas not assessed by the CERAD. RESULTS: The FTD and VaD groups differed significantly on the mental status examination measures. FTD patients performed significantly better than the VaD patients on digit span and constructions, despite comparable performance by both groups on calculations. Although not statistically significant, the FTD group performed worse than the VaD group on verbal fluency and abstractions. These differences were not explained by group differences in age and education. CONCLUSION: These results suggest that cognitive differences between FTD and VaD groups reflect greater frontal pathology in contrast to relative sparing of posterior cortex and subcortical white matter in FTD. These cognitive differences as measured by a mental status examination may help distinguish between these two dementia syndromes. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RI Pachana, Nancy/C-6807-2016 OI Pachana, Nancy/0000-0002-8927-4205 NR 51 TC 18 Z9 19 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAY PY 1997 VL 45 IS 5 BP 579 EP 583 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WZ009 UT WOS:A1997WZ00900006 PM 9158578 ER PT J AU Zoja, C Liu, XH Donadelli, R Abbate, M Testa, D Corna, D Taraboletti, G Vecchi, A Dong, QG Rollins, BJ Bertani, T Remuzzi, G AF Zoja, C Liu, XH Donadelli, R Abbate, M Testa, D Corna, D Taraboletti, G Vecchi, A Dong, QG Rollins, BJ Bertani, T Remuzzi, G TI Renal expression of monocyte chemoattractant protein-1 in lupus autoimmune mice SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; HUMAN MESANGIAL CELLS; BLOOD MONONUCLEAR LEUKOCYTES; GLOMERULAR ENDOTHELIAL-CELLS; GENE-EXPRESSION; EXPERIMENTAL GLOMERULONEPHRITIS; CHEMOTACTIC PROTEIN-1; KAPPA-B; MCP-1; NEPHRITIS AB Mononuclear cell infiltration in glomeruli and renal interstitium is a prominent feature of some types of glomerulonephritis, including lupus nephritis. The mechanism(s) underlying monocyte influx into the kidney is not fully understood. Recently, monocyte chemoattractant protein-1 (MCP-1) has been identified as a chemotactic factor involved in the recruitment of monocytes/macrophages in the glomeruli of rats with mesangioproliferative as well as anti-glomerular basement membrane glomerulonephritis. In the study presented here, renal MCP-1 mRNA expression in New Zealand Black x New Zealand White (NZB/W) F1 mice, a model of genetically determined immune complex disease that mimics systemic lupus in humans, was investigated. Northern blot analysis revealed a single 0.7 kb MCP-1 transcript of very low intensity in kidneys from 2-month-old NZB/W mice that had not yet developed proteinuria nor renal damage. Message levels, which increased markedly with the progression of nephritis and in association with mononuclear cell infiltration, were 10- and 15- fold higher in 8-10-month-old mice than in 2-month-old mice. By in situ hybridization, increased expression of MCP-1 mRNA was demonstrated in glomeruli and, even more striking, in tubular epithelial cells. Western blot analysis demonstrated increased expression of MCP-1 protein in kidneys of 10-month-old NZB/W mice, consistent with MCP-1 mRNA data. When NZB/W mice were treated with cyclophosphamide up to 12 months of age, expression of MCP-1 in the renal tissue remained low, the influx of inflammatory cells did not appear, and glomerular and tubular structures remained well preserved. These data suggest that elevated MCP-1 might act as a signal for inflammatory cells to infiltrate the kidney in lupus nephritis. C1 OSPED RIUNITI BERGAMO,DIV NEPHROL & DIALYSIS,I-24100 BERGAMO,ITALY. DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. RP Zoja, C (reprint author), MARIO NEGRI INST PHARMACOL RES,VIA GAVAZZENI 11,I-24125 BERGAMO,ITALY. NR 56 TC 71 Z9 81 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD MAY PY 1997 VL 8 IS 5 BP 720 EP 729 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA XB644 UT WOS:A1997XB64400003 PM 9176841 ER PT J AU ElSaden, SM Grant, EG Sayre, J Vinuela, F Duckwiler, G AF ElSaden, SM Grant, EG Sayre, J Vinuela, F Duckwiler, G TI Transcranial color Doppler imaging of brain arteriovenous malformations in adults SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Article DE arteries, abnormalities; arteriovenous malformations, cerebral; blood, flow dynamics; brain, abnormalities; ultrasonography, Doppler studies ID ULTRASOUND; SONOGRAPHY; DIAGNOSIS; DISORDERS; STENOSIS; ARTERY; FLOW; US AB This study was performed to investigate the utility of transcranial color Doppler sonography in evaluating adult cerebral arteriovenous malformations. Twelve patients with such malformations underwent sonography. Spectral Doppler sonographic assessment included peak systolic velocity, end diastolic velocity, and resistive index within the intracranial and extracranial vessels. Color Doppler sonography was used to visualize the site of shunting. Paired and unpaired Student's t-tests were used to determine significance of spectral findings. The nidus was seen in eight of 10 pial malformations. The nidi in two patients were located in the parietal region and not visualized. When compared with the corresponding contralateral artery, feeding arteries (identified in all 10 of the pial lesions) demonstrated diminished resistive indices (P = 0.09). Similarly, the end diastolic velocity was increased in all feeding arteries (P = 0.03). When compared with published normal values, the peak systolic and end diastolic velocities were significantly elevated and the resistive indices were low (P < 0.0003). Transcranial color Doppler sonography depicted the nidi of pial arteriovenous malformations in 80% of cases. Feeding arteries demonstrated abnormal peak systolic velocity, end diastolic velocity, and resistive index in all cases when compared with published values. Transcranial color Doppler sonography is not a good screening tool due to limited acoustical window, but it may be useful for noninvasive study of the physiology of arteriovenous malformations as they are treated. C1 UNIV CALIF LOS ANGELES,MED CTR,DEPT RADIOL,LOS ANGELES,CA 90024. RP ElSaden, SM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT RADIOL,BLDG 500,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 14 TC 8 Z9 8 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD MAY PY 1997 VL 16 IS 5 BP 327 EP 334 PG 8 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA XT749 UT WOS:A1997XT74900003 PM 9315170 ER PT J AU Tearney, GJ Brezinski, ME Southern, JF Bouma, BE Boppart, SA Fujimoto, JG AF Tearney, GJ Brezinski, ME Southern, JF Bouma, BE Boppart, SA Fujimoto, JG TI Optical biopsy in human urologic tissue using optical coherence tomography SO JOURNAL OF UROLOGY LA English DT Article DE optics; endoluminal; urology; imaging; transurethral prostatectomy ID REFLECTOMETRY; ULTRASOUND AB Optical Coherence Tomography (OCT) is a recently developed non-invasive technique for obtaining high resolution, cross-sectional images of human tissue. This work investigated the capability of OCT to differentiate the architectural morphology of urologic tissue with the long term aim of using OCT as an adjunct to endoscopic imaging and to improve the efficiency of interventional procedures such as transurethral prostatectomy (TURF). Urologic tissues were taken postmortem, dissected, and imaged using OCT. Microstructure was delineated in different urologic tissues, including the prostatic urethra, prostate, bladder, and ureter, with an axial resolution of 16 +/- mu m., higher than any clinically available endoscopic intraluminal imaging technology. The ability of OCT to provide non-contact high resolution imaging of urologic tissue architectural morphology (i.e. optical biopsy), without the need for excisional biopsy, suggests the potential of using OCT to obtain information on tissue microstructure that could only previously be obtained with conventional biopsy. C1 MIT,ELECT RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Tearney, GJ (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,BLDG 36-357,50 VASSAR ST,CAMBRIDGE,MA 02139, USA. RI Boppart, Stephen/C-7338-2009 FU NEI NIH HHS [9-RO1-EY11289-10] NR 19 TC 104 Z9 106 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAY PY 1997 VL 157 IS 5 BP 1915 EP 1919 DI 10.1016/S0022-5347(01)64900-0 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA WU178 UT WOS:A1997WU17800111 PM 9112562 ER PT J AU Kowalski, CM Kaufman, JA Rivitz, SM Geller, SC Waltman, AC AF Kowalski, CM Kaufman, JA Rivitz, SM Geller, SC Waltman, AC TI Migration of central venous catheters: Implications for initial catheter tip positioning SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE catheters and catheterization central venous access; catheters and catheterization, complications ID ACCESS; PERFORATION; PLACEMENT; HEART AB PURPOSE: To evaluate the change in position of chest wall central venous access catheters (CVACs) after placement. Complication rates associated with catheter tip position were reviewed. PATIENTS AND METHODS: Fifty patients (36 women, 14 men) with chest wall CVACs placed in the angiography suite were studied, Catheter migration was calculated as the difference between the carina-catheter tip measurements on immediate supine and upright postprocedure (within 24 hours) chest radiographs, Catheter-related complication data were gathered via telephone interview and review of the medical records. RESULTS: Peripheral catheter migration occurred in 49 of 50 patients (average, 3.2 cm +/- 1.8); central catheter migration occurred in one of 50 patients (3.9 cm). Catheter type was the only significant factor that affected the amount of migration; side of insertion or the patient's gender were not significant. Catheter malfunction and symptomatic upper extremity venous thrombosis rates tended to be lower in patients with right atrial versus superior vena cava catheters (18% vs 34%), but differences were not significant (P = .202). CONCLUSION: Catheter migration after chest wall CVAC placement is a common event. The catheter tip should be initially positioned approximately 3-4 cm more centrally than the desired final position. Further study is necessary of catheter-related complication rates relative to the final position of the catheter tip. C1 MASSACHUSETTS GEN HOSP,SECT VASC RADIOL,BOSTON,MA 02114. NR 10 TC 61 Z9 62 U1 0 U2 1 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 MAY-JUN PY 1997 VL 8 IS 3 BP 443 EP 447 DI 10.1016/S1051-0443(97)70586-4 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA WY512 UT WOS:A1997WY51200019 PM 9152919 ER PT J AU Engelman, A Liu, Y Chen, HM Farzan, M Dyda, F AF Engelman, A Liu, Y Chen, HM Farzan, M Dyda, F TI Structure-based mutagenesis of the catalytic domain of human immunodeficiency virus type 1 integrase SO JOURNAL OF VIROLOGY LA English DT Article ID HIV-1 INTEGRASE; VIRAL REPLICATION; ESCHERICHIA-COLI; GENETIC-ANALYSIS; PROTEIN INVITRO; I INTEGRASE; DNA-BINDING; IDENTIFICATION; RESIDUES; MUTATIONS AB Two different crystal structures of the human immunodeficiency virus type 1 (HIV-1) integrase (IN) catalytic domain were analyzed for interactions at the enzyme active site, Gln-62 and Glu-92 interact with active-site residue Asp-64, and Lys-136 interacts with active-site residue Asp-116 across a dimer interface, Conservative and nonconservative substitutions were introduced at these positions to probe the roles of these interactions in HIV-1 integration, Purified mutant proteins were assayed for in vitro 3' processing, DNA strand transfer, and disintegration activities, and HIV-1 mutants were assayed for virion protein composition, reverse transcription, and infectivities in human cell lines. Each of the mutant IN proteins displayed wild-type disintegration activity, indicating that none of the interactions is essential for catalysis, Mutants carrying Gin or Ala for Glu-92 displayed wild-type activities, but substituting Lys for Glu-92 reduced in vitro 3' processing and DNA strand transfer activities 5- to 10-fold and yielded a replication-defective IN active-site mutant viral phenotype. Substituting Glu for Gln-62 reduced in vitro 3' processing and DNA strand transfer activities 5- to 10-fold without grossly affecting viral replication kinetics, suggesting that HIV-1 can replicate in T-cell lines with less than the wild-type level of IN activity, The relationship between IN solubility and HIV-I replication was also investigated, We previously showed that substituting Lys for Phe-185 dramatically increased the solubility of recombinant IN but caused an HIV-1 particle assembly defect. Mutants carrying His at this position displayed increased solubility and wild-type replication kinetics, showing that increased IN solubility per se is not detrimental to virus growth. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NIDDKD,MOL BIOL LAB,BETHESDA,MD 20892. RP Engelman, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI39394] NR 50 TC 51 Z9 51 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAY PY 1997 VL 71 IS 5 BP 3507 EP 3514 PG 8 WC Virology SC Virology GA WT189 UT WOS:A1997WT18900018 PM 9094622 ER PT J AU Hardwicke, MA Schaffer, PA AF Hardwicke, MA Schaffer, PA TI Differential effects of nerve growth factor and dexamethasone on herpes simplex virus type 1 oriL- and oriS-dependent DNA replication in PC12 cells SO JOURNAL OF VIROLOGY LA English DT Article ID ORIGIN-BINDING-PROTEIN; EPSTEIN-BARR-VIRUS; GLUCOCORTICOID HORMONES; REGULATORY REGION; GENE; REACTIVATION; RECEPTOR; SEQUENCE; ELEMENT; IDENTIFICATION AB The herpes simplex virus type 1 (HSV-1) genome contains three origins of DNA replication, one copy of oriL and two copies of oriS, Although oriL and oriS are structurally different, they have extensive nucleotide sequence similarity and can substitute for each other to initiate viral DNA replication, A fundamental question that remains to be answered is why the HSV-1 genome contains two types of origin, We have recently identified a novel glucocorticoid response element (GRE) within oriL that is not present in oriS and have shown by gel mobility shift assays that purified glucocorticoid receptor (GR), as well as GR present in cellular extracts, can bind to the GRE in oriL, To determine whether glucocorticoids and the CRE affect the efficiency of oril-dependent DNA replication, we performed transient DNA replication assays in the presence and absence of dexamethasone (DEX), Because HSV-I is a neurotropic virus and establishes latency in cells of neural origin, these tests were conducted in PC12 cells, which assume the properties of sympathetic neurons when differentiated with nerve growth factor (NGF), In NGF-differentiated PC12 cells, oril-dependent DNA replication was enhanced 5-fold by DEX, whereas in undifferentiated cells, DEX enhanced replication similar to 2-fold. Notably, the enhancement of oriL function by DEX was abolished when the GRE was mutated, NGF-induced differentiation alone had no effect, In contrast to oriL, oriS-dependent DNA replication was reduced similar to 5-fold in NGF-differentiated PC12 cells and an additional 4-fold in differentiated cells treated with DEX, In undifferentiated PC12 cells, DEX had only a minor inhibitory effect (similar to 2-fold) on oriS function. Although the cis-acting elements that mediate the NGF- and DEX-specific repression of oriS-dependent DNA replication are unknown, a functional GRE is critical for the DEX-induced enhancement of oriL function in NGF-differentiated PC12 cells, The enhancement of oril-dependent DNA replication by DEX in differentiated PC12 cells suggests the possibility that glucocorticoids, agents long recognized to enhance reactivation of latent herpesvirus infections, act through the GRE in oriL to stimulate viral DNA replication and reactivation in terminally differentiated neurons in vivo. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOL GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOL GENET,BOSTON,MA 02115. FU NIAID NIH HHS [F32AI08878]; PHS HHS [R0IA128537] NR 54 TC 42 Z9 43 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAY PY 1997 VL 71 IS 5 BP 3580 EP 3587 PG 8 WC Virology SC Virology GA WT189 UT WOS:A1997WT18900026 PM 9094630 ER PT J AU Olsen, JG Salih, MA Harrison, JL Herrera, I Luther, MF Kalu, DN Lifschitz, MD Katz, MS Yeh, CK AF Olsen, JG Salih, MA Harrison, JL Herrera, I Luther, MF Kalu, DN Lifschitz, MD Katz, MS Yeh, CK TI Modulation by food restriction of intracellular calcium signaling in parotid acinar cells of aging Fischer 344 rats SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID AGED RATS; RECEPTOR STIMULATION; SALIVARY SECRETION; GLAND MEMBRANES; TRANSDUCTION; ACTIVATION; MECHANISMS; CA-2+; RESPONSIVENESS; G(ALPHA-Q/11) AB Previous studies suggest that alpha(1)-adrenergic (alpha(1)-AR)-induced intracellular calcium ([Ca2+](i)) mobilization in rat parotid acinar cells declines with age. In this study, we examined the effects of food restriction on alpha(1)-AR- and muscarinic-stimulated [Ca2+](i) mobilization in parotid acinar cells during aging. [Ca2+](i) levels in response to the (alpha(1)-AR agonist epinephrine and the muscarinic agonist carbachol were evaluated in Fura-2-loaded parotid acinar cells from ad libitum-fed (AL) and food-restricted (FR) Fisher 344 male rats at 4, 6, 14, and 24 months of age. [Ca2+](i) responses to epinephrine and carbachol 110 mu M) were significantly reduced (48% and 35%, respectively; p < .05) in cells from 24-month-old AL rats as compared to younger AL rats. In contrast, no significant reduction of epinephrine and carbachol responses was observed in 24-month-old FR animals. An age-related increase in basal [Ca2+](i) (peak around 14 months; p < .02) was observed in both AL and FR rats. In addition, basal [Ca2+](i) was higher in FR than in AL rats at 14 and 24 months of age (p < .02). These studies suggest that FR partially attenuates or delays age-related impairments in alpha(1)-AR- and muscarinic-cholinergic signal transduction systems of parotid acinar cells. Basal [Ca2+](i) also appears to be altered during aging and by FR. C1 S TEXAS VET HLTH CARE SYST, AUDIE L MURPHY DIV, GRECC, SAN ANTONIO, TX 78284 USA. S TEXAS VET HLTH CARE SYST, RES SERV, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PHYSIOL, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT DENT DIAGNOST SERV, SAN ANTONIO, TX USA. RI Salih, Mustafa/C-1222-2014 OI Salih, Mustafa/0000-0002-4379-2111 FU NIA NIH HHS [AG-01188] NR 39 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1079-5006 EI 1758-535X J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD MAY PY 1997 VL 52 IS 3 BP B152 EP B158 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WZ219 UT WOS:A1997WZ21900004 PM 9158549 ER PT J AU Vitiello, MV Wilkinson, CW Merriam, GR Moe, KE Prinz, PN Ralph, DD Colasurdo, EA Schwartz, RS AF Vitiello, MV Wilkinson, CW Merriam, GR Moe, KE Prinz, PN Ralph, DD Colasurdo, EA Schwartz, RS TI Successful 6-month endurance training does not alter insulin-like growth factor-I in healthy older men and women SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID BODY-FAT DISTRIBUTION; SOMATOMEDIN-C; IGF-I; HORMONE; EXERCISE; YOUNG; RESPONSES; AGE; SECRETION; DISEASE AB Background. Lean body mass, strength, and endurance decline with advancing age, changes paralleled by declines in anabolic hormones, including growth hormone (GH) and insulin-like growth factor-I (IGF-I). Acute exercise has been shown to stimulate the GH/IGF-I axis, and long-term exercise increases GH. This study examined the effect of endurance training on IGF-I in healthy older men and women. Methods. Thirty-one healthy older men (66.9 +/- 1.0 yrs, mean +/- SEM) and 21 healthy older women (67.1 +/- 1.7 yrs) were randomized to either 3d/wk, 6-month endurance (ET3) or stretching/flexibility (SF3) protocols. Another group of 15 healthy older men (69.0 +/- 1.3 yrs) participated in a more intensive 5d/wk, 6-month endurance protocol (ET5). Before and after training, subjects were weight stabilized and participated in maximal exercise tolerance testing, body composition assessment, and fasting blood sampling. Results. ET3 training resulted in a significant increase (14%) in maximal aerobic power (VO(2)max), significant decreases in body weight (BW), fat mass (FM), and wais/hip ratio (WHR), and a significant increase in fat-free mass (FFM). No significant VO(2)max or body composition changes were observed in the SF3 group. For the ET5 group, a significant increase (22%) in VO(2)max and significant decreases in BW, FM, and WHR were observed. No significant changes in IGF-I were observed for any of the three groups. Pre- versus post-training IGF-I values were very stable (r = .86, p < .001) across subjects. Conclusions. Within-subject basal levels of IGF-I in healthy seniors were extremely stable between pre- and posttraining assessments. Two endurance training protocols of magnitudes sufficient to significantly increase aerobic capacity and decrease measures of body adiposity did not significantly increase basal levels of IGF-I in healthy older men and women. C1 UNIV WASHINGTON,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. VA PUGET SOUND HLTH CARE SYST,AMER LAKE DIV,TACOMA,WA. FU NIMH NIH HHS [R01-MH45186, K02-MH1158, R01-MH53575] NR 25 TC 28 Z9 28 U1 0 U2 2 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD MAY PY 1997 VL 52 IS 3 BP M149 EP M154 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WZ219 UT WOS:A1997WZ21900011 PM 9158556 ER PT J AU Sugimori, T Griffith, DL Arnaout, MA AF Sugimori, T Griffith, DL Arnaout, MA TI Emerging paradigms of integrin ligand binding and activation SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT ISN Forefronts in Nephrology Symposium on Cytokines and Adhesion Molecules in Tissue Injury and Repair CY SEP 12-15, 1996 CL SNOWBIRD, UT SP ISN ID FUNCTION-ASSOCIATED ANTIGEN-1; PLATELET GLYCOPROTEIN-IIB; DIVALENT-CATION REGULATION; CELL-ADHESION MOLECULE-1; I-DOMAIN; CRYSTAL-STRUCTURE; GPIIB-IIIA; CYTOPLASMIC DOMAIN; FIBRONECTIN RECEPTOR; MONOCLONAL-ANTIBODY AB Adhesion of cells to each other or to the extracellular matrix provides essential signals that regulate many cellular functions including cell migration, proliferation, differentiation and apoptosis. The integrin superfamily orchestrates many of these complex adhesive events through regulated interactions with a large variety of ligands. Crystallization of some ligands and of a ligand binding integrin domain, reviewed here, together with extensive mutagenesis studies are beginning to shed light on the inner workings of these receptors. C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,DEPT MED,LEUKOCYTE BIOL & INFLAMMAT PROGRAM,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA. NR 135 TC 34 Z9 34 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAY PY 1997 VL 51 IS 5 BP 1454 EP 1462 DI 10.1038/ki.1997.199 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA WX906 UT WOS:A1997WX90600019 PM 9150458 ER PT J AU Goodman, WG Veldhuis, JD Belin, TR Juppner, H Salusky, IB AF Goodman, WG Veldhuis, JD Belin, TR Juppner, H Salusky, IB TI Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT ISN Forefronts in Nephrology Symposium on Cytokines and Adhesion Molecules in Tissue Injury and Repair CY SEP 12-15, 1996 CL SNOWBIRD, UT SP ISN ID GLAND FUNCTION; HEMODIALYSIS-PATIENTS; PEDIATRIC-PATIENTS; FAILURE; HYPERCALCEMIA; HYPERPLASIA; SECRETION; TUMORS; ASSAY; CAPD AB Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2 degrees HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2 degrees HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2 degrees HPT and in 20 NL. Basal serum PTH levels were 88 +/- 51, 536 +/- 395, and 26 +/- 6 pg/ml, respectively, in AD, 2 degrees HPT and NL, whereas basal ionized calcium levels did nor differ. When expressed as a percentage of pre-infusion values, PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 +/- 5.6%) and in 2 degrees HPT (27.8 +/- 12.3%) than in NL, (11.9 +/- 5.8%, P < 0.001). Both the amplitude of suppression (%) and the rate of decline (min(-1)) in serum PTH were less in AD and 2 degrees HPT than in NL, P < 0.05 for each parameter: corresponding values for each group, with 95% confidence intervals, were 77% (73 to 52) and 0.039 min(-1) (0.030 to 0.018) in AD, 72% (68 to 76) and 0.031 min(-1) (0.025 to 0.036) in 2 degrees HPT and 87% (84 to 89) and 0.070 min(-1) (0.058 to 0.089) in NL. Neither variable differed between AD and 2 degrees HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2 degrees HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2 degrees HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20% of pre-infusion values in fewer subjects with AD (1 of 6) or 2 degrees HPT (9 of 31) than in NL (17 of 20) (chi(2) = 17.51, P < 0.005). The results indicate thai the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2 degrees HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2 degrees HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD. 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. UNIV VIRGINIA,DEPT MED,CHARLOTTESVILLE,VA. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. FU NCRR NIH HHS [RR-00865, RR-00847]; NIDDK NIH HHS [DK-35423] NR 27 TC 15 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAY PY 1997 VL 51 IS 5 BP 1590 EP 1595 DI 10.1038/ki.1997.218 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA WX906 UT WOS:A1997WX90600037 PM 9150477 ER PT J AU Meehan, SM McCluskey, RT Pascual, M Preffer, FI Anderson, P Schlossman, SF Colvin, RB AF Meehan, SM McCluskey, RT Pascual, M Preffer, FI Anderson, P Schlossman, SF Colvin, RB TI Cytotoxicity and apoptosis in human renal allografts: Identification, distribution, and quantitation of cells with a cytotoxic granule protein GMP-17 (TIA-1) and cells with fragmented nuclear DNA SO LABORATORY INVESTIGATION LA English DT Article ID NATURAL-KILLER-CELLS; MEDIATED CYTOTOXICITY; ACUTE REJECTION; T-LYMPHOCYTES; BIOPSIES; DEATH; FAS; SUBPOPULATION; EXPRESSION; MECHANISMS AB In the present study, we analyzed human renal allografts using immunohistochemical techniques to determine the site, identity, and frequency of (a) cytotoxic and apoptotic cells, as identified by staining for GMP-17 (TIA-1), a component of cytotoxic granules; and (b) DNA fragmentation in situ, as detected by the TUNEL method. In acute cellular rejection (n = 15), GMP-17(+) mononuclear cells accounted for 29% +/- 12% of the infiltrating cells in the interstitium (341 +/- 164/mm(2)) and were significantly more concentrated in tubulitis lesions, where they amounted to 65% +/- 14% of the mononuclear cells (96 +/- 61/mm(2)) (p < 0.01 versus interstitium). GMP-17(+) mononuclear cells were also found in sites of endothelialitis. An estimated 80% of the GMP-17(+) lymphocytes expressed CD8, and 10% to 20% expressed either CD4 or the macrophage marker CD14. The latter finding led us to analyze normal peripheral blood monocytes by flow cytometry, all of which were found to contain GMP-17. NK cells and neutrophils, which are known to express GMP-17, were detected only rarely in allografts. Specimens with cyclosporine A toxicity (n = 7) or acute tubular necrosis (n = 13) showed fewer GMP-17(+) cells in the interstitium (22 +/- 46/mm(2) and 62 +/- 50/mm(2), respectively) and tubules (2 +/- 6/mm(2) and 10 +/- 10/mm(2), respectively) (all p < 0.01 versus rejection). These differences were due largely to less intense mononuclear cell infiltration. In cyclosporine A toxicity, however, the percentages of GMP-17(+) mononuclear cells within tubules and the interstitium were significantly lower than in rejection (p = 0.02), whereas in acute tubular necrosis significantly tower percentages were found in the tubules (p = 0.04) but not in the interstitium. Native kidneys with end-stage diabetic nephropathy (n = 5) had very low proportions of GMP-17(+) cells in interstitial infiltrates (7% +/- 6%) and in tubules (11% +/- 15%), although the infiltrates were focally intense (517 +/- 355/mm(2)). TUNEL+ cells were found in acute cellular rejection, predominantly in areas with intense mononuclear infiltrates and also within lesions of tubulitis and endothelialitis. Although some TUNEL+ cells were intrinsic renal cells, most appeared to be infiltrating mononuclear cells, and we were able to detect CD3 in some. In areas of intense cellular infiltration, the percentages of TUNEL+ cells (range, 0.5% to 4.2%) were comparable to those seen in the rat thymus, indicating a high level of apoptosis. Overall, in the allograft samples, the numbers of GMP-17(+) cells and TUNEL+ cells were significantly correlated (r = 0.79; p < 0.01). These data provide new evidence that T cell (and possibly macrophage)-mediated cytotoxicity plays an important role in acute renal allograft rejection, particularly in the case of tubular injury, and furthermore suggest that apoptosis may be a mechanism not only for graft cell destruction, but also for elimination of activated T cells in the infiltrate. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,TRANSPLANTAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,IMMUNOPATHOL UNIT,BOSTON,MA 02114. DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. FU NCI NIH HHS [T32-CA-09216]; NHLBI NIH HHS [P01-HL-18646] NR 49 TC 77 Z9 84 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD MAY PY 1997 VL 76 IS 5 BP 639 EP 649 PG 11 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA XA306 UT WOS:A1997XA30600005 PM 9166283 ER PT J AU Weichselbaum, RR Kufe, D AF Weichselbaum, RR Kufe, D TI Gene therapy of cancer SO LANCET LA English DT Article ID TUMOR-REGRESSION; EXPRESSION; DNA; MICE; COMPLEXES; VECTORS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. RP Weichselbaum, RR (reprint author), UNIV CHICAGO,CTR RADIAT THERAPY,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637, USA. NR 31 TC 1 Z9 2 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAY PY 1997 VL 349 SU 2 BP S10 EP S12 DI 10.1016/S0140-6736(97)90013-1 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA WZ895 UT WOS:A1997WZ89500005 ER PT J AU Fried, MP Kleefield, J Gopal, H Reardon, E Ho, BT Kuhn, FA AF Fried, MP Kleefield, J Gopal, H Reardon, E Ho, BT Kuhn, FA TI Image-guided endoscopic surgery: Results of accuracy and performance in a multicenter clinical study using an electromagnetic tracking system SO LARYNGOSCOPE LA English DT Article; Proceedings Paper CT COSM Meeting CY MAY 08, 1996 CL ORLANDO, FL SP COSM ID SINUS SURGERY; COMPLICATIONS AB Image-guided surgery has recently been described in the literature as a useful technology for improved functional endoscopic sinus surgery localization. image-guided surgery yields accurate knowledge of the surgical field boundaries, allowing safer and more thorough sinus surgery. We have previously reviewed our initial experience with The InstaTrak System. This article presents a multicenter clinical study (n=55) that assesses the system's capability for localizing structures in critical surgical sites. The purpose of this paper is to present quantitative data on accuracy and performance. We describe several new advances including an automated registration technique that eliminates the redundant computed tomography scan, compensation for head movement, and the ability to use interchangeable instruments. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. BETH ISRAEL DEACONNESS MED CTR,JOINT CTR OTOLARYNGOL,BOSTON,MA. BETH ISRAEL DEACONNESS MED CTR,DIV OTOLARYNGOL,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BETH ISRAEL DEACONNESS MED CTR,DEPT RADIOL,BOSTON,MA. CARNEY HOSP,DEPT OTOL & LARYNGOL,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA. MEM MED CTR,GEORGIA EAR INST,DEPT OTOLARYNGOL,SAVANNAH,GA. NR 10 TC 141 Z9 143 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD MAY PY 1997 VL 107 IS 5 BP 594 EP 601 DI 10.1097/00005537-199705000-00008 PG 8 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA WX657 UT WOS:A1997WX65700007 PM 9149159 ER PT J AU LevRam, V Nebyelul, Z Ellisman, MH Huang, PL Tsien, RY AF LevRam, V Nebyelul, Z Ellisman, MH Huang, PL Tsien, RY TI Absence of cerebellar long-term depression in mice lacking neuronal nitric oxide synthase SO LEARNING & MEMORY LA English DT Article ID PURKINJE NEURONS; GENE; DEFICIENT; CELLS AB Extensive pharmacological evidence suggests that nitric oxide (NO) is a crucial transmitter for cerebellar long-term depression (LTD), a long-lasting decrease in efficacy of the synapses from parallel fibers onto Purkinje neurons, triggered by coincident presynaptic activity and postsynaptic depolarization. We now show that LTD cannot be induced in Purkinje neurons under whole-cell patch clamp in cerebellar slices from young adult mice genetically lacking neuronal nitric oxide synthase (nNOS). This genetic evidence confirms the essentiality of NO and nNOS for LTD in young adult rodents, Surprisingly, LTD in cells from nNOS knockout mice cannot be rescued by photolytic uncaging of NO and cGMP inside Purkinje neurons, although such stimuli circumvent acute pharmacological inhibition of nNOS and soluble guanylate cyclase in normal rodents. Also slices from knockout mice show no deficit in cGMP elevation in response to exogenous NO. Therefore, prolonged absence of nNOS allows atrophy of the signaling pathway downstream of cGMP. C1 UNIV CALIF SAN DIEGO,DEPT PHARMACOL,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,HOWARD HUGHES MED INST,LA JOLLA,CA 92093. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,CHARLESTOWN,MA 02129. FU NCRR NIH HHS [RR04050]; NINDS NIH HHS [NS27177, NS33335] NR 24 TC 45 Z9 49 U1 1 U2 4 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 1072-0502 J9 LEARN MEMORY JI Learn. Mem. PD MAY-JUN PY 1997 VL 4 IS 1 BP 169 EP 177 DI 10.1101/lm.4.1.169 PG 9 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA XP549 UT WOS:A1997XP54900011 PM 10456061 ER PT J AU Stone, RM AF Stone, RM TI Bryostatin 1: Differentiating agent from the depths SO LEUKEMIA RESEARCH LA English DT Article ID PROTEIN-KINASE-C; PROMYELOCYTIC LEUKEMIA-CELLS; RETINOIC ACID; PHASE-I; MYELODYSPLASTIC SYNDROMES; ACTIVATOR BRYOSTATIN-1; ANTICANCER AGENT; INVIVO ACTIVITY; HL-60 CELLS; INVITRO RP Stone, RM (reprint author), DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 32 TC 23 Z9 23 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD MAY PY 1997 VL 21 IS 5 BP 399 EP 401 DI 10.1016/S0145-2126(96)00123-3 PG 3 WC Oncology; Hematology SC Oncology; Hematology GA XH854 UT WOS:A1997XH85400006 PM 9225066 ER PT J AU Kelly, K AF Kelly, K TI Natural woman, natural menopause: Complete program for healthy menopause - Laux,M, Conrad,C SO LIBRARY JOURNAL LA English DT Book Review RP Kelly, K (reprint author), MASSACHUSETTS GEN HOSP,TREADWELL LIB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD MAY 1 PY 1997 VL 122 IS 8 BP 133 EP 134 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA WV949 UT WOS:A1997WV94900201 ER PT J AU Kelly, K AF Kelly, K TI The MEND clinic guide to natural medicine for menopause and beyond - Maas,P SO LIBRARY JOURNAL LA English DT Book Review RP Kelly, K (reprint author), MASSACHUSETTS GEN HOSP,TREADWELL LIB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD MAY 1 PY 1997 VL 122 IS 8 BP 133 EP 134 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA WV949 UT WOS:A1997WV94900200 ER PT J AU Kelly, K AF Kelly, K TI Estrogen: The natural way - Shandler,N SO LIBRARY JOURNAL LA English DT Book Review RP Kelly, K (reprint author), MASSACHUSETTS GEN HOSP,TREADWELL LIB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD MAY 1 PY 1997 VL 122 IS 8 BP 133 EP 134 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA WV949 UT WOS:A1997WV94900199 ER PT J AU Elias, AD Skarin, AT Leong, T Mentzer, S Strauss, G Lynch, T Shulman, L Jacobs, C Abner, A Baldini, EH Frei, E Sugarbaker, DJ AF Elias, AD Skarin, AT Leong, T Mentzer, S Strauss, G Lynch, T Shulman, L Jacobs, C Abner, A Baldini, EH Frei, E Sugarbaker, DJ TI Neoadjuvant therapy for surgically staged IIIA N2 non-small cell lung cancer (NSCLC) SO LUNG CANCER LA English DT Article DE neoadjuvant therapy; non-small cell lung cancer; staging ID PREOPERATIVE CHEMOTHERAPY; RANDOMIZED TRIAL; PHASE-II; INDUCTION CHEMOTHERAPY; RADIATION-THERAPY; RADIOTHERAPY; CARCINOMA; CISPLATIN; SURGERY; 5-FLUOROURACIL AB Introduction: Neoadjuvant therapy in patients with Stage IIIA NSCLC is associated with a 50-70% resection rate and a 3-5 year survival of 20-32%, but few trials have required meticulous staging of the mediastinum to ensure homogeneity of the study population. Continuous infusion cisplatin 25 mg/m(2)/day 1-5, 5-fluorouracil 800 mg/m(2)/day 2-5, and high-dose leukovorin 500 mg/m(2)/day 1-5 (PFL) given every 4 weeks achieved a 41% response rate in metastatic NSCLC (Lynch TJ, Kalish LA, Kass F, Strauss G, Elias A, Skarin A, Shulman L, Sugarbaker D, Frei E. Continuous infusion cisplatin, 5-fluorouracil, and leukovorin for advanced non-small cell lung cancer. Cancer 1994; 73: 1171-1176). The regimen was therefore evaluated in 34 patients with pathologic Stage IIIA N2 disease between 3/91 and 10/92. Methods: Staging consisted of chest, liver, brain computerized tomography and bone scan, bronchoscopy and surgical mediastinal node mapping. Patients received PFL for 3 cycles, followed by thoracotomy and thoracic radiotherapy (TRT) to 54-60 Gy. Results: Median age was 57 (42-68) years. Demographic factors included: male 56%; adenocarcinoma 59%, squamous cell carcinoma 24%; Stage T3N2 26%, T2N2 56%, and T1N2 18%. No treatment related deaths occurred. Radiographically defined response to PFL was 65% (6% complete). Thoracotomy was performed in 28 patients (82%) (6 had no attempt due to disease progression). Complete resection was achieved in 21 (75%) and seven were unresectable. Pathologic complete response was observed in five patients (15%) and an additional unresectable patient had fibrosis-only documented at thoracotomy for an overall clinicopathologic response rate of 76% (18% pathologic CR). Another ten patients had residual primary with or without hilar disease with resolution of previously documented mediastinal involvement. Sis (18%) patients remain alive and disease-free with a median follow-up of 46 (33-50) months, four of whom had achieved pathologic complete response at time of surgery. Conclusions: Long-term event-foe survival was associated with complete surgical resection which in turn was associated with clinical response to chemotherapy. There was a possible trend associating pathologic downstaging (absent residual disease in mediastinal nodes), particularly pathologic complete response observed in patients with non-bulky mediastinal disease, with improved event-free survival. Pathologic downstaging might therefore be a useful surrogate endpoint in trials evaluating the preoperative activity of new chemotherapy regimens. While radiographic response generally correlated with findings at surgery, response as determined by histologic examination of resected tissue was generally more extensive and may more accurately reflect the systemic impact of the chemotherapy regimen. (C) 1997 Elsevier Science Ireland Ltd. RP Elias, AD (reprint author), BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 27 TC 69 Z9 72 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-5002 J9 LUNG CANCER-J IASLC JI Lung Cancer PD MAY PY 1997 VL 17 IS 1 BP 147 EP 161 DI 10.1016/S0169-5002(97)00658-2 PG 15 WC Oncology; Respiratory System SC Oncology; Respiratory System GA XE169 UT WOS:A1997XE16900009 PM 9194034 ER PT J AU Fried, LF Palevsky, PM AF Fried, LF Palevsky, PM TI Hyponatremia and hypernatremia SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Review ID ANTIDIURETIC-HORMONE SECRETION; ANTI-DIURETIC HORMONE; INDUCED WATER-INTOXICATION; CENTRAL-NERVOUS-SYSTEM; THIAZIDE-INDUCED HYPONATREMIA; CHRONIC HEART-FAILURE; VASOPRESSIN SECRETION; INAPPROPRIATE SECRETION; RAPID CORRECTION; ARGININE VASOPRESSIN AB Hyponatremia and hypernatremia are common electrolyte disorders that are associated with increased morbidity and mortality. Both disturbances result from disorders of water homeostasis. This article reviews normal water homeostasis and the pathophysiology of hypo- and hypernatremia. A rationale for treatment recommendation is provided. C1 UNIV PITTSBURGH,SCH MED,DEPT MED,RENAL ELECTROLYTE DIV,PITTSBURGH,PA 15213. VA PITTSBURGH HLTH CARE SYST,MED SERV,RENAL SECT,PITTSBURGH,PA. NR 121 TC 87 Z9 95 U1 3 U2 6 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAY PY 1997 VL 81 IS 3 BP 585 EP & DI 10.1016/S0025-7125(05)70535-6 PG 26 WC Medicine, General & Internal SC General & Internal Medicine GA XA501 UT WOS:A1997XA50100002 PM 9167647 ER PT J AU Curhan, GC AF Curhan, GC TI Dietary calcium, dietary protein, and kidney stone formation SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 8th International Congress on Renal Nutrition and Metabolism CY OCT 09-12, 1996 CL NAPLES, ITALY SP Baxter Healthcare Corp, Sigma Tau Pharm Inc, Second Univ Naples DE animal protein; calcium; diet; kidney stones; prospective studies ID HEALTHY-SUBJECTS; UROLITHIASIS; FREQUENCY; RISK AB Kidney stone disease is common and is a major cause of morbidity involving the urinary tract. Rising incidence rates of calcium oxalate stone disease, the most common type of kidney stone, have focused attention on dietary habits and their potential role in the development of nephrolithiasis. Traditionally, calcium restriction had been recommended to reduce the likelihood of calcium stone formation, but recent evidence suggests that dietary calcium restriction may actually increase the risk. Observational and experimental data suggest that restriction of animal protein may lower the risk of stone formation, but a randomized trial did not confirm this finding. Dietary modification may play an important role in reducing the likelihood of stone recurrence. Notably, dietary calcium restriction should be avoided in patients who have had a calcium oxalate kidney stone. C1 BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. RP Curhan, GC (reprint author), HARVARD UNIV,RENAL UNIT,MASSACHUSETTS GEN HOSP,SCH MED,FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 21 Z9 21 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD MAY-DEC PY 1997 VL 23 IS 3-6 BP 261 EP 264 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YE344 UT WOS:A1997YE34400029 PM 9387129 ER PT J AU Sandhu, C Garbe, J Bhattacharya, N Daksis, J Pan, CH Yaswen, P Koh, J Slingerland, JM Stampfer, MR AF Sandhu, C Garbe, J Bhattacharya, N Daksis, J Pan, CH Yaswen, P Koh, J Slingerland, JM Stampfer, MR TI Transforming growth factor beta stabilizes p15(INK4B) protein, increases p15(INK4B)-cdk4 complexes, and inhibits cyclin D1 cdk4 association in human mammary epithelial cells SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DEPENDENT KINASE INHIBITOR; TUMOR-SUPPRESSOR GENE; TGF-BETA; RETINOBLASTOMA-PROTEIN; DNA-REPLICATION; POTENTIAL MEDIATOR; MAMMALIAN-CELLS; CANCER-CELLS; P21; EXPRESSION AB The effects of transforming growth factor beta (TGF-beta) were studied in closely related human mammary epithelial cells (HMEC), both finite-life-span 184 cells and immortal derivatives, 184A1(S), and 184A1L5(R), which differ in their cell cycle responses to TGF-beta but express type I and type II TGF-beta receptors and retain TGF-beta induction of extracellular matrix. The arrest-resistant phenotype was not due to loss of cyclin-dependent kinase (cdk) inhibitors. TGF-beta was shown to regulate p15(INK4B) expression at at least two levels: mRNA accumulation and protein stability. In TGF-beta-arrested HMEC, there was not only an increase in p15 mRNA but also a major increase in p15(INK4B) protein stability. As cdk4- and cdk6-associated p15(INK4B) increased during TGF-beta arrest of sensitive cells, there was a loss of cyclin D1, p21(Cip1), and p27(Kip1) from these kinase complexes, and cyclin E-cdk2-associated p27(Kip1) increased. In HMEC, p15(INK4B) complexes did not contain detectable cyclin. p15(INK4B) from both sensitive and resistant cells could displace in vitro cyclin D1, p21(Cip1), and p27(Kip1) from cdk4 isolated from sensitive cells. Cyclin D1 could not be displaced from cdk4 in the resistant 184A1L5(R) cell lysates. Thus, in TGF-beta arrest, p15(INK4B) may displace already associated cyclin D1 from cdks and prevent new cyclin D1-cdk complexes from forming. Furthermore, p27(Kip1) binding shifts from cdk4 to cyclin E-cdk2 during TGF-beta-mediated arrest. The importance of posttranslational regulation of p15(INK4B) by TGF-beta is underlined by the observation that in TGF-beta-resistant 184A1L5(R), although the p15 transcript increased, p15(INK4B) protein was not stabilized and did not accumulate, and cyclin D1-cdk association and kinase activation were not inhibited. C1 TORONTO SUNNYBROOK REG CANC CTR, DIV CANC BIOL RES, TORONTO, ON M4N 3M5, CANADA. UNIV CALIF BERKELEY, LAWRENCE BERKELEY LAB, BERKELEY, CA 94720 USA. MASSACHUSETTS GEN HOSP, CTR CANC, CHARLESTOWN, MA 02129 USA. FU NCI NIH HHS [CA-24844] NR 77 TC 148 Z9 154 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1997 VL 17 IS 5 BP 2458 EP 2467 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WV199 UT WOS:A1997WV19900011 PM 9111314 ER PT J AU Sharma, S Jhala, US Johnson, T Ferreri, K Leonard, J Montminy, M AF Sharma, S Jhala, US Johnson, T Ferreri, K Leonard, J Montminy, M TI Hormonal regulation of an islet-specific enhancer in the pancreatic homeobox gene STF-1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TRANSCRIPTION FACTOR; INSULIN GENE; RAT PANCREAS; EXPRESSION; RECEPTOR; CELLS; HEAD AB The homeobox protein STF-1 appears to function as a master control switch for expression of the pancreatic program during development. Here we characterize a composite enhancer which directs STF-1 expression to pancreatic islet cells via two functional elements that recognize the nuclear factors HNF-3 beta and BETA-2. In keeping with their inhibitory effects on islet cell maturation, glucocorticoids were found to repress STF-1 gene expression by interfering with HNF-3 beta activity on the islet-specific enhancer, Overexpression of HNF-3 beta suppressed glucocorticoid receptor-mediated inhibition of the STF-1 gene, and our results suggest that the expansion of pancreatic islet precursor cells during development may be restricted by hormonal cues which regulate STF-1 gene expression. C1 BOSTON UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,DEPT CELL BIOL,BOSTON,MA 02215. VIVORX INC,SANTA MONICA,CA 90404. STRANG CORNELL RES LAB,NEW YORK,NY 10021. RP Sharma, S (reprint author), UNIV CALIF SAN DIEGO,DEPT BIOL,LA JOLLA,CA 92037, USA. OI Ferreri, Kevin/0000-0003-0379-0389 FU NIDDK NIH HHS [DK 49777] NR 18 TC 89 Z9 90 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1997 VL 17 IS 5 BP 2598 EP 2604 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WV199 UT WOS:A1997WV19900026 PM 9111329 ER PT J AU Fiorentini, P Huang, KN Tishkoff, DX Kolodner, RD Symington, LS AF Fiorentini, P Huang, KN Tishkoff, DX Kolodner, RD Symington, LS TI Exonuclease I of Saccharomyces cerevisiae functions in mitotic recombination in vivo and in vitro SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SINGLE-STRANDED-DNA; EXCISION-REPAIR GENE; DIRECT-REPEAT RECOMBINATION; SCHIZOSACCHAROMYCES-POMBE; MEIOTIC RECOMBINATION; ESCHERICHIA-COLI; INITIATION SITE; BREAK REPAIR; RAD52 GENES; RECJ-GENE AB We previously described a 5'-3' exonuclease required for recombination in vitro between linear DNA molecules with overlapping homologous ends. This exonuclease, referred to as exonuclease I (Exo I), has been purified more than 300-fold from vegetatively grown cells and copurifies with a 42-kDa polypeptide. The activity is nonprocessive and acts preferentially on double-stranded DNA. The biochemical properties are quite similar to those of Schizosaccharomyces pombe fro I. Extracts prepared from cells containing a mutation of the Saccharomyces cerevisiae EXO1 gene, a homolog of S. pombe exo1, had decreased in vitro recombination activity and when fractionated were found to lack the peak of activity corresponding to the 5'-3' exonuclease. The role of EXO1 on recombination in vivo was determined by measuring the rate of recombination in an exo1 strain containing a direct duplication of mutant ade2 genes and was reduced sixfold. These results indicate that EXO1 is required for recombination in vivo and in vitro in addition to its previously identified role in mismatch repair. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT MICROBIOL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,CANC RES INST,NEW YORK,NY 10032. HARVARD UNIV,DANA FARBER CANC INST,CHARLES A DANA DIV HUMAN CANC GENET,SCH MED,BOSTON,MA 02115. FU NIGMS NIH HHS [GM50006, GM08224, GM41784] NR 67 TC 146 Z9 148 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1997 VL 17 IS 5 BP 2764 EP 2773 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WV199 UT WOS:A1997WV19900044 PM 9111347 ER PT J AU Mecocci, P Beal, MF Cecchetti, R Polidori, MC Cherubini, A Chionne, F Avellini, L Romano, G Senin, U AF Mecocci, P Beal, MF Cecchetti, R Polidori, MC Cherubini, A Chionne, F Avellini, L Romano, G Senin, U TI Mitochondrial membrane fluidity and oxidative damage to mitochondrial DNA in aged and AD human brain SO MOLECULAR AND CHEMICAL NEUROPATHOLOGY LA English DT Article DE membrane fluidity; mitochondrial DNA; aging brain; Alzheimer disease (AD); oxidation ID CYTOCHROME-OXIDASE ACTIVITY; ALZHEIMERS-DISEASE; LIPID-PEROXIDATION; RADICALS; PROTEIN; INVITRO; CORTEX; AMYLOIDOGENICITY; RESTRICTION; INCREASES AB Oxidative damage on biological molecules has been proposed as a major cause of alterations observed in aging brain as well as in neurodegenerative diseases. In this study, we measured membrane fluidity in mitochondria extracted from three cerebral regions and cerebellum of Alzheimer disease (AD) patients and age-matched controls by means of fluorescence polarization technique. A significant reduction of mitochondrial membrane fluidity was found in AD, except in cerebellum. In controls, a decrease of membrane fluidity was observed along with age, and it was also related to the content of the oxidized nucleoside 8-hydroxy-2'-deoxyguanosine (OH(8)dG) in mitochondrial DNA (mtDNA). Alteration in membrane fluidity seems to be a result of lipid peroxidation, since it dramatically decreased when mitochondria were exposed to FeCl2 and H2O2. The parallel increase of viscosity in mitochondrial membrane and the amount of OH(8)dG in mtDNA is suggestive of a relationship between these biological markers of oxidative stress. These results provide further evidence that oxidative stress may play a role in the pathogenesis of AD. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA. UNIV PERUGIA,MONTELUCE POLICLIN,DEPT MED PHYS,I-06100 PERUGIA,ITALY. UNIV PERUGIA,INST MED CHEM & BIOCHEM,I-06100 PERUGIA,ITALY. RP Mecocci, P (reprint author), UNIV PERUGIA,DEPT CLIN MED PATHOL & PHARMACOL,I-06100 PERUGIA,ITALY. OI Cherubini, Antonio/0000-0003-0261-9897 NR 50 TC 108 Z9 110 U1 0 U2 5 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 1044-7393 J9 MOL CHEM NEUROPATHOL JI Mol. Chem. Neuropathol. PD MAY PY 1997 VL 31 IS 1 BP 53 EP 64 DI 10.1007/BF02815160 PG 12 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA XN180 UT WOS:A1997XN18000005 PM 9271005 ER PT J AU Iliopoulos, O Kaelin, WG AF Iliopoulos, O Kaelin, WG TI The molecular basis of von Hippel Lindau disease SO MOLECULAR MEDICINE LA English DT Review ID TUMOR-SUPPRESSOR GENE; RENAL-CELL CARCINOMA; SOMATIC MUTATIONS; IDENTIFICATION; ELONGATION; PHENOTYPE; FEATURES; PRODUCT; BINDING; PROTEIN C1 DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 43 TC 30 Z9 30 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 1076-1551 J9 MOL MED JI Mol. Med. PD MAY PY 1997 VL 3 IS 5 BP 289 EP 293 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA XC147 UT WOS:A1997XC14700001 PM 9205944 ER PT J AU Blum, K Braverman, ER Wu, S Cull, JG Chen, TJH Gill, J Wood, R Eisenberg, A Sherman, M Davis, KR Matthews, D Fischer, L Schnautz, N Walsh, W Pontius, AA Zedar, M Kaats, G Comings, DE AF Blum, K Braverman, ER Wu, S Cull, JG Chen, TJH Gill, J Wood, R Eisenberg, A Sherman, M Davis, KR Matthews, D Fischer, L Schnautz, N Walsh, W Pontius, AA Zedar, M Kaats, G Comings, DE TI Association of polymorphisms of dopamine D-2 receptor (DRD2), and dopamine transporter (DAT(1)) genes with schizoid/avoidant behaviors (SAB) SO MOLECULAR PSYCHIATRY LA English DT Article DE schizoid/avoidant behavior; polymorphisms; dopamine D-2 receptor gene (DRD2); dopamine transporter gene (DAT(1)) ID PROLONGED P300 LATENCY; PERSONALITY-DISORDERS; BETA-HYDROXYLASE; D2 RECEPTOR; ALLELIC ASSOCIATION; SUBSTANCE-ABUSE; ALCOHOLISM; LINKAGE; LOCUS; VULNERABILITY AB The dopaminergic system, and in particular the dopamine D-2 receptor, has been implicated in reward mechanisms in the brain. Dysfunction of the D-2 dopamine receptors leads to aberrant substance-seeking behaviors (ethanol, drugs, tobacco, and food) and other related behaviors (pathological gambling, Tourette's disorder, attention-deficit/hyperactivity disorder). This is the first study supporting a strong association between the dopamine D-2 receptor Tag A(1) allele with schizoid/avoidant behavior (SAB). Additionally, an albeit weaker association between the 480-bp VNTR 10/10 allele of the dopamine transporter (DAT(1)) gene with SAB was similarly found. C1 NYU,SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10010. CITY HOPE NATL MED CTR,DEPT MED GENET,DUARTE,CA 91010. KANTROLL INC,SAN ANTONIO,TX 78209. CHANG JUNG UNIV,TAINAN,TAIWAN. UTHSC,DEPT COMP RESOURCES,SAN ANTONIO,TX. UNIV N TEXAS,CTR HLTH SCI,DEPT PATHOL,DNA IDENT LAB,FT WORTH,TX 76107. COMPREHENS NEUROBEHAV SYST,AUSTIN,TX 78246. SAN MARCOS TREATMENT CTR,SAN MARCOS,TX 78667. HLTH RES INST,PFEIFFER TREATMENT CTR,NAPERVILLE,IL 60563. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. HLTH & MED RES FDN,SAN ANTONIO,TX 78209. RP Blum, K (reprint author), UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH HOUSTON,DEPT BEHAV SCI,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDA NIH HHS [R01-DA08417] NR 79 TC 75 Z9 79 U1 1 U2 5 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD MAY PY 1997 VL 2 IS 3 BP 239 EP 246 DI 10.1038/sj.mp.4000261 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA WY048 UT WOS:A1997WY04800013 PM 9152988 ER PT J AU Sikorski, R Peters, R AF Sikorski, R Peters, R TI World Wide Web sites in biotechnology SO NATURE BIOTECHNOLOGY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1087-0156 J9 NAT BIOTECHNOL JI Nat. Biotechnol. PD MAY PY 1997 VL 15 IS 5 BP 475 EP 475 PG 1 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA WX237 UT WOS:A1997WX23700035 PM 9131630 ER PT J AU Liaw, D Marsh, DJ Li, J Dahia, PLM Wang, SI Zheng, ZM Bose, S Call, KM Tsou, HC Peacocke, M Eng, C Parsons, R AF Liaw, D Marsh, DJ Li, J Dahia, PLM Wang, SI Zheng, ZM Bose, S Call, KM Tsou, HC Peacocke, M Eng, C Parsons, R TI Germline mutations of the PTEN gene in Cowden disease, an inherited breast and thyroid cancer syndrome SO NATURE GENETICS LA English DT Article ID LHERMITTE-DUCLOS DISEASE AB Cowden disease (CD) is an autosomal dominant cancer predisposition syndrome associated with an elevated risk for tumours of the breast, thyroid and skin(1-2). Lhermitte-Duclos disease (LDD) cosegregates with a subset of CD families and is associated with macrocephaly, ataxia and dysplastic cerebellar gangliocytomatosis(3-4). The common feature of these diseases is a predisposition to hamartomas, benign tumours containing differentiated but disorganized cells indigenous to the tissue of origin. Linkage analysis has determined that a single locus within chromosome 10q23 is likely to be responsible for both of these diseases(5). A candidate tumour suppressor gene (PTEN) within this region is mutated in sporadic brain, breast and prostate cancer(6). Another group has independently isolated the same gene, termed MMAC1, and also found somatic mutations throughout the gene in advanced sporadic cancers(7). Mutational analysis of PTEN in CD kindreds has identified germline mutations in four of five families, We found nonsense and missense mutations that are predicted to disrupt the protein tyrosine/dual-specificity phosphatase domain of this gene. Thus, PTEN appears to behave as a tumour suppressor gene in the germline. Our data also imply that PTEN may play a role in organizing the relationship of different cell types within an organ during development. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. COLUMBIA UNIV,COLL PHYS & SURG,DEPT PATHOL,NEW YORK,NY 10032. COLUMBIA UNIV,COLL PHYS & SURG,DEPT MED,NEW YORK,NY 10032. COLUMBIA UNIV,COLL PHYS & SURG,DEPT DERMATOL,NEW YORK,NY 10032. CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE CB2 2QQ,ENGLAND. GENOME THERAPEUT CORP,WALTHAM,MA. RI Marsh, Deborah/I-1491-2014; OI Marsh, Deborah/0000-0001-5899-4931; Eng, Charis/0000-0002-3693-5145 NR 16 TC 1309 Z9 1335 U1 7 U2 52 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD MAY PY 1997 VL 16 IS 1 BP 64 EP 67 DI 10.1038/ng0597-64 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA WX024 UT WOS:A1997WX02400023 PM 9140396 ER PT J AU Blumenthal, D Causino, N Campbell, EG AF Blumenthal, D Causino, N Campbell, EG TI Academic industry research relationships in genetics: A field apart SO NATURE GENETICS LA English DT Article AB Academic-industry research relationships (AIRRS) have become widely accepted and increasingly common in the life sciences. Using nationwide surveys from the United States, we found significant differences between the AIRRs of genetics firms and faculty and those of other firms and faculty, Significantly more genetics than nongenetics firms funded AIRRs, and genetics firms' AIRRs were larger and longer, Genetics faculty with AIRRs were significantly more likely than non-genetics faculty to report that patents, licenses, new companies and trade secrets had resulted from their university research; and that they had refused to share research results or biomaterials with colleagues. RP Blumenthal, D (reprint author), MASSACHUSETTS GEN HOSP,HLTH POLICY RES & DEV UNIT,50 STANIFORD ST,BOSTON,MA 02114, USA. FU NHGRI NIH HHS [HG00724-01] NR 6 TC 20 Z9 21 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 MAY PY 1997 VL 16 IS 1 BP 104 EP 108 DI 10.1038/ng0597-104 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA WX024 UT WOS:A1997WX02400032 PM 9140405 ER PT J AU Gong, JL Chen, DS Kashiwaba, M Kufe, D AF Gong, JL Chen, DS Kashiwaba, M Kufe, D TI Induction of antitumor activity by immunization with fusions of dendritic and carcinoma cells SO NATURE MEDICINE LA English DT Article ID CYTOTOXIC T-LYMPHOCYTES; COLONY-STIMULATING FACTOR; IN-VITRO; ANTIGEN; GENERATION; PEPTIDE AB Dendritic cells (DCs) are potent antigen-presenting cells that prime naive cytotoxic T-cells (CTLs)(1). In this study, we have fused DCs with MC38 carcinoma cells. The fusion cells were positive for major histocompatibility (MHC) class I and II, costimulating molecules and intercellular cell adhesion molecule-1 (ICAM-1). The results show that the fusion cells stimulate naive T cells in the primary mixed lymphocyte reaction (MLR) and induce MC38 tumor-specific CTLs in vivo. Antibody-mediated depletion experiments demonstrate that induction of CD4(+) and CD8(+) CTLs protects against challenge with tumor cells. We also show that immunization with the fusion cells induces rejection of established metastases. These findings represent the first demonstration that fusions of DCs and tumor cells can be used in the treatment of cancer. RP Gong, JL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 22 TC 489 Z9 517 U1 2 U2 10 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 MAY PY 1997 VL 3 IS 5 BP 558 EP 561 DI 10.1038/nm0597-558 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA WX543 UT WOS:A1997WX54300038 PM 9142127 ER PT J AU Pekary, AE Sattin, A Lloyd, RL AF Pekary, AE Sattin, A Lloyd, RL TI Electroconvulsive seizures increase levels of PS4, the TRH-enhancing peptide [prepro-TRH(160-169)], in rat brain SO NEUROENDOCRINOLOGY LA English DT Article DE seizures; thyrotropin-releasing hormone; thyrotropin-releasing hormone enhancing peptide; limbic system; swim test; stress ID THYROTROPIN-RELEASING-HORMONE; GENE-EXPRESSION; INHIBITING FACTOR; FUTURE-RESEARCH; PRECURSOR; PITUITARY; PREPRO-TRH-(160-169); HYPOTHALAMUS; SECRETION; BINDING AB We report the development of a radioimmunoassay for prepro-TRH(160-169) (PS4), a thyrotropin-releasing hormone (TRH) enhancing peptide, and its use in characterizing the effect of electroconvulsive seizures on the levels of this peptide in various brain regions of male Wistar rats. We found that electroconvulsive seizures significantly elevated the PS4 levels in hippocampus, amygdala, pyriform (olfactory) cortex, and anterior cortex but not in striatum, motor cortex, locus ceruleus, or ventral lateral medulla. The levels of PS4 were highly correlated with the corresponding TRH (p-Glu-His-Pro-NH2) and TRH-Gly (p-Glu-His-Pro-Gly) levels in hippocampus, amygdala, and pyriform cortex, consistent with the prepro-TRH source of all of these peptides. The PS4 levels in hippocampus and amygdala were significantly correlated with the immobility time in the Porsolt forced swim test, an established animal model for antidepressant effects. The PS4 levels in peripheral blood, hypothalamus, anterior cortex, amygdala, and eyes increased severalfold at 20 min following intracisternal injection of 228 mu g of this peptide, suggesting that it readily crosses the blood-brain barrier. The pituitary levels of PS4 and TRH-Gly, on the other hand, were decreased within 20 min by intracisternal PS4, suggesting PS4 stimulated the release of prepro-TRH peptides from the pituitary. Fresh rat and human serum rapidly degraded PS4, indicating that it may act primarily as a paracrine modulator of TRH effects in pituitary, brain, and reproductive system. C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. RP Pekary, AE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,11301 WILSHIRE BLVD,BLDG 114,RM 200,LOS ANGELES,CA 90073, USA. NR 44 TC 17 Z9 17 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD MAY PY 1997 VL 65 IS 5 BP 377 EP 384 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA WY144 UT WOS:A1997WY14400009 PM 9158070 ER PT J AU Ueki, K Ramaswamy, S Billings, SJ Mohrenweiser, HW Louis, DN AF Ueki, K Ramaswamy, S Billings, SJ Mohrenweiser, HW Louis, DN TI ANOVA, a putative astrocytic RNA-binding protein gene that maps to chromosome 19q13.3 SO NEUROGENETICS LA English DT Article DE chromosome 19; glioma; NOVA; RNA-binding ID TUMOR-SUPPRESSOR GENE; FRAGILE-X SYNDROME; EXON AMPLIFICATION; ANTI-RI; REGION; 19Q; IDENTIFICATION; ANTIBODIES; EXPRESSION; CLONING AB Exon amplification from cosmids mapping to the glioma tumor suppressor gene candidate region on chromosome 19q13.3 yielded an exon with high homology to a portion of the NOVA1 gene, which encodes a neuron-specific RNA-binding protein recognized by the paraneoplastic syndrome antibody anti-Ri. Screening of a human brain cDNA library with this exon identified a 1.9 kb cDNA with extensive homology to NOVA1, including three nearly identical KH domains characteristic of a subtype of RNA-binding proteins. Northern blots demonstrated expression of a 2.5 kb mRNA in brain, but in no other tissues. In situ hybridization on human cerebral cortex showed mRNA expression restricted to astrocytes. We have therefore named the gene ANOVA, for astrocytic NOVA1-like gene. Southern blotting and single strand conformation polymorphism analyses did not show tumor-specific alterations of this gene in gliomas and RT-PCR studies showed expression in glioma cell lines, suggesting that ANOVA is not the chromosome 19q glioma tumor suppressor gene. Given that two cloned paraneoplastic antigens are neuronal RNA-binding proteins and that glial proteins may act as paraneoplastic antigens, the ANOVA product may be a target antigen in one of the undefined human paraneoplastic syndromes. C1 Massachusetts Gen Hosp, Mol Neurooncol Lab, Dept Pathol Neuropathol & Neurosurg Serv, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. Univ Calif Lawrence Livermore Natl Lab, Ctr Human Genome, Livermore, CA 94550 USA. RP Louis, DN (reprint author), Massachusetts Gen Hosp, Mol Neurooncol Lab, Dept Pathol Neuropathol & Neurosurg Serv, Charlestown, MA 02129 USA. FU NCI NIH HHS [CA 69285] NR 28 TC 11 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 1364-6745 J9 NEUROGENETICS JI Neurogenetics PD MAY PY 1997 VL 1 IS 1 BP 31 EP 36 DI 10.1007/s100480050005 PG 6 WC Genetics & Heredity; Clinical Neurology SC Genetics & Heredity; Neurosciences & Neurology GA 135ZP UT WOS:000076833200006 PM 10735272 ER PT J AU Kaye, JA Swihart, T Howieson, D Dame, A Moore, MM Karnos, T Camicioli, R Ball, M Oken, B Sexton, G AF Kaye, JA Swihart, T Howieson, D Dame, A Moore, MM Karnos, T Camicioli, R Ball, M Oken, B Sexton, G TI Volume loss of the hippocampus and temporal lobe in healthy elderly persons destined to develop dementia SO NEUROLOGY LA English DT Article ID MINI-MENTAL-STATE; ALZHEIMERS-DISEASE; OLDEST-OLD; ATROPHY; POPULATION; DIAGNOSIS; AMYGDALA; MEMORY; SCALE; BRAIN AB Objective: To determine initial locus and rate of degeneration of temporal lobe structures (total lobe, hippocampus and parahippocampus) in preclinical dementia. Background: Postmortem studies suggest that the earliest changes in Alzheimer's disease are neurofibrillary tangle formation in hippocampus and adjacent cortex. MRI volume analysis of temporal lobe structures over time in subjects prior to developing dementia may allow the identification of when these processes begin, the rate they develop, and which areas are key to symptom development. Methods: 30 nondemented (NoD), healthy, elderly individuals enrolled in a prospective study of healthy aging evaluated annually over a mean of 42 months. Twelve subjects with subsequent cognitive decline were assigned to the preclinical dementia group (PreD). All 120 annual MRI studies analyzed by volumetric techniques assessed group differences in temporal lobe volumes and rates of brain loss. Results: NoD as well as PreD subjects had significant, time-dependent decreases in hippocampal and parahippocampal volume. Rates of volume loss between the groups did not significantly differ. PreD cases had significantly smaller hippocampi when asymptomatic. Parahippocampal volume did not differ between PreD and NoD cases. Significant time-dependent temporal lobe atrophy was present only in PreD. Conclusions: Hippocampal and parahippocampal atrophy occurs at a similar rate regardless of diagnostic group. Those who develop dementia may have smaller hippocampi to begin with, but become symptomatic because of accelerated loss of temporal lobe volume. Temporal lobe volume loss may mark the beginning of the disease process within six years prior to dementia onset. C1 OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT SURG & MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP Kaye, JA (reprint author), OREGON HLTH SCI UNIV,DEPT NEUROL,CDW2,3181 SAM JACKSON PK RD,PORTLAND,OR 97201, USA. OI Kaye, Jeffrey/0000-0002-9971-3478; Camicioli, Richard/0000-0003-2977-8660 FU NIA NIH HHS [AG08017] NR 47 TC 284 Z9 291 U1 2 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAY PY 1997 VL 48 IS 5 BP 1297 EP 1304 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA WZ778 UT WOS:A1997WZ77800027 PM 9153461 ER PT J AU Krings, T Buchbinder, BR Butler, WE Chiappa, KH Jiang, HJ Cosgrove, GR Rosen, BR AF Krings, T Buchbinder, BR Butler, WE Chiappa, KH Jiang, HJ Cosgrove, GR Rosen, BR TI Functional magnetic resonance imaging and transcranial magnetic stimulation: Complementary approaches in the evaluation of cortical motor function SO NEUROLOGY LA English DT Article ID CEREBRAL BLOOD-FLOW; HUMAN BRAIN ACTIVATION; HAND MUSCLES; EVOKED-POTENTIALS; NEURAL ACTIVITY; NITRIC-OXIDE; CORTEX; REORGANIZATION; RESPONSES; MRI AB Functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulation (TMS) represent different approaches to mapping the motor cortex. fMRI identifies areas of hemodynamic changes during task performance while TMS provides electrophysiologic data concerning the localization and density of cortical motoneurons. Here we define the spatial correlation between fMRI and TMS maps and compared them with direct electrical cortical stimulation (ECS). We performed fMRI at 1.5 T on 3 normal subjects and 2 patients with mass lesions near the central sulcus using a multislice, asymmetric, spin-echo, echo-planar pulse sequence during the performance of a motor task, We also performed focal TMS with surface EMG recordings from the muscles primarily involved in the fMRI task. We coregistered the stimulation sites in real time with the fMRI maps using a frameless stereotactic system. In both patients we also performed ECS of the cortex during surgery under local anesthesia. fMRI maps were validated by the electrophysiologic data both pre- and intraoperatively. Our results suggest that regions of fMRI activation correspond spatially to areas of highest motoneuron density as demonstrated by electrophysiologic techniques. C1 MASSACHUSETTS GEN HOSP, CLIN NEUROPHYSIOL LAB, NEUROL SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROSURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DIV NEURORADIOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, MGH NMR CTR, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 64 TC 106 Z9 107 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAY PY 1997 VL 48 IS 5 BP 1406 EP 1416 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA WZ778 UT WOS:A1997WZ77800048 PM 9153482 ER PT J AU Cummings, JL AF Cummings, JL TI The neuropsychiatric inventory: Assessing psychopathology in dementia patients SO NEUROLOGY LA English DT Article ID PROBABLE ALZHEIMERS-DISEASE; NURSING-HOME; PSYCHIATRIC-SYMPTOMS; EXTRAPYRAMIDAL SIGNS; DELUSIONS; PSYCHOSIS; SPECT; DEPRESSION; CAREGIVERS; PREDICTORS AB The Neuropsychiatric Inventory (NPI) was developed to assess psychopathology in dementia patients. It evaluates 12 neuropsychiatric disturbances common in dementia: delusions, hallucinations, agitation, dysphoria, anxiety, apathy, irritability, euphoria, disinhibition, aberrant motor behavior, night-time behavior disturbances, and appetite and eating abnormalities. The severity and frequency of each neuropsychiatric symptom are rated on the basis of scripted questions administered to the patient's caregiver. The NPI also assesses the amount of caregiver distress engendered by each of the neuropsychiatric disorders. A total NPI score and a total caregiver distress score are calculated, in addition to the scores for the individual symptom domains. Content validity, concurrent validity, inter-rater reliability, and test-retest reliability of the NPI are established. Different neurologic disorders have characteristic neuropsychiatric manifestations and distinctive NPI profiles. The NPI is sensitive to treatment effects and has demonstrated the amelioration of behavioral symptoms in Alzheimer's disease by cholinergic agents. The NPI is a useful instrument for characterizing the psychopathology of dementia syndromes, investigating the neurobiology of brain disorders with neuropsychiatric manifestations, distinguishing among different dementia syndromes, and assessing the efficacy of treatment. C1 UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90095. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,NEUROBEHAV & NEUROPSYCHIAT PROGRAM,LOS ANGELES,CA 90073. RP Cummings, JL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,710 WESTWOOD PLAZA,LOS ANGELES,CA 90095, USA. FU NIA NIH HHS [AG10123] NR 62 TC 536 Z9 553 U1 3 U2 27 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAY PY 1997 VL 48 IS 5 SU 6 BP S10 EP S16 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA XA096 UT WOS:A1997XA09600003 PM 9153155 ER PT J AU Hsueh, YP Kim, E Sheng, M AF Hsueh, YP Kim, E Sheng, M TI Disulfide-linked head-to-head multimerization in the mechanism of ion channel clustering by PSD-95 SO NEURON LA English DT Article ID TUMOR-SUPPRESSOR PROTEIN; GUANYLATE KINASES; K+ CHANNELS; SYNAPSES; HOMOLOG; SAP90 AB The PSD-95/SAP90 family of PDZ-containing proteins is directly involved in the clustering of specific ion channels at synapses. We report that channel clustering depends on a conserved N-terminal domain of PSD-95 that mediates multimerization and disulfide linkage of PSD-95 protomers. This N-terminal multimerization domain confers channel clustering activity on a single PDZ domain. Thus, channel clustering depends on aggregation of PDZ domains achieved by head-to-head multimerization of PSD-95, rather than by concatenation of PDZ domains in PSD-95 monomers. This mechanism predicts that PSD-95 can organize heterogeneous membrane protein clusters via differential binding specificities of its three PDZ domains. PSD-95 and its relative chapsyn-110 exist as disulfide-linked complexes in rat brain, consistent with head-to-head multimerization of these proteins in vivo. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROBIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Hsueh, YP (reprint author), MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114, USA. RI Kim, Eunjoon/C-1566-2011; OI Hsueh, Yi-Ping/0000-0002-0866-6275 NR 29 TC 165 Z9 166 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD MAY PY 1997 VL 18 IS 5 BP 803 EP 814 DI 10.1016/S0896-6273(00)80319-0 PG 12 WC Neurosciences SC Neurosciences & Neurology GA XB722 UT WOS:A1997XB72200013 PM 9182804 ER PT J AU Chauhan, N Siegel, G AF Chauhan, N Siegel, G TI Na,K-ATPase: Increases in alpha 1-messenger RNA and decreases in alpha 3-messenger RNA levels in aging rat cerebral cortex SO NEUROSCIENCE LA English DT Article DE in situ hybridization; gene expression; brain ID DIFFERENTIAL DISTRIBUTION; ALZHEIMERS-DISEASE; NERVOUS-SYSTEM; NA+,K+-ATPASE; ISOFORMS; BRAIN AB Age-related changes in the expression of Na,K-ATPase catalytic (alpha) subunit isoform messenger RNAs were investigated by in situ hybridization in frontal-parietal cortex of Fischer-344 male rats, It was found that the density of alpha 1-messenger RNA, present in glia and some neurons, increases dramatically in the neuropil of cortex and in the corpus callosum of the aged (24 months) as compared to young (three months) rats. In contrast, levels of alpha 3-messenger RNA, which is neuron-specific, decrease dramatically over the neurons of layers III and V and retrosplenial cortex in the aged as compared to the young animals, despite no changes in cellular density. The declines in the levels of neuron-specific alpha 3-messenger RNA may constitute a very early change in age-related differentiation of brain, These changes in Na,K-ATPase isoform expression may represent a candidate for an age-related factor predisposing to or potentiating certain neurodegenerative diseases. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MOL & CELLULAR NEUROSCI LAB,HINES,IL 60141. LOYOLA UNIV,DEPT NEUROL,MAYWOOD,IL 60153. LOYOLA UNIV,DEPT MOL & CELLULAR BIOCHEM,MAYWOOD,IL 60153. NR 15 TC 4 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD MAY PY 1997 VL 78 IS 1 BP 7 EP 11 PG 5 WC Neurosciences SC Neurosciences & Neurology GA WR750 UT WOS:A1997WR75000002 PM 9135086 ER PT J AU Markowitz, C Mann, FC Labow, BI Abcouwer, SF Souba, WW AF Markowitz, C Mann, FC Labow, BI Abcouwer, SF Souba, WW TI The role of the lung in the metabolism of fat - Is the lung an organ of nutrition and metabolism? SO NUTRITION LA English DT Article ID ARTERY ENDOTHELIAL-CELLS; GLUTAMINE-SYNTHETASE EXPRESSION; TRANSPORT; ENDOTOXIN; GLUCOCORTICOIDS C1 MASSACHUSETTS GEN HOSP,DEPT SURG,NUTR SUPPORT SERV,BOSTON,MA 02214. HARVARD UNIV,SCH MED,BOSTON,MA. RP Markowitz, C (reprint author), MASSACHUSETTS GEN HOSP,DIV SURG ONCOL,COX 626,100 BLOSSOM ST,BOSTON,MA 02214, USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0899-9007 J9 NUTRITION JI Nutrition PD MAY PY 1997 VL 13 IS 5 BP 492 EP 495 DI 10.1016/S0899-9007(97)84179-2 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA XJ082 UT WOS:A1997XJ08200025 PM 9225353 ER PT J AU Alpert, JE Fava, M AF Alpert, JE Fava, M TI Nutrition and depression: The role of folate SO NUTRITION REVIEWS LA English DT Review ID FOLIC-ACID DEFICIENCY; S-ADENOSYLMETHIONINE; CELL FOLATE; TETRAHYDROBIOPTERIN; ILLNESS; SERUM; METABOLISM; THERAPY; BRAIN; RAT AB A relationship between folate and neuropsychiatric disorders has been inferred from clinical observation and from the enhanced understanding of the role of folate in critical brain metabolic pathways. Depressive symptoms are the most common neuropsychiatric manifestation of folate deficiency. Conversely, borderline low or deficient serum or red blood cell folate levels have been defected in 15-38% of adults diagnosed with depressive disorders. Recently, low folate levels have been linked to poorer antidepressant response to selective serotonin reuptake inhibitors. Factors contributing to low serum folate levels among depressed patients as well as the circumstances under which folate and ifs derivatives may have a role in antidepressant pharmacotherapy must be further clarified. C1 MASSACHUSETTS GEN HOSP,DEPRESS CLIN & RES PROGRAM,BOSTON,MA 02114. RP Alpert, JE (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X NR 38 TC 95 Z9 98 U1 1 U2 7 PU INT LIFE SCIENCES INST PI LAWRENCE PA 810 EAST 10TH ST SUBSCRIPTION OFFICE, LAWRENCE, KS 66044 SN 0029-6643 J9 NUTR REV JI Nutr. Rev. PD MAY PY 1997 VL 55 IS 5 BP 145 EP 149 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA XG608 UT WOS:A1997XG60800001 PM 9212690 ER PT J AU HuberGieseke, T Pernin, A Huber, O Burger, AG Meier, CA AF HuberGieseke, T Pernin, A Huber, O Burger, AG Meier, CA TI Lack of loss of heterozygosity at the c-erbA beta locus in gastrointestinal tumors SO ONCOLOGY LA English DT Article DE thyroid hormone receptor; loss of heterozygosity; gastrointestinal tumors ID THYROID-HORMONE RECEPTOR; RENAL-CELL CARCINOMA; CHAIN-REACTION PCR; V-ERBA; LUNG-CANCER; SHORT ARM; CHROMOSOME 3P; GENE; DELETION; POLYMORPHISM AB The cellular homologues of the viral oncogene c-erbA encode for the nuclear thyroid hormone receptor c-erbA (TR). The gene for the human TR beta subtype is located on chromosome 3p24, and a loss of heterozygosity around this region has been reported in breast and small cell lung cancers. suggesting that TR beta might act as a tumor suppressor gene. In the present study, we used PCR-based restriction fragment length polymorphisms to examine the 3p24 region of 19 patients with gastrointestinal tumors for loss of heterozygosity (LOH). Interestingly, only 1 of the patients had an LOH at this locus, while 4 patients had a microdeletion of both alleles in the 3p24 region. These results suggest that, in contrast to previous reports on lung and breast cancers, a loss of heterozygosity of the TR locus at 3p24 is a rare event. A critical review of the literature, however, suggests, that some of the earlier studies have used markers whose location is only imprecisely mapped and may hence point to a tumor suppressor gene candidate other than TR beta. However, a selective microdeletion of both alleles was detected in the tumors of 4 of the 19 patients, indicating that this region on chromosome 3p may be genetically unstable in gastrointestinal tumors. C1 MASSACHUSETTS GEN HOSP,DIV ENDOCRINOL,THYROID UNIT,BOSTON,MA 02114. UNIV HOSP GENEVA,DEPT MED,MED CLIN 2,GENEVA,SWITZERLAND. UNIV HOSP GENEVA,DEPT ABDOMINAL SURG,GENEVA,SWITZERLAND. NR 42 TC 14 Z9 14 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0030-2414 J9 ONCOLOGY JI Oncology PD MAY-JUN PY 1997 VL 54 IS 3 BP 214 EP 219 PG 6 WC Oncology SC Oncology GA WV697 UT WOS:A1997WV69700007 PM 9143402 ER PT J AU Anderson, CA Wilkening, GN Filley, CM Reardon, MS Kleinschmidt-DeMasters, BK AF Anderson, CA Wilkening, GN Filley, CM Reardon, MS Kleinschmidt-DeMasters, BK TI Neurobehavioral outcome in pediatric craniopharyngioma SO PEDIATRIC NEUROSURGERY LA English DT Article DE neurobehavior; craniopharyngioma, pediatric; outcome, neurobehavioral ID CHILDHOOD CRANIOPHARYNGIOMA; SURGICAL-MANAGEMENT; RADIATION-THERAPY; CHILDREN; SURGERY; RADIOTHERAPY; RECURRENCE; SURVIVORS; SYMPTOMS; REMOVAL AB Neurobehavioral dysfunction occurs in children with craniopharyngioma, both before and after treatment, and its impact on outcome may not be fully appreciated. Also unclear is whether neurobehavioral outcome relates more to tumor location or surgical factors. We reviewed the records of 20 children with craniopharyngioma who were seen between 1983 and 1995. All children had subfrontal craniotomy and either partial (14 children) or gross total (6 children) resection of their tumors. In addition to traditional neuropsychological testing, we assessed social behavior and school performance using standardized ratings based on family interviews and school records. Over a mean follow-up period of 38 months, only 3 of 20 children had a good outcome in all three categories, and 12 of 20 had moderate or severe impairment in at least one category. Outcome did not differ between those who had partial and those with gross total resection. We conclude that neurobehavioral disorders are common and cause important morbidity in children after treatment for craniopharyngioma. To evaluate these impairments in future outcome studies, standard neuropsychological testing should be supplemented by specific behavioral assessments to capture the full range of neurobehavioral disability. In this series, partial versus gross total resection did not influence outcome, implying that tumor location in diencephalic and limbic regions is a more important factor. C1 Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Sch Med, Denver, CO 80262 USA. Childrens Hosp, Denver, CO 80218 USA. Denver Vet Affairs Med Ctr, Denver, CO USA. RP Anderson, CA (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Neurol, 4200 E 9th Ave, Denver, CO 80262 USA. NR 50 TC 39 Z9 39 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PD MAY PY 1997 VL 26 IS 5 BP 255 EP 260 PG 6 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA YP821 UT WOS:000071318500004 PM 9440495 ER PT J AU Neuhauser, TS Lancaster, K Haws, R Drehner, D Gulley, ML Lichy, JH Taubenberger, JK AF Neuhauser, TS Lancaster, K Haws, R Drehner, D Gulley, ML Lichy, JH Taubenberger, JK TI Rapidly progressive T cell lymphoma presenting as acute renal failure: Case report and review of the literature SO PEDIATRIC PATHOLOGY & LABORATORY MEDICINE LA English DT Article DE lymphoma; renal failure; T cell ID NON-HODGKINS-LYMPHOMA; MALIGNANT-LYMPHOMA; KIDNEY; INVOLVEMENT; CHILDREN; TUMOR AB We describe a case of peripheral T cell lymphoma that is remarkable fro its fulminate course and selective targeting of both kidneys. The patient was a 6-year-old girl who was in her usual state of good health until the onset of abdominal pain and fever. She was treated for acute oliguric renal failure and visual disturbances. A renal biopsy was performed. Biopsy findings were interpreted as suggestive of a vasculitic process, and treatment was initiated for a presumptive diagnosis of Wegener's granulomatosis. The patient died 3 days following admission, and autopsy revealed extensive bilateral kidney infiltration by a peripheral T cell lymphoma. The remainder of the body was spared with the exception of mild infiltration of the pulmonary parenchyma and choroid plexus by neoplastic lymphocytes. The neoplastic nature of the disease was confirmed utilizing immunoperoxidase stains and T cell receptor gene rearrangement. Primary renal lymphoma and renal failure attributable to involvement by lymphoma are rare findings that should be considered when other more common causes of renal insufficiency have been excluded. The presenting clinical complaints are generally of short duration, nonspecific, and atypical. Most patients exhibit oliguria. Physical examination may reveal hepatosplenomegaly, lymphadenopathy, and flank and/or abdominal mass(es). Laboratory findings frequently include an elevated serum creatinine, blood urea nitrogen, lactate dehydrogenase, and a mild proteinuria. Electrolyte abnormalities are variably present. Possible radiographic findings include hypodense or hypoechoic renal lesions and diffuse bilateral renal enlargement. Although the prognosis is dismal, survival may be prolonged utilizing current treatment modalities, and rare patients may be ''cured'' of disease. The clinical presentation, radiological findings, and prognosis of patients with clinically evident renal involvement by non-Hodgkin's lymphoma are discussed. C1 WILFORD HALL USAF MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78236. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. ARMED FORCES INST PATHOL,MOL DIAGNOST LAB,WASHINGTON,DC 20306. RP Neuhauser, TS (reprint author), WILFORD HALL USAF MED CTR,DEPT PATHOL,13754 MORNINGBLUFF DR,SAN ANTONIO,TX 78216, USA. NR 47 TC 16 Z9 16 U1 0 U2 3 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 1077-1042 J9 PEDIATR PATHOL LAB M JI Pediatr. Pathol. Lab. Med. PD MAY-JUN PY 1997 VL 17 IS 3 BP 449 EP 460 DI 10.1080/107710497174741 PG 12 WC Pathology; Pediatrics SC Pathology; Pediatrics GA XC161 UT WOS:A1997XC16100007 PM 9185223 ER PT J AU Keyes, LE Majack, R Dempsey, EC Moore, LG AF Keyes, LE Majack, R Dempsey, EC Moore, LG TI Pregnancy stimulation of DNA synthesis and uterine blood flow in the guinea pig SO PEDIATRIC RESEARCH LA English DT Article ID ESTROUS-CYCLE; ARTERIES AB Pregnancy stimulates DNA synthesis in uterine artery smooth muscle cells. Unknown is whether DNA synthesis increases in all layers of the vessel wall in uterine or nonuterine vessels, the distribution and time course of the proliferative response in relation to the rise in uterine blood flow, and the extent to which a pregnancy-induced rise in DNA synthesis can be mimicked by chronic estradiol treatment. To measure DNA synthesis, we implanted bromodeoxyuridine (BrdU, 400 mg) s.c. for 14-d periods in three nonpregnant, nine pregnant, three vehicle, and five estradiol (2.5 mg/14 d)-treated guinea pigs. Uterine blood flow was measured in four nonpregnant and 18 pregnant animals using radiolabeled microspheres. Pregnancy stimulated DNA synthesis in the adventitia, media, and intima of the uterine artery, radial artery (the vessels deriving from the main uterine artery and entering the uterine wall), and uterine vein but not in the aorta or mesenteric artery. Maximal uterine artery medial area and labeling indices in all layers of the uterine artery, uterine vein, and the radial artery adventitia were attained by mid-pregnancy (d 28-42 of the guinea pig's 63-day gestation), whereas DNA synthesis increased progressively until term in the radial artery media and intima. The greatest rise in uterine artery blood flow (y) occurred after peak proliferation in the uterine artery and in concert with radial artery medial and intimal proliferation (y = 1.99.10(0.023x) where x is day postconception). (17)beta-Estradiol treatment for 14 d in ovariectomized guinea pigs increased DNA synthesis in the radial artery adventitia and tended (p = 0.08) to increase labeling indices in the media of all vessels examined but did not fully reproduce the effects of pregnancy. We concluded that pregnancy-related, possibly hormonal stimuli prompted growth in all layers of the uterine artery wall by mid-pregnancy and served to initiate a rise in uterine blood flow. The resultant increase in flow and shear stress likely stimulated DNA synthesis in the radial artery which helped sustain the rise in flow near term. C1 UNIV COLORADO,HLTH SCI CTR,CVP RES LAB,DENVER,CO 80262. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. UNIV COLORADO,HLTH SCI CTR,WOMENS HLTH RES CTR,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PEDIAT,DENVER,CO 80262. DENVER VA MED CTR,RESP CARE SECT,DENVER,CO 80220. UNIV COLORADO,DEPT ANTHROPOL,DENVER,CO 80217. FU NHLBI NIH HHS [HL 14985] NR 24 TC 21 Z9 21 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD MAY PY 1997 VL 41 IS 5 BP 708 EP 715 DI 10.1203/00006450-199705000-00017 PG 8 WC Pediatrics SC Pediatrics GA WV663 UT WOS:A1997WV66300017 PM 9128295 ER PT J AU Stark, LJ Mulvihill, MM Jelalian, E Bowen, AM Powers, SW Tao, SJ Creveling, S Passero, MA Harwood, I Light, M Lapey, A Hovell, MF AF Stark, LJ Mulvihill, MM Jelalian, E Bowen, AM Powers, SW Tao, SJ Creveling, S Passero, MA Harwood, I Light, M Lapey, A Hovell, MF TI Descriptive analysis of eating behavior in school-age children with cystic fibrosis and healthy control children SO PEDIATRICS LA English DT Article DE cystic fibrosis; oral intake; behavior; eating ID INCREASING CALORIE CONSUMPTION; NUTRITIONAL SUPPLEMENTATION; PARENTERAL-NUTRITION; BODY-COMPOSITION; GROWTH; REHABILITATION; EXPENDITURE; DISEASE; ENERGY; OBESE AB Study Objective. To investigate calorie intake, behavioral eating styles, and parent perception of eating behavior of school-age children with cystic fibrosis (CF) compared with healthy peers. Design. A two-group comparison study. Setting. A clinical sample of 28 school-age children with CF and a community sample of 28 healthy peers matched for age (6 to 12 years) and socioeconomic status. Measurements and Main Results. The children with CF consumed more calories per day (2175 cal/d) than the control children (1875 cal/d) and achieved a significantly higher recommended daily allowance (RDA) of energy (128% of the RDA) than the control children (91.61% of the RDA). Fifty-four percent of the CF sample were achieving the CF dietary recommendations of 120% of the RDA. Despite this energy intake, the CF sample was significantly below the control sample on weight (24.56 vs 31.23 kg), height (125.48 vs 133.06 cm), and z score for weight (-0.811 vs 0.528) and height (-0.797 vs 0.371). On measures of behavioral eating style, the CF sample had significantly longer meals (23.90 min) than the control sample (17.34 min) and had a significantly slower pace of eating (43.27% 10-second intervals with bites) than the control sample (51.29% 10-second intervals with bites) but did not differ significantly on the number of calories consumed during dinner. On a measure of parent report of mealtime behaviors, parents of the children with CF rated mealtime behavior problems of ''dawdles'' and ''refuses food'' as more intense (mean, 3.46) than did the parents of control children (mean, 2.67). For the CF sample, a significant correlation was found between the parent intensity ratings of problem behavior in general and meal duration (r = .48), and a significant negative correlation was found between the parent intensity ratings of problem mealtime behaviors and the percentage of intervals with bites (pace of meal) (r = -.533). Conclusions. Although the school-age children with CF were consuming more calories per day than their healthy peers, and more than 50% of the children in the CF sample were at or above the CF dietary recommendations, the children in the CF sample were significantly below the control children on measures of weight and height. The behavioral data suggest that increased caloric intake is not without cost, because the CF sample spent an additional 7 minutes per day at dinner and ate their meals at a slower pace than their healthy peers. These data were associated with higher intensity ratings of mealtime behaviors by parents of children with CF. These findings point to the need for individualized assessment of energy needs for school-age children with CF and comprehensive programs that teach parents behavioral strategies to motivate their children to meet these higher energy requirements in an adaptive manner. C1 BROWN UNIV,RHODE ISL HOSP,SCH MED,DEPT PEDIAT,PROVIDENCE,RI 02903. UNIV CALIF SAN DIEGO,MED CTR,DEPT PEDIAT,SAN DIEGO,CA 92103. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SAN DIEGO STATE UNIV,GRAD SCH PUBL HLTH,SAN DIEGO,CA 92182. RP Stark, LJ (reprint author), BROWN UNIV,RHODE ISL HOSP,SCH MED,DEPT PSYCHIAT & HUMAN BEHAV,593 EDDY ST,PROVIDENCE,RI 02903, USA. NR 35 TC 43 Z9 44 U1 0 U2 2 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1997 VL 99 IS 5 BP 665 EP 671 PG 7 WC Pediatrics SC Pediatrics GA WX728 UT WOS:A1997WX72800003 PM 9113942 ER PT J AU GillBody, KM Popat, RA Parker, SW Krebs, DE AF GillBody, KM Popat, RA Parker, SW Krebs, DE TI Rehabilitation of balance in two patients with cerebellar dysfunction SO PHYSICAL THERAPY LA English DT Article DE balance; balance rehabilitation; cerebellar rehabilitation; postural control ID ATAXIA; DEGENERATION AB The treatment of two patients with cerebellar disfunction is described. One patient was a 36-year-old woman with a 7-month history of dizziness and unsteadiness following surgical resection of a recurrent pilocystic astrocytoma located in the cerebellar vermis. The other patient was a 48-year-old man with cerebrotendinous xanthamatosis (CTX) and diffuse cerebellar atrophy, and a 10-year history of progressive gait and balance difficulties. Each patient was treated with a 6-week course of physical therapy that emphasized the practice of activities that challenged stability. The patient with the cerebellar tumor resection also performed eve-head coordination exercises. Each patient had weekly therapy and performed selected balance retraining exercises oil a daily basis at home. Measurements taken before and after treatment for each patient included self-perception of symptoms, clinical balance tests, and stability during selected standing and gait activities; for the patient with the cerebellar tumor resection, vestibular function tests and posturography were also performed. Both patients reported improvements in symptoms and demonstrated similar improvements on several kinematic indicators of stability during gait. The patient with the cerebellar tumor resection improved on posturography following treatment, whereas the patient with CTS improved on clinical balance tests. This case report describes two individualized treatment programs and documents functional improvements in two patients with different etiologies, durations, and clinical presentations of cerebellar dysfunction. The outcomes suggest that patients with cerebellar lesions, acute or chronic, may be able to learn to improve their postural stability. C1 MASSACHUSETTS GEN HOSP, PHYS THERAPY SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, BIOMOT LAB, BOSTON, MA 02114 USA. MIT, CAMBRIDGE, MA 02139 USA. RP GillBody, KM (reprint author), MASSACHUSETTS GEN HOSP, INST HLTH PROFESS, GRAD PROGRAMS PHYS THERAPY, 101 MERRIMAC ST, BOSTON, MA 02114 USA. FU NIA NIH HHS [R01AG11255]; PHS HHS [H133G60045] NR 41 TC 44 Z9 46 U1 3 U2 8 PU AMER PHYSICAL THERAPY ASSOC PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD MAY PY 1997 VL 77 IS 5 BP 534 EP 552 PG 19 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA WY502 UT WOS:A1997WY50200008 PM 9149763 ER PT J AU Ahn, DK Sims, CD Randolph, MA OConnor, D Butler, PEM Amarante, MTJ Yaremchuk, MJ AF Ahn, DK Sims, CD Randolph, MA OConnor, D Butler, PEM Amarante, MTJ Yaremchuk, MJ TI Craniofacial skeletal fixation using biodegradable plates and cyanoacrylate glue SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article; Proceedings Paper CT Symposium on Resolving Controversies in Craniomaxillofacial Surgery: Symposium for Clinicians and Investigators of the American-Society-of-Maxillofacial Surgeons CY SEP 23, 1994 CL SAN DIEGO, CA SP Amer Soc Maxillofacial Surgeons ID MANDIBULAR FRACTURES; CELL-CULTURES; BONE; SURGERY; GROWTH; SCREWS; ASSAY AB This study examined the feasibility of fixation of craniofacial bone using Lactosorb biodegradable plates adhered to bone with butyl-2-cyanoacrylate adhesive (Histoacryl) in a pig. The stability and bone-healing characteristics of this rigid fixation method were studied and compared with standard rigid fixation using metal plates and screws on osteotomy sites in the frontal bones and infraorbital rims. Rectangular osteotomies (2.0 x 3.0 cm) were per formed on the right and left sides of the frontal bone and wedge-shaped osteotomies (1.5 x 1.7 cm) were made on the left and right infraorbital rims in seven Yorkshire pigs. Metal plates were applied with screws to the osteotomies on one side, and the other side was fixed with a biodegradable plate and butyl-2-cyanoacrylate. The animals were sacrificed at 8 weeks, and both sides were compared biomechanically and histologically. Radiographic, biomechanical, and histologic analyses were performed to evaluate skeletal stability, contour, accurate positioning of bon) fragments, bone healing, and maximum torque to failure of the repair sites. Clinical and radiographic observations demonstrated stability of the bone fragments without any evidence of displacement. According to Student's t test for paired data, no statistical difference was found in the maximum torque to failure of fragments fixed with biodegradable plates and glue compared with those fixed with metal plates and screws (P > 0.05), whether or not a gap existed at the osteosynthesis site. Although the sample size was small, no differences were noted between the two types of treatment groups. This study, demonstrates that rigid internal fixation of osteotomized cranial bone fragments using biodegradable plates and butyl-2-cyanoacrylate is as effective as metal plate and screw fixation in this animal model. C1 MASSACHUSETTS GEN HOSP,DIV PLAST SURG ACC 4,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 37 TC 36 Z9 37 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD MAY PY 1997 VL 99 IS 6 BP 1508 EP 1515 DI 10.1097/00006534-199705000-00005 PG 8 WC Surgery SC Surgery GA WW902 UT WOS:A1997WW90200005 PM 9145117 ER PT J AU Bergeron, B AF Bergeron, B TI Agents for change SO POSTGRADUATE MEDICINE LA English DT Article C1 MIT,BOSTON,MA. RP Bergeron, B (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD MAY PY 1997 VL 101 IS 5 BP A20 EP A20 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA WY649 UT WOS:A1997WY64900024 ER PT J AU Glazer, WM AF Glazer, WM TI Diagnosis and treatment of chronic depression - Kocsis,JH, Klein,DN SO PSYCHIATRIC SERVICES LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Glazer, WM (reprint author), HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138, 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 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD MAY PY 1997 VL 48 IS 5 BP 720 EP 721 PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA WY168 UT WOS:A1997WY16800033 ER PT J AU Alpert, JE Uebelacker, LA McLean, NE Nierenberg, AA Pava, JA Worthington, JJ Tedlow, JR Rosenbaum, JF Fava, M AF Alpert, JE Uebelacker, LA McLean, NE Nierenberg, AA Pava, JA Worthington, JJ Tedlow, JR Rosenbaum, JF Fava, M TI Social phobia, avoidant personality disorder and atypical depression: Co-occurrence and clinical implications SO PSYCHOLOGICAL MEDICINE LA English DT Article; Proceedings Paper CT 149th Annual Meeting of the American-Psychiatric-Association CY MAY 04-09, 1996 CL NEW YORK, NY SP Amer Psychiat Assoc ID MAJOR DEPRESSION; ANXIETY DISORDERS; COMORBIDITY; PREVALENCE; DYSTHYMIA; SUBTYPES; OUTPATIENTS; VALIDITY AB Background. Increasing attention has been directed in recent years to the detection and treatment of psychiatric co-morbidity among depressed individuals. The overlap of social phobia (SP) and avoidant personality disorder (APD) has been well recognized and a relationship between these disorders and depression has been suggested. Methods. The pattern and clinical implications of co-morbidity of SP and APD with major depressive disorder (MDD), diagnosed by DSM-III-R criteria, were studied among 243 out-patients presenting with depression. Results. Overall, 26.7% of adults in our sample with MDD met criteria for SP and 28.4% for APD. Almost two-thirds of depressed adults meeting criteria for social phobia or avoidant personality disorder met criteria for both (SP+APD). Depressed adults who met criteria for both SP+APD exhibited a significantly higher proportion of atypical depression (54.8%) compared with those with neither SP nor APD (31.1%). Among depressed patients, the co-occurrence of SP with APD was also associated with an earlier age of onset of MDD, a greater number of comorbid Axis I diagnoses, and greater impairment of social adjustment and assertiveness. Conclusions. Results confirm the overlap of SP and APD in a depressed population and the high prevalence of these disorders in MDD. They suggest that depressed individuals with both SP and APD but not SP alone are at particularly high risk for atypical depression and for social dysfunction in excess of that caused by a current major depression. RP Alpert, JE (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS CLIN & RES PROGRAM,WACC 815,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [R01 MH 48483-01] NR 32 TC 79 Z9 81 U1 2 U2 9 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD MAY PY 1997 VL 27 IS 3 BP 627 EP 633 DI 10.1017/S0033291797004765 PG 7 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA XD047 UT WOS:A1997XD04700014 PM 9153683 ER PT J AU Greenberg, DB AF Greenberg, DB TI Neuropsychiatry - Fogel,BS, Schiffer,RB, Rao,SM SO PSYCHOSOMATICS LA English DT Book Review RP Greenberg, DB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,AVERY D WEISMAN PSYCHIAT CONSULTAT SERV,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 MAY-JUN PY 1997 VL 38 IS 3 BP 295 EP 296 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA WW177 UT WOS:A1997WW17700011 ER PT J AU Viguera, AC AF Viguera, AC TI Theoretical approaches to obsessive-compulsive disorder - Jakes,I SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Viguera, AC (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, 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 MAY-JUN PY 1997 VL 38 IS 3 BP 298 EP 298 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA WW177 UT WOS:A1997WW17700013 ER PT J AU Pogue, BW Hasan, T AF Pogue, BW Hasan, T TI A theoretical study of light fractionation and dose-rate effects in photodynamic therapy SO RADIATION RESEARCH LA English DT Article ID MULTICELL TUMOR SPHEROIDS; MURINE TUMOR; MOUSE-TUMORS; BLOOD-FLOW; OXYGEN-TENSION; FLUENCE RATE; BPD-MA; MODEL; MESOTHELIOMA; DESTRUCTION AB The efficacy of photodynamic therapy is dependent upon the optical dose rate or upon the fractionation schedule of the light, These effects are thought to be limited by the time required for oxygen diffusion from the capillaries, since this therapy can consume oxygen faster than it can be supplied to tissues distant from the blood vessels, Oxygen diffusion and consumption by metabolic and photochemical mechanisms have been modeled here to compare theoretical predictions with experimental results of varying light fractionations and delivered dose rates, The mathematics of the problem have been described in the literature, and the present study extends these calculations to allow a more direct and quantitative comparison with fractionation experiments, using both analytical and numerical arguments, The optimum fraction time was found to depend only on the intercapillary spacing and not on the intensity of irradiation or the concentration of photosensitizer, The calculations indicate that experimentally observed optimum fractionation times of 30 and 60 s correspond to a distance from capillary to cell of approximately 1 mm, These results suggest that the fractionated light irradiation experiments need careful interpretation, and some possible reasons for longer optimum fractionation times are discussed, (C) 1997 by Radiation Research Society. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 36 TC 47 Z9 47 U1 0 U2 7 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD MAY PY 1997 VL 147 IS 5 BP 551 EP 559 DI 10.2307/3579621 PG 9 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA WY053 UT WOS:A1997WY05300004 PM 9146700 ER PT J AU Ontell, FK Moore, EH Shepard, JO Shelton, DK AF Ontell, FK Moore, EH Shepard, JO Shelton, DK TI The costal cartilages in health and disease SO RADIOGRAPHICS LA English DT Article DE cartilage; thorax, calcification; thorax, diseases; thorax, neoplasms AB The costal margin, although imaged in many routine radiologic examinations, has been ignored in the radiology literature, Calcification of the costal cartilages follows gender-related patterns and is generally not evident radiographically until after the age of 30 years, Diffuse enlargement of the costochondral junctions may alert the astute observer to the presence of systemic diseases such as acromegaly and rickets, Focal masses have a subtle appearance on plain radiographs and may be better imaged with computed tomography (CT) or magnetic resonance imaging, Chondrosarcoma of the costal margin typically appears as an expansile mass with coarse calcifications and an associated soft-tissue mass, Radiographic and CT features of costochondritis include chondral enlargement or destruction, low-attenuation cartilage at CT, associated soft-tissue swelling, and localized peripheral cartilage calcification, There appears to be an association between heavy premature costal cartilage calcification and certain systemic conditions, such as malignancy, autoimmune disorders, chronic renal failure, and thyroid disease, particularly Graves disease. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP Ontell, FK (reprint author), UNIV CALIF DAVIS,MED CTR,DEPT RADIOL,TICON 2 BLDG,RM 216,2516 STOCKTON BLVD,SACRAMENTO,CA 95817, USA. NR 8 TC 21 Z9 25 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD MAY-JUN PY 1997 VL 17 IS 3 BP 571 EP 577 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WY172 UT WOS:A1997WY17200005 PM 9153697 ER PT J AU Slanetz, PJ Moore, RH Hulka, CA Halpern, EF Habunek, DA Whitman, GJ McCarthy, KA Hall, DA Kopans, DB AF Slanetz, PJ Moore, RH Hulka, CA Halpern, EF Habunek, DA Whitman, GJ McCarthy, KA Hall, DA Kopans, DB TI Screening mammography: Effect of national guidelines on current physician practice SO RADIOLOGY LA English DT Article DE breast neoplasms, radiography; breast radiography, utilization; cancer screening; radiology and radiologists, socioeconomic issues ID BREAST AB PURPOSE: To evaluate the effect of natural breast cancer screening guidelines on current physician attitudes toward and practice of screening mammography. MATERIALS AND METHODS: Questionnaire responses from 278 physicians were analyzed. The questionnaire had four sections: general information on physician practice and experience, current use of breast cancer screening, perceptions of screening mammography, and physician awareness of and response to the controversy in breast cancer screening. RESULTS: In women aged 40-49 years, 144 (52%) of 278 physicians performed annual clinical breast examination and screening mammography every 2 years; 57 (21%) favored annual mammography and clinical breast examination. In women aged 50 years and older, 232 (83%) physicians screened patients annually with clinical breast examination and mammography. Two hundred seventeen (78%) physicians were aware of the recommended changes in screening guidelines; 54 (19%) were not aware of the changes. Of those aware of the changes, 56 (26%) changed to the new guidelines, 150 (69%) did not change, and six (3%) modified their practice somewhat. CONCLUSION: Physician practice as regards screening mammography is influenced by national guidelines. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,DIV BREAST IMAGING,BOSTON,MA 02114. OI Slanetz, Priscilla/0000-0003-1248-5116 NR 6 TC 12 Z9 12 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAY PY 1997 VL 203 IS 2 BP 335 EP 338 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WU532 UT WOS:A1997WU53200013 PM 9114084 ER PT J AU Ryan, JM Hahn, PF Boland, GW McDowell, RK Saini, S Mueller, PR AF Ryan, JM Hahn, PF Boland, GW McDowell, RK Saini, S Mueller, PR TI Percutaneous gastrostomy with T-fastener gastropexy: Results of 316 consecutive procedures SO RADIOLOGY LA English DT Article DE gastrojejunostomy; gastrostomy; stomach, interventional procedure ID FEEDING GASTROSTOMY; EXPERIENCE; GASTROJEJUNOSTOMY; GASTROENTEROSTOMY; COMPLICATIONS AB PURPOSE: To assess the rates of technical success and complications associated with radiologic gastrostomy or gastrojejunostomy performed with T-fastener gastropexy. MATERIALS AND METHODS: In 316 consecutive patients, radiologic gastrostomy or gastrojejunostomy with T-fastener gastropexy was performed over a 10-year period. Results of the procedures were reviewed. Results of follow-up were available for all patients. RESULTS: Of 316 procedures, 314 were successful (technical success rate, 99.4%). Six (1.9%) major complications occurred; 50% occurred in patients with peritoneal involvement from ovarian carcinoma. Ten (3.2%) minor complications occurred, Four minor complications occurred in patients with ovarian cancer and ascites, The 30-day mortality rate was 3.8% (12 patients) with one procedure-related death (0.3%). CONCLUSION: A T-fastener gastropexy may have a protective role in prevention of leakage of gastric contents into the peritoneum in patients with ascites. Ascites need no longer be considered a contraindication for radiologic gastrostomy. A gastropexy enables routine use of larger gastrostomy tubes and ready replacement of a displaced tube even before the development of a mature tract. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV ABDOMINAL IMAGING & INTERVENT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 15 TC 60 Z9 60 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 MAY PY 1997 VL 203 IS 2 BP 496 EP 500 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WU532 UT WOS:A1997WU53200040 PM 9114111 ER PT J AU Amin, MB Young, RH AF Amin, MB Young, RH TI Intraepithelial lesions of the urinary bladder with a discussion of the histogenesis of urothelial neoplasia SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Article DE urinary bladder; neoplasms; transitional cell carcinoma; papillary transitional cell carcinoma; papilloma; papillary hyperplasia; inverted papilloma; urothelial dysplasia; atypical hyperplasia; atypia; carcinoma in situ ID TRANSITIONAL CELL-CARCINOMA; INVERTED PAPILLOMA; INTESTINAL METAPLASIA; IN-SITU; DYSPLASIA; CANCER; TRACT; ADENOCARCINOMA; VARIANT; BENIGN AB Bladder neoplasia of the transitional cell type progresses by two distinct, but occasionally interrelated, pathways characterized morphologically by a papillary or nonpapillary configuration. In this review, the authors discuss intraepithelial lesions of the urinary bladder, ie, those lesions confined within the basement membrane of the urothelium. The emphasis is on histogenesis of bladder neoplasia, its putative precursor lesions, and its noninvasive forms. Areas of controversies are highlighted, and the pertinent clinical features, histological findings, and biological potential of these lesions examined. Copyright (C) 1997 by W.B. Saunders Company. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP Amin, MB (reprint author), HENRY FORD HOSP,DEPT PATHOL,2799 W GRAND BLVD,DETROIT,MI 48202, USA. NR 56 TC 38 Z9 38 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD MAY PY 1997 VL 14 IS 2 BP 84 EP 97 PG 14 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA XK974 UT WOS:A1997XK97400002 PM 9179970 ER PT J AU Eble, JN Young, RH AF Eble, JN Young, RH TI Carcinoma of the urinary bladder: A review of its diverse morphology SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Review DE urinary bladder; carcinoma; urothelium; adenocarcinoma; squamous cell carcinoma; sarcomatoid carcinoma ID TRANSITIONAL-CELL-CARCINOMA; HUMAN CHORIONIC-GONADOTROPIN; MALIGNANT FIBROUS HISTIOCYTOMA; PRIMARY ADENOCARCINOMA; VERRUCOUS CARCINOMA; UNDIFFERENTIATED CARCINOMA; INTESTINAL METAPLASIA; VILLOUS ADENOMA; RHABDOID TUMOR; BONE-FORMATION AB The microscopic appearances of carcinomas of the urinary bladder are reviewed, with emphasis on patterns that have been highlighted only recently or account for major problems in differential diagnosis. Approximately 90% of bladder cancers are of urothelial (transitional cell) type. The major new information pertaining to that category is the appreciation of the extent to which they may have unusual patterns that, on occasion, lead to their misinterpretation as benign. The homology between some of these variants and benign epithelial abnormalities is emphasized and helps in understanding them: nested carcinomas and von Brunn's nests, small tubules and nephrogenic adenoma, carcinomatous glands and cystitis glandularis, cystic carcinomas and cystitis cystica. Other peculiar patterns seen in urothelial carcinoma include slit-like spaces, clefts, and angulated nests with spikes. Differences in opinion have been apparent in recent contributions concerning carcinomas of the bladder with a prominent component of spindle cells (sarcomatoid carcinomas) and whether they represent a category distinct from carcinosarcoma. Irrespective of this academic distinction, the potential for some epithelial-derived tumors of the bladder to be dominated by or even have an exclusive component of spindle cells is important. Three other major categories of primary bladder cancer are squamous cell carcinoma, adenocarcinoma, and undifferentiated carcinoma. The differences in the frequency of subtypes of adenocarcinoma originating in the bladder mucosa and urachus has recently been emphasized, as has the spectrum of undifferentiated carcinomas. In some bladder cancers, the stroma has unusual features. These are carcinomas with pseudosarcomatous stroma, osseous or cartilaginous metaplasia, or osteoclast-type giant cells. The diversity of appearances of bladder cancer has important implications in differential diagnosis. Copyright (C) 1997 by W.B. Saunders Company. C1 INDIANA UNIV,SCH MED,DEPT PATHOL,INDIANAPOLIS,IN 46202. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RP Eble, JN (reprint author), RICHARD L ROUDEBUSH VET ADM MED CTR,1481 W 10TH ST,INDIANAPOLIS,IN 46202, USA. NR 108 TC 64 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 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD MAY PY 1997 VL 14 IS 2 BP 98 EP 108 PG 11 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA XK974 UT WOS:A1997XK97400003 PM 9179971 ER PT J AU Young, RH AF Young, RH TI Pseudoneoplastic lesions of the urinary bladder and urethra: A selective review with emphasis on recent information SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Article DE urinary bladder; urethra; pseudotumor; cystitis glandularis; mucin extravasation; nephrogenic adenoma; papillary-polypoid cystitis; endosalpingiosis; endocervicosis; mullerianosis; inflammatory pseudotumor; urethral caruncle; papillary-polypoid urethritis; prostatic-type polyp; transitional cell hyperplasia ID CLEAR-CELL ADENOCARCINOMA; PSEUDOSARCOMATOUS FIBROMYXOID TUMOR; METAPLASIA NEPHROGENIC ADENOMA; PROSTATIC URETHRA; INFLAMMATORY PSEUDOTUMOR; POLYPOID CYSTITIS; INTESTINAL METAPLASIA; MYOFIBROBLASTIC TUMOR; FEMALE URETHRA; BRUNNS NESTS AB Selected tumor-like lesions of the urinary bladder and urethra, particularly those that have been the subject of recent attention in the literature, are reviewed. Within the category of epithelial abnormalities, it has recently been appreciated that cystitis glandularis of the intestinal ?rpe is occasionally associated with prominent mucin extravasation into the stroma, a finding that should not lead to the misdiagnosis of adenocarcinoma. Additionally, the problems that nephrogenic adenoma may cause have been the subject of recent study, and a detailed microscopic analysis of this lesion has shed light on the relative frequency of its common, and uncommon, features. Within the category of tumor-like lesions of the bladder, the inflammatory pseudotumor has been the subject of much interest as have mullerian lesions. It has recently been appreciated that endosalpingiosis is rarely seen at this site, usually in association with endocervicosis or endometriosis, leading to the suggested usage of the designation ''mullerianosis.'' Selected other tumor-like lesions of the urinary bladder and urethra are also reviewed, including the problems nephrogenic adenoma may cause when it involves the prostatic urethra in men or a urethral diverticulum in females as well as the peculiar stromal cells that have recently been described within some urethral caruncles. Copyright (C) 1997 by W.B. Saunders Company. RP Young, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 83 TC 40 Z9 42 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD MAY PY 1997 VL 14 IS 2 BP 133 EP 146 PG 14 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA XK974 UT WOS:A1997XK97400006 PM 9179974 ER PT J AU Amin, MB Young, RH AF Amin, MB Young, RH TI Primary carcinomas of the urethra SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Article DE urethra; carcinoma; adenocarcinoma; squamous cell carcinoma; transitional cell carcinoma; clear cell carcinoma ID CLEAR-CELL ADENOCARCINOMA; PROSTATE-SPECIFIC ANTIGEN; FEMALE URETHRA; PAPILLARY ADENOCARCINOMA; ACID-PHOSPHATASE; GLANDS; ORIGIN; APPEARANCE; FEATURES; WOMEN AB Urethral carcinomas are rare, and information reported in the literature is relatively limited. In this review, the authors present separate discussions on the pathology of carcinomas occurring in men and women with emphasis on the diverse histological subtypes. Because tumor type and prognosis correspond to anatomic location, normal anatomy and histology have been given due consideration. Of particular note in the recent literature is an expanded experience with clear cell carcinoma, a distinctive tumor primarily of the female urethra that has generated considerable interest with respect to its prognosis and relationship to urethral diverticulum. The authors use this review to illustrate several features of the pathology of these neoplasms synthesize the literature, and place into perspective the clinical, pathological, and prognostic features. Copyright (C) 1997 by W.B. Saunders Company. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP Amin, MB (reprint author), HENRY FORD HOSP,DEPT PATHOL,2799 W GRAND BLVD,DETROIT,MI 48202, USA. NR 55 TC 28 Z9 29 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD MAY PY 1997 VL 14 IS 2 BP 147 EP 160 PG 14 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA XK974 UT WOS:A1997XK97400007 PM 9179975 ER PT J AU Lukaszewicz, GC Souba, WW Abcouwer, SF AF Lukaszewicz, GC Souba, WW Abcouwer, SF TI Induction of muscle glutamine synthetase gene expression during endotoxemia is adrenal gland dependent SO SHOCK LA English DT Article ID AMINO-ACID METABOLISM; TUMOR-NECROSIS-FACTOR; SKELETAL-MUSCLE; MEDIATED INDUCTION; TREATED RATS; LIPOPOLYSACCHARIDE; GLUCOCORTICOIDS; CELLS; INTERLEUKIN-1 AB Skeletal muscle plays a crucial role in maintaining nitrogen homeostasis during health and critical illness by exporting glutamine, the most abundant amino acid in the blood. We hypothesized that induction of glutamine synthetase (GS) expression, the principal enzyme of de novo glutamine biosynthesis, in skeletal muscle after endotoxin administration was adrenal gland dependent. We studied the expression of GS in normal and adrenalectomized rats after intraperitoneal administration of Escherichia coli lipopolysaccharide (LPS). Treatment of normal rats with LPS resulted in a marked increase in GS mRNA that was dose and time dependent, and preceded the increase in GS protein and specific activity. The increase in muscle GS mRNA observed in normal rats in response to LPS was abrogated in adrenalectomized rats at 3 h after high dose LPS treatment and markedly attenuated at 5.5 h after low dose LPS treatment. These and other studies implicate glucocorticoid hormones as a key, but not exclusive, regulator of skeletal muscle GS expression after a catabolic insult. C1 HARVARD UNIV,SCH MED,DIV SURG ONCOL,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OI Abcouwer, Steven F/0000-0003-2580-1288 FU NHLBI NIH HHS [R01 HL44986] NR 29 TC 5 Z9 6 U1 0 U2 0 PU BIOMEDICAL PRESS PI AUGUSTA PA 1021 15TH ST, BIOTECH PARK STE 9, AUGUSTA, GA 30901 SN 1073-2322 J9 SHOCK JI Shock PD MAY PY 1997 VL 7 IS 5 BP 332 EP 338 DI 10.1097/00024382-199705000-00004 PG 7 WC Critical Care Medicine; Hematology; Surgery; Peripheral Vascular Disease SC General & Internal Medicine; Hematology; Surgery; Cardiovascular System & Cardiology GA WZ715 UT WOS:A1997WZ71500004 PM 9165667 ER PT J AU Gonzalez, S Alcaraz, MV Diaz, F Flotte, TJ deVargas, IP Anderson, RR Kollias, N AF Gonzalez, S Alcaraz, MV Diaz, F Flotte, TJ deVargas, IP Anderson, RR Kollias, N TI DNA ploidy changes in rhino mouse skin induced by all-trans retinoic acid and retinol SO SKIN PHARMACOLOGY LA English DT Article DE all-trans retinoic acid; retinol; rhino mouse; epidermal cell kinetics; DNA content ID VITAMIN-A; EPIDERMIS; INVITRO; GROWTH AB Objective: In order to assess the proliferative changes induced by all-trans retinoic acid (RA) and retinol (ROL), we have carried out a study of the DNA content of basal and suprabasal keratinocytes after epicutaneous application on the rhino mouse. Study Design: Skin sections were analyzed stereologically and cytophotometrically using the Feulgen technique. The diploid DNA value (2C) was obtained from hepatocyte nuclei of control animals. Whereas cells in phase G(0)-G(1) will show a 2C content, cells during phase S and in phase G(2)-M will show DNA values ranging from 2C to 4C and 4C, respectively. Results: Although epidermal thickness (ET) increased significantly in all treated animals, surface density only increased in animals treated with all-trans RA. Quantification of DNA content of basal keratinocytes showed reduction of 2C and 2C-4C populations with a commensurate increase in proportions of cells with 4C and >4C in the animals treated with 0.025% all-trans RA and ROL. Suprabasal keratinocytes of mice treated with 0.025% all-trans showed a decrease of the 2C population and an increased proportion of cells with 4C. Whereas 0.025% all-trans RA induced an increase of both basal and suprabasal DNA indices, ROL enhanced only the basal DNA index significantly. Conclusion: Animals treated with 0.025% ROL showed a significant increase in the basal proliferative index (PI) while the suprabasal PI remained constant; treatment with 0.025% all-trans RA produced a significant increase of both basal and suprabasal PIs and parakeratotic hyperkeratosis probably due to incomplete differentiation. C1 UNIV MALAGA,FAC MED,DEPT NORMAL & PATHOL MORPHOL,E-29071 MALAGA,SPAIN. RP Gonzalez, S (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT DERMATOL,SCH MED,WELLMAN LABS PHOTOMED,BARLETT 707,BOSTON,MA 02114, USA. NR 25 TC 6 Z9 6 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1011-0283 J9 SKIN PHARMACOL JI Skin Pharmacol. PD MAY-JUN PY 1997 VL 10 IS 3 BP 135 EP 143 PG 9 WC Dermatology; Pharmacology & Pharmacy SC Dermatology; Pharmacology & Pharmacy GA XT021 UT WOS:A1997XT02100003 PM 9287394 ER PT J AU Sullivan, G Young, AS Morgenstern, H AF Sullivan, G Young, AS Morgenstern, H TI Behaviors as risk factors for rehospitalization: Implications for predicting and preventing admissions among the seriously mentally ill SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY LA English DT Article ID SCHIZOPHRENIA; RELAPSE; SYSTEM AB This case-control study investigated the extent to which aberrant behaviors, in contrast to more traditional clinical factors (such as symptoms and alcohol abuse), place individuals with schizophrenia at increased risk for rehospitalization. One hundred and one recidivists (cases) were matched to 101 non-recidivists (controls) on gender, race, and time since index hospitalization. Key informants, usually family members, were interviewed to assess behaviors during a 2-week period. After controlling for possible confounding variables, we found that each aberrant behavior increased the risk for rehospitalization, but highly disruptive or dangerous behaviors (such as threatening others, acting very bizarrely, or attempting suicide) conveyed a markedly high degree of risk (adjusted odds ratio = 83.9). It is possible that service providers may be able to avert the fiscal and emotional cost of hospitalization by collaborating more closely with family members to identify these behaviors and intervene before hospitalization becomes unavoidable. C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,NEUROPSYCHIAT HOSP,W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT EPIDEMIOL,LOS ANGELES,CA 90024. RP Sullivan, G (reprint author), RAND CORP,1700 MAIN ST,POB 2138,SANTA MONICA,CA 90407, USA. RI Young, Alexander/A-1523-2009 OI Young, Alexander/0000-0002-9367-9213 FU NIMH NIH HHS [MH47907, MH49199] NR 27 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0933-7954 J9 SOC PSYCH PSYCH EPID JI Soc. Psychiatry Psychiatr. Epidemiol. PD MAY PY 1997 VL 32 IS 4 BP 185 EP 190 DI 10.1007/BF00788237 PG 6 WC Psychiatry SC Psychiatry GA WZ122 UT WOS:A1997WZ12200002 PM 9184463 ER PT J AU Jones, RM MacDonald, ME Branda, J Altherr, MR Louis, DN Schmidt, EV AF Jones, RM MacDonald, ME Branda, J Altherr, MR Louis, DN Schmidt, EV TI Assignment of the human gene encoding eukaryotic initiation factor 4E (EIF4E) to the region q21-25 on chromosome 4. SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID CAP-BINDING PROTEIN; RNA 5' CAP; TRANSLATIONAL CONTROL; EIF-4E; TRANSFORMATION; FACTOR-EIF-4E; EXPRESSION; RECEPTOR; MYC AB We recently cloned genomic sequences containing the promoter region for the messenger RNA cap binding protein (eIF4E). As the rate-limiting step in translation, eukaryotic initiation factor 4E is important in cellular growth control. Using oligonucleotide primers specific for the promoter region in polymerase chain reactions (PCR), we amplified the human gene in a chromosome 4-specific human/rodent somatic cell panel. This panel mapped single copy genomic sequences for eIF4E in the region 4q21 to 4q25. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,CHARLESTOWN,MA 02129. LOS ALAMOS NATL LAB,GENOM & STRUCT BIOL GRP,LOS ALAMOS,NM 87545. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP Jones, RM (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,CHARLESTOWN,MA 02129, USA. FU NCI NIH HHS [R01-CA63117]; NHGRI NIH HHS [HG 00169]; NINDS NIH HHS [T32NS07340-04] NR 23 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD MAY PY 1997 VL 23 IS 3 BP 221 EP 223 DI 10.1007/BF02721373 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA XZ594 UT WOS:A1997XZ59400005 PM 9330633 ER PT J AU Ueki, K Ramaswamy, S Billings, SJ Mohrenweiser, HW Louis, DN AF Ueki, K Ramaswamy, S Billings, SJ Mohrenweiser, HW Louis, DN TI Chromosomal localization to 19q13.3, partial genomic structure and 5' cDNA sequence of the human symplekin gene SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID TUMOR-SUPPRESSOR GENE; 19Q; PROTEIN; MAP AB Exon trapping from cosmids mapping to chromosome 19q13.3 yielded 6 exonic sequences that matched the human symplekin gene, which encodes a tight junction-related protein. One exonic sequence identified a 4.0 kb brain cDNA clone, R6E1, which contained 302 bp 5' to the originally reported 3.7 kb symplekin cDNA. A portion of this novel 5' sequence matched an additional trapped exonic sequence which was obtained from the most telomeric cosmid analyzed. The symplekin gene thus lies in a telomeric-to-centromeric direction on 19q13.3. Only three cosmids from a large 19q13.3 contig hybridized with R6E1, thereby assigning the symplekin gene to a 40 kb region immediately telomeric to gene 59 and the DM protein kinase gene. The 5' end of the R6E1 clone has a potential initiation codon with a strong Kozak sequence and Northern blot analysis detected a 4.2 kb signal in most human tissues, indicating that R6E1 may be a complete cDNA sequence. Based on the trapped exonic sequences, twelve exon-intron boundaries were predicted. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. LAWRENCE LIVERMORE NATL LAB,CTR HUMAN GENOME,LIVERMORE,CA 94550. RP Ueki, K (reprint author), MASSACHUSETTS GEN HOSP,MOL NEUROONCOL LAB,DEPT PATHOL NEUROPATHOL,CHARLESTOWN,MA 02129, USA. FU NCI NIH HHS [CA 69285] NR 8 TC 6 Z9 7 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD MAY PY 1997 VL 23 IS 3 BP 229 EP 231 DI 10.1007/BF02721375 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA XZ594 UT WOS:A1997XZ59400007 PM 9330635 ER PT J AU Schaefer, PW Buonanno, FS Gonzalez, RG Schwamm, LH AF Schaefer, PW Buonanno, FS Gonzalez, RG Schwamm, LH TI Diffusion-weighted imaging discriminates between cytotoxic and vasogenic edema in a patient with eclampsia SO STROKE LA English DT Article DE brain edema; eclampsia; hypertension; magnetic resonance imaging ID HYPERTENSIVE ENCEPHALOPATHY; CEREBRAL-ISCHEMIA; MR; BRAIN; CT; BLINDNESS; PREGNANCY; GLIOMAS; WATER AB Background The pathophysiology of eclampsia remains unclear. While the majority of patients develop reversible T2 hyperintense signal abnormalities on MR scans and reversible neurological deficits, some patients do develop infarctions (permanent T2 hyperintense abnormalities) and permanent neurological impairment. Routine MRI cannot prospectively differentiate between these two patient groups. Echo-planar diffusion-weighted imaging however, is a new technique that clearly differentiates between cytotoxic and vasogenic edema. Case Description A 30-year-old woman developed symptoms consistent with eclampsia 24 hours after delivering premature twins. An MRI demonstrated extensive, diffuse T2 hyperintense signal abnormalities involving subcortical white matter and adjacent gray matter with a posterior predominance, consistent with either infarction or hypertensive ischemic encephalopathy. Diffusion-weighted images demonstrated increased diffusion, consistent with vasogenic edema and hypertensive ischemic encephalopathy. Conclusions Unlike routine MRI, diffusion-weighted imaging reliably differentiates between vasogenic edema and cytotoxic edema. Consequently, in eclamptic patients diffusion-weighted imaging can afford clear differentiation between hypertensive ischemic encephalopathy and infarction, two very different entities with very different treatment protocols. Diffusion-weighted imaging should be performed in all eclamptic patients and should greatly affect their management. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP Schaefer, PW (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,GRAY 285,FRUIT ST,BOSTON,MA 02114, USA. OI Schwamm, Lee/0000-0003-0592-9145 NR 26 TC 234 Z9 240 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAY PY 1997 VL 28 IS 5 BP 1082 EP 1085 PG 4 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA WZ267 UT WOS:A1997WZ26700041 PM 9158653 ER PT J AU Ciulla, TA Bains, RA Jakobiec, FA Topping, TM Gragoudas, ES AF Ciulla, TA Bains, RA Jakobiec, FA Topping, TM Gragoudas, ES TI Uveal lymphoid neoplasia: A clinical-pathologic correlation and review of the early form SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE choroid; corticosteroid; cryotherapy; Dutcher bodies; lymphoid hyperplasia; lymphoma; radiation; uveal lymphoid neoplasia ID MANAGEMENT; TUMORS; MELANOMA; CANCER; EYES AB We report three cases of uveal lymphoid neoplasia that were diagnosed early in their course. One case exhibited a posterior form, presenting with progressive hyperopia from a serous macular detachment and choroidal involvement along with retrobulbar involvement. This patient was treated with proton beam irradiation. Two cases displayed an anterior form, with fixed fleshy epibulbar masses resembling salmon patches, and choroidal involvement. The histologic findings from biopsy of these anterior masses are presented. One of these patients was treated with complete excision of the mass and double freeze-thaw cryotherapy of the scleral bed, and the other patient was treated with conventional photon beam irradiation. The clinical features of uveal lymphoid neoplasia in its early form are discussed. Evaluation and treatment strategies for these early forms of uveal lymphoid neoplasia are reviewed. (C) 1997 by Elsevier Science Inc. All rights reserved. C1 VICTORIA HOSP,IVEY INST OPHTHALMOL,LONDON,ON N6A 4G5,CANADA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. OPHTHALM CONSULTANTS BOSTON,BOSTON,MA. RP Ciulla, TA (reprint author), INDIANA UNIV,SCH MED,DEPT OPHTHALMOL,RETINA SECT,702 ROTARY CIRCLE,INDIANAPOLIS,IN 46202, USA. NR 24 TC 21 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD MAY-JUN PY 1997 VL 41 IS 6 BP 467 EP 476 DI 10.1016/S0039-6257(97)00015-5 PG 10 WC Ophthalmology SC Ophthalmology GA XH333 UT WOS:A1997XH33300003 PM 9220569 ER PT J AU Bergeron, BP Bailin, MT AF Bergeron, BP Bailin, MT TI The contribution of hypermedia link authoring SO TECHNICAL COMMUNICATION LA English DT Article AB Linking, when properly executed, enhances the value of content by providing a consistent perspective and organizational scheme that enriches the user's experience. Link authoring, like content authoring, is a creative process of making connections between disparate yet related information. Effective link authoring requires intellect, creativity, and domain knowledge to define the relationships among concepts that can support a particular pedagogical objective. The contribution of hypermedia link authoring is often poorly understood and unrecognized by traditional academic and publishing communities. Publishers of commercial and academic hypermedia typically neither formally recognize link authoring as something that should be protected by copyright, nor do they extend to those involved in link authoring the same degree of credit or remuneration given conventional content authors or illustrators. However, with the recent explosive growth in hypermedia publishing via the World Wide Web, CD-ROM, and other digital forms, the significance of link authoring is becoming more apparent. Clearly, a new paradigm is in order, one that recognizes the contribution of link authoring in the communication of thoughts, emotions, and information. C1 Massachusetts Gen Hosp, Dept Anesthesiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. RP Bergeron, BP (reprint author), Massachusetts Gen Hosp, Dept Anesthesiol, Boston, MA 02114 USA. NR 23 TC 0 Z9 0 U1 0 U2 0 PU SOC TECHNICAL COMMUNICATION PI ARLINGTON PA 901 NORTH STUART ST, STE 904, ARLINGTON, VA 22203 USA SN 0049-3155 J9 TECH COMMUN JI Tech. Commun. PD MAY PY 1997 VL 44 IS 2 BP 121 EP 128 PG 8 WC Communication SC Communication GA ZE665 UT WOS:000072817600008 ER PT J AU WurglerMurphy, SM Saito, H AF WurglerMurphy, SM Saito, H TI Two-component signal transducers and MAPK cascades SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Review ID 2-COMPONENT REGULATORS; BACILLUS-SUBTILIS; RESPONSE PATHWAY; MAMMALIAN-CELLS; FISSION YEAST; ARABIDOPSIS; ENCODES; GENE; KINASES; BINDING AB Two-component signal transducers, which are characterized by the histidine-to-aspartate phospho-transfer mechanism, were once thought to be restricted to prokaryotes. They have, however, now been identified in diverse eukaryotic species including plant, fungus, yeast and slime mold. In yeast, a two-component osmosensor has been found to regulate a mitogen-activated protein kinase (MAPK) cascade, a ubiquitous eukaryotic signaling module. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOL PHARMACOL,BOSTON,MA 02115. RP WurglerMurphy, SM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 38 TC 225 Z9 236 U1 0 U2 8 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD MAY PY 1997 VL 22 IS 5 BP 172 EP 176 DI 10.1016/S0968-0004(97)01036-0 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WZ504 UT WOS:A1997WZ50400012 PM 9175476 ER PT J AU Stoffers, DA Thomas, MK Habener, JF AF Stoffers, DA Thomas, MK Habener, JF TI Homeodomain protein IDX-1 - A master regulator of pancreas development and insulin gene expression SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID TRANSCRIPTION FACTOR EXPRESSION; BETA-CELL MASS; ISLET CELLS; GLUCOSE-CONCENTRATION; DIABETES-MELLITUS; HOMEOBOX FACTOR; FACTOR STF-1; EXOCRINE; PROMOTER; REDUCTION AB The homeodomain protein IDX-1 appears to be a ''master regulator'' of pancreas development and beta-cell differentiation and function. In murine gene inactivation models and in a human subject with a homozygous mutation of the IDX-1 gene, the pancreas fails to develop. In the adult endocrine pancreas, IDX-1 is primarily expressed in beta cells, where it is a key factor in the upregulation of insulin gene transcription and appears to have a role in the regulation of the somatostatin, glucokinase, glucose transporter-2, and islet amyloid polypeptide genes. Recent studies also suggest a role for IDX-1 in the neogenesis and proliferation of beta cells. The observed functions of IDX-1 and its downregulation in parallel with insulin in glucose-toxicity models implicate IDX-1 as a potential factor contributing to the pathogenesis of diabetes mellitus. Future directions include the use of conditional gene inactivation to determine more precisely the role of IDX-1 throughout endocrine pancreas differentiation and the exploration of IDX-1 as a potential target for gene therapy of diabetes mellitus. (C) 1997, Elsevier Science Inc. RP Stoffers, DA (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, MOL ENDOCRINOL LAB, HOWARD HUGHES MED INST, BOSTON, MA 02114 USA. RI Stoffers, Doris/H-6157-2012 NR 63 TC 72 Z9 73 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD MAY-JUN PY 1997 VL 8 IS 4 BP 145 EP 151 DI 10.1016/S1043-2760(97)00008-8 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XG345 UT WOS:A1997XG34500004 PM 18406800 ER PT J AU Auchincloss, H AF Auchincloss, H TI Xenotransplantation literature update SO XENOTRANSPLANTATION LA English DT Review RP Auchincloss, H (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,WHITE 510B,BOSTON,MA 02114, USA. NR 128 TC 0 Z9 0 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0908-665X J9 XENOTRANSPLANTATION JI Xenotransplantation PD MAY PY 1997 VL 4 IS 2 BP 120 EP 125 DI 10.1111/j.1399-3089.1997.tb00174.x PG 6 WC Medicine, Research & Experimental; Transplantation SC Research & Experimental Medicine; Transplantation GA XN862 UT WOS:A1997XN86200007 ER PT J AU Catalano, PJ AF Catalano, PJ TI Bivariate modelling of clustered continuous and ordered categorical outcomes SO STATISTICS IN MEDICINE LA English DT Article; Proceedings Paper CT Workshop on Statistical Methods for Multiple Events Data in Clinical Trials CY JUN 01-02, 1995 CL HARVARD UNIV, SCH PUBLIC HLTH, BOSTON, MA SP Harvard Univ, Sch Public Hlth, Schering Plough HO HARVARD UNIV, SCH PUBLIC HLTH ID QUANTITATIVE RISK ASSESSMENT; LONGITUDINAL DATA-ANALYSIS; DEVELOPMENTAL TOXICITY; ESTIMATING EQUATIONS; MULTIPLE ENDPOINTS; DISCRETE; REGRESSION; RESPONSES AB Simultaneous observation of continuous and ordered categorical outcomes for each subject is common in biomedical research but multivariate analysis of the data is complicated by the multiple data types. Here we construct a model for the joint distribution of bivariate continuous and ordinal outcomes by applying the concept of latent variables to a multivariate normal distribution. The approach is then extended to allow for clustering of the bivariate outcomes. The model can be parameterized in a way that allows writing the joint distribution as a product of a standard random effects model for the continuous variable and a correlated cumulative probit model for the ordinal outcome. This factorization suggests convenient parameter estimation using estimating equations. Foetal weight and malformation data from a developmental toxicity experiment illustrate the results. (C) 1997 by John Wiley & Sons, Ltd. Stat. Med., Vol. 16, 883-900 (1997). C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP Catalano, PJ (reprint author), HARVARD UNIV,SCH PUBL HLTH,DIV BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIEHS NIH HHS [ES06900] NR 26 TC 19 Z9 19 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 30 PY 1997 VL 16 IS 8 BP 883 EP 900 DI 10.1002/(SICI)1097-0258(19970430)16:8<883::AID-SIM542>3.0.CO;2-E PG 18 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA WY902 UT WOS:A1997WY90200012 PM 9160486 ER PT J AU Finkelstein, DM Schoenfeld, DA Stamenovic, E AF Finkelstein, DM Schoenfeld, DA Stamenovic, E TI Analysis of multiple failure time data from an aids clinical trial SO STATISTICS IN MEDICINE LA English DT Article; Proceedings Paper CT Workshop on Statistical Methods for Multiple Events Data in Clinical Trials CY JUN 01-02, 1995 CL HARVARD UNIV, SCH PUBLIC HLTH, BOSTON, MA SP Harvard Univ, Sch Public Hlth, Schering Plough HO HARVARD UNIV, SCH PUBLIC HLTH ID COX REGRESSION-ANALYSIS AB The primary endpoint of AIDS prophylaxis trials is the occurrence of opportunistic infections. While the treatments are not expected to have an effect on the underlying HIV disease, an effect of treatments on mortality cannot be ruled out. Therefore, the primary analysis of these trials must be based on a combined endpoint of infection and survival times. There are several methods available for analysis of multiple failure time data. However, there is no standard method for combining mortality and other failures in these analyses. This paper explores the analysis of multiple infections in the context of a study in which treatments may have an effect on mortality. The methods are applied to an AIDS clinical trial of prophylaxis for fungal infections. (C) 1997 by John Wiley & Sons, Ltd. Stat. Med., Vol. 16, 951-961 (1997). C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ACTG,STATA & DATA ANAL CTR,BOSTON,MA 02115. RP Finkelstein, DM (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI 30885, AI 95030] NR 7 TC 14 Z9 16 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 30 PY 1997 VL 16 IS 8 BP 951 EP 961 PG 11 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA WY902 UT WOS:A1997WY90200017 PM 9160491 ER PT J AU Boppart, SA Tearney, GJ Bouma, BE Southern, JF Brezinski, ME Fujimoto, JG AF Boppart, SA Tearney, GJ Bouma, BE Southern, JF Brezinski, ME Fujimoto, JG TI Noninvasive assessment of the developing Xenopus cardiovascular system using optical coherence tomography SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE microscopy; imaging; embryology; development ID MICROSCOPY AB Studies investigating normal and abnormal cardiac development are frequently limited by an inability to assess cardiovascular function within the intact organism, Tn this work, optical coherence tomography (OCT), a new method of micron-scale, noninvasive imaging based on the measurement of backscattered infrared light, was introduced for the high resolution assessment of structure and function in the developing Xenopus laevis cardiovascular system. Microstructural details, such as ventricular size and wall positions, were delineated with OCT at 16-mu m resolution and correlated with histology. Three-dimensional representation of the cardiovascular system also was achieved by repeated cross-sectional imaging at intervals of 25 mu m. In addition to structural information, OCT provides high speed in vivo axial ranging and imaging, allowing quantitative dynamic activity, such as ventricular ejection fraction, to be assessed. The sensitivity of OCT for dynamic assessment was demonstrated with an inotropic agent that altered cardiac function and dimensions, Optical coherence tomography is an attractive new technology for assessing cardiovascular development because of its high resolution, its ability to image through nontransparent structures, and its Inexpensive portable design, in vivo and in vitro imaging are performed at a resolution approaching that of histopathology without the need for animal killing. C1 MIT,DEPT ELECT ENGN & COMP SCI,ELECT RES LAB,CAMBRIDGE,MA 02139. MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. SINAI SAMARITAN MED CTR,DEPT PATHOL,MILWAUKEE,WI 53201. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RI Boppart, Stephen/C-7338-2009 FU NEI NIH HHS [9-RO1-EY11289-10, R01 EY011289]; NHLBI NIH HHS [R29 HL055686, NIH-1-R29-HL55686-01A1] NR 26 TC 134 Z9 136 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 29 PY 1997 VL 94 IS 9 BP 4256 EP 4261 DI 10.1073/pnas.94.9.4256 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WX362 UT WOS:A1997WX36200006 PM 9113976 ER PT J AU Davis, RE Miller, S Herrnstadt, C Ghosh, SS Fahy, E Shinobu, LA Galasko, D Thal, LJ Beal, MF Howell, N Parker, WD AF Davis, RE Miller, S Herrnstadt, C Ghosh, SS Fahy, E Shinobu, LA Galasko, D Thal, LJ Beal, MF Howell, N Parker, WD TI Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID AMYLOID PRECURSOR PROTEIN; FIRST-DEGREE RELATIVES; BRAIN; OXIDATION; DEMENTIA; MEDICINE; DNA; TAU AB yMounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). Cytochrome c oxidase (CO) is kinetically abnormal, and its activity is decreased in brain and peripheral tissue in late-onset AD, CO is encoded by both the mitochondrial and the nuclear genomes, Its catalytic centers, however, are encoded exclusively by two mitochondrial genes, CO1 and CO2 (encoding CO subunits I and II, respectively). We searched these genes, as well as other mitochondrial genes, for mutations that might alter CO activity and cosegregate with AD. In the present study, specific missense mutations in the mitochondrial CO1 and CO2 genes but not the CO3 gene were found to segregate at a higher frequency with AD compared with other neurodegenerative or metabolic diseases, These mutations appear together in the same mitochondrial DNA molecule and define a unique mutant mitochondrial genome, Asymptomatic offspring of AD mothers had higher levels of these mutations than offspring of AD fathers, suggesting that these mutations can be maternally inherited. Cell lines expressing these mutant mitochondrial DNA molecules exhibited a specific decrease in CO activity and increased production of reactive oxygen species, We suggest that specific point mutations in the CO1 and CO2 genes cause the CO defect in AD, A CO defect may represent a primary etiologic event, directly participating in a cascade of events that results in AD. C1 UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92161. VET AFFAIRS MED CTR,DEPT NEUROL,SAN DIEGO,CA 92161. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV TEXAS,MED BRANCH,DIV BIOL,GALVESTON,TX 77550. UNIV VIRGINIA,SCH MED,DEPT NEUROL & PEDIAT,CHARLOTTESVILLE,VA 22908. RP Davis, RE (reprint author), MITOKOR,11494 SORRENTO VALLEY RD,SAN DIEGO,CA 92121, USA. NR 43 TC 265 Z9 278 U1 1 U2 4 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 APR 29 PY 1997 VL 94 IS 9 BP 4526 EP 4531 DI 10.1073/pnas.94.9.4526 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WX362 UT WOS:A1997WX36200053 PM 9114023 ER PT J AU Baker, K Warren, KS Yellen, G Fishman, MC AF Baker, K Warren, KS Yellen, G Fishman, MC TI Defective ''pacemaker'' current (I-h) in a zebrafish mutant with a slow heart rate SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CALF PURKINJE-FIBERS; SINO-ATRIAL NODE; ACTIVATED CURRENT IF; PACE-MAKER CURRENT; SINOATRIAL NODE; VENTRICULAR MYOCYTES; HYPERPOLARIZATION; CELLS; MECHANISMS; BLOCK AB At a cellular level, cardiac pacemaking, which sets the rate and rhythm of the heartbeat, is produced by the slow membrane depolarization that occurs between action potentials, Several ionic currents could account for this pacemaker potential, but their relative pi-eminence is controversial, and it is not known which ones actually play a pacemaking role ire vivo. To correlate currents in individual heart cells with the rhythmic properties of the int-act heart, we have examined slow mo (smo), a recessive mutation we discovered in the zebrafish Danio I el io. This mutation causes a reduced heart rate in the embryo, a property we can quantitate because the embryo is transparent, We developed methods for culture of cardiocytes from zebrafish embryos and found that, even in culture, cells from smo continue to beat relatively slowly, By patch-clamp analysis, we discovered that a large repertoire of cardiac currents noted in other species are present in these cultured cells, including sodium, T-type, and L-type calcium and several potassium currents, all of which appear normal in the mutant, The only abnormality appears to be in a hyperpolarization-activated inward current with the properties of I-h, a current described previously in the nervous system, pacemaker, and other cardiac tissue, smo cardiomyocytes have a reduction in I-h that appears to result from severe diminution of one kinetic component of the I-h current. This provides strong evidence that I-h is an important contributor to the pacemaking behavior of the intact heart. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CARDIOVASC RES CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OI Yellen, Gary/0000-0003-4228-7866 FU NCRR NIH HHS [R01 RR08888]; NHLBI NIH HHS [R01 HL49579, T32 HL07208, R01 HL049579, T32 HL007208]; NINDS NIH HHS [R01 NS029693] NR 31 TC 117 Z9 121 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 APR 29 PY 1997 VL 94 IS 9 BP 4554 EP 4559 DI 10.1073/pnas.94.9.4554 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WX362 UT WOS:A1997WX36200058 PM 9114028 ER PT J AU Delmonico, FL Cosimi, AB Colvin, R Farrell, ML Thistlethwaite, R Spargo, B OLaughlin, R Matas, AJ Burke, B McHugh, L Lindblad, AS Stablein, DM CarterCampbell, S Salomon, DR Quinn, S Haverty, T Knowles, R Kale, R AF Delmonico, FL Cosimi, AB Colvin, R Farrell, ML Thistlethwaite, R Spargo, B OLaughlin, R Matas, AJ Burke, B McHugh, L Lindblad, AS Stablein, DM CarterCampbell, S Salomon, DR Quinn, S Haverty, T Knowles, R Kale, R TI Murine OKT4A immunosuppression in cadaver donor renal allograft recipients - A cooperative clinical trial in a transplantation pilot study SO TRANSPLANTATION LA English DT Article ID ANTI-CD4 MONOCLONAL-ANTIBODY; HUMAN ORGAN-TRANSPLANTATION; TOLERANCE; REJECTION; SURVIVAL; MICE; CD4 AB Background. A phase I study of anti-CD4 immunosuppression of cadaver donor rend allograft recipients was conducted by the NIH Cooperative Clinical Trials in Transplantation to assess safety, tolerability, immunoactivity, and pharmacokinetics of multiple infusions of murine anti-human CD4 monoclonal antibody OKT4A. Methods. Thirty patients were enrolled (August 1992 to October 1993) and received OKT4A at dosages of 0.5 mg/kg (24 patients), 1.0 mg/kg (3 patients), and 2.0 mg/kg (3 patients), beginning and continuing for 12 consecutive days with a standard regimen of cyclosporine, azathioprine, and prednisone. OKT4A treatment was continued after surgery if serum creatinine 24 hr after transplantation was <85% of pretransplantation baseline creatinine. Results. Ninety-three percent of patients treated at 0.5 mg/kg OKT4A and all patients at higher doses had mean peak CD4 saturations in excess of 90%. A human anti-mouse antibody response of >3 times pretreatment levels was observed in 84% of patients. There was no evidence of CD4 T cell depletion. OKT4A was well tolerated without first-dose side effects. For the 19 eligible patients treated with 0.5 mg/kg OKT4A with initial graft function, the 3-month treated rejection rate was 37%. The 2-year graft survival rate for all 30 patients enrolled was 83%, and for the 19 eligible patients, 95%. Conclusions. The high percentage of CD4 saturation, the minimal side effects, the observation of a low 3-month rejection rate, and an excellent 2-year graft survival rate in patients treated with 0.5 mg/kg OKT4A support the continued investigation of an anti-CD4 approach to immunosuppressive therapy. C1 UNIV CHICAGO,MED CTR,CHICAGO,IL 60637. UNIV MINNESOTA,MINNEAPOLIS,MN. EMMES CORP,CLIN COORDINATING CTR,POTOMAC,MD. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ 08869. RP Delmonico, FL (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,32 FRUIT ST,BOSTON,MA 02114, USA. NR 25 TC 3 Z9 3 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 APR 27 PY 1997 VL 63 IS 8 BP 1087 EP 1095 PG 9 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA WW660 UT WOS:A1997WW66000007 ER PT J AU Lee, RS Grusby, MJ Laufer, TM Colvin, R Glimcher, LH Auchincloss, H AF Lee, RS Grusby, MJ Laufer, TM Colvin, R Glimcher, LH Auchincloss, H TI Cd8+ effector cells responding to residual class I antigens, with help from CD4(+) cells stimulated indirectly, cause rejection of ''major histocompatibility complex-deficient'' skin grafts SO TRANSPLANTATION LA English DT Article ID T-CELLS; MONOCLONAL-ANTIBODIES; ALLOGRAFT-REJECTION; INVIVO; LYMPHOCYTES; SURVIVAL; DETERMINANTS; RECOGNITION; MICE; DESTRUCTION AB Background. Skin grafts from mice that are deficient in the expression of both class I and class II major histocompatibility complex (MHC) antigens are rejected rapidly by normal recipients. Methods. To determine the mechanism of this rejection, MHC-deficient skin grafts were placed on recipients with different degrees of antigenic disparity and on recipients depleted of selected T cell subpopulations, In addition, the recipient's T cells were examined in vitro for their responses before and after graft rejection. Results. The results indicate that (1) CD4(+) cells provide help for this rejection by recognizing donor antigens presented by recipient class II antigens, and (2) CD8(+) cells can participate as effector cells, recognizing residual class I antigens expressed by the MHC-deficient grafts. Conclusions. The primary conclusion from these studies is that the supposedly MHC-deficient mice actually do have sufficient class I antigen expression to cause skin graft rejection, This finding prevents the use of these mice to answer definitively the question of whether grafts entirely lacking MHC antigens would be rejected, However, these studies do illustrate two important (although previously recognized) features of allogeneic skin graft rejection: (1) that rejection can be initiated by help provided entirely through the indirect pathway, and (2) that help provided through the indirect pathway is available for effector T cells sensitized directly by donor cells, However, the results from these and other studies suggest that indirect effector mechanisms would probably be able to destroy truly MHC-deficient grafts under some circumstances. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN SURG SERV,TRANSPLANTAT UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL36372, HL18646] NR 36 TC 46 Z9 46 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD APR 27 PY 1997 VL 63 IS 8 BP 1123 EP 1133 DI 10.1097/00007890-199704270-00012 PG 11 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA WW660 UT WOS:A1997WW66000012 PM 9133474 ER PT J AU Kim, TW Pettingell, WH Hallmark, OG Moir, RD Wasco, W Tanzi, RE AF Kim, TW Pettingell, WH Hallmark, OG Moir, RD Wasco, W Tanzi, RE TI Endoproteolytic cleavage and proteasomal degradation of presenilin 2 in transfected cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FAMILIAL ALZHEIMERS-DISEASE; MISSENSE MUTATIONS; AMYLOID PRECURSOR; GENE; CYTOSKELETON; PROTEIN; UBIQUITIN; ASSOCIATION; INHIBITION; MOLECULES AB Mutations in the presenilin genes, PS1 and PS2, cause a major portion of early onset familial Alzheimer's disease (FAD), The biological roles of the presenilins and how their pathological mutations confer FAD are unknown, In this study, we set out to examine the processing and degradation pathways of PS2. For regulated expression of PS2, we have established inducible cell lines expressing PS2 under the tight control of the tetracycline-responsive transactivator. Western blot analysis revealed that PS2 was detected as an similar to 53-55-kDa polypeptide (54-kDa PS2) as well as a high molecular mass form (HMW-PS2). Using a stably transfected, inducible cell system, we have found that PS2 is proteolytically cleaved into two stable cellular polypeptides including an similar to 20-kDa C-terminal fragment and an similar to 34-kDa N-terminal fragment. PS2 is polyubiquitinated in vivo, and the degradation of PS2 is inhibited by proteasome inhibitors, N-acetyl-L-leucinal-L-norleucinal and lactacystin. Our studies suggest that PS2 normally undergoes endoproteolytic cleavage and is degraded via the proteasome pathway. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,GENET & AGING UNIT,CHARLESTOWN,MA 02129. NR 44 TC 201 Z9 205 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 APR 25 PY 1997 VL 272 IS 17 BP 11006 EP 11010 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WW009 UT WOS:A1997WW00900007 PM 9110991 ER PT J AU Godwin, SL Soltoff, SP AF Godwin, SL Soltoff, SP TI Extracellular calcium and platelet-derived growth factor promote receptor-mediated chemotaxis in osteoblasts through different signaling pathways SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID G-PROTEIN; DNA-SYNTHESIS; CELLS; MOBILIZATION; MECHANISM; MONOCYTES; MC3T3-E1; CA2+; BETA; OSTEOCLASTS AB The discovery of a calcium receptor has stimulated interest in the signaling events underlying extracellular calcium ([Ca2+](o))-induced cell-specific responses, In osteoblasts, elevated levels of extracellular calcium mediate both mitogenesis and chemotaxis. Here we provide evidence that [Ca2+](o)-stimulated chemotaxis of MC3T3-E1 osteoblast-like cells involves a G-protein-linked calcium-sensing receptor, [Ca2+](o) promotes chemotaxis in a concentration-dependent manner. Pertussis toxin blocked almost all of [Ca2+](o)-stimulated chemotaxis but had only a small effect on platelet-derived growth factor (PDGF)-stimulated chemotaxis. Consistent with the signaling model for PDGF mediated chemotaxis, activation of phospholipase C played a critical role in [Ca2+](o)-initiated chemotaxis: U-73122, an inhibitor of the activation of phospholipase C, blocked approximately 50% of PDGF-stimulated chemotaxis but blocked nearly all of the [Ca2+](o)-stimulated chemotaxis, Down-regulation of protein kinase C also blocked about 50% of PDGF-stimulated chemotaxis but aid riot block [Ca2+](o)-stimulated chemotaxis. Thus, unlike PDGF-mediated chemotaxis, chemotaxis stimulated by [Ca2+](o) does not appear to require protein kinase C activation. This finding suggests events downstream of inositol 1,4,5-trisphosphate production rather than diacylglycerol production are critical to [Ca2+](o)-promoted chemotaxis of MC3T3-E1 cells. The signal transduction mechanism underlying PDGF-induced chemotaxis involves the activation of phosphoinositide 3-kinase, as judged by the in vivo production of phosphatidylinositol 3,4-diphosphate and 3,4,5-trisphosphate and the partial sensitivity of chemotaxis to wortmannin, an inhibitor of phosphoinositide 3-kinase, In contrast, [Ca2+](o)-stimulated chemotaxis was not blocked by wortmannin and elevations in [Ca2+](o) did not increase the production of lipid products of phosphoinositide 3-kinase, Overall, [Ca2+](o)-promoted chemotaxis of osteoblasts appears to utilize a unique signaling mechanism via a calcium-sensing receptor. C1 HARVARD UNIV,INST MED,DEPT MED,BETH ISRAEL DEACONNESS MED CTR,DIV SIGNAL TRANSDU,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT ORTHODONT,BOSTON,MA 02115. FU NIDCR NIH HHS [DE00275, DE10877] NR 42 TC 80 Z9 80 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 APR 25 PY 1997 VL 272 IS 17 BP 11307 EP 11312 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WW009 UT WOS:A1997WW00900052 PM 9111036 ER PT J AU Sandrock, AW Dryer, SE Rosen, KM Gozani, SN Kramer, R Theill, LE Fischbach, GD AF Sandrock, AW Dryer, SE Rosen, KM Gozani, SN Kramer, R Theill, LE Fischbach, GD TI Maintenance of acetylcholine receptor number by neuregulins at the neuromuscular junction in vivo SO SCIENCE LA English DT Article ID BUNGAROTOXIN-TREATED RATS; ORIGINAL SYNAPTIC SITES; EPSILON-SUBUNIT GENE; ADULT MUSCLE-FIBERS; DIFFERENTIAL EXPRESSION; REGENERATING MUSCLE; CARDIAC DEVELOPMENT; MYASTHENIA-GRAVIS; CHICK MYOTUBES; MESSENGER-RNA AB ARIA (for acetylcholine receptor-inducing activity), a protein purified on the basis of its ability to stimulate acetylcholine receptor (AChR) synthesis in cultured myotubes, is a member of the neuregulin family and is present at motor endplates. This suggests an important role for neuregulins in mediating the nerve-dependent accumulation of AChRs in the postsynaptic membrane. Nerve-muscle synapses have now been analyzed in neuregulin-deficient animals. Mice that are heterozygous for the deletion of neuregulin isoforms containing an immunoglobulin-like domain are myasthenic. Postsynaptic AChR density is significantly reduced, as judged by the decrease in the mean amplitude of spontaneous miniature endplate potentials and bungarotoxin binding. On the other hand, the mean amplitude of evoked end plate potentials was not decreased, due to an increase in the number of quanta released per impulse, a compensation that has been observed in other myasthenic states. Thus, the density of AChRs in the postsynaptic membrane depends on immunoglobulin-containing neuregulin isoforms throughout the life of the animal. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. AMGEN INC,THOUSAND OAKS,CA 91320. FU NINDS NIH HHS [R01-NS18458, K08-NS01580] NR 49 TC 217 Z9 218 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 25 PY 1997 VL 276 IS 5312 BP 599 EP 603 DI 10.1126/science.276.5312.599 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WV721 UT WOS:A1997WV72100047 PM 9110980 ER PT J AU Dranoff, G AF Dranoff, G TI Gene therapy 1996 SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Editorial Material RP Dranoff, G (reprint author), DANA FARBER CANC INST,DANA 710E,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD APR 18 PY 1997 VL 1332 IS 2 BP R21 EP R24 DI 10.1016/S0304-419X(96)00046-7 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA WY130 UT WOS:A1997WY13000006 PM 9141465 ER PT J AU Livingston, DM AF Livingston, DM TI Cancer genetics and tumor suppressor genes - Sponsored by Cold Spring Harbor Laboratory - August 14-18, 1996 SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Editorial Material RP Livingston, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD APR 18 PY 1997 VL 1332 IS 2 BP R25 EP R31 DI 10.1016/S0304-419X(97)00003-6 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA WY130 UT WOS:A1997WY13000007 PM 9141466 ER PT J AU Qureshi, N Kaltashov, I Walker, K Doroshenko, V Cotter, RJ Takayama, K Sievert, TR Rice, PA Lin, JSL Golenbock, DT AF Qureshi, N Kaltashov, I Walker, K Doroshenko, V Cotter, RJ Takayama, K Sievert, TR Rice, PA Lin, JSL Golenbock, DT TI Structure of the monophosphoryl lipid a moiety obtained from the lipopolysaccharide of Chlamydia trachomatis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; RHODOPSEUDOMONAS-SPHAEROIDES; SALMONELLA-TYPHIMURIUM; NEISSERIA-GONORRHOEAE; MASS-SPECTROMETRY; FATTY-ACIDS; INFECTION; PURIFICATION; DESORPTION; MUTANT AB Monophosphoryl lipid A was prepared from the lipopolysaccharide of Chlamydia trachomatis, converted to the methyl ester, and fractionated by reverse-phase high-performance liquid chromatography. The peak fractions were collected and analyzed by mass spectrometry. Matrix-assisted laser desorption/ionization and liquid secondary ion mass spectrometry of the first of two major high-performance liquid chromatographic fractions showed multiple quasi-molecular ions of MNa+ at m/z 1780, 1794, 1808, 1822, and 1836. The positive-ion Liquid secondary ion mass spectrometry spectrum also showed a minor series of peaks at mit 1916, 1930, 1944, 1958, and 1971, consistent with the formation of matrix adducts with 3-nitrobenzyl alcohol. Oxonium ions representing the distal subunit were observed at mit 1057, 1071, 1085, 1099, and 1113. The second fraction was similarly analyzed and found to contain structural homologs of the first fraction. Based on this study, the major lipid A component of chlamydial lipopolysaccharide is a glucosamine disaccharide that contains five fatty acids and a phosphate in the distal segment. Three fatty acyl groups are in the distal segment, and two are in the reducing end segment. The acyloxyacyl group is located in the distal segment in amide linkage. Two structural series, differing by 14 atomic mass units in the reducing subunit, were observed. Chlamydial lipid A is complex and consists of at least 20 homologous structural components. The relatively low potency of Chlamydia trachomatis lipopolysaccharide in activating lipopolysaccharide-responsive cells might be related to the unusual fatty acid composition of the lipid A moiety. C1 UNIV WISCONSIN,DEPT BACTERIOL,MADISON,WI 53706. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOL SCI,BALTIMORE,MD 21205. BOSTON MED CTR,MAXWELL FINLAND LAB INFECT DIS,BOSTON,MA 02118. BOSTON UNIV,SCH MED,BOSTON,MA 02118. RP Qureshi, N (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERRACE,RM D-2215,MADISON,WI 53705, USA. FU NIAID NIH HHS [AI-38515, AI-33087]; NIGMS NIH HHS [GM-50870] NR 22 TC 52 Z9 52 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 18 PY 1997 VL 272 IS 16 BP 10594 EP 10600 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WV262 UT WOS:A1997WV26200040 PM 9099706 ER PT J AU Puder, M Soberman, RJ AF Puder, M Soberman, RJ TI Glutathione conjugates recognize the Rossmann fold of glyceraldehyde-3-phosphate dehydrogenase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN LEUKOTRIENE-C(4) SYNTHASE; HUMAN-LEUKOCYTES; PROTEIN; 5-LIPOXYGENASE; CELLS; EXPRESSION; IDENTIFICATION; TRANSLOCATION; PURIFICATION; ASSOCIATION AB Leukotriene (LT) C-4 and other glutathione conjugates are synthesized intracellularly and then move to the plasma membrane for export. The intracellular proteins that bind these molecules and the significance of these interactions are poorly understood. To identify the binding sites of membrane-associated proteins that recognize these molecules, we utilized photoaffinity probes to label the inner leaflet of erythrocytes. The predominant molecule labeled with S-(p-nitrobenzyl)glutathione-[I-125]4-azidosalicylic acid (PNBG-[I-125]ASA) or LTC4[I-125]4-azidosalicylic acid (LTC4-[I-125]ASA) was 38 kDa, The protein was labeled with PNBG-[I-125]ASA, electroblotted to polyvinylidene difluoride membranes, digested in situ with lysyl endopeptidase, and two radiolabeled peptides isolated by reverse phase-high performance liquid chromatography, These contained an identity of 7/11 with amino acids 119-129, and 11/11 with amino acids 67-77 of human Liver glyceraldehyde-3-phosphate dehydrogenase (GAPDH), respectively. Photoaffinity labeling with PNBG-[I-125]ASA was blocked completely by 100 mu M ATP and greater than 50% with 100 mu M NAD(+). LTC4-[I-125]ASA binding to the NAD(+) site was confirmed by V8 protease digestion of purified GAPDH labeled with LTC4-[I-125]ASA or PNBG-[I-125]ASA, with both labels localized to the 6.8-kDa N-terminal fragment. Photoaffinity labeling of ML-60 cells with (LTC4HI)-I-125-ASA identified GAPDH as the predominant cytoplasmic binding protein in these cells. These data indicate that GAPDH is a membrane-associated and cytoplasmic protein which binds glutathione conjugates including LTC4. C1 MASSACHUSETTS GEN HOSP EAST,MASSACHUSETTS GEN HOSP,ARTHRIT UNIT,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP EAST,MASSACHUSETTS GEN HOSP,DEPT MED,CHARLESTOWN,MA 02129. FU NCI NIH HHS [CA-09031, CA-09580]; NIEHS NIH HHS [ES-50859] NR 31 TC 16 Z9 17 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 APR 18 PY 1997 VL 272 IS 16 BP 10936 EP 10940 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WV262 UT WOS:A1997WV26200086 PM 9099752 ER PT J AU Frazier, JA AlaghbandRad, J Jacobsen, L Lenane, MC Hamburger, S Albus, K Smith, A McKenna, K Rapoport, JL AF Frazier, JA AlaghbandRad, J Jacobsen, L Lenane, MC Hamburger, S Albus, K Smith, A McKenna, K Rapoport, JL TI Pubertal development and onset of psychosis in childhood onset schizophrenia SO PSYCHIATRY RESEARCH LA English DT Article DE psychotic symptoms; pubarche; menarche ID GENDER DIFFERENCES; LIFE EVENTS; PHENOMENOLOGY AB In this study, pubertal development was examined for a sample of children and adolescents with childhood onset schizophrenia (COS) defined as psychosis by age 12. Developmental and psychiatric histories were obtained for 28 adolescents (mean age 14.5 +/- 2.3 years) with severe, treatment refractory COS (14 males, 14 females). Age of onset of psychosis was also examined in relation to menarche and development of secondary sex characteristics. Girls had a trend towards developing secondary sex characteristics earlier than boys (P = 0.06), consistent with North American norms. Males (N = 14) and females (N = 14) had similar age of onset of psychosis. The age of development of secondary sex characteristics was associated with onset of psychosis for girls, but this finding was driven by one outlier. There was no significant correlation between development of psychosis and menarche. Neither male nor female probands differed significantly from their well siblings or from North American norms in their age of onset of pubertal development. There was no evidence of early onset of secondary sex characteristics for this sample. Finally, there was an absence of a clear relationship between onset of psychosis and indices of sexual development for these very early onset cases. (C) 1997 Elsevier Science Ireland Ltd. C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. UNIV DELAWARE,GRAD SCH CLIN PSYCHOL,NEWARK,DE. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL. RP Frazier, JA (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 28 TC 21 Z9 21 U1 6 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD APR 18 PY 1997 VL 70 IS 1 BP 1 EP 7 DI 10.1016/S0165-1781(97)03062-X PG 7 WC Psychiatry SC Psychiatry GA WZ834 UT WOS:A1997WZ83400001 PM 9172272 ER PT J AU Kloen, P Visker, MHPW Olijve, W vanZoelen, EJJ Boersma, CJC AF Kloen, P Visker, MHPW Olijve, W vanZoelen, EJJ Boersma, CJC TI Cell-type-specific modulation of Hox gene expression by members of the TGF-beta superfamily: A comparison between human osteosarcoma and neuroblastoma cell lines SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID BONE MORPHOGENETIC PROTEINS; HOMEOBOX-CONTAINING GENE; GROWTH-FACTOR-BETA; RETINOIC ACID; SEQUENTIAL ACTIVATION; ADHESION MOLECULE; DIFFERENTIATION; TISSUES AB Homeobox gene expression in osteoblast-like cells was investigated using the polymerase chain reaction (PCR). A total of 13 homeobox genes was detected in U-2 OS (human osteosarcoma) and MC3T3-E1 (mouse osteoblast) cells by sequencing cloned PCR products, Using specific primers, a different pattern of Hox gene expression was shown for the neuroblastoma cell line SK-N-SH relative to U-2 OS and MC3T3-E1. Additionally, we showed that expression of HOXC6 in U-2 OS and SK-N-SH was differentially regulated by rhBMP-2, TGF-beta and activin-A. This suggests that specific Hox genes may be target genes for TGF-beta superfamily members, and allows us to further understand the complex functions of these growth factors and how they relate to growth and development. (C) 1997 Academic Press. C1 UNIV NIJMEGEN,DEPT CELL BIOL,NIJMEGEN,NETHERLANDS. UNIV NIJMEGEN,DEPT APPL BIOL,NIJMEGEN,NETHERLANDS. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. RI Visker, Marleen/E-1394-2012 NR 37 TC 11 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 17 PY 1997 VL 233 IS 2 BP 365 EP 369 DI 10.1006/bbrc.1997.6458 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA WW748 UT WOS:A1997WW74800014 PM 9144540 ER PT J AU Kharbanda, S Pandey, P Jin, SF Inoue, S Bharti, A Yuan, ZM Weichselbaum, R Weaver, D Kufe, D AF Kharbanda, S Pandey, P Jin, SF Inoue, S Bharti, A Yuan, ZM Weichselbaum, R Weaver, D Kufe, D TI Functional interaction between DNA-PK and c-Abl in response to DNA damage SO NATURE LA English DT Article ID DEPENDENT PROTEIN-KINASE; STRAND-BREAK REPAIR; V(D)J RECOMBINATION; TYROSINE KINASE; KU-AUTOANTIGEN; SH3 DOMAINS; COMPLEMENTATION; SENSITIVITY; BINDING; ANTIGEN AB How DNA damage is converted into intracellular signals that can control cell behaviour is unknown. The c-Abl protein tyrosine kinase is activated by ionizing radiation and certain other DNA-damaging agents(1-5), whereas the DNA-dependent protein kinase (DNA-PK), consisting of a serine/threonine kinase and Ku DNA-binding subunits, requires DNA double-strand breaks or other DNA lesions for activation(6-8). Here we demonstrate that c-Abl interacts constitutively with DNA-PK. Ionizing radiation stimulates binding of c-Abl to DNA-PK and induces an association of c-Abl with Ku antigen. We show that DNA-PK phosphorylates and activates c-Abl in vitro. Cells deficient in DNA-PK are defective in c-Abl activation induced by ionizing radiation. In a potential feedback mechanism, c-Abl phosphorylates DNA-PK, but not Ku, in vitro. Phosphorylation of DNA-PK by c-Abl inhibits the ability of DNA-PK to form a complex with DNA. We also show that treatment of cells with ionizing radiation results in phosphorylation of DNA-PK that is dependent on c-Abl. Our results support the hypothesis that there are functional interactions between c-Abl and DNA-PK in the response to DNA damage. C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. NR 23 TC 210 Z9 214 U1 0 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 17 PY 1997 VL 386 IS 6626 BP 732 EP 735 DI 10.1038/386732a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WU387 UT WOS:A1997WU38700060 PM 9109492 ER PT J AU Ivanchuk, SM Eng, C Cavenee, WK Mulligan, LM AF Ivanchuk, SM Eng, C Cavenee, WK Mulligan, LM TI The expression of RET and its multiple splice forms in developing human kidney SO ONCOGENE LA English DT Article DE RET; kidney; alternative splicing ID GROWTH-FACTOR RECEPTORS; ADULT-RAT TISSUES; TYROSINE KINASE; PROTO-ONCOGENE; PROTOONCOGENE PRODUCT; MESSENGER-RNA; CELL-LINE; VARIANTS; TRANSFORMATION; SPECIFICITY AB A series of inductive events between two different cell groups, the ureteric bud epithelium and metanephric mesenchyme, gives rise to the functional mammalian kidney, These reciprocal inductive interactions involve a number of molecules, one of which is the RET receptor tyrosine kinase, The phenotype of mice lacking functional RET includes kidney agenesis or severe dysgenesis, indicating a requirement for RET in kidney organogenesis, To investigate RET expression in human kidney development, we used a semi-quantitative RT-PCR-based strategy to examine a panel of kidney RNA samples ranging from 8-24 weeks gestational age, We found RET expression was highest earlier in development (14 weeks) with expression decreasing through to 24 weeks gestation, While three alternative RET transcripts generated by exon skipping at the 5' end of the gene were all detected throughout kidney development, expression of one transcript, RET2/6, where exon 2 was spliced to exon 6, varied relative to full length RET during this period, Levels of RET2/6 were highest at the earliest age of fetal kidney examined (8 weeks) and decreased relative to all other RET transcripts to low adult levels, The period of high expression coincides with a period of rapid bud bifurcation, Thus, it is possible that RET2/6 has a role in the early growth and differentiation of the human kidney. C1 QUEENS UNIV,DEPT PATHOL,KINGSTON,ON K7L 3N6,CANADA. QUEENS UNIV,DEPT PAEDIAT,KINGSTON,ON K7L 3N6,CANADA. HARVARD UNIV,SCH MED,DEPT MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTRO,BOSTON,MA 02115. LUDWIG INST CANC RES,SAN DIEGO BRANCH,LA JOLLA,CA 92093. OI Eng, Charis/0000-0002-3693-5145 NR 43 TC 29 Z9 29 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 17 PY 1997 VL 14 IS 15 BP 1811 EP 1818 DI 10.1038/sj.onc.1201016 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA WW166 UT WOS:A1997WW16600007 PM 9150387 ER PT J AU Mekeel, KL Tang, W Kachnic, LA Luo, CM DeFrank, JS Powell, SN AF Mekeel, KL Tang, W Kachnic, LA Luo, CM DeFrank, JS Powell, SN TI Inactivation of p53 results in high rates of homologous recombination SO ONCOGENE LA English DT Article DE p53; genetic stability; homologous recombination; plasmid ID CELL-CYCLE CONTROL; C-TERMINAL DOMAIN; WILD-TYPE P53; DNA-DAMAGE; ATAXIA-TELANGIECTASIA; INDUCED MUTATION; HAMSTER-CELLS; COLON-CANCER; GENE; APOPTOSIS AB Using a plasmid substrate which integrates into the genome, we determined that the rate of homologous recombination was suppressed by p53, Human tumor cell lines, mutant or null for p53 had recombination rates 10 000-times greater than primary fibroblasts. When isogenic cell pairs from tumor cells or primary fibroblasts were compared, differing only in one genetic change which inactivated p53, the recombination rate increased >100-fold. Functional inactivation of p53 by dominant mutant p53, by large T antigen of SV40 virus, by E6 protein of human papilloma virus, or by genetic deletion led to the same result. Our results suggest that p53 suppresses spontaneous homologous recombination, and that p53 is not required for recombination to proceed, The mechanism of recombination suppression may be related to the reported association of p53 with Rad 51, but the functional consequences of this association are not yet established. It is suggested that suppression of homologous recombination is the means by which p53 maintains genetic stability. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. FU NCI NIH HHS [CA58985] NR 45 TC 180 Z9 182 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 17 PY 1997 VL 14 IS 15 BP 1847 EP 1857 DI 10.1038/sj.onc.1201143 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA WW166 UT WOS:A1997WW16600011 PM 9150391 ER PT J AU Blumenthal, D Campbell, EG Anderson, MS Causino, N Louis, KS AF Blumenthal, D Campbell, EG Anderson, MS Causino, N Louis, KS TI Withholding research results in academic life science - Evidence from a national survey of faculty SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article AB Objectives.-To identify the prevalence and determinants of data-withholding behaviors among academic life scientists. Design.-Mailed survey of 3394 life science faculty in the 50 universities that received the most funding from the National Institutes of Health in 1993. Participants.-A total of 2167 faculty responded to the survey, a 64% response rate. Outcome Measures.-Whether respondents delayed publication of their research results for more than 6 months and whether respondents refused to share research results with other university scientists in the last 3 years. Results.-A total of 410 respondents (19.8%) reported that publication of their research results had been delayed by more than 6 months at least once in the last 3 years to allow for patent application, to protect their scientific lead, to slow the dissemination of undesired results, to allow time to negotiate a patent, or to resolve disputes over the ownership of intellectual property. Also, 181 respondents (8.9%) reported refusing to share research results with other university scientists in the last 3 years, in multivariate analysis, participation in an academic-industry research relationship and engagement in the commercialization of university research were significantly associated with delays in publication. Odds ratios (ORs) and 95% confidence intervals (Cls) were 1.34 (1.07-1.59) and 3.15 (2.88-3.41), respectively. Variables associated with refusing to share results were conducting research similar to the Human Genome Project (OR, 2.09; 95% CI, 1.75-2.42), publication rate (OR, 1.02; 95% CI, 1.01-1.03), and engagement in commercialization of research (OR, 2.45; 95% CI, 2.08-2.82). Conclusions.-Withholding of research results is not a widespread phenomenon among life-science researchers, However, withholding is more common among the most productive and entrepreneurial faculty, These results also suggest that data withholding has affected a significant number of life-science faculty and further study on data-withholding practices is suggested. C1 PARTNERS HEALTHCARE SYST,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA. UNIV MINNESOTA,COLL EDUC & HUMAN DEV,MINNEAPOLIS,MN 55455. RP Blumenthal, D (reprint author), MASSACHUSETTS GEN HOSP,DIV GEN INTERNAL MED,HLTH POLICY RES & DEV UNIT,50 STANIFORD ST,BOSTON,MA 02114, USA. FU NHGRI NIH HHS [HG00724-01] NR 11 TC 320 Z9 327 U1 5 U2 41 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 16 PY 1997 VL 277 IS 15 BP 1224 EP 1228 DI 10.1001/jama.277.15.1224 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA WT403 UT WOS:A1997WT40300034 PM 9103347 ER PT J AU Peters, R Sikorski, R AF Peters, R Sikorski, R TI Digital dialogue - Sharing information and interests on the Internet SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA. NATL CANC INST,BETHESDA,MD. RP Peters, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,WANG BLDG,ACC-1,FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 24 Z9 24 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 APR 16 PY 1997 VL 277 IS 15 BP 1258 EP 1260 DI 10.1001/jama.277.15.1258 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA WT403 UT WOS:A1997WT40300045 PM 9103353 ER PT J AU Johnson, JM Meiering, EM Wright, JE Pardo, J Rosowsky, A Wagner, G AF Johnson, JM Meiering, EM Wright, JE Pardo, J Rosowsky, A Wagner, G TI NMR solution structure of the antitumor compound PT523 and NADPH in the ternary complex with human dihydrofolate reductase SO BIOCHEMISTRY LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; ESCHERICHIA-COLI; CRYSTAL-STRUCTURES; CROSS-RELAXATION; ROTATING-FRAME; BIOLOGICAL-ACTIVITY; HETERONUCLEAR NMR; PRACTICAL ASPECTS; COENZYME BINDING; METHOTREXATE AB The antitumor compound PT523 [N-alpha-(4-amino-4-deoxypteroyl)-N-delta-hemiphthaloyl-L-ornithine] was found to have an inhibition constant (K-i) of 0.35 +/- 0.10 pM against human dihydrofolate reductase (hDHFR), 15-fold lower than that of the classical antifolate drug methotrexate (MTX). The structure of PT523 bound to hDHFR and hDHFR-NADPH was investigated using multinuclear NMR techniques. NMR data indicate that the binary complex has two distinct conformations in solution which are in slow exchange and that the addition of NADPH stabilizes the ternary complex in a single bound state. Comparison of resonance assignments in the PT523 and MTX ternary complexes revealed that substantial protein chemical shift differences are limited to small regions of hDHFR tertiary structure. A restrained molecular dynamics and energy minimization protocol was performed for the hDHFR-PT523-NADPH complex, using 185 NOE restraints (33 intermolecular) to define the ligand-binding region. The positions of the pteridine and pABA rings of PT523 and the nicotinamide and ribose rings of NADPH are well defined in the solution structures (RMSD = 0.59 Angstrom) and are consistent with previously determined structures of DHFR complexes. The N-delta-hemiphthaloyl-L-omithine group of PT523 is less well defined, and the calculated model structures suggest the hemiphthaloyl ring may adopt more than one conformation in solution. Contacts between the hemiphthaloyl ring and hDHFR, which are not possible in the hDHFR-MTX-NADPH complex, may explain the greater inhibition potency of PT523. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOL PHARMACOL,PROGRAM HIGHER DEGREES BIOPHYS,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [R01-CA 25394] NR 76 TC 33 Z9 33 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 15 PY 1997 VL 36 IS 15 BP 4399 EP 4411 DI 10.1021/bi963039i PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU189 UT WOS:A1997WU18900005 PM 9109647 ER PT J AU Wilson, CJ Husain, SS Stimson, ER Dangott, LJ Miller, KW Maggio, JE AF Wilson, CJ Husain, SS Stimson, ER Dangott, LJ Miller, KW Maggio, JE TI p-(4-hydroxybenzoyl)phenylalanine: A photoreactive amino acid analog amenable to radioiodination for elucidation of peptide-protein interaction application to substance P receptor SO BIOCHEMISTRY LA English DT Article ID HUMAN NEUROKININ-1 RECEPTOR; NICOTINIC ACETYLCHOLINE-RECEPTOR; PHOTOAFFINITY CROSS-LINKING; BINDING-SITE; NONPEPTIDE ANTAGONISTS; NK-1 RECEPTOR; SH2 DOMAIN; BIOCHEMICAL-CHARACTERIZATION; BIMOLECULAR INTERACTIONS; ANGIOTENSIN RECEPTOR AB Benzoylphenylalanine, a photoreactive phenylalanine analog that can be incorporated into a peptide during solid-phase synthesis, is a useful probe for investigating the interactions of bioactive peptides with their receptors. This probe, however, lacks versatility because it is not detectable by Edman sequencing and because it cannot be labeled with radioiodine, requiring radiolabeling of the peptide ligand at a site distal to the photoreactive amino acid. The separation of the radioisotope and photoaffinity labels along the primary sequence limits identification of the photoinsertion site to a peptide fragment rather than a specific amino acid of the receptor protein. We have now synthesized p-(4-hydroxybenzoyl)phenylalanine by a synthetic route involving reaction of 4-(chloromethyl)benzoic anhydride with phenol in polyphosphoric acid to give the 4-(chloromethyl)benzoyl ester of 4-(chloromethyl)-4'-hydroxybenzophenone followed by reaction of the benzophenone derivative with ethyl acetamidocyanoacetate and subsequent hydrolysis of the product to give p-(4-hydroxybenzoyl)phenylalanine. The novel photolabile amino acid was incorporated into substance P (replacing Phe(8) or Lys(3)) to give 11-mer peptides that bind with high (nM) affinity and specificity to the substance P receptor. Radioiodination of the substance P analogs resulted in the incorporation of I-125 at the photoreactive amino acid residue, yielding probes of high (similar to 2000 Ci/mmol) specific activity. Subsequent photolysis of the radiolabeled peptides in the presence of substance P receptor caused covalent attachment of the peptide to the receptor with high photoinsertion yield (approximate to 30%); photolabeling was abolished in the presence of excess unlabeled SP. p-(4-Hydroxybenzoyl)phenylalanine retains p-benzoylphenylalanine's high insertion yield and low reactivity with water, but in contrast allows placement of radioiodine and the photoactive moieties within the same residue, providing the ability to identify the specific site(s) of interaction, and identification of the residue by Edman sequencing. This novel amino acid may be useful in the elucidation of the interaction of a variety of peptides with their receptors. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOL PHARMACOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT NEUROBIOL, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT ANESTHESIA, BOSTON, MA 02115 USA. FU NIGMS NIH HHS [GM-15904] NR 67 TC 20 Z9 20 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 15 PY 1997 VL 36 IS 15 BP 4542 EP 4551 DI 10.1021/bi962299x PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU189 UT WOS:A1997WU18900021 PM 9109663 ER PT J AU Suzuki, T Ando, K Isohara, T Oishi, M Lim, GS Satoh, Y Wasco, W Tanzi, RE Nairn, AC Greengard, P Gandy, SE Kirino, Y AF Suzuki, T Ando, K Isohara, T Oishi, M Lim, GS Satoh, Y Wasco, W Tanzi, RE Nairn, AC Greengard, P Gandy, SE Kirino, Y TI Phosphorylation of Alzheimer beta-amyloid precursor-like proteins SO BIOCHEMISTRY LA English DT Article ID MESSENGER-RNA; MOLECULAR-CLONING; KINASE-C; DISEASE; CDNA; HOMOLOG; GENE; APLP2; APP AB Amyloid precursor-like proteins (APLPs), APLP1 and APLP2, are members of a gene family which include the Alzheimer beta-amyloid precursor protein (APP). APLP1, APLP2, and APP contain highly homologous amino acid sequences, especially in their cytoplasmic domains, although APLPs lack the beta-amyloid domain derived by proteolytic processing from APP. APP is phosphorylated at three sites in the cytoplasmic domain in cultured cells and adult rat brain [Suzuki et al. (1994) EMBO J. 13, 1114-1122; Oishi, et al. (1997) Mel. Med. 3, 109-121] and at sites in the extracellular domain in cultured cells [Knops et al. (1993) Biochem. Biophys. Res. Commun. 197, 380-385; Hung & Selkoe (1994) EMBO J. 13, 534-542; Waiter et al. (1997) J. Biol. Chem. 272, 1896-1903]. We report here that a cytoplasmic domain peptide from APLP1 is phosphorylated in vitro by protein kinase C and that a cytoplasmic domain peptide from APLP2 is phosphorylated in vitro by protein kinase C and cdc2 kinase. APLP2 is phosphorylated by cdc2 kinase at a site homologous to the cdc2 kinase site phosphorylated in APP. Furthermore, phosphorylation of this site occurs in a cell cycle-dependent manner in cultured cells. These findings indicate that in intact cells the phosphorylation of APLP2 appears to be regulated in a similar fashion to that of APP. C1 NIPPON STEEL CORP LTD,ADV TECHNOL RES LABS,LIFE SCI RES CTR,NAKAMURA KU,KAWASAKI,KANAGAWA 211,JAPAN. ROCKEFELLER UNIV,MOL & CELLULAR NEUROSCI LAB,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,LAB GENET & AGING,CHARLESTOWN,MA 02129. NEW YORK HOSP,CORNELL MED CTR,DEPT NEUROL & NEUROSCI,NEW YORK,NY 10021. RP Suzuki, T (reprint author), UNIV TOKYO,FAC PHARMACEUT SCI,LAB NEUROBIOPHYS,GRAD SCH PHARMACEUT SCI,BUNKYO KU,HONGO 7-3-1,TOKYO,JAPAN. RI Suzuki, Toshiharu/B-5342-2013 FU NIA NIH HHS [AG11508, AG10491, AG09464] NR 23 TC 40 Z9 41 U1 2 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 15 PY 1997 VL 36 IS 15 BP 4643 EP 4649 DI 10.1021/bi962618k PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU189 UT WOS:A1997WU18900033 PM 9109675 ER PT J AU Renshaw, PF Lafer, B Babb, SM Fava, M Stoll, AL Christensen, JD Moore, CM YurgelunTodd, DA Bonello, CM Pillay, SS Rothschild, AJ Nierenberg, AA Rosenbaum, JF Bruce, BM AF Renshaw, PF Lafer, B Babb, SM Fava, M Stoll, AL Christensen, JD Moore, CM YurgelunTodd, DA Bonello, CM Pillay, SS Rothschild, AJ Nierenberg, AA Rosenbaum, JF Bruce, BM TI Basal ganglia choline levels in depression and response to fluoxetine treatment: An in vivo proton magnetic resonance spectroscopy study SO BIOLOGICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Meeting of the Society-of-Biological-Psychiatry CY 1994 CL PHILADELPHIA, PA SP Soc Biol Psychiat DE major depression; fluoxetine; magnetic resonance spectroscopy; magnetic resonance imaging; choline; basal ganglia ID HUMAN-BRAIN INVIVO; SIGNAL TRANSDUCTION; METABOLITES; MANIA; HYPOTHESIS; NEURONS; SPECTRA; NUCLEI; RAT AB We have investigated proton magnetic resonance spectra of the basal ganglia in 41 medication-free outpatients with major depression, prior to starting an 8-week standardized trial of open-label fluoxetine, and 22 matched comparison subjects. Upon completing the trial, depressed subjects were classified as treatment responders (n = 18) or nonresponders (n = 23), based on changes in the Hamilton Depression Rating Scale. Depressed subjects had a lower area ratio of the choline resonance to the creatine resonance (Cho/Cr) than comparison subjects. This statistically significant difference between the depressed subjects and comparison subjects was more pronounced in the treatment responders than in the nonresponders. There were no differences in the relative volumes of gray matter or white matter in the voxel used for proton spectroscopy in depressed subjects relative to comparison subjects. These results are consistent with an alteration in the metabolism of cytosolic choline compounds in the basal ganglia of depressed subjects and, in particular, those who are responsive to fluoxetine. (C) 1997 Society of Biological Psychiatry. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,PSYCHOPHARMACOL UNIT,BOSTON,MA. MCLEAN HOSP,AFFECT DISORDERS PROGRAM,BELMONT,MA 02178. HARVARD UNIV,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. RP Renshaw, PF (reprint author), MCLEAN HOSP,BRAIN IMAGING CTR,115 MILL ST,BELMONT,MA 02178, USA. RI Lafer, Beny/C-1055-2012; Lafer, Beny/F-9390-2015 OI Lafer, Beny/0000-0002-6132-9999; Lafer, Beny/0000-0002-6132-9999 FU NIMH NIH HHS [MH-47457] NR 39 TC 84 Z9 86 U1 3 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1997 VL 41 IS 8 BP 837 EP 843 DI 10.1016/S0006-3223(96)00256-9 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WT661 UT WOS:A1997WT66100001 PM 9099409 ER PT J AU Cardenas, VA Gill, P Fein, G AF Cardenas, VA Gill, P Fein, G TI Human P50 suppression is not affected by variations in wakeful alertness SO BIOLOGICAL PSYCHIATRY LA English DT Article DE singular value decomposition; C-T ratio; event-related potentials; beta power; auditory P50 ID AUDITORY-EVOKED-RESPONSES; SCHIZOPHRENIA; RELIABILITY; SLEEP; NORMALIZATION; POTENTIALS; WAVE; CAT AB The amplitude and suppression of the auditory P50 event-related potential may be useful for studying schizophrenia and drug abuse; however, the low reliability of the P50 suppression measure limits its value for correlation with clinical measures. Reliability can be increased either by improving measurement methods or by reducing or eliminating sources of variance in the recordings. In this paper the effect on P50 amplitude and suppression of variation in wakeful alertness within an experimental session was examined in 20 normal subjects. The percentage of beta power in the interval immediately prior to the P50 stimuli was used as an index of alertness. P50 amplitudes or C-T ratios were estimated using peak-picking and using the singular value decomposition (SVD) method. No effects of variation of wakeful alertness were observed on arty P50 amplitude or suppression measure. Comparing the peak-picking vs SVD estimates replicated our prior results showing markedly higher reliabilities with SVD. We conclude: 1) that variation within an experimental session in wakeful alertness level as indexed by the percentage of beta power does not affect P50 amplitude or suppression, and 2) the SVD method brings the reliability of the C-T ratio up to levels where its usefulness in clinical studies can be examined. (C) 1997 Society of Biological Psychiatry. C1 UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,SAN FRANCISCO,CA 94143. SAN FRANCISCO VET ADM MED CTR,PSYCHIAT SERV,SAN FRANCISCO,CA. FU NIDA NIH HHS [R01DA08365] NR 41 TC 20 Z9 20 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1997 VL 41 IS 8 BP 891 EP 901 DI 10.1016/S0006-3223(96)00186-2 PG 11 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WT661 UT WOS:A1997WT66100008 PM 9099416 ER PT J AU DunussiJoannopoulos, K Krenger, W Weinstein, HJ Ferrara, JLM Croop, JM AF DunussiJoannopoulos, K Krenger, W Weinstein, HJ Ferrara, JLM Croop, JM TI CD8(+) T cells activated during the course of murine acute myelogenous leukemia elicit therapeutic responses to late B7 vaccines after cytoreductive treatment SO BLOOD LA English DT Article ID TUMOR-ANTIGENS; ANTITUMOR IMMUNITY; MYELOID-LEUKEMIA; HUMAN-MELANOMA; LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; CD28 RECEPTOR; GENE-TRANSFER; COSTIMULATION; CANCER AB We have previously shown in a murine acute myelogenous leukemia (AML) model that leukemic mice can be cured with a B7 vaccine if immunized early in the disease and that CD8(+) T cells are necessary for tumor rejection. However, when B7 vaccine is administered 2 weeks after leukemia inoculation, the effect is only prolonged survival, ending in death virtually of all the mice. To distinguish between tumor kinetics and tumor-induced immunosuppression as potential mechanisms eliminating the therapeutic potential of late B7 vaccines, we performed in vitro T-cell studies during leukemia progression and in vivo studies on the clinical outcome of late B7 vaccines in combination with prior cytoreductive chemotherapy. Our results show that CD8(+) T cells from leukemic mice 1 and 2 weeks after leukemia inoculation proliferate more vigorously in response to in vitro activation than cells from normal mice and produce Th1-type cytokines interleukin-2 and interferon-gamma. Cytotoxic T lymphocyte (CTL) assays demonstrate that cells from week-2 vaccinated mice (which succumb to their leukemia), surprisingly develop a stronger CTL activity than cells from week-1 vaccinated mice (which reject their leukemia), Finally, the combination of late chemotherapy and late B7 vaccine administration can cure only 20% of leukemic mice, whereas early chemotherapy and the same late B7 vaccine administration cure 100% of leukemic mice. These results demonstrate that in murine AML tumor growth does not induce T-cell anergy or a Th2 cytokine profile and suggest that tumor growth is most likely to be the limiting factor in the curative potential of late B7 vaccines. (C) 1997 by The American Society of Hematology. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,DIV PEDIAT ONCOL,BOSTON,MA. RP DunussiJoannopoulos, K (reprint author), DANA FARBER CANC INST,DEPT PEDIAT,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 55 TC 22 Z9 22 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1997 VL 89 IS 8 BP 2915 EP 2924 PG 10 WC Hematology SC Hematology GA WV146 UT WOS:A1997WV14600034 PM 9108412 ER PT J AU Soiffer, RJ Fairclough, D Robertson, M Alyea, E Anderson, K Freedman, A BartlettPandite, L Fisher, D Schlossman, RL Stone, R Murray, C Freeman, A Marcus, K Mauch, P Nadler, L Ritz, J AF Soiffer, RJ Fairclough, D Robertson, M Alyea, E Anderson, K Freedman, A BartlettPandite, L Fisher, D Schlossman, RL Stone, R Murray, C Freeman, A Marcus, K Mauch, P Nadler, L Ritz, J TI CD6-depleted allogeneic bone marrow transplantation for acute leukemia in first complete remission SO BLOOD LA English DT Article ID VERSUS-HOST DISEASE; T-CELL DEPLETION; ACUTE LYMPHOBLASTIC-LEUKEMIA; CYTOMEGALO-VIRUS INFECTION; ACUTE MYELOGENOUS LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA; CAMPATH-1 PLUS COMPLEMENT; RECOMBINANT INTERLEUKIN-2; SELECTIVE DEPLETION; MYELOID-LEUKEMIA AB The appropriate timing of bone marrow transplantation (BMT) for adults with acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL) is controversial. Although allogeneic transplantation results in a lower risk of disease recurrence than intensive chemotherapy alone, overall outcome following BMT may not be improved due to the higher incidence of therapy-related fatal complications, frequently as a result of the development of graft-versus-host disease (GVHD). Selective T-cell depletion of donor marrow can reduce the incidence of GVHD and thereby limit transplant-related toxicity. Herein we report the risk of GVHD, incidence of transplant related mortality (TRM), likelihood of disease relapse, and overall survival in adult patients undergoing BMT with CD6 depleted allogeneic marrow for acute leukemia in first remission. Forty-one consecutive allogeneic transplants were performed on patients with acute leukemia and high-risk features (28 AML, 13 ALL) using T12 monoclonal antibody and complement to remove CD6+ T cells from donor marrow. No pre- or posttransplant immune suppressive medications for GVHD prophylaxis were administered. The actuarial estimated risk of grade 2 to 4 acute GVHD was 15% in patients receiving HLA identical grafts. Chronic GVHD developed in five patients. The estimated risk of TRM for patients in first complete remission was 5% at Day + 100 and 16% at 2 years. Fatalities attributable to infection with cytomegalovirus or Epstein-Barr virus occurred in only three patients. Estimated probabilities of relapse, overall survival, and event-free survival at 4 years were 25%, 71%, and 63%, respectively. No significant differences in GVHD, TRM, relapse rate, or survival was observed for patients with AML compared with those with ALL. Allogeneic transplantation with CD6 depleted bone marrow is effective in consolidating remissions of high-risk patients with acute leukemia in first remission without excessive toxicity. (C) 1997 by The American Society of Hematology. C1 DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP Soiffer, RJ (reprint author), DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 NR 60 TC 59 Z9 59 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1997 VL 89 IS 8 BP 3039 EP 3047 PG 9 WC Hematology SC Hematology GA WV146 UT WOS:A1997WV14600047 PM 9108425 ER PT J AU Oken, MM Harrington, DP Abramson, N Kyle, RA Knospe, W Glick, JH AF Oken, MM Harrington, DP Abramson, N Kyle, RA Knospe, W Glick, JH TI Comparison of melphalan and prednisone with vincristine, carmustine, melphalan, cyclophosphamide, and prednisone in the treatment of multiple myeloma - Results of Eastern Cooperative Oncology Group Study E2479 SO CANCER LA English DT Article; Proceedings Paper CT Meeting of the Education Program of the American-Society-of-Hematology CY DEC, 1993 CL ST LOUIS, MO SP Amer Soc Hematol DE multiple myeloma; treatment; chemotherapy; hematologic malignancy; plasma cell neoplasms ID COMBINATION CHEMOTHERAPY; REGRESSION-MODELS; SURVIVAL; TABLES AB BACKGROUND. The Eastern Cooperative Oncology Group (ECOG) performed a Phase III comparison of melphalan and prednisone (MP) with vincristine, carmustine (BCNU), melphalan, cyclophosphamide, and prednisone (VBMCP) in an attempt to determine which of these regimens should be the standard treatment for multiple myeloma. METHODS. Four hundred seventy-nine previously untreated patients with multiple myeloma from 23 ECOG institutions were enrolled. Treatment, assigned by randomization, consisted of either 4-week cycles of MP or 5-week cycles of VBCMP. After 1 year of induction therapy, patients received MP or VBMCP maintenance therapy at 6- and 8-week intervals, respectively, until relapse. Patients who experienced treatment failure with MP were eligible for crossover therapy with VBMCP. RESULTS. Objective responses were obtained for 51% of patients receiving MP, as compared with 72% of patients receiving VBMCP (P < 0.001). Response duration was also longer with VBMCP (median, 18 months with MP vs. 24 months with VBMCP; P = 0.007). Overall survival was not significantly different between MP and VBMCP (P = 0.30). The 5-year survival for VBMCP was 26%, as compared with 19% for MP. VBMCP was associated with more nausea, peripheral nerve toxicity, alopecia, and neutropenia, but the infection rate was equal to that observed with MP. Both regimens were generally well tolerated. The main exception was that elderly patients who were confined to bed had a higher risk of death with VBMCP. The two regimens produced a similar incidence of late secondary myelodysplastic syndrome and acute leukemia. Crossover VBMCP for patients failing with MP was only minimally effective, with an objective response rate of 20% and median survival of 11 months after crossover. CONCLUSIONS. VBMCP is more effective than MP in producing and sustaining remission of multiple myeloma. It is associated with a marginal survival advantage and an apparently greater chance of surviving 5 years for patients who can tolerate moderately intensive combination chemotherapy. (C) 1997 American Cancer Society. C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. BAPTIST REG CANC INST,JACKSONVILLE,FL. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV PENN,PHILADELPHIA,PA 19104. RP Oken, MM (reprint author), ABBOTT NW HOSP,VIRGINIA PIPER CANC INST,800 E 28TH ST,MINNEAPOLIS,MN 55407, USA. FU NCI NIH HHS [CA 13650, CA23318, CA 25988] NR 22 TC 58 Z9 65 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 15 PY 1997 VL 79 IS 8 BP 1561 EP 1567 DI 10.1002/(SICI)1097-0142(19970415)79:8<1561::AID-CNCR18>3.0.CO;2-W PG 7 WC Oncology SC Oncology GA WR200 UT WOS:A1997WR20000018 PM 9118039 ER PT J AU Guidi, AJ Connolly, JL Harris, JR Schnitt, SJ AF Guidi, AJ Connolly, JL Harris, JR Schnitt, SJ TI The relationship between shaved margin and inked margin status in breast excision specimens SO CANCER LA English DT Article DE breast carcinoma; ductal carcinoma in situ; margins; breast conservation ID CARCINOMA IN-SITU; CONSERVATION THERAPY; CONSERVING SURGERY; RADIATION-THERAPY; LOCAL RECURRENCE; RISK-FACTORS; CANCER; LUMPECTOMY AB BACKGROUND, The presence of tumor at the inked margins (IMs) of breast specimens is associated with an increased risk of local recurrence after breast-conserving therapy for invasive breast carcinoma and ductal carcinoma in situ (DCIS). Given the importance of margin status, some have advocated the use of shaved margins (SMs) as a means of conducting a more complete examination of the specimen margins than could be done with sections taken perpendicular to the IMs. However, it is not known whether these two methods of margin assessment provide comparable information. METHODS. To address this issue, the authors studied 22 consecutive breast reexcision specimens (10 DCIS, 6 infiltrating ductal carcinomas, and 6 infiltrating lobular carcinomas) in which the specimen surfaces were inked, the margins were shaved, and tumor was present in at least one of the SM sections. A total of 199 SMs were examined. The SMs were originally embedded in a way that permitted histologic sections to be cut opposite the inked surface. Sections of SM stained with hematoxylin and eosin (H & E) were reviewed and scored for the presence and extent (number of low-power fields) of cancer. The remaining tissue from the SM was then removed from the blocks, cut perpendicular to the IM, and reembedded to permit visualization of tumor in relation to the IM. Sections were then cut from two different levels of each reembedded block and stained with H & E. An SM was considered positive if tumor was present anywhere on the section. An IM was considered positive when tumor extended to the inked surface. RESULTS. Although all 22 excisions had at least 1 positive SM, tumor was present at an IM in only 12 specimens (55%). Among 69 positive SMs, the corresponding IM was positive in only 42 (61%). The likelihood of a positive IM increased with the number of low-power fields of involvement by invasive carcinoma or DCIS on the SM, as follows: 19% with 1 low power-field, 67% with 2 low-power fields, and 97% with greater than or equal to 3 low-power fields (all P < 0.02). When the SM was negative, the corresponding IM was negative in 98% of cases. CONCLUSIONS. Many patients with positive SMs do not have positive IMs. A positive SM more reliably predicts a positive IM when tumor involves greater than or equal to 3 low-power fields of the SM. The authors conclude that the clinical implications of a positive SM may not be the same as those of a positive IM. Clinical outcome studies are needed to define further the implications of positive SMs. (C) American Cancer Society. C1 BETH ISRAEL DEACONNESS MED CTR,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA. NR 18 TC 46 Z9 46 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 15 PY 1997 VL 79 IS 8 BP 1568 EP 1573 DI 10.1002/(SICI)1097-0142(19970415)79:8<1568::AID-CNCR19>3.0.CO;2-W PG 6 WC Oncology SC Oncology GA WR200 UT WOS:A1997WR20000019 PM 9118040 ER PT J AU Englert, C Maheswaran, S Garvin, AJ Kreidberg, J Haber, DA AF Englert, C Maheswaran, S Garvin, AJ Kreidberg, J Haber, DA TI Induction of p21 by the Wilms' tumor suppressor gene WT1 SO CANCER RESEARCH LA English DT Article ID CYCLIN-DEPENDENT KINASES; TRANSCRIPTION FACTOR; CELL-PROLIFERATION; KIDNEY DEVELOPMENT; PROTEIN; INHIBITION; P53; DIFFERENTIATION; EXPRESSION; PRODUCT AB WT1 encodes a zinc finger transcription factor that is expressed in the developing kidney and the inactivation of which leads to Wilms' tumor, a pediatric kidney cancer, We have recently shown that inducible expression of WT1 in osteosarcoma cells triggers programmed cell death, an effect that is associated with transcriptional repression of the endogenous epidermal growth factor receptor, We now show that WT1-mediated apoptosis is preceded by induction of the cyclin-dependent kinase inhibitor p21, associated with G(1) phase arrest, This effect is only demonstrated by WT1 isoforms with an intact DNA binding domain, and it is associated with increased expression of endogenous p21 mRNA, WT1-mediated induction of p21 is independent of p53, another tumor suppressor gene known to regulate p21 expression, In the kidney, p21 is expressed in differentiating glomerular podocytes along with WT1, We conclude that induction of p21 expression may contribute to WT1-dependent differentiation pathways in the kidney and potentially to the function of WT1 as a tumor suppressor gene. C1 MASSACHUSETTS GEN HOSP,CTR CANC,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29325. CHILDRENS HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. FU NCI NIH HHS [CA 37887, CA 58596] NR 39 TC 99 Z9 101 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1997 VL 57 IS 8 BP 1429 EP 1434 PG 6 WC Oncology SC Oncology GA WT723 UT WOS:A1997WT72300007 PM 9108440 ER PT J AU Simons, JW Jaffee, EM Weber, CE Levitsky, HI Nelson, WG Carducci, MA Lazenby, AJ Cohen, LK Finn, CC Clift, SM Hauda, KM Beck, LA Leiferman, KM Owens, AH Piantadosi, S Dranoff, G Mulligan, RC Pardoll, DM Marshall, FF AF Simons, JW Jaffee, EM Weber, CE Levitsky, HI Nelson, WG Carducci, MA Lazenby, AJ Cohen, LK Finn, CC Clift, SM Hauda, KM Beck, LA Leiferman, KM Owens, AH Piantadosi, S Dranoff, G Mulligan, RC Pardoll, DM Marshall, FF TI Bioactivity of autologous irradiated renal cell carcinoma vaccines generated by ex vivo granulocyte-macrophage colony-stimulating factor gene transfer SO CANCER RESEARCH LA English DT Article ID CYTOLYTIC T-LYMPHOCYTES; TUMOR-INFILTRATING LYMPHOCYTES; HUMAN PROSTATE-CANCER; MAJOR BASIC-PROTEIN; HUMAN-MELANOMA; HUMAN EOSINOPHILS; HLA-A2 MELANOMAS; ANTIGEN GP100; IMMUNITY; THERAPY AB Granulocyte-macrophage colony-stimulating factor (GM-CSF) gene-transduced, irradiated tumor vaccines induce potent, T-cell-mediated antitumor immune responses in preclinical models. We report the initial results of a phase I trial evaluating this strategy for safety and the induction of immune responses in patients with metastatic renal cell carcinoma (RCC). Patients were treated in a randomized, double-blind dose-escalation study with equivalent doses of autologous, irradiated RCC vaccine cells with or without ex vivo human GM-CSF gene transfer, The replication-defective retroviral vector MFG was used for GM-CSF gene transfer, No dose-limiting toxicities were encountered in 16 fully evaluable patients, GM-CSF gene-transduced vaccines were equivalent in toxicity to nontransduced vaccines up to the feasible limits of autologous tumor vaccine yield, No evidence of autoimmune disease was observed, Biopsies of intradermal sites of injection with GM-CSF gene-transduced vaccines contained distinctive macrophage, dendritic cell, eosinophil, neutrophil, and T-cell infiltrates similar to those observed in preclinical models of efficacy, Histological analysis of delayed-type hypersensitivity responses in patients vaccinated with GM-CSF-transduced vaccines demonstrated an intense eosinophil infiltrate that was not observed in patients who received nontransduced vaccines. An objective partial response was observed in a patient treated with GM-CSF gene-transduced vaccine who displayed the largest delayed-type hypersensitivity conversion, No replication-competent retrovirus was detected in vaccinated patients, This Phase I study demonstrated the feasibility, safety, and bioactivity of an autologous GM-CSF gene-transduced tumor vaccine for RCC patients. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT UROL,BALTIMORE,MD 21205. JAMES BUCHANAN BRADY UROL INST,BALTIMORE,MD. UNIV ALABAMA,BIRMINGHAM,AL 35294. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. HARVARD UNIV,SCH MED,CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. SOMATIX THERAPY CORP,ALAMEDA,CA 94501. RP Simons, JW (reprint author), JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,720 N WOLFE ST,BALTIMORE,MD 21205, USA. NR 50 TC 349 Z9 353 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1997 VL 57 IS 8 BP 1537 EP 1546 PG 10 WC Oncology SC Oncology GA WT723 UT WOS:A1997WT72300024 PM 9108457 ER PT J AU Sato, N Vatner, SF Shen, YT Kudej, RK GhalehMarzban, B Uechi, M Asai, K Mirsky, I Patrick, TA Shannon, RP Vatner, DE AF Sato, N Vatner, SF Shen, YT Kudej, RK GhalehMarzban, B Uechi, M Asai, K Mirsky, I Patrick, TA Shannon, RP Vatner, DE TI Effects of cardiac denervation on development of heart failure and catecholamine desensitization SO CIRCULATION LA English DT Article DE ventricular denervation; catecholamines; receptors, beta, adrenergic; heart failure; physiology ID IDIOPATHIC DILATED CARDIOMYOPATHY; BETA-ADRENERGIC-BLOCKADE; DOWN-REGULATION; LEFT-VENTRICLE; DOUBLE-BLIND; EXERCISE; SYSTEM; ABNORMALITIES; METOPROLOL; CARVEDILOL AB Background Two signatures of heart failure are activation of the sympathetic nervous system and catecholamine desensitization. However, whether or not the elimination of cardiac nerves affects either the progression of heart failure or catecholamine desensitization is not clear. Methods and Results We studied 8 dogs with selective ventricular denervation (VD) (surgical technique) and 10 intact dogs, chronically instrumented for measurement of left ventricular (LV) and arterial pressures, IV dP/dt, LV internal diameter, and wall thickness before and after heart failure was induced by rapid pacing (240 bpm) for 3 to 4 weeks. VD was confirmed by the absence of reflex effects induced by intracardiac veratrine and depletion of tissue norepinephrine and by supersensitive responses to norepinephrine. During the development of heart failure, LV end-systolic and end-diastolic stresses and heart rate increased, while myocardial contractility, as reflected by LV dP/dt and mean velocity of circumferential fiber shortening corrected for heart rate (Vcf(c)), decreased in both intact and VD dogs. However, the increases in LV end-diastolic stress and decreases in LV dP/dt as well as the relationship between LV systolic stress and Vcf(c) in heart failure were less (P<.05) in VD dogs. The responses of LV dP/dt and heart rate to both isoproterenol and norepinephrine in intact dogs were reduced in heart failure. The physiological desensitization to the inotropic effects of isoproterenol and norepinephrine was less in dogs with VD (P<.05), but chronotropic responses were similar because atrial innervation remained intact. Plasma norepinephrine levels were not different in VD dogs (592+/-79 pg/mL) compared with intact dogs (576+/-81 pg/mL) in heart failure. Conclusions Dogs with selective VD tolerated the development of heart failure better than intact dogs and demonstrated significantly less catecholamine desensitization. The latter indicates that intact ventricular innervation is required for physiological expression of catecholamine desensitization despite comparable elevation of plasma catecholamines during the development of heart failure. C1 NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. ALLEGHENY UNIV HLTH SCI,PITTSBURGH,PA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-33107, HL-38070, HL-37404] NR 32 TC 21 Z9 21 U1 1 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR 15 PY 1997 VL 95 IS 8 BP 2130 EP 2140 PG 11 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA WU760 UT WOS:A1997WU76000028 PM 9133524 ER PT J AU Sluder, AE Lindblom, T Ruvkun, G AF Sluder, AE Lindblom, T Ruvkun, G TI The Caenorhabditis elegans orphan nuclear hormone receptor gene nhr-2 functions in early embryonic development SO DEVELOPMENTAL BIOLOGY LA English DT Article ID C-ELEGANS; DNA-BINDING; TRANSCRIPTION FACTOR; RETINOIC ACID; GLUCOCORTICOID RECEPTOR; DROSOPHILA EMBRYO; SEQUENCE-ANALYSIS; ESCHERICHIA-COLI; LEADER SEQUENCE; CELL LINEAGE AB We have identified a Caenorhabditis elegans gene, nhr-2 that is a member of the nuclear hormone receptor superfamily of transcription factors and defines a new subclass of the superfamily. nhr-2 messenger RNA is expressed in the maternal germline and during the first half of embryogenesis. Zygotic expression of nhr-2 begins by the 16-cell stage, making it one of the earliest genes known to be transcribed in the embryo. Immunolocalization detects NHR-2 protein in embryonic nuclei as early as the 2-cell stage. The protein is present in every nucleus until the 16- to 20-cell stage. Subsequently, expression continues in many, but not all, cell lineages, becoming progressively restricted to the anterior and dorsal regions of the embryo and disappearing during the initial stages of morphogenesis. Disruption of nhr-2 function with antisense RNA results in embryonic and early larval arrest, indicating that the gene has an essential function in embryonic development. nhr-2 does not correspond to known mutations mapped to the same genetic interval, and will provide an entry point for further study of a heretofore uncharacterized zygotic gene regulatory pathway. (C) 1997 Academic Press. C1 MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP Sluder, AE (reprint author), UNIV GEORGIA,DEPT CELLULAR BIOL,724 BIOL SCI BLDG,ATHENS,GA 30602, USA. NR 92 TC 21 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD APR 15 PY 1997 VL 184 IS 2 BP 303 EP 319 DI 10.1006/dbio.1997.8544 PG 17 WC Developmental Biology SC Developmental Biology GA WX472 UT WOS:A1997WX47200009 PM 9133437 ER PT J AU Morgan, B Sun, L Avitahl, N Andrikopoulos, K Ikeda, T Gonzales, E Wu, P Neben, S Georgopoulos, K AF Morgan, B Sun, L Avitahl, N Andrikopoulos, K Ikeda, T Gonzales, E Wu, P Neben, S Georgopoulos, K TI Aiolos, a lymphoid restricted transcription factor that interacts with Ikaros to regulate lymphocyte differentiation SO EMBO JOURNAL LA English DT Article DE Aiolos; Ikaros; lymphoid progenitors; stem cells; transcription factors ID NATURAL-KILLER-CELLS; GENE; PROTEIN; DOMAIN; MICE; PRECURSORS; LEUKEMIA; FAMILY; MEMBER AB Development of the lymphoid system is dependent on the activity of zinc finger transcription factors encoded by the Ikaros gene, Differences between the phenotypes resulting from a dominant-negative and a null mutation in this gene suggest that Ikaros proteins act in concert with another factor with which they form heterodimers. Here we report the cloning of Aiolos, a gene which encodes an Ikaros homologue that heterodimerizes with Ikaros proteins. In contrast to Ikaros-which is expressed from the pluripotent stem cell to the mature lymphocyte-Aiolos is first detected in more committed progenitors with a lymphoid potential and is strongly up-regulated as these differentiate into pre-T and pre-B cell precursors. The expression patterns of Aiolos and Ikaros, the relative transcriptional activity of their homo- and heteromeric complexes, and the dominant interfering effect of mutant Ikaros isoforms on Aiolos activity all strongly suggest that Aiolos acts in concert with Ikaros during lymphocyte development, We therefore propose that increasing levels of Ikaros and Aiolos home- and heteromeric complexes in differentiating lymphocytes are essential for normal progression to a mature and immunocompetent state. C1 GENET INST INC,HEMOPOIESIS UNIT,CAMBRIDGE,MA 02138. SHOWA UNIV,SCH DENT,TOKYO 142,JAPAN. RP Morgan, B (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA 02129, USA. FU NIAID NIH HHS [R01-AI33062] NR 30 TC 226 Z9 232 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR 15 PY 1997 VL 16 IS 8 BP 2004 EP 2013 DI 10.1093/emboj/16.8.2004 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WV896 UT WOS:A1997WV89600020 PM 9155026 ER PT J AU Kaya, G Rodriguez, I Jorcano, JL Vassalli, P Stamenkovic, I AF Kaya, G Rodriguez, I Jorcano, JL Vassalli, P Stamenkovic, I TI Selective suppression of CD44 in keratinocytes of mice bearing an antisense CD44 transgene driven by a tissue-specific promoter disrupts hyaluronate metabolism in the skin and impairs keratinocyte proliferation SO GENES & DEVELOPMENT LA English DT Article DE CD44 glycoprotein; hyaluronate disruption; transgenic mice; keratinocyte proliferation ID CELL-ADHESION; GROWTH-FACTOR; RECEPTOR; BINDING; GLYCOPROTEIN; EXPRESSION; LOCALIZATION; FIBROBLASTS; DEGRADATION; RECOGNITION AB CD44 is a broadly distributed polymorphic glycoprotein that serves as the principal cell-surface receptor for hyaluronate. Although CD44-mediated cell interaction with hyaluronate has been implicated in a variety of physiologic events, including cell-cell and cell-substrate adhesion, cell migration, proliferation, and activation, as well as hyaluronate uptake and degradation, the biologic role of CD44 in vivo in various tissues remains to be determined. In the present work we have developed transgenic mice that express an antisense CD44 cDNA driven by the keratin-5 promoter. These mice lack detectable CD44 expression in skin keratinocytes and corneal epithelium and display abnormal hyaluronate accumulation in the superficial dermis and corneal stroma, distinct morphologic alterations of basal keratinocytes and cornea, and defective keratinocyte proliferation in response to mitogen and growth factors. These alterations are reflected by a decrease in skin elasticity, impaired local inflammatory response and tissue repair, delayed hair regrowth, and failure of the epidermis to undergo hyperplasia in response to carcinogen. Our observations indicate that two major functions of CD44 in skin are the regulation of keratinocyte proliferation in response to extracellular stimuli and the maintenance of local hyaluronate homeostasis. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. CIEMAT,DEPT CELL & MOL BIOL,E-28040 MADRID,SPAIN. UNIV GENEVA,MED CTR,DEPT PATHOL,CH-1211 GENEVA,SWITZERLAND. FU NCI NIH HHS [CA55735] NR 43 TC 169 Z9 173 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD APR 15 PY 1997 VL 11 IS 8 BP 996 EP 1007 DI 10.1101/gad.11.8.996 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA WY940 UT WOS:A1997WY94000004 PM 9136928 ER PT J AU Gerecke, DR Olson, PF Koch, M Knoll, JHM Taylor, R Hudson, DL Champliaud, MF Olsen, BR Burgeson, RE AF Gerecke, DR Olson, PF Koch, M Knoll, JHM Taylor, R Hudson, DL Champliaud, MF Olsen, BR Burgeson, RE TI Complete primary structure of two splice variants of collagen XII, and assignment of alpha 1(XII) collagen (COL12A1), alpha 1(IX) collagen (COL9A1), and alpha 1(XIX) collagen (COL19A1) to human chromosome 6q12-q13 SO GENOMICS LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; EMBRYONIC-DEVELOPMENT; FACIT COLLAGENS; IX COLLAGEN; CHAIN; MOLECULES; COMPONENT; DOMAINS; REGION; UNIQUE AB Overlapping cDNA clones that encode the full-length human alpha 1(XII) collagen polypeptides were isolated. The long variant molecule cDNA of 9750 nucleotides (nt) contains a 9189-nt open reading frame encoding 3063 amino acid residues. The short variant molecule cDNA of 6258 nt contains a 5697-nt open reading frame encoding 1899 amino acid residues. At the amino terminus of each variant is a 24-residue signal peptide that is followed by the mature polypeptides of 3039 amino acid residues with a calculated molecular mass of 330,759 Da for the long variant and 1875 amino acid residues with a calculated molecular mass of 203,163 Da for the short variant polypeptide. The human collagen XII chains are predicted to have all the structural domains described for the molecules in chicken and mouse, including, fibronectin type III repeats, von Willebrand factor A domains, and two triple-helical domains similar to those of all the other collagen family members. The amino acid residue sequence of human alpha 1(XII) collagen showed 92% identity to the mouse chain and 78% identity to the chicken chain. The sequence of three peptide fragments of collagen XII isolated from human placenta was identical to the sequence predicted from the deduced cDNA sequence and confirms that the cDNA encodes human alpha 1(XII) collagen. An isolated genomic clone was used to map the locus of the COL12A1 gene to chromosome 6q12-q13, very close to the locus of the FACIT collagen genes COL9A1 and COL19A1. RT-PCR on a variety of cDNAs demonstrates that both variant transcripts appear in human amnion, chorion, skeletal muscle, small intestine, and in cell cultures of human dermal fibroblasts, keratinocytes, and endothelial cells. Only the small. variant transcript is apparent in human lung, placenta, kidney, and a squamous cell carcinoma cell line. These results confirm the previous observations showing that collagen XII is found in collagen I-containing tissues. (C) 1997 Academic Press. C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,CHARLESTOWN,MA 02129. CHILDRENS HOSP,DIV GENET,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL DEACONESS MED CTR,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV ALABAMA,SCH DENT,BIRMINGHAM,AL 35294. HARVARD UNIV,SCH MED,DEPT BIOL CELULAR,BOSTON,MA 02115. RP Gerecke, DR (reprint author), MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BLDG 149,13TH ST,CHARLESTOWN,MA 02129, USA. FU NIAMS NIH HHS [AR35689]; NICHD NIH HHS [HD18568] NR 28 TC 30 Z9 32 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR 15 PY 1997 VL 41 IS 2 BP 236 EP 242 DI 10.1006/geno.1997.4638 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA WU556 UT WOS:A1997WU55600012 PM 9143499 ER PT J AU Cohen, RD Castellani, LW Qiao, JH VanLenten, BJ Lusis, AJ Reue, K AF Cohen, RD Castellani, LW Qiao, JH VanLenten, BJ Lusis, AJ Reue, K TI Reduced aortic lesions and elevated high density lipoprotein levels in transgenic mice overexpressing mouse apolipoprotein A-IV SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE apo A-IV; atherosclerosis; lipoproteins; cellular cholesterol efflux; transgene ID LECITHIN-CHOLESTEROL ACYLTRANSFERASE; GENETICALLY-ENGINEERED MICE; HUMAN-PLASMA; APOA-I; INTESTINAL EXPRESSION; INTERSTITIAL FLUID; MESENTERIC LYMPH; TANDEM REPEATS; MESSENGER-RNA; III GENE AB Transgenic mouse lines carrying several copies of the mouse apo A-IV gene were produced. Lipoprotein composition and function, and aortic lesion development were examined. Apo A-IV levels in the plasma of transgenic mice were elevated threefold compared with nontransgenic littermates on a chow diet, and sixfold in mice fed an atherogenic diet. Plasma concentrations of total cholesterol, HDL cholesterol, triglycerides, and free fatty acids were similar in transgenic and control mice fed a chow diet. However, with the atherogenic diet, male transgenic mice exhibited significantly higher levels of plasma triglycerides (P < 0.05), total cholesterol (P < 0.01), HDL cholesterol (P < 0.0001), and free fatty acids (P < 0.05), and lower levels of unesterified cholesterol (P < 0.05), than nontransgenic littermates. Expression of the apo A-IV transgene had a protective effect against the formation of diet-induced aortic lesions, with transgenics exhibiting lesion scores of similar to 30% those seen in control mice. HDL-sized lipoproteins isolated from transgenic mice fed the atherogenic diet promoted cholesterol efflux from cholesterol-loaded human monocytes more efficiently than comparable lipoproteins from nontransgenic counterparts. Plasma from transgenics also exhibited higher endogenous cholesterol esterification rates. Taken together, these results suggest that apo A-IV levels influence the metabolism and antiatherogenic properties of HDL. C1 W LOS ANGELES VET AFFAIRS MED CTR,LIPID RES LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,DEPT MICROBIOL & MOL GENET,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,INST MOL BIOL,LOS ANGELES,CA 90095. FU NHLBI NIH HHS [HL-30568, HL-28481] NR 59 TC 119 Z9 121 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 15 PY 1997 VL 99 IS 8 BP 1906 EP 1916 DI 10.1172/JCI119358 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA WV360 UT WOS:A1997WV36000014 PM 9109435 ER PT J AU He, JL deCastro, CM Vandenbark, GR Busciglio, J Gabuzda, D AF He, JL deCastro, CM Vandenbark, GR Busciglio, J Gabuzda, D TI Astrocyte apoptosis induced by HIV-1 transactivation of the c-kit protooncogene SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; SUPPRESSES APOPTOSIS; NEF; RECEPTOR; LIGAND; KINASE; CELLS; ENCEPHALITIS; ACTIVATION; INFECTION AB HIV-1 infection of the central nervous system (CNS) frequently causes dementia and other neurological disorders. The mechanisms of CNS injury in HIV-1 infection are poorly understood. Apoptosis of neurons and astrocytes is induced by HIV-1 infection ira vitro and in brain tissue from AIDS patients, but the apoptotic stimuli have not been identified. We report herein that HIV-1 infection of primary brain cultures induces the receptor tyrosine kinase protooncogene c-kit and that high levels of c-Kit expression are associated with astrocyte apoptosis. Overexpression of c-Kit in an astrocyte-derived cell line in the absence of HIV-1 induces rapid apoptotic death. The apoptotic mechanism requires the c-Kit tyrosine kinase domain. The mechanism of c-kit induction by HIV-1 involves transactivation of the c-kit promoter by the HIV-1 Nef protein. These studies demonstrate that c-Kit can induce astrocyte apoptosis and suggest that this mechanism may play a role in CNS injury caused by HIV-1 infection. We propose that c-Kit can serve dual functions as a growth factor receptor or apoptosis inducer. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. DUKE UNIV,MED CTR,DEPT MED,DIV HEMATOL ONCOL,DURHAM,NC 27710. CHILDRENS HOSP,DEPT NEUROL,MED CTR,BOSTON,MA 02115. FU NIAID NIH HHS [AI28691, AO6514, P30 AI028691]; NINDS NIH HHS [NS35734, R01 NS035734] NR 39 TC 51 Z9 52 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 APR 15 PY 1997 VL 94 IS 8 BP 3954 EP 3959 DI 10.1073/pnas.94.8.3954 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WW810 UT WOS:A1997WW81000087 PM 9108086 ER PT J AU Homanics, GE DeLorey, TM Firestone, LL Quinlan, JJ Handforth, A Harrison, NL Krasowski, MD Rick, CEM Korpi, ER Makela, R Brilliant, MH Hagiwara, N Ferguson, C Snyder, K Olsen, RW AF Homanics, GE DeLorey, TM Firestone, LL Quinlan, JJ Handforth, A Harrison, NL Krasowski, MD Rick, CEM Korpi, ER Makela, R Brilliant, MH Hagiwara, N Ferguson, C Snyder, K Olsen, RW TI Mice devoid of gamma-aminobutyrate type A receptor beta 3 subunit have epilepsy, cleft palate, and hypersensitive behavior SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene targeting; benzodiazepine; Angelman syndrome; anesthesia ID A RECEPTOR; ACID RECEPTOR; GABA(A) RECEPTOR; MESSENGER-RNAS; ANGELMAN SYNDROME; GROWTH-FACTORS; RETINOIC ACID; RAT-BRAIN; P-LOCUS; MOUSE AB gamma-Aminobutyric acid type A receptors (GABA(A)-Rs) mediate the bulk of rapid inhibitory synaptic transmission in the central nervous system. The beta 3 subunit is an essential component of the GABA(A)-R in many brain regions, especially during development, and is implicated in several pathophysiologic processes. We examined mice harboring a beta 3 gene inactivated by gene targeting. GABA(A)-R density is approximately halved in brain of beta 3-deficient mice, and GABA(A)-R function is severely impaired. Most beta-deficient mice die as neonates; some neonatal mortality, but not all, is accompanied by cleft palate. beta 3-deficient mice that survive are runted until weaning but achieve normal body size by adulthood, although with reduced life span. These mice are fertile but mothers fail to nurture offspring. Brain morphology is grossly normal, but a number of behaviors are abnormal, consistent with the widespread location of the beta 3 subunit. The mice are very hyperactive and hyperresponsive to human contact and other sensory stimuli, and often run continuously in tight circles. When held by the tail, they hold all paws in like a ball, which is frequently a sign of neurological impairment. They have difficulty swimming, walking on grids, and fall off platforms and rotarods, although they do not have a jerky gait. beta 3-deficient mice display frequent myoclonus and occasional epileptic seizures, documented by electroencephalographic recording. Hyperactivity, lack of coordination, and seizures are consistent with reduced presynaptic inhibition in spinal cord and impaired inhibition in higher cortical centers and/or pleiotropic developmental defects. C1 UNIV CALIF LOS ANGELES, DEPT MOL & MED PHARMACOL, LOS ANGELES, CA 90095 USA. W LOS ANGELES VET AFFAIRS MED CTR, NEUROL SERV, LOS ANGELES, CA 90073 USA. UNIV CHICAGO, DEPT ANESTHESIA & CRIT CARE, CHICAGO, IL 60637 USA. UNIV TURKU, DEPT PHARMACOL & CLIN PHARMACOL, FIN-20520 TURKU, FINLAND. NATL PUBL HLTH INST, DEPT ALCOHOL RES, FIN-00101 HELSINKI, FINLAND. UNIV TAMPERE, SCH MED, FIN-33101 TAMPERE, FINLAND. FOX CHASE CANC CTR, INST CANC RES, PHILADELPHIA, PA 19111 USA. RP Homanics, GE (reprint author), UNIV PITTSBURGH, SCH MED, DEPT ANESTHESIOL CRIT CARE MED, W1356 BIOMED SCI TOWER, PITTSBURGH, PA 15261 USA. OI Homanics, Gregg/0000-0003-3641-8153 FU NIAAA NIH HHS [AA10422, R01 AA010422, R37 AA010422]; NIGMS NIH HHS [GM43840, GM52035] NR 39 TC 313 Z9 321 U1 0 U2 7 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 APR 15 PY 1997 VL 94 IS 8 BP 4143 EP 4148 DI 10.1073/pnas.94.8.4143 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA WW810 UT WOS:A1997WW81000120 PM 9108119 ER PT J AU Pins, MR Saidman, SL Cosimi, AB Jennings, LD Stowell, CP AF Pins, MR Saidman, SL Cosimi, AB Jennings, LD Stowell, CP TI Accelerated acute rejection of an apparent A(2) renal allograft in an O recipient - Report of a case with flow cytometric analysis SO TRANSPLANTATION LA English DT Article ID BLOOD GROUP-A; ABO-INCOMPATIBLE A2; KIDNEY-TRANSPLANTATION; SECRETOR STATUS; ANTIGENS; LEWIS AB We report a case of accelerated acute rejection of a renal allograft from a presumed ABO histo-blood group A(2) donor in an O recipient, in which all of the published criteria for compatibility had been met. Flow cytometric analysis of the A and H antigen expression on the kidney donor's erythrocytes suggested that this donor did not have an A(2) phenotype, but rather another subgroup of A. Some of the reported cases of accelerated acute rejection of A(2) renal allografts in O recipients may have resulted from misapplication of the results of standard lectin agglutination to the transplant setting. The current case suggests that a more sophisticated method of ABO phenotyping, such as erythrocyte Bow cytometric analysis, may be necessary in the transplant setting. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 15 TC 14 Z9 14 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 APR 15 PY 1997 VL 63 IS 7 BP 984 EP 988 DI 10.1097/00007890-199704150-00014 PG 5 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA WU375 UT WOS:A1997WU37500014 PM 9112352 ER PT J AU Mittleman, MA Maclure, M Nachnani, M Sherwood, JB Muller, JE AF Mittleman, MA Maclure, M Nachnani, M Sherwood, JB Muller, JE TI Educational attainment, anger, and the risk of triggering myocardial infarction onset SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CORONARY HEART-DISEASE; CARDIOVASCULAR REACTIVITY; CYNICAL HOSTILITY; BLOOD-PRESSURE; SOCIAL SUPPORT; CASE-CROSSOVER; MENTAL STRESS; PLAQUES; LEVEL AB Background: While it has recently been shown that anger may trigger the onset of acute myocardial infarction, there has been no study of the role of socioeconomic factors in such triggering. Socioeconomic factors, such as educational attainment, may modulate the risk of triggering because of their influence on individual reactivity to external stressors and on the prevalence of traditional cardiac risk factors. Objective: To evaluate the influence of educational attainment on the relative risk of myocardial infarction onset following episodes of anger. Methods: We interviewed 1623 patients (501 women) an average of 4 days following a myocardial infarction. Data were collected on standard demographic variables as well as risk factors for coronary artery disease. Educational attainment was categorized into 3 levels: less than high school, completed high school, and at least some college. Anger was assessed by the Onset Anger Scale, a single-item, 7-level, self-report scale. Occurrence of anger in the 2 hours preceding the onset of myocardial in farction was compared with its expected frequency using self-matched control data based on the case-crossover study design. Results: The risk of having a myocardial infarction triggered by isolated episodes of anger declined consistently and significantly with increasing levels of educational attainment (P=.03). The relative risk was twice as high among those with less than high school education (relative risk, 3.3; 95% confidence interval, 2.0-5.4) compared with patients with at least some college education (relative risk, 1.6; 95% confidence interval, 0.9-2.9). Conclusions: These findings indicate that socioeconomic factors are potent modulators of the risk of triggering acute cardiovascular disease onset. A better understanding of the physiological mechanisms underlying this association may lead to novel approaches to prevent acute cardiovascular events. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. UNIV KENTUCKY,MED CTR,DEPT MED,DIV CARDIOL,LEXINGTON,KY 40536. RP Mittleman, MA (reprint author), HARVARD UNIV,BETH ISRAEL DEACONNESS MED CTR,SCH MED,DIV CARDIOVASC,INST PREVENT CARDIOVASC DIS,BOSTON,MA 02215, USA. FU NHLBI NIH HHS [HL41016] NR 40 TC 71 Z9 74 U1 0 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD APR 14 PY 1997 VL 157 IS 7 BP 769 EP 775 DI 10.1001/archinte.157.7.769 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA WR999 UT WOS:A1997WR99900007 PM 9125009 ER PT J AU Fischer, GS Alpert, HR Stoeckle, JD Emanuel, LL AF Fischer, GS Alpert, HR Stoeckle, JD Emanuel, LL TI Can goals of care be used to predict intervention preferences in an advance directive? SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID TREATMENT CHOICES; VALUES HISTORY; MEDICAL-CARE; PATIENT; PHYSICIANS; DECISIONS AB Background: Some have suggested that advance directives elicit goals of care from patients, instead of or in addition to specific intervention preferences, but little is known about whether goals of care can be used in a meaningful way on documents or whether they can predict preferences for specific interventions. Methods: Attending physicians (n=716) at the Massachusetts General Hospital in Boston were surveyed to elicit general goals of care leg, treat everything or comfort measures only) along with specific preferences for 11 medical interventions in 6 scenarios. In each scenario, each goal was classified as an adequate predictor of acceptance or rejection of an intervention if its predictive value of the preference for that intervention was at least 80%. Results: Goals varied with scenarios (P<.001) in a predictable manner. The goal treat everything was an adequate predictor of acceptance of each intervention, and comfort was an adequate predictor of rejection for nearly every intervention. Attempt cure adequately predicted acceptance of almost every nonaggressive intervention, but did not predict acceptance of aggressive interventions. Quality of life predicted rejection of aggressive interventions in 3 scenarios, but was not useful in other cases. When goals were predictors of preferences, the mean range of 95% confidence intervals for their predictive values was generally 20% or less. Conclusions: Goals have a valid role in advance directives, since the goal choices had a logical relationship to scenarios and intervention choices. However, the 2 goals attempt cure and choose quality of life were not predictive in many instances. If these findings hold true for more general populations of patients, then advance directive documents will need to rely on more than these general goal statements if they are to adequately represent patient preferences. C1 UNIV PITTSBURGH,SCH MED,CTR MED ETH,PITTSBURGH,PA 15261. HARVARD UNIV,SCH MED,DIV MED ETH,BOSTON,MA. MASSACHUSETTS GEN HOSP,DIV GEN INTERNAL MED,BOSTON,MA 02114. RP Fischer, GS (reprint author), UNIV PITTSBURGH,SCH MED,DIV GEN INTERNAL MED,120 LYTTON ST,PITTSBURGH,PA 15261, USA. NR 32 TC 34 Z9 34 U1 3 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD APR 14 PY 1997 VL 157 IS 7 BP 801 EP 807 DI 10.1001/archinte.157.7.801 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA WR999 UT WOS:A1997WR99900013 PM 9125014 ER PT J AU Burton, MD Kawashima, A Brayer, JA Kazemi, H Shannon, DC Schuchardt, A Costantini, F Pachnis, V Kinane, TB AF Burton, MD Kawashima, A Brayer, JA Kazemi, H Shannon, DC Schuchardt, A Costantini, F Pachnis, V Kinane, TB TI RET proto-oncogene is important for the development of respiratory CO2 sensitivity SO JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM LA English DT Article DE control of respiration; respiratory chemosensitivity; ret proto-oncogene; knockout mouse; genetics ID SUDDEN-INFANT-DEATH; CENTRAL HYPOVENTILATION SYNDROME; HIRSCHSPRUNGS-DISEASE; ARCUATE NUCLEUS; NEWBORN RAT; HEART-RATE; PROTOONCOGENE; MUTATIONS; ACETYLCHOLINE; PERTURBATIONS AB Brain stem muscarinic cholinergic pathways are important in respiratory carbon dioxide (CO2) chemosensitivity. Defects in the muscarinic system have been reported in children with congenital/developmental disorders of respiratory control such as sudden infant death syndrome (SIDS) and congenital central hypoventilation syndrome (CCHS). This early onset of disease suggests a possible genetic basis. The muscarinic system is part of the autonomic nervous system which develops from the neural crest. Ret proto-oncogene is important for this development. Thus, a potential role for ret in the development of respiratory CO2 chemosensitivity was considered. Using plethysmography, we assessed the ventilatory response to inhaled CO2 in the unanesthetized offsprings of ret(+/-) mice. Fractional increases in minute ventilation during hypercapnia relative to isocapnia were 5.1 +/- 3.2, 3.0 +/- 1.6 and 1.4 +/- 0.8 for the ret(+/+), ret(+/-) and ret(-/-) mice, respectively. The ret knockout mice have a depressed ventilatory response to inhaled CO2. Therefore, the ret gene is an important factor in the pathway of neuronal development which allow respiratory CO2 chemosensitivity. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PEDIAT PULM UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. MILLENNIUM PHARMACEUT,CAMBRIDGE,MA 02139. NATL INST MED RES,GENE STRUCT & EXPRESS LAB,LONDON NW7 1AA,ENGLAND. COLUMBIA UNIV COLL PHYS & SURG,DEPT GENET & DEV,NEW YORK,NY 10032. RP Burton, MD (reprint author), MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 02271-03] NR 33 TC 80 Z9 83 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1838 J9 J AUTONOM NERV SYST JI J. Auton. Nerv. Syst. PD APR 14 PY 1997 VL 63 IS 3 BP 137 EP 143 DI 10.1016/S0165-1838(97)00002-7 PG 7 WC Neurosciences SC Neurosciences & Neurology GA WU783 UT WOS:A1997WU78300004 PM 9138245 ER PT J AU Mundinger, TO Boyle, MR Taborsky, GJ AF Mundinger, TO Boyle, MR Taborsky, GJ TI Activation of hepatic sympathetic nerves during hypoxic, hypotensive and glucopenic stress SO JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM LA English DT Article DE norepinephrine; epinephrine; hemorrhage; 2-deoxyglucose ID HYPERGLYCEMIC RESPONSE; LIVER; DOGS; HYPOGLYCEMIA; STIMULATION; HEMORRHAGE; METABOLISM; NOREPINEPHRINE; INNERVATION; INFUSION AB To investigate the potential for neural regulation of liver function, we sought to determine whether hepatic sympathetic nerves are activated during stress. Hepatic norepinephrine spillover (HNESO) was measured in halothane-anesthetized dogs before, during and after glucopenia, hypoxia and hemorrhage. HNESO increased during 2-deoxyglucose (2-DG, 600 mg/kg plus 13.5 mg/kg/min, IV)-induced glucopenia from a baseline of 9 +/- 3 ng/min to 83 +/- 24 ng/min (Delta = +74 +/- 23 ng/min, p < 0.01). During hypoxia (partial pressure of oxygen in arterial blood = 23 +/- 2 mmHg), HNESO increased by 142 +/- 47 ng/min (p < 0.025), and HNESO increased by 84 +/- 22 ng/min (p < 0.01) during hemorrhage (mean arterial blood pressure = 40 +/- 1 mmHg), suggesting activation of hepatic sympathetic nerves during all three stresses. To validate the use of HNESO as an index of hepatic sympathetic nerve activity, we repeated the stresses of hypoxia and hemorrhage in dogs following chemical sympathetic denervation of the liver induced by prior intraportal 6-hydroxy dopamine infusion. Hepatic denervation reduced the HNESO responses to hypoxia and hemorrhage by more than 90%. In addition to hepatic neural responses to stress, the sympathetic responses of the adrenal medulla and of systemic sympathetic nerves were monitored using changes in the arterial concentration of epinephrine and norepinephrine, respectively. Arterial epinephrine and norepinephrine increased by varying degrees during all three stresses, suggesting general sympatho-adrenal activation. As expected, 6-hydroxydopamine pretreatment did not alter the epinephrine response to hypoxia or hemorrhage. The arterial norepinephrine responses to hypoxia and hemorrhage were modestly reduced in hepatically sympathectomized animals, suggesting a small hepatic contribution to the elevated arterial level of norepinephrine during these stresses. We conclude that: (1) the stresses of glucopenia, hypoxia and hemorrhage activate the sympathetic nerves of the liver and (2) HNESO is a valid index of hepatic sympathetic nerve activity. Finally, we speculate that such activation may influence liver function. C1 VET AFFAIRS PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. RP Mundinger, TO (reprint author), UNIV WASHINGTON,DEPT MED,DIV ENDOCRINOL & METAB 151,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. FU NIDDK NIH HHS [DK 12829, DK 17047] NR 28 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1838 J9 J AUTONOM NERV SYST JI J. Auton. Nerv. Syst. PD APR 14 PY 1997 VL 63 IS 3 BP 153 EP 160 DI 10.1016/S0165-1838(97)00004-0 PG 8 WC Neurosciences SC Neurosciences & Neurology GA WU783 UT WOS:A1997WU78300006 PM 9138247 ER PT J AU Wucherpfennig, K AF Wucherpfennig, K TI Hot papers - Autoimmunity molecular mimicry - Molecular mimicry in T cell-mediated autoimmunity: Viral peptides activate human T cell clones specific for myelin basic protein by K.W. Wucherpfennig, J.L. Strominger - Comments SO SCIENTIST LA English DT Editorial Material AB Molecular biologist Kai Wucherpfennig reports on molecular mimicry in T cell-mediated autoimmunity. RP Wucherpfennig, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CAMBRIDGE,MA 02138, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD APR 14 PY 1997 VL 11 IS 8 BP 11 EP 11 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA WX946 UT WOS:A1997WX94600010 ER PT J AU Torchilin, VP Trubetskoy, VS AF Torchilin, VP Trubetskoy, VS TI Amphiphilic polyethyleneglycol derivatives: Long-circulating micellar carriers for therapeutic and diagnostic agents. SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 13 PY 1997 VL 213 BP 59 EP POLY PN 2 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA WP187 UT WOS:A1997WP18702796 ER PT J AU Huang, Z Szostak, JW AF Huang, Z Szostak, JW TI RNA terminal modification. SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MOL BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 13 PY 1997 VL 213 BP 109 EP CARB PN 1 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA WP185 UT WOS:A1997WP18501003 ER PT J AU Wang, Y ParhamiSeren, B Gallagher, RT Berova, N Nakanishi, K Kim, S Corey, EJ Haupert, GT AF Wang, Y ParhamiSeren, B Gallagher, RT Berova, N Nakanishi, K Kim, S Corey, EJ Haupert, GT TI High yield purification of a hypothalamic Na, K-ATPase inhibitor and its structural characterization. SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. BION INC,RIVERSIDE TECHNOL CTR,CAMBRIDGE,MA 02139. COLUMBIA UNIV,DEPT CHEM,NEW YORK,NY 10032. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 13 PY 1997 VL 213 BP 127 EP ANYL PN 1 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA WP185 UT WOS:A1997WP18500482 ER PT J AU Bhatia, SN Yarmush, ML Toner, M AF Bhatia, SN Yarmush, ML Toner, M TI Probing the heterotypic interface: Parenchymal-mesenchymal cell communication. SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,LAB SURG SCI & ENGN,CTR ENGN MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 13 PY 1997 VL 213 BP 334 EP COLL PN 1 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA WP185 UT WOS:A1997WP18502574 ER PT J AU Symes, A Gearan, T Eby, J Fink, JS AF Symes, A Gearan, T Eby, J Fink, JS TI Integration of Jak-Stat and AP-1 signaling pathways at the vasoactive intestinal peptide cytokine response element regulates ciliary neurotrophic factor-dependent transcription SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LEUKEMIA-INHIBITORY FACTOR; NEUROBLASTOMA CELL-LINE; CULTURED SYMPATHETIC NEURONS; TRIPARTITE CNTF RECEPTOR; C-FOS; JUN-B; ONCOSTATIN-M; TYROSINE PHOSPHORYLATION; GENE-EXPRESSION; TRANSDUCER GP130 AB Ciliary neurotrophic factor (CNTF)-dependent induction of expression of the neuropeptide vasoactive intestinal peptide (VIP) gene is mediated by a 180-base pair cytokine response clement (CyRE) in the VIP promoter, To elucidate the molecular mechanisms mediating the transcriptional activation by CNTF, intracellular signaling to the CyRE has been studied in a neuroblastoma cell line, It has been shown previously that CNTF induces Stat proteins to bind to a site within the CyRE, CNTF also induces a second protein to bind to a C/EBP-like site within the CyRE. In this report, we show that this inducible CyRE binding protein is composed of the AP I proteins c-Fos, JuuB, and JunD., These proteins bind to a non-canonical AP-P site located near the previously characterized C/EBP site, The serine/threonine kinase inhibitor H7 prevents CNTF-dependent induction of AP-1 binding and CyRE-mediated transcription, suggesting that an H7-sensitive kinase is important to mediating CNTF effects on VIP transcription, The integration at the VIP CyRE of the Jak-Stat and AP-I signaling pathways with other pre-existing proteins provides a cellular mechanism for cell- and cytokine-specific signaling. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,MOL NEUROBIOL LAB,BOSTON,MA 02114. RI Symes, Aviva/S-7471-2016 OI Symes, Aviva/0000-0003-2557-9939 FU NINDS NIH HHS [NS27514] NR 70 TC 50 Z9 50 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 11 PY 1997 VL 272 IS 15 BP 9648 EP 9654 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU039 UT WOS:A1997WU03900012 PM 9092493 ER PT J AU Sattler, M Salgia, R Shrikhande, G Verma, S Pisick, E Prasad, KVS Griffin, JD AF Sattler, M Salgia, R Shrikhande, G Verma, S Pisick, E Prasad, KVS Griffin, JD TI Steel factor induces tyrosine phosphorylation of CRKL and binding of CRKL to a complex containing c-Kit, phosphatidylinositol 3-kinase, and p120(CBL) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SPOTTING W LOCUS; CELL FACTOR; PROTO-ONCOGENE; SH3 DOMAIN; HEMATOPOIETIC-CELLS; SIGNALING PATHWAYS; CBL PROTOONCOGENE; KINASE RECEPTOR; PI 3-KINASE; PC12 CELLS AB Steel factor (SF) is a growth and survival factor for hematopoietic cells, The receptor for SF, c-Kit, contains intrinsic tyrosine kinase activity, and binding of SF induces rapid tyrosine phosphorylation of several cellular proteins, including c-ait itself, Activation of C-Kit is shown here to induce tyrosine phosphorylation of CRKL, and CRKL coprecipitated with c-Kit through an interaction that required the CRKL SH3 domains and not the SH2 domain, CRKL associated with c-Kit indirectly as part of a larger complex of proteins, Two proteins in this complex were identified as the p85 regulatory subunit of phosphatidylinositol 3-kinase (p85(PI3K)) and the proto-oncoprotein p120(CBL). Because p85(PI3K) is known to bind to the activated c-Kit receptor, the possibility that CRKL interacted with c-Kit indirectly through p85(PI3K) was investigated, Far Western blotting with a CRKL-SH3 glutathione S-transferase fusion protein showed that CRKL binds directly to p85(PI3K) in vitro, However, although a small amount of CRKL was preassociated with p85(PI3K), the interaction was increased after SF stimulation, suggesting that the interactions of these three proteins are complex, We conclude that SF induces the formation of a signaling complex potentially containing CRKL and p120(CBL), of which bind to c-Kit through p85PI3K. These data suggest that one function of CRKL in normal cells might be to recruit signaling molecules such as CBL into a complex with PI3K, Such complexes could be important in propagating signals involving PI3K such as gene expression and adhesion. C1 DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FU NCI NIH HHS [CA01730]; NIDDK NIH HHS [DK50654] NR 62 TC 90 Z9 92 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 APR 11 PY 1997 VL 272 IS 15 BP 10248 EP 10253 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU039 UT WOS:A1997WU03900093 PM 9092574 ER PT J AU Guan, GM Dai, PH Osborne, TF Kim, JB Shechter, I AF Guan, GM Dai, PH Osborne, TF Kim, JB Shechter, I TI Multiple sequence elements are involved in the transcriptional regulation of the human squalene synthase gene SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIPOPROTEIN RECEPTOR GENE; LEUCINE ZIPPER PROTEIN; MOLECULAR-CLONING; BINDING PROTEIN-1; STEROL REGULATION; NF-Y; PROMOTER; SREBP-1; IDENTIFICATION; EXPRESSION AB The expression of human squalene synthase (HSS) gene is transcriptionally regulated in HepG-2 cells, up to 10-fold, by variations in cellular cholesterol homeostasis, An earlier deletion analysis of the 5'-flanking region of the HSS gene demonstrated that most of the HSS promoter activity is detected within a 69-base pair sequence located between nucleotides -131 and -200, ADD1/SREBP-1c, a rat homologue of sterol regulatory element binding protein (SREBP)-1c binds to sterol regulatory element (SRE)-1-like sequence (HSS-SRE-1) present in this region (Guan, G., Jiang, G., Koch, R. L. and Shechter, I. (1995) J. Biol. Chem. 270, 21958-21965), In our present study, we demonstrate that mutation of this HSS-SRE-1 element significantly reduced, but did not abolish, the response of HSS promoter to change in sterol concentration, Mutation scanning indicates that two additional DNA promoter sequences are involved in sterol-mediated regulation, The first sequence contains an inverted SRE-3 element (Inv-SRE-3) and the second contains an inverted Y-box (Inv-Y-box) sequence, A single mutation in any of these sequences reduced, but did not completely remove, the response to sterols, Combination mutation studies showed that the HSS promoter activity was abolished only when all three elements were mutated simultaneously, Go-expression of SRE-1- or SRE-2-binding proteins (SREBP-1 or SREBP-2) with HSS promoter-luciferase reporter resulted in a dramatic increase of HSS promoter activity, Gel mobility shift studies indicate differential binding of the SREBPs to regulatory sequences in the HSS promoter. These results indicate that the transcription of the HSS gene is regulated by multiple regulatory elements in the promoter. C1 UNIFORMED SERV UNIV HLTH SCI,F EDWARD HEBERT SCH MED,DEPT BIOCHEM,BETHESDA,MD 20814. UNIV CALIF IRVINE,DEPT MOL BIOL & BIOCHEM,IRVINE,CA 92717. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL48540, HL50628] NR 32 TC 89 Z9 94 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 11 PY 1997 VL 272 IS 15 BP 10295 EP 10302 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WU039 UT WOS:A1997WU03900100 PM 9092581 ER PT J AU Marcon, L Sodroski, J AF Marcon, L Sodroski, J TI High degree of sensitivity of the simian immunodeficiency virus (SIVmac) envelope glycoprotein subunit association to amino acid changes in the glycoprotein 41 ectodomain SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID T-LYMPHOTROPIC RETROVIRUS; HTLV-III; OLIGOMERIC STRUCTURE; RHESUS-MONKEYS; MACROPHAGE TROPISM; VARIABLE REGIONS; SYNDROME AIDS; CELL-LINE; TYPE-1; INFECTION AB The infection of macaques by simian immunodeficiency virus (SIVmac) represents an attractive model to study the pathogenic determinants of primate and human immunodeficiency viruses, The utility of this model would be enhanced if genetic changes in human immunodeficiency virus (HIV-1) associated with interesting in vitro properties would, when introduced into SIVmac, result in similar phenotypes, In this study, we introduced amino acid changes into the SIV(mac)239 envelope glycoproteins that, in the context of the HIV-1 envelope glycoproteins, disproportionately attenuated in vitro cytopathic effects compared with the viral replication rate, Amino acid changes in the SIV(mac)239 gp41 ectodomain altered the noncovalent association of the gp120 and gp41 glycoproteins significantly more than did analogous changes in the HIV-1 envelope glycoproteins, Decreases in the affinity of the gp120-gp41 interaction were observed and were associated with a dramatic attenuation of virus replication not seen in the HIV-X studies, The increased sensitivity of the SIVmac gp120-gp41 interaction to amino acid changes presents an obstacle to the direct extension of results obtained with the HIV-1 envelope glycoproteins to the SIV-macaque model. 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 PADUA,SCH MED,INST MICROBIOL,I-35121 PADUA,ITALY. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA 06516]; NIAID NIH HHS [AI24755, AI28691] NR 60 TC 10 Z9 10 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR 10 PY 1997 VL 13 IS 6 BP 441 EP 447 DI 10.1089/aid.1997.13.441 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA WT421 UT WOS:A1997WT42100001 PM 9100985 ER PT J AU Zhang, D Johnson, RP AF Zhang, D Johnson, RP TI Molecular cloning and comparative analysis of the rhesus macaque costimulatory molecules CD80 (B7-1) and CD86 (B7-2) SO CELLULAR IMMUNOLOGY LA English DT Article ID T-CELL PROLIFERATION; B-CELLS; ACTIVATION ANTIGEN-B7; COUNTER-RECEPTOR; DENDRITIC CELLS; LYMPHOCYTES-T; CD28; CTLA-4; EXPRESSION; SIGNALS AB To facilitate analysis of the role of costimulatory molecules in a nonhuman primate model, we cloned and sequenced the CD80 (B7-1) and CD86 (B7-2) costimulatory molecules from rhesus macaques, Rhesus CD80 and CD86 were highly homologous to their human counterparts, with overall amino acid homologies of greater than 90%, and were specifically recognized by murine antihuman CD80 or CD86 monoclonal antibodies. Stable cell lines expressing rhesus CD80 or CD86 induced proliferation of suboptimally activated CD4(+) T cells and transcription of cytokine mRNA. Both CD80 and CD86 were able to provide costimulation for interferon-gamma and IL-2 synthesis by rhesus CD4(+) T cells, but CD80 costimulation also resulted in synthesis of IL-4 and IL-10. The high degree of homology between the rhesus and the human CD80 and CD86 molecules should facilitate analysis of therapeutic interventions directed at this costimulatory pathway in nonhuman primates. (C) 1997 Academic Press. C1 HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,DIV IMMUNOL,SOUTHBOROUGH,MA 01772. MASSACHUSETTS GEN HOSP,CTR AIDS RES,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. FU NCRR NIH HHS [NCRR 00055, NCRR 00168] NR 41 TC 7 Z9 7 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 10 PY 1997 VL 177 IS 1 BP 9 EP 17 DI 10.1006/cimm.1997.1098 PG 9 WC Cell Biology; Immunology SC Cell Biology; Immunology GA WW325 UT WOS:A1997WW32500002 PM 9140091 ER PT J AU Redmond, RW Kochevar, IE Krieg, M Smith, G McGimpsey, WG AF Redmond, RW Kochevar, IE Krieg, M Smith, G McGimpsey, WG TI Excited state relaxation in cyanine dyes: A remarkably efficient reverse intersystem crossing from upper triplet levels SO JOURNAL OF PHYSICAL CHEMISTRY A LA English DT Article ID MEROCYANINE 540-MEDIATED PHOTOSENSITIZATION; PHOTOPHYSICAL PROPERTIES; 3,3'-DIALKYLTHIACARBOCYANINE DYES; STRUCTURAL MODIFICATIONS; LEUKEMIC-CELLS; MECHANISM; PHOTOCHEMISTRY; FLUORESCENCE; ISOMERIZATION; SENSITIVITY AB The upper triplet states of Merocyanine 540 and related cyanine dyes have been generated by a two-color, two-pulse method. The decay of this state partitions between internal conversion to T-1 and remarkably efficient reverse intersystem crossing to the singlet manifold. Thus, UV or visible laser generation of the T-1 state (either directly or by a sensitized route) followed by excitation with a 640 nm pulse ultimately results in fluorescence and isomerization from the lowest excited singlet state (S-1), as evidenced by the production of the ground state photoisomer absorption and emission coincident with the second laser pulse. Since identical behavior (isomerization and fluorescence) is observed for direct excitation into the singlet manifold, we conclude that both the singlet and triplet states are of the same geometry and that isomerization does not occur directly from either T-1 or T-n. C1 MED COLL WISCONSIN,MACC FUND RES CTR,DEPT PEDIAT,MILWAUKEE,WI 53226. WORCESTER POLYTECH INST,DEPT CHEM & BIOCHEM,WORCESTER,MA 01609. RP Redmond, RW (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 37 TC 42 Z9 42 U1 1 U2 18 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1089-5639 J9 J PHYS CHEM A JI J. Phys. Chem. A PD APR 10 PY 1997 VL 101 IS 15 BP 2773 EP 2777 DI 10.1021/jp963001f PG 5 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA WT888 UT WOS:A1997WT88800007 ER PT J AU Sandrock, AW Cros, DP Louis, DN AF Sandrock, AW Cros, DP Louis, DN TI A 51-year-old man with chronic obstructive pulmonary disease and generalized muscle weakness - Acute critical-illness myopathy, with loss of myosin filaments, ? induced by corticosteroid treatment SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID GUILLAIN-BARRE-SYNDROME; HYPERKALEMIC PERIODIC PARALYSIS; ACUTE QUADRIPLEGIC MYOPATHY; ILL PATIENTS; NEUROMUSCULAR-JUNCTION; PROLONGED PARALYSIS; BLOCKING-AGENTS; NORTHERN CHINA; POLYNEUROPATHY; ANTIBODIES C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Sandrock, AW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 45 TC 16 Z9 16 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 10 PY 1997 VL 336 IS 15 BP 1079 EP 1088 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA WT161 UT WOS:A1997WT16100008 ER PT J AU Komatsuzaki, K Murayama, Y Giambarella, U Ogata, E Seino, S Nishimoto, I AF Komatsuzaki, K Murayama, Y Giambarella, U Ogata, E Seino, S Nishimoto, I TI A novel system that reports the G-proteins linked to a given receptor: A study of type 3 somatostatin receptor SO FEBS LETTERS LA English DT Article DE G-protein; subtype specificity; somatostatin receptor; reporting system; adenylyl cyclase; G(s) chimera ID ADENYLYL-CYCLASE; PHOSPHOLIPASE-C; ACTIVATION; ALPHA; IDENTIFICATION; SPECIFICITY; DOMAINS; INHIBITION; SECRETION; SUBUNITS AB SSTR3, a somatostatin (SST) receptor, is an adenylyl cyclase (AC)-inhibiting receptor, To assign the G-protein alpha-subunit (G alpha) linked to this receptor, we created a novel reporter system which utilizes the well-established facts that the C-terminal 5 residues of G alpha are the receptor contact site and G alpha(s) stimulates all subtypes of AC, We constructed chimeric G alpha(s), the C-terminal 5 residues of which were replaced with the corresponding C-terminus of each known G alpha, and examined which chimera confers SSTR3-induced activation of AC, Cellular transfection of SSTR3 and measurement of SST-dependent AC activity through co-transfected chimeric G alpha(s) revealed that SSTR3 recognizes the C-termini of G alpha(i1/2) hut not of G alpha(o) or G alpha(z), and those of G alpha(14) and G alpha(16), but not of G alpha(q) or G alpha(11). As predicted by the chimeric G alpha(s), SST-bound SSTR3 stimulated polyphosphoinositide turnover only when G alpha(16) or G alpha(14) was co-transfected, We conclude that the chimeric G alpha(s), system provides a new approach towards the assignment of G-proteins linked to a given receptor. (C) 1997 Federation of European Biochemical Societies. C1 KEIO UNIV,SCH MED,DEPT PHARMACOL & NEUROSCI,SHINJUKU KU,TOKYO 160,JAPAN. HARVARD UNIV,SCH MED,CARDIOVASC RES CTR,MASSACHUSETTS GEN HOSP,DEPT MED,CHARLESTOWN,MA 02129. UNIV TOKYO,SCH MED,DEPT MED 4,BUNKYO KU,TOKYO 113,JAPAN. CANC RES INST,TOKYO 170,JAPAN. CANC RES INST,TOSHIMA KU,TOKYO 170,JAPAN. CHIBA UNIV,SCH MED,DIV DEV PHYSIOL,CTR BIOMED SCI,CHIBA 280,JAPAN. NR 25 TC 31 Z9 32 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD APR 7 PY 1997 VL 406 IS 1-2 BP 165 EP 170 DI 10.1016/S0014-5793(97)00257-3 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA WT548 UT WOS:A1997WT54800037 PM 9109410 ER PT J AU Lloyd, GM Minto, AW Dorf, ME Proudfoot, A Wells, TNC Salant, DJ GutierrezRamos, JC AF Lloyd, GM Minto, AW Dorf, ME Proudfoot, A Wells, TNC Salant, DJ GutierrezRamos, JC TI RANTES and monocyte chemoattractant protein-1 (MCP-1) play an important role in the inflammatory phase of crescentic nephritis, but only MCP-1 is involved in crescent formation and interstitial fibrosis SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID COLONY-STIMULATING FACTOR; COLLAGEN MESSENGER-RNA; CYTOKINE RANTES; BOWMAN CAPSULE; MURINE RANTES; GROWTH-FACTOR; EXPRESSION; GLOMERULONEPHRITIS; CELLS; MACROPHAGE AB The involvement of chemokines in inflammation is well established, but their functional role in disease progression, and particularly in the development of fibrosis, is not yet understood. To investigate the functional role that the chemokines monocyte chemoattractant protein-1 (MCP-1) and RANTES play in inflammation and the progression to fibrosis during crescentic nephritis we have developed and characterized a murine model for this syndrome. Significant increases in T-lymphocytes and macrophages were observed within glomeruli and interstitium, paralleled by an induction of mRNA expression of MCP-1 and RANTES, early after disease initiation. Blocking the function of MCP-1 or RANTES resulted in significant decreases in proteinuria as well as in numbers of infiltrating leukocytes, indicating that both MCP-1 and RANTES (regulated upon activation in normal T cells expressed and secreted) play an important role in the inflammatory phase of crescentic nephritis. In addition, neutralization of MCP-1 resulted in a dramatic decrease in both glomerular crescent formation and deposition of type I collagen. These results highlight a novel role for MCP-1 in crescent formation and development of interstitial fibrosis, and indicate that in addition to recruiting inflammatory cells this chemokine is critically involved in irreversible tissue damage. C1 MILLENNIUM PHARMACEUT INC,CAMBRIDGE,MA 02139. BOSTON UNIV,MED CTR,DEPT MED,BOSTON,MA 02118. HARVARD UNIV,SCH MED,CTR BLOOD RES INC,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. GLAXO INST MOL BIOL SA,CH-1228 GENEVA,SWITZERLAND. NR 40 TC 51 Z9 51 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 7 PY 1997 VL 185 IS 7 BP 1371 EP 1380 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA WU183 UT WOS:A1997WU18300022 ER PT J AU Deutsch, JC AF Deutsch, JC TI Ascorbic acid and dehydroascorbic acid interconversion without net oxidation or reduction SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; HUMAN-BLOOD PLASMA; LIPID-PEROXIDATION; BIOLOGICAL SAMPLES; VITAMIN-C; ANTIOXIDANT AB The interconversion of ascorbic acid and dehydroascorbic acid was examined in aqueous solution using unlabeled dehydroascorbic acid and nonlabile, stable isotope-labeled ascorbic acid by gas chromatographic/mass spectrometric analysis. Although the formation of unlabeled ascorbic acid from unlabeled dehydroascorbic acid or labeled dehydroascorbic acid from labeled ascorbic acid did not occur to any significant extent when either solutions of unlabeled dehydroascorbic acid or labeled ascorbic acid were incubated alone, significant amounts of both labeled dehydroascorbic acid and unlabeled ascorbic acid formed when unlabeled dehydroascorbic acid was incubated with labeled ascorbic acid at acid pH. At alkaline pH, interconversion did not occur to any appreciable extent. Likewise, interconversion did not appear to occur in plasma at physiologic concentrations of ascorbic acid, but did occur with pharmacologic concentrations. These data show that ascorbic acid and dehydroascorbic acid interconvert in acidic solution, suggesting the reducing hydrogen atoms are delocalized when ascorbic acid is paired with dehydroascorbic acid under these circumstances. Alkaline pH and plasma inhibit the interconversion. (C) 1997 Academic Press. C1 UNIV COLORADO,HLTH SCI CTR,DEPT MED,DIV HEMATOL,DENVER,CO 80220. DENVER VET AFFAIRS HOSP,DENVER,CO 80220. RP Deutsch, JC (reprint author), UNIV COLORADO,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,4200 E 9TH AVE,CAMPUS BOX B-170,DENVER,CO 80220, USA. NR 18 TC 12 Z9 12 U1 0 U2 19 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR 5 PY 1997 VL 247 IS 1 BP 58 EP 62 DI 10.1006/abio.1997.2035 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA WT591 UT WOS:A1997WT59100009 PM 9126371 ER PT J AU Li, XG Haluska, P Hsiang, YH Bharti, AK Kufe, DW Liu, LF Rubin, EH AF Li, XG Haluska, P Hsiang, YH Bharti, AK Kufe, DW Liu, LF Rubin, EH TI Involvement of amino acids 361 to 364 of human topoisomerase I in camptothecin resistance and enzyme catalysis SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE topoisomerase; camptothecin; DNA binding; DNA cleavage; drug resistance; enzyme mutations ID ACTIVE-SITE TYROSINE; PROTEIN-KINASE-C; DNA TOPOISOMERASES; POINT MUTATION; DUPLEX DNA; PHOSPHORYLATION; IDENTIFICATION; BINDING; MECHANISM; POISONS AB Camptothecins are antineoplastic drugs that specifically target the enzyme DNA topoisomerase I. Prior work has identified a human topoisomerase I mutation, F361S, that confers resistance to camptothecin. We now demonstrate that substitutions in the 361-364 region can alter DNA cleavage/ligation by the enzyme. The defective catalysis exhibited by certain mutants likely relates to an impaired interaction with DNA, since these enzymes are more sensitive to the inhibitory effects of DNA binding ligands. Moreover, studies with peptides and fusion proteins suggest that the 361-364 region may bind DNA directly. The finding that the 361-364 region is involved in both enzyme catalysis and camptothecin resistance suggests that this region is part of the active site of human topoisomerase I and that camptothecin may interact with the enzyme at this site. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT PHARMACOL,PISCATAWAY,NJ 08854. CANC INST NEW JERSEY,PISCATAWAY,NJ 08854. DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA70981] NR 36 TC 36 Z9 36 U1 0 U2 1 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 APR 4 PY 1997 VL 53 IS 7 BP 1019 EP 1027 DI 10.1016/S0006-2952(96)00899-4 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WW920 UT WOS:A1997WW92000015 PM 9174116 ER PT J AU Lee, FJS Lin, LW Smith, JA AF Lee, FJS Lin, LW Smith, JA TI A N-alpha-acetyltransferase selectively transfers an acetyl group to NH2-terminal methionine residues: Purification and partial characterization SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEIN STRUCTURE AND MOLECULAR ENZYMOLOGY LA English DT Article DE amino-terminal processing; protein modification; yeast; (S-cerevisiae) ID AMINO-TERMINAL ACETYLATION; SACCHAROMYCES-CEREVISIAE; MICROGRAM QUANTITIES; ACID-SEQUENCE; RAT-LIVER; PROTEINS; YEAST; SPECIFICITY; PEPTIDES; IDENTIFICATION AB Methionine N-alpha-acetyltransferase (M-N(alpha)AT), which selectively catalyzes the transfer of an acetyl group from acetyl coenzyme A to the alpha-NH2 group of methionine residues in proteins and peptides, was isolated from Saccharomyces cerevisiae. The enzyme was purified 22 000-fold to apparent homogeneity by successive purification steps using DEAE-Sepharose, DE-52 cellulose, CM-52 cellulose, Affi-Gel Blue gel and hydroxyapatite. The M(r) of the native enzyme was estimated to be 70 000 +/- 5000 by gel filtration chromatography. The enzyme has a pI near 8.3 as determined by chromatofocusing on Mono P. The enzyme catalyzed the transfer of an acetyl group to a synthetic peptide mimicking the first 24 residues of yeast proteinase A inhibitor 3 (Met-Asn-Thr...) and 3 of its 19 penultimately substituted analogues ([Asp(2)], [Glu(2)], and [Gln(2)]). Based on the estimated molecular weight and amino-acid sequence, The enzyme is different from two other recently identified methionine N-alpha-acetyltransferases, NAT2 (Kulkarni, M.S. and Sherman, F. (1994) J. Biol. Chem. 269, 13141-13147) and MAK3 (Tercero, J.C. and Wickner, R.B. (1992) J. Biol. Chem. 267, 20277-20281). Among these three enzymes, M-N(alpha)AT and NAT2 have similar substrate specificity, however, only purified M-N(alpha)AT, but not recombinant NAT2 gene product, can catalyze the transfer of acetyl group to NH2-terminal methionine residues. The availability of this methionine N-alpha-acetyltransferase will advance the understanding of protein co-translational processing. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NATL TAIWAN UNIV,SCH MED,INST MOL MED,TAIPEI 10764,TAIWAN. RP Lee, FJS (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114, USA. OI LEE, FANG-JEN/0000-0002-2167-2426 NR 49 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4838 J9 BBA-PROTEIN STRUCT M JI Biochim. Biophys. Acta-Protein Struct. Molec. Enzym. PD APR 4 PY 1997 VL 1338 IS 2 BP 244 EP 252 DI 10.1016/S0167-4838(96)00200-2 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA WT626 UT WOS:A1997WT62600011 PM 9128142 ER PT J AU Ferrante, RJ Schulz, JB Kowall, NW Beal, MF AF Ferrante, RJ Schulz, JB Kowall, NW Beal, MF TI Systemic administration of rotenone produces selective damage in the striatum and globus pallidus, but not in the substantia nigra SO BRAIN RESEARCH LA English DT Article DE mitochondrion; Parkinson's; 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP); basal ganglion; complex I; NADPH-diaphorase; substantia nigra ID NADH DEHYDROGENASE; 1-METHYL-4-PHENYLPYRIDINIUM ION; PARKINSONS-DISEASE; METABOLITE; PIERICIDIN; DEFICIENCY; INHIBITION; NEUROTOXIN; TOXICITY; ANALOGS AB Complex I dysfunction has been implicated in the pathogenesis of Parkinson's disease and in the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces a Parkinsonian syndrome in experimental animals and humans. Rotenone is an insecticide which is a specific inhibitor of complex I. We examined the pattern of central nervous system damage produced by i.v. systemic administration of rotenone in rats. Rotenone produced selective damage in the striatum and the globus pallidus, but the substantia nigra was spared. These results are consistent with prior reports suggesting that the selective vulnerability of the substantia nigra to MPTP involves both uptake by the dopamine transporter as well as complex I inhibition, and they show that rotenone produces a unique pattern of central nervous system damage. (C) 1997 Elsevier Science B.V. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,BEDFORD,MA 01730. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. UNIV TUBINGEN,DEPT NEUROL,D-7400 TUBINGEN,GERMANY. RI Schulz, Jorg/D-9786-2012; Kowall, Neil/G-6364-2012 OI Schulz, Jorg/0000-0002-8903-0593; Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [AG12922, 1P30AG13846]; NINDS NIH HHS [NS16367] NR 21 TC 125 Z9 139 U1 1 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 4 PY 1997 VL 753 IS 1 BP 157 EP 162 DI 10.1016/S0006-8993(97)00008-5 PG 6 WC Neurosciences SC Neurosciences & Neurology GA WT662 UT WOS:A1997WT66200019 PM 9125443 ER PT J AU Perrimon, N Perkins, LA AF Perrimon, N Perkins, LA TI There must be 50 ways to rule the signal: The case of the Drosophila EGF receptor SO CELL LA English DT Review ID PROTEIN; TRIGGERS; PATHWAY C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,BOSTON,MA 02114. RP Perrimon, N (reprint author), HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115, USA. NR 17 TC 121 Z9 123 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 4 PY 1997 VL 89 IS 1 BP 13 EP 16 DI 10.1016/S0092-8674(00)80177-4 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WR685 UT WOS:A1997WR68500004 PM 9094709 ER PT J AU Ditzel, HJ Parren, PWHI Binley, JM Sodroski, J Moore, JP Barbas, CF Burton, DR AF Ditzel, HJ Parren, PWHI Binley, JM Sodroski, J Moore, JP Barbas, CF Burton, DR TI Mapping the protein surface of human immunodeficiency virus type 1 gp120 using human monoclonal antibodies from phage display libraries SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE human antibody repertoires; epitope mapping; HIV infection; combinatorial libraries; gp120 topology ID CD4 BINDING-SITE; COMBINATORIAL LIBRARIES; NEUTRALIZING ANTIBODY; GLYCOPROTEIN GP120; VARIABLE REGIONS; FAB FRAGMENTS; EPITOPES; HIV-1; PANEL; IDENTIFICATION AB Panels of hybridoma-derived monoclonal antibodies against diverse epitopes are widely used in defining protein surface topography, particularly in the absence of crystal or NMR structural information. Here we show that recombinant monoclonal antibodies from phage display libraries provide a rapid alternative for surface epitope mapping. Diverse epitopes are accessed by presenting antigen to the library in different forms, such as sequential masking of epitopes with existing antibodies or ligands prior to selection and selection on peptides. The approach is illustrated for a recombinant form of the human immunodeficiency virus type 1 (HIV-1) surface glycoprotein gp120 which has been extensively mapped by rodent and human monoclonal antibodies derived by cellular methods. Human recombinant Fab fragments to most of the principal epitopes on gp120 are selected including Fabs to the C1 region, a C1/C5 epitope, a C1/C2 epitope, the V2 loop, the V3 loop and the CD4 binding domain. In addition an epitope linked to residues in the V2 loop and CD4 binding domain is identified. Most of these specificities are associated with epitopes presented poorly on native multimeric envelope, consistent with the notion that these antibodies are associated with immunization by forms of gp120 differing in conformation from that found on whole virus or infected cells. (C) 1997 Academic Press Limited. C1 Scripps Res Inst, DEPT IMMUNOL, LA JOLLA, CA 92037 USA. Scripps Res Inst, DEPT MOL BIOL, LA JOLLA, CA 92037 USA. ODENSE UNIV, SCH MED, DEPT MED MICROBIOL, ODENSE, DENMARK. UNIV COPENHAGEN HOSP, RIGSHOSP, DEPT CLIN IMMUNOL, DK-2100 COPENHAGEN, DENMARK. NYU, SCH MED, AARON DIAMOND AIDS RES CTR, NEW YORK, NY 10016 USA. DANA FARBER CANC INST, DIV HUMAN RETROVIROL, BOSTON, MA 02115 USA. OI Ditzel, Henrik J./0000-0003-3927-5135; Parren, Paul/0000-0002-4365-3859 FU NCI NIH HHS [CA06516]; NIAID NIH HHS [AI24755, AI31783] NR 45 TC 52 Z9 52 U1 1 U2 2 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD APR 4 PY 1997 VL 267 IS 3 BP 684 EP 695 DI 10.1006/jmbi.1997.0912 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WT334 UT WOS:A1997WT33400017 PM 9126846 ER PT J AU Zhang, R Zhang, H Zhu, WM Pardee, AB Coffey, RJ Liang, P AF Zhang, R Zhang, H Zhu, WM Pardee, AB Coffey, RJ Liang, P TI Mob-1, a Ras target gene, is overexpressed in colorectal cancer SO ONCOGENE LA English DT Article DE ras oncogene; chemokines; colorectal cancer; cell transformation ID DIFFERENTIAL DISPLAY; MESSENGER-RNA; EXPRESSION; CELLS; INDUCTION; PROTEINS AB Mutations in the ras oncogenes have been linked to many different cancers, In contrast to the extensive body of knowledge related to the genetics of ras activation, relatively little is known of the transcriptional events triggered by ras, In previous work we have used differential display to identify Mob-1, a member of alpha-chemokine family, as one of the immediate transcriptional targets following Ras activation, Here, we provide additional experimental evidence to support this finding by the use of an inducible H-ras expression system, the treatment of Ras farnesyl transferase inhibitor and activation of endogenous Ras by serum growth factors, We further demonstrate that IP-10, the human homolog of Mob-1, is overexpressed in the majority of colorectal cancers. C1 VANDERBILT UNIV,DEPT CELL BIOL,SCH MED,VANDERBILT CANC CTR,NASHVILLE,TN 37232. VANDERBILT UNIV,DEPT MED & CELL BIOL,NASHVILLE,TN 37232. VANDERBILT UNIV,VET AFFAIRS MED CTR,NASHVILLE,TN 37232. DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. FU NCI NIH HHS [R01 CA46413, R01 CA61232] NR 17 TC 26 Z9 26 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 3 PY 1997 VL 14 IS 13 BP 1607 EP 1610 DI 10.1038/sj.onc.1200957 PG 4 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA WQ548 UT WOS:A1997WQ54800012 PM 9129152 ER PT J AU Dan, L Laposata, M AF Dan, L Laposata, M TI Ethyl palmitate and ethyl oleate are the predominant fatty acid ethyl esters in the blood after ethanol ingestion and their synthesis is differentially influenced by the extracellular concentrations of their corresponding fatty acids SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE fatty acid ethyl ester; ethanol; fatty acid; Hep G2 cells ID METABOLISM; RAT; SYNTHASE; IDENTIFICATION; ARACHIDONATE; PURIFICATION; LIPASE AB The possibility that fatty acid ethyl esters (FAEEs), esterification products of fatty acids and ethanol, are mediators of ethanol-induced organ damage was suggested by an autopsy study in which individuals who died while acutely intoxicated were found to have FAEEs predominantly in the organs damaged by ethanol abuse, We initially observed in human subjects after ethanol consumption that there is a marked preference for the synthesis of ethyl palmitate and ethyl oleate over other FAEEs. To investigate the basis for this relative fatty acid specificity for FAEE synthesis, we used an in vitro system of Hep G2 cells incubated with ethanol. The cells were capable of synthesizing FAEEs upon exposure to ethanol and they showed a preference for synthesis of ethyl palmitate and ethyl oleate, as was found in human plasma after ethanol ingestion, This finding allowed us to explore the metabolic preference for palmitate and oleate in FAEE synthesis at the biochemical level using intact cells, We demonstrated that the preferential selection of palmitate and oleate for FAEE synthesis was not likely to be the result of specificity for palmitate and oleate by FAEE synthase or preferential uptake of palmitate and oleate by Hep G2 cells, In studies to determine whether the preference for ethyl palmitate and ethyl oleate synthesis was a result of higher concentrations of palmitate and oleate in the extracellular medium, we observed that the synthesis of ethyl oleate, ethyl linoleate, and ethyl arachidonate, but not ethyl palmitate, is influenced by the extracellular concentration of its corresponding fatty acid. The results of our studies indicate that ethyl palmitate and ethyl oleate are the predominant ethyl esters synthesized, that there is no preferential uptake or enzyme affinity for their fatty acid precursors to explain the predominance, and that ethyl palmitate synthesis is uniquely unaffected by the concentration of palmitate in the extracellular medium. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,DIV CLIN LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 31 TC 32 Z9 33 U1 0 U2 2 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 APR PY 1997 VL 21 IS 2 BP 286 EP 292 DI 10.1097/00000374-199704000-00016 PG 7 WC Substance Abuse SC Substance Abuse GA WU258 UT WOS:A1997WU25800016 PM 9113265 ER PT J AU Sontag, SJ Robinson, M Roufail, W Hirschowitz, BI Sabesin, SM Wu, WC Behar, J Peterson, WL Kranz, KR Tarnawski, A Dayal, Y Berman, R Simon, TJ AF Sontag, SJ Robinson, M Roufail, W Hirschowitz, BI Sabesin, SM Wu, WC Behar, J Peterson, WL Kranz, KR Tarnawski, A Dayal, Y Berman, R Simon, TJ TI Daily omeprazole surpasses intermittent dosing in preventing relapse of oesophagitis: A US multi-centre double-blind study SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article ID LONG-TERM TREATMENT; REFLUX ESOPHAGITIS; RANITIDINE AB Introduction: Relapse of erosive oesophagitis occurs in almost all patients if treatment is stopped after initial healing. Aim: To assess the potential of different therapeutic regimens of omeprazole to prevent relapse of erosive reflux oesophagitis after initial healing with omeprazole, Patients and methods: Patients whose active erosive reflux oesophagitis (grade greater than or equal to 2) had healed (grade 0 or 1) after 4-8 weeks of open-label omeprazole 40 mg daily (phase I) were eligible to join a multi-centre, 6-month double-blind, placebo-controlled maintenance study (phase II), which included endoscopy, symptom assessments, serum gastrin measurements, and gastric fundic biopsies. During phase I, endoscopy was performed at weeks 0, 4, and 8. At the end of phase I, 429 of 472 patients (91%) were healed, and there were significant reductions in heartburn, dysphagia and acid regurgitation. Of the 429 patients who healed, 406 joined phase II and were randomized to one of three groups: 20 mg omeprazole daily (n = 138), 20 mg omeprazole for 3 consecutive days each week (n = 137), or placebo (n = 131). During phase II, endoscopy was performed at months 1, 3, and 6 or at symptomatic relapse. Results: The percentages of patients still in endoscopic remission at 6 months were 11% for placebo, 34% for omeprazole 3-days-a-week, and 70% for omeprazole daily, Both omeprazole regimens were superior to placebo in preventing recurrence of symptoms (P < 0.001); however, omeprazole 20 mg daily was superior to omeprazole 20 mg 3-days-a-week (P < 0.001). Compared to baseline, omeprazole therapy resulted in no significant differences among treatment groups in the distribution of gastric endocrine cells. Conclusions: These results show that after healing of erosive oesophagitis with 4-8 weeks of omeprazole, relapse of oesophagitis and recurrence of reflux symptoms can be prevented in 70% of patients with a maintenance regimen of 20 mg daily, but that intermittent dosing comprising 3 consecutive days each week significantly compromises efficacy. C1 UNIV TEXAS,SW MED CTR,DEPT MED,DALLAS,TX 75230. RP Sontag, SJ (reprint author), US DEPT VET AFFAIRS,MED SERV,POB 5000,BLDG 1 151B,HINES,IL 60141, USA. NR 12 TC 18 Z9 18 U1 0 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PD APR PY 1997 VL 11 IS 2 BP 373 EP 380 DI 10.1046/j.1365-2036.1997.141317000.x PG 8 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA WX244 UT WOS:A1997WX24400021 PM 9146778 ER PT J AU Samore, MH Wessolossky, MA Lewis, SM Shubrooks, SJ Karchmer, AW AF Samore, MH Wessolossky, MA Lewis, SM Shubrooks, SJ Karchmer, AW TI Frequency, risk factors, and outcome for bacteremia after percutaneous transluminal coronary angioplasty SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID TRANS-LUMINAL ANGIOPLASTY; SEPTIC ENDARTERITIS; CARDIAC-CATHETERIZATION; EPIDURAL ABSCESS; FEMORAL-ARTERY; INFECTION; COMPLICATIONS AB The objectives of this study were to examine bacteremias after percutaneous transluminal coronary angioplasty (PTCA) with respect to incidence, outcome, and risk factors. Patients undergoing PTCA from January 1990 through April 1994 were studied; during this period a total of 4,217 PTCAs were performed in 3,473 patients. With use of predefined clinical and microbiologic criteria, bacteremias were divided into 3 categories according to the relation to the PTCA procedure: PTCA-related, unrelated, and indeterminate. Ninety-one patients with at least 1 positive blood culture during a 7-week period after PTCA were identified. The bacteremia was classified as unrelated to the PTCA procedure in 32 patients, PTCA-related in 27, and indeterminant in the remaining 32 patients. The attack rate of PTCA-related bacteremia during the 52-month period was 0.64%. The most common organisms causing PTCA-related bacteremia were Staphylococcus aureus (14 patients), coagulase-negative staphylococci (9 patients) and group B streptococci (6 patients). Septic complications, which included femoral artery mycotic aneurysm, septic arthritis, and septic thrombosis, occurred in 10 patients (0.24%). Independent risk factors for PTCA-related bacteremia included duration of procedure (odds ratio [OR] 2.9; p = 0.04), number of catheterizations at the same site (OR 4.0; p = 0.015), difficult vascular access (OR 14.9; p = 0.007), arterial sheath in place >1 day (OR 6.8; p = 0.025), congestive heart failure (OR 43.3; p = 0.002). Thus, PTCA-related bacteremia is an infrequent complication of PTCA but can be associated with significant morbidity, particularly when the infecting organism is S. aureus. Four of the 5 risk factors for PTCA-related bacteremia appear to correlate directly with increased vascular injury or maintenance of the arterial entry for the procedure. (C) 1997 by Excerpta Medica, Inc. C1 BETH ISRAEL DEACONESS MED CTR,DIV INFECT DIS,DEPT MED,BOSTON,MA 02215. BETH ISRAEL DEACONESS MED CTR,DIV CARDIOVASC MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 19 TC 47 Z9 49 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD APR 1 PY 1997 VL 79 IS 7 BP 873 EP 877 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA WT426 UT WOS:A1997WT42600006 PM 9104897 ER PT J AU Kahrilas, PJ Orlando, RC Sontag, SJ Lechago, J Richter, JE Freston, JW Peura, DA Hirschowitz, BI AF Kahrilas, PJ Orlando, RC Sontag, SJ Lechago, J Richter, JE Freston, JW Peura, DA Hirschowitz, BI TI The pathogenesis of GERD: The relationship between epithelial defense, dysmotility, and acid exposure - Panel discussion SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material C1 NW MEM HOSP,DEPT GASTROENTEROL,GASTROINTESTINAL DIAGNOST LAB,CHICAGO,IL 60611. TULANE UNIV,SCH MED,DEPT PHYSIOL & MED,NEW ORLEANS,LA 70112. TULANE UNIV,MED CTR,DEPT MED,SECT GASTROENTEROL & HEPATOL,NEW ORLEANS,LA 70112. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,ENDOSCOPY LAB,HINES,IL 60141. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. METHODIST HOSP,DEPT LAB MED,HOUSTON,TX 77030. CLEVELAND CLIN FDN,DEPT GASTROENTEROL,CLEVELAND,OH 44195. UNIV CONNECTICUT,SCH MED,DEPT MED,FARMINGTON,CT. JOHN DEMPSEY HOSP,DEPT MED,FARMINGTON,CT. UNIV VIRGINIA,SCH MED,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,HLTH SCI CTR,DEPT INTERNAL MED,DIV GASTROENTEROL,CHARLOTTESVILLE,VA 22908. UNIV ALABAMA,SCH MED,DEPT PHYSIOL & MED,BIRMINGHAM,AL. MCMASTER UNIV,MED CTR,DIV GASTROENTEROL,HAMILTON,ON,CANADA. RP Kahrilas, PJ (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT MED,CHICAGO,IL 60611, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD APR PY 1997 VL 92 IS 4 SU S BP S5 EP S7 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WW683 UT WOS:A1997WW68300003 ER PT J AU Lechago, J McGuigan, JE Freston, JW Richter, JE Sontag, SJ Parkinson, A AF Lechago, J McGuigan, JE Freston, JW Richter, JE Sontag, SJ Parkinson, A TI Long-term acid control and proton pump inhibitors: Interactions and safety issues in perspective SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material C1 METHODIST HOSP,DEPT LAB MED,HOUSTON,TX 77030. UNIV FLORIDA,SHANDS HOSP,J HILLIS MILLER HLTH CTR,COLL MED,DEPT MED,GAINESVILLE,FL. UNIV CONNECTICUT,SCH MED,DEPT MED,FARMINGTON,CT. JOHN DEMPSEY HOSP,DEPT MED,FARMINGTON,CT. CLEVELAND CLIN FDN,DEPT GASTROENTEROL,CLEVELAND,OH 44195. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,ENDOSCOPY LAB,HINES,IL 60141. UNIV KANSAS,SCH MED,DEPT PHARMACOL TOXICOL & THERAPEUT,KANSAS CITY,KS. RP Lechago, J (reprint author), BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD APR PY 1997 VL 92 IS 4 SU S BP S56 EP S57 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WW683 UT WOS:A1997WW68300022 ER PT J AU Maton, PN Howden, CW Freston, JW Tolman, KG Hunt, RH Hirschowitz, BI Sontag, SJ Orlando, RC AF Maton, PN Howden, CW Freston, JW Tolman, KG Hunt, RH Hirschowitz, BI Sontag, SJ Orlando, RC TI Optimizing the pharmacology of acid control in acid-related disorders - Panel discussion SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material C1 UNIV S CAROLINA,SCH MED,DEPT INTERNAL MED,DIV DIGEST DIS & NUTR,COLUMBIA,SC. RICHLAND MEM HOSP,DEPT INTERNAL MED,COLUMBIA,SC. UNIV CONNECTICUT,SCH MED,DEPT MED,FARMINGTON,CT. JOHN DEMPSEY HOSP,DEPT MED,FARMINGTON,CT. UNIV UTAH,SCH MED,DEPT GASTROENTEROL INTERNAL MED,SALT LAKE CITY,UT. UNIV HOSP,DEPT GASTROENTEROL,SALT LAKE CITY,UT. MCMASTER UNIV,MED CTR,DIV GASTROENTEROL,HAMILTON,ON,CANADA. UNIV ALABAMA,SCH MED,DEPT PHYSIOL & MED,BIRMINGHAM,AL. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,ENDOSCOPY LAB,HINES,IL 60141. TULANE UNIV,SCH MED,DEPT PHYSIOL & MED,NEW ORLEANS,LA 70112. TULANE UNIV,MED CTR,DEPT MED,SECT GASTROENTEROL & HEPATOL,NEW ORLEANS,LA 70112. RP Maton, PN (reprint author), PRESBYTERIAN HOSP,OKLAHOMA FDN DIGEST RES,OKLAHOMA CITY,OK 73104, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD APR PY 1997 VL 92 IS 4 SU S BP S20 EP S21 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WW683 UT WOS:A1997WW68300009 ER PT J AU Weinrauch, LA Gleason, RE Keough, J DElia, JA AF Weinrauch, LA Gleason, RE Keough, J DElia, JA TI Relationship between autonomic function and plasma fibrinogen, viscosity, and elements of fibrinolytic activity in diabetic nephropathy SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article; Proceedings Paper CT Annual National Meeting of the American Federation for Clinical Research CY MAY 05-08, 1995 CL SAN DIEGO, CA SP Amer Fed Clin Res DE insulin-dependent diabetes mellitus; autonomic function; plasma fibrinogen ID HEART-RATE-VARIABILITY; CORONARY-ARTERY DISEASE; ACUTE MYOCARDIAL-INFARCTION; CARDIOVASCULAR-DISEASE; RENAL-TRANSPLANTATION; MORNING INCREASE; RISK; MELLITUS; MORTALITY AB Twenty-three insulin-dependent diabetics with proteinuria (3.3 g/day: range 0.3 to 8.9) and azotemia (creatinine clearance: 58 mL/min, range 30 to 112) were tested for 24-h mean arterial blood pressure; instantaneous heart rate variations to a computerized protocol involving timed ventilation, assumption of upright posture, and Valsalva maneuver; plasma fibrinogen, viscosity, fibrinolytic activity, and plasminogen activator inhibitor. These were to test the hypothesis that autonomic dysfunction is associated with altered concentrations of plasma fibrinogen, fibrinolytic activity, viscosity, and plasminogen activator inhibitor. We have previously shown the absence of a correlation between level of blood pressure, clinical and standard laboratory testing, and the results of the autonomic function testing protocol used in this study. In this group of patients, plasma fibrinogen concentration was correlated (positively) with mean arterial pressure and (negatively) with heart rate variation in response to the Valsalva maneuver. The greater the mean arterial pressure or the worse the Valsalva results, the higher the plasma fibrinogen concentration. In addition, patients with one or no abnormal autonomic function tests had a mean fibrinogen of less than 400 mg/dL compared to the group of patients with two or more abnormal tests who had a mean fibrinogen of 500 mg/dL. In patients with demonstrated parasympathetic abnormalities, postural heart rate variation testing also discerned a differential in plasma fibrinogen. Lower concentration of plasminogen activator inhibitor throughout the day, and greater fibrinolytic activity in the morning were also noted to be present in patients with abnormal heart rate response to the Valsalva maneuver. We conclude that there are relationships between high blood pressure, autonomic function, and hemostatic factors favoring thrombogenesis that may be related by common mechanisms and treatments in the diabetic with kidney disease. (C) 1997 American Journal of Hypertension, Ltd. C1 JOSLIN DIABET CTR,JOHN COOK RENAL UNIT,BOSTON,MA 02215. OI Weinrauch, Larry/0000-0003-1357-9528 NR 33 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1997 VL 10 IS 4 BP 454 EP 461 PN 1 PG 8 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA WV881 UT WOS:A1997WV88100012 PM 9128213 ER PT J AU Chynn, EW Rubin, PAD AF Chynn, EW Rubin, PAD TI Metastatic Ewing cell sarcoma of the sinus and osteoid osteoma of the orbit SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article AB PURPOSE: To familiarize ophthalmologists with the management of a ''solitary hot lesion'' on bone scan as part of a metastatic examination. METHODS: Case report of a 27-year-old man with primary Ewing sarcoma of the fibula. Bone scan as part of a metastatic evaluation showed increased uptake in the left orbit. A metastatic lesion could not be ruled out radiologically. RESULTS: A biopsy was performed, and the lesion was found to be osteoid osteoma; therefore, the patient received only local radiation therapy to the fibula. Eight months later, the patient developed metastatic Ewing cell sarcoma of the sphenoid sinus and subsequently died. CONCLUSIONS: Because of the high,sensitivity but low specificity of bone scan, secondary lesions on bone scan are not necessarily metastases. A biopsy specimen is often required for pathologic diagnosis. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,EYE PLAST & ORBIT SERV,BOSTON,MA 02114. NR 5 TC 4 Z9 5 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD APR PY 1997 VL 123 IS 4 BP 565 EP 567 PG 3 WC Ophthalmology SC Ophthalmology GA WT005 UT WOS:A1997WT00500025 PM 9124264 ER PT J AU Xia, MQ Qin, SX McNamara, M Mackay, C Hyman, BT AF Xia, MQ Qin, SX McNamara, M Mackay, C Hyman, BT TI Interleukin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer's disease SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HUMAN ASTROCYTES; CYTOKINES; PROTEIN; PLASTICITY; PATTERNS; GROWTH; GAP-43; IL-8; GENE; TAU AB Cytokines mediate inflammatory responses through their receptors in the hematopoietic system. III a search for potential mediators of inflammatory responses in Alzheimer's disease, we examined brain for cytokine receptors. Herein we describe interleukin-8 receptor B (IL-8RB, also termed CXCR2) immunoreactivity in the central nervous system, Strong IL-8RB immunoreactivity is present in both Alzheimer's disease and control brains, Neurons, dendrites, and axons are clearly immunoreactive. lit Alzheimer's disease, IL-8RB immunoreactive is also present ill some swollen dystrophic neurites of neuritic plaques. Double staining and confocal microscopic analysis reveals that these IL-8RB-positive neurites in plaques are neurofilament positive and are distinct from astrocytic or microglial processes. In general, these IL-8RB-positive neurites no not co-localize with PHF-1 or AT8 (hyperphosphorylated tau) immunoreactive neurites but instead co-localize with beta PP-positive neurites, These results demonstrate for the first time IL-8RB immunoreactivity in the central nervous system and imply a new role for this receptor outside the hematopoietic system. The strong presence of IL-8RB on neurons and the potential of glial cells to produce IL-8 suggest that this system might mediate neuronal-glial interactions. C1 LEUKOSITE INC, CAMBRIDGE, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROL, CAMBRIDGE, MA 02138 USA. RI Mackay, Charles/A-9673-2008 OI Mackay, Charles/0000-0002-6338-7340 FU NIA NIH HHS [AG08487, AG05134] NR 31 TC 95 Z9 98 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9440 EI 1525-2191 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1997 VL 150 IS 4 BP 1267 EP 1274 PG 8 WC Pathology SC Pathology GA WR012 UT WOS:A1997WR01200014 PM 9094983 ER PT J AU Darling, JM Goldring, SR Harada, Y Handel, ML Glowacki, J Gravallese, EM AF Darling, JM Goldring, SR Harada, Y Handel, ML Glowacki, J Gravallese, EM TI Multinucleated cells in pigmented villonodular synovitis and giant cell tumor of tendon sheath express features of osteoclasts SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID RESISTANT ACID-PHOSPHATASE; MESSENGER-RNA EXPRESSION; BONE-MARROW CULTURES; CALCITONIN RECEPTOR; MOUSE BONE; MACROPHAGE POLYKARYONS; MONOCLONAL-ANTIBODIES; VITRONECTIN RECEPTOR; DIFFERENTIATION; IDENTIFICATION AB Pigmented villonodular synovitis (PVNS) and the histologically related lesion giant cell tumor of tendon sheath (GCTTS) are idiopathic, proliferative lesions that can induce osteolysis and formation of bone cysts, These lesions contain two predominant cell types: mononuclear polyhedral cells and multinucleated cells (MNCs). Previous studies demonstrated that the mononuclear cells exhibit phenotypic features consistent with derivation from a monocyte/macrophage lineage. The cell lineage of the MNCs and their relationship to osteoclasts are not known. To characterize the MNCs in these lesions and to establish the relationship of these MNCs to osteoclasts, histological sections from six cases of PVNs and two cases of GCTTS were studied, Mononuclear cells expressed CD14 and HLA-DR, in keeping with their relationship to cells of the monocyte/macrophage lineage, Characterization of the MNCs revealed features associated with an osteoclast phenotype, Seven of the eight specimens contained MNCs that were intensely tartrate-resistant acid phosphatase positive approximately 5% of the mononuclear cells were tartrate-resistant acid phosphatase positive and these tended to surround MNCs, MNCs in both lesions reacted strongly with the 23C6 monoclonal antibody that recognizes the alpha V beta(3) integrin (the vitronectin receptor), as did several mononuclear cells surrounding the MNCs, Most MNCs did not express CD14 or HLA-DR, Expression of-receptors for calcitonin, a marker for osteoclasts, was detected ora MNCs after incubation of sections with I-125-labeled salmon calcitonin and emulsion autoradiography, MNCs in four of six PVNS and two of two GCTTS samples demonstrated specific calcitonin binding Expression of mRNA for calcitonin receptor was confirmed in all cases by reverse transcriptase polymerase chain reaction, These results demonstrate that MNCs in PVNS and GCTTS express phenotypic features of authentic osteoclasts and suggest that osteoclast-like multinucleated cells can arise in synovial soft tissues remote from bone. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV RHEUMATOL IMMUNOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RHEUMATOL,BOSTON,MA 02114. BETH ISRAEL MED CTR,BOSTON,MA. FU NIAMS NIH HHS [AR-03564, AR-01824]; NIDDK NIH HHS [DK-46773] NR 52 TC 48 Z9 50 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1997 VL 150 IS 4 BP 1383 EP 1393 PG 11 WC Pathology SC Pathology GA WR012 UT WOS:A1997WR01200025 PM 9094994 ER PT J AU Virtanen, I Lohi, J Tani, T Korhonen, M Burgeson, RE Lehto, VP Leivo, I AF Virtanen, I Lohi, J Tani, T Korhonen, M Burgeson, RE Lehto, VP Leivo, I TI Distinct changes in the laminin composition of basement membranes in human seminiferous tubules during development and degeneration SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID ADULT-MOUSE TISSUES; MONOCLONAL-ANTIBODIES; SERTOLI CELLS; DIFFERENTIAL EXPRESSION; EXTRACELLULAR-MATRIX; HUMAN TESTIS; A-CHAIN; NEUROMUSCULAR-JUNCTION; SCHWANN-CELLS; BETA-1 AB We studied the distribution of laminin (Ln) chains and their integrin (Int) receptors in normal developing and adult and in atrophied human testes by using immunohistochemistry. Immunostaining for EHS Ln and type IV collagen was used to identify basement membranes (BMs). In the BM of seminiferous epithelium of fetal testis, a panel of monoclonal antibodies showed immunoreactivity for Ln alpha 1-, alpha 2-, beta 1-, beta 2- and gamma 1-chains, suggestive of the presence of Lns 1 to 3. In BM of adult seminiferous epithelium with active spermatogenesis, immunoreactivity for Ln beta 2- and gamma 1-chains was found but not for Ln alpha-chains, suggesting a complex of Ln chains not compatible with any known trimers. Instead, with polyclonal In antiserum and monoclonal antibody to type IV collagen, a distinct BM-like reactivity was seen. In atrophied testes, prominent immunoreactivities for Ln chains, compatible with Ins I to 3, were seen in the thickened BM of seminiferous tubules, hence suggesting of reappearance of fetal Lns. Among the subunits of Ln-binding Int receptors in fetal seminiferous tubules, a strong immunoreactivity for Int beta(1)- and Int alpha 6-subunits was seen throughout the seminiferous epithelium, other Int subunits being found in interstitial cells, In the adult and atrophied testes, immunoreactivities for Int beta(1)- and Int alpha(6)-subunits were seen to be confined to the basal aspect of the seminiferous epithelium whereas immunoreactivities for Int alpha(1)-, alpha(2)-, alpha(3)(-) and beta(4)-subunits were seen in the myoid cells. The results show that both maturation and degenerative changes of human testes are accompanied by distinct changes in the In expression of BM of seminiferous epithelium, which appears to accompany epithelial differentiation of the Sertoli cells. Furthermore, they suggest the presence of a novel Ln trimer in BM of adult human seminiferous tubules. C1 UNIV HELSINKI,HAARTMAN INST,DEPT PATHOL,FIN-00014 HELSINKI,FINLAND. UNIV OULU,DEPT PATHOL,OULU,FINLAND. UNIV OULU,BIOCTR,OULU,FINLAND. UNIV OULU,DEPT PATHOL,OULU,FINLAND. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA. RP Virtanen, I (reprint author), UNIV HELSINKI,DEPT ANAT,INST BIOMED,POB 9,SILTAVUORENPENGER 20A,FIN-00014 HELSINKI,FINLAND. NR 66 TC 55 Z9 58 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 APR PY 1997 VL 150 IS 4 BP 1421 EP 1431 PG 11 WC Pathology SC Pathology GA WR012 UT WOS:A1997WR01200028 PM 9094997 ER PT J AU Berdiev, BK Shlyonsky, VG Senyk, O Keeton, D Guo, Y Matalon, S Cantiello, HF Prat, AG Ausiello, DA Ismailov, II Benos, DJ AF Berdiev, BK Shlyonsky, VG Senyk, O Keeton, D Guo, Y Matalon, S Cantiello, HF Prat, AG Ausiello, DA Ismailov, II Benos, DJ TI Protein kinase A phosphorylation and G protein regulation of type II pneumocyte Na+ channels in lipid bilayers SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE amiloride; ion transport; pertussis toxin ID LUNG LIQUID CLEARANCE; SODIUM-TRANSPORT; PERTUSSIS TOXIN; ALVEOLAR; REABSORPTION; CONSUMPTION; INHIBITION; CLONING; CELLS AB Protein kinase A (PKA)- and G protein-mediated regulation of immunopurified adult rabbit alveolar epithelial type II (ATII) cell proteins that exhibit amiloride-sensitive Na+ channel activity was studied in planar lipid bilayers and freshly isolated ATII cells. Addition of the catalytic subunit of PKA + ATP increased single channel open probability from 0.42 +/- 0.05 to 0.82 +/- 0.07 in a voltage-independent manner, without affecting unitary conductance. This increase in open probability of the channels was mainly due to a decrease in the time spent by the channel in its closed state. The apparent inhibition constant for amiloride increased from 8.0 +/- 1.8 mu M under control conditions to 15 +/- 3 mu M after PKA-induced phosphorylation; that for ethylisopropylamiloride increased from 1.0 +/- 0.4 to 2.0 +/- 0.5 mu M. Neither pertussis toxin (PTX) nor guanosine 5'-O-(3-thiotriphosphate) affected ATII Na+ channel activity in bilayers. Moreover, PTX failed to affect amiloride-inhibitable Na-22(+) uptake in freshly isolated ATII cells. In vitro, ADP ribosylation induced by PTX revealed the presence of a specifically ribosylated band at 40-45 kDa in the total solubilized ATII cell protein fraction, but not in the immunopurified fraction. Moreover, the immunopurified channel was downregulated in response to guanosine 5'-O-(3-thiotriphosphate)-mediated activation of the exogenous G alpha(i-2), but not G(oA), G alpha(i-1), or G alpha(i-3), protein added to the channel. This effect occurred only in the presence of actin. These results suggest that amiloride-sensitive Na+ channels in adult alveolar epithelia regulated by PKA-mediated phosphorylation also retain the ability to be regulated by G alpha(i-2), but not G alpha(i-1) or G alpha(i-3), protein. C1 UNIV ALABAMA, DEPT PHYSIOL & BIOPHYS, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT PULM MED, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT ANESTHESIOL, BIRMINGHAM, AL 35294 USA. MASSACHUSETTS GEN HOSP, RENAL UNIT, CHARLESTOWN, MA 02129 USA. NR 34 TC 18 Z9 18 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD APR PY 1997 VL 272 IS 4 BP C1262 EP C1270 PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA WU497 UT WOS:A1997WU49700021 ER PT J AU Ismailov, II Berdiev, BK Shlyonsky, VG Fuller, CM Prat, AG Jovov, B Cantiello, HF Ausiello, DA Benos, DJ AF Ismailov, II Berdiev, BK Shlyonsky, VG Fuller, CM Prat, AG Jovov, B Cantiello, HF Ausiello, DA Benos, DJ TI Role of actin in regulation of epithelial sodium channels by CFTR SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE cystic fibrosis transmembrane conductance regulator; amiloride; protein kinase A; phosphorylation; cytoskeleton ID FIBROSIS RESPIRATORY EPITHELIUM; HUMAN NASAL EPITHELIUM; CYSTIC-FIBROSIS; NA+ CHANNEL; CHLORIDE CHANNELS; APICAL MEMBRANE; TRANSPORT; PROTEIN; PHOSPHORYLATION; LOCALIZATION AB Cystic fibrosis (CF) airway epithelia exhibit enhanced Na+ reabsorption in parallel with diminished Cl- secretion. We tested the hypothesis that actin plays a role in the regulation of a cloned epithelial Na+ channel (ENaC) by the cystic fibrosis transmembrane conductance regulator (CFTR). We found that immunopurified bovine tracheal CFTR coreconstituted into a planar lipid bilayer with alpha,beta,gamma-rat ENaC (rENaC) decreased single-channel open probability (P-o) of rENaC in the presence of actin by over 60%, a significantly greater effect than was observed in the absence of actin (similar to 20%). In the presence of actin, protein kinase A plus ATP activated both CFTR and rENaC, but CFTR was activated in a sustained manner, whereas the activation of rENaC was transitory. ATP alone could also activate ENaC transiently in the presence of actin but had no effect on CFTR. Stabilizing short actin filaments at a fixed length with gelsolin (at a ratio to actin of 2:1) produced a sustained activation of alpha,beta,gamma-rENaC in both the presence or absence of CFTR. Gelsolin alone (i.e., in the absence of actin) had no effect on the conductance or P-o of either CFTR or rENaC. We have also found that short actin filaments produced their modulatory action on alpha-rENaC independent of the presence of the beta- or gamma-rENaC subunits. In contrast, CFTR did not affect any properties of the channel formed by alpha-rENaC alone, i.e., in the absence of beta- or gamma-rENaC. These results indicate that CFTR can directly downregulate single Na+ channel activity, which may account for the observed differences between Na+ transport in normal and CF-affected airway epithelia. Moreover, the presence of actin confers an enhanced modulatory ability of CFTR on Na+ channels. C1 UNIV ALABAMA, DEPT PHYSIOL & BIOPHYS, BIRMINGHAM, AL 35294 USA. MASSACHUSETTS GEN HOSP EAST, RENAL UNIT, CHARLESTOWN, MA 02129 USA. RI Fuller, Cathy/B-4046-2011 NR 36 TC 66 Z9 67 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD APR PY 1997 VL 272 IS 4 BP C1077 EP C1086 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA WU497 UT WOS:A1997WU49700002 ER PT J AU Hocker, M Zhang, ZS Merchant, JL Wang, TC AF Hocker, M Zhang, ZS Merchant, JL Wang, TC TI Gastrin regulates the human histidine decarboxylase promoter through an AP-1-dependent mechanism SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE c-fos; c-jun; DNA element ID PROTEIN-KINASE-C; ENTEROCHROMAFFIN-LIKE CELLS; SIGNALING PATHWAY; FOS; EXPRESSION; GENE; JUN; TRANSCRIPTION; ACTIVATION; PROLIFERATION AB The histidine decarboxylase (HDC) gene is regulated transcriptionally by gastrin and phorbol 12-myristate 13-acetate (PMA) through a protein kinase C (PKC)-related pathway. To determine the role of AP-I (fosljun) in the regulation of the HDC promoter, gastric cancer (AGS-B) cells stably expressing the cholecystokinin-B/gastrin receptor and the 1.8-kb human (h) HDC-luciferase (luc) construct were cotransfected with constructs expressing c-fos and c-jun. Overexpression of c-fos and c-jun activated the HDC promoter in a dose-dependent fashion in 1.8-kb hHDC-luc/AGS-B cells as well as in transfected F9 embryonal carcinoma cells, which lack: endogenous AP-1 activity. PMA was unable to activate the HDC promoter in F9 cells, which were not transfected with c-fos and c-jun. Gastrin stimulation increased c-fos and c-jun mRNA abundance and AP-1-dependent transcriptional activity, as assessed by a reporter construct in which the CAT reporter gene is under the control of a 12-O-tetradecanoylphorbol-13-acetate response element multimer. Gastrin-stimulated HDC promoter activity was blocked by transfection of c-fos antisense and dominant negative c-jun expression constructs. Finally, overexpression of c-fos and c-jun activated the hHDC promoter through a downstream cis-acting element (gastrin response element), which does not bind AP-1. In conclusion, activation of AP-1 is essential far gastrin-stimulated HDC transcription, but the mechanism appears to be indirect. C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. UNIV MICHIGAN, HOWARD HUGHES MED INST, ANN ARBOR, MI 48109 USA. UNIV MICHIGAN, DEPT MED, ANN ARBOR, MI 48109 USA. FU NIDDK NIH HHS [R37 DK045729, R01 DK045729, R01-DK-45729, R01-DK-48077] NR 33 TC 32 Z9 32 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD APR PY 1997 VL 272 IS 4 BP G822 EP G830 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA WU499 UT WOS:A1997WU49900018 PM 9142914 ER PT J AU Kanai, M Rosenberg, I Podolsky, DK AF Kanai, M Rosenberg, I Podolsky, DK TI Cytokine regulation of fibroblast growth factor receptor 3 IIIb in intestinal epithelial cells SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE Caco-2; intestinal cell; cytokine; peptide growth factor ID FACTOR-BETA; DOMAIN-III; EXPRESSION; BINDING; DIFFERENTIATION; PROLIFERATION; KERATINOCYTE; SECRETION; MIGRATION; GAMMA AB Proliferation and function of the intestinal epithelium is modulated by a range of regulatory peptides, including cytokines and peptide growth factors. To define mechanisms integrating these regulatory systems, the effects of growth factors and cytokines on the expression of the fibroblast growth factor (FGF) receptor 3 (FGFRS) IIIb expressed on intestinal epithelial cells were examined in Caco-2 cells. Regulated expression of FGFRS IIIb was associated with acquisition of the differentiated state. Keratinocyte growth factor (KGF), a ligand of another member of the FGF receptor family, enhanced expression of FGFR3 IIIb, but acidic FGF, the ligand for FGFR3 IIIb itself, had no effect. Epidermal growth factor and transforming growth factor-beta also markedly enhanced FGFR3 IIIb expression in a different temporal pattern. In addition, FGFRS IIIb expression was increased 10-fold by the cytokine interleukin-2. These studies demonstrate integration between cytokines and growth factor ligand-receptor systems in intestinal epithelial cells. C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-43351, DK-41557] NR 46 TC 31 Z9 31 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD APR PY 1997 VL 272 IS 4 BP G885 EP G893 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA WU499 UT WOS:A1997WU49900026 PM 9142922 ER PT J AU Schulz, JB Panahian, N Chen, YI Beal, MF Moskowitz, MA Rosen, BR Jenkins, BG AF Schulz, JB Panahian, N Chen, YI Beal, MF Moskowitz, MA Rosen, BR Jenkins, BG TI Facilitation of postischemic reperfusion with alpha-PBN: Assessment using NMR and Doppler flow techniques SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE N-tert-butyl-alpha-phenylnitrone; free radicals; flow; volume; magnetic resonance imaging ID CONJUGATED SUPEROXIDE-DISMUTASE; FOCAL CEREBRAL-ISCHEMIA; TERT-BUTYL-NITRONE; FREE-RADICALS; BLOOD-FLOW; ANTIOXIDANT TIRILAZAD; HUMAN-NEUTROPHILS; OXYGEN RADICALS; BRAIN INJURY; RAT-BRAIN AB We examined the effects of the free radical spin trap N-tert-butyl-alpha-phenylnitrone (PBN) on focal cerebral ischemia/reperfusion injury in halothane-anesthetized rats. Ninety minutes after middle cerebral artery occlusion by an intraluminal filament, the artery was reperfused. Intravenous injections of 25 mg/kg PBN 5 min before and 30 min after insertion of the filament significantly attenuated the lesion volume measured 24 h after ischemia. During ischemia and during the first 30 min after reperfusion, cerebral blood volume and blood flow were measured by volume-sensitive and newly developed flow-sensitive magnetic resonance imaging (MRI) techniques and by laser-Doppler flowmetry. In all animals the area of decreased blood flow was larger than the area of decreased volume by a factor of 2.2. The area of the postreperfusion flow deficits matched the final lesion volumes at 24 h measured histologically much better than did the blood volume deficits in both saline and PBN-treated animals. Reperfusion led to a return of blood flow and volume to values close to the contralateral side in the PBN-treated animals, in contrast to the saline-treated control group. We conclude that in focal ischemia/reperfusion PBN provides protection of the vascular endothelium, leading to enhanced postischemic reperfusion. The implication of this is that the vascular endothelium may be a primary target for the damaging action of free radicals given the protection afforded by putative spin traps. C1 Massachusetts Gen Hosp, MGH, NMR Ctr, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Stroke Lab & Neurosurg Serv, Boston, MA 02114 USA. Massachusetts Gen Hosp, Neurochem Lab & Neurol Serv, Boston, MA 02114 USA. RP Jenkins, BG (reprint author), Massachusetts Gen Hosp, MGH, NMR Ctr, Bldg 149,13th St, Charlestown, MA 02129 USA. RI Moskowitz, Michael/D-9916-2011; Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 NR 34 TC 30 Z9 30 U1 0 U2 2 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 APR PY 1997 VL 272 IS 4 BP H1986 EP H1995 PG 10 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA WU852 UT WOS:A1997WU85200052 ER PT J AU Raff, H Jankowski, BM Goodfriend, TL Baker, JE Papanek, PE AF Raff, H Jankowski, BM Goodfriend, TL Baker, JE Papanek, PE TI Effect of exposure to hypoxia from birth an aldosterone in rabbits: Role of unesterified fatty acids SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE adrenal cortex; zona glomerulosa cell; oleic acid; development; corticosterone ID ATRIAL-NATRIURETIC-FACTOR; ADRENOCORTICAL FUNCTION; GLOMERULOSA CELLS; ZONA GLOMERULOSA; HYPOXEMIA; RATS; INHIBITION; SECRETION; CORTICOSTERONE; MECHANISM AB Hypoxia and fluid and electrolyte disturbances are serious risks to normal postnatal development. Because a decrease in inspired O-2 (hypoxic hypoxia) inhibits aldosterone synthesis in the adult and aldosterone controls water and electrolyte balance, we studied adrenocortical function in rabbits exposed to normobaric normoxia or hypoxic hypoxia (fraction of inspired O-2 0.09) from birth. At 21 days of age, rabbits were anesthetized, the adrenals were rapidly removed, and the adrenal capsules containing mostly zona glomerulosa cells were separated. Cells were dispersed with collagenase and studied in vitro. Hypoxia in vivo resulted in a 73% decrease in basal aldosterone release and a 86% decrease in adenosine 3',5'-cyclic monophosphate-stimulated aldosterone release in vitro. We hypothesized that increased unesterified fatty acids could be partly responsible for inhibition of aldosterone synthesis. Total serum unesterified fatty acids in hypoxic kits were significantly increased (298 +/- 14 mu mol/l) compared with normoxic kits (184 +/- 31 mu mol/l). When cells from hypoxic rabbits were washed with fatty acid-free albumin and studied under conditions devoid of fatty acids, aldosterone production was partially restored. Corticosterone production was not affected by washing. Washing had no effect on aldosterone synthesis by cells from normoxic rats. Finally, exposing washed zona glomerulosa cells to oleic acid (10-50 mu M) inhibited aldosteronogenesis. We conclude that exposure to hypoxia from birth attenuates aldosterone production in part due to an increase in levels of unesterified fatty acid levels. C1 ST LUKES HOSP, ENDOCRINE RES LAB, MILWAUKEE, WI 53215 USA. MED COLL WISCONSIN, DEPT MED, MILWAUKEE, WI 53226 USA. MED COLL WISCONSIN, DEPT CARDIOTHORAC SURG, MILWAUKEE, WI 53226 USA. MARQUETTE UNIV, PROGRAM PHYS THERAPY, MILWAUKEE, WI 53201 USA. UNIV WISCONSIN, SCH MED, DEPT MED, MADISON, WI 53705 USA. UNIV WISCONSIN, SCH MED, DEPT PHARMACOL, MADISON, WI 53705 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. NR 36 TC 9 Z9 9 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 EI 1522-1490 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD APR PY 1997 VL 272 IS 4 BP R1084 EP R1087 PG 4 WC Physiology SC Physiology GA WT588 UT WOS:A1997WT58800011 PM 9140005 ER PT J AU Brown, D AF Brown, D TI Polarity, function, and dysfunction of renal epithelial cells SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP Brown, D (reprint author), MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD APR PY 1997 VL 272 IS 4 BP F423 EP F423 PG 1 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA WU837 UT WOS:A1997WU83700001 ER PT J AU Tondo, L Baldessarini, RJ Floris, G Rudas, N AF Tondo, L Baldessarini, RJ Floris, G Rudas, N TI Effectiveness of restarting lithium treatment after its discontinuation in bipolar I and bipolar II disorders SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PROPHYLAXIS; RISK AB Objective: This study tested the hypothesis that resumption of lithium treatment of bipolar disorders may be less effective after maintenance treatment has been discontinued. Method: Eighty-six patients with type I or II bipolar disorder, not selected according to response to treatment, were followed prospectively during two periods of lithium maintenance treatment averaging 4.6 and 4.4 years. Morbidity (illness episodes per year, hospitalizations per year, percentage of time ill) was assessed, and use of adjunctive medication was rated. Results: Morbidity was similar in the first and second treatment periods (mean number of episodes=0.83 and 0.94 per year, respectively; mean percentage of time ill=18.0% and 24.2%), with no differences in numbers of manic and depressive episodes or differences by gender, diagnostic type, length of first treatment, interval between treatments, or discontinuation rate. There was 12.8% more use of adjunctive medication in the second period. Conclusions: The efficacy of lithium did not differ significantly between the first and second treatment periods. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,BOSTON,MA 02114. UNIV CAGLIARI,CTR LUCIO BINI,I-09124 CAGLIARI,SARDINIA,ITALY. UNIV CAGLIARI,DEPT PSYCHIAT,I-09124 CAGLIARI,SARDINIA,ITALY. FU NIMH NIH HHS [MH-31142, MH-47370] NR 12 TC 48 Z9 48 U1 0 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1997 VL 154 IS 4 BP 548 EP 550 PG 3 WC Psychiatry SC Psychiatry GA WQ183 UT WOS:A1997WQ18300018 PM 9090344 ER PT J AU Seage, GR Gatsonis, C Weissman, JS Haas, JS Cleary, PD Fowler, FJ Massagli, MP Stone, VE Craven, DE Makadon, H Goldberg, J Coltin, K Levin, KS Epstein, AM AF Seage, GR Gatsonis, C Weissman, JS Haas, JS Cleary, PD Fowler, FJ Massagli, MP Stone, VE Craven, DE Makadon, H Goldberg, J Coltin, K Levin, KS Epstein, AM TI The Boston AIDS survival score (BASS): A multidimensional AIDS severity instrument SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; FUNCTIONAL STATUS; EXPERIENCE; DIAGNOSIS; INFECTION; HEALTH AB Objectives. This study developed a new acquired immunodeficiency syndrome (AIDS) severity system by including diagnostic, physiological, functional, and sociodemographic factors predictive of survival. Methods. Three-hundred five persons with AIDS in Boston were interviewed; their medical records were reviewed and vital status ascertained. Results. Overall median (+/-SD) survival for the cohort from the first interview until death was 560 +/- 14.4 days. The best model for predicting survival, the Boston AIDS Survival Score, included-the Justice score (stage 2 relative hazard [RH] = 1.25, 95% confidence interval [CI] = 0.80, 1.96; stage 3 RH = 1.76, 95% CI = 1.15, 2.70), a newly developed opportunistic disease; score (Boston opportunistic Disease Survival Score; stage 2 RH = 1.35, 95% CI = 0.90, 2.02; stage 3 RH = 2.10, 95% CI = 1.38, 3.18), and measures of activities of daily living (any intermediate limitations, RH = 1.84, 95% CI = 1.05, 3.21; any basic limitations, RH = 2.60, 95% CI = 1.44, 4.69). This model had substantially greater predictive power (R-2 = .17, C statistic = .68) than the Justice score alone (R-2 = .09, C statistic = .61). Conclusions. Incorporating data on clinically important events and functional: status into a physiologically based system can-improve the prediction of survival with AIDS. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,BOSTON,MA 02115. BOSTON DEPT HLTH & HOSP,INST URBAN HLTH POLICY & RES,BOSTON,MA. BOSTON UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BROWN UNIV,CTR STAT SCI,PROVIDENCE,RI 02912. HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,HLTH POLICY RES & DEV UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV GEN MED,SECT HLTH SERV & POLICY RES,BOSTON,MA 02115. UNIV MASSACHUSETTS,SURVEY RES CTR,BOSTON,MA 02125. BOSTON UNIV,BOSTON CITY HOSP,SCH MED,BOSTON,MA 02118. BETH ISRAEL HOSP,DIV GEN MED,BOSTON,MA 02215. HARVARD COMMUNITY HLTH PLAN,BOSTON,MA. FU PHS HHS [R01-H506239] NR 30 TC 9 Z9 9 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1997 VL 87 IS 4 BP 567 EP 573 DI 10.2105/AJPH.87.4.567 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA WY039 UT WOS:A1997WY03900010 PM 9146433 ER PT J AU Korent, VA Conhaim, RL McGrath, AM DeAngeles, DA Harms, BA AF Korent, VA Conhaim, RL McGrath, AM DeAngeles, DA Harms, BA TI Molecular distribution of hetastarch in plasma and lung lymph of unanesthetized sheep SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID AWAKE SHEEP; LIQUID; HYPOPROTEINEMIA; EXCHANGE; PRESSURE; NODES AB We used high performance size exclusion chromatography (HPSEC) to measure concentrations and molecular masses of hetastarch (Het) in plasma and lung lymph of unanesthetized sheep. Our goal was to assess the osmotic effectiveness of Het in the pulmonary circulation as judged by its exclusion from lung lymph. Sheep (n = 5) received 35 ml/kg of Hat (6%) over 90 min. At the end of the infusion, Het concentrations in plasma reached a peak value of 2.9 +/- 0.1% (mean +/- SD). Lymph concentrations reached a peak value of 1.3 +/- 0.3% at 4.5 h. Het molecular masses in plasma averaged 650 +/- 36 kD at 90 min, hut ranged from 31 to 2,942 +/- 187 kD. Masses in lung lymph averaged 373 +/- 71 kD, and ranged from TB +/- 2 to 1,693 +/- 514 kD (p less than or equal to 0.05 vs. plasma). Het contributed 6.7 +/- 1,5 mm Hg to the plasma macromolecular osmotic pressure, and 3.7 +/- 1.8 mm Hg to the lymph osmotic pressure. Despite the fact that Het has the largest molecular mass of any of the current macromolecular plasma volume expanders, we found that it filtered readily into lymph, raising the lymph osmotic pressure. These findings suggest that the rationale for the osmotic performance of such solutions may need to be reconsidered. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SURG,MADISON,WI 53705. UNIV WISCONSIN,DEPT SURG,MADISON,WI. FU NHLBI NIH HHS [HL46236] NR 28 TC 5 Z9 5 U1 0 U2 0 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 APR PY 1997 VL 155 IS 4 BP 1302 EP 1308 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA WR657 UT WOS:A1997WR65700020 PM 9105071 ER PT J AU Koch, JS Whitman, GJ Chew, FS AF Koch, JS Whitman, GJ Chew, FS TI Bronchus-associated lymphoid tissue hyperplasia of the lung SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID BALT C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. UNIV TEXAS,MD ANDERSON HOSP & TUMOR INST,DIV DIAGNOST IMAGING,HOUSTON,TX 77030. NR 5 TC 3 Z9 3 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 APR PY 1997 VL 168 IS 4 BP 1044 EP 1044 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WQ211 UT WOS:A1997WQ21100035 PM 9124112 ER PT J AU Yang, CF Wu, MT Chiang, AA Lai, RS Chen, C Tiao, WM McLoud, TC Wang, JS Pan, HB AF Yang, CF Wu, MT Chiang, AA Lai, RS Chen, C Tiao, WM McLoud, TC Wang, JS Pan, HB TI Correlation of high-resolution CT and pulmonary function in bronchiolitis obliterans: A study based on 24 patients associated with consumption of Sauropus androgynus SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID LUNG TRANSPLANTATION PATIENTS; CONSTRICTIVE BRONCHIOLITIS; SMALL AIRWAYS; DISEASES; BRONCHIECTASIS; ADULTS AB OBJECTIVE. An outbreak of Sauropus androgynus-associated bronchiolitis obliterans occurred in Taiwan in the summer of 1995. We undertook a study of the correlation between high-resolution CT findings and pulmonary function testing in patients from this outbreak. MATERIALS AND METHODS. We evaluated inspiratory-expiratory high-resolution CT scans of 24 patients with S. androgynus-associated bronchiolitis obliterans. The presence of bronchiectasis was assessed by two visual scores (a bronchial dilatation score and a bronchiectasis extent score). Extent of air-trapping was assessed visually and given a score. We also used computer software to assess the extent of air-trapping and generate scores of dynamic attenuation. Spirometry, plethysmography, and diffusion capacity of each patient were also obtained. RESULTS. All four scores had statistically significant correlation with forced expiratory volume in 1 sec (FEV(1)) (p < .05 for both bronchiectasis scores; p < .001 for both air-trapping scores). The two air-trapping scores had statistically significant correlation with forced vital capacity and diffusion capacity. We found the scores for dynamic attenuation had the greatest correlation with FEV(1) (r = .85). We also found that mosaic attenuation was notable on expiratory CT scans alone in nine patients (type 1 air-trapping) and on both inspiratory and expiratory CT scans in 15 patients (type 2 air-trapping). In the latter group, FEV(1) was significantly lower (p < .01). CONCLUSION. Findings from high-resolution CT of air-trapping were more important than findings of bronchiectasis when correlating pulmonary function with S. androgynus-associated bronchiolitis obliterans. Type 2 air-trapping suggested a more severe air-flow obstruction than did type 1. Scores for quantitative attenuation generated by computer software were helpful in assessing air-trapping and correlating it with pulmonary function. These findings may apply to patients with bronchiolitis obliterans from other causes. C1 NATL YANG MING UNIV,TAIPEI 112,TAIWAN. NATL DEF MED CTR,TAIPEI 100,TAIWAN. VET GEN HOSP KAOHSIUNG,DEPT MED,KAOHSIUNG 813,TAIWAN. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. VET GEN HOSP KAOHSIUNG,DEPT PATHOL,KAOHSIUNG 813,TAIWAN. RP Yang, CF (reprint author), VET GEN HOSP KAOHSIUNG,DEPT RADIOL,386 TA CHUNG 1ST RD,KAOHSIUNG 813,TAIWAN. NR 27 TC 20 Z9 23 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 APR PY 1997 VL 168 IS 4 BP 1045 EP 1050 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WQ211 UT WOS:A1997WQ21100036 PM 9124113 ER PT J AU Hulka, CA Slanetz, PJ Halpern, EF Hall, DA McCarthy, KA Moore, R Boutin, S Kopans, DB AF Hulka, CA Slanetz, PJ Halpern, EF Hall, DA McCarthy, KA Moore, R Boutin, S Kopans, DB TI Patients' opinion of mammography screening services: Immediate results versus delayed results due to interpretation by two observers SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID LOW-COST; PATIENTS PREFERENCES; OPERATE AB OBJECTIVE. The purpose of this study was to evaluate by random questionnaire mailings the preferences of women who have undergone mammography in our region regarding communication of mammography screenign results. MATERIALS AND METHODS. Questionnaires were mailed to 400 randomly selected women who were more than 35 years old and who had been treated at our institution for medical or surgical reasons. Questions regarding use of mammography screening at our institution versus services at other locations were included. The questionnaire described two possible mammography services; either a double reading service that would provide delayed reports (DRDR) with the benefit of extra cancers detected, and a service that provides immediate reports given directly to the patient by an on-site radiologist, The presentation of the services was reversed in half the questionnaires to avoid bias. Patients' choices were collected, as were demographic data. The choice of one system over the other was evaluated using the one-sample test for binomial probability, The chi-square test was used to determine if the order of questions on the survey or the site of patients' screening mammography affected responses. RESULTS. The response rate was 42% (n = 168). Of these, one response informed us of the death of a patient. Of the remaining 167 respondents, 75% (n = 126) preferred the DRDR system, 13% (n = 22) preferred the system providing immediate results (p < .0001), and the other 19 respondents did not select a preference. Of the 167 respondents, 156 answered the question regarding previous screening mammography experience. Of the 105 patients who had undergone screening mammography at our institution, 78% (n = 82) pre preferred the DRDR system. Of the 51 patients who had undergone mammography elsewhere or who had never undergone mammography, 75% (n = 38) preferred the DRDR system. We found that ordering of presentation of the systems in the questionnaire had no effect on responses. Likewise, whether a respondent had undergone mammography at our institution had no effect on responses (p = 1.0). CONCLUSION. A statistically significant number of women who responded to our questionnaire preferred the DRDR system of reporting screening mammographic results. Educational material about double reading that we included with each patient's questionnaire could account for these results, If the use of a second interpreter is feasible and is done for batch interpretation of screening mammograms, then education of patients about this process may increase acceptance of a delayed mammographic report. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. BROWN UNIV,PROVIDENCE,RI 02912. RP Hulka, CA (reprint author), BETH ISRAEL HOSP,DEPT RADIOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. OI Slanetz, Priscilla/0000-0003-1248-5116 NR 15 TC 19 Z9 20 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 APR PY 1997 VL 168 IS 4 BP 1085 EP 1089 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA WQ211 UT WOS:A1997WQ21100043 PM 9124120 ER PT J AU Misdraji, J delCastillo, CF Ferry, JA AF Misdraji, J delCastillo, CF Ferry, JA TI Follicle center lymphoma of the ampulla of Vater presenting with jaundice - Report of a case SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE follicle center lymphoma; duodenum; ampulla of vater; jaundice; biliary obstruction ID NON-HODGKINS-LYMPHOMA; PRIMARY GASTROINTESTINAL LYMPHOMA; BILE-DUCT OBSTRUCTION; MALIGNANT-LYMPHOMA; BILIARY OBSTRUCTION; SMALL-BOWEL; TRACT; CLASSIFICATION; DIAGNOSIS; SECONDARY AB We report the case of a 56-year-old woman who presented with biliary obstruction due to a neoplasm involving the duodenum in the area of the ampulla of Vater and the head of the pancreas. Clinically and radiographically: she was thought to have pancreatic carcinoma. Histologic examination of the specimen from a Whipple procedure revealed malignant lymphoma, follicle center type, follicular, grade 1 of 3 (follicular, predominantly small cleaved cell type), arising in the duodenum and invading the pancreas. Five peripancreatic lymph nodes were partially involved by lymphoma. Follicle center lymphoma presenting as a mass involving the ampulla of Vater with jaundice has not been described previously. Our case indicates that this type of lymphoma can occur in this location and can present with features that mimic pancreatic carcinoma. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP Misdraji, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 37 TC 42 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 APR PY 1997 VL 21 IS 4 BP 484 EP 488 DI 10.1097/00000478-199704000-00016 PG 5 WC Pathology; Surgery SC Pathology; Surgery GA WW277 UT WOS:A1997WW27700016 PM 9130997 ER PT J AU Okamoto, H Meng, W Ma, JY Ayata, C Roman, RJ Bosnjak, ZJ Kampine, JP Huang, PL Moskowitz, MA Hudetz, AG AF Okamoto, H Meng, W Ma, JY Ayata, C Roman, RJ Bosnjak, ZJ Kampine, JP Huang, PL Moskowitz, MA Hudetz, AG TI Isoflurane-induced cerebral hyperemia in neuronal nitric oxide synthase gene deficient mice SO ANESTHESIOLOGY LA English DT Article DE anesthetics, volatile, isoflurane; brain, cerebral blood flow, laser-Doppler flowmetry; gases, nitric oxide; genetics, nitric oxide synthase; pharmacology, nitric oxide synthase inhibitor ID ARGININE METHYL-ESTER; BLOOD-FLOW; VOLATILE ANESTHETICS; HALOTHANE; RAT; BRAIN; RECEPTORS; MICROCIRCULATION; ENDOTHELIUM; DISRUPTION AB Background: Nitric oxide (NO) has been reported to play an important role in isoflurane-induced cerebral hyperemia in vivo. In the brain, there are two constitutive isoforms of NO synthase (NOS), endothelial NOS (eNOS), and neuronal NOS (nNOS). Recently, the mutant mouse deficient in nNOS gene expression (nNOS knockout) has been developed The present study was designed to examine the role of the two constitutive NOS isoforms in cerebral blood flow (CBF) response to isoflurane using this nNOS knockout mouse. Methods: Regional CBF (rCBF) in the cerebral cortex was measured with laser-Doppler flowmetry in wild-type mice (129/SV or C57BL/6) and nNOS knockout mice during stepwise increases in the inspired concentration of isoflurane from 0.6 vol% to 1.2, 1.8, and 2.4 vol%. Subsequently, a NOS inhibitor, N-omega-nitro-L-arginine (L-NNA), was administered intravenously (20 mg/kg), and 45 min later, the rCBF response to isoflurane was tested again In separate groups of wild-type mice and the knockout mice, the inactive enantiomer, N-omega-nitro-D-arginine (D-NNA) was administered intravenously in place of L-NNA. Brain NOS activity was measured with radio-labeled L-arginine to L-citrulline conversion after treatment with L-NNA and D-NNA. Results: Isoflurane produced dose-dependent increases in rCBF by 25 +/- 3%, 74 +/- 10%, and 108 +/- 14% (SEM) in 129/SV mice and by 32 +/- 2%, 71 +/- 3%, and 96 +/- 7% in C57BL/6 mice at 1.2, 1.8, and 2.4 vol%, respectively. These increases were attenuated at every anesthetic concentration by L-NNA but not by D-NNA. Brain NOS activity was decreased by 92 +/- 2% with L-NNA compared with D-NNA. In nNOS knockout mice, isoflurane increased rCBF by 67 +/- 8%, 88 +/- 12%, and 112 +/- 18% at 1.2, 1.8, and 2.4 vol%, respectively. The increase in rCBF at 1.2 vol% was significantly greater in the nNOS knockout mice than that in the wild-type mice. Administration of L-NNA in the knockout mice attenuated the rCBF response to isoflurane at 1.2 and 1.8 vol% but had no effect on the response at 2.4 vol%. Conclusions: In nNOS knockout mice, the cerebral hyperemic response to isoflurane is preserved by compensatory mechanism(s) that is NO-independent at 2.4 vol%, although it may involve eNOS at 1.2 and 1.8 vol%. It is suggested that in wild-type mice, eNOS and nNOS contribute to isoflurane-induced increase in rCBF. At lower concentrations (1.2 and 1.8 vol%), eNOS may be involved, whereas at 2.4 vol%, nNOS may be involved. C1 MED COLL WISCONSIN,DEPT ANESTHESIOL,MILWAUKEE,WI 53226. MED COLL WISCONSIN,DEPT PHYSIOL,MILWAUKEE,WI 53226. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE & NEUROVASC REGULAT LAB,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC RES CTR,BOSTON,MA. RI Moskowitz, Michael/D-9916-2011 FU NIGMS NIH HHS [GM 08377] NR 42 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1997 VL 86 IS 4 BP 875 EP 884 DI 10.1097/00000542-199704000-00018 PG 10 WC Anesthesiology SC Anesthesiology GA WT008 UT WOS:A1997WT00800020 PM 9105232 ER PT J AU Curhan, GC Willett, WC Speizer, FE Spiegelman, D Stampfer, MJ AF Curhan, GC Willett, WC Speizer, FE Spiegelman, D Stampfer, MJ TI Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; OXALATE NEPHROLITHIASIS; EXCRETION; FORMERS; REPRODUCIBILITY; HYPERCALCIURIA; MAGNESIUM; VALIDITY AB Background: Calcium intake is believed to play an important role in the formation of kidney stones, but data on the risk factors for stone formation in women are limited. Objective: To examine the association between intake of dietary and supplemental calcium and the risk for kidney stones in women. Design: Prospective cohort study with 12-year follow-up. Setting: Several U.S. states. Participants: 91 731 women participating in the Nurses' Health Study I who were 34 to 59 years of age in 1980 and had no history of kidney stones, Measurements: Self-administered food-frequency questionnaires were used to assess diet in 1980, 1984, 1986, and 1990. The main outcome measure was incident symptomatic kidney stones. Results: During 903 849 person-years of follow-up, 864 cases of kidney stones were documented. After adjustment for potential risk factors, intake of dietary calcium was inversely associated with risk for kidney stones and intake of supplemental calcium was positively associated with risk. The relative risk for stone formation in women in the highest quintile of dietary calcium intake compared with women in the lowest quintile was 0.65 (95% CI, 0.50 to 0.83). The relative risk in women who took supplemental calcium compared with women who did not was 1.20 (CI, 1.02 to 1.41), In 67% of women who took supplemental calcium, the calcium either was not consumed with a meal or was consumed with meals whose oxalate content was probably low. Other dietary factors showed the following relative risks among women in the highest quintile of intake compared with those in the lowest quintile: sucrose, 1.52 (CI, 1.18 to 1.96); sodium, 1.30 (CI, 1.05 to 1.62); fluid, 0.61 (CI, 0.48 to 0.78); and potassium, 0.65 (CI, 0.51 to 0.84). Conclusions: High intake of dietary calcium appears to decrease risk for symptomatic kidney stones, whereas intake of supplemental calcium may increase risk. Because dietary calcium reduces the absorption of oxalate, the apparently different effects caused by the type of calcium may be associated with the timing of calcium ingestion relative to the amount of oxalate consumed. However, other factors present in dairy products (the major source of dietary calcium) could be responsible for the decreased risk seen with dietary calcium. C1 BRIGHAM & WOMENS HOSP, CHANNING LAB, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, DEPT EPIDEMIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. RP Curhan, GC (reprint author), HARVARD UNIV, SCH PUBL HLTH, DEPT NUTR, 665 HUNTINGTON AVE, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA40356, CA55075]; NIDDK NIH HHS [DK45362] NR 33 TC 334 Z9 349 U1 0 U2 3 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 EI 1539-3704 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1997 VL 126 IS 7 BP 497 EP + PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA WQ195 UT WOS:A1997WQ19500010 PM 9092314 ER PT J AU Mazurek, MF Garside, S Beal, MF AF Mazurek, MF Garside, S Beal, MF TI Cortical peptide changes in Huntington's disease may be independent of striatal degeneration SO ANNALS OF NEUROLOGY LA English DT Article ID CEREBRAL-CORTEX; MORPHOMETRIC ANALYSIS; ALZHEIMERS-DISEASE; ENERGY-METABOLISM; NEUROPEPTIDE-Y; HUMAN-BRAIN; CHOLECYSTOKININ; NEURONS; SOMATOSTATIN; RAT AB Patients with Huntington's disease (HD) develop pathological changes in cerebral cortex as well as in striatum. We studied levels of neuropeptide immunoreactivity in 13 areas of postmortem cerebral cortex dissected from 24 cases of HD and 12 controls. Concentrations of immunoreactive cholecystokinin (CCK-LI) were consistently elevated 57 to 153% in HD cortex. Levels of vasoactive intestinal polypeptide (VIP-LI) and neuropeptide Y (NPY-LI) were significantly increased in 10 and 8 of the 13 cortical regions, respectively, Concentrations of somatostatin (SRIF-LI) were increased in only 3 areas, while substance P (SP-LI) was, for the most part, unchanged. Detailed analyses of the CCK-LI and VIP-LI data showed there to be no relationship between the increased cortical peptide levels and the degree of striatal atrophy. We studied the same cortical peptides in rats with long-standing striatal lesions and found no significant changes of CCK-LI, NPY-LI, VIP-LI, or SRIF-LI in any of the 8 cortical regions that were examined. These results indicate that there are widespread and differential changes in cortical neuropeptide systems in HD and that these changes occur independently of the striatal pathology that characterizes the illness. C1 MCMASTER UNIV, MED CTR, DEPT PSYCHIAT, HAMILTON, ON L8N 3Z5, CANADA. MCMASTER UNIV, MED CTR, DEPT BIOMED SCI NEUROSCI, HAMILTON, ON L8N 3Z5, CANADA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. RP Mazurek, MF (reprint author), MCMASTER UNIV, MED CTR, DEPT MED NEUROL, NEUROL 4U2, 1200 MAIN ST W, HAMILTON, ON L8N 3Z5, CANADA. FU NINDS NIH HHS [NS 16367] NR 34 TC 14 Z9 15 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1997 VL 41 IS 4 BP 540 EP 547 DI 10.1002/ana.410410418 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA WT994 UT WOS:A1997WT99400017 PM 9124812 ER PT J AU Acquadro, MA Salman, SD Joseph, MP AF Acquadro, MA Salman, SD Joseph, MP TI Analysis of pain and endoscopic sinus surgery for sinusitis SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE endoscopic sinus surgery; sinus pain; sinusitis ID PHYSICAL-EXAMINATION; HISTORY; DIAGNOSIS AB This prospective clinical descriptive study was designed to see whether patients who had endoscopic sinus surgery for sinusitis had relief of pain, and whether they had new pain postoperatively. The sample was 252 consecutive patients who underwent endoscopic sinus surgery after presenting with inflammatory sinus disorders meeting specific clinical definitions of sinusitis and criteria for surgically treatable sinus disorders developed by the treating surgeon. Of the 252 consecutive endoscopic sinus surgery patients, 106 (42%) had no preoperative pain and 146 (58%) patients had preoperative sinus pain. At 6- to 12-month postoperative evaluations, patients with no preoperative pain did not develop any new postoperative pain. Among the 146 patients with preoperative pain, 82 (56%) had no pain, residual symptoms, or further sequelae, and were considered cured; 42 (29%) reported a marked improvement of pain or discomfort; 9 (6%) had the same degree of pain or discomfort as before; 3 (2%) reported worse pain or discomfort; and 10 (7%) reported new pain or discomfort. These results suggest that the application of consistent definitions and clinical criteria for various forms of surgically treatable sinusitis will more likely predict improvement of pain and discomfort following surgical treatment. The risk of developing new pain and discomfort following endoscopic sinus surgery in individuals without preoperative pain or discomfort is negligible. The risk of worsening pain or new pain was less than 10% in patients with preoperative pain. Ongoing efforts such as the International Conference on Sinus Disease in the development of consistent terminology, staging, and therapy, and future modifications from additional clinical experience, should result in more predictable and effective care in the surgical treatment for pain of sinus disease. C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA. RP Acquadro, MA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT ANESTHESIA,243 CHARLES ST,BOSTON,MA 02114, USA. NR 11 TC 18 Z9 18 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD APR PY 1997 VL 106 IS 4 BP 305 EP 309 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA WT836 UT WOS:A1997WT83600008 PM 9109721 ER PT J AU Canver, CC Armstrong, VM Cooler, SD Nichols, RD AF Canver, CC Armstrong, VM Cooler, SD Nichols, RD TI Assessment of internal thoracic artery vasoreactivity in response to sublingual nitroglycerin SO ANNALS OF THORACIC SURGERY LA English DT Article ID MAMMARY ARTERY; NONINVASIVE ASSESSMENT; SURGERY; BYPASS; GRAFT AB Background. We have previously shown the feasibility of assessing internal thoracic artery (ITA) size and blood now hemodynamics before and after coronary artery bypass grafting using color-flow duplex ultrasound. This noninvasive method would be an ideal diagnostic tool for the evaluation of ITA graft status after therapeutic interventions in a patient with angina after coronary artery bypass grafting. The purpose of this study was to investigate the effects of nitroglycerin on the diameter and blood flow velocities of the left native ITA before coronary artery bypass grafting and the ITA graft postoperatively. Methods. The study consisted of 24 male patients (mean age, 59 +/- 2.3 years) who had undergone elective coronary artery bypass grafting using a left ITA graft to the left anterior descending artery, with additional saphenous vein grafts. Color-flow duplex ultrasound (5.0-MHz transducer) was used for both the preoperative imaging of native ITAs and the postoperative study of ITA grafts before patient discharge. Repeated-measures analysis of variance was used to compare measurements of the ITA size and flow velocities (peak systolic velocity and end-diastolic velocity) at 5, 10, and 15 minutes after a single dose of sublingual nitroglycerin (0.4 mg) with the baseline values obtained without nitroglycerin. Results. The preoperative native left ITA and the postoperative left ITA graft diameters responded to sublingual nitroglycerin by showing a rapid and significant increase beginning at 5 minutes and lasting up to 15 minutes (p = 0.0001). Sublingual nitroglycerin caused the peak systolic velocity of the native left ITA to be augmented at 5 minutes (p = 0.0002), and this effect was still apparent at 10 minutes (p = 0.0001) and 15 minutes (p = 0.0192). However, postoperative left ITA graft peak systolic velocities remained unaffected by the sublingual nitroglycerin (p = not significant). Conclusions. We conclude that instantaneous noninvasive measurement of ITA graft size and blood flow velocities after a therapeutic drug intervention may be clinically useful, particularly in a post-coronary artery bypass grafting patient with recurrent angina. (C) 1997 by The Society of Thoracic Surgeons. RP Canver, CC (reprint author), UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,SCH MED,CLIN SCI CTR H4 352,MADISON,WI 53792, USA. NR 7 TC 7 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1997 VL 63 IS 4 BP 1041 EP 1043 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA WT197 UT WOS:A1997WT19700027 PM 9124902 ER PT J AU Paithankar, DY Chen, AU Pogue, BW Patterson, MS SevickMuraca, EM AF Paithankar, DY Chen, AU Pogue, BW Patterson, MS SevickMuraca, EM TI Imaging of fluorescent yield and lifetime from multiply scattered light reemitted from random media SO APPLIED OPTICS LA English DT Article DE fluorescence imaging; biomedical optics; image reconstruction; fluorescence lifetime; fluorescence yield ID LASER-INDUCED FLUORESCENCE; IN-VIVO PH; TURBID MEDIA; SPECTROSCOPY; TOMOGRAPHY; TISSUE; LOCALIZATION; ABSORBERS AB The feasibility of employing fluorescent contrast agents to perform optical imaging in tissues and other scattering media has been examined through computational studies. Fluorescence lifetime and yield can give crucial information about local metabolite concentrations or environmental conditions within tissues. This information can be employed toward disease detection, diagnosis, and treatment if noninvasively quantitated from reemitted optical signals. However, the problem of inverse image reconstruction of fluorescence yield and lifetime is complicated because of the highly scattering nature of the tissue. Here a light propagation model employing the diffusion equation is used to account for the scattering of both the excitation and fluorescent light. Simulated measurements of frequency-domain parameters of fluorescent modulated ac amplitude and phase lag are used as inputs to an inverse image-reconstruction algorithm, which employs the diffusion model to predict frequency-domain measurements resulting from a modulated input at the phantom periphery. In the inverse image-reconstruction algorithm, a Newton-Raphson technique combined with a Marquardt algorithm is employed to converge on the fluorescent properties within the medium. The successful reconstruction of both the fluorescence yield and lifetime in the case of a heterogeneous fluorophore distribution within a scattering medium has been demonstrated without a priori information or without the necessity of obtaining absence images. (C) 1997 Optical Society of America. C1 MCMASTER UNIV,HAMILTON,ON L8V 5C2,CANADA. HAMILTON REG CANC CTR,HAMILTON,ON L8V 5C2,CANADA. PURDUE UNIV,SCH CHEM ENGN,W LAFAYETTE,IN 47907. RP Paithankar, DY (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,50 BLOSSOM ST,BOSTON,MA 02111, USA. RI Patterson, Michael/A-9882-2010; Sevick-Muraca, Eva/A-4152-2017 OI Patterson, Michael/0000-0002-6398-0742; Sevick-Muraca, Eva/0000-0002-8152-4847 NR 34 TC 155 Z9 158 U1 0 U2 3 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD APR 1 PY 1997 VL 36 IS 10 BP 2260 EP 2272 DI 10.1364/AO.36.002260 PG 13 WC Optics SC Optics GA WQ039 UT WOS:A1997WQ03900036 PM 18253202 ER PT J AU Sims, KB Irvine, AR Good, WV AF Sims, KB Irvine, AR Good, WV TI Norrie disease in a family with a manifesting female carrier SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID CANDIDATE GENE; MUTATION; TRANSLOCATION; LINKAGE AB Objectives: To show that Norrie disease can occur in a girl and to describe her ophthalmologic and genetic features. Methods: Amplification of DNA polymerase chain reaction and sequencing of asymmetric polymerase chain reaction for exon 3 were performed on the blood specimen obtained from a girl born with bilateral retinal detachments. Patient: A female child with bilateral retinal detachment who had 2 uncles in whom Norrie disease had already been diagnosed. Results: The child had a mutation in the third exon (T776-->A; Ile 123-->Asn) identical to the mutation found in her uncles. Conclusions: Norrie disease can occur in girls. The most likely explanation is nonrandom or unfavorable X inactivation, although timing of development of the peripheral retina and its blood supply could render it vulnerable to effects of the mutant allele at a critical developmental phase. C1 UNIV CINCINNATI,COLL MED,DEPT OPHTHALMOL,CINCINNATI,OH 45267. MASSACHUSETTS GEN HOSP,DEV NEUROGENET LABS,CHARLESTOWN,MA. UNIV CALIF SAN FRANCISCO,DEPT OPHTHALMOL,SAN FRANCISCO,CA 94143. NR 20 TC 20 Z9 20 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 APR PY 1997 VL 115 IS 4 BP 517 EP 519 PG 3 WC Ophthalmology SC Ophthalmology GA WT596 UT WOS:A1997WT59600011 PM 9109762 ER PT J AU Li, KK Lucarelli, MJ Bilyk, JR Joseph, MP AF Li, KK Lucarelli, MJ Bilyk, JR Joseph, MP TI Optic nerve decompression for compressive neuropathy secondary to neoplasia SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID FIBROUS DYSPLASIA; CANAL DECOMPRESSION; BLINDNESS; MENINGIOMAS; TRAUMA; SINUS AB Objective: To evaluate the outcome of extracranial optic nerve decompression in patients with compressive optic neuropathy secondary to intracranial, paranasal sinus, or orbital neoplastic processes. Design: A retrospective chart review and clinical followup of patients who underwent optic nerve decompression. Setting: Tertiary care referral center. Patients: During an 8-year period, 95 extracranial optic nerve decompressions were performed by one of us (M.P.J.) for optic neuropathy resulting from traumatic, inflammatory, infectious, iatrogenic, neoplastic, and idiopathic processes. Thirty patients with compressive optic neuropathy secondary to histopathologically confirmed tumors were identified. Intervention: Optic nerve decompression via external ethmoidectomy approach. Result: Twenty (67%) of 30 patients showed improvement in vision. Improvement in 17 of the 20 patients has been stable. Seven patients (23%) showed no improvement but there was no further worsening of vision after surgery. In 3 patients (10%) vision deteriorated following surgery. Conclusion: Extracranial optic nerve decompression may be considered for the preservation or improvement of vision in selected patients with compressive optic neuropathy from neoplasms. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL HEAD & NECK SURG,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 37 TC 13 Z9 13 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 APR PY 1997 VL 123 IS 4 BP 425 EP 429 PG 5 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA WT849 UT WOS:A1997WT84900012 PM 9109792 ER PT J AU Nah, EH King, DE Craig, FE AF Nah, EH King, DE Craig, FE TI CD4 and CD8 antigen coexpression - A flow cytometric study of peripheral blood, bone marrow, body fluid, and solid lymphoreticular specimens SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID T-CELL LYMPHOMAS; INTERLEUKIN-4; CLONES AB Objective.-CD4 and CD8 antigen coexpression occurs not only on blastic T-cell malignancies, but also on a small subset of mature lymphocytes. The aim of this study was to determine the prevalence of this population of cells and to identify features that can be used to differentiate them from T lymphoblasts. Design.-All specimens submitted to the clinical flow cytometry laboratory from August 1, 1994, through July 31, 1995, were analyzed for CD4 and CD8 coexpression. Main Outcome Measure.-Percentage of lymphocytes coexpressing the CD4 and CD8 antigens. Results.-Four percent (22/526) of all specimens contained a population of CD4/CD8 coexpressing cells. Five cases represented CD4 and CD8 antigen expression on neoplastic cells. In 17 cases, the CD4/CD8 coexpressing cells appeared to represent a population of mature lymphocytes with a normal phenotype. The immature cells of T-cell acute lymphocytic leukemia and lymphoblastic lymphoma represented a dominant uniform population of cells demonstrating strong staining with both the CD4 and CD8 antigens. Cases containing a mature population of CD4/CD8 coexpressing cells were characterized by fewer coexpressing cells and variable expression of CD8. There were cases where distinction of this population of mature CD4/CD8 coexpressing lymphoid cells from a blastic malignancy was not possible using immunophenotyping alone. Conclusion.-Correlation of clinical, morphologic, and immunophenotypic data is recommended to prevent the misdiagnosis of subtle involvement by a blastic T-cell malignancy. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78384. CHONNAM UNIV HOSP,DEPT CLIN PATHOL,KWANGJU,SOUTH KOREA. AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78284. NR 17 TC 2 Z9 3 U1 0 U2 0 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 APR PY 1997 VL 121 IS 4 BP 381 EP 384 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA WW544 UT WOS:A1997WW54400011 PM 9140307 ER PT J AU Bodis, S Hemesath, T Fisher, DE AF Bodis, S Hemesath, T Fisher, DE TI Highly conserved asparagine in the basic domain of Myc is dispensable for DNA binding, transformation, and apoptosis SO BIOCHEMICAL AND MOLECULAR MEDICINE LA English DT Article ID LOOP-HELIX PROTEIN; TRANSCRIPTIONAL ACTIVATION; CRYSTAL-STRUCTURE; B/HLH/Z DOMAIN; MYOD; RECOGNITION; REGION; DIMER; FIBROBLASTS; MUTATIONS AB The basic region of c-Myc and other basic helix-loop-helix (b-HLH)-containing proteins bind to the palindromic DNA sequences CANNTG. For the myogenic factor MyoD, a member of the b-HLH family, mutation of several basic region residues abrogates muscle differentiation, but not DNA binding, One of the amino acid positions displaying this behavior in MyoD aligns with a highly conserved asparagine in Myc. This conserved asparagine displays complete tolerance for alanine substitution as measured by DNA binding. To test the possibility of whether the basic region of Myc encodes a second biological function, the conserved asparagine in c-Myc (N360) was mutated to alanine and tested for the Myc-dependent functions of cellular transformation and apoptosis. In contrast to the deleterious effects of such mutations in MyoD, the alanine mutant functions normally for both Myc-dependent cellular transformation and apoptosis induction. Therefore, a basic region function distinct from DNA binding may not be a general feature of HLH transcription factors. (C) 1997 Academic Press. C1 DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. NR 23 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1077-3150 J9 BIOCHEM MOL MED JI Biochem. Mol. Med. PD APR PY 1997 VL 60 IS 2 BP 102 EP 107 DI 10.1006/bmme.1997.2575 PG 6 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA WW752 UT WOS:A1997WW75200003 PM 9169089 ER PT J AU Renshaw, P Kaufman, MJ Pollack, MH Rose, SL Kukes, TJ Mendelson, JH Lukas, SE Cohen, BM AF Renshaw, P Kaufman, MJ Pollack, MH Rose, SL Kukes, TJ Mendelson, JH Lukas, SE Cohen, BM TI Abnormal cerebral metabolism in opiate-dependent polydrug abusers SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MCLEAN HOSP,BRAIN IMAGING CTR,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,ANXIETY DISORDERS PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 19 EP 19 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900021 ER PT J AU Ames, D Wirshing, WC Brammer, G Pashdag, J Yuwiler, A AF Ames, D Wirshing, WC Brammer, G Pashdag, J Yuwiler, A TI Variability in whole blood serotonin as a marker for suicidality in schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. PEPPERDINE UNIV,GRAD SCH EDUC & PSYCHOL,CULVER CITY,CA 90230. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 28 EP 28 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900030 ER PT J AU Altshuler, L Bartzokis, G Grieder, T Curran, J Mintz, J AF Altshuler, L Bartzokis, G Grieder, T Curran, J Mintz, J TI Specific limbic differences in MRI of schizophrenic and bipolar subjects SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT RADIOL,LOS ANGELES,CA 90024. RI Bartzokis, George/K-2409-2013; Mintz, Jim/N-7385-2014 OI Mintz, Jim/0000-0002-8299-5851 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 33 EP 33 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900035 ER PT J AU Tsai, G vanKammen, DP Chen, S Kelley, ME Coyle, JT AF Tsai, G vanKammen, DP Chen, S Kelley, ME Coyle, JT TI Glutamatergic transmission and structural deficits in schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,LAB MOL & DEV NEUROSCI,CHARLESTOWN,MA. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,CHARLESTOWN,MA. MASSACHUSETTS GEN HOSP,CHARLESTOWN,MA. HIGHLAND DRIVE VA MED CTR,PITTSBURGH,PA. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 38 EP 38 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900040 ER PT J AU Wilkins, RT Rojas, D Teale, P Sheeder, J Aasal, R Wahlberg, LJ Marquardt, JE Sandberg, EJ Simon, J Arciniegas, D Laudenslager, M Taylor, D Montgomery, P Reite, M AF Wilkins, RT Rojas, D Teale, P Sheeder, J Aasal, R Wahlberg, LJ Marquardt, JE Sandberg, EJ Simon, J Arciniegas, D Laudenslager, M Taylor, D Montgomery, P Reite, M TI Reduced hippocampal volume in PTSD: Is it PTSD, or alcohol? SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 DENVER VET AFFAIRS MED CTR,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. RI Arciniegas, David/A-3792-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 41 EP 41 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900043 ER PT J AU Arciniegas, D Rojas, D Sheeder, J Aasal, R Teale, P Sandberg, E Reite, M Beresford, T AF Arciniegas, D Rojas, D Sheeder, J Aasal, R Teale, P Sandberg, E Reite, M Beresford, T TI Alcohol and the pituitary in hippocampal volume loss in PTSD SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. DENVER VET AFFAIRS MED CTR,DENVER,CO 80220. RI Arciniegas, David/A-3792-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 42 EP 42 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900044 ER PT J AU Bartzokis, G Altshuler, L Grieder, T Curran, J AF Bartzokis, G Altshuler, L Grieder, T Curran, J TI Medial temporal lobe volume measurement reliability using reformatted 3D images SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT RADIOL,LOS ANGELES,CA 90024. RI Bartzokis, George/K-2409-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 49 EP 49 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900051 ER PT J AU Amin, F Stroe, AE Adebogun, O Silverman, JM Smith, CJ Knott, PJ Siever, LJ Davis, KL AF Amin, F Stroe, AE Adebogun, O Silverman, JM Smith, CJ Knott, PJ Siever, LJ Davis, KL TI Attenuated diurnal dopamine rhythm in non-psychotic relatives of schizophrenic probands SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON VAMC,HOUSTON,TX 77030. MT SINAI SCH MED,BRONX VAMC,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 229 EP 229 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900231 ER PT J AU Ames, D Wirshing, WC Marshall, BD Green, MF McGurk, SR Mintz, J Marder, SR AF Ames, D Wirshing, WC Marshall, BD Green, MF McGurk, SR Mintz, J Marder, SR TI Treatment resistant schizophrenia: Evaluation of risperidone vs. haloperidol SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Mintz, Jim/N-7385-2014 OI Mintz, Jim/0000-0002-8299-5851 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 245 EP 245 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900247 ER PT J AU George, MS Speer, AM Stallings, L Wassermann, EM Kimbrell, TA Epstein, C Risch, SC Post, RM AF George, MS Speer, AM Stallings, L Wassermann, EM Kimbrell, TA Epstein, C Risch, SC Post, RM TI Combining transcranial magnetic stimulation with functional imaging SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PSYCHIAT,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT RADIOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT NEUROL,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,DEPT PSYCHIAT,CHARLESTON,SC. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. EMORY UNIV,DEPT NEUROL,ATLANTA,GA 30322. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 261 EP 261 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900262 ER PT J AU Yehuda, R Siever, LJ AF Yehuda, R Siever, LJ TI Persistent effects of stress in trauma survivors and their descendants SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI SCH MED,NEW YORK,NY 10029. BRONX VET ADM MED CTR,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 265 EP 265 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900266 ER PT J AU Bauer, M McBride, L Chase, C Sachs, G AF Bauer, M McBride, L Chase, C Sachs, G TI Manual-based group psychotherapy for bipolar disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. VET ADM MED CTR,PROVIDENCE,RI 02806. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 272 EP 272 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900273 ER PT J AU Amsterdam, J GarciaEspana, F Fawcett, J Quitkin, F Reimherr, F Rosenbaum, J HornigRohan, M AF Amsterdam, J GarciaEspana, F Fawcett, J Quitkin, F Reimherr, F Rosenbaum, J HornigRohan, M TI Fluoxetine-induced blood pressure changes - Do SSRIs cause hypertension? SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV PENN,MED CTR,PHILADELPHIA,PA 19104. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. UNIV UTAH,SCH MED,SALT LAKE CITY,UT. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 318 EP 318 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900319 ER PT J AU Fava, M Dunner, D Greist, J HornigRohan, M Preskorn, S Trivedi, M Zajecka, J Cohen, M Wingard, P AF Fava, M Dunner, D Greist, J HornigRohan, M Preskorn, S Trivedi, M Zajecka, J Cohen, M Wingard, P TI An open-label study of mirtazapine in depressed patients who failed treatment with an SSRI SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV WASHINGTON,MED CTR,SEATTLE,WA 98105. DEAN FDN HLTH, RES & EDUC,MADISON,WI 53717. UNIV PENN,MED CTR,PHILADELPHIA,PA 19104. INST PSYCHIAT RES,WICHITA,KS 67214. SW MED SCH,DALLAS,TX 75235. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. ORGANON INC,W ORANGE,NJ 07052. RI Preskorn, Sheldon/L-9839-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 330 EP 330 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900330 ER PT J AU Roitman, SEL Keefe, RSE Mitropoulou, V Dupre, RL Siever, LJ AF Roitman, SEL Keefe, RSE Mitropoulou, V Dupre, RL Siever, LJ TI Visuospatial working memory in schizotypal personality disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY. DUKE UNIV,MED CTR,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 355 EP 355 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900355 ER PT J AU Kirrane, R Trestman, R Mitropoulou, V Nunn, M Siever, L AF Kirrane, R Trestman, R Mitropoulou, V Nunn, M Siever, L TI Effects of amphetamine on cognitive impairment in schizotypal personality disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY 10029. BRONX VET ADM MED CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 356 EP 356 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900356 ER PT J AU Yao, JK Reddy, RD vanKammen, DP AF Yao, JK Reddy, RD vanKammen, DP TI Reduced level of the antioxidant uric acid in schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 VA PITTSBURGH HLTH CARE SYST,PITTSBURGH,PA 15206. UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,MED CTR,PITTSBURGH,PA 15213. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 391 EP 391 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900390 ER PT J AU Yaffe, K Ettinger, B Pressman, A Seeley, D Whooley, M Schaefer, C Cummings, S AF Yaffe, K Ettinger, B Pressman, A Seeley, D Whooley, M Schaefer, C Cummings, S TI Neuropsychiatric function and DHEAS in elderly women: A prospective study SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. SAN FRANCISCO VET AFFAIRES MED CTR,SAN FRANCISCO,CA. KAISER PERMANENTE MED CARE PROGRAM,DIV RES,OAKLAND,CA 94611. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 409 EP 409 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900407 ER PT J AU WooMing, AM Trestman, RL Mitropoulou, V Siever, LJ AF WooMing, AM Trestman, RL Mitropoulou, V Siever, LJ TI Role of menstrual cycle status in noradrenergic studies SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MT SINAI VA MED CTR,NEW YORK,NY. BRONX VET ADM MED CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 416 EP 416 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900414 ER PT J AU Smoller, JW Halbreich, U AF Smoller, JW Halbreich, U TI Intermittent luteal phase sertraline treatment of dysphoric premenstrual syndrome SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1997 VL 41 SU 7 BP 418 EP 418 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WQ709 UT WOS:A1997WQ70900416 ER PT J AU Cantiello, HF AF Cantiello, HF TI Nucleotide transport through the cystic fibrosis transmembrane conductance regulator SO BIOSCIENCE REPORTS LA English DT Review DE CFTR; ABC transporters; P-glycoprotein; ATP channels; ATP release ID RESISTANCE P-GLYCOPROTEIN; SHARK RECTAL GLAND; LIVER ECTO-ATPASE; PROTEIN-KINASE-C; MULTIDRUG-RESISTANCE; CHLORIDE CHANNELS; PLASMA-MEMBRANE; FUNCTIONAL RECONSTITUTION; EXTRACELLULAR ATP; COMPLEMENTARY-DNA AB The cystic fibrosis transmembrane conductance regulator (CFTR) is a member of the superfamily of ATP-binding cassette (ABC) transporters, also known as traffic ATPases, which are implicated in the movement of various substrates. Recent studies indicate that CFTR and other closely related ABC transporters are also implicated in the movement of cellular ATP. This is the subject of current controversy. Therefore, evidence for the movement of cellular nucleotides by expression of CFTR and related molecules, as well as the potential significance of ATP-permeable channels in cell physiology, are reviewed in this study. The hypothesis is thus forwarded for the improper delivery of cellular ATP to the extracellular milieu by a dysfunctional CFTR, to be a relevant factor in the onset of cystic fibrosis. RP Cantiello, HF (reprint author), MASSACHUSETTS GEN HOSP, RENAL UNIT, 149 13TH ST, CHARLESTOWN, MA 02129 USA. NR 102 TC 15 Z9 15 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND SN 0144-8463 EI 1573-4935 J9 BIOSCIENCE REP JI Biosci. Rep. PD APR PY 1997 VL 17 IS 2 BP 147 EP 171 DI 10.1023/A:1027381412574 PG 25 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XH104 UT WOS:A1997XH10400004 PM 9217964 ER PT J AU Lee, BSJ Wegner, SA McGarigle, CJ Bierer, BE Antin, JH AF Lee, BSJ Wegner, SA McGarigle, CJ Bierer, BE Antin, JH TI Treatment of chronic graft-versus-host disease with clofazimine SO BLOOD LA English DT Article ID MARROW TRANSPLANTATION; PYODERMA GANGRENOSUM; LUPUS-ERYTHEMATOSUS; B663; CHEMOTHERAPY; THALIDOMIDE; ULTRAVIOLET; ENHANCEMENT; PREDNISONE; MECHANISM AB Clofazimine (Lamprene) is an antimycobacterial drug that has antiinflammatory activity in a number of chronic autoimmune skin disorders. We report 22 patients treated with clofazimine for chronic graft-versus-host disease (cGVHD). The initial dose was 300 mg orally in a single daily dose for 90 days. After 90 days, the dose was lowered to 100 mg orally each day and the medication continued indefinitely as tolerated. Treatment courses lasted 7 to 835 days and were generally well tolerated. Gastrointestinal side effects occurred in eight of 22 patients (36%) and hyperpigmentation was noted in 12 of 22 patients (55%), which resolved upon decrease or discontinuation of the drug. Over 50% of patients with skin involvement, flexion contractures, or oral manifestations achieved complete or partial responses. Seven of 22 patients (32%) were able to reduce other immunosuppressive medications. Thus, clofazimine is safe and has encouraging efficacy in cGVHD, particularly if sclerodermatous skin, joint contractures, or oral manifestations are present. The mechanism by which clofazimine induces a response is unknown, but might be secondary to suppression of alloreactive T-cell function in cGVHD target organs. Clofazimine deserves further study for the treatment of cGVHD. (C) 1997 by The American Society of Hematology. C1 BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,DEPT MED,BOSTON,MA 02115. DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FU NCI NIH HHS [CA 39542, CA 58661] NR 40 TC 43 Z9 48 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1997 VL 89 IS 7 BP 2298 EP 2302 PG 5 WC Hematology SC Hematology GA WQ359 UT WOS:A1997WQ35900007 PM 9116272 ER PT J AU Lehmann, LE Guinan, EC Halpern, SL Donovan, MJ Bierer, BE Parsons, SK AF Lehmann, LE Guinan, EC Halpern, SL Donovan, MJ Bierer, BE Parsons, SK TI Isolated testicular relapse in an adolescent 5 years following allogeneic bone marrow transplantation for acute myelogenous leukemia SO BONE MARROW TRANSPLANTATION LA English DT Article DE bone marrow transplant; AML; testicular relapse ID ACUTE NONLYMPHOBLASTIC LEUKEMIA; ACUTE MONOBLASTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; CHILDREN; INFILTRATION AB A case of isolated testicular relapse occurring 5 years after allogeneic bone marrow transplantation (BMT) for acute myelogenous leukemia (AML) is reported. The patient presented with M4 AML at age 13 and underwent allogeneic BMT in first remission, 5 months after diagnosis. He had no acute graft-versus-host disease (GVHD) but developed mild chronic GVHD 5 months following transplant and received immunosuppressive therapy for the next 2 years, Five years posttransplant he had an isolated testicular relapse that was treated with chemotherapy and testicular radiation, The patient remains in remission 17 months following relapse and more than 15 months following the cessation of therapy. C1 CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,DIV PATHOL,BOSTON,MA 02115. OVERLOOK HOSP,VALERIE FUND CHILDRENS CTR,SUMMIT,NJ. RP Lehmann, LE (reprint author), DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [5PO1 CA 39542] NR 17 TC 4 Z9 4 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD APR PY 1997 VL 19 IS 8 BP 849 EP 851 DI 10.1038/sj.bmt.1700753 PG 3 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA WV986 UT WOS:A1997WV98600017 PM 9134181 ER PT J AU Louis, DN AF Louis, DN TI A molecular genetic model of astrocytoma histopathology SO BRAIN PATHOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; TUMOR-SUPPRESSOR GENE; FACTOR RECEPTOR GENE; HUMAN-MALIGNANT ASTROCYTOMA; CELL-CYCLE INHIBITION; HUMAN BRAIN-TUMORS; GLIOBLASTOMA-MULTIFORME; HUMAN GLIOMAS; RETINOBLASTOMA-PROTEIN; HUMAN CANCERS AB As the molecular events responsible for astrocytoma formation and progression are being clarified, it is becoming possible to correlate these alterations with the specific histopathological and biological features of astrocytoma, anaplastic astrocytoma and glioblastoma multiforme. In WHO grade II astrocytomas, autocrine stimulation by the platelet-derived growth factor system coupled with inactivation of the p53 gene may lead to a growth stimulus in the face of decreased cell death with slow net growth ensuing. Such cells would also have defective responses to DNA damage and impaired DNA repair, setting the stage for future malignant change. Such biological scenarios recapitulate many of the clinicopathological features of WHO grade II astrocytomas. Anaplastic astrocytomas further display release of a critical cell cycle brake that involves the CDKN2/p16, RB and CDK4 genes. This results in mitoses seen histologically; clinically, there is more conspicuous, rapid growth. Finally, glioblastomas may emerge from the microenvironmental outgrowth of more malignant clones in a complex vicious cycle that involves necrosis, hypoxia, growth factor release, angiogenesis and clonal selection; growth signals mediated by activation of epidermal growth factor receptors may precipitate glioblastomas. It is clear as well that glioblastoma multiforme can arise via a number of independent genetic pathways, although the clinical significance of these distinctions remains unclear. C1 MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA. RP Louis, DN (reprint author), MASSACHUSETTS GEN HOSP,MOL NEUROONCOL LAB,DEPT PATHOL,CNY6,143 13TH ST,CHARLESTOWN,MA 02129, USA. FU NCI NIH HHS [CA69280, CA57683] NR 82 TC 166 Z9 169 U1 1 U2 2 PU INT SOC NEUROPATHOLOGY PI PITTSBURGH PA 200 LOTHROP ST A506, PITTSBURGH, PA 15213 SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD APR PY 1997 VL 7 IS 2 BP 755 EP 764 DI 10.1111/j.1750-3639.1997.tb01062.x PG 10 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA WV764 UT WOS:A1997WV76400005 PM 9161727 ER PT J AU Zaretsky, AE Fava, M Davidson, KG Pava, JA Matthews, J Rosenbaum, JF AF Zaretsky, AE Fava, M Davidson, KG Pava, JA Matthews, J Rosenbaum, JF TI Are dependency and self-criticism risk factors for major depressive disorder? SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Article DE dysfunctional attitudes; dependency; self-criticism; depression; life events ID LIFE EVENTS; DYSFUNCTIONAL ATTITUDES; EXPERIENCES QUESTIONNAIRE; VULNERABILITY FACTORS; SOCIOTROPY-AUTONOMY; UNIPOLAR DEPRESSION; DRUG-TREATMENT; BECK CONCEPTS; PERSONALITY; TEMPERAMENT AB Objective: To determine whether dependent and self-critical personality traits are associated with specific types of life events and whether these traits change with pharmacotherapy. Method: Overall, 142 depressed outpatients completing 8 weeks of fluoxetine treatment were administered the Life Experiences Survey (LES) at baseline and the Dysfunctional Attitude Scale (DAS) and Hamilton Depression Rating Scale (HDRS) at baseline and endpoint. Results: The DAS dependency subscale, but not the self-criticism subscale, showed significant correlations with life events regardless of congruency. Baseline HDRS scores were positively correlated with both DAS subscales and total score. The DAS subscales, the total DAS score, and the HDRS all improved significantly with treatment. Conclusions: These results confirm a growing body of research that has found an association between sociotropic or dependent personality traits and life events. C1 UNIV TORONTO,DEPT PSYCHIAT,TORONTO,ON,CANADA. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPRESS CLIN & RES PROGRAM,BOSTON,MA 02114. RP Zaretsky, AE (reprint author), MT SINAI HOSP,DEPT PSYCHIAT,COGNIT BEHAV THERAPY CLIN,SUITE 941A,600 UNIV AVE,TORONTO,ON M5G 1X5,CANADA. NR 55 TC 4 Z9 4 U1 1 U2 4 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD APR PY 1997 VL 42 IS 3 BP 291 EP 297 PG 7 WC Psychiatry SC Psychiatry GA WU692 UT WOS:A1997WU69200007 PM 9114945 ER PT J AU Berg, J Gebhardt, MC Rand, WM AF Berg, J Gebhardt, MC Rand, WM TI Effect of timing of postoperative chemotherapy on survival of dogs with osteosarcoma SO CANCER LA English DT Article; Proceedings Paper CT 6th Annual Symposium of the American-College-of-Veterinary-Surgeons CY NOV 03-06, 1996 CL SAN FRANCISCO, CA SP Amer Coll Vet Surgeons DE animal models; osteosarcoma; canine; metastases; chemotherapy ID PRIMARY TUMOR REMOVAL; APPENDICULAR OSTEOSARCOMA; ADJUVANT CHEMOTHERAPY; OSTEOGENIC-SARCOMA; RESIDUAL TUMOR; CISPLATIN; METASTASES; AMPUTATION; KINETICS; SURGERY AB BACKGROUND. After excision of primary tumors, initiation of chemotherapy for micrometastases is often delayed for 2 to 4 weeks to permit patient recovery and early healing of the surgical wound. However, studies using murine tumors have indicated that removal of a primary tumor may cause increased cell proliferation within micrometastases during the first 7 to 10 days after surgery, potentially rendering the micrometastases more susceptible to chemotherapy. Clinical trials assessing the value of early postoperative initiation of chemotherapy for human breast carcinoma have yielded conflicting results. Osteosarcoma of dogs is a naturally occurring model for human tumors likely to have micrometastases at the time of diagnosis. METHODS. Before surgery, 102 dogs with osteosarcoma were randomized to receive cisplatin and doxorubicin chemotherapy beginning either 2 days or 10 days after amputation. Survival analysis was performed for each treatment group and for a historic control group comprised of 162 dogs treated by amputation alone. RESULTS. Median survival times for dogs treated by amputation alone and for dogs receiving chemotherapy beginning 2 or 10 days after surgery were 5.5, 11.5, and 11.0 months, respectively. Survival was significantly longer for each of the two groups of dogs receiving chemotherapy than for control dogs (P < 0.0001). There was no significant difference in survival between treatment groups (P = 0.727). CONCLUSIONS. These results do not disprove the theory that removal of a primary tumor alters the growth kinetics of metastases, but do imply that there is no substantial advantage to early postoperative initiation of adjuvant chemotherapy for spontaneous tumors of large species. (C) 1997 American Cancer Society. C1 MASSACHUSETTS GEN HOSP,ORTHOPED RES LAB,BOSTON,MA. TUFTS UNIV,SCH MED,DEPT COMMUNITY HLTH,BOSTON,MA 02111. RP Berg, J (reprint author), TUFTS UNIV,SCH VET MED,DEPT SURG,200 WESTBORO RD,NORTH GRAFTON,MA 01536, USA. NR 31 TC 49 Z9 51 U1 2 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1997 VL 79 IS 7 BP 1343 EP 1350 DI 10.1002/(SICI)1097-0142(19970401)79:7<1343::AID-CNCR11>3.0.CO;2-# PG 8 WC Oncology SC Oncology GA WP130 UT WOS:A1997WP13000011 PM 9083156 ER PT J AU Gollamudi, SV Gelman, RS Peiro, G Schneider, LJ Schnitt, SJ Recht, A Silver, BJ Harris, JR Connolly, JL AF Gollamudi, SV Gelman, RS Peiro, G Schneider, LJ Schnitt, SJ Recht, A Silver, BJ Harris, JR Connolly, JL TI Breast-conserving therapy for stage I-II synchronous bilateral breast carcinoma SO CANCER LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the American-Society-for-Therapeutic-Radiology-and-Oncology CY OCT 07-11, 1995 CL MIAMI BEACH, FL SP Amer Soc Therapeut Radiol & Oncol DE radiotherapy; breast neoplasms; synchronous; adenocarcinoma; bilateral ID PRIMARY RADIATION-THERAPY; OPPOSITE BREAST; CANCER; POPULATION; SURVIVAL; DISEASE; RISKS AB BACKGROUND. Synchronous bilateral breast carcinoma (SBBC) is an uncommon presentation, and the management of patients with this disease is not well established. METHODS. In order to evaluate whether patients with early-stage SBBC could be safely and effectively treated with bilateral breast-conserving therapy (BCT), the authors retrospectively reviewed the records of 24 patients with clinical Stage I-II SBBC treated during the period 1977-1989 with bilateral BCT. SBBC was defined as bilateral invasive carcinomas diagnosed no more than 1 month apart. The median age at diagnosis was 56 years (range, 32-85 years), and the median follow-up for surviving patients was 95 months (range, 68-157 months). Pathology slides were available for review in 19 cases. Cosmetic results and complications after BCT were scored. Outcome was compared with that of 1314 patients with unilateral Stage I or II breast carcinoma, within the same age range, treated during the same time period. RESULTS. There were no significant differences between the SBBC and unilateral groups in actuarial disease free survival (70% and 74%, respectively, at 5 years), overall survival (88% and 87%, respectively, at 5 years), or crude distribution of sites of first failure. Multivariate analysis of overall survival and disease free survival also did not show bilaterality to be a significant factor, The cosmetic results fur the SBBC group were not significantly different from those for the unilateral group. Physician assessment of cosmetic outcome was excellent in 57% and good in 43% of SBBC patients evaluated 25-48 months after BCT. Long term complications were rare in both groups. CONCLUSIONS. Patients with early-stage SBBC can be safely treated with carefully planned, bilateral BCT, with outcome that appears to be comparable to that of patients with early-stage unilateral breast carcinoma. (C) 1997 American Cancer Society. C1 HARVARD UNIV, SCH MED, JOINT CTR RADIAT THERAPY, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT RADIAT ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BETH ISRAEL HOSP, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. DANA FARBER CANC INST, DIV BIOSTAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. NR 25 TC 34 Z9 34 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1997 VL 79 IS 7 BP 1362 EP 1369 DI 10.1002/(SICI)1097-0142(19970401)79:7<1362::AID-CNCR14>3.0.CO;2-Y PG 8 WC Oncology SC Oncology GA WP130 UT WOS:A1997WP13000014 PM 9083159 ER PT J AU Strobel, T Swanson, L Cannistra, SA AF Strobel, T Swanson, L Cannistra, SA TI In vivo inhibition of CD44 limits intra-abdominal spread of a human ovarian cancer xenograft in nude mice: A novel role for CD44 in the process of peritoneal implantation SO CANCER RESEARCH LA English DT Article ID TUMOR-GROWTH INVIVO; CELL-LINES; VARIANT; EXPRESSION AB Ovarian cancer cells frequently metastasize by implanting onto the peritoneal mesothelial lining of the abdominal cavity. Data obtained from in vitro adhesion studies have suggested a possible role for the CD44 molecule in this process. The purpose of the present study was to determine the in vivo role of CD44 in ovarian cancer metastasis by using a nude mouse xenograft model of peritoneal implantation. Three groups of 10 athymic female nude mice each received an i.p. inoculum of 10 x 10(6) cells from a CD44-positive human ovarian cancer cell line (36M2) in the presence of either anti-D144 antibody (Ab; nonreactive IgG1), anti-DP3 Ab (reactive IgG1 Ab that does not inhibit in vitro binding), or neutralizing anti-CD44 Ab (IgG1), The number of peritoneal and diaphragmatic implants at 5 weeks for anti-D144 and anti-DF3-treated groups was 103 +/- 17 and 120 +/- 20, respectively (mean +/- SE; P > 0.2), In contrast, animals treated with anti-CD44 Ab experienced a significant reduction in the number of tumor implants (35 +/- 4; P < 0.002). Anti-CD44 Ab was not inhibitory to the growth of 36M2 cells in vitro and did not inhibit s.c. tumor growth in vivo, suggesting that the observed effect was related to inhibition of peritoneal implantation. These data suggest that the CD44 molecule plays an important in vivo role in ovarian cancer cell implantation and that strategies to inhibit CD44 function may represent a novel approach to limiting the intra-abdominal spread of this highly lethal tumor. C1 HARVARD UNIV,DIV NEOPLAST DIS MECHANISMS,DANA FARBER CANC INST,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 60670] NR 13 TC 88 Z9 92 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1997 VL 57 IS 7 BP 1228 EP 1232 PG 5 WC Oncology SC Oncology GA WQ625 UT WOS:A1997WQ62500004 PM 9102203 ER PT J AU Chmura, SJ Nodzenski, E Beckett, MA Kufe, DW Quintans, J Weichselbaum, RR AF Chmura, SJ Nodzenski, E Beckett, MA Kufe, DW Quintans, J Weichselbaum, RR TI Loss of ceramide production confers resistance to radiation-induced apoptosis SO CANCER RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; SIGNAL-TRANSDUCTION PATHWAY; DOUBLE-STRAND BREAKAGE; PROGRAMMED CELL-DEATH; IONIZING-RADIATION; SURVIVAL; FAS AB Ionizing radiation mediates cell death, in part, through chromosomal damage following one or more cell divisions, X-rays also induce programmed cell death (apoptosis) in some cell types both in vitro and in vivo, Both neutral and acidic sphingomyelinases, which generate the lipid second messenger ceramide, are reported to induce apoptosis following ionizing radiation and other death signals such as tumor necrosis factor Lu and Fas ligand, Herein we report that a loss of ceramide production from a neutral sphingomyelinase generates a radioresistant phenotype as measured by a marked decrease in apoptosis, A WEHI-231 subline made deficient in ceramide production was found to be resistant to apoptosis compared with the parental subline following treatment with X-rays, The resistant subline underwent two to three subsequent cell divisions following X-irradiation, confirming that X-rays induce cell death through both mitotic and apoptotic mechanisms, These data suggest that loss of ceramide production following X-rays represents an extranuclear mechanism for the development of radioresistance, Modulation of extranuclear signals may increase tumor cell killing following radiation and represent new cellular targets for cancer therapy. C1 UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,DIV BIOL SCI,CHICAGO,IL 60637. UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [5-R01-CA42596, 5-R01-CA41068]; NIGMS NIH HHS [GM07183] NR 28 TC 138 Z9 141 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1997 VL 57 IS 7 BP 1270 EP 1275 PG 6 WC Oncology SC Oncology GA WQ625 UT WOS:A1997WQ62500013 PM 9102212 ER PT J AU Tilly, JL Tilly, KI Perez, GI AF Tilly, JL Tilly, KI Perez, GI TI The genes of cell death and cellular susceptibility to apoptosis in the ovary: A hypothesis SO CELL DEATH AND DIFFERENTIATION LA English DT Article DE apoptosis; Bcl-2; Bax; Bcl-x; p53; ICE; caspase; oocyte; granulosa cell; atresia ID FOLLICLE-STIMULATING-HORMONE; EPIDERMAL GROWTH-FACTOR; PRIMORDIAL GERM-CELLS; TUMOR-SUPPRESSOR P53; GRANULOSA-CELLS; BCL-2 GENE; IN-VIVO; PREOVULATORY FOLLICLES; CHORIONIC-GONADOTROPIN; ENDONUCLEASE ACTIVITY AB Recent advances in the field of cell death, primarily derived from gene-transfer experiments and manipulation of tumor cell lines in vitro, have identified key genes responsible for determining whether or not a given cell will initiate apoptosis, However, comparatively less is known of the role that the products of these genes play in physiological settings of cell death, In the ovary, a tremendous level of normal cell death takes place in the germline throughout the later stages of fetal development, This process is responsible for setting the absolute number of oocytes ('eggs') available for subsequent development and ovulation during adult life, Interestingly, death remains the fate of the vast majority of oocytes that survive the waves of attrition during fetal life and are endowed in the post-natal ovary as primordial follicles, This pool of oocytes is lost indirectly as a consequence of the death of the somatic (granulosa) cells that, in the case of a small percentage of the total follicles, support and nourish the oocyte until its release at ovulation, Due to the magnitude of cell death that occurs normally within the female gonad during both fetal development and post-natal life, the ovary has proven to be an excellent model to study the role of cell death genes in a physiological setting of endocrine-regulated apoptosis, It is now known that a diverse spectrum of pro and anti apoptosis susceptibility genes, including members of the bcl-2 and CASP(ced-3/lce) gene families, are expressed in germ cells and/or somatic cells of the ovary, Many, but not all, of these genes are regulated by specific survival factors, such as gonadotropins and growth factors, and changes in the temporal patterns of cell death gene expression suggest an intimate association exists between the products of these genes and activation of cellular suicide, Moreover, pathological oocyte destruction, such as that triggered by exposure of female germ cells to chemotherapeutic compounds or environmental toxicants, may also be dependent upon gene-driven apoptosis, As such, this review will discuss data supporting the hypothesis that the susceptibility of ovarian cells to death induction is dependent upon the pattern of cell death gene expression occurring within those cells prior to and/or concomitant with receipt of the stimulus for apoptosis, Elucidation of the relationship between germ cell loss and cell death genes may allow future intervention into the process of oocyte depletion associated with normal and pathophysiological reproductive senescence. C1 MASSACHUSETTS GEN HOSP,VINCENT CTR REPROD BIOL,BOSTON,MA 02114. RP Tilly, JL (reprint author), HARVARD UNIV,SCH MED,DEPT OBSTET GYNECOL & REPROD BIOL,55 FRUIT ST,BOSTON,MA 02114, USA. NR 87 TC 57 Z9 57 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1350-9047 J9 CELL DEATH DIFFER JI Cell Death Differ. PD APR PY 1997 VL 4 IS 3 BP 180 EP 187 DI 10.1038/sj.cdd.4400238 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WR528 UT WOS:A1997WR52800003 PM 16465227 ER PT J AU Cutrer, FM Limmroth, V Moskowitz, MA AF Cutrer, FM Limmroth, V Moskowitz, MA TI Possible mechanisms of valproate in migraine prophylaxis SO CEPHALALGIA LA English DT Article ID CORTICAL SPREADING DEPRESSION; RAT SPINAL-CORD; PROTEIN-LIKE IMMUNOREACTIVITY; TRIGEMINAL NUCLEUS CAUDALIS; D-ASPARTATE NMDA; SODIUM VALPROATE; EXPERIMENTAL ARTHRITIS; ANTICONVULSANT ACTION; GABA RECEPTORS; DURA-MATER AB Valproate has been shown to be an effective prophylactic treatment in migraine. Investigation of the mechanism of its antimigraine action is difficult due to the broad range of its biochemical effects and the complex nature of migraine pathophysiology. Valproate increases brain GABA levels and, in doing so, may suppress migraine-related events in the cortex, perivascular parasympathetics or trigeminal nucleus caudalis. There is experimental evidence that it suppresses neurogenic inflammation and directly attenuates nociceptive neurotransmission. In addition, valproate reportedly alters levels of excitatory and inhibitory neurotransmitters and exerts direct effects on neuronal membranes in vitro. Valproate's observed effect may ultimately result from a combination of actions at different loci. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,CHARLESTOWN,MA 02129. RP Cutrer, FM (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,149 13TH ST CNY 6403,CHARLESTOWN,MA 02129, USA. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [K08 NS 01803] NR 84 TC 80 Z9 83 U1 2 U2 3 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0333-1024 J9 CEPHALALGIA JI Cephalalgia PD APR PY 1997 VL 17 IS 2 BP 93 EP 100 DI 10.1046/j.1468-2982.1997.1702093.x PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA WU666 UT WOS:A1997WU66600006 PM 9137844 ER PT J AU Bunburaphong, T Imanaka, H Nishimura, M Hess, D Kacmarek, RM AF Bunburaphong, T Imanaka, H Nishimura, M Hess, D Kacmarek, RM TI Performance characteristics of bilevel pressure ventilators - A lung model study SO CHEST LA English DT Article DE bilevel pressure ventilators; expiratory resistance; inspiratory demand; noninvasive positive pressure ventilators; ventilator performance ID OBSTRUCTIVE PULMONARY-DISEASE; ACUTE RESPIRATORY-FAILURE; SUPPORT VENTILATION; MECHANICAL VENTILATION; NASAL MASK; FACE MASK; ACUTE EXACERBATIONS; INSPIRATORY WORK; DEVICES; BIPAP AB Bilevel pressure ventilators are being used increasingly to provide noninvasive ventilatory support in the management of obstructive sleep apnea, chronic ventilatory failure, and acute respiratory failure. However, the ability of these ventilators to respond to inspiratory demand without imposing expiratory loads has not been evaluated extensively. We evaluated the performance of nine bilevel pressure ventilators in a lung model, as compared with the Nellcor Puritan-Bennett 7200ae adult critical care ventilator. All ventilators were set to provide pressure support ventilation (PSV) and positive end-expiratory pressure (PEEP) at a rate of 10 breaths/min with an inspiratory time of 1.0 s. Simulated pleural pressure, airway pressure, and flow at airway opening were continuously monitored. We studied the effects of three PSV levels (5, 10, and 15 cm H2O) with 5 cm H2O PEEP at two lung compliances (50 and 80 mL/cm H2O) and four peak inspiratory flow demands (20, 40, 60, and 80 L/unin) on seven dependent variables: inspiratory delay time (D-I), inspiratory trigger pressure (P-I), inspiratory area percent (Area I%), expiratory delay time (D-E), supraplateau expiratory pressure change (P-E), expiratory area (Area E), and ventilator peak flow (VPF). Most ventilators performed as well as or significantly (p<0.05) better than the 7200ae in all studied variables. Compliance did not significantly affect ventilator performance. Increasing inspiratory flow demand significantly (p<0.05) increased D-I, P-I, P-E, and VPF and decreased Area I% with most ventilators. As ventilatory demand increased, D-E and Area E significantly (p<0.05) changed. With some units, D-E and Area E increased, while with others they decreased. Most bilevel pressure ventilators evaluated were able to respond to high ventilatory demands and outperformed the Nellcor Puritan-Bennett 7200ae ventilator. C1 MASSACHUSETTS GEN HOSP,RESP CARE DEPT LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 32 TC 60 Z9 65 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD APR PY 1997 VL 111 IS 4 BP 1050 EP 1060 DI 10.1378/chest.111.4.1050 PG 11 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA WT736 UT WOS:A1997WT73600037 PM 9106588 ER PT J AU Rauch, SL Bates, JF Grachev, ID AF Rauch, SL Bates, JF Grachev, ID TI Obsessive-compulsive disorder SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID GLUCOSE METABOLIC RATES; CEREBRAL BLOOD-FLOW; NUCLEAR MAGNETIC-RESONANCE; BASAL GANGLIA; TOURETTES-SYNDROME; CAUDATE-NUCLEUS; BEHAVIORAL PSYCHOTHERAPY; HUNTINGTONS-DISEASE; SYMPTOM PROVOCATION; IN-VIVO AB Although neuroimaging has a limited role in the diagnostic assessment of obsessive-compulsive disorder (OCD), neuroimaging research has contributed crucial information regarding the pathophysiology of OCD and related diseases. OCD may be one of a spectrum of disorders that all involve corticostriatal pathology, in which the clinical presentation reflects the topography of dysfunction within the striatum. Structural neuroimaging studies of OCD have indicated volumetric abnormalities in the caudate nucleus. Functional imaging studies of OCD have shown increased activity in the corticostriatal pathway involving anterior orbitofrontal cortex and the caudate nucleus, both at rest and during symptom provocation, which is attenuated following effective treatment. Paralimbic elements, such as the anterior cingulate and posterior orbitofrontal cortex, may play a role in mediating anxiety or arousal nonspecifically. Taken together, these imaging data support the ''striatal topography'' model of OCD and suggest directions for future research, focusing on processes involving anterior orbitofrontal cortex and the caudate nucleus. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 87 TC 10 Z9 10 U1 9 U2 11 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD APR PY 1997 VL 6 IS 2 BP 365 EP & PG 18 WC Psychiatry SC Psychiatry GA WX109 UT WOS:A1997WX10900009 ER PT J AU Gold, HK Garabedian, HD Dinsmore, RE Guerrero, LJ Cigarroa, JE Palacios, IF Leinbach, RC AF Gold, HK Garabedian, HD Dinsmore, RE Guerrero, LJ Cigarroa, JE Palacios, IF Leinbach, RC TI Restoration of coronary flow in myocardial infarction by intravenous chimeric 7E3 antibody without exogenous plasminogen activators - Observations in animals and humans SO CIRCULATION LA English DT Article; Proceedings Paper CT 69th Annual Scientific Session of the American-Heart-Association CY NOV 09-16, 1996 CL NEW ORLEANS, LA SP Amer Heart Assoc, Hoechst Marion Roussel Inc, Kansas City DE 7E3; myocardial infarction; platelet aggregation inhibitors; reperfusion ID MONOCLONAL-ANTIBODY; THROMBOLYSIS; REPERFUSION; REDUCTION; THERAPY AB Background Corollary thrombus is composed of platelets and fibrin, and during thrombolytic treatment, reflow may be slowed by platelet deposition. It may be possible to initiate coronary reflow without exogenous plasminogen activators by blocking platelet aggregation while fibrin generation is impeded with heparin. Methods and Results In 14 dogs, left anterior descending coronary artery thrombosis was produced by endothelial trauma and thrombin instillation in the presence of stenosis distally. Reflow was monitored by flow probe during treatment with (1) heparin, (2) heparin and aspirin, and (3) heparin, aspirin, and intravenous 7E3. Eighty percent of dogs treated with the third combination showed stable reflow (greater than or equal to 25% of prestenotic flow) in 50+/-9 minutes. In addition, 13 patients were studied during intravenous administration of c7E3 10 minutes before primary angioplasty for acute myocardial infarction and Thrombolysis In Myocardial Infarction (TIMI) grade 0 or 1 flow. Pretreatment included heparin and oral aspirin. Flow increased during a 10-minute period by at least one TIMI grade in 11 (85%) of 13 and reached TIMI grade 2 or 3 in 7 (54%) of 13 patients. Average TIMI grade flow increased from 0.31+/-0.5 to 1.54+/-0.8 (P<.001). Thrombus length 10 minutes after c7E3 was 5.1+/-3.5 mm. All but 1 patient then underwent angioplasty. There were no complications. Conclusions Coronary reflow can be initiated by intravenous 7E3 administration in the presence of heparin and aspirin. In human patients, this flow can be observed in 10 minutes without exogenous thrombolytic agents. RP Gold, HK (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,CTR AMBULATORY CARE,SUITE 480,BOSTON,MA 02114, USA. NR 20 TC 127 Z9 128 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 APR 1 PY 1997 VL 95 IS 7 BP 1755 EP 1759 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA WR519 UT WOS:A1997WR51900004 PM 9107158 ER PT J AU Butte, AN Houng, AK Jang, IK Reed, GL AF Butte, AN Houng, AK Jang, IK Reed, GL TI alpha(2)-Antiplasmin causes thrombi to resist fibrinolysis induced by tissue plasminogen activator in experimental pulmonary embolism SO CIRCULATION LA English DT Article DE alpha 2-antiplasmin; fibrinolysis; embolism; plasminogen activators ID HUMAN-PLASMA; CLOT LYSIS; ALPHA-2-PLASMIN INHIBITOR; CANINE MODEL; FACTOR-XIIIA; THROMBOLYSIS; ALPHA-2-ANTIPLASMIN; HEMOSTASIS; DEFICIENCY; MECHANISM AB Background In patients with pulmonary embolism, thrombi resist fibrinolysis induced by plasminogen activators. Because the molecular basis of this thrombus resistance is poorly understood, we used a potent inhibitor to examine the potential role of alpha(2)-antiplasmin (alpha 2AP) in experimental pulmonary embolism. Methods and Results Lysis of experimental pulmonary emboli was measured 4 hours after embolization in anesthetized ferrets. All animals received heparin (100 U/kg). Five experimental groups were studied: (1) no recombinant tissue plasminogen activator (rTPA); (2) rTPA at 1 mg/kg; (3) rTPA at 2 mg/kg; (4) rTPA at 1 mg/kg plus a control monoclonal antibody (MAb); and (5) rTPA at 1 mg/kg plus an alpha 2AP inhibitor (MAb 77A3). In comparison with ferrets receiving no rTPA (15.6+/-10.5% lysis, mean+/-SD), rTPA-treated groups showed significantly greater lysis (P<.01). Animals treated with rTPA and alpha 2AP inhibitor (56.2+/-4.7% lysis) showed significantly greater lysis than all other treatment groups. including ferrets treated with the same dose of rTPA alone (38.5+/-6.3%, P<.01), with twice the rTPA dose alone (45.0+/-6.5%. P<.05), or with a control MAb (35.2+/-4.6%, P<.01). The combination of rTPA treatment and (alpha 2AP inhibition caused no consumption of fibrinogen. Conclusions Inhibition of alpha 2AP significantly amplified the lysis of experimental pulmonary emboli by rTPA without increasing fibrinogen consumption. These results suggest that alpha 2AP may play an important role in thrombus resistance in patients with venous thromboembolism. C1 HARVARD UNIV,SCH PUBL HLTH,CARDIOVASC BIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-02348] NR 37 TC 18 Z9 19 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 APR 1 PY 1997 VL 95 IS 7 BP 1886 EP 1891 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA WR519 UT WOS:A1997WR51900023 PM 9107177 ER PT J AU Skopicki, HA Lyons, GE Schatteman, G Smith, RC Andres, V Schirm, S Isner, J Walsh, K AF Skopicki, HA Lyons, GE Schatteman, G Smith, RC Andres, V Schirm, S Isner, J Walsh, K TI Embryonic expression of the Gax homeodomain protein in cardiac, smooth, and skeletal muscle SO CIRCULATION RESEARCH LA English DT Article DE homeobox gene; Gax; cardiac muscle; smooth muscle; skeletal muscle ID HOMEOBOX GENE; MOUSE EMBRYOGENESIS; TRANSCRIPTION FACTORS; MOLECULAR-CLONING; PROGENITOR CELLS; NERVOUS-SYSTEM; NEURAL CREST; HEART; SPECIFICATION; GROWTH AB Gax is a homeobox-containing gene that has been detected in adult cardiovascular tissues and exhibits a growth arrest-specific pattern of expression in cultured vascular myocytes. To study the regulation of gar during development, we performed immunohistochemistry and in situ hybridization on mouse embryos. Gax was present in mesodermally and, as with other homeobox genes, neuroectodermally derived tissues. Early mesodermal protein expression was limited to the lateral plate and semitic mesoderm. Gax in the cardiac muscle lineage exhibited a biphasic pattern of expression. Expression was prominent in the heart tube of the earliest cardiomyocytes and remained prominent through the looping stage (day 12.5 post coitum [pc]) but fell below the threshold of detection in atria and ventricles by day 13.5 pc. At day 15.5 pc, Gax protein was again detectable but restricted to cells within the compact layer of the ventricular myocardium. Gax expression was also noted in smooth muscle cells as early as day 9.5 pc. In the skeletal muscle lineage, Gax protein was expressed at the onset of somitogenesis before the expression of the myogenic basic helix-loop-helix and MEF2/RSRF family proteins. Subsequently, it was noted at day 9.5 pc in premyogenic cells migrating into head, trunk, and limb buds. Gax was detected in myotomes, premuscle masses, and mature muscle groups. These data suggest an important developmental role for Gax in all muscle lineages. C1 ST ELIZABETHS MED CTR,DIV CARDIOVASC RES,BOSTON,MA 02135. TUFTS UNIV,SCH MED,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. UNIV WISCONSIN,SCH MED,DEPT ANAT,MADISON,WI 53706. BERLEX BIOSCI,DEPT CARDIOVASC RES,RICHMOND,CA. RI Andres, Vicente/I-6440-2014 OI Andres, Vicente/0000-0002-0125-7209 FU NHLBI NIH HHS [HL-02824, HL-50692]; NIAMS NIH HHS [AR-40197] NR 51 TC 29 Z9 32 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD APR PY 1997 VL 80 IS 4 BP 452 EP 462 PG 11 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA WQ093 UT WOS:A1997WQ09300003 PM 9118475 ER PT J AU Durante, W Kroll, MH Christodoulides, N Peyton, KJ Schafer, AI AF Durante, W Kroll, MH Christodoulides, N Peyton, KJ Schafer, AI TI Nitric oxide induces heme oxygenase-1 gene expression and carbon monoxide production in vascular smooth muscle cells SO CIRCULATION RESEARCH LA English DT Article DE nitric oxide; carbon monoxide; heme oxygenase ID CYCLIC GUANOSINE-MONOPHOSPHATE; L-ARGININE; RAT; SYNTHASE; INDUCTION; BILIRUBIN; ENZYME; LIVER; BLOOD; INTERLEUKIN-1-BETA AB Since recent studies demonstrate that vascular smooth muscle cells synthesize two distinct guanylate cyclase-stimulatory gases, NO and CO, we examined possible regulatory interactions between these two signaling molecules. Treatment of rat aortic smooth muscle cells with the NO donors, sodium nitroprusside, S-nitroso-N-acetyl-penicillamine, or 3-morpholinosydnonimine, increased heme oxygenase-1 (HO-1) mRNA and protein levels in a concentration- and time-dependent manner. Both actinomycin D and cycloheximide blocked NO-stimulated HO-1 mRNA and protein expression. Nuclear run-on experiments demonstrated that NO donors increased HO-1 gene transcription between 3- and 6-fold. In contrast, NO donors had no effect on the stability of HO-1 mRNA. Incubation of vascular smooth muscle cells with the membrane-permeable cGMP analogues, dibutyryl cGMP and 8-bromo-cGMP, failed to induce HO-1 gene expression. Treatment of vascular smooth muscle cells with NO donors also stimulated the production and release of CO, as demonstrated by the CO-dependent increase in intracellular cGMP levels in coincubated platelets. Finally, incubating vascular smooth muscle cells with interleukin-1 beta and tumor necrosis factor-alpha induced NO synthesis and also significantly increased the level of HO-1 protein. The cytokine-stimulated production of both NO and HO-1 protein in smooth muscle cells was blocked by the NO synthase inhibitor methyl-L-arginine. These results demonstrate that exogenously administered or endogenously released NO stimulates HO-1 gene expression and CO production in vascular smooth muscle cells. The ability of NO to induce HO-catalyzed CO release from vascular smooth muscle cells provides a novel mechanism by which NO might modulate soluble guanylate cyclase and, thereby, vascular smooth muscle cell and platelet function. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT PHARMACOL,HOUSTON,TX 77030. RP Durante, W (reprint author), HOUSTON VA MED CTR,BLDG 109,ROOM 116,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NHLBI NIH HHS [HL-36045] NR 49 TC 252 Z9 270 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD APR PY 1997 VL 80 IS 4 BP 557 EP 564 PG 8 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA WQ093 UT WOS:A1997WQ09300015 PM 9118487 ER PT J AU Oates, JC Ruiz, P Alexander, A Pippen, AMM Gilkeson, GS AF Oates, JC Ruiz, P Alexander, A Pippen, AMM Gilkeson, GS TI Effect of late modulation of nitric oxide production on murine lupus SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID ARTHRITIS-LIKE DISEASE; MONOMETHYL-L-ARGININE; SYNTHASE EXPRESSION; AUTOIMMUNE-DISEASE; IMMUNE-RESPONSE; MRL/1 MICE; GLOMERULONEPHRITIS; MANIFESTATIONS; ANTIBODIES; CELLS AB MRL/MpJ-Fas(lpr) (MRL-lpr) and New Zealand Black/White (NZB/W) mice develop spontaneous autoimmune disease characterized by autoantibody production and glomerulonephritis that progresses in parallel with increasing systemic nitric oxide (NO) production. A previously published study from our laboratory indicated that oral administration of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine (NMMA) before the onset of clinical disease significantly decreased renal and joint pathology in MRL-lpr mice, To characterize the effect of late modulation of NO production in murine SLE, we administered oral NMMA and/or restricted dietary arginine after disease onset in two murine models of SLE. When receiving combined NMMA and arginine restriction, MRL-Epr mice had reduced joint pathology scores and NZB/W mice had lower renal pathology scores than control mice. These results indicate that modulating NO production after the onset of disease diminishes disease severity in two models of SLE, although not as effectively as treating before disease onset. (C) 1997 Academic Press. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. UNIV MIAMI,MED CTR,MIAMI,FL 33152. DUKE UNIV,MED CTR,DURHAM,NC. RP Oates, JC (reprint author), RALPH H JOHNSON VAMC,MED RES SERV,CHARLESTON,SC 29425, USA. FU NIAMS NIH HHS [AR39162, K08 AR002193] NR 35 TC 46 Z9 48 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1997 VL 83 IS 1 BP 86 EP 92 DI 10.1006/clin.1997.4332 PG 7 WC Immunology; Pathology SC Immunology; Pathology GA WP273 UT WOS:A1997WP27300017 PM 9073540 ER PT J AU Lipsky, BA Baker, PD Landon, GC Fernau, R AF Lipsky, BA Baker, PD Landon, GC Fernau, R TI Antibiotic therapy for diabetic foot infections: Comparison of two parenteral-to-oral regimens SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID LOWER-EXTREMITY INFECTIONS; SKIN-STRUCTURE; SOFT-TISSUE; OFLOXACIN; DISEASE; CIPROFLOXACIN; MANAGEMENT AB This prospective, randomized, multicenter trial compared the efficacy of two antibiotic regimens for treatment of foot infections in diabetic adults. Patients with infections requiring hospitalization were randomized to receive either intravenous ofloxacin followed by oral ofloxacin or intravenous ampicillin/sulbactam followed by oral amoxicillin/clavulanate (the aminopenicillin regimen) for 14-28 days. Patients with osteomyelitis were eligible for the study if the infected bone was to be removed. Of 108 patients enrolled in the study, 88 who were evaluable had various skin and soft-tissue infections, and 24% had osteomyelitis. For the ofloxacin and aminopenicillin regimens, the mean duration of intravenous therapy was 7.8 and 7.1 days, respectively, the mean duration of oral therapy was 13.2 and 12.0 days, respectively, the rate of eradication of pathogens was 78% and 88%, respectively, and the overall rate of clinical cure or improvement was 85% and 83%, respectively. Thus, about 3 weeks of therapy with either regimen was well tolerated and effective in treating these diabetic foot infections. C1 UNIV WASHINGTON,SCH MED,DEPT MED,DIV GEN INTERNAL MED,SEATTLE,WA 98195. HOUSTON VET AFFAIRS MED CTR,SECT ORTHOPED SURG,HOUSTON,TX. RP Lipsky, BA (reprint author), VET AFFAIRS PUGET SOUND HLTH CARE SYST,ANTIBIOT RES CLIN,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. OI Lipsky, Benjamin A./0000-0001-9886-5114 NR 14 TC 69 Z9 71 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 APR PY 1997 VL 24 IS 4 BP 643 EP 648 DI 10.1093/clind/24.4.643 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA WT725 UT WOS:A1997WT72500015 PM 9145738 ER PT J AU Mulroy, WF Harris, WH AF Mulroy, WF Harris, WH TI Acetabular and femoral fixation 15 years after cemented total hip surgery SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID REPLACEMENT; COMPONENT AB Total hip arthroplasty in patients younger than 51 years of age remains controversial. The authors report results in 47 hips in 40 patients at an average followup of 15 years, Second generation femoral cementing techniques were used. Special attention was given to studying the differences between the outcome of acetabular versus femoral fixation. The patient group included 11 in whom custom components were used and 13 who had structural autografts for severe acetabular dysplasia. One femoral component and 10 acetabular components were revised for aseptic loosening, After 15 years, improved cementing techniques produced a marked reduction in the rate of femoral aseptic loosening. Loss of fixation of cemented acetabular components was common. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 30 TC 24 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD APR PY 1997 IS 337 BP 118 EP 128 PG 11 WC Orthopedics; Surgery SC Orthopedics; Surgery GA WT707 UT WOS:A1997WT70700014 PM 9137183 ER PT J AU Lee, MS Silver, PA AF Lee, MS Silver, PA TI RNA movement between the nucleus and the cytoplasm SO CURRENT OPINION IN GENETICS & DEVELOPMENT LA English DT Article ID REV ACTIVATION DOMAIN; MESSENGER-RNA; SACCHAROMYCES-CEREVISIAE; BINDING-PROTEINS; HIV-1 REV; HNRNP A1; IN-VITRO; NUCLEOCYTOPLASMIC TRANSPORT; REGULATORY PROTEINS; EXPORT PATHWAY AB The past year has seen significant advances in our understanding of the mechanism of RNA movement between the nucleus and the cytoplasm. The emerging view is that proteins bind to and escort RNAs to their proper subcellular location. The discovery of peptide signals that target nuclear export and the identification of novel protein mediators of RNA export are examples of significant recent discoveries. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOL BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOL PHARMACOL,BOSTON,MA 02115. NR 79 TC 34 Z9 34 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-437X J9 CURR OPIN GENET DEV JI Curr. Opin. Genet. Dev. PD APR PY 1997 VL 7 IS 2 BP 212 EP 219 DI 10.1016/S0959-437X(97)80131-1 PG 8 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA WW570 UT WOS:A1997WW57000010 PM 9115427 ER PT J AU Lee, JT Jaenisch, R AF Lee, JT Jaenisch, R TI The (epi)genetic control of mammalian X-chromosome inactivation SO CURRENT OPINION IN GENETICS & DEVELOPMENT LA English DT Article ID IMPRINTED XIST EXPRESSION; DOSAGE COMPENSATION; GENE; METHYLATION; MOUSE; DROSOPHILA; REPEATS; NUCLEUS; REGION; CELLS AB In mammals, the X chromosome is uniquely capable of complete inactivation. Research in the past two years has validated the long-held hypothesis that the 'X-inactivation center' (Xic) controls events of X inactivation and that its resident gene Xist is not only required but is at least partially responsible for the cis-restriction of X inactivation. Progress has also been made in identifying genes within the Xic. Although Xist remains the only known required element, evidence now suggests that a separate element for X counting must exist and that the Xic may be entirely contained within a 450 kb sequence. This small region may be sufficient for both initiation and establishment of X inactivation. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP Lee, JT (reprint author), MIT,DEPT BIOL,WHITEHEAD INST BIOMED RES,9 CAMBRIDGE CTR,CAMBRIDGE,MA 02142, USA. NR 42 TC 59 Z9 60 U1 0 U2 3 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-437X J9 CURR OPIN GENET DEV JI Curr. Opin. Genet. Dev. PD APR PY 1997 VL 7 IS 2 BP 274 EP 280 DI 10.1016/S0959-437X(97)80138-4 PG 7 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA WW570 UT WOS:A1997WW57000017 PM 9115428 ER PT J AU Georgopoulos, K AF Georgopoulos, K TI Transcription factors required for lymphoid lineage commitment SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID T-CELL DEVELOPMENT; DENDRITIC CELLS; MOUSE THYMUS; IKAROS GENE; EXPRESSION; FAMILY; PU.1; E2A AB Intimate interactions between multipotential hemopoietic stem cells and their microenvironment work towards redefining the identity and the differentiative fate of these primitive cells. Molecular cues delivered by the microenvironment frequently act in an instructive fashion by initiating intracellular signaling pathways that ultimately target a select group of transcription factors. These transcriptional regulators in turn trigger a cascade of genetic changes that ultimately determine the course of the cells during differentiation. Gene inactivation studies on the PU.1, Ikaros and GATA-3 genes have revealed that their encoded factors are essential for the earliest commitment step into the B and T lymphoid lineages. RP Georgopoulos, K (reprint author), HARVARD UNIV,SCH MED,CUTANEOUS BIOL RES CTR,MASSACHUSETTS GEN HOSP,CHARLESTOWN,MA 02129, USA. NR 40 TC 59 Z9 60 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1997 VL 9 IS 2 BP 222 EP 227 DI 10.1016/S0952-7915(97)80139-2 PG 6 WC Immunology SC Immunology GA WV040 UT WOS:A1997WV04000009 PM 9099800 ER PT J AU Abdelilah, S Driever, W AF Abdelilah, S Driever, W TI Pattern formation in janus-mutant zebrafish embryos SO DEVELOPMENTAL BIOLOGY LA English DT Article ID BONE MORPHOGENETIC PROTEIN-4; XENOPUS-LAEVIS EMBRYOS; VENTRAL MESODERM; CELL MOVEMENTS; MARGINAL ZONE; FATE MAP; INDUCTION; BMP-4; GENE; EXPRESSION AB Mechanisms that underlie the formation of the vertebrate body appear to be highly conserved between amphibia and teleosts. For teleosts, however, mesoderm induction and the establishment of dorsoventral polarity are poorly understood. In this study, we present an analysis of early pattern formation in the zebrafish maternal-effect mutation janus. This mutation frequently results in a separation of the cleavage stage blastoderm into two halves that undergo separate development until fusion occurs at the end of gastrulation. Here, we employ janus-mutant embryos to analyze the mechanisms of mesoderm formation and ventral specification in a teleost. Analysis of the expression of the panmesodermal marker no tail in janus-mutant embryos indicates that mesoderm induction depends on a marginal position. In an analysis of ventral specification, we show that the early expression of the ventral marker GATA-2 is confined to the area on both blastodermal halves opposite the dorsal shield region. Since, in janus-mutant embryos, the dorsal position is random with respect to the division plane bisecting the two blastodermal halves, a variety of dorsoventral asymmetries arise within individual embryos. In one constellation, the dorsal position is localized to the plane of bisection and two ventral positions develop at opposite ends of the blastodermal halves. Hence, ventral fates can be specified at any position around the blastodermal margins and are excluded from the dorsal position. The diblastodermic system of the janus-mutant embryo allows for the study of the interactions of dorsal and ventral determinants in varying spatial arrangements. We have studied pattern formation in dorsal half-blastoderms that contain the entire shield region but only a reduced ventrolateral marginal zone. As assessed by the presence of the most ventral cell type, blood, ventral specification within a dorsal half-blastoderm is not suppressed. (C) 1997 Academic Press. C1 MASSACHUSETTS GEN HOSP,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. FU NICHD NIH HHS [R01-HD29761] NR 64 TC 6 Z9 7 U1 0 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD APR 1 PY 1997 VL 184 IS 1 BP 70 EP 84 DI 10.1006/dbio.1997.8517 PG 15 WC Developmental Biology SC Developmental Biology GA WV156 UT WOS:A1997WV15600008 PM 9142985 ER PT J AU Bosserhoff, AK Kondo, S Moser, M Dietz, UH Copeland, NG Gilbert, DJ Jenkins, NA Buettner, R Sandell, LJ AF Bosserhoff, AK Kondo, S Moser, M Dietz, UH Copeland, NG Gilbert, DJ Jenkins, NA Buettner, R Sandell, LJ TI Mouse CD-RAP/MIA gene: Structure, chromosomal localization, and expression in cartilage and chondrosarcoma SO DEVELOPMENTAL DYNAMICS LA English DT Article DE MIA; melanoma; CD-RAP; chondrogenesis; mouse gene ID MESSENGER-RNA; DIFFERENTIAL EXPRESSION; RAT CHONDROSARCOMA; COLLAGEN GENE; PROCOLLAGEN; PROTEIN; IDENTIFICATION; ORGANIZATION; PROPEPTIDE; SEQUENCE AB A cDNA encoding a novel protein has been previously isolated from two independent sources: melanoma cell cultures and chondrocytes. The protein from human melanoma cell lines and tumors is called melanoma inhibitory activity (MIA) (Blesch et al. [1994] Cancer Res. 54:5695-5701) and the protein from primary bovine chondrocytes and cartilaginous tissues is called cartilage-derived retinoic acid-sensitive protein (CD-RAP) (Dietz and Sandell [1996] J. Biol. Chem. 271:3311-3316). In order to investigate the gene regulation and function of CD-RAP/MIA, the mouse gene locus was isolated and analyzed, Developmental expression was determined by in situ hybridization to mouse embryos. Expression was limited to cartilaginous tissues and was initiated with the advent of chondrogenesis, remaining abundant throughout development. The mouse gene was isolated and sequenced from a 129Sv library and sequenced directly from an additional strain, B6C3Fe. The mouse CD-RAP/MIA gene is 1.5 kbp and consists of four exons. The promoter sequence of the gene contains many potential regulatory domains including 8 basic helix-loop-helix protein-binding domains and an AT-rich domain, both motifs shown to be present in the cartilage-specific enhancer of the type II procollagen gene. Other potential cis-acting motifs include binding sites for GATA-1, NF-IL6, PEA3, w-elements, NF kappa B, Zeste and Spl. The gene, called cdrap, was localized to the end of an arm of chromosome 7 at the same site as the transforming growth factor beta 1 (Tgf-beta 1) and the glucose phosphate isomerase 1 (Gpi1) genes. Potential mouse mutants that mapped to the same region of chromosome 7 mere identified. Two of the potential mutants with skeletal phenotypes were sequenced, pudgy (pu) and extra toes with spotting (Xs(J)); however, no mutations were found in the coding sequence. To determine whether CD-RAP/MIA is associated with tumors of cartilage, mRNAs from a variety of rodent tissues and cell lines were screened, Expression was detected in a rodent tumor, the Swarm rat chondrosarcoma and a chondrosarcoma cell line derived from it, but not in other tissues or tumors of non-cartilage origin. Immunolocalization revealed CD-RAP/MIA protein localized in cartilage only, These results show that the normal expression of CD-RAP/MIA is limited to cartilage; however, pathologically, it is expressed both in melanoma and chondrosarcoma. The restricted expression of CD-RAP/MIA may provide an opportunity to monitor cartilage metabolic activity as well as the tumor activity of melanoma and chondrosarcoma. (C) 1997 Wiley-Liss, Inc. C1 UNIV WASHINGTON,DEPT ORTHOPED ORT 112,VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. UNIV WASHINGTON,DEPT BIOCHEM,VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. UNIV REGENSBURG,DEPT PATHOL,D-93053 REGENSBURG,GERMANY. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NIAMS NIH HHS [R01AR36994] NR 31 TC 95 Z9 105 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD APR PY 1997 VL 208 IS 4 BP 516 EP 525 DI 10.1002/(SICI)1097-0177(199704)208:4<516::AID-AJA7>3.0.CO;2-L PG 10 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA WQ842 UT WOS:A1997WQ84200007 PM 9097023 ER PT J AU Ho, M Marger, M Beart, J Yip, I Shekelle, P AF Ho, M Marger, M Beart, J Yip, I Shekelle, P TI Is the quality of diabetes care better in a diabetes clinic or in a general medicine clinic? SO DIABETES CARE LA English DT Article; Proceedings Paper CT 18th Annual Meeting of the National-Society-of-General-Internal-Medicine CY MAY 04-06, 1995 CL SAN DIEGO, CA SP Natl Soc Gen Internal Med ID MANAGED CARE; MELLITUS; PROTEINURIA; KIDNEY AB OBJECTIVE - To compare the quality of ambulatory diabetes care delivered by physicians in the diabetes clinic versus the general medicine clinic of a university-affiliated Veterans Administration medical center. RESEARCH DESIGN AND METHODS - This is a retrospective study that involved the review of medical records against predetermined process-of-care criteria. A total of 112 patients with diabetes were randomly selected, of whom 56 were cared for in the general medicine clinic and 56 in the diabetes clinic. The following main outcome measures were examined: 1) the compliance with individual criteria; and 2) the proportion of patient visits in each clinic receiving minimally acceptable quality, defined as a blood pressure measurement, a record of type of hypoglycemic medication, a glycated hemoglobin measurement within the past year, a urinalysis within the past year, an ophthalmologist or optometrist eye examination within the past year or scheduled in the next six months, a record of change in therapeutic management, and a scheduled return visit. RESULTS - The diabetes clinic performed significantly better than the general medicine clinic on the following criteria: a record of a patient's self-monitoring of blood glucose levels; a foot examination; a comprehensive eye examination; a glycated hemoglobin measurement; and a referral for diabetic education. The proportion of patient visits meeting the minimally acceptable levels of quality was better in the diabetes clinic than the general medicine clinic (73 vs. 52%, P = 0.02). CONCLUSIONS - Patients cared for by physicians in the diabetes clinic receive better quality of diabetes care than do patients cared for by physicians in the general medical clinic. If patient care is to be shifted from specialists to generalists, additional attention needs to be paid to ensure that generalists have the knowledge and system resources necessary to deliver an acceptable quality of diabetes care. C1 W LOS ANGELES VET AFFAIRS MED CTR, ENDOCRINOL SECT, MED SERV, LOS ANGELES, CA 90073 USA. VET ADM HLTH SERV, RES & DEV FIELD PROGRAM, CTR STUDY HEALTHCARE PROVIDER BEHAV, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. RP Ho, M (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DIV GEN INTERNAL MED, 111G, GEN INTERNAL MED SECT, MED SERV, LOS ANGELES, CA 90073 USA. NR 26 TC 106 Z9 106 U1 1 U2 4 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 EI 1935-5548 J9 DIABETES CARE JI Diabetes Care PD APR PY 1997 VL 20 IS 4 BP 472 EP 475 DI 10.2337/diacare.20.4.472 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP645 UT WOS:A1997WP64500003 PM 9096962 ER PT J AU Simonson, DC Kourides, IA Feinglos, M Shamoon, H Fischette, CT Aronoff, S Blonde, L Cefalu, W Clement, S Greenberg, C Levin, S Lucas, CP Macy, C Manning, J Marbury, TC McAdams, MJ Mezitis, NHE Miller, S Owens, D Sandler, J Schwartz, SL Shamoon, H Sosenko, J AF Simonson, DC Kourides, IA Feinglos, M Shamoon, H Fischette, CT Aronoff, S Blonde, L Cefalu, W Clement, S Greenberg, C Levin, S Lucas, CP Macy, C Manning, J Marbury, TC McAdams, MJ Mezitis, NHE Miller, S Owens, D Sandler, J Schwartz, SL Shamoon, H Sosenko, J TI Efficacy, safety, and dose-response characteristics of glipizide gastrointestinal therapeutic system on glycemic control and insulin secretion in NIDDM - Results of two multicenter, randomized, placebo-controlled clinical trials SO DIABETES CARE LA English DT Article; Proceedings Paper CT American-Diabetes-Association Annual Meeting and Scientific Sessions CY JUN 11-14, 1994 CL NEW ORLEANS, LA SP Amer Diabet Assoc ID DEPENDENT DIABETES-MELLITUS; ORAL HYPOGLYCEMIC AGENTS; HEPATIC GLUCOSE-PRODUCTION; SULFONYLUREA THERAPY; GLYBURIDE THERAPY; TYPE-2 DIABETICS; PHARMACOKINETICS; PATHOGENESIS; PHARMACOLOGY; METABOLISM AB OBJECTIVE - To investigate the efficacy, safety, and dose-response characteristics of an extended-release preparation of glipizide using the gastrointestinal therapeutic system (GITS) on plasma glucose, glycosylated hemoglobin (HbA(1c)), and insulin secretion to a liquid-mixed meal in NIDDM patients. RESEARCH DESIGN AND METHODS - Two prospective, randomized, double-blind, placebo-controlled, multicenter clinical trials were performed in 22 sites and 347 patients with NIDDM (aged 59 +/- 0.6 years; BMI, 29 +/- 0.3 kg/m(2); known diabetes duration, 8 +/- 0.4 years) were studied. Each clinical trial had a duration of 16 weeks with a 1-week washout, 3-week single-blind placebo phase, 4-week titration to a fixed dose, and 8-week maintenance phase at the assigned dose. In the first trial, once-daily doses of 5, 20, 40, or 60 mg glipizide GITS were compared with placebo in 143 patients. In the second trial, doses of 5, 10, 15, or 20 mg of glipizide GITS were compared with placebo in 204 patients. HbA(1c), fasting plasma glucose (FPG), insulin, C-peptide, and glipizide levels were determined at regular intervals throughout the study Postprandial plasma glucose (PPG), insulin, and C-peptide also were determined at 1 and 2 h after a mixed meal (Sustacal). RESULTS - All doses of glipizide GITS in both trials produced significant reductions from placebo in FPG (range -57 to - 74 mg/dl) and HbA(1c) (range - 1.50 to -1.82%). Pharmacodynamic analysis indicated a significant relationship between plasma glipizide concentration and reduction in FPG and HbA(1c) over a dose range of 5-60 mg, with maximal efficacy achieved at a dose of 20 mg for FPG and at 5 mg for HbA(1c). PPG levels were significantly lower, and both postprandial insulin and C-peptide levels significantly higher in patients treated with glipizide GITS compared with placebo. The percent reduction in FPG was comparable across patients with diverse demographic and clinical characteristics, including those with entry FPG greater than or equal to 250 mg/dl, resulting in greater absolute decreases in FPG and HbA(1c) in patients with the most severe hyperglycemia. Despite the forced titration to a randomly assigned dose, only ii patients in both studies discontinued therapy because of hypoglycemia. Glipizide GITS did not alter lipids levels or produce weight gain. CONCLUSIONS - The once-daily glipizide GITS 1) lowered HbA(1c), FPG, and PPG over a dose range of 5-60 mg, 2) was maximally effective at 5 mg (using HbA(1c)) or 20 mg (using FPG) based on pharmacokinetic and pharmacodynamic relationships, 3) maintained its effectiveness in poorly controlled patients (those with entry FPG greater than or equal to 250 mg/dl), 4) was safe and well tolerated in a wide variety of patients with NIDDM, and 5) did not produce weight gain or adversely affect lipids. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. PFIZER INC,NEW YORK,NY. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10467. ENDOCRINE ASSOCIATES DALLAS,DALLAS,TX. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT INTERNAL MED,WINSTON SALEM,NC 27103. WALTER REED ARMY MED CTR,ENDOCRINE METABOL SERV,WASHINGTON,DC 20307. DUKE UNIV,DURHAM,NC 27706. NW RES ASSOCIATES INC,PORTLAND,DORSET,ENGLAND. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. BEAUMONT HOSP,BIRMINGHAM,AL. LANSDALE MED GRP,LANSDALE,PA. ORLANDO CLIN RES CTR,ORLANDO,FL. ST LUKES ROOSEVELT HOSP,DIV ENDOCRINOL DIABET & METAB,NEW YORK,NY. CLIN RES CTR,SAN ANTONIO,TX. CTR STRESS STUDIES,SAN DIEGO,CA. DIABET & GLANDULAR DIS CLIN,SAN ANTONIO,TX. MONTEFIORE MED CTR,BRONX,NY 10467. JACKSON MEM HOSP,MIAMI,FL 33136. NW RES ASSOCIATES INC,PORTLAND,OR. OI Shamoon, Harry/0000-0002-5014-5211 NR 62 TC 93 Z9 98 U1 0 U2 6 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1997 VL 20 IS 4 BP 597 EP 606 DI 10.2337/diacare.20.4.597 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP645 UT WOS:A1997WP64500027 PM 9096986 ER PT J AU Scavini, M Galli, L Reich, S Eaton, RP Charles, MA Dunn, FL Micossi, P Torri, M Petrella, G Galimberti, G Cristallo, M Vai, S Pozza, G Olsen, C Turner, D Nolleman, C LavinTompkins, J Selam, JL Haardt, MJ Dorange, C Jeandidier, N Ortega, F Boivin, S Nathan, D Larkin, M McKitrick, C Schwarz, S Fisher, J Kipnes, S Walz, B Vague, P Reeves, ML Goudner, M Thomson, GP Jaffiol, C Renard, E Lauton, D JacquesApostol, D Bringer, J Tauber, JP HanaireBroutin, H ReesJones, R Adolff, S Bays, HA Pfeifer, M Clarke, D Irsigler, K Feinboch, C Hutter, R Mendel, H Diglas, J AF Scavini, M Galli, L Reich, S Eaton, RP Charles, MA Dunn, FL Micossi, P Torri, M Petrella, G Galimberti, G Cristallo, M Vai, S Pozza, G Olsen, C Turner, D Nolleman, C LavinTompkins, J Selam, JL Haardt, MJ Dorange, C Jeandidier, N Ortega, F Boivin, S Nathan, D Larkin, M McKitrick, C Schwarz, S Fisher, J Kipnes, S Walz, B Vague, P Reeves, ML Goudner, M Thomson, GP Jaffiol, C Renard, E Lauton, D JacquesApostol, D Bringer, J Tauber, JP HanaireBroutin, H ReesJones, R Adolff, S Bays, HA Pfeifer, M Clarke, D Irsigler, K Feinboch, C Hutter, R Mendel, H Diglas, J TI Catheter survival during long-term insulin therapy with an implanted programmable pump SO DIABETES CARE LA English DT Article; Proceedings Paper CT AIDSPIT Meeting CY JAN, 1994 CL IGLS, AUSTRIA SP AIDSPIT ID DELIVERY; MULTICENTER; SYSTEMS; TRIAL AB OBJECTIVE - To survey catheter complications and to analyze catheter survival during long-term intraperitoneal and intravenous insulin therapy with an implanted programmable pump with a sideport. RESEARCH DESIGN AND METHODS - Catheter occlusions were documented by measuring dynamic catheter resistance. Catheter migrations or breaks were demonstrated by X ray. When flushing the catheter with buffer solution through the sideport failed to clear the occlusion, catheters were replaced or laparoscopy was performed for the excision of fibrous tissue growth. Broken or migrated catheters were replaced. RESULTS - Occlusions were the most common catheter complications, and the majority of them (79% intraperitoneal and 84% intravenous) were cleared by flushing the catheter. Survival at 3 years was significantly higher for intraperitoneal catheters compared with intravenous catheters (60% intraperitoneal and 22% intravenous). CONCLUSIONS - Nonsurgical management of catheter occlusions contributed to extend catheter lifetime. Intraperitoneal catheters have a lower morbidity and a higher survival than intravenous catheters. C1 STRATO INFUSAID,NORWOOD,MA. UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. UNIV CALIF IRVINE,DIABET RES PROGRAM,IRVINE,CA 92717. DUKE UNIV,MED CTR,DURHAM,NC. HOP HOTEL DIEU,PARIS,FRANCE. UNIV STRASBOURG,STRASBOURG,FRANCE. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SAN ANTONIO REG MED CTR,SAN ANTONIO,TX. HOP ENFANTS LA TIMONE,MARSEILLE,FRANCE. E RIDGE HOSP,CHATTANOOGA,TN. HOP LAPEYRONIE,MONTPELLIER,FRANCE. HOP RANGUEIL,TOULOUSE,FRANCE. AURORA REG MED CTR,AURORA,CO. HUMANA LEXINGTON,LEXINGTON,KY. DIABET HLTH CTR,SALT LAKE CITY,UT. VIENNA LAINZ HOSP,VIENNA,AUSTRIA. RP Scavini, M (reprint author), SAN RAFFAELE SCI INST,VIA OLGETTINA 60,I-20132 MILAN,ITALY. NR 14 TC 16 Z9 16 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1997 VL 20 IS 4 BP 610 EP 613 DI 10.2337/diacare.20.4.610 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP645 UT WOS:A1997WP64500029 PM 9096988 ER PT J AU Aronson, D AF Aronson, D TI Pharmacologic modulation of autonomic tone: Implications for the diabetic patient SO DIABETOLOGIA LA English DT Article ID HEART-RATE-VARIABILITY; ACUTE MYOCARDIAL-INFARCTION; SUDDEN CARDIAC DEATH; FREQUENCY-DOMAIN MEASURES; CORONARY-ARTERY DISEASE; POWER SPECTRAL-ANALYSIS; BETA-BLOCKERS; PANCREAS TRANSPLANTATION; CARDIORESPIRATORY ARREST; CIRCADIAN PATTERN RP Aronson, D (reprint author), JOSLIN DIABET CTR,DIV RES,METAB SECT,1 JOSLIN PL,BOSTON,MA 02215, USA. RI Aronson, Doron/F-3390-2010 NR 62 TC 16 Z9 16 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD APR PY 1997 VL 40 IS 4 BP 476 EP 481 DI 10.1007/s001250050704 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WR840 UT WOS:A1997WR84000016 PM 9112027 ER PT J AU Garrison, MW Malone, CL Eiland, J Anderson, DE AF Garrison, MW Malone, CL Eiland, J Anderson, DE TI Influence of pH on the antimicrobial activity of clarithromycin and 14-hydroxyclarithromycin against Haemophilus influenzae using an in vitro pharmacodynamic model SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article; Proceedings Paper CT 7th European Congress of Clinical Microbiology and Infectious Diseases CY MAR 26-30, 1995 CL VIENNA, AUSTRIA ID OTITIS-MEDIA; INVITRO; METABOLITE; PNEUMONIA; MACROLIDE; CHILDREN AB Clarithromycin activity can be influenced by the pH of the surrounding environment. Evidence supports a reduced pH of middle ear fluid (MEF) and lung tissues in patients with otitis media and pneumonia, respectively. To evaluate the influence of pH on clarithromycin activity, an in vitro pharmacodynamic chamber model (PDCM) was used to generate bacterial time-kill curves for clarithromycin and a 2:1 ratio of clarithromycin and 14-hydroxyclarithromycin (HC) against Haemophilus influenzae at three different pH values: 7.2, 6.8, 6.4. Concentrations observed in MEF and lung tissues were simulated for clarithromycin alone and clarithromycin plus HC. Differences in activity at each pH were identified by com paring initial kill curve slopes and total log reduction. Experiments with amoxicillin-clavulanate were conducted as a reference. In simulated MEF regimens at pH 7.2, activity of clarithromycin alone improved by adding HC (additional 2 log(10) reduction at 8 h); however, at pH values of 6.8 and 6.4, kill curves resembled growth controls. In simulated lung regimens, differences between clarithromycin alone and clarithromycin plus HC were insignificant; both produced a 2 log(10) reduction at pH 7.2, and activity dramatically dropped to <0.4 log(10) as pH declined. In contrast, amoxicillin-clavulanate consistently produced a 3 log(10) reduction over each pH value with more rapid initial kill relative to all clarithromycin regimens. These findings suggest the activity of clarithromycin against H. influenzae may be significantly compromised in respiratory tract infections involving a reduced pH. Trials with emphasis on clinical outcomes analysis will assist further in determining the significance of these experimental findings. (C) 1997 Elsevier Science Inc. C1 DEACONESS MED CTR,SPOKANE,WA. SACRED HEART MED CTR,DEPT MICROBIOL,SPOKANE,WA. RP Garrison, MW (reprint author), WASHINGTON STATE UNIV,COLL PHARM,601 W 1ST AVE,SPOKANE,WA 99204, USA. NR 25 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD APR PY 1997 VL 27 IS 4 BP 139 EP 145 DI 10.1016/S0732-8893(97)00026-6 PG 7 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA WY200 UT WOS:A1997WY20000007 PM 9154410 ER PT J AU Silverman, SL AF Silverman, SL TI Nasal calcitonin SO ENDOCRINE LA English DT Article DE calcitonin; osteoporosis therapy ID SALMON-CALCITONIN; POSTMENOPAUSAL OSTEOPOROSIS; ESTABLISHED OSTEOPOROSIS; HIP FRACTURE; BONE MASS; PREVENTION; ANTIBODIES; THERAPY; SPRAY AB Nasal calcitonin is a newly approved treatment for established osteoporosis that increases lumbar spine bone mass, is safe, and well tolerated. Fracture efficacy data is not yet available, although preliminary results are promising. The dose for established osteoporosis is 200 IU. The dose for prevention of postmenopausal osteoporosis has not been established. Nasal calcitonin may be analgesic to bone and may be of benefit in glucocorticoid-induced vertebral osteoporosis. Nasal spray calcitonin may be of benefit to the symptomatic patient with acute vertebral fracture, the complex patient, or the patient with established osteoporosis who is intolerant of bisphosphonates or estrogen. C1 OSTEOPOROSIS MED CTR,LOS ANGELES,CA. RP Silverman, SL (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DEPT RHEUMATOL,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 30 TC 5 Z9 5 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0969-711X J9 ENDOCRINE JI Endocrine PD APR PY 1997 VL 6 IS 2 BP 199 EP 202 DI 10.1007/BF02738965 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XB143 UT WOS:A1997XB14300014 PM 9225136 ER PT J AU Hu, SB Johnson, L Roche, PC Keutmann, HT AF Hu, SB Johnson, L Roche, PC Keutmann, HT TI A functional determinant in human luteinizing hormone and chorionic gonadotropin: Differential effect of mutations about beta-GLN-S4 SO ENDOCRINOLOGY LA English DT Article ID HUMAN CHORIOGONADOTROPIN-BETA; LEYDIG TUMOR-CELLS; FOLLICLE-STIMULATING-HORMONE; GLYCOPROTEIN HORMONES; PRECOCIOUS PUBERTY; SUBUNIT; RECEPTOR; MUTAGENESIS; LUTROPIN; HYPOGONADISM AB There is evidence that the conserved glutamine at residue 54 in the beta-subunit of human LH and and CG (hCG) is important for biological activity. Mutation to Arg in LH has been reported to impair receptor binding, leading to a documented case of hypogonadism, whereas in hCG the mutation has been shown to result in defective subunit association. Functional distinctions between LH and hCG have been described, but the significance of peptide-chain differences between the two has not been investigated systematically. We therefore compared the role of Gln-54 and its neighboring residues in both hormones, through replacement by amino acids with contrasting properties using site-directed mutagenesis. The mutant subunits were coexpressed with alpha-subunit in mammalian (Chinese hamster ovary) cells and the secreted hormones assayed for heterodimer formation, receptor binding, and steroidogenesis in murine Leydig cell tumor (MA-10) cells. Basic (Arg, Lys) substitution for Gln-54 in either hormone markedly impaired subunit association (<20% of wild-type) and the heterodimers that were formed were inactive (<5% or wild-type) in both assays. Arg-substituted hCG was also inactive in an adenylate cyclase assay using HEK-293 cells expressing rat LH/hCG receptor. After acidic (Glu) or neutral (Ala) substitution, heterodimer formation was less impaired (50-60% of wild-type), but effects on receptor interaction differed between the two hormones. The LH mutants still lacked binding activity, whereas the hCG products were fully active. The importance of residue 54 for receptor interaction appears to be sharply localized because mutation at adjacent positions (Pro-53 and Val-55) did not impair the activity of either hormone. Diminished heterodimer formation by Ile-53 mutation in LH (but not hCG), together with the similar effects of basic mutations at 54, imply long-distance effects as these residues are remote from alpha in the crystal structure. Our findings indicate that position 54 in LH and hCG is a determinant for both subunit association and receptor interaction. The differing responses between LH and hCG to certain mutations suggest that structural characteristics of the peptide chains may confer functional differences despite their close sequence homology. C1 MASSACHUSETTS GEN HOSP, ENDOCRINE UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, REPROD ENDOCRINE SCI CTR, DEPT MED, BOSTON, MA 02114 USA. MAYO CLIN & MAYO GRAD SCH MED, DEPT LAB MED & PATHOL, ROCHESTER, MN 55905 USA. NR 46 TC 2 Z9 2 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 APR PY 1997 VL 138 IS 4 BP 1627 EP 1633 DI 10.1210/en.138.4.1627 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP335 UT WOS:A1997WP33500036 PM 9075724 ER PT J AU Scaglia, L Cahill, CJ Finegood, DT BonnerWeir, S AF Scaglia, L Cahill, CJ Finegood, DT BonnerWeir, S TI Apoptosis participates in the remodeling of the endocrine pancreas in the neonatal rat SO ENDOCRINOLOGY LA English DT Article ID BETA-CELL MASS; GROWTH-FACTOR; INSULIN; POPULATIONS; EXPRESSION; FETAL; PROTEINS; GLUCAGON; DYNAMICS; ISLETS AB In rodents, shortly after birth a lack of increase in pancreatic weight and in islet mass have been reported during a time of overall body weight increase. To understand this regulation of the neonatal growth of the beta cell mass, we studied Sprague Dawley rats at 2,9, 13, 17, 20, 24, and 31 days of age for beta cell replication, beta cell mass, and cell size and for the presence of beta cell apoptosis. beta cell mass was stable from 2-20 days (range: 0.91 +/- 0.2 to 1.33 +/- 0.23 mg) and increased thereafter. beta cell replication progressively decreased. Condensed apoptotic nuclei were identified and counted on paraffin sections using the fluorescent dye propidium iodide. Apoptotic beta cell nuclei were found at a basal rate (1.54 +/-: 0.22%) at 2, 9, and again after 20 days of age. However, at 13 and 17 days, the incidence of apoptosis was significantly increased (3.64 +/- 0.45%). The decreased replication and the increased incidence of apoptosis in the beta cells strongly suggest a wave of neogenesis of beta cells to maintain the constant beta cell mass. These data show that the endocrine pancreas undergoes significant modification during neonatal life and that apoptosis is an important mechanism in this remodeling of the beta cell mass. Whether a selective deletion of some population of beta cells occurs is unclear, but a dysregulation of this remodeling process could have important affects on the pancreatic beta cell mass. C1 JOSLIN DIABET CTR,EP JOSLIN RES LABS,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. UNIV ALBERTA,DEPT MED,EDMONTON,AB T6G 2H7,CANADA. UNIV ALBERTA,DEPT PHYSIOL,EDMONTON,AB T6G 2H7,CANADA. FU NIDDK NIH HHS [DK-35449, DK-36836] NR 27 TC 287 Z9 294 U1 0 U2 5 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1997 VL 138 IS 4 BP 1736 EP 1741 DI 10.1210/en.138.4.1736 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP335 UT WOS:A1997WP33500050 PM 9075738 ER PT J AU Joun, H Lanske, B Karperien, M Qian, F Defize, L AbouSamra, A AF Joun, H Lanske, B Karperien, M Qian, F Defize, L AbouSamra, A TI Tissue-specific transcription start sites and alternative splicing of the parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor gene: A new PTH/PTHrP receptor splice variant that lacks the signal peptide SO ENDOCRINOLOGY LA English DT Article ID FUNCTIONAL EXPRESSION; CLONING; CELLS; RAT; MOUSE; PROTEINS; ACIDS AB The PTH/PTHrP receptor gene is expressed in bone and kidney as well as in many other tissues. Using primer extension followed by rapid cloning of amplified complementary DNA ends, we have isolated new PTH/PTHrP receptor complementary DNAs with different splicing patterns and have characterized a new upstream transcription start site. Three 5' nontranslated exons, U3, U2 and U1, located 4.8, 2.5, and 1.2 kb upstream of the exon that encodes the putative signal peptide of the classical receptor (exon S), have been characterized. Four types of splicing patterns were recognized. Type I splicing pattern is transcribed from exon U1 and is spliced to exons S and E1; this pattern was found in most tissues tested. Types II, III, and IV splicing patterns are transcribed from exon U3 and have a restricted tissue distribution. Type II splice pattern, containing exons U3, U2, and S and type III splicing pattern, containing exon U3, U2, and El (skipping exon S), was found only in kidney. Type IV splice pattern, containing exon U3 and S was found both in kidney and ovary. Because the type III splice variant skips exon S, translation of this splice Variant initiates at a different AUG codon. The type III splice variant was weakly expressed on the cell surface of COS-7 cells, as assessed by double antibody binding assay, and no detectable ligand binding was observed on intact cells. The type III splice variant, however, increased cAMP accumulation in COS-7 cells when challenged with PTH(1-34), PTH(1-84) and hPTHrP(1-36) with EC50s that are similar to those observed in COS-7 cells expressing the type I variant but with a maximum stimulation that was lower than that observed in COS-7 cells expressing the type I variant. These data indicate low levels of cell surface expression of the type III splice variant. Treatment of COS-7 cells with tunicamycin decreased the size of the type I splice variant from a broad band of 85 kDa to a compact band of about 60 kDa. The type III splice variant did not change in size in COS-7 cells treated with tunicamycin, indicating that the type III splice variant did not undergo any glycosylation step. In conclusion, the PTH/PTHrP receptor gene uses alternate promoters in a tissue-specific manner that results in several tissue-specific alternatively spliced transcripts. One of these transcripts, the type III splice variant, is expressed in kidney and lacks the signal peptide. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NETHERLANDS INST DEV BIOL,UTRECHT,NETHERLANDS. OI Abou-Samra, Abdul/0000-0001-8735-1142 FU NIAMS NIH HHS [AR-45485] NR 24 TC 62 Z9 62 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1997 VL 138 IS 4 BP 1742 EP 1749 DI 10.1210/en.138.4.1742 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WP335 UT WOS:A1997WP33500051 PM 9075739 ER PT J AU Zietman, AL Shipley, WU AF Zietman, AL Shipley, WU TI Progress in the management of T3-4 adenocarcinoma of the prostate SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID RANDOMIZED COMPARATIVE TRIAL; HIGH-DOSE IRRADIATION; RADIATION-THERAPY; RADICAL PROSTATECTOMY; LOCALIZED CARCINOMA; CLINICAL STAGE; INTERIM-REPORT; FOLLOW-UP; CANCER; ANTIGEN C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114. NR 33 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD APR PY 1997 VL 33 IS 4 BP 555 EP 559 DI 10.1016/S0959-8049(96)00442-X PG 5 WC Oncology SC Oncology GA WZ557 UT WOS:A1997WZ55700020 PM 9274434 ER PT J AU Kosinski, CM Cha, JH Young, AB Persichetti, F MacDonald, M Gusella, JF Penney, JB Standaert, DG AF Kosinski, CM Cha, JH Young, AB Persichetti, F MacDonald, M Gusella, JF Penney, JB Standaert, DG TI Huntingtin immunoreactivity in the rat neostriatum: Differential accumulation in projection and interneurons SO EXPERIMENTAL NEUROLOGY LA English DT Article ID DISEASE GENE HOMOLOG; IT15 PROTEIN PRODUCT; WIDESPREAD EXPRESSION; TARGETED DISRUPTION; EMBRYONIC LETHALITY; PREFERENTIAL LOSS; CAG REPEAT; NEURONS; BRAIN; LOCALIZATION AB Huntington's disease is caused by a mutation of the gene encoding the protein huntingtin. Features of the human disease, characterized by selective loss of neurons from the neostriatum, can be replicated in rodents by administration of excitotoxins. In both affected individuals and the rodent model, there is massive loss of striatal projection neurons with selective sparing of interneurons. Furthermore, in the human disease the earliest evidence of striatal injury is found in striosomal regions of the striatum. The mRNA encoding huntingtin is known to be expressed by neurons throughout the brain, a distribution which does not account for the selective patterns of neuronal death which are observed. Using fluorescence immunocytochemistry and confocal microscopy with an antibody to huntingtin, we have observed that in rats a subset of striatal projection neurons contains dense accumulations of huntingtin immunoreactivity (HT-ir), while most neurons in the striatum contain much smaller amounts. The intensely stained neurons are concentrated within the striatal striosomes, as defined by calbindin-D-28K staining. In the matrix regions, relatively few neurons contain dense accumulations of HT-ir, and these cells always lack perikaryal staining for calbindin-D-28K. Striatal interneurons, identified by the presence of immunoreactivity for choline acetyltransferase, parvalbumin, calretinin, or neuronal nitric oxide synthase, exhibit little or no HT-ir. The paucity of HT-ir in striatal interneurons, as well as the prominence of staining in a subset of striosomal neurons, mirrors the selective vulnerability of these different types of cells in early stages of human Huntington's disease and in rodent excitotoxic models of the disorder. Our observations suggest that mechanisms which modulate the accumulation of huntingtin may play a central role in the neuronal degeneration of Huntington's disease. (C) 1997 Academic Press. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,CHARLESTOWN,MA 02129. RP Kosinski, CM (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,FRUIT ST,BOSTON,MA 02114, USA. OI Standaert, David/0000-0003-2921-8348 FU NINDS NIH HHS [NS16367, NS31579, NS32765] NR 38 TC 47 Z9 47 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD APR PY 1997 VL 144 IS 2 BP 239 EP 247 DI 10.1006/exnr.1997.6441 PG 9 WC Neurosciences SC Neurosciences & Neurology GA XH046 UT WOS:A1997XH04600001 PM 9168825 ER PT J AU Schapiro, RH AF Schapiro, RH TI Image of the month - The patient has Peutz-Jeghers syndrome SO GASTROENTEROLOGY LA English DT Article RP Schapiro, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 BP 1068 EP & PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WT504 UT WOS:A1997WT50400005 PM 10465624 ER PT J AU Geissler, M Tokushige, K Chante, CC Zurawski, VR Wands, JR AF Geissler, M Tokushige, K Chante, CC Zurawski, VR Wands, JR TI Cellular and humoral immune response to hepatitis B virus structural proteins in mice after DNA-based immunization SO GASTROENTEROLOGY LA English DT Article ID DIRECT GENE-TRANSFER; CYTOTOXIC T-LYMPHOCYTES; SURFACE-ANTIGEN; NUCLEOCAPSID ANTIGEN; TRANSGENIC MICE; VIRAL-INFECTION; PRE-S(2) REGION; SKELETAL-MUSCLE; PLASMID DNA; EPITOPE AB Background & Aims: Development of a broad-based cellular immune response to hepatitis B viral structural proteins may be important for recovery from infection, and lack of such responses may lead to persistent viral infection and chronic liver disease. Strategies designed to enhance the hepatitis B virus (HBV)-specific immune response may be able to reduce persistent viral infection of the liver, The aim of this study was to induce HBV-specific cellular and humoral immune responses in mice using DNA-based immunizations with the large and middle envelope and nucleocapsid proteins, Methods: Antibodies to HBV structural proteins, T-helper-cell proliferation, and cytokine release and generation of cytotoxic T lymphocyte (CTL) activity were measured in vaccinated mice, Results: Immunized mice developed high-titer antibodies against envelope and core proteins in serum. More importantly, 93% of the immunized mice produced strong inflammatory CD4(+) T-cell and CD8(+) CTL responses to viral proteins, Conclusions: This study shows that DNA-based vaccination will generate broad-based CTL activity as well as strong T-helper cell responses with the production of TH1-type cytokines to HBV structural proteins. Such constructs are promising candidates as antiviral agents, and these studies have defined some of the most immunogenic antigens for an immunotherapeutic approach of chronic HBV infection. C1 MASSACHUSETTS GEN HOSP,MOL HEPATOL LAB,CTR CANC,CHARLESTOWN,MA 02129. CARDINAL SANTOS MED CTR,MANILA,PHILIPPINES. APOLLON INC,MALVERN,PA 19355. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02169] NR 66 TC 72 Z9 84 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 BP 1307 EP 1320 DI 10.1016/S0016-5085(97)70145-8 PG 14 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WT504 UT WOS:A1997WT50400035 PM 9098017 ER PT J AU Jacoby, RF Schlack, S Cole, CE Skarbek, M Harris, C Meisner, LF AF Jacoby, RF Schlack, S Cole, CE Skarbek, M Harris, C Meisner, LF TI A juvenile polyposis tumor suppressor locus at 10q22 is deleted from nonepithelial cells in the lamina propria SO GASTROENTEROLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Gastroenterology-Association CY MAY 19-22, 1996 CL SAN FRANCISCO, CA SP Amer Gastroenterol Assoc ID COLI; CANCER; PATHOGENESIS; CARCINOMA; RISK; FISH AB Background & Aims: Juvenile polyps are characterized by an abundant lamina propria that lacks smooth muscle and may contain cystically dilated glands, with epithelium that seems normal and is nondysplastic. Rarely, an autosomal dominant inheritance pattern occurs. The aim of this study was to test the hypothesis that the genetic defect in both sporadic juvenile polyps and hereditary juvenile polyposis involves loss of function for a tumor suppressor gene. Methods: Allelic losses were detected by comparing normal DNA with tumor DNA from a series of 47 juvenile polyps from 16 patients using polymerase chain reaction amplification of microsatellite markers and fluorescent in situ hybridization (FISH). Results: Somatic deletions at 10q22 were detected in 39 of 47 juvenile polyps (83%) from 16 unrelated patients with either hereditary or sporadic juvenile polyps, and the minimum overlap localized juvenile polyposis coli to the 3-cM interval D10S219-D10S1696. Fluorescent in situ hybridization shows that the cells affected by deletion mutation reside exclusively in the lamina propria, not in the epithelium. Conclusions: The location of a novel tumor suppressor gene on chromosome 10 that is affected by deletion mutation in the majority of juvenile polyps was mapped. Unlike adenomas and carcinomas of the colonic epithelium, juvenile polyps originate in the lamina propria. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,GASTROENTEROL SECT,MADISON,WI. UNIV WISCONSIN,CTR COMPREHENS CANC,DEPT MED,MADISON,WI. UNIV WISCONSIN,CTR COMPREHENS CANC,DEPT CYTOGENET,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. FU NCI NIH HHS [U01 CA59352, P30 CA14520] NR 26 TC 94 Z9 95 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 BP 1398 EP 1403 DI 10.1016/S0016-5085(97)70156-2 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WT504 UT WOS:A1997WT50400046 PM 9098028 ER PT J AU Aleynik, S Leo, MA Takeshige, U Aleynik, M Lieber, CS AF Aleynik, S Leo, MA Takeshige, U Aleynik, M Lieber, CS TI Dilinoleoylphosphatidylcholine (DLPC) is the active antioxidant of polyenylphosphatidylcholine (PPC) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, ALCOHOL RES CTR, SECT LIVER DIS & NUTR, NEW YORK, NY USA. MT SINAI SCH MED, NEW YORK, NY USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1209 EP A1209 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904819 ER PT J AU Aleynik, S Leo, MA Aleynik, M Lieber, CS AF Aleynik, S Leo, MA Aleynik, M Lieber, CS TI Polyenylphosphatidylcholine protects rat pancreas against alcohol/iron-induced oxidative stress SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, LIVER DIS SECT, NEW YORK, NY USA. BRONX VET ADM MED CTR, NUTR & ALCOHOL RES CTR, NEW YORK, NY USA. MT SINAI SCH MED, NEW YORK, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A424 EP A424 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901689 ER PT J AU Arora, S Baraona, E Lieber, CS AF Arora, S Baraona, E Lieber, CS TI Ranitidine increases blood alcohol levels in social drinkers. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, CTR ALCOHOL RES & TREATMENT, BRONX, NY USA. MT SINAI SCH MED, NEW YORK, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1214 EP A1214 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904841 ER PT J AU Awane, M MacDermott, RP Podolsky, DK Reinecker, HC AF Awane, M MacDermott, RP Podolsky, DK Reinecker, HC TI Intestinal epithelial cells express functional IL-17 receptors. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. LAHEY HITCHCOCK CLIN, BURLINGTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A860 EP A860 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903427 ER PT J AU Beck, PL Hilsden, R Meddings, J Lee, SS AF Beck, PL Hilsden, R Meddings, J Lee, SS TI Sucrose permeability can detect portal hypertensive gastropathy in cirrhotic rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALGARY, GI RES GRP, CALGARY, AB T2N 1N4, CANADA. MASSACHUSETTS GEN HOSP, IBD, RES GRP, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1224 EP A1224 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904878 ER PT J AU BelkindGerson, J Kaplan, LM AF BelkindGerson, J Kaplan, LM TI The cRet ligand GNDF, an enteric neurotrophin, is specifically expressed by rat intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1131 EP A1131 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904510 ER PT J AU BelkindGerson, J Choi, RS Vacanti, JP Kaplan, LM AF BelkindGerson, J Choi, RS Vacanti, JP Kaplan, LM TI Intestinal epithelial cells direct their own innervation in a co-culture system. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. CHILDRENS HOSP, DEPT SURG, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A697 EP A697 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902777 ER PT J AU Beltinger, J Makh, S Goke, M Podolsky, DK Hawkey, CJ Mahida, YR AF Beltinger, J Makh, S Goke, M Podolsky, DK Hawkey, CJ Mahida, YR TI Expression of cyclooxygenase (COX) enzymes & extracellular matrix (ECM) proteins by human colonic subepithelial myofibroblasts. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV NOTTINGHAM HOSP, DIV GASTROENTEROL, NOTTINGHAM NG7 2UH, ENGLAND. MASSACHUSETTS GEN HOSP, GI UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1132 EP A1132 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904511 ER PT J AU Chang, L Saba, L Silverman, DHS Matin, K Mandelkern, MA Mayer, EA AF Chang, L Saba, L Silverman, DHS Matin, K Mandelkern, MA Mayer, EA TI Differences in perception and brain activation in response to visceral stimuli in IBS patient and non-patient twins. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, HARBOR MED CTR, DIV GASTROENTEROL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, NEUROENTER BIOL GRP, CURE, DIG DIS CTR, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT PHYSIOL, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT NUCL MED, LOS ANGELES, CA 90073 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A709 EP A709 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902827 ER PT J AU Chung, DC Brown, SB Smith, AP Graemecook, F Warshaw, AL Jensen, RT Arnold, A AF Chung, DC Brown, SB Smith, AP Graemecook, F Warshaw, AL Jensen, RT Arnold, A TI Genome-wide allelotyping of pancreatic endocrine tumors. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, LAB ENDOCRINE ONCOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NIH, DIGEST DIS BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A434 EP A434 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901727 ER PT J AU Chung, RT Han, CJ Kaplan, LM AF Chung, RT Han, CJ Kaplan, LM TI Purified hepatitis C virus NS5b binds the 3'-terminal region of the HCV genome in a sequence-specific manner. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1244 EP A1244 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904961 ER PT J AU Chung, RT Han, CJ Kaplan, LM AF Chung, RT Han, CJ Kaplan, LM TI Expressed hepatitis C virus NS5b RNA polymerase is a non-processive enzyme. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1244 EP A1244 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904960 ER PT J AU Chung, RT Monto, A Dienstag, JL Kaplan, LM AF Chung, RT Monto, A Dienstag, JL Kaplan, LM TI NS5a mutations do not predict response to interferon in American patients infected with genotype 1 hepatitis C virus. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1244 EP A1244 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904959 ER PT J AU ChyangWu, D Taupin, D Podolsky, DK AF ChyangWu, D Taupin, D Podolsky, DK TI Gene expression of the gastric trefoil peptide SP is mediated by intestinal trefoil factor. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 KAOHSIUNG MED COLL HOSP, TAIPEI, TAIWAN. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A90 EP A90 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900355 ER PT J AU Darmoul, D Huttner, KM Ouellette, AJ AF Darmoul, D Huttner, KM Ouellette, AJ TI A repeated sequence element upstream of the mouse cryptdin-4 gene transcription start site. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. CHILDRENS HOSP, JOINT PROGRAM NEONATAL, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A869 EP A869 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903462 ER PT J AU Deng, W Kaneko, H Tache, Y Mitsuma, T AF Deng, W Kaneko, H Tache, Y Mitsuma, T TI Central and peripheral actions of amylin to prevent ethanol-induced gastric injury in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, DEPT MED,W LOS ANGELES VAMC,CURE, DIGEST DIS RES CTR, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. AICHI MED UNIV, DEPT INTERNAL MED 4, AICHI, JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1141 EP A1141 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904550 ER PT J AU FernandezdelCastillo, C Rattner, DW Mostafavi, A McGrath, D Warshaw, AL AF FernandezdelCastillo, C Rattner, DW Mostafavi, A McGrath, D Warshaw, AL TI Debridement and closed packing for the treatment of necrotizing pancreatitis. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1440 EP A1440 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905738 ER PT J AU Fox, JG Dangler, C Edelman, W Kucherlapati, R Wang, TC AF Fox, JG Dangler, C Edelman, W Kucherlapati, R Wang, TC TI Decreased Helicobacter felis-associated proliferative body gastritis and systemic immune responses in C57BL/6 mice carrying a truncated APC gene. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MIT, DIV COMPARAT MED, CAMBRIDGE, MA 02139 USA. ALBERT EINSTEIN COLL MED, DEPT MOL GENET, BRONX, NY 10467 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A562 EP A562 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902240 ER PT J AU Fujimoto, M Nishimura, A MacDermott, RP Sanderson, IR AF Fujimoto, M Nishimura, A MacDermott, RP Sanderson, IR TI Short chain fatty acids alter IGF-binding protein secretion by intestinal epithelial cells through histone-dependent and histone-independent pathways SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA 02114 USA. LAHEY HITCHCOCK CLIN, GASTROINTESTINAL SECT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A363 EP A363 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901446 ER PT J AU Gilbert, RJ Reese, TG Napadow, VJ Wedeen, VJ AF Gilbert, RJ Reese, TG Napadow, VJ Wedeen, VJ TI Three-dimensional myoarchitecture of the intact mammalian tongue. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST ELIZABETHS MED CTR, DEPT MED, BOSTON, MA USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. MIT, DEPT MECH ENGN, BOSTON, MA USA. TUFTS UNIV, SCH MED, BOSTON, MA 02111 USA. MASSACHUSETTS GEN HOSP, NMR CTR, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A737 EP A737 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902938 ER PT J AU Goke, M Kanai, M Podolsky, DK AF Goke, M Kanai, M Podolsky, DK TI Repair of wounded intestinal epithelium is mediated by MAP kinase signaling pathways induced by TGF alpha. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A981 EP A981 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903911 ER PT J AU Goke, M Kanai, M Podolsky, DK AF Goke, M Kanai, M Podolsky, DK TI Fibroblasts stimulate intestinal epithelial cell proliferation: Importance of hepatocyte growth factor (HGF). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD MED SCH, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A876 EP A876 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903492 ER PT J AU Gschossmann, JM Raybould, H Ennes, H Young, S Lembo, T Mayer, EA AF Gschossmann, JM Raybould, H Ennes, H Young, S Lembo, T Mayer, EA TI Different types of cation channels mediate mechanical and chemical activation of DRG neurons SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE DIG DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A740 EP A740 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902951 ER PT J AU Han, CJ Chung, RT Kaplan, LM AF Han, CJ Chung, RT Kaplan, LM TI Activation of hepatitis C virus NS5b RNA polymerase activity by host cell factors. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1277 EP A1277 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905093 ER PT J AU Henihan, RDJ Zhensheng, Z Wang, TC AF Henihan, RDJ Zhensheng, Z Wang, TC TI Overexpression of the somatostatin type 2 (SSTR2) receptor in gastric (AGS-B) cells inhibits HDC promoter activity. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROENTEROL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1154 EP A1154 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904601 ER PT J AU Hocker, M Waigand, K Rosewicz, S OConnor, DT Riecken, EO Wiedenmann, B Wang, TC AF Hocker, M Waigand, K Rosewicz, S OConnor, DT Riecken, EO Wiedenmann, B Wang, TC TI Gastrin regulates chromogranin a promoter activity in AGS-B gastric carcinoma cells and transgenic mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 FREE UNIV BERLIN, BENJAMIN FRANKLIN MED CTR, D-1000 BERLIN, GERMANY. UCSD, SAN DIEGO, CA USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1155 EP A1155 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904605 ER PT J AU Hocker, M Rosenberg, I Xavier, R Podolsky, DK Merchant, JL Wang, TC AF Hocker, M Rosenberg, I Xavier, R Podolsky, DK Merchant, JL Wang, TC TI H2O2 stimulates tyrosine phosphorylation, ERK-activity and transactivation of the histidine decarboxylase (HDC) promoter in AGS-B human gastric carcinoma cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 FREE UNIV BERLIN, BENJAMIN FRANKLIN MED CTR, DEPT GASTROENTEROL, D-1000 BERLIN, GERMANY. UNIV MICHIGAN, DEPT MED, ANN ARBOR, MI 48109 USA. UNIV MICHIGAN, HOWARD HUGHES MED INST, ANN ARBOR, MI 48109 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1155 EP A1155 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904604 ER PT J AU Hoppin, AG Jasper, MS Kaplan, LM AF Hoppin, AG Jasper, MS Kaplan, LM TI Ovariectomy estrogen replacement: A pharmacological model of leptin deficiency. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD MED SCH, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A880 EP A880 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903507 ER PT J AU Hoppin, AG Kaplan, LM Leichtner, AM Zurakowski, D Bousvaros, A AF Hoppin, AG Kaplan, LM Leichtner, AM Zurakowski, D Bousvaros, A TI Leptin overexpression does not mediate growth failure in children with inflammatory bowel disease. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD MED SCH, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A880 EP A880 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903505 ER PT J AU Inomoto, T Yan, YX Togawa, K Ouellette, A Rustgi, AK AF Inomoto, T Yan, YX Togawa, K Ouellette, A Rustgi, AK TI The intestinal crypt kinase, ick, has a dual phosphorylation site that is present in MAP kinases SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, HEMATOL ONCOL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A583 EP A583 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902321 ER PT J AU Jacoby, RF Potter, D Cole, C Bosch, A AF Jacoby, RF Potter, D Cole, C Bosch, A TI Presymptomatic screening for HNPCC by detection of the phenotype of microsatellite instability in benign colon adenomas SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN, DEPT MED, MADISON, WI USA. UNIV WISCONSIN, DEPT BIOSTAT, MADISON, WI USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, PATHOL & LAB MED SERV, MADISON, WI 53705 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A585 EP A585 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902332 ER PT J AU Jacoby, RF Cole, C Clipson, L Gould, K Luongo, C Loser, A Newton, M Dove, WF AF Jacoby, RF Cole, C Clipson, L Gould, K Luongo, C Loser, A Newton, M Dove, WF TI Intestinal neoplasia in the Min mouse adenoma model is not strongly influenced by the enteric microbial status (normal flora vs germ-free) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN, SCH MED, DEPT MED, MADISON, WI USA. UNIV WISCONSIN, SCH MED, DEPT BIOSTAT, MADISON, WI USA. UNIV WISCONSIN, SCH MED, DEPT ONCOL, MADISON, WI USA. UNIV WISCONSIN, SCH MED, DEPT GENET, MADISON, WI USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, PATHOL & LAB MED SERV, MADISON, WI 53705 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A585 EP A585 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902331 ER PT J AU Jacoby, RF Stoltenberg, RL Madsen, JA Schlack, SC Harms, BA AF Jacoby, RF Stoltenberg, RL Madsen, JA Schlack, SC Harms, BA TI Neoplasia in ileal pouch mucosa after total proctocolectomy for juvenile polyposis. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN, DEPT MED, MADISON, WI USA. UNIV WISCONSIN, DEPT ONCOL, MADISON, WI USA. UNIV WISCONSIN, DEPT GENET, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, PATHOL & LAB MED SERV, MADISON, WI 53705 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A585 EP A585 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902330 ER PT J AU Jasper, MS Koo, LJ Kaplan, LM AF Jasper, MS Koo, LJ Kaplan, LM TI Leptin modulates insulin secretion from insulinoma cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1158 EP A1158 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904617 ER PT J AU Jenkins, TD Rustgi, AK AF Jenkins, TD Rustgi, AK TI Cis-regulatory sequences in the Epstein-Barr Virus BNLF-2 promoter under the influence of phorbol ester bind specific nuclear proteins from esophageal squamous epithelial cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, HEMATOL ONCOL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A586 EP A586 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902336 ER PT J AU Jensen, DM Gornbein, J Jensen, ME King, J Cheng, S AF Jensen, DM Gornbein, J Jensen, ME King, J Cheng, S TI Effects of alcohol, aspirin, and other potential risk factors on outcomes of severe ulcer hemorrhage. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, CURE, HEMOSTASIS RES GRP, LOS ANGELES, CA 90073 USA. NR 0 TC 5 Z9 5 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A160 EP A160 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900636 ER PT J AU Jensen, DM Cheng, S Jensen, ME Gornbein, J Jutabha, R Kovacs, TOG Machicado, GA AF Jensen, DM Cheng, S Jensen, ME Gornbein, J Jutabha, R Kovacs, TOG Machicado, GA TI Risk factors and recurrence of ulcer hemorrhage. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, CURE, LOS ANGELES, CA 90073 USA. NR 0 TC 5 Z9 5 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A160 EP A160 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900635 ER PT J AU Jensen, G Feitelson, M Farci, P Liang, TJ Wright, T Munoz, S AF Jensen, G Feitelson, M Farci, P Liang, TJ Wright, T Munoz, S TI Serum hepatitis C RNA in fulminant hepatitis: Evaluation by multiple laboratories. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ALBERT EINSTEIN MED CTR, PHILADELPHIA, PA 19141 USA. THOMAS JEFFERSON UNIV, PHILADELPHIA, PA 19107 USA. NIH, BETHESDA, MD 20892 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. UNIV CALIF SAN FRANCISCO, VA HOSP, SAN FRANCISCO, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1294 EP A1294 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905158 ER PT J AU Jeon, WK Koh, TJ Wu, DC Wang, TC AF Jeon, WK Koh, TJ Wu, DC Wang, TC TI Human spasmolytic polypeptide gene expression is regulated by serum in the human gastric carcinoma cell line KATO III. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, DIV GASTROENTEROL, BOSTON, MA 02114 USA. KAOHSIUNG MED COLL HOSP, DEPT MED, DIV GASTROENTEROL, KAOHSIUNG, TAIWAN. RI Wu, Deng-Chyang/D-2337-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A881 EP A881 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903512 ER PT J AU Joshi, V Lentz, M Fox, JG Wang, TC Goldenring, JR AF Joshi, V Lentz, M Fox, JG Wang, TC Goldenring, JR TI Aberrant mucous neck cell lineages associated with fundic H-pylori gastritis. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MIT, DIV COMPARAT MED, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, GI UNIT, BOSTON, MA 02114 USA. MED COLL GEORGIA, DEPT PATHOL, AUGUSTA, GA 30912 USA. MED COLL GEORGIA, INST MOL MED, AUGUSTA, GA 30912 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A163 EP A163 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900648 ER PT J AU Kanai, M Goke, M Tsunekawa, S Podolsky, DK AF Kanai, M Goke, M Tsunekawa, S Podolsky, DK TI Signal transduction pathway of colonic epithelial cell fibroblast growth factor receptor 3: Identification of a novel 66 kDa phosphoprotein. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A588 EP A588 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902343 ER PT J AU Kaneko, H Deng, W Mori, S Tache, Y Mitsuma, T AF Kaneko, H Deng, W Mori, S Tache, Y Mitsuma, T TI Central action of adrenomedullin (AM) to prevent ethanol-induced gastric injury is not mediated through CGRP1- and TRH-receptors in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 AICHI MED UNIV, DEPT INTERNAL MED 4, AICHI 48011, JAPAN. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, CURE, DIGEST DIS RES CTR, DEPT MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1160 EP A1160 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904626 ER PT J AU Keates, S Kelly, CP Mizoguchi, E Bhan, A Keates, AC AF Keates, S Kelly, CP Mizoguchi, E Bhan, A Keates, AC TI Production of ENA-78, and enterocyte derived chemokine, is upregulated in ulcerative colitis. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, BETH ISRAEL DEACONESS MED CTR, GI, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1010 EP A1010 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904027 ER PT J AU Keshavarzian, A Jacyno, M Winship, D Sanderson, IR AF Keshavarzian, A Jacyno, M Winship, D Sanderson, IR TI IL-8 in colonic lumen of patients with ulcerative colitis (UC) is responsible for priming of neutrophils (PMN): A possible mechanism of PMN activation & tissue damage in UC. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 LOYOLA UNIV, SCH MED, DEPT MED, GI DIV & PHARM, MAYWOOD, IL 60153 USA. HINES VA, HINES, IL USA. MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PED GI & NUTR, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1011 EP A1011 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904029 ER PT J AU Kim, HS Rogers, SA Liang, TJ Blumberg, RS AF Kim, HS Rogers, SA Liang, TJ Blumberg, RS TI Identifying CD1d interacting proteins by yeast two hybrid system. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1012 EP A1012 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904035 ER PT J AU Koh, TJ Dockray, GJ Varro, A Cahill, RJ Fox, JG Wang, TC AF Koh, TJ Dockray, GJ Varro, A Cahill, RJ Fox, JG Wang, TC TI Overexpression of glycine-extended progastrin results in gastric ulceration and colonic goblet cell hyperplasia. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. UNIV LIVERPOOL, PHYSIOL LAB, LIVERPOOL L69 3BX, MERSEYSIDE, ENGLAND. MIT, DIV COMPARAT MED, CAMBRIDGE, MA 02139 USA. RI Varro, Andras/M-2647-2016 OI Varro, Andras/0000-0003-0745-3603 NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1163 EP A1163 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904636 ER PT J AU Kovacs, TOG Sytnik, B Walsh, JH AF Kovacs, TOG Sytnik, B Walsh, JH TI The effects of Helicobacter pylori infection on gastric distention-induced acid and gastrin secretion SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, CURE, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A183 EP A183 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900727 ER PT J AU Kovacs, TOG Sytnik, B Walsh, JH AF Kovacs, TOG Sytnik, B Walsh, JH TI Helicobacter pylori infection decreases parietal cell sensitivity to gastrin SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, CURE, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A183 EP A183 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900729 ER PT J AU Krishnarao, ASM Hirsch, R Rogers, RA Averboukh, L Pardee, AB Frendl, G AF Krishnarao, ASM Hirsch, R Rogers, RA Averboukh, L Pardee, AB Frendl, G TI Macrophage activated genes from an experimental mice colitis model SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP, DEPT ANESTHESIA, CTR EXPT THERAPEUT & REPERFUS INJURY, BOSTON, MA 02115 USA. HARVARD UNIV, CTR DIGEST DIS, BOSTON, MA USA. HARVARD UNIV, SCH PUBL HLTH, DEPT ENVIRONM HLTH, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CELL GROWTH & REGULAT, BOSTON, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1019 EP A1019 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904062 ER PT J AU Lembo, T Naliboff, B Saba, L Matin, K Mayer, EA AF Lembo, T Naliboff, B Saba, L Matin, K Mayer, EA TI Differential effects of somatostatin analogue and opioid on perception of rectal pain. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,DIG DIS RES CTR,CURE, NEUROENTER BIOL GRP, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A773 EP A773 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903082 ER PT J AU Lencer, WI Strohmeier, GR Currie, MG Ouellette, AJ Selsted, M Madara, JL AF Lencer, WI Strohmeier, GR Currie, MG Ouellette, AJ Selsted, M Madara, JL TI Induction of epithelial secretion by channel forming cryptdins SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF IRVINE, IRVINE, CA 92717 USA. CHILDRENS HOSP, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. SEARLE RES & DEV, ST LOUIS, MO USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A379 EP A379 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901510 ER PT J AU Mashimo, H Ashegh, EJ Goyal, RK AF Mashimo, H Ashegh, EJ Goyal, RK TI Distinct roles of neuronal and endothelial nitric oxide synthases in NANC inhibitory neurotransmission. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BROCKTON W ROXBURY VET AFFAIRS MED CTR, CTR SWALLOWING & MOTIL DISORDERS, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A784 EP A784 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903125 ER PT J AU Matin, K Mayer, EA Munakata, J Naliboff, B Lembo, T AF Matin, K Mayer, EA Munakata, J Naliboff, B Lembo, T TI Intravenous octreotide (OCT) affects visceral discomfort thresholds but not stimulus-response functions in IBS patients. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, DEPT MED,SCH MED,NEUROENTER BIOL GRP, DIG DIS RES CTR,CURE, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A785 EP A785 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903129 ER PT J AU Mizoguchi, A Mizoguchi, E Bhan, AK AF Mizoguchi, A Mizoguchi, E Bhan, AK TI The appendix is a priming site for the development of chronic colitis in TCR alpha-mutant mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1043 EP A1043 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904159 ER PT J AU Mizoguchi, E Mizoguchi, A Bhan, AK AF Mizoguchi, E Mizoguchi, A Bhan, AK TI Role of the cytokines in the early stages of inflammatory bowel disease in TCR alpha-mutant mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1044 EP A1044 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904162 ER PT J AU Mizoguchi, E Mizoguchi, A Chiba, C Niles, JL Bhan, AK AF Mizoguchi, E Mizoguchi, A Chiba, C Niles, JL Bhan, AK TI Anti-neutrophil cytoplasmic antibodies producing B cells in TCR alpha-mutant mice with inflammatory bowel disease. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1044 EP A1044 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904160 ER PT J AU Moser, AJ Abedin, ZR Weber, P Abedin, MZ Roslyn, JJ AF Moser, AJ Abedin, ZR Weber, P Abedin, MZ Roslyn, JJ TI Na+/Ca2+ exchange by the gallbladder: A potential cause of gallstones. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ALLEGHENY UNIV HLTH SCI, DEPT SURG, PHILADELPHIA, PA 19102 USA. PHILADELPHIA VA MED CTR, RES SERV, PHILADELPHIA, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1460 EP A1460 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905817 ER PT J AU Muller, A Odze, R Jenkins, T Shahsesfaei, A Nakagawa, H Inomoto, T Rustgi, AK AF Muller, A Odze, R Jenkins, T Shahsesfaei, A Nakagawa, H Inomoto, T Rustgi, AK TI The induction of epidermal growth factor receptor expression in the esophageal squamous epithelium of cyclin D1 transgenic mice SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, HEMATOL ONCOL UNIT, BOSTON, MA USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, DEPT PATHOL, BOSTON, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A621 EP A621 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902472 ER PT J AU Munakata, J Mayer, EA FitzGerald, L Matin, K Tougas, G Naliboff, B AF Munakata, J Mayer, EA FitzGerald, L Matin, K Tougas, G Naliboff, B TI Autonomic responses to visceral stimulation are downregulated in irritable bowel syndrome (IBS) patients. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE DIG DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90024 USA. MCMASTER UNIV, HAMILTON, ON, CANADA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A794 EP A794 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903165 ER PT J AU Munakata, J Silverman, DHS Naliboff, B Matin, K Mayer, EA AF Munakata, J Silverman, DHS Naliboff, B Matin, K Mayer, EA TI Anterior cingulate cortical activity levels during expected pain correlate with sensitized rectal perception thresholds in IBS and healthy subjects. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, DEPT MED,NEUROENTER BIOL GRP,CURE,DIG DIS RES CTR, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A794 EP A794 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903163 ER PT J AU Naliboff, B Munakata, J Matin, K FitzGerald, L Mayer, EA AF Naliboff, B Munakata, J Matin, K FitzGerald, L Mayer, EA TI Symptom severity and predominant symptom are associated with rectal sensitivity before and after sigmoid stimulation. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE DIG DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A797 EP A797 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903175 ER PT J AU Naliboff, B Saba, L Fullerton, S Mayer, EA AF Naliboff, B Saba, L Fullerton, S Mayer, EA TI Altered sensitivity to medications in functional bowel disease SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE,DIGEST DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A796 EP A796 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903174 ER PT J AU Ness, SL Edelman, W Jenkins, TD Rustgi, AK Kucherlapati, R AF Ness, SL Edelman, W Jenkins, TD Rustgi, AK Kucherlapati, R TI Targeted disruption of the keratin 4 gene in mice causes basal hyperplasia and impaired differentiation in esophageal squamous epithelium SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ALBERT EINSTEIN COLL MED, DEPT MOL GENET, NEW YORK, NY USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A626 EP A626 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902493 ER PT J AU Ogata, H Podolsky, DK AF Ogata, H Podolsky, DK TI Identification of a goblet cell-specific enhancer element in the rat intestinal trefoil factor gene promoter bound by a goblet cell nuclear protein. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. RI Ogata, Haruhiko/B-3964-2014 NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A392 EP A392 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901560 ER PT J AU Porch, JV Ferguson, CM AF Porch, JV Ferguson, CM TI Expanding the indications for laparoscopic cholecystectomy SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1466 EP A1466 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905839 ER PT J AU Quirk, DM Barry, MJ Aserkoff, B Podolsky, DK AF Quirk, DM Barry, MJ Aserkoff, B Podolsky, DK TI Physician specialty and variations in the cost of treating patients with acute upper gastrointestinal bleeding. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A36 EP A36 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41900142 ER PT J AU Rattner, D Dawson, S Birkett, D Forse, A Freund, W Isaacson, K Satava, R Torma, M Zeitels, S Zucker, K AF Rattner, D Dawson, S Birkett, D Forse, A Freund, W Isaacson, K Satava, R Torma, M Zeitels, S Zucker, K TI The biotechnology roadmap in minimally invasive therapy SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CTR PROCEDURAL MED, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1466 EP A1466 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905840 ER PT J AU Raybould, HE Bitticaca, M Caan, S Tabrizi, Y Wong, H Walsh, JH Meyer, JH Sternini, C AF Raybould, HE Bitticaca, M Caan, S Tabrizi, Y Wong, H Walsh, JH Meyer, JH Sternini, C TI 5-HT3 receptors (5HT(5)R) localized on vagal afferents innervating the stomach and duodenum contribute to intestinal inhibition of gastric emptying. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE DIG DIS RES CTR, W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90095 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROBIOL & PHYSIOL, LOS ANGELES, CA 90095 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A811 EP A811 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903232 ER PT J AU Raybould, HE Tabrizi, Y Meyer, JH Tso, P AF Raybould, HE Tabrizi, Y Meyer, JH Tso, P TI Lipid-induced inhibition of gastric emptying is dependent on chylomicron formation in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED,DEPT MED,CURE DIG DIS RES CTR, W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90095 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90095 USA. UNIV CINCINNATI, DEPT PATHOL, CINCINNATI, OH 45267 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A811 EP A811 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41903231 ER PT J AU Reinecker, HC Mehta, A Li, DJ Manion, DJ Podolsky, DK MacDermott, RP AF Reinecker, HC Mehta, A Li, DJ Manion, DJ Podolsky, DK MacDermott, RP TI Expression of a cytomegalovirus derived chemokine receptor regulates protein kinase A activity in intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 LAHEY HITCHCOCK CLIN, BURLINGTON, MA USA. MASSACHUSETTS GEN HOSP, DEPT MED, INFECT DIS UNIT, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1070 EP A1070 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904266 ER PT J AU Sands, BE Podolsky, DK Peppercorn, MA Marshall, A Warner, AS MacDermott, RP GraemeCook, F Dykens, JA AF Sands, BE Podolsky, DK Peppercorn, MA Marshall, A Warner, AS MacDermott, RP GraemeCook, F Dykens, JA TI Urinary 8-hydroxydeoxyguanosine (8-OHdGUA) excretion as a non-invasive marker of disease activity in ulcerative colitis (UC). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 WARNER LAMBERT PARKE DAVIS, PHARMACEUT RES, ANN ARBOR, MI 48105 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. BETH ISRAEL MED CTR, BOSTON, MA USA. LAHEY HITCHCOCK CLIN, BURLINGTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1081 EP A1081 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904309 ER PT J AU Seensalu, R Avedian, D Barbuti, R Slice, L Walsh, JH AF Seensalu, R Avedian, D Barbuti, R Slice, L Walsh, JH TI Inactivation of rho p21 by Cl-botulinum C3 exoenzyme enhances gastrin release from isolated canine G-cells in primary culture SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, DEPT MED, CURE, DIGEST DIS RES CTR, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1187 EP A1187 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904731 ER PT J AU So, JBY Rattner, DW AF So, JBY Rattner, DW TI Outcomes of atypical reflux symptoms after laparoscopic fundoplication. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1474 EP A1474 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905872 ER PT J AU Srivastava, MD Srivastava, BIS AF Srivastava, MD Srivastava, BIS TI Effect of erythromycin (E), azithromycin (A), clarithromycin (C) and omeprazole (O) on chemokines and IL-10 production in human cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, BOSTON, MA 02115 USA. CHILDRENS HOSP, BOSTON, MA 02115 USA. ROSWELL PK CANC INST, BUFFALO, NY 14263 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1095 EP A1095 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904365 ER PT J AU Syngal, S Fox, E Eng, C Garber, JE Kolodner, RD AF Syngal, S Fox, E Eng, C Garber, JE Kolodner, RD TI Presence of more than one hMSH2 or hMLHI mutation in four hereditary non polyposis colon cancer (HNPCC) kindreds. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BRIGHAM & WOMENS HOSP, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A664 EP A664 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902647 ER PT J AU Syngal, S Weeks, JC Schrag, D Garber, JE Kuntz, KM AF Syngal, S Weeks, JC Schrag, D Garber, JE Kuntz, KM TI Benefits of colonoscopic surveillance and prophylactic colectomy in mutation carriers for hereditary nonpolyposis colorectal cancer (HNPCC) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, BRIGHAM & WOMENS HOSP,SCH MED,SECT CLIN EPIDEMIOL, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, GI DIV, BOSTON, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A664 EP A664 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902645 ER PT J AU Tanaka, S Engel, E Guth, PH Wenby, RB Meiselman, HJ Lee, J Kaunitz, JD AF Tanaka, S Engel, E Guth, PH Wenby, RB Meiselman, HJ Lee, J Kaunitz, JD TI Regional differences in H+, HCO3, and CO2 diffusion through native porcine gastroduodenal mucus SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOMATH, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV SO CALIF, DEPT PHYSIOL & BIOPHYS, LOS ANGELES, CA 90089 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A308 EP A308 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901228 ER PT J AU Tanaka, S Guth, PH Kaunitz, JD AF Tanaka, S Guth, PH Kaunitz, JD TI Pentagastrin gastroprotection against acid-induced injury is related to H-2 receptor activation but not acid secretion SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A308 EP A308 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901226 ER PT J AU Tanaka, S Chu, S Montrose, MH Kaunitz, JD AF Tanaka, S Chu, S Montrose, MH Kaunitz, JD TI Confocal microscopic study of rat esophageal interstitial pH during luminal and basolateral acid challenge SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT MED, BALTIMORE, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A307 EP A307 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901225 ER PT J AU Tanaka, S Engel, E Guth, PH Wenby, RB Meiselman, HJ Lee, J Kaunitz, JD AF Tanaka, S Engel, E Guth, PH Wenby, RB Meiselman, HJ Lee, J Kaunitz, JD TI CO2 and HCO3 diffusion through porcine gastric mucin SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV SO CALIF, DEPT PHYSIOL & BIOPHYS, LOS ANGELES, CA 90089 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT BIOMATH, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A307 EP A307 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901223 ER PT J AU Taupin, D Zhang, Z Wang, TC Podolsky, DK AF Taupin, D Zhang, Z Wang, TC Podolsky, DK TI Genomic cloning and identification of enhancer activity within intron 1 of the gastric trefoil peptide, mouse SP SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A310 EP A310 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901237 ER PT J AU Tearney, GJ Brezinski, ME Boppart, SA Pitris, C Bouma, BE Southern, JF Fujimoto, JG AF Tearney, GJ Brezinski, ME Boppart, SA Pitris, C Bouma, BE Southern, JF Fujimoto, JG TI High resolution imaging of pathologic gastrointestinal tissues using optical coherence tomography. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MIT, DEPT ELECT ENGN & COMP SCI, ELECT RES LAB, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, DEPT INTERNAL MED, BOSTON, MA 02114 USA. RI Boppart, Stephen/C-7338-2009 NR 0 TC 1 Z9 1 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A667 EP A667 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902658 ER PT J AU Togawa, K Inomoto, T Marcus, D DeFoe, D Brooks, S Edelmann, W Kucherlapati, R Smith, S Rustgi, AK AF Togawa, K Inomoto, T Marcus, D DeFoe, D Brooks, S Edelmann, W Kucherlapati, R Smith, S Rustgi, AK TI Targeted disruption of the adenomatous polyposis coli (APC) gene in mice leads to abnormalities of the retinal pigment epithelium. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, HEMATOL ONCOL UNIT, BOSTON, MA USA. MED COLL GEORGIA, AUGUSTA, GA 30912 USA. E TENNESSEE STATE UNIV, JOHNSON CITY, TN 37614 USA. ALBERT EINSTEIN MED UNIV, BRONX, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A669 EP A669 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902665 ER PT J AU Warshaw, AL Zgraggen, K Rattner, DW FernandezdelCastillo, C AF Warshaw, AL Zgraggen, K Rattner, DW FernandezdelCastillo, C TI Middle segment pancreatectomy: A novel technique for conserving pancreatic tissue SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1484 EP A1484 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905914 ER PT J AU Werner, J Saghir, M FernandezdelCastillo, C Laposata, M Warshaw, AL AF Werner, J Saghir, M FernandezdelCastillo, C Laposata, M Warshaw, AL TI Fatty acid ethyl esters from both intrapancreatic and extrapancreatic metabolism or ethanol play a role in alcohol-induced pancreatic injury in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A494 EP A494 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901967 ER PT J AU Wiedenmann, B Wang, T Eichhorn, I Niesar, M Hocker, M Henry, JP Solimena, M Riecken, EO AF Wiedenmann, B Wang, T Eichhorn, I Niesar, M Hocker, M Henry, JP Solimena, M Riecken, EO TI Molecular dissection of regulated secretory pathways in human gastric enterochromaffin-like cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT INTERNAL MED, DIV GASTROENTEROL, D-12200 BERLIN, GERMANY. HARVARD UNIV, SCH MED, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. INST BIOL PHYSICOCHIM, PARIS, FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A330 EP A330 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901314 ER PT J AU Yan, YX Nakagawa, H Lee, MH Rustgi, AK AF Yan, YX Nakagawa, H Lee, MH Rustgi, AK TI Transforming growth factor-alpha (TGF alpha) enhances cyclin D1 transcription through the early growth response (EGR-1) protein SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,HEMATOL ONCOL UNIT, GASTROINTESTINAL UNIT, BOSTON, MA USA. BOSTON UNIV, MED CTR, DEPT MED, BOSTON, MA 02215 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A685 EP A685 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41902728 ER PT J AU Yang, HT Wu, SV Song, M Pichuantes, S Nguyen, A Quan, S Polito, A Walsh, JH AF Yang, HT Wu, SV Song, M Pichuantes, S Nguyen, A Quan, S Polito, A Walsh, JH TI High prevalence of cagA, picB-positive H-pylori strains in China. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, CURE, DIGEST DIS RES CTR, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. CHIRON CORP, EMERYVILLE, CA 94608 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A337 EP A337 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901345 ER PT J AU Zgraggen, K Warshaw, AL Sigala, H Rattner, DW FernandezdelCastillo, C AF Zgraggen, K Warshaw, AL Sigala, H Rattner, DW FernandezdelCastillo, C TI Metastases to the pancreas and their surgical extirpation. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1487 EP A1487 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41905923 ER PT J AU Zgraggen, K Rivera, JA GraemeCook, F Werner, J Centeno, BA Rattner, DW Rustgi, AK Warshaw, AL FernandezdelCastillo, C AF Zgraggen, K Rivera, JA GraemeCook, F Werner, J Centeno, BA Rattner, DW Rustgi, AK Warshaw, AL FernandezdelCastillo, C TI Detailed characterization of the DMBA rat model of pancreatic ductal adenocarcinoma SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A496 EP A496 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901976 ER PT J AU Zgraggen, K Rivera, JA Pins, M Werner, J delCastillo, CF Compton, CC Rustgi, AK Warshaw, AL AF Zgraggen, K Rivera, JA Pins, M Werner, J delCastillo, CF Compton, CC Rustgi, AK Warshaw, AL TI Intraductal papillary mucinous tumors of the pancreas: The frequency of activating k-ras mutations correlates to the degree of histopathologic abnormality SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A497 EP A497 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41901977 ER PT J AU Zhang, ZS Koh, TJ Henihan, RDJ Wang, TC AF Zhang, ZS Koh, TJ Henihan, RDJ Wang, TC TI Activation of human histidine decarboxylase (HDC) gene transcription by gastrin through a 75/80-kDa sequence-specific nuclear protein complex. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1997 VL 112 IS 4 SU S BP A1203 EP A1203 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WV419 UT WOS:A1997WV41904794 ER PT J AU Tearney, GJ Brezinski, ME Bouma, BE Boppart, SA Pitris, C Southern, JF Fujimoto, JG AF Tearney, GJ Brezinski, ME Bouma, BE Boppart, SA Pitris, C Southern, JF Fujimoto, JG TI In vivo high resolution imaging of gastrointestinal tissue using optical coherence tomography. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MIT,ELECT RES LAB,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RI Boppart, Stephen/C-7338-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 63 EP 63 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400063 ER PT J AU Fox, VL CarrLocke, DL Hardy, S Israel, E Share, J AF Fox, VL CarrLocke, DL Hardy, S Israel, E Share, J TI Transient bile duct obstruction mimicking choledochal cyst in infants. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DIV GASTROENTEROL,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,DIV PEDIAT GASTROENTEROL,WORCESTER,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 141 EP 141 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400141 ER PT J AU Jensen, DM Machicado, GA Hirabayashi, K AF Jensen, DM Machicado, GA Hirabayashi, K TI Prospective clinical and laboratory studies of rubber band ligators for obliteration of medium and small esophageal varices. SO GASTROINTESTINAL ENDOSCOPY 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 MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 188 EP 188 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400188 ER PT J AU Carroll, N Quirk, D Centeno, B Warshaw, A Brugge, W AF Carroll, N Quirk, D Centeno, B Warshaw, A Brugge, W TI Accuracy of EUS-guided pancreatic biopsies SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 580 EP 580 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400577 ER PT J AU Quirk, D Lynch, T Grossbard, M Brugge, W AF Quirk, D Lynch, T Grossbard, M Brugge, W TI Prospective study of pre- and post-adjuvant treatment EUS in patients with esophageal cancer SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 612 EP 612 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400609 ER PT J AU Quirk, D Lewandrowski, K Centeno, B Warshaw, A Brugge, W AF Quirk, D Lewandrowski, K Centeno, B Warshaw, A Brugge, W TI The use of linear-array endoscopic ultrasonography in fine needle aspiration of pancreatic cystic lesions. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 613 EP 613 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400614 ER PT J AU Quirk, D Kelsey, P Schapiro, R Brugge, W AF Quirk, D Kelsey, P Schapiro, R Brugge, W TI The use of linear-array endoscopic ultrasonography in the detection of common bile duct stones. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1997 VL 45 IS 4 SU S BP 614 EP 614 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WU214 UT WOS:A1997WU21400611 ER PT J AU Xie, JW Quinn, A Zhang, XL Bare, J Rothman, A Collins, C Cutone, S Rutter, M McCormick, MK Epstein, E AF Xie, JW Quinn, A Zhang, XL Bare, J Rothman, A Collins, C Cutone, S Rutter, M McCormick, MK Epstein, E TI Physical mapping of the 5 Mb D9S196-D9S180 interval harboring the basal cell nevus syndrome gene and localization of six genes in this region SO GENES CHROMOSOMES & CANCER LA English DT Article ID ANEMIA GROUP-C; CARCINOMA-SYNDROME; RAPID METHOD; CONSTRUCTION; SEQUENCES; LIBRARY; CLONES; DNA AB The basal cell nevus syndrome (Gorlin syndrome) is characterized by multiple basal cell carcinomas and diverse developmental defects. The gene responsible for this syndrome has been mapped previously to a 2 cM interval between D9S196 and D9S180 at 9q22.3, and very recently mutations of a candidate gene in this region-the human homolog of the Drosophila patched gene-have been identified. We report here on physical mapping studies integrating a contig of yeast artificial chromosomes and bacterial artificial chromosomes with a long-range map spanning approximately 5 Mb between the recombination-determined flanking markers. Six genes have been mapped to this interval. (C) 1997 Wiley-Liss, Inc. C1 SAN FRANCISCO GEN HOSP,DEPT DERMATOL,SAN FRANCISCO,CA 94110. SAN FRANCISCO GEN HOSP,DEPT LAB MED,SAN FRANCISCO,CA 94110. MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOL NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CHARLESTOWN,MA. FU NIAMS NIH HHS [AR-39959]; NINDS NIH HHS [NS-32675] NR 15 TC 8 Z9 8 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD APR PY 1997 VL 18 IS 4 BP 305 EP 309 PG 5 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA WQ873 UT WOS:A1997WQ87300009 PM 9087571 ER PT J AU LaBaer, J Garrett, MD Stevenson, LF Slingerland, JM Sandhu, C Chou, HS Fattaey, A Harlow, E AF LaBaer, J Garrett, MD Stevenson, LF Slingerland, JM Sandhu, C Chou, HS Fattaey, A Harlow, E TI New functional activities for the p21 family of CDK inhibitors SO GENES & DEVELOPMENT LA English DT Article DE CDK inhibitors; D-type cyclin; immunodepletion; p21 and p27 families; complex assembly; adaptors ID CYCLIN-DEPENDENT KINASES; MAMMARY EPITHELIAL-CELLS; RETINOBLASTOMA PROTEIN; G1 PHASE; BINDING DOMAINS; DNA-REPLICATION; T-ANTIGEN; IDENTIFICATION; G(1); EXPRESSION AB The association of cdk4 with D-type cyclins to form functional kinase complexes is comparatively inefficient. This has led to the suggestion that assembly might be a regulated step. In this report we demonstrate that the CDK inhibitors p21(CIP), p27(KIP), and p57(KIP2) all promote the association of cdk4 with the D-type cyclins. This effect is specific and does not occur with other cdk inhibitors or cdk-binding proteins. Both in vivo and in vitro, the abundance of assembled cdk4/cyclin D complex increases directly with increasing inhibitor levels. The promotion of assembly is not attributable to a simple cell cycle block and requires the function of both the cdk and cyclin-binding domains. Kinetic studies demonstrate that p21 and p27 lead to a 35- and 80-fold increase in K-a, respectively, mostly because of a decrease in K-off. At low concentrations, p21 promotes the assembly of active kinase complexes, whereas at higher concentrations, it inhibits activity. Moreover, immunodepletion experiments demonstrate that most of the active cdk4-associated kinase activity also associates with p21. To confirm these results in a natural setting, we examine the assembly of endogenous complexes in mammary epithelial cells after release from a G(0) arrest. In agreement with our other data, cyclin D1 and p21 bind concomitantly to cdk4 during the in vivo assembly of cdk4/cyclin D1 complexes. This complex assembly occurs in parallel to an increase in cyclin D1-associated kinase activity. Immunodepletion experiments demonstrate that most of the cellular cyclin D1-associated kinase activity is also p21 associated. Finally, we find that all three CIP/KIP inhibitors target cdk4 and cyclin D1 to the nucleus. We suggest that in addition to their roles as inhibitors, the p21 family of proteins, originally identified as inhibitors, may also have roles as adaptor proteins that assemble and program kinase complexes for specific functions. C1 ONYX PHARMACEUT,RICHMOND,CA 94806. SUNNYBROOK HLTH SCI CTR,DIV CANC BIOL RES,TORONTO,ON M4N 3M5,CANADA. RP LaBaer, J (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,CHARLESTOWN,MA 02129, USA. FU NCI NIH HHS [CA64166] NR 66 TC 1051 Z9 1066 U1 0 U2 21 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD APR 1 PY 1997 VL 11 IS 7 BP 847 EP 862 DI 10.1101/gad.11.7.847 PG 16 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA WU794 UT WOS:A1997WU79400004 PM 9106657 ER PT J AU Teoh, SW Flandermeyer, DT Rosowski, JJ AF Teoh, SW Flandermeyer, DT Rosowski, JJ TI Effects of pars flaccida on sound conduction in ears of Mongolian gerbil: Acoustic and anatomical measurements SO HEARING RESEARCH LA English DT Article DE pars flaccida; tympanic membrane; middle ear; models; acoustics; anatomy ID MIDDLE-EAR; TYMPANIC MEMBRANE; TRANSMISSION; MECHANICS; EARDRUM; CAT; IMPEDANCE; PRESSURE; BEHAVIOR; HEARING AB This paper presents evidence on how the pars flaccida of the tympanic membrane affects the acoustic input to the middle and inner ear. Measurements of middle-ear acoustic input admittance and sound-pressure levels in both the ear canal and the middle-ear cavity were made in ears of eight gerbils before and after manipulations of the middle ear and tympanic membrane. The results are interpreted in terms of a model proposed by Kohlloffel [Hear. Res. 13 (1984) 83-88]. The input-admittance measurements show that the pars flaccida of gerbil acts as a resonator with a resonance frequency of approx. 500 Hz. The admittance of this resonator appears in parallel with the input admittance of the pars tensa and its ossicular and cochlear load. At frequencies below the resonance, the pars flaccida admittance is compliance-like and its magnitude is comparable to that of the pars tensa and its load; consequently, the presence of pars flaccida increases the overall middle-ear input admittance and decreases the pressure difference across the tympanic membrane. At higher frequencies, the admittance of pars flaccida is mass-like and small in magnitude, and it has negligible influence on the overall middle-ear input admittance and the pressure difference across the tympanic membrane. These results suggest that the presence of pars flaccida reduces low-frequency acoustic input to the middle- and inner-ear and consequently decreases hearing sensitivity in this frequency range. Our measurements suggest that with a constant sound pressure stimulus, stiffening the gerbil pars flaccida would increase the motion of the pars tensa by 3-10 dB at frequencies below the normal flaccida resonance. C1 MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,SPEECH & HEARING SCI PROGRAM,CAMBRIDGE,MA 02139. MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. FU NIDCD NIH HHS [T32-DC-00038, R01-DC00194] NR 60 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1997 VL 106 IS 1-2 BP 39 EP 65 DI 10.1016/S0378-5955(97)00002-6 PG 27 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WT378 UT WOS:A1997WT37800005 PM 9112106 ER PT J AU Emmons, KM Kawachi, I Barclay, G AF Emmons, KM Kawachi, I Barclay, G TI Tobacco control: A brief review of its history and prospects for the future SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID NICOTINE CHEWING-GUM; CIGARETTE-SMOKING; PASSIVE SMOKING; UNITED-STATES; LUNG-CANCER; TRANSDERMAL NICOTINE; HEART-DISEASE; ILLEGAL SALE; CALIFORNIA; EXPOSURE AB Significant strides have been made in tobacco control in the United States. This article highlights key events in the history of tobacco control, and looks toward the future to identify tobacco control strategies that are likely to have maximal public health impact in the next decade. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP Emmons, KM (reprint author), DANA FARBER CANC INST,CTR COMMUNITY BASED RES,44 BINNEY ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [1RO1HL50017, 1RO1HL48180] NR 102 TC 19 Z9 19 U1 3 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1997 VL 11 IS 2 BP 177 EP & DI 10.1016/S0889-8588(05)70425-1 PG 20 WC Oncology; Hematology SC Oncology; Hematology GA WX529 UT WOS:A1997WX52900002 PM 9137965 ER PT J AU Shaffer, K AF Shaffer, K TI Imaging and medical staging of lung cancer SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID DIGITAL CHEST RADIOGRAPHY; BEAM EQUALIZATION RADIOGRAPHY; COMPUTER-AIDED DIAGNOSIS; BRONCHOGENIC-CARCINOMA; PERFLUBRON EMULSION; MAGNETIC-RESONANCE; CT; TOMOGRAPHY; MR; SCINTIGRAPHY AB Plain films and CT remain the mainstays of imaging for staging of most thoracic malignancies. New developments in both areas may allow more sensitive and specific diagnoses at lower cost in the future. Magnetic resonance imaging plays a role in certain parts of the chest, particularly the lung apices and diaphragms, but offers no clear advantage over CT in nodal staging. Newer, more functional, imaging agents are becoming available using positron-emitting radioisotopes and radio-labeled antibodies which may provide the most specific staging possible using imaging methods. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP Shaffer, K (reprint author), DANA FARBER CANC INST,DEPT RADIOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 47 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 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1997 VL 11 IS 2 BP 197 EP & DI 10.1016/S0889-8588(05)70426-3 PG 18 WC Oncology; Hematology SC Oncology; Hematology GA WX529 UT WOS:A1997WX52900003 PM 9137966 ER PT J AU Miller, YE Franklin, WA AF Miller, YE Franklin, WA TI Molecular events in lung carcinogenesis SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID CANCER CELL-LINE; OBSTRUCTIVE PULMONARY-DISEASE; CHROMOSOMAL REGION 3P21; NONSMALL-CELL; SHORT ARM; HOMOZYGOUS DELETION; PRENEOPLASTIC LESIONS; CIGARETTE SMOKERS; CARCINOMA; EXPRESSION AB Genetic alterations seen in established lung cancers are also often found in premalignant respiratory epithelium. The frequency, usual order, biologic consequences, and prognostic import of the alterations are only beginning to be studied. Increased knowledge regarding pulmonary premalignancy may provide earlier, more treatable endpoints for early detection and therapy. C1 DENVER VET AFFAIRS MED CTR, DIV MED ONCOL, DENVER, CO 80220 USA. UNIV COLORADO, HLTH SCI CTR, DENVER, CO USA. UNIV COLORADO, CTR CANC, DENVER, CO 80262 USA. RP DENVER VET AFFAIRS MED CTR, DIV PULM & CRIT CARE MED, 1055 CLERMONT ST, DENVER, CO 80220 USA. FU NCI NIH HHS [P50 CA58187, P30 CA46934]; NHLBI NIH HHS [R01 HL45745] NR 92 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0889-8588 EI 1558-1977 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1997 VL 11 IS 2 BP 215 EP + DI 10.1016/S0889-8588(05)70427-5 PG 1 WC Oncology; Hematology SC Oncology; Hematology GA WX529 UT WOS:A1997WX52900004 PM 9137967 ER PT J AU Bataille, R Manolagas, SC Berenson, JR AF Bataille, R Manolagas, SC Berenson, JR TI Pathogenesis and management of bone lesions in multiple myeloma SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID COLONY-STIMULATING FACTOR; B-CELL MALIGNANCIES; OSTEOCLAST-ACTIVATING FACTOR; LEUKEMIA INHIBITORY FACTOR; TUMOR NECROSIS FACTOR; DICHLOROMETHYLENE DIPHOSPHONATE; QUANTITATIVE HISTOLOGY; RESORBING CYTOKINE; OSTEOTROPIC FACTOR; SIGNAL TRANSDUCER AB Osteolytic lesions are among the hallmarks of multiple myeloma (MM). On the other hand, they are rare in B cell malignancies other than MM. Data have shown a close relationship between myeloma cell. growth factors and factors involved in the occurrence of bone lesions in MM. Biophosphonates, which are potent inhibitors of bone resorption to control MM-induced hypercalcemia, are of interest due to their ability to slow the progression of MM bone disease. C1 UNIV ARKANSAS MED SCI HOSP,CTR OSTEOPOROSIS & METAB BONE DIS,LITTLE ROCK,AR 72205. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. RP Bataille, R (reprint author), INST BIOL,HEMATOL LAB,9 QUAI MONCOUSU,F-44035 NANTES 01,FRANCE. NR 80 TC 45 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1997 VL 11 IS 2 BP 349 EP & DI 10.1016/S0889-8588(05)70435-4 PG 14 WC Oncology; Hematology SC Oncology; Hematology GA WX529 UT WOS:A1997WX52900012 PM 9137974 ER PT J AU Elias, AD AF Elias, AD TI Multidisciplinary care of lung cancer patients .1. Preface SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Editorial Material RP Elias, AD (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1997 VL 11 IS 2 BP R13 EP R15 DI 10.1016/S0889-8588(05)70424-X PG 3 WC Oncology; Hematology SC Oncology; Hematology GA WX529 UT WOS:A1997WX52900001 ER PT J AU Kawamura, T Furusaka, A Koziel, MJ Chung, RT Wang, TC Schmidt, EV Liang, TJ AF Kawamura, T Furusaka, A Koziel, MJ Chung, RT Wang, TC Schmidt, EV Liang, TJ TI Transgenic expression of hepatitis C virus structural proteins in the mouse SO HEPATOLOGY LA English DT Article ID NON-B-HEPATITIS; HEPATOCELLULAR-CARCINOMA; NON-A; RECOMBINANT VACCINIA; ENVELOPE PROTEINS; VIRAL-HEPATITIS; CORE PROTEIN; INFECTION; MICE; GLYCOPROTEIN AB Although hepatitis C virus (HCV) is a leading cause of morbidity and mortality worldwide, the role of viral cytopathic effects remains unclear. To study the biosynthesis of HCV structural proteins and their pathogenic role, we constructed transgenic mice, expressing type 1b HCV structural proteins (core, E1, and E2) in Liver tissues. Two liver-specific promoters were used. The mouse major urinary protein (MUP) promoter has been shown to be developmentally regulated with little or no expression in utero but high-level expression after birth. The albumin (Alb) promoter provides constitutive, high levels of transgenes in liver. Expression of both HCV transgenes was detected in several Lines by Northern blots, HCV-specific reverse transcriptase-polymerase chain reactions (RT-PCR), and Western immunoblotting. Alb HCV lines showed higher levels of HCV expression than the MUP HCV Lines. Immunohistochemical analysis revealed a predominantly cytoplasmic presence of core protein with occasional nuclear staining, and both cytoplasmic and membrane expression of the E2 protein in the transgenic livers. In both transgenes, the highest levels of both antigens were seen in perivenular hepatocytes, suggesting potential processing specificity in those cells. At six months of age, the Livers of all transgenic lineages remained histologically normal. We concluded that HCV structural proteins are not directly cytopathic in this animal model. C1 MASSACHUSETTS GEN HOSP,CTR CANC,LAB TUMOR BIOL,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NIDDK,LIVER DIS SECT,NIH,BETHESDA,MD. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02129. FU NCI NIH HHS [R01-CA63117, CA 54524]; NIDDK NIH HHS [DK01952] NR 47 TC 111 Z9 116 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1997 VL 25 IS 4 BP 1014 EP 1021 DI 10.1002/hep.510250437 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA WT540 UT WOS:A1997WT54000037 PM 9096613 ER PT J AU Oberley, TD Oberley, LW AF Oberley, TD Oberley, LW TI Antioxidant enzyme levels in cancer SO HISTOLOGY AND HISTOPATHOLOGY LA English DT Review DE antioxidant enzymes; reactive oxygen species; superoxide dismutase; carcinogenesis; malignant phenotype ID MANGANESE-SUPEROXIDE-DISMUTASE; ORNITHINE DECARBOXYLASE INDUCTION; GLUTATHIONE-PEROXIDASE ACTIVITY; SYRIAN-HAMSTER TISSUES; TUMOR NECROSIS FACTOR; RENAL-CELL CARCINOMA; MOUSE-LIVER CELLS; FREE-RADICALS; MULTISTAGE CARCINOGENESIS; XANTHINE-OXIDASE AB Normal cells are protected by antioxidant enzymes from the toxic effects of high concentrations of reactive oxygen species generated during cellular metabolism. Even though cancer cells generate reactive oxygen species, it has been demonstrated biochemically that antioxidant enzyme levels are low in most animal and human cancers. However, a few cancer types have been found to have elevated levels of antioxidant enzymes, particularly manganese superoxide dismutase. Morphologic studies of animal and human cancer have confirmed that although the majority of tumor cell types from several organ systems have low antioxidant enzymes, adenocarcinomas may have elevated manganese superoxide dismutase and catalase levels. However, all cancers examined to date have some imbalance in antioxidant enzyme levels compared with the cell of origin. Antioxidant enzyme importance in cancer genesis has been difficult to evaluate in early cancerous lesions using biochemical techniques because such lesions are small and therefore below the level of detection. Using immunohistochemical techniques, early lesions of human and animal cancers were demonstrated to have low antioxidant enzymes, thus suggesting a role for these enzymes both in the genesis of cancer and the malignant phenotype. All but one human cancer cell type (the granular cell variant of human renal adenocarcinoma) examined showed both low catalase and glutathione peroxidase levels, suggesting that most cancer cell types cannot detoxify hydrogen peroxide. Our results to date are used to propose new cancer therapies based on modulation of cellular redox state. C1 UNIV WISCONSIN,SCH MED,DEPT PATHOL & LAB MED,MADISON,WI. UNIV IOWA,RADIAT RES LAB,COLL MED,IOWA CITY,IA 52242. RP Oberley, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL & LAB MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA 41267]; NIDCR NIH HHS [DE 10758] NR 82 TC 257 Z9 264 U1 2 U2 12 PU F HERNANDEZ PI MURCIA PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN SN 0213-3911 J9 HISTOL HISTOPATHOL JI Histol. Histopath. PD APR PY 1997 VL 12 IS 2 BP 525 EP 535 PG 11 WC Cell Biology; Pathology SC Cell Biology; Pathology GA WR423 UT WOS:A1997WR42300024 PM 9151141 ER PT J AU Ma, LD Penfornis, A Wang, XL Schoenfeld, D Akerblom, HK Tuomilehto, J Lounamaa, R Toivanen, L Fagerlund, A Flittner, M Gustafsson, B Haggqvist, C Hakulinen, A Herva, L Hiltunen, P Huhtamaki, T Huttunan, NP Huupponen, T Hyttinen, M Joki, T Jokisalo, R Kaar, ML Kallio, S Kaprio, EA Kaski, U Knip, M Laine, L Lappalainen, J Maenpaa, J Makela, AL Niemi, K Niiranen, A Nuuja, A Ojajarvi, P Otonkoski, T Pihlajamaki, K Pontynen, S Rajantie, J Sankala, J Schumacher, J Sillanpaa, M Stahlberg, MR Strahlmann, CH Uotila, T Vare, M Varimo, P Wettenstrand, G TuomilehtoWolf, E Metcalfe, K Hitman, G Faustman, D AF Ma, LD Penfornis, A Wang, XL Schoenfeld, D Akerblom, HK Tuomilehto, J Lounamaa, R Toivanen, L Fagerlund, A Flittner, M Gustafsson, B Haggqvist, C Hakulinen, A Herva, L Hiltunen, P Huhtamaki, T Huttunan, NP Huupponen, T Hyttinen, M Joki, T Jokisalo, R Kaar, ML Kallio, S Kaprio, EA Kaski, U Knip, M Laine, L Lappalainen, J Maenpaa, J Makela, AL Niemi, K Niiranen, A Nuuja, A Ojajarvi, P Otonkoski, T Pihlajamaki, K Pontynen, S Rajantie, J Sankala, J Schumacher, J Sillanpaa, M Stahlberg, MR Strahlmann, CH Uotila, T Vare, M Varimo, P Wettenstrand, G TuomilehtoWolf, E Metcalfe, K Hitman, G Faustman, D TI Evaluation of TAP1 polymorphisms with insulin dependent diabetes mellitus in Finnish diabetic patients SO HUMAN IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-II REGION; LINKAGE DISEQUILIBRIUM; GENETIC SUSCEPTIBILITY; MULTIPLE-SCLEROSIS; TRANSPORTERS TAP1; ASSOCIATION; DISEASE; ANTIGEN; IDDM AB Insulin dependent diabetes mellitus (IDDM) is an autoimmune disease with a strong association between disease and the HLA class II region. Because abnormal antigen processing, in part characterized by altered class I processing, has been identified in patients with IDDM, the TAP (transporter associated with antigen processing) genes located in the HLA class II region make attractive candidate genes for IDDM. Five coding region variants of TAP1 were typed in a cohort of well characterized Finnish patients with diabetes (n = 119) and compared to racially matched control subjects (n = 92). We found that although no single TAP1 polymorphism was associated with IDDM, a genotypic combination of Ile/Val at codon 333 with Asp/Asp at codon 637 was found more frequently in subjects with IDDM (9.4%) compared to controls (1.2%; P = 0.025). This could not be accounted for by an association with any particular haplotype defined by class I or class II serology. (C) American Society for Histocompatibility and Immunogenetics, 1997. C1 MASSACHUSETTS GEN HOSP,IMMUNOBIOL LAB,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,DEPT BIOSTAT,CHARLESTOWN,MA. ST BARTHOLOMEWS & ROYAL LONDON SCH MED,MED UNIT,LONDON,ENGLAND. NATL PUBL HLTH INST,DEPT EPIDEMIOL & HLTH PROMOT,HELSINKI,FINLAND. FU NIDCR NIH HHS [DE11023-02, DE11151-03]; NIDDK NIH HHS [P30-DK4056-1] NR 52 TC 14 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 1 PY 1997 VL 53 IS 2 BP 159 EP 166 DI 10.1016/S0198-8859(97)00030-X PG 8 WC Immunology SC Immunology GA WV914 UT WOS:A1997WV91400005 PM 9129974 ER PT J AU Mark, EJ Flieder, DB Matsubara, O AF Mark, EJ Flieder, DB Matsubara, O TI Treated Wegener's granulomatosis: Distinctive pathological findings in the lungs of 20 patients and what they tell us about the natural history of the disease SO HUMAN PATHOLOGY LA English DT Article DE Wegener's granulomatosis; palisading granuloma; vasculitis; capillaritis; bronchiolitis; corticosteroids; cyclophosphamide ID DIFFUSE PULMONARY HEMORRHAGE; PATHERGIC GRANULOMATOSIS; CAPILLARITIS; VASCULITIS; BIOPSIES; LESIONS AB Patients with an established diagnosis of Wegener's granulomatosis (WG) sometimes undergo lung biopsy when the disease does not behave in the expected manner. Treatment affects the tissue reaction. The microscopic recognition of partially treated disease is important, as the absence of expected lesions may lead to nonspecific diagnoses and inappropriate management. The appearance of treated disease over time may offer insight into its histogenesis and natural history. We correlated clinical features and pulmonary histology in 20 patients with WG after they had been treated with corticosteroids or cyclophosphamide or both. All patients had inflammatory or fibrotic pulmonary disease resulting from WG, but only 4 (20%) had macronodular necrosis typical of WG. Serum antineutrophil cytoplasmic antibody (ANCA) was elevated in all patients in whom it was measured. We divided the pathological findings into (1) vasculitis, (2) extravascular necrosis, (3) bronchiolitis, and (4) other lesions, and further divided them into (a) diagnostic for active disease, (b) suspicious for active disease, (c) suspicious for healing disease, (d) suspicious for residual disease, and (e) possible disease. Diagnostic or suspicious vascular lesions occurred in 15 patients (75%) and included granulomatous vasculitis, capillaritis or suspicious capillaritis, and neutrophilic vasculitis. Diagnostic or suspicious extravascular lesions occurred in 12 patients (60%) and included palisading granuloma, microabscess, macronodular pathergic necrosis, giant cell nodules, and micronodular scars. The giant cell nodules and nodular scars were an unusual healing pattern of palisading granulomas. Diagnostic bronchiolar lesions occurred in 1 patient (6%) and suspicious lesions in 13 patients (65%), including three novel patterns of bronchiolitis fibrosa (BF): (1) BF with giant cells, (2) BF crith hemosiderin, and (3) BF with micronodular scars. Other features related to WG included diffuse alveolar damage, peculiar alveolar fibrin, interstitial fibrosis, pneumonitis resembling usual interstitial pneumonitis, and lipoid pneumonia. Classic necrotic nodules and vasculitis of WG should not be anticipated after therapy, but the diagnosis of pulmonary WG after treatment may be made if the effects of treatment on histology are considered. Changes in anticipated histology are found after therapy as short as 6 days. The histology typically has muted features. BF develops in most patients and may reflect a salutary effect of therapy. Palisading granuloma may convert to giant cell nodule or micronodular scar. Interstitial fibrosis is common, and pneumonitis resembling usual interstitial pneumonitis can develop. If only healing or residual disease is encountered, one should search further clinically and pathologically for active disease. Dampened inflammatory lesions represent smoldering disease that presumably needs: additional therapy. Scarring presumably represents successfully treated but permanent disease. Copyright (C) 1997 by W.B. Saunders Company. C1 HARVARD UNIV,SCH MED,BOSTON,MA. NATL DEF MED COLL,DEPT PATHOL,TOKOROZAWA,SAITAMA,JAPAN. RP Mark, EJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 27 TC 26 Z9 28 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD APR PY 1997 VL 28 IS 4 BP 450 EP 458 DI 10.1016/S0046-8177(97)90034-4 PG 9 WC Pathology SC Pathology GA WV186 UT WOS:A1997WV18600011 PM 9104945 ER PT J AU Corless, CL Kibel, AS Iliopoulos, O Kaelin, WG AF Corless, CL Kibel, AS Iliopoulos, O Kaelin, WG TI Immunostaining of the von Hippel-Lindau gene product in normal and neoplastic human tissues SO HUMAN PATHOLOGY LA English DT Article DE vonHippel Lindau disease; kidney; renal cell carcinoma; pheochromocytoma; immunohistochemistry ID TUMOR-SUPPRESSOR GENE; RENAL-CELL CARCINOMA; SOMATIC MUTATIONS; PAPILLARY CYSTADENOMA; DISEASE; VHL; MANIFESTATIONS; IDENTIFICATION; PHENOTYPE; PROTEIN AB Alterations in the von Hippel-Lindau (VHL) gene are correlated with a diverse group of neoplasms including hemangioblastoma, clear cell renal carcinoma (RCC), and pheochromocytoma. Molecular genetic studies suggest that VHL is a tumor-suppressor gene; corresponding ly, reintroduction of a VHL complementary DNA (cDNA) into RCC cells inhibits their ability to form tumors in nude mice. Recently, it was discovered that the VHL gene product (pVHL) binds to two subunits of the transcription elongation complex Elongin (SIII), resulting in decreased activity of this complex in vitro. It is proposed that pVHL functions in vivo as a negative regulator of transcription elongation; however, the intracellular localization of pVHL has not been clearly delineated. Epitope-tagged pVHL has been observed in either the nucleus or the cytoplasm of cultured cells, depending on the density of the cell culture. In this article, the cellular localization of pVHL in normal and neoplastic human tissues is documented using three different monoclonal antibodies. Strong expression of pVHL was observed in the epithelial cells of all organs examined, particularly in renal tubules, and was exclusively cytoplasmic. Lesser degrees of staining, also cytoplasmic, were observed in other cell types. A variety of carcinomas (lung, prostate, colon, breast, bladder, and thyroid) showed strong cytoplasmic staining for pVHL including four of five sporadic clear cell RCC. Of the nonepithelial neoplasms examined, only one tumor, an embryonal rhabdomyosarcoma, failed to stain for pVHL. The findings establish widespread expression of VHL at the protein level and provide strong evidence that most, if not all, pVHL is localized to the cytoplasm of cells in vivo. C1 OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. DANA FARBER CANC INST,BOSTON,MA 02115. RP Corless, CL (reprint author), DEPT VET AFFAIRS MED CTR,DEPT PATHOL 113,3710 SW US VET HOSP RD,PORTLAND,OR 97207, USA. NR 25 TC 84 Z9 86 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 APR PY 1997 VL 28 IS 4 BP 459 EP 464 DI 10.1016/S0046-8177(97)90035-6 PG 6 WC Pathology SC Pathology GA WV186 UT WOS:A1997WV18600012 PM 9104946 ER PT J AU Greferath, R Nehls, P AF Greferath, R Nehls, P TI Monoclonal antibodies to thymidine glycol generated by different immunization techniques SO HYBRIDOMA LA English DT Article ID THYMINE GLYCOL; DNA; QUANTITATION; RESIDUES; DAMAGE AB Monoclonal antibodies specific for thymidine glycol in oxidized DNA were generated by immunization with thymidine glycol monophosphate (TMP-OH) or thymidine glycol (T-OH), respectively, conjugated to keyhole limpet hemocyanin (KLH) or thyreoglobulin (TG), Forty-five clones (TMP-OH) and 70 clones (T-OH) were examined upon antibody production in ELISA. Four clones secreting IgG1, kappa, were characterized further, In several studies the antibodies derived from the immunization with TMP-OH were inhibited by various inhibitors, In descending order of effectiveness, they were thymidine glycol monophosphate (TMP-OH), thymidine glycol (T-OH), thymidine monophosphate (TMP), and thymidine (Thn), After immunization with T-OH, antibodies were inhibited in following order: T-OH > TMP-OH > TMP > Thn, Inhibition by the bases thymine, adenine, cytosine, and guanine were negligible, In ISB (Immuno Slot Blot) performed with OsO4-treated DNA (Poly-[dA-dT]) and amount of 70 fmol thymidine glycol was detectable, DNA had to be irradiated at a level of at least 20 Gy to detect any damage in ELISA but at a lower level of irradiation (10 Gy) in ISB by one of these antibodies, TPS-1, The antibodies obtained after immunization with hapten-protein are therefore capable of the detection of low frequency lesions in DNA generated by free radicals after radiation or oxidative stress. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02135. HARVARD UNIV,SCH MED,DEV LABS,BOSTON,MA 02135. UNIV ULM,INST PATHOL & RECHTSMED,D-89081 ULM,GERMANY. UNIV ESSEN GESAMTHSCH KLINIKUM,INST HYG & ARBEITSMED,D-45122 ESSEN,GERMANY. NR 18 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0272-457X J9 HYBRIDOMA JI Hybridoma PD APR PY 1997 VL 16 IS 2 BP 189 EP 193 DI 10.1089/hyb.1997.16.189 PG 5 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Immunology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Immunology GA WX606 UT WOS:A1997WX60600008 PM 9145322 ER PT J AU Cegielski, JP Goetz, MB Jacobson, JM Cohn, SE Weinstein, RA DeHovitz, JA Bennett, CL AF Cegielski, JP Goetz, MB Jacobson, JM Cohn, SE Weinstein, RA DeHovitz, JA Bennett, CL TI Gender differences in early suspicion of tuberculosis in hospitalized, high-risk patients during 4 epidemic years, 1987 to 1990 SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID RESISTANT MYCOBACTERIUM-TUBERCULOSIS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA; PULMONARY TUBERCULOSIS; DELAYED DIAGNOSIS; VIRUS INFECTION; HIV-INFECTION; UNITED-STATES; NEW-YORK; AIDS AB Objectives: To assess the degree to which, from 1987 to 1990, physicians suspected tuberculosis (TB) in the first 2 hospital days in human immunodeficiency virus (HIV)-infected patients with pulmonary disease. Design: Retrospective cohort study. Setting: 96 hospitals in five US cities. Patients: 2174 adult patients with acquired immunodeficiency syndrome discharged with a diagnosis of Pneumocystis carinii pneumonia from 1987 to 1990. The diagnosis generally was not known on admission. Results: Physicians suspected TB in the first 2 hospital days in 66% of these patients in 1987, a rate that increased steadily to 74% in 1990. However, the extent to which physicians considered TB among female patients decreased from 76% to 71% over the 4 years. Controlling for confounding variables by multiple logistic regression, the odds that TB would be suspected early increased 1.8-fold among men (odds ratio [OR], 1.8; 95% confidence interval [CI95], 1.4-2.4), but not in women (OR, 0.6; CI95, 0.2-1.9). Among the five cities, the odds of early suspicion of TB increased most in New York City (OR, 3.9; CI95, 2.0-7.9). Conclusions: Physicians considered TB in a timely manner in an increasing majority of male, but not female, high-risk patients during the first years of TB resurgence in the United States. Physicians must be aware of the changing epidemiology of HIV and TB, as well as their practice patterns, to prevent nosocomial transmission of this disease. C1 UNIV TEXAS,CTR HLTH,CTR PULM INFECT DIS CONTROL,TYLER,TX 75710. UNIV TEXAS,CTR HLTH,DEPT MED,TYLER,TX 75710. VET ADM MED CTR,DEPT MED,LOS ANGELES,CA. BRONX VET ADM MED CTR,DEPT MED,NEW YORK,NY. MT SINAI SCH MED,NEW YORK,NY. UNIV ROCHESTER,DEPT MED,ROCHESTER,NY. RUSH MED COLL,DEPT MED,CHICAGO,IL 60612. COOK CTY HOSP,CHICAGO,IL 60612. SUNY HLTH SCI CTR,DEPT MED,BROOKLYN,NY 11203. LAKESIDE VET ADM MED CTR,DEPT MED,CHICAGO,IL 60611. NW UNIV,CHICAGO,IL. RAND CORP,SANTA MONICA,CA. RI Bennett, Charles/C-2050-2008; OI Goetz, Matthew/0000-0003-4542-992X FU AHRQ HHS [1R01HS06494-01, 1R03HS07846-01, HS-00032032] NR 40 TC 9 Z9 10 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD APR PY 1997 VL 18 IS 4 BP 237 EP 243 PG 7 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA WV963 UT WOS:A1997WV96300004 PM 9131365 ER PT J AU Shlaes, DM Gerding, DN John, JF Craig, WA Bornstein, DL Duncan, RA Eckman, MR Farrer, WE Greene, WH Lorian, V Levy, S McGowan, JE Paul, SM Ruskin, J Tenover, FC Watanakunakorn, C AF Shlaes, DM Gerding, DN John, JF Craig, WA Bornstein, DL Duncan, RA Eckman, MR Farrer, WE Greene, WH Lorian, V Levy, S McGowan, JE Paul, SM Ruskin, J Tenover, FC Watanakunakorn, C TI Society for Healthcare Epidemiology of America and Infectious Diseases Society of America Joint Committee on the Prevention of Antimicrobial Resistance: Guidelines for the prevention of antimicrobial resistance in hospitals SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID GRAM-NEGATIVE BACILLI; STAPHYLOCOCCUS-AUREUS; ANTIBIOTIC USE; AMIKACIN USE; AMINOGLYCOSIDE RESISTANCE; CIPROFLOXACIN RESISTANCE; CEPHALOSPORIN USE; ACTIVE EFFLUX; USAGE; SURVEILLANCE AB Antimicrobial resistance results in increased morbidity, mortality, and costs of health care. Prevention of the emergence of resistance and the dissemination of resistant microorganisms will reduce these adverse effects and their attendant costs. Appropriate antimicrobial stewardship that includes optimal selection, dose, and duration of treatment, as well as control of antibiotic use, will prevent or slow the emergence of resistance among microorganisms. A comprehensively applied infection control program will interdict the dissemination of resistant strains. C1 VET AFFAIRS LAKESIDE MED CTR,CHICAGO,IL. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,NEW BRUNSWICK,NJ. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. LAHEY CLIN FDN,BURLINGTON,MA. DULUTH CLIN LTD,DULUTH,MN. ST ELIZABETH HOSP,ELIZABETH,NJ. SUNY STONY BROOK,UNIV HOSP,STONY BROOK,NY 11794. BRONX LEBANON HOSP CTR,BRONX,NY 10456. TUFTS UNIV,SCH MED,BOSTON,MA 02111. GRADY MEM HOSP,ATLANTA,GA. NEW JERSEY STATE DEPT HLTH,TRENTON,NJ 08625. KAISER PERMANENTE MED CTR,LOS ANGELES,CA 90034. CTR DIS CONTROL & PREVENT,ATLANTA,GA. ST ELIZABETH HOSP,MED CTR,YOUNGSTOWN,OH 44501. RP Shlaes, DM (reprint author), WYETH AYERST RES,401 N MIDDLETOWN RD,PEARL RIVER,NY 10965, USA. RI mcgowan jr, john/G-5404-2011 NR 85 TC 163 Z9 170 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD APR PY 1997 VL 18 IS 4 BP 275 EP 291 PG 17 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA WV963 UT WOS:A1997WV96300013 PM 9131374 ER PT J AU Bani, L David, D Moreau, JL Cayota, A Nakarai, T Ritz, J Theze, J AF Bani, L David, D Moreau, JL Cayota, A Nakarai, T Ritz, J Theze, J TI Expression of the IL-2 receptor gamma subunit in resting human CD4 T lymphocytes: MRNA is constitutively transcribed and the protein stored as an intracellular component SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE CD4 T cells; cytokine responsiveness; IL-2; IL-2 receptor gamma chain ID BETA-CHAIN GENE; INTERLEUKIN-2 RECEPTOR; PERIPHERAL-BLOOD; HUMAN MONOCYTES; ENDOPLASMIC-RETICULUM; INTERFERON-GAMMA; ALPHA-CHAIN; CELLS; ACTIVATION; IDENTIFICATION AB IL-2 receptor (IL-2R) is composed of three subunits named IL-2R alpha, IL-2R beta and IL-2R gamma. Here, we study the expression of the IL-2R gamma in highly purified, resting peripheral human CD4 T lymphocytes. We show by FACS analysis that the IL-2R gamma subunit is not detectable at the cell surface of peripheral CD4 T lymphocytes. This result has been verified after acid treatment of the cell surface and analysis with three specific anti-IL-2R gamma mAb. Using RT-PCR and intracellular FACS analysis, we demonstrate that IL-2R gamma is constitutively expressed at the mRNA level and the protein is stored as an intracellular component in resting CD4 T lymphocytes. IL-2R alpha and beta subunits are not detectable by these methods. In addition, we show that CD4 T cells remain insensitive to a variety of cytokines that share IL-2R gamma as a common subunit of their receptors (e.g. IL-2, IL-4, IL-7 and IL-15). The kinetics of cell surface expression of IL-2R gamma have been studied after activation of CD4 T lymphocytes and compared with induction of IL-2R alpha and IL-2R beta. Maximum expression of IL-2R gamma is observed after 2 days of stimulation, and remains constant and comparable to IL-2R beta up to day 5. We conclude from these studies that IL-2R gamma is translocated to the membrane only after T cell activation and induction of the IL-2R alpha and IL-2R beta genes. We hypothesize that in CD4 T cells a large intracellular pool of IL-2R gamma is present but that its cell surface translocation depends on the expression of alpha and/or beta chains specific for IL-2, IL-4, IL-7, IL-9 or IL-15. C1 INST PASTEUR,UNITE IMMUNOGENET CELLULAIRE,F-75724 PARIS 15,FRANCE. INST PASTEUR,UNITE IMMUNOL & IMMUNOPATHOL,F-75724 PARIS 15,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES & TUMOR IMMUNOL,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619] NR 38 TC 28 Z9 28 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD APR PY 1997 VL 9 IS 4 BP 573 EP 580 DI 10.1093/intimm/9.4.573 PG 8 WC Immunology SC Immunology GA WV965 UT WOS:A1997WV96500013 PM 9138018 ER PT J AU Tsuji, K Uwano, T Yoshida, Y Kikuchi, K Okamoto, T Yamamoto, S Ichiki, M Hayashi, I Ohno, T Kufe, DW AF Tsuji, K Uwano, T Yoshida, Y Kikuchi, K Okamoto, T Yamamoto, S Ichiki, M Hayashi, I Ohno, T Kufe, DW TI Detection of the circulating lung cancer marker LCAP with a new monoclonal antibody TRD-L1 SO INTERNATIONAL JOURNAL OF BIOLOGICAL MARKERS LA English DT Article DE monoclonal antibody; adenocarcinoma; double-determinant immunoassay ID CARCINOEMBRYONIC ANTIGEN; BREAST-CANCER; TUMOR-MARKER; CARCINOMA; DF3 AB Lung Cancer Associated Protein (LCAP) is a high molecular weight glycoprotein defined by the monoclonal antibody (MAb) DF-L1 prepared against a primary adenocarcinoma of the lung. Previous studies have demonstrated that LCAP circulates at elevated levels in patients with lung cancer. However a suitable assay for monitoring LCAP levels has not been available. The present work describes the development of a double-determinant LCAP assay using MAb TRD-L1 as the capture antibody and MAb DF-L1 as the tracer. In 60 normal subjects, the mean LCAP level was 4.8 U/ml with 2 (3.3%) subjects having values >12 U/ml (mean + 2SDS). By contrast, 37 of 67 (55.2%) patients with lung cancer had LCAP levels >12 U/ml. Moreover, only 14 of 203 (6.9%) patients with benign lung disease had elevated levels. LCAP levels were most commonly elevated (62.7%) in patients with adenocarcinoma of the lung and with advanced disease. These results indicate that LCAP as detected by MAb TRD-L1 is a potentially useful marker for the evaluation of patients with lung cancer. C1 CANC INST HOSP,DEPT INTERNAL MED,TOKYO,JAPAN. JIKEI UNIV,SCH MED,DEPT MICROBIOL,TOKYO,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. RP Tsuji, K (reprint author), TERUMO CO LTD,CTR RES & DEV,1500 INOKUCHI,NAKAI,KANAGAWA 25901,JAPAN. NR 14 TC 0 Z9 0 U1 0 U2 0 PU WICHTIG EDITORE PI MILAN PA 72/74 VIA FRIULI, 20135 MILAN, ITALY SN 0393-6155 J9 INT J BIOL MARKER JI Int. J. Biol. Markers PD APR-JUN PY 1997 VL 12 IS 2 BP 49 EP 54 PG 6 WC Biotechnology & Applied Microbiology; Oncology SC Biotechnology & Applied Microbiology; Oncology GA XY513 UT WOS:A1997XY51300002 PM 9342632 ER PT J AU Lerner, LH Lerner, EA Bello, YM AF Lerner, LH Lerner, EA Bello, YM TI Co-existence of cutaneous and presumptive pulmonary alternariosis SO INTERNATIONAL JOURNAL OF DERMATOLOGY LA English DT Article AB A 71-year-old man presented with an asymptomatic lesion on the arm. He was born in rural West Virginia, spent several years in military service in the South Pacific, and is a long-term resident of Maine. He has chronic obstructive pulmonary disease, coronary artery disease, and noninsulin-dependent diabetes melitus. He was evaluated for episodes of hemoptysis by bronchoscopy in 1980 and 1984, but no cause was established. His usual medications included prednisone 10 mg daily. One month prior to the dermatology consultation the patient had been admitted to another hospital because of a flare-up of his lung disease. He was treated for 10 days with intravenous steroids and bronchodilators, resulting in improvement of his respiratory status. A cardiac pacemaker was inserted because of arrythmias. By the time of discharge, 1 week later, the prednisone dose had been tapered to his usual 10 mg daily. One week prior to the dermatology consultation, he was admitted to this institution for evaluation of recurrent atrial fibrillation. On admission, his chest X-ray revealed a pulmonary nodule which had not been present 1 month previously (Fig. 1a). The dermatology service was asked to evaluate an enlarging lesion on the right arm. The arm lesion began 2 weeks earlier as a group of papules which grew and coalesced. Two days prior to evaluation, the lesion had spontaneously drained purulent material. There was no pruritus or pain. The patient did not recall any similar skin problem in the past and had no history of trauma to the area. He reported a 30 lb weight loss in the 2 months prior to admission despite a good appetite. There was no history of fever or malaise. On examination, a 3.3 x 1.5 cm plaque was noted on the right extensor forearm just above the wrist (Fig. 2). The plaque was erythematous with a shiny atrophic epidermis and fine scale. One portion of the plaque had a red-yellow hue and was indurated while the other had a grey-blue pigmented appearance. The remainder of his skin examination was unremarkable. There was no adenopathy or hepatosplenomegaly. Routine laboratory tests were significant for hyperglycemia, a mildly elevated white blood cell count of 11.5 K/UL with a normal differential; lactate dehydrogenase was 325 U/L (normal, 88-196) and alkaline phosphatase 113 U/L (normal, 16-95). CT scan of the chest revealed emphysema and multiple bilateral pulmonary nodules with cavitation (Fig. 1b). A low attenuation region in the spleen was interpreted as representing an inflammatory or infectious focus, or, less likely, a cyst. CT scan of the abdomen revealed a normal liver and no abdominal adenopathy. Bone scan and ophthalmologic examination revealed no evidence of bony or ocular involvement. A 4-mm punch biopsy from the plaque on the wrist revealed suppurative granulomatous inflammation extending from the lower papillary dermis down to the deep dermis at the base of the biopsy specimen (Fig. 3a). Many multinucleated giant cells were observed. The overlying epidermis showed slight acanthosis with compaction and focal parakeratosis of the stratum corneum. In the dermis, numerous rounded structures and septate hyphae, measuring 5-9 microns in diameter, were present both within giant cells and extracellularly (Fig. 3b). These structures were stained by a Grocott methenamine silver stain, consistent with fungi (Fig. 3c). These findings, and the lack of encapsulation typically seen in subcutaneous phaeohyphomycosis, suggest a systemic fungal disease rather than direct cutaneous inoculation.(8) A second specimen was sent for culture to the University of Texas Health Science Center in San Antonio and grew Alternaria alternata (no further description is available). In retrospect, the pigment seen clinically may have resulted either from the fungus, which is typically pigmented, or from an ecchymosis. Sensitivity testing revealed that the fungus was susceptible to amphotericin 0.29 mu g/mL, itraconazole 0.07 mu g/mL, and ketoconazole 0.1 mu g/mL. Serum titers for complement-fixing antibodies to aspergillus and blastomyces were negative. Although no specific antifungal therapy was started, follow-up chest X-rays showed a dramatic decrease in the size of the pulmonary nodules (Fig. Ic). During the same week, the plaque on the arm also decreased in size to 2.7 x 1.4 cm. The alkaline phosphatase decreased to normal and the lactate dehydrogenase decreased to 261. The patient was discharged home without antifungal therapy, and prednisone was discontinued 10 days after discharge. The skin lesion resolved spontaneously. In the 2 years since presentation there has not been a recurrence of skin or lung lesions. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV DERMATOL,BOSTON,MA 02115. NR 12 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0011-9059 J9 INT J DERMATOL JI Int. J. Dermatol. PD APR PY 1997 VL 36 IS 4 BP 285 EP 288 PG 4 WC Dermatology SC Dermatology GA XA675 UT WOS:A1997XA67500012 PM 9169329 ER PT J AU Jones, MA Young, RH AF Jones, MA Young, RH TI Atypical oxyphilic metaplasia of the endocervical epithelium: A report of six cases SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE oxyphilic metaplasia; endocervical atypia ID UTERINE CERVIX; TUBAL METAPLASIA; ADENOCARCINOMA; DIAGNOSIS; LESIONS AB We report six examples of a hitherto undescribed atypical metaplastic change of the endocervical glandular epithelium that we have designated atypical oxyphilic metaplasia of the endocervical epithelium. The patients ranged in age from 41 to 62 (mean 47.8) years; one was postmenopausal. Gravidity ranged from one to five (mean 2.8) and parity from one to four (mean 2.7). At the time of diagnosis one patient was taking combined oral contraceptives and one was taking tamoxifen for breast cancer. All of the lesions were incidental findings and were unassociated with a gross abnormality. Microscopically, affected endocervical glands were lined by large cuboidal or polygonal epithelial cells with dense, eosinophilic, focally vacuolated cytoplasm and varying degrees of nuclear atypia. Nuclei were enlarged, hyperchromatic, and frequently multilobated or multinucleated. Rare apical snouts were present in two cases. Stratification and mitotic activity were absent. Rare, focal periodic acid-Schiff positivity with and without diastase predigestion was present in three of three cases. Mucin staining was negative in two of three cases and focally stained luminal secretions in one of three cases. Three of three cases were negative for GCDFP-15 and carcinoembryonic antigen. Meaningful follow-up in four patients ranged from 1 to 15 (mean 5.5) years and was uneventful in all of them. Atypical oxyphilic metaplasia of endocervical epithelium represents yet another benign endocervical glandular atypia that must be distinguished from more serious lesions. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02115. RP Jones, MA (reprint author), MAINE MED CTR,DEPT PATHOL,PORTLAND,ME 04102, USA. NR 17 TC 7 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1997 VL 16 IS 2 BP 99 EP 102 DI 10.1097/00004347-199704000-00003 PG 4 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA WQ673 UT WOS:A1997WQ67300002 PM 9100061 ER PT J AU OConnell, JX Young, RH Nielsen, GP Rosenberg, AE Bainbridge, TC Clement, PB AF OConnell, JX Young, RH Nielsen, GP Rosenberg, AE Bainbridge, TC Clement, PB TI Nodular fasciitis of the vulva: A study of six cases and literature review SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Review DE vulva; nodular fasciitis; pseudosarcoma ID SMOOTH-MUSCLE TUMORS; AGGRESSIVE ANGIOMYXOMA; ANGIOMYOFIBROBLASTOMA; NEOPLASM AB We report six cases of histologically typical nodular fasciitis that each presented as a vulvar soft tissue mass. The diagnosis of nodular fasciitis had not been considered by the referring pathologist in any of the five consultation cases. The patients' ages ranged from 7 to 51 years (mean 34). The lesion was confined to the labia in the four cases in which a specific site was noted, The masses ranged from 1.5 to 3.5 cm (mean 2.2) in maximal dimension. All of them were locally excised, and the resection margins were involved in each case. In addition to the typical features of nodular fasciitis, a noteworthy finding in two of the six cases was the presence of cleftlike spaces lined by plump synovial-like cells, Follow-up ranged from 3 months to 7 years (mean 24 months). A local recurrence developed in one patient at 4 months and was reexcised; there have been no recurrences in any other case. The literature contains only five additional examples of vulvar nodular fasciitis. Although all were pathologically typical, the diagnosis was often not considered, evidently because of the unusual location. Awareness that nodular fasciitis may occur in the vulva and the features that allow its distinction from other mesenchymal ''tumors'' occurring at this site will facilitate its correct diagnosis. C1 BRITISH COLUMBIA CANC AGCY,VANCOUVER CLIN,DEPT LAB MED,VANCOUVER,BC V5Z 4E6,CANADA. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP OConnell, JX (reprint author), VANCOUVER HOSP & HLTH SCI CTR,DEPT LAB MED,DIV ANAT PATHOL,910 W 10TH AVE,VANCOUVER,BC V5Z 4E3,CANADA. NR 17 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1997 VL 16 IS 2 BP 117 EP 123 DI 10.1097/00004347-199704000-00006 PG 7 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA WQ673 UT WOS:A1997WQ67300005 PM 9100064 ER PT J AU Quinn, TR Young, RH AF Quinn, TR Young, RH TI Epidermolytic hyperkeratosis in the lower female genital tract: An uncommon simulant of mucocutaneous papillomavirus infection - A report of two cases SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE vulva; vagina; epidermolytic hyperkeratosis; isolated epidermolytic acanthoma ID PAPULAR ACANTHOLYTIC DYSKERATOSIS; DISEASE AB Two examples of epidermolytic hyperkeratosis (EH) involving the female genital tract are described. The first case, an isolated epidermolytic acanthoma, involved the vulva of a 75-year-old woman. The second case involved the vaginal wall of a 40-year-old woman who had similar lesions of the oral mucosa. EH is characterized by epidermal acanthosis, compact papillomatous hyperkeratosis, and dissolution of the suprabasilar epithelium, resulting in perinuclear clear zones. Granular keratohyalin clumping, hypergranulosis, and dyskeratosis resulting in intracellular eosinophilic globules (''cell within a cell'' appearance) are additional distinctive findings. Because of the rarity of the lesion in the female genital tract, it may be confused with other lesions that more commonly affect this region. Correct recognition of EH may have significant clinical implications. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 33 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1997 VL 16 IS 2 BP 163 EP 168 DI 10.1097/00004347-199704000-00013 PG 6 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA WQ673 UT WOS:A1997WQ67300012 PM 9100071 ER PT J AU Tenner, S FernandezdelCastillo, C Warshaw, A Steinberg, W HermonTaylor, J Valenzuela, JE Hariri, M Hughes, M Banks, PA AF Tenner, S FernandezdelCastillo, C Warshaw, A Steinberg, W HermonTaylor, J Valenzuela, JE Hariri, M Hughes, M Banks, PA TI Urinary trypsinogen activation peptide (TAP) predicts severity in patients with acute pancreatitis SO INTERNATIONAL JOURNAL OF PANCREATOLOGY LA English DT Article DE acute pancreatitis; trypsinogen activation peptide; prognostic signs in acute pancreatitis ID APACHE-II; SYSTEM AB Conclusions. Urinary TAP obtained within the first 48 h of the onset of symptoms can distinguish patients with severe acute pancreatitis. Background. Urinary trypsinogen activation peptide (TAP) has recently been described as an early marker of severity in acute pancreatitis. Methods. In a multicenter study, urine samples were collected for TAP concentration at 6-12, 24, and 48 h after admission from 139 patients with acute pancreatitis (99 with mild disease, 40 with severe disease) and from 50 control patients. Severity of acute pancreatitis was defined by the presence of organ failure and/ or pancreatic necrosis on dynamic contrast-enhanced computed tomography. Results. Median urinary TAP in the 139 patients with acute pancreatitis compared to the 50 control patients was significantly higher at admission, 4.6 vs 0.8 ng/mL (p < 0.001), and 6-12 h, 1.9 vs 0.55 ng/mL (p = 0.04). Among patients who presented within 48 h of the onset of symptoms, the median urinary TAP for severe pancreatitis (9 patients) compared to mild pancreatitis (40 patients) was significantly higher at admission, 29.6 vs. 3.6 ng/mL (p = 0.0001). Also, when obtained within 48 h of the onset of symptoms, all patients with severe pancreatitis had an admission urinary TAP level > 10 ng/mL. The sensitivity and specificity of an admission urinary TAP greater than or equal to 10 for severe pancreatitis was 100 and 85%, respectively. Given a cutoff of 10 ng/mL for an admission urinary TAP obtained within 48 h of the onset of symptoms, the negative predictive value was 100% for mild pancreatitis. C1 BRIGHAM & WOMENS HOSP,DEPT MED,CTR PANCREAT DIS,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. ST GEORGE HOSP,SCH MED,LONDON,ENGLAND. UNIV SO CALIF,LOS ANGELES,CA. NR 16 TC 70 Z9 70 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0169-4197 J9 INT J PANCREATOL JI Int. J. Pancreatol. PD APR PY 1997 VL 21 IS 2 BP 105 EP 110 PG 6 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA XF635 UT WOS:A1997XF63500002 PM 9209951 ER PT J AU Shankar, P Serulneck, TM Dezube, BJ Lieberman, J AF Shankar, P Serulneck, TM Dezube, BJ Lieberman, J TI Drugs that inhibit herpesvirus DNA synthesis block in vitro activation of the Kaposi's Sarcoma-associated herpes virus (KSHV) in peripheral blood mononuclear cells. SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR 1 PY 1997 VL 14 IS 4 BP 40 EP 40 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA WU251 UT WOS:A1997WU25100074 ER PT J AU Hsu, YY Rasmussen, RA Trantolo, DJ Gresser, JD Wise, DL AF Hsu, YY Rasmussen, RA Trantolo, DJ Gresser, JD Wise, DL TI Antiretroviral DNA vaccine controlled release system from poly(D,L-lactide-co-glycolide) microparticles against HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NORTHEASTERN UNIV,DEPT CHEM ENGN,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR 1 PY 1997 VL 14 IS 4 BP 57 EP 57 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA WU251 UT WOS:A1997WU25100088 ER PT J AU Gill, PS Scadden, DT Groopman, J Tulpule, A Hajdenberg, J Mocharnuk, R Espina, BM Ilaw, M Bresnahan, J Cabriales, S Levine, AM Huybensz, S Winograd, B AF Gill, PS Scadden, DT Groopman, J Tulpule, A Hajdenberg, J Mocharnuk, R Espina, BM Ilaw, M Bresnahan, J Cabriales, S Levine, AM Huybensz, S Winograd, B TI Low dose paclitaxel (Taxol(R)) is highly effective in the treatment of patients with advanced AIDS-related Kaposi's sarcoma SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV SO CALIF,SCH MED,LOS ANGELES,CA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DEACONESS HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,WALLINGFORD,CT. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR 1 PY 1997 VL 14 IS 4 BP 77 EP 77 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA WU251 UT WOS:A1997WU25100108 ER PT J AU Mijailovich, SM Treppo, S Venegas, JG AF Mijailovich, SM Treppo, S Venegas, JG TI Effects of lung motion and tracer kinetics corrections on PET imaging of pulmonary function SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE regional lung function; respiratory gating; motion artifacts; nitrogen-13; positron emission tomography; alveolar ventilation; perfusion; ventilation-perfusion ratio ID POSITRON EMISSION TOMOGRAPHY; REGIONAL V/Q RATIOS; GAS-TRANSPORT; HIGH-FREQUENCY; SUPINE HUMANS; BLOOD-FLOW; VENTILATION; QUANTIFICATION; VOLUME AB A method to assess the three-dimensional distribution of alveolar ventilation-perfusion ratio ((V) over A/(Q) over dot) by imaging the lungs with positron emission tomography (PET) during a constant-rate intravenous infusion of (NN)-N-13-labeled saline solution was developed by C. G. Rhodes, S. O. Valind, L. H. Brudin, P. E. Wollmer, T. Jones, P. D. Buckingham, and J. M. B. Hughes (J. Appl. Physiol. 66: 1896-1904 and 1905-1913, 1989). We have modified this methodology to obtain high-resolution, low-noise PET images of local (V) over dot A/(Q) over dot where lung motion artifact was eliminated by respiratory gating of image collection. In addition, we have refined and implemented the methods to assess local alveolar ventilation by imaging the washout of equilibrated (NN)-N-13 and local perfusion by imaging the distribution of an intravenous bolus of (NN)-N-13-labeled saline solution during apnea. This paper experimentally evaluates the effect of the implemented modifications in mechanically ventilated and anesthetized dogs. We found that the lack of gating had no significant effect on the average recovered (V) over dot A/(Q) over dot, but the spatial heterogeneity [pixel-by-pixel coefficient of variation squared (CV2) = SD2/mean(2)] was underestimated by 14%. The lack of gating during the washout underestimated the average specific ventilation by 11% and decreased the corresponding CV2 by 50%. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 15 TC 38 Z9 38 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1997 VL 82 IS 4 BP 1154 EP 1162 PG 9 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA WT038 UT WOS:A1997WT03800019 PM 9104852 ER PT J AU Treppo, S Mijailovich, SM Venegas, JG AF Treppo, S Mijailovich, SM Venegas, JG TI Contributions of pulmonary perfusion and ventilation to heterogeneity in VA/Q measured by PET SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE positron emission tomography; body position; gas exchange; regional ventilation-perfusion ratio; dog; pulmonary heterogeneity; functional imaging ID POSITRON EMISSION TOMOGRAPHY; BLOOD-FLOW DISTRIBUTION; REGIONAL V/Q RATIOS; GAS-TRANSPORT; SPATIAL HETEROGENEITY; LUNG EXPANSION; SUPINE HUMANS; QUANTIFICATION; GRAVITY; VOLUME AB To estimate the contributions of the heterogeneity in regional perfusion ((Q) over dot) and alveolar ventilation ((V) over dot A) to that of ventilation-perfusion ratio ((V) over dot A/(Q) over dot), we have refined positron emission tomography (PET) techniques to image local distributions of (Q) over dot and VA per unit of gas volume content (s(Q) over dot and s(V) over dot A, respectively) and VA/(Q) over dot in dogs. s(V) over dot A was assessed in two ways: 1) the washout of (NN)-N-13 tracer after equilibration by rebreathing (s(V) over dot A(i)), and 2) the ratio of an apneic image after a bolus intravenous infusion of (NN)-N-13-saline solution to an image collected during a steady-state intravenous infusion of the same solution (s(V) over dot A(p)). s(V) over dot A(p) was systematically higher than s(V) over dot A(i) in all animals, and there was a high spatial correlation between s(Q) over dot and s(V) over dot A(p) in both body positions (mean correlation was 0.69 prone and 0.81 supine) suggesting that ventilation to well-perfused units was higher than to those poorly perfused. In the prone position, the spatial distributions of s(Q) over dot, s(V) over dot A(p), and (V) over dot A/(Q) over dot were fairly uniform with no significant gravitational gradients; however, in the supine position, these variables were significantly more heterogeneous, mostly because of significant gravitational gradients (15, 5.5, and -10%/cm, respectively) accounting for 73, 33, and 66% of the corresponding coefficient of variation (CV)(2) values. We conclude that, in the prone position, gravitational forces in blood and lung tissues are largely balanced out by dorsoventral differences in lung structure. In the supine position, effects of gravity and structure become additive, resulting in substantial gravitational gradients in s(Q) over dot and s(V) over dot A(p), with the higher heterogeneity in (V) over dot A/(Q) over dot caused by a gravitational gradient in s(Q) over dot, only partially compensated by that in s(V) over dot A. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Treppo, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-38267] NR 31 TC 68 Z9 69 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1997 VL 82 IS 4 BP 1163 EP 1176 PG 14 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA WT038 UT WOS:A1997WT03800020 PM 9104853 ER PT J AU Nosek, MT Martyn, JAJ AF Nosek, MT Martyn, JAJ TI Na+ channel and acetylcholine receptor changes in muscle at sites distant from burns do not simulate denervation SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE acetylcholine receptors in burns; sodium channel in burns; muscle weakness in burns; transcripts of muscle receptors in burns ID SKELETAL-MUSCLE; SODIUM-CHANNEL; MESSENGER-RNA; PROTEIN-KINASE; RAT-BRAIN; SUBUNIT; MODULATION; RESISTANCE; EXPRESSION; MYOGENIN AB Muscle weakness and aberrant responses to neuromuscular relaxants after burn injury are associated with upregulation of acetylcholine receptors (AChRs). Typically, these functional, pharmacological, and biochemical changes occur after denervation, in which transcriptionally mediated qualitative changes in AChRs and Na+ channels and of myogenic regulatory proteins MyoD and myogenin also occur. This study in rats, by an examination of changes in the above-enumerated proteins or their transcripts in the gastrocnemius muscle distant from the burn, verifies whether a denervation-like state exists after burns. Scatchard analysis of [H-3]saxitoxin binding revealed no changes in the affinity (K-d) and total number (B-max) of Na+ channels between control and burn-injured animals at both 7 and 14 days after injury. The mRNA levels of the immature proteins, SkM2 of the Na+ channels and the gamma-subunits of AChRs, the increase of which is pathognomic of denervation, were assessed by Northern analysis and were unchanged. The transcripts of mature Na+ channels, SkM1, were significantly increased at day 14 after the burn (1.24 +/- 0.10 in burn-injured vs. 1.06 +/- 0.12 in sham animals, arbitrary units, P = 0.006). Although MyoD levels were increased in burn-injured animals at 14 days (0.21 +/- 0.02 vs. 0.15 +/- 0.07 arbitrary units, P = 0.05), myogenin levels were unaltered. The absence of changes in AChR transcripts, including alpha-, delta-, and gamma-subunits, indicates that the upregulation of AChR in burns is not transcriptionally mediated. The unaltered levels of transcripts of myogenin, SkM2 of Na+ channels and gamma-subunit of AChR, confirm that there is no denervation-like prejunctional (nerve-related) component to explain the muscle weakness or the upregulation of AChRs at sites distant from burns. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANESTHESIA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT CRIT CARE,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. FU NIGMS NIH HHS [GM-31569-14, GM-55082-01] NR 32 TC 10 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1997 VL 82 IS 4 BP 1333 EP 1339 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA WT038 UT WOS:A1997WT03800040 PM 9104873 ER PT J AU McGrory, BJ Shinar, AA Freiberg, AA Harris, WH AF McGrory, BJ Shinar, AA Freiberg, AA Harris, WH TI Enhancement of the value of hip questionnaires by telephone follow-up evaluation SO JOURNAL OF ARTHROPLASTY LA English DT Article DE total hip arthroplasty; outcome studies; MOS 36-Item Short-Form Health Survey (SF-36); WOMAC osteoarthritis index; telephone call AB Errors, omissions, false understanding, and contradictory answers can compromise the use of questionnaires to generate follow-up data. To assess the utility of and effort involved in adding routinely a telephone interview to clarify the questionnaire, a study of total hip arthroplasty patients was carried out. Thirty-six patients with 37 primary and 13 revision total hip arthroplasties filled out a standardized questionnaire (which asks a number of demographic questions as well as questions that allow calculation of the Medical Outcome Studies [MOS] 36-Item Short-form Health Survey [SF-36], Western Ontario MacMaster Arthritis Center [WOMAC] osteoarthritis index, and Harris hip score) prior to returning for routine follow-up evaluation a minimum of 1 year after surgery. Two hundred thirty-two of a possible 4,350 responses (5.3%) were missing, contradictory, or answered with two or more answers on the questionnaire. Only eight such defects occurred following the telephone interview by a skilled orthopaedic surgeon, representing a significant reduction in these defects (P < .005). The average time of the telephone call was 2.8 minutes (range, 1-12 minutes), and the average number of attempts to contact the patient was 1.4 (range, 1-6). All questionnaire data and questionnaire data plus telephone data were compared with data obtained from a subsequent face-to-face interview by a different skilled orthopaedic surgeon who was blinded to the data from both the questionnaire and the telephone interview. It is demonstrated that a telephone call to follow up a standardized, self-administered questionnaire is a very effective way to augment the quality and quantity of questionnaire responses. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. NR 10 TC 32 Z9 33 U1 0 U2 2 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0883-5403 J9 J ARTHROPLASTY JI J. Arthroplast. PD APR PY 1997 VL 12 IS 3 BP 340 EP 343 DI 10.1016/S0883-5403(97)90033-4 PG 4 WC Orthopedics SC Orthopedics GA WU688 UT WOS:A1997WU68800016 PM 9113551 ER PT J AU Bal, BS Jiranek, WA Jasty, M Harris, WH AF Bal, BS Jiranek, WA Jasty, M Harris, WH TI Periprosthetic femoral osteolysis around an uncemented nonmodular Moore prosthesis SO JOURNAL OF ARTHROPLASTY LA English DT Article DE periprosthetic osteolysis; joint arthroplasty; Moore prosthesis AB Periprosthetic osteolysis is a major problem in total joint arthroplasty surgery today. The particulate debris from ultrahigh-molecular-weight polyethylene, polymethyl methacrylate, and corrosion products from modular connections have been implicated in this process. A case of femoral osteolysis at the tip of a nonmodular Moore prosthesis, in the absence of polyethylene, polymethyl methacrylate, and modular connections, is reported. In the area of osteolysis, histochemical and in situ hybridization techniques established the expression of messenger ribonucleic acid encoding for certain cytokines implicated in bone resorption, preferentially in the area of osteolysis. This case illustrates that the etiology of periprosthetic osteolysis is multifactorial and can occur in the absence of polyethylene, methacrylate, or modular components. All joint implants should be monitored for the development of this complication. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. OI Bal, B. Sonny/0000-0002-9615-8632 NR 15 TC 5 Z9 5 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0883-5403 J9 J ARTHROPLASTY JI J. Arthroplast. PD APR PY 1997 VL 12 IS 3 BP 346 EP 349 DI 10.1016/S0883-5403(97)90035-8 PG 4 WC Orthopedics SC Orthopedics GA WU688 UT WOS:A1997WU68800018 PM 9113553 ER PT J AU Chapman, MW Bucholz, R Cornell, C AF Chapman, MW Bucholz, R Cornell, C TI Treatment of acute fractures with a collagen-calcium phosphate graft material - A randomized clinical trial SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID BONE; DEFECTS AB A prospective, randomized clinical trial was conducted concurrently at eighteen medical centers in order to compare the safety and efficacy of two types of graft material for the treatment of fractures of long bones: autogenous bone graft obtained from the iliac crest, and a composite material composed of purified bovine collagen, a biphasic calcium-phosphate ceramic, and autogenous marrow, Two hundred and thirteen patients (249 fractures) were followed for a minimum of twenty-four months to monitor healing and the occurrence of complications. We observed no significant differences between the two treatment groups with respect to rates of union (p = 0.94, power = 88 per cent) or functional measures (use of analgesics, pain with activities of daily living, and impairment in activities of daily living; p > 0.10). The prevalence of complications did not differ between the treatment groups except for the rate Of infection, which was higher in the patients who were managed with an autogenous graft. Twelve patients who were managed with a synthetic graft had a positive antibody titer to bovine collagen; seven of them agreed to have intradermal challenge with bovine collagen, One patient had a positive skin response to the challenge but had no complications with regard to healing of the fracture. We concluded that, for traumatic defects of long bones that necessitate grafting, use of the composite graft material appears to be justified on the grounds of safety, efficacy, and elimination of the increased operative time and risk involved in obtaining an autogenous graft from the iliac crest. C1 ST PAUL RAMSEY MED CTR,ST PAUL,MN 55101. HERMANN HOSP,HOUSTON,TX. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. HENNEPIN CTY MED CTR,MINNEAPOLIS,MN. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. HAMOT MED CTR,ERIE,PA. SAN BERNARDINO CTY MED CTR,SAN BERNARDINO,CA. ERIE CTY MED CTR & LABS,ERIE,PA. WILLIAM WISHARD MEM HOSP,INDIANAPOLIS,IN. REG MED CTR,MEMPHIS,TN. UNIV LOUISVILLE,HUMANA HOSP,LOUISVILLE,KY 40292. GERMANTOWN HOSP & MED CTR,PHILADELPHIA,PA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. TAMPA GEN HOSP,TAMPA,FL 33606. UNIV CALIF DAVIS,MED CTR,DEPT ORTHOPAED SURG,SACRAMENTO,CA 95817. UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. HOSP SPECIAL SURG,NEW YORK,NY 10021. RP Chapman, MW (reprint author), UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103, USA. NR 15 TC 130 Z9 140 U1 1 U2 5 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 APR PY 1997 VL 79A IS 4 BP 495 EP 502 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA WU515 UT WOS:A1997WU51500004 PM 9111393 ER PT J AU Jupiter, JB Gerhard, HJ Guerrero, J Nunley, JA Levin, LS AF Jupiter, JB Gerhard, HJ Guerrero, J Nunley, JA Levin, LS TI Treatment of segmental defects of the radius with use of the vascularized osteoseptocutaneous fibular autogenous graft SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID FLAP; TRANSPLANT AB Nine patients who had a complex, combined skeletal and sofa-tissue defect involving the radius were managed with operative reconstruction with use of a vascularized osteoseptocutaneous fibular autogenous graft, All of the patients were male, and the average age was thirty-two Sears (range, twenty-one to forty-two years). Three patients sustained the injury as the result of a gunshot wound and two each, as the result of a motor-vehicle accident, a fall from a height, or a machinery-related accident. Five patients had a concomitant fracture of the ulna. The average length of the radial defect was seven centimeters. Six patients had a deep osseous infection. The average length of the fibular autogenous graft was 7.9 centimeters, and the average size of the associated fasciocutaneous component was 11.8 by 5.9 centimeters, Two patients had a concomitant arthrodesis of the wrist, A split-thickness skin graft was used to close the donor site in six patients, Two patients had postoperative vascular complications that necessitated revision with an autogenous vein graft. One patient had a second operation six months postoperatively to correct an angular deformity that had developed secondary to a non-union at the graft-host hone junction. After an average duration of follow-up of twenty-four months, all hut one of the patients had radiographic evidence of osseous union at both the proximal and the distal graft-host bone junction, No patient had evidence of resorption of tile graft or symptoms referable to the donor leg at the time of the most recent examination, Six patients had returned to their preinjury occupation. C1 DUKE UNIV,MED CTR,DEPT SURG,DIV ORTHOPAED SURG,DURHAM,NC 27710. CTR MEDICO CARACAS,CARACAS,VENEZUELA. RP Jupiter, JB (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,WAC-527,BOSTON,MA 02114, USA. NR 32 TC 68 Z9 70 U1 0 U2 2 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 APR PY 1997 VL 79A IS 4 BP 542 EP 550 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA WU515 UT WOS:A1997WU51500009 PM 9111398 ER PT J AU Buckwalter, JA Mankin, HJ AF Buckwalter, JA Mankin, HJ TI Articular cartilage .1. Tissue design and chondrocyte-matrix interactions SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID FETAL EPIPHYSEAL CARTILAGE; AGE-RELATED-CHANGES; PROTEIN COMP; PROTEOGLYCANS; COLLAGEN; OSTEOARTHRITIS; FIBROMODULIN; BEHAVIOR; JOINT; TENASCIN C1 MASSACHUSETTS GEN HOSP, OSRTHOPAED SERV, BOSTON, MA 02114 USA. RP Buckwalter, JA (reprint author), UNIV IOWA, COLL MED, DEPT ORTHOPAED, 01013 PAPPAJOHN PAVIL, IOWA CITY, IA 52242 USA. NR 78 TC 309 Z9 321 U1 3 U2 40 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 USA SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD APR PY 1997 VL 79A IS 4 BP 600 EP 611 PG 12 WC Orthopedics; Surgery SC Orthopedics; Surgery GA WU515 UT WOS:A1997WU51500021 ER PT J AU Buckwalter, JA Mankin, HJ AF Buckwalter, JA Mankin, HJ TI Articular cartilage .2. Degeneration and osteoarthrosis, repair, regeneration, and transplantation SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Review ID CONTINUOUS PASSIVE MOTION; FULL-THICKNESS DEFECTS; GROWTH-FACTOR-I; OSTEOCHONDRAL ALLOGRAFTS; FIBRONECTIN FRAGMENTS; PERIOSTEAL GRAFTS; KNEE-JOINT; POSTTRAUMATIC DEFECTS; ARTHROSCOPIC LAVAGE; SUBCHONDRAL BONE C1 MASSACHUSETTS GEN HOSP, ORTHOPAED SERV, BOSTON, MA 02114 USA. RP Buckwalter, JA (reprint author), UNIV IOWA, COLL MED, DEPT ORTHOPAED, 01013 PAPPAJOHN PAVIL, IOWA CITY, IA 52242 USA. NR 168 TC 543 Z9 551 U1 8 U2 48 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 USA SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD APR PY 1997 VL 79A IS 4 BP 612 EP 632 PG 21 WC Orthopedics; Surgery SC Orthopedics; Surgery GA WU515 UT WOS:A1997WU51500022 ER PT J AU Samuels, MH Veldhuis, JD Kramer, P Urban, RJ Bauer, R Mundy, GR AF Samuels, MH Veldhuis, JD Kramer, P Urban, RJ Bauer, R Mundy, GR TI Episodic secretion of parathyroid hormone in postmenopausal women: Assessment by deconvolution analysis and approximate entropy SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID FREQUENCY-MODULATION; CIRCADIAN-RHYTHM; PULSE AMPLITUDE; IMMUNORADIOMETRIC ASSAY; OSTEOPOROTIC PATIENTS; PULSATILE SECRETION; TRABECULAR BONE; DOWN-REGULATION; PTH-RECEPTOR; CALCIUM AB In healthy young subjects, parathyroid hormone (PTH) is secreted presumptively in a dual fashion,,vith low amplitude pulses apparently superimposed on tonic secretion, In contrast, PTH secretion has not been as well characterized in postmenopausal women, and relationships among bone density, estrogen status, and PTH release have not been explored, It is possible that a pulsatile pattern of PTH secretion is important for bone remodeling, since exogenous PTH administered in a pulsatile manner stimulates bone formation, To assess the importance of pulsatile PTH secretion as a determinant of bone mass,,ve measured PTH in blood sampled every 2 minutes for 6 h in four groups of older women: (1) high bone density receiving estrogen (n = 6), (2) high bone density not receiving estrogen (n = 5), (3) low bone density receiving estrogen (n = 6), and (4) low bone density not receiving estrogen (n = 8), The plasma PTH release profiles were subjected to deconvolution analysis, which resolves measured hormone concentrations into secretion and clearance components, and to an approximate entropy (ApEn) estimate, which provides an ensemble measure of the serial regularity or orderliness of the release process, In postmenopausal subjects, PTH was secreted in a fashion similar to that observed in young adults, with significant tonic secretion and PTH pulse occurrences averaging every 18-19 minutes, Pulsatile PTH secretion accounted for approximately 25% of the total secreted PTH, There were no differences in the amplitude or frequency of pulsatile PTH secretory parameters or in ApEn values among the four groups or compared,vith young controls, We conclude that in postmenopausal women, PTH secretory patterns and temporal organization are similar to those in healthy young subjects and are not altered in states of low bone density or estrogen deficiency, This suggests that abnormalities in orderly pulsatile PTH secretion are unlikely to play a major role in established postmenopausal osteoporosis. C1 UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA. NSF,CTR BIOL TIMING,CHARLOTTESVILLE,VA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. RP Samuels, MH (reprint author), OREGON HLTH SCI UNIV,DIV ENDOCRINOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NCRR NIH HHS [M01-RR01346, M01-RR00334]; NICHD NIH HHS [K04-HD-00634] NR 35 TC 12 Z9 13 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1997 VL 12 IS 4 BP 616 EP 623 DI 10.1359/jbmr.1997.12.4.616 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WR370 UT WOS:A1997WR37000014 PM 9101373 ER PT J AU Hadjis, TA Stevenson, WG Harada, T Friedman, PL Sager, P Saxon, LA AF Hadjis, TA Stevenson, WG Harada, T Friedman, PL Sager, P Saxon, LA TI Preferential locations for critical reentry circuit sites causing ventricular tachycardia after inferior wall myocardial infarction SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY LA English DT Article DE ventricular tachycardia; inferior wall myocardial infarction; reentry circuits ID HUMAN HEART; SLOW CONDUCTION; ACTIVATION; ORIGIN; ENTRAINMENT; ABLATION; ISTHMUS AB Reentrant VT Post MI. Introduction: For relatively slow monomorphic ventricular tachycardia (VT) after myocardial infarction, entrainment can be used to identify reentry circuit ''isthmus sites'' (exit sites and sites proximal to the exit) where radiofrequency (RF) catheter ablation has the greatest likelihood of interrupting reentry, Similarities in coronary and ventricular anatomy may cause such sites to form in preferential locations, The objective of this study is to determine if there are preferential locations for reentry circuit isthmus regions in chronic inferior wall infarctions causing VT. Methods and Results: Catheter mapping and RF catheter ablation was performed in 21 patients with an old inferior wall myocardial infarction and VT, The inferior wall was divided into 9 anatomic regions: 3 apical, 3 mid, and 3 basal segments, Of 46 different VTs, an endocardial isthmus site was identified in one or more zones in 28 (61%), with 10 VTs having isthmus sites in two or more adjacent regions, Isthmus zones were found in a basal region of the left ventricle in 24 (86%) of 28 VTs, in a mid segment in 9 (32%) VTs, and in an apical segment in 1 (4%) (P = 0.002), Of 30 RF current applications that terminated VT, 21 (70%) were at basal isthmus sites. Conclusion: The high prevalence of endocardial isthmus zones near the base of the left ventricle suggests that the mitral annulus often plays a role in defining the margins of reentry circuits that cause relatively slow VTs after inferior wall myocardial infarction. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. NR 17 TC 34 Z9 34 U1 1 U2 3 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 1045-3873 J9 J CARDIOVASC ELECTR JI J. Cardiovasc. Electrophysiol. PD APR PY 1997 VL 8 IS 4 BP 363 EP 370 DI 10.1111/j.1540-8167.1997.tb00801.x PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA WT367 UT WOS:A1997WT36700001 PM 9106421 ER PT J AU Sattler, M Salgia, R Durstin, MA Prasad, KV Griffin, JD AF Sattler, M Salgia, R Durstin, MA Prasad, KV Griffin, JD TI Thrombopoietin induces activation of the phosphatidylinositol-3' kinase pathway and formation of a complex containing p85(PI3K) and the protooncoprotein p120(CBL) SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID C-CBL PROTOONCOGENE; GROWTH-FACTOR RECEPTOR; MPL LIGAND; TYROSINE PHOSPHORYLATION; SH3 DOMAIN; MOLECULAR-CLONING; PROTEIN PRODUCT; LEUKEMIA-VIRUS; ERYTHROID PROGENITORS; HEMATOPOIETIC-CELLS AB Thrombopoietin (TPO) promotes megakaryocyte growth and development. Its receptor, c-MPL, is restricted to cells of megakaryocytic lineage and stem cells. We have previously shown that activation of c-MPL by thrombopoietin rapidly activates at least two cytoplasmic tyrosine kinases, JAK2 and TYK2, after ligand binding. Phosphatidylinositol-3' kinase (PI3K) has been shown to play an important role in downstream signaling for many receptors. Thrombopoietin was found to also rapidly activate phosphatidylinositol-3' kinase, and the phosphatidylinositol-3' kinase inhibitor wortmannin decreased proliferation of thrombopoietin-stimulated cells, implying that phosphatidylinosilol-3' kinase may have a regulatory role in thrombopoietin signaling. In immunoprecipitation studies, the regulatory subunit of phosphatidylinositol-3' kinase, p85(PI3K), associated With several tyrosine phosphoproteins, and the major phosphoprotein was a 120 kDa protein identified as p120(CBL). The phosphatidylinositol-3' kinase-enzyme activity in p120(CBL) immunoprecipitates was elevated in thrombopoietin-stimulated cells as compared to immunoprecipitates from unstimulated cells. p120(CBL) may be involved in signaling pathways activated by c-MPL which involve phosphatidylinositol-3' kinase. (C) 1997 Wiley-Liss, Inc. C1 DANA FARBER CANC INST, DIV HEMATOL MALIGNANCIES, BOSTON, MA 02115 USA. DANA FARBER CANC INST, DIV TUMOR IMMUNOL, BOSTON, MA 02115 USA. NR 49 TC 31 Z9 31 U1 0 U2 2 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1997 VL 171 IS 1 BP 28 EP 33 PG 6 WC Cell Biology; Physiology SC Cell Biology; Physiology GA WQ865 UT WOS:A1997WQ86500004 PM 9119889 ER PT J AU Hara, H Fink, K Endres, M Friedlander, RM Gagliardini, V Yuan, JY Moskowitz, MA AF Hara, H Fink, K Endres, M Friedlander, RM Gagliardini, V Yuan, JY Moskowitz, MA TI Attenuation of transient focal cerebral ischemic injury in transgenic mice expressing a mutant ICE inhibitory protein SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE DNA fragmentation; infarction; interleukin-1 beta converting enzyme; mutant mice; neurological deficit; transient focal ischemia ID DNA FRAGMENTATION; CYSTEINE PROTEASE; BRAIN INJURY; CELL-DEATH; APOPTOSIS; RAT; INTERLEUKIN-1; MECHANISMS; CLEAVES; DAMAGE AB We used transgenic mice expressing a dominant negative mutation of interleukin-1 beta converting enzyme (ICE) (C285G) in a model of transient focal ischemia in order to investigate the role of ICE in ischemic brain damage. Transgenic mutant ICE mice (n = 11) and wild-type littermates (n = 9) were subjected to 3 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Cerebral infarcts and brain swelling were reduced by 44% and 46%, respectively. Neurological deficits were also significantly reduced. Regional CBF, blood pressure, core temperature, and heart rate did not differ between groups when measured for up to 1 h after reperfusion. Increases in immunoreactive IL-1 beta levels, observed in ischemic wild-type brain at 30 min after repel-fusion, were 77% lower in the mutant strain, indicating that proLL-1 beta cleavage is inhibited in the mutants. DNA fragmentation was reduced in the mutants 6 and 24 h after reperfusion. Hence, endogenous expression of an ICE inhibitor confers resistance to cerebral ischemia and brain swelling. Our results indicate that downregulation of ICE expression might provide a useful therapeutic target in cerebral ischemia. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,NEUROSURG SERV,STROKE & NEUROVASC REGULAT,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT NEUROL,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT MED,CARDIOVASC RES CTR,CHARLESTOWN,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROSURG SERV,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,CHARLESTOWN,MA. RI Moskowitz, Michael/D-9916-2011; Friedlander, Robert/A-2845-2016 OI Friedlander, Robert/0000-0003-4423-9219 FU NINDS NIH HHS [NS10828] NR 35 TC 199 Z9 208 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD APR PY 1997 VL 17 IS 4 BP 370 EP 375 DI 10.1097/00004647-199704000-00002 PG 6 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA WW738 UT WOS:A1997WW73800002 PM 9143219 ER PT J AU Kelly, SJ Macaruso, P Sokol, SM AF Kelly, SJ Macaruso, P Sokol, SM TI Mental calculation in an autistic savant: A case study SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID IDIOT SAVANT; CALENDRICAL CALCULATORS; ABILITY; MEMORY AB We present a detailed investigation of mental calculation in RH. an autistic savant. In Experiment 1 RH performed faster anti more accurately than control subjects in mentally solving multi-digit multiplication problems. However, we found no evidence that RH employed short-cut strategies to solve these problems. His response times were consistent with application of a left-to-right computational procedure employed by expert calculators. He also responded extremely quickly to 2-digit squares, suggesting that he may have memorized the answers. In Experiment 2 we taught RH a new computational algorithm for converting temperatures from Celsius to Fahrenheit. RH was able to learn the new algorithm. but required much assistance and made only slight gains with practice. RH did not recognize an easy solution strategy based on inverting steps in the conversion algorithm. We suggest that the inflexible nature of RH's performance may reflect his autistic tendencies coupled with limited intelligence. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,GRAD PROGRAM COMMUN SCI & DISORDERS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,NEUROLINGUIST LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,CAMBRIDGE,MA 02138. NR 31 TC 11 Z9 11 U1 0 U2 5 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD APR PY 1997 VL 19 IS 2 BP 172 EP 184 DI 10.1080/01688639708403848 PG 13 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA XC634 UT WOS:A1997XC63400002 PM 9240477 ER PT J AU Kotlar, TJ Young, RH Albanese, C Crowley, WF Scully, RE Jameson, JL AF Kotlar, TJ Young, RH Albanese, C Crowley, WF Scully, RE Jameson, JL TI A mutation in the follicle-stimulating hormone receptor occurs frequently in human ovarian sex cord tumors SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GRANULOSA-CELL TUMOR; CLINICOPATHOLOGICAL ANALYSIS; PRECOCIOUS PUBERTY; TSH-RECEPTOR; GENE; INHIBIN; PURIFICATION; NEOPLASMS; ALPHA; MICE AB A subset of ovarian tumors, referred to as sex cord-stromal tumors, produce endocrine manifestations due to the secretion of estrogens or androgens. Because gonadotropins induce the growth, differentiation, and function of the steroid-producing cells of the ovary, we hypothesized that mutations in the FSH receptor (FSH-R) might occur in this group of tumors. Ovarian sex cord tumors (n = 13), small cell carcinomas of the ovary (n = 3), and control DNA specimens (n = 116) were screened for mutations in the transmembrane domains of the FSH-R. A heterozygous T-->C mutation was found at nucleotide 1777 that converts codon 591 from phenylalanine to serine (F591S). This sixth transmembrane domain mutation was found in 9 of 13 (69%) sex cord tumors and 2 of 3 ovarian small cell carcinomas, but it was not present in control specimens, including 5 normal ovaries, 5 nonsex cord ovarian tumors, 16 thyroid tumors, or 90 specimens of peripheral blood leukocyte DNA, suggesting that this nucleotide change is not a polymorphism. The functional effects of identified mutations were assessed by expression of the wild-type or the F591S mutant FSH-R in COS-7 cells. The F591S mutation eliminated FSH-stimulated cAMP production, and a similar effect was observed when this mutation was introduced into the homologous location of the LH receptor. The high prevalence of the F591S mutation in the FSH-R suggests that it plays a role in the development of ovarian sex cord tumors. C1 NORTHWESTERN UNIV, SCH MED, DIV ENDOCRINOL METAB & MOL MED, CHICAGO, IL 60611 USA. HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [U54-HD-29164] NR 37 TC 51 Z9 56 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1997 VL 82 IS 4 BP 1020 EP 1026 DI 10.1210/jc.82.4.1020 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WT034 UT WOS:A1997WT03400009 PM 9100567 ER PT J AU Chaidarun, SS Klibanski, A Alexander, JM AF Chaidarun, SS Klibanski, A Alexander, JM TI Tumor-specific expression of alternatively spliced estrogen receptor messenger ribonucleic acid variants in human pituitary adenomas SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID BREAST TISSUES; GROWTH; CELLS; TRANSCRIPTION; GENE AB The well documented mitogenic and hormone regulatory effects of estrogen (E(2)) on pituitary cells are mediated via its nuclear receptor (ER), a cellular homolog of v-erbA oncogene. ER isoforms generated by alternative exon splicing, termed ER variants Delta 2ER to Delta 7ER, have been identified in breast cancer and have been postulated to have important pathogenetic and clinical implications in tumorigenesis and/or development of hormone resistance. Because pituitary tumors, particularly prolactinomas, are known to be E(2)-dependent, we investigated alternatively spliced ER variant messenger ribonucleic acid expression in 40 human pituitary tumors of various phenotypes and normal pituitary tissues, using reverse transcription-PCR and Southern blot analyses. Nine of 11 prolactinomas readily expressed multiple ER variants (Delta 2ER, Delta 4ER, Delta 5ER, and Delta 7ER), whereas 6 of 11 tumors showed faint expression of Delta 3ER. Four of 7 glycoprotein hormone-producing tumors that synthesized FSH beta expressed Delta 2ER, Delta 5ER, and Delta 7ER. In 9 GH- and 10 ACTH-secreting tumors examined, the expression of normal and variant ER was restricted to tumors that also exhibited scattered PRL immunoreactivity. Variant and normal ER were not found in three null cell tumors (oncocytomas) that showed negative immunoreactivity for all pituitary hormones or their subunits. In contrast, only Delta 4ER and Delta 7ER were uniformly detected in normal pituitaries. Delta 6ER was not detected in any normal or neoplastic pituitary specimen studied. We conclude that multiple alternatively spliced ER variants are coexpressed with normal ER in a tumor phenotype-specific manner. In addition, ER variants Delta 2ER and Delta 5ER were found to be tumor specific. Future functional studies will be required to determine whether coexpression of multiple ER variants along with normal ER confers a pathophysiological role in pi pituitary hormone regulation and/or tumor cell proliferation. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP Chaidarun, SS (reprint author), MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, DEPT MED, BULFINCH 457, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-40947] NR 26 TC 36 Z9 38 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1997 VL 82 IS 4 BP 1058 EP 1065 DI 10.1210/jc.82.4.1058 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WT034 UT WOS:A1997WT03400015 PM 9100573 ER PT J AU McHorney, CA Haley, SM Ware, JE AF McHorney, CA Haley, SM Ware, JE TI Evaluation of the MOS SF-36 physical functioning scale (PF-10) .2. Comparison of relative precision using Likert and Rasch scoring methods SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE health status assessment; physical functioning; measurement precision; item response theory; Rasch rating scale analysis ID HEALTH-STATUS MEASURES; APPLYING PSYCHOMETRIC CRITERIA; QUALITY-OF-LIFE; MEDICAL REHABILITATION; PRIMARY CARE; RELIABILITY; FRAMEWORK; VALIDITY; UNIDIMENSIONALITY; REPRODUCIBILITY AB This study examined the relative precision (RP) of two methods of scoring the 10-item Physical Functioning Scale (PF-10) from a large sample of patients (n = 3445) of the Medical Outcomes Study. Based on a Likert scaling model, the PF-10 summated scoring method was compared with a Rasch Item Response Theory (IRT) scaling model in which raw scores were transformed into a latent trait variable of physical functioning. Potential differences between scoring methods were hypothesized to be attributed to: (1) the logarithmic nature of the Rasch transformation; (2) the unevenness of the PF-10 item distributions; and (3) reduction of within-group variance. RP ratios favored the Rasch model in discriminating between patients who differed in disease severity. The Rasch and Likert scoring models performed similarly for tests involving sensitivity to change over a two-year follow up period. In all comparisons, differences between methods were most apparent in clinical groups whose scores most approximated the extremes of the score distribution. Further research is necessary to test for differences between scoring models in discrimination and sensitivity to change among clinical groups whose scores are sufficiently spread across thr continuum of physical functioning, in particular patients with either very high or low physical functioning. The Rasch model of scoring may have important implications for the clinical interpretation of individual scores at all ranges of the scale. (C) 1997 Elsevier Science Inc. C1 UNIV WISCONSIN,SCH MED,DEPT PREVENT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53705. NEW ENGLAND REHABIL HOSP,WOBURN,MA 01801. TUFTS UNIV,NEW ENGLAND MED CTR HOSP,HLTH INST,BOSTON,MA 02111. RP McHorney, CA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HLTH SERV RES & DEV PROGRAM,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. RI Page, Andrew/G-5438-2012 OI Page, Andrew/0000-0003-3133-2844 NR 55 TC 142 Z9 145 U1 1 U2 10 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD APR PY 1997 VL 50 IS 4 BP 451 EP 461 DI 10.1016/S0895-4356(96)00424-6 PG 11 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA WX076 UT WOS:A1997WX07600011 PM 9179104 ER PT J AU Tsukaguchi, H Shayakul, C Berger, UV Tokui, T Brown, D Hediger, MA AF Tsukaguchi, H Shayakul, C Berger, UV Tokui, T Brown, D Hediger, MA TI Cloning and characterization of the urea transporter UT3 - Localization in rat kidney and testis SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE urea transport; urinary concentration; kidney; testis; spermatocyte ID MEDULLARY COLLECTING DUCT; DESCENDING VASA-RECTA; FUNCTIONAL EXPRESSION; WATER CHANNEL; CELLS AB Urea transport in the kidney plays an important role in urinary concentration and nitrogen balance. Recently, three types of urea transporters have been cloned, UT1 and UT2 from rat and rabbit kidney and HUT11 from human bone marrow, To elucidate the physiological role of the latter urea transporter, we have isolated the rat homologue (UT3) of HUT11 and studied its distribution of expression and functional characteristics. UT3 cDNA encodes a 384 amino acid residue protein, which has 80% identity to the human HUT11 and 62% identity to rat UT2. Functional expression in Xenopus oocytes induced a large (similar to 50-fold) increase in the uptake of urea compared with water-injected oocytes. The uptake was inhibited by phloretin (0.75 mM) and pCMBS (0.5 mM) (55 and 32% inhibition, respectively). Northern analysis gave a single band of 3.8 kb in kidney inner and outer medulla, testis, brain, bone marrow, spleen, thymus, and lung, In situ hybridization of rat kidney revealed that UT3 mRNA is expressed in the inner stripe of the outer medulla, inner medulla, the papillary surface epithelium, and the transitional urinary epithelium of urinary tracts. Co-staining experiments using antibody against van Willebrand factor showed that UT3 mRNA in the inner stripe of the outer medulla is expressed in descending vasa recta. These data suggest that UT3 in kidney is involved in counter current exchange between ascending and descending vasa recta, to enhance the cortico-papillary osmolality gradient, In situ hybridization of testis revealed that UT3 is located in Sertoli cells of seminiferous tubules. The signal was only detected in Sertoli cells associated with the early stages of spermatocyte development, suggesting that urea may play a role in spermatogenesis. C1 HARVARD UNIV,DIV RENAL,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02129. FU NIDDK NIH HHS [R01-DK 70784, R01-DK 42956] NR 38 TC 92 Z9 93 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 1 PY 1997 VL 99 IS 7 BP 1506 EP 1515 DI 10.1172/JCI119313 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA WT444 UT WOS:A1997WT44400009 PM 9119994 ER PT J AU Lilly, CM Nakamura, H Kesselman, H NaglerAnderson, C Asano, K GarciaZepeda, EA Rothenberg, ME Drazen, JM Luster, AD AF Lilly, CM Nakamura, H Kesselman, H NaglerAnderson, C Asano, K GarciaZepeda, EA Rothenberg, ME Drazen, JM Luster, AD TI Expression of eotaxin by human lung epithelial cells - Induction by cytokines and inhibition by glucocorticoids SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE chemokine; eosinophil; cytokine; asthma; allergic disease ID COLONY-STIMULATING FACTOR; GUINEA-PIG MODEL; AIRWAY INFLAMMATION; MESSENGER-RNA; BRONCHOALVEOLAR LAVAGE; ENDOTHELIAL-CELLS; RICH SEQUENCES; ASTHMA; INTERLEUKIN-8; DEXAMETHASONE AB Eotaxin is a potent and specific eosinophil chemoattractant that is mobilized in the respiratory epithelium after allergic stimulation. Pulmonary levels of eotaxin mRNA are known to increase after allergen exposure in sensitized animals. Pn this study we demonstrate that TNF alpha and IL-1 beta induce the accumulation of eotaxin mRNA in the pulmonary epithelial cell lines A549 and BEAS 2B in a dose-dependent manner, Cytokine-induced A549 cell mRNA accumulation was maximal at 4 h and was significantly enhanced when the cells were costimulated with IFN gamma. TNF alpha- and IL-1 beta-induced increases in eotaxin mRNA were diminished in a dose-dependent manner by the glucocorticoid dexamethasone and were augmented by the protein synthesis inhibitor cycloheximide. Cytokine-induced increases in eotaxin mRNA expression correlated with increased eotaxin protein production and secretion, and dexamethasone inhibition of cytokine-induced eotaxin mRNA augmentation was associated with diminished eotaxin protein secretion. These findings, together with the known kinetics of TNF alpha and IL-1 beta mobilization in asthmatic airways and the potent eosinophil chemotactic effects of eotaxin, define a mechanism linking inflammatory cytokine mobilization to eosinophil recruitment that may be relevant to the pathogenesis of asthma. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,MUCOSAL IMMUNOL LAB,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. RP Lilly, CM (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,COMBINED PROGRAM PULM & CRIT CARE MED,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-03283]; NIAID NIH HHS [AI 40618]; NIDDK NIH HHS [DK-43551] NR 42 TC 281 Z9 288 U1 0 U2 5 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 1 PY 1997 VL 99 IS 7 BP 1767 EP 1773 DI 10.1172/JCI119341 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA WT444 UT WOS:A1997WT44400037 PM 9120022 ER PT J AU CastiglioneGertsch, M Goldhirsch, A Gusterson, B Bettelheim, R Reed, R Gusset, H Geiser, K Hurny, C Bernhard, J Hangartner, A Maibach, R Pedowski, R Gelber, R Price, K Peterson, H Zelen, M Isley, M Hinkle, R Kay, RG Holdaway, IM Harvey, VJ Jagusch, MF Neave, L Mason, BM Evans, B Benjamin, CS Carter, JF Gillman, JC Mack, D BensonCooper, D Monfardini, S Galligioni, E Crivellari, D Buonadonna, A Massarut, S Rossi, C Candiani, E Carbone, A Volpe, R Trovo, MG Roncadin, M Santini, GF Villalta, D Coran, F Morassut, S Marini, G Simoncini, E Marpicati, P Zaniboni, A Sartori, U Barni, A Cerutti, L Alghisi, A Raffaglio, E Garattini, MP Albertini, A Grigolato, F Morassi, L Bergonzini, R Lauriola, C Gudgeon, A Dent, DM Tiltman, A Hacking, A Dowdle, E Steynor, P Toop, J Schnurch, HG Mosny, D Bender, HG Bojar, H Veronesi, A Foladore, S Pamich, G Bianchi, G Torretta, A Rudenstam, CM Wallgren, A Persson, S Mattsson, J Cahlin, E Hafstrom, LO Holmberg, S Hultborn, R ColldahlJaderstrom, G Gustavsson, B Carlsson, G Ivarsson, L Thoren, O Ruusvik, O Nicklasson, LG Dahlin, S Karlsson, G Lindberg, B Sundback, A Bergegardh, S Salander, H Andersson, C Hessman, Y Nelzen, O Heideman, M Ramhult, T Svensson, JH Lidberg, P Bjork, S Lindtner, J Erzen, D Cerar, O Stabuc, B Golouh, R Lamovec, J Sebek, S Kramberger, M Vrhovec, I CortesFunes, H MartinezTello, F Mendiola, C CruzVigo, F Larrodera, ML Sierra, A Miranda, P Alonso, S Collins, J Snyder, R Gregory, P Buras, WI Green, M Gale, T Henderson, M Hart, S Neil, S Kitchen, P Lovell, R McLennan, R Reed, R Russell, I Schwarz, M Basser, R Robertson, A Gill, P Carter, ML Malycha, P Yeoh, E Ward, G Leong, ASY LommaxSmith, J Hoosfall, D DAngelo, R Byrne, M vanHazel, G Dewar, J Buck, M Sheiner, HJ Ingram, D Sterrett, G Hahnel, R Forbes, JF Steward, J Darbar, SW Bishop, JM Simms, B Ziogas, V Tattersall, MHN Coates, A Niesche, F West, R Renwick, S Donovan, J Duval, P Simes, RJ Ng, A Glenn, D North, RA Beith, J OConnor, RG Rice, M Stevens, G Fey, M Barth, A Dreher, E Isenschmid, M Schneider, H Buser, K Ludin, J Luthi, JM Altermatt, HJ Laissue, JA Markwalder, R Burgi, H Senn, HJ Thurlimann, B Jungi, WF Morant, R Oehlschlegel, C Hardmeier, T Luscher, K Ries, G Topfer, M Lorenz, U Benz, D Schiltknecht, O Spati, B Schmid, L Cavalli, F Sessa, C Bronz, L Martinelli, G Muller, W Luscieti, P Passega, E Pedrinis, E Rey, P Martinoli, S Spinelli, A Galfetti, MA Lombardi, A Pedrazzini, A Losa, G Varini, M Ginier, M Herrmann, R Harder, JF Laffer, U Almendral, AC Eppenberger, U Torhorst, J Siegenthaler, P Piguet, D Barrelet, V Baumann, RP Joss, R Sauter, C Metzger, U Engeler, V Haller, U Kochli, O Leyvraz, S Perey, L Anani, P Gomez, F Mirimanoff, RO Chapuis, G DeGrandi, P Reymond, P Alberto, P Schafer, P Krauer, F Forni, M Aapro, M Egeli, R Megevand, R JacotdesCombes, E Schindler, A Noseda, G Weber, W Lehmann, W AF CastiglioneGertsch, M Goldhirsch, A Gusterson, B Bettelheim, R Reed, R Gusset, H Geiser, K Hurny, C Bernhard, J Hangartner, A Maibach, R Pedowski, R Gelber, R Price, K Peterson, H Zelen, M Isley, M Hinkle, R Kay, RG Holdaway, IM Harvey, VJ Jagusch, MF Neave, L Mason, BM Evans, B Benjamin, CS Carter, JF Gillman, JC Mack, D BensonCooper, D Monfardini, S Galligioni, E Crivellari, D Buonadonna, A Massarut, S Rossi, C Candiani, E Carbone, A Volpe, R Trovo, MG Roncadin, M Santini, GF Villalta, D Coran, F Morassut, S Marini, G Simoncini, E Marpicati, P Zaniboni, A Sartori, U Barni, A Cerutti, L Alghisi, A Raffaglio, E Garattini, MP Albertini, A Grigolato, F Morassi, L Bergonzini, R Lauriola, C Gudgeon, A Dent, DM Tiltman, A Hacking, A Dowdle, E Steynor, P Toop, J Schnurch, HG Mosny, D Bender, HG Bojar, H Veronesi, A Foladore, S Pamich, G Bianchi, G Torretta, A Rudenstam, CM Wallgren, A Persson, S Mattsson, J Cahlin, E Hafstrom, LO Holmberg, S Hultborn, R ColldahlJaderstrom, G Gustavsson, B Carlsson, G Ivarsson, L Thoren, O Ruusvik, O Nicklasson, LG Dahlin, S Karlsson, G Lindberg, B Sundback, A Bergegardh, S Salander, H Andersson, C Hessman, Y Nelzen, O Heideman, M Ramhult, T Svensson, JH Lidberg, P Bjork, S Lindtner, J Erzen, D Cerar, O Stabuc, B Golouh, R Lamovec, J Sebek, S Kramberger, M Vrhovec, I CortesFunes, H MartinezTello, F Mendiola, C CruzVigo, F Larrodera, ML Sierra, A Miranda, P Alonso, S Collins, J Snyder, R Gregory, P Buras, WI Green, M Gale, T Henderson, M Hart, S Neil, S Kitchen, P Lovell, R McLennan, R Reed, R Russell, I Schwarz, M Basser, R Robertson, A Gill, P Carter, ML Malycha, P Yeoh, E Ward, G Leong, ASY LommaxSmith, J Hoosfall, D DAngelo, R Byrne, M vanHazel, G Dewar, J Buck, M Sheiner, HJ Ingram, D Sterrett, G Hahnel, R Forbes, JF Steward, J Darbar, SW Bishop, JM Simms, B Ziogas, V Tattersall, MHN Coates, A Niesche, F West, R Renwick, S Donovan, J Duval, P Simes, RJ Ng, A Glenn, D North, RA Beith, J OConnor, RG Rice, M Stevens, G Fey, M Barth, A Dreher, E Isenschmid, M Schneider, H Buser, K Ludin, J Luthi, JM Altermatt, HJ Laissue, JA Markwalder, R Burgi, H Senn, HJ Thurlimann, B Jungi, WF Morant, R Oehlschlegel, C Hardmeier, T Luscher, K Ries, G Topfer, M Lorenz, U Benz, D Schiltknecht, O Spati, B Schmid, L Cavalli, F Sessa, C Bronz, L Martinelli, G Muller, W Luscieti, P Passega, E Pedrinis, E Rey, P Martinoli, S Spinelli, A Galfetti, MA Lombardi, A Pedrazzini, A Losa, G Varini, M Ginier, M Herrmann, R Harder, JF Laffer, U Almendral, AC Eppenberger, U Torhorst, J Siegenthaler, P Piguet, D Barrelet, V Baumann, RP Joss, R Sauter, C Metzger, U Engeler, V Haller, U Kochli, O Leyvraz, S Perey, L Anani, P Gomez, F Mirimanoff, RO Chapuis, G DeGrandi, P Reymond, P Alberto, P Schafer, P Krauer, F Forni, M Aapro, M Egeli, R Megevand, R JacotdesCombes, E Schindler, A Noseda, G Weber, W Lehmann, W TI Effectiveness of adjuvant chemotherapy in combination with tamoxifen for node-positive postmenopausal breast cancer patients SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID GROWTH AB Purpose: Adjuvant tamoxifen has been shown to reduce relapse and mortality among node-positive postmenopausal breast cancer patients. The value of adding chemotherapy to tamoxifen is controversial. Patients and Methods: Between July 1986 and April 1993, 1,266 postmenopausal breast cancer patients with node-positive disease were randomly assigned to receive one of four adjuvant therapy regimens: (A) tamoxifen alone for 5 years; (B) tamoxifen plus three courses of early cyclophosphamide, methotrexate, and fluorouracil (CMF) on months 1, 2, and 3; (C) tamoxifen plus delayed single courses of CMF on months 9, 12, and 15; (D) tamoxifen plus early and delayed CMF on months 1, 2, 3, 9, 12, and 15. The two-by-two factorial design allowed two direct comparisons: early CMF (B and D) versus no early CMF (A and C), and delayed CMF (C and D) versus no delayed CMF (A and B). Estrogen receptor (ER) status was known for all patients and was used to stratify the randomization. A total of 1,212 patients (96%) were eligible and assessable. The median followup duration was 60 months. Results: The results of the two-by-two factorial comparison were as follows: (1) early CMF added to tamoxifen significantly improved 5-year disease-free survival (DFS; 64% v 57%; hazards ratio [HR], 0.79; 95% confidence interval [CI], 0.66 to 0.95; P = .01); and (2) delayed CMF added to tamoxifen did not improve DFS (5-year DFS, 61% v 60%; HR, 0.97; 95% CI, 0.81 to 1.17; P = .77). For patients with ER-positive tumors, the addition of CMF, either early or delayed or both, reduced the relative risk of relapse by 22% to 36%. In contrast, for patients with ER-negative tumors, tamoxifen with delayed CMF was associated with a nonsignificant increased risk of relapse (HR, 1.27; 95% CI, 0.92 to 1.76; P = .15). Conclusion: Postmenopausal patients with node-positive breast cancer should be offered combination chemotherapy in addition to tamoxifen. Tamoxifen should not be initiated before CMF, as this might be detrimental, especially for patients with ER-negative tumors. (C) 1997 by American Society of Clinical Oncology. C1 DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. FRONTIER SCI & TECHNOL RES FDN INC,AMHERST,MA. AUCKLAND BREAST CANC STUDY GRP,AUCKLAND,NEW ZEALAND. CTR RIFERIMENTO ONCOL,I-33081 AVIANO,ITALY. SPEDALI CIVIL BRESCIA,I-25125 BRESCIA,ITALY. FDN BERETTA,BRESCIA,ITALY. GROOTE SCHUUR HOSP,ZA-7925 CAPE TOWN,SOUTH AFRICA. UNIV DUSSELDORF,D-4000 DUSSELDORF,GERMANY. PRESIDIO OSPED,GORIZIA,ITALY. W SWEDISH BREAST CANC STUDY GRP,GOTHENBURG,SWEDEN. INST ONCOL,LJUBLJANA,SLOVENIA. MADRID BREAST CANC GRP,MADRID,SPAIN. ANTICANC COUNCIL VICTORIA,MELBOURNE,VIC,AUSTRALIA. ROYAL ADELAIDE HOSP,ADELAIDE,SA 5000,AUSTRALIA. SIR CHARLES GAIRDNER HOSP,NEDLANDS,WA 6009,AUSTRALIA. UNIV NEWCASTLE,WARATAH,AUSTRALIA. UNIV SYDNEY,SYDNEY,NSW 2006,AUSTRALIA. ROYAL PRINCE ALFRED HOSP,SYDNEY,NSW,AUSTRALIA. UNIV BERN,INSELSPITAL,SWISS GRP CLIN CANC RES,CH-3010 BERN,SWITZERLAND. KANTONSSPITAL,CH-9007 ST GALLEN,SWITZERLAND. OSPED SAN GIOVANNI BELLINZONA,BELLINZONA,SWITZERLAND. HOP CADOLLES,NEUCHATEL,SWITZERLAND. KANTONSSPITAL,CH-4031 BASEL,SWITZERLAND. KANTONSSPITAL,LUZERN,SWITZERLAND. KANTONSSPITAL,ZURICH,SWITZERLAND. CTR HOP UNIV,LAUSANNE,SWITZERLAND. UNIV GENEVA,HOP CANTONAL,CH-1211 GENEVA,SWITZERLAND. SWISS CANC LEAGUE,BERN,SWITZERLAND. RP CastiglioneGertsch, M (reprint author), INT BREAST CANC STUDY GRP,COORDINATING CTR,EFFINGERSTR 40,CH-3008 BERN,SWITZERLAND. RI gusterson, barry/D-3752-2009; Simes, Robert/P-1497-2014 NR 22 TC 95 Z9 95 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1997 VL 15 IS 4 BP 1385 EP 1394 PG 10 WC Oncology SC Oncology GA WX651 UT WOS:A1997WX65100013 ER PT J AU Krischer, JP Epstein, S Cuthbertson, DD Goorin, AM Epstein, ML Lipshultz, SE AF Krischer, JP Epstein, S Cuthbertson, DD Goorin, AM Epstein, ML Lipshultz, SE TI Clinical cardiotoxicity following anthracycline treatment for childhood cancer: The Pediatric Oncology Group experience SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID IDIOPATHIC DILATED CARDIOMYOPATHY; ACUTE LYMPHOBLASTIC-LEUKEMIA; ADRIAMYCIN NSC-123127 CARDIOMYOPATHY; BONE-MARROW TRANSPLANTATION; CONGESTIVE HEART-FAILURE; BLACK-WHITE DIFFERENCES; LONG-TERM SURVIVORS; DOWNS-SYNDROME; RISK-FACTORS; DOXORUBICIN THERAPY AB Purpose: To determine the incidence of clinical cardiotoxicity from anthracycline chemotherapy in children with cancer and to identify associated risk factors. Patients and Methods: The study population consisted of 6,493 children with cancer who had received anthracycline chemotherapy on pediatric Oncology Group (POG) protocols from 1974 to 1990. Cardiotoxicity, defined as congestive heart failure not due to other causes, abnormal measurements of cardiac function that prompted discontinuation of therapy, or sudden death from presumed cardiac causes, was determined by a review of protocol records. Results: Cardiotoxicity was confirmed in 106 patients (1.6%): 58 had congestive heart failure, 43 had changes in measures of cardiac function that prompted the discontinuation of therapy, and five died suddenly From presumed cardiac causes. In a multivariate analysis, factors that contributed to the relative risk (RR) of toxicity were a cumulative anthracycline dose greater than or equal to 550 mg/m(2) of body-surface area (RR = 5.2), maximal dose greater than or equal to 50 mg/m(2) (RR = 2.8), female sex (RR = 1.9), black race (RR = 1.7), presence of trisomy 21 (RR = 3.4), and exposure to amsacrine (RR = 2.6). Cardiotoxicity within I year after the completion of anthracycline treatment (early cardiotoxicity) represented 89.5% of all cases. Conclusion: Early clinical cardiotoxicity in children treated with anthracycline is rare. A high maximal dose, or cumulative dose of anthracycline, female sex, black race, presence of trisomy 21, and treatment with amsacrine increase the risk for anthracycline-associated cardiotoxicity. (C) 1997 by American Society of Clinical Oncology. C1 UNIV S FLORIDA,DEPT PEDIAT,TAMPA,FL 33612. DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT CARDIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP MICHIGAN,DIV CARDIOL,DETROIT,MI 48201. WAYNE STATE UNIV,DEPT PEDIAT,DETROIT,MI 48202. RP Krischer, JP (reprint author), UNIV S FLORIDA,H LEE MOFFIT CANC CTR & RES INST,DEPT PEDIAT,MDC 44,12902 MAGNOLIA DR,TAMPA,FL 33612, USA. FU NCI NIH HHS [CA06516, CA29139, CA34183] NR 70 TC 251 Z9 262 U1 1 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1997 VL 15 IS 4 BP 1544 EP 1552 PG 9 WC Oncology SC Oncology GA WX651 UT WOS:A1997WX65100034 PM 9193351 ER PT J AU Vose, JM Pandite, AN Beveridge, RA Geller, RB Schuster, MW Anderson, JE LeMaistre, CF Ahmed, T Granena, A Keating, A Ranada, JMF Stiff, PJ Tabbara, I Longo, W Copelan, EA Nichols, C Smith, A Topolsky, DL Bierman, PJ Lebsack, ME Lange, M Garrison, L AF Vose, JM Pandite, AN Beveridge, RA Geller, RB Schuster, MW Anderson, JE LeMaistre, CF Ahmed, T Granena, A Keating, A Ranada, JMF Stiff, PJ Tabbara, I Longo, W Copelan, EA Nichols, C Smith, A Topolsky, DL Bierman, PJ Lebsack, ME Lange, M Garrison, L TI Granulocyte-macrophage colony-stimulating factor interleukin-3 fusion protein versus granulocyte-macrophage colony-stimulating factor after autologous bone marrow transplantation for non-Hodgkin's lymphoma: Results of a randomized double-blind trial SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID HIGH-DOSE CHEMOTHERAPY; RECOMBINANT HUMAN INTERLEUKIN-3; PROGENITOR CELLS; PLATELET RECOVERY; CYCLOPHOSPHAMIDE; MULTICENTER; THERAPY; PRIMATES; DISEASE; CANCER AB Purpose: A phase III trial to compare PIXY321 with granulocyte-macrophage colony-stimulating factor (GM-CSF) following high-dose therapy and autologous bone marrow transplant (ABMT) was conducted to evaluate the time to hematopoietic recovery. Patients and Methods: One hundred seventy-seven patients with non-Hodgkin's lymphoma (NHL) receiving ABMT were randomized to receive either PIXY321 750 mu g/m(2)/d divided into two subcutaneous (SC) doses or GM-CSF 250 mu g/m(2)/d as a 2-hour intravenous (IV) infusion starting on day 0 post-ABMT for a maximum of 28 days. Results: The median time to reach an absolute neutrophil count (ANC) greater than or equal to 500/mu L in the PIXY321 group was 17 days versus 19 days in the GM-CSF group (P = .07) and the median time to reach platelet transfusion independence in the PIXY321 group was 25 days versus 23 days in the GM-CSF group (P = .30). the toxicity profiles of the two agents appeared to be equivalent with the exception of more patients in the PIXY321 group with a rash (64%) compared with the GM-CSF group (48%) (P = .028). A logistic regression model identified the use of a non-total-body irradiation (TBI) regimen and/or receipt of unpurged marrow and a body-surface area greater than 2.0 m(2) as predictive of faster neutrophil engraftment, and those three factors, as well as the receipt of less than or equal to two prior chemotherapy regimens as predictive for rapid platelet engraftment. Conclusion: There was a trend toward a slight improvement in neutrophil engraftment post-ABMT with the PIXY321 administered by an SC route compared with GM-CSF administered by an IV route. However, no differences could be identified between the two agents with respect to the time to platelet transfusion independence. Patient, regimen, and graft characteristics were most predictive of the engraftment tempo. (C) 1997 by American Society of Clinical Oncology. C1 DANA FARBER CANC INST,BOSTON,MA 02115. FAIRFAX HEMATOL ONCOL ASSOCIATES,FAIRFAX,VA. EMORY UNIV,ATLANTA,GA 30322. N SHORE UNIV,MANHASSET,NY. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. S TEXAS CANC INST,SAN ANTONIO,TX. NEW YORK MED COLL,VALHALLA,NY 10595. LOYOLA UNIV,NEW ORLEANS,LA 70118. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. UNIV WISCONSIN,MADISON,WI 53706. OHIO STATE UNIV,COLUMBUS,OH 43210. INDIANA UNIV,BLOOMINGTON,IN 47405. HOSP DURAN I REYNALS,BARCELONA,SPAIN. HOSP PRINCESA,MADRID,SPAIN. TORONTO GEN HOSP,TORONTO,ON,CANADA. LONDON REG CANC CTR,LONDON,ON N6A 4L6,CANADA. MED COLL PENN & HAHNEMANN UNIV,PHILADELPHIA,PA. IMMUNEX CORP,SEATTLE,WA. RP Vose, JM (reprint author), UNIV NEBRASKA,MED CTR,600 S 42ND ST,OMAHA,NE 68198, USA. NR 29 TC 11 Z9 11 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1997 VL 15 IS 4 BP 1617 EP 1623 PG 7 WC Oncology SC Oncology GA WX651 UT WOS:A1997WX65100044 PM 9193361 ER PT J AU Janicek, M Kaplan, W Neuberg, D Canellos, GP Shulman, LN Shipp, MA AF Janicek, M Kaplan, W Neuberg, D Canellos, GP Shulman, LN Shipp, MA TI Early restaging gallium scans predict outcome in poor-prognosis patients with aggressive non-Hodgkin's lymphoma treated with high-dose CHOP chemotherapy SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LARGE-CELL LYMPHOMA; STANDARD REGIMEN CHOP; GA-67 SCINTIGRAPHY; M-BACOD; THERAPY; TRIAL; SPECT AB Purpose: This prospective study assessed the predictive value of early restaging gallium (Ga) and computed tomographic (CT) scans in poor-prognosis patients with aggressive non-Hodgkin's lymphoma (NHL) who were treated with high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy. Patients and Methods: Thirty newly diagnosed patients with bulky (greater than or equal to 10 cm) advanced-stage aggressive NHL were treated with a four-cycle high-dose CHOP regimen (22 patients at maximum-tolerated dose [MTD]: cyclophosphamide 4 g/m(2), doxorubicin 70 mg/m(2), vincristine 2 mg, and prednisone 100 mg orally for 5 days), All patients had chest/abdominol/pelvic CT scans and 10-mCi Ga scans at baseline and following two and four cycles of therapy. Scans were reviewed in a blinded manner for CT-documented rates of response and sizes of residual masses and Ga avidity of residual masses, The results of early (post-cycle 2) and final (post-cycle 4) restaging were subsequently associated with clinical outcome. Results: CT-documented rates of response and residual-moss sizes were indistinguishable in complete responders who remained continuously disease-free (CR-Cont), complete responders who subsequently relapsed (CR-Rel), and partial responders who then progressed (PR/Prog), In marked contrast, early restaging (post-cycle 2) Ga scans accurately delineated these three categories of patients: CR-Cont 90% Ga-negative (18 of 20 patients) versus CR-Rel 25% Ga-negative (one of four patients) versus PR/Prog 0% Ga-negative (zero of six patients) (P = .000014). At a median follow-vp duration of 31 months (range, 21 to 46), 94% of patients who had negative early restaging Ga scans remain free from progression (FFP), whereas only 18% of patients who had positive early restaging Ga scans remain FFP (P = .000007). Early restaging Ga scans were more predictive for FFP than final restaging Ga scans because patients who required four full cycles of therapy to become Ga-negative were more likely to develop recurrent disease. Conclusion: Early restaging Ga scans delineate patients who are likely to have prolonged disease-free survival from those who fail to respond to intensive induction therapy. Patients whose tumors remain Ga-positive midway through high-dose CHOP therapy have a poor outcome and may be candidates for alternative treatment. (C) 1997 by American Society of Clinical Oncology. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 21 TC 73 Z9 73 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1997 VL 15 IS 4 BP 1631 EP 1637 PG 7 WC Oncology SC Oncology GA WX651 UT WOS:A1997WX65100046 PM 9193363 ER PT J AU Vonderheide, RH Fleming, MD Carter, G Singer, S Demetri, G AF Vonderheide, RH Fleming, MD Carter, G Singer, S Demetri, G TI Angiosarcoma SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID SOFT-TISSUE RP Vonderheide, RH (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BRIGHAM & WOMENS HOSP,44 BINNEY ST,BOSTON,MA 02115, USA. NR 3 TC 3 Z9 3 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1997 VL 15 IS 4 BP 1708 EP 1709 PG 2 WC Oncology SC Oncology GA WX651 UT WOS:A1997WX65100055 PM 9193372 ER PT J AU Berenson, JR Rosen, L Vescio, R Lau, HS Woo, M Sioufi, A Kowalski, O Knight, RD Seaman, JJ AF Berenson, JR Rosen, L Vescio, R Lau, HS Woo, M Sioufi, A Kowalski, O Knight, RD Seaman, JJ TI Pharmacokinetics of pamidronate disodium in patients with cancer with normal or impaired renal function SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article ID BONE METASTASES AB Pamidronate is a second-generation bisphosphonate that undergoes negligible biodegradation and is eliminated exclusively by renal excretions. Nineteen cancer patients were stratified according to baseline creatinine clearance (Cl-cr): group I, Cl-cr >90 mL/min (n = 6); group II, Cl-cr 61 mL/min to 90 mL/min (n = 6); group III, Cl-cr 30 mL/min to 60 mL/min (n = 3); group IV, Cl-cr <30 mL/min (n = 4). All patients received a single, 90-mg dose of pamidronate disodium administered in a 4-hour intravenous infusion. Plasma and urine samples were collected at intervals up to 36 and 120 hours, respectively, after the start of infusion and were assayed for pamidronate, using validated high-performance liquid chromatography. Pamidronate's pharmacokinetics were characterized by a short distribution phase (2-3 hours) followed by rapid elimination of the drug in urine. Elimination of pamidronate was slower in patients in group IV with a mean +/- standard deviation area under the plasma concentration-time curve (AUC(0-36)) of 19.0 +/- 4.60 mu g.hr/mL compared with 8.1 +/- 3.13 mu g.hr/mL in patients in group I. A linear relationship in Cl-cr was observed for AUC(0-36) (r = 0.67), urinary excretion (r = 0.69), and renal clearance (r = 0.81). Renal clearance was proportional to Cl-cr for patients in all four renal-function groups. In the treatment of bone metastases of malignancy, successive doses of pamidronate are generally separated by weeks; thus, plasma accumulation in patients with renal impairment is not expected to be clinically relevant. A reduction in dose of pamidronate disodium should not be necessary in cancer patients with renal impairment. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90024. DEPT CLIN DEV,RUEIL MALMAISON,FRANCE. DEPT BIOPHARMACEUT & PHARMACOKINET,RUEIL MALMAISON,FRANCE. CIBA GEIGY CORP,DEPT CLIN DEV,SUMMIT,NJ 07901. NR 11 TC 66 Z9 67 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD APR PY 1997 VL 37 IS 4 BP 285 EP 290 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WU254 UT WOS:A1997WU25400003 PM 9115053 ER PT J AU Bodkin, JA Lasser, RA Wines, JD Gardner, DM Baldessarini, RJ AF Bodkin, JA Lasser, RA Wines, JD Gardner, DM Baldessarini, RJ TI Combining serotonin reuptake inhibitors and bupropion in partial responders to antidepressant monotherapy SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; SEXUAL DYSFUNCTION; PANIC DISORDER; FLUOXETINE; PHARMACOLOGY; FLUVOXAMINE; DEPRESSION; EFFICACY; THERAPY; PLACEBO AB Background: Many patients with affective illness show partial or otherwise unsatisfactory responses to standard treatments, encouraging trials of combinations of pharmacologically dissimilar antidepressants. Method: Records of consecutive outpatients with affective disorders only partially responsive to treatment with a serotonin reuptake inhibitor (SRI) or bupropion, alone, were reviewed for changes in specific symptoms and risks of adverse events when an SRI and bupropion were combined. Results: Greater symptomatic improvement was found in 19 (70%) of 27 subjects during a mean +/- SD of 11 +/- 14 months of combined daily use of bupropion (243 +/- 99 mg) with an SRI (31 +/- 16 mg fluoxetine-equivalents) than with either agent alone. Adverse effect risks were similar to those associated with each monotherapy, with a > 10% incidence of sexual dysfunction (N = 11, 41%), insomnia (N = 6, 22%), anergy (N = 4, 15%), and tremor (N = 3, 11%) during combined therapy; there were no seizures. Conclusion: With conservative dosing and close monitoring, combinations of SRIs with bupropion in this uncontrolled clinical series appeared to be safe and often more effective than monotherapy. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,INT CONSORTIUM PSYCHIAT RES,BELMONT,MA. MASSACHUSETTS GEN HOSP,BIPOLAR & PSYCHOT DISORDERS PROGRAM,PSYCHIAT RES LABS,BELMONT,MA. FU NIMH NIH HHS [MH-47370, MH-31154] NR 41 TC 121 Z9 124 U1 1 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD APR PY 1997 VL 58 IS 4 BP 137 EP 145 DI 10.4088/JCP.v58n0401 PG 14 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA WX131 UT WOS:A1997WX13100001 PM 9164423 ER PT J AU Frazer, A AF Frazer, A TI Pharmacology of antidepressants SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT Proceedings of the Satellite Symposium to the XX Collegium Internationale Neuro-Psychopharmacologicum (CINP) Congress on Neurotransmitters in Depression CY JUN 23, 1996 CL MELBOURNE, AUSTRALIA SP Collegium Int Neuro-Psychopharm (CINP) ID SEROTONIN REUPTAKE INHIBITORS; MONOAMINE-OXIDASE INHIBITORS; LOCUS-CERULEUS NEURONS; LONG-TERM TREATMENT; MAJOR DEPRESSION; DOUBLE-BLIND; ATYPICAL DEPRESSION; PHARMACOKINETIC PROPERTIES; PLASMA TRYPTOPHAN; LIMBIC FOREBRAIN AB This review covers mechanisms of action, efficacy, side effects, and toxicity of various classes of antidepressants: tricyclic antidepressants, monoamine oxidase inhibitors, second-generation antidepressants including the selective inhibitors of serotonin reuptake, and novel drugs such as mirtazapine, nefazodone, and venlafaxine. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP Frazer, A (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIMH NIH HHS [MH 29094] NR 158 TC 69 Z9 69 U1 1 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1997 VL 17 IS 2 SU 1 BP S2 EP S18 DI 10.1097/00004714-199704001-00002 PG 17 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA WQ891 UT WOS:A1997WQ89100002 PM 9090573 ER PT J AU Gorski, PA AF Gorski, PA TI Presidential address - A broad reach for health SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Gorski, PA (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 1997 VL 18 IS 2 BP 138 EP 140 DI 10.1097/00004703-199704000-00027 PG 3 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA WV151 UT WOS:A1997WV15100019 ER PT J AU Vadakekalam, J Rabaglia, ME Metz, SA AF Vadakekalam, J Rabaglia, ME Metz, SA TI Roles of GTP and phospholipase C in the potentiation of Ca2+-induced insulin secretion by glucose in rat pancreatic islets SO JOURNAL OF ENDOCRINOLOGY LA English DT Article ID SENSITIVE K+ CHANNELS; MOUSE B-CELLS; PHOSPHOINOSITIDE METABOLISM; RELEASE; HYDROLYSIS; LANGERHANS; MECHANISMS; CALCIUM; CA-2+; TIME AB Glucose can augment insulin secretion independently of K+ channel closure, provided cytoplasmic free Ca2+ concentration is elevated. A role for phospholipase C (PLC) in this phenomenon has been both claimed and refuted. Recently, we have shown a role for GTP in the secretory effect of glucose as well as in glucose-induced PLC activation, using islets pre-treated with GTP synthesis inhibitors such as mycophenolic acid (MPA). Therefore, in the current studies, we examined first, whether glucose augments Ca2+-induced PLC activation and second, whether GTP is required for this effect, when K+(ATP) channels are kept open using diazoxide. Isolated rat islets pre-labeled with [H-3]myo-inositol were studied with or without first priming with glucose. There was a 98% greater augmentation of insulin secretion by 16.7 mM glucose (in the presence of diazoxide and 40 mM K+) in primed islets; however, the ability of high glucose to augment PLC activity bore no relationship to the secretory response. MPA markedly inhibited PLC in both conditions; however, insulin secretion was only inhibited (by 46%) in primed islets. None of these differences were attributable to alterations in labeling of phosphoinositides or levels of GTP or ATP. These data indicate that an adequate level of GTP is critical for glucose's potentiation of Ca2+-induced insulin secretion in primed islets but that PLC activation can clearly be dissociated from insulin secretion and therefore cannot be the major cause of glucose's augmentation of Ca2+-induced insulin secretion. C1 UNIV WISCONSIN,DEPT MED,WILLIAM S MIDDLETON MEM VET ADM HOSP,MADISON,WI 53792. UNIV WISCONSIN,ENDOCRINOL SECT,MADISON,WI 53792. FU NIDDK NIH HHS [DK 37312] NR 26 TC 11 Z9 11 U1 0 U2 2 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0022-0795 J9 J ENDOCRINOL JI J. Endocrinol. PD APR PY 1997 VL 153 IS 1 BP 61 EP 71 DI 10.1677/joe.0.1530061 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WR278 UT WOS:A1997WR27800007 PM 9135570 ER PT J AU Boyle, LL Brownfield, MS Lent, SJ Goodman, B VoHill, H Litwin, J Carnes, M AF Boyle, LL Brownfield, MS Lent, SJ Goodman, B VoHill, H Litwin, J Carnes, M TI Intensive venous sampling of adrenocorticotropic hormone in rats with sham or paraventricular nucleus lesions SO JOURNAL OF ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING FACTOR; ACTH-SECRETION; VASOPRESSIN SECRETION; ARGININE VASOPRESSIN; MEDIAN-EMINENCE; RHYTHMS; BLOOD; CRF AB Adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary is predominantly regulated by corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) synthesized in neurons of the paraventricular nucleus (PVN) of the hypothalamus. Secretion of ACTH occurs in pulsatile bursts. To explore the relationship between hypothalamic control and the pulsatile pattern of ACTH secretion, we measured ACTH in 2 min blood samples over 4 h in rats with intact and lesioned PVN during hypovolemic-stress or control conditions and also measured median eminence (ME) levels of CRH, AVP, and oxytocin (OT). Mean plasma ACTH was highest in the sham lesioned-hypovolemic group, lowest in the sham lesioned-control soup and intermediate in the two PVN-lesioned groups. CRH in the ME was negligible in the lesioned animals and correlated with OT and AW. Pulsatile secretion was observed despite PVN ablation. Visual inspection of composite time series suggested different temporal patterns of ACTH secretion. Principal components analysis of the individual ACTH time series revealed three significant eigenvectors which correlated differentially with the three treatment groups. Neither lesioned group had the steep rise over 10 min seen in plasma ACTH in the non-lesioned groups. Delayed ACTH rise after 30-60 min occurred in all but the sham control group. Our data suggest that CRH is responsible for immediate secretion of ACTH in response to hypovolemic stress and that regulators from non-PVN sites may be responsible for more delayed secretion of ACTH in this setting. The persistence of ME AVP and OT levels in the face of >90% reduction in ME CRH levels leaves open the question of a role for one or both of these peptides in the delayed ACTH response following stress onset and in the generation of pulsatile ACTH secretory bursts. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR CLIN,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,MADISON,WI 53706. UNIV WISCONSIN,SCH VET MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. FU NIDDK NIH HHS [R29DK40759] NR 24 TC 11 Z9 11 U1 0 U2 0 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0022-0795 J9 J ENDOCRINOL JI J. Endocrinol. PD APR PY 1997 VL 153 IS 1 BP 159 EP 167 DI 10.1677/joe.0.1530159 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WR278 UT WOS:A1997WR27800018 PM 9135580 ER PT J AU Kirikae, T Kirikae, F Tominaga, K Qureshi, N Yamamoto, S Nakano, M AF Kirikae, T Kirikae, F Tominaga, K Qureshi, N Yamamoto, S Nakano, M TI Rhodobacter sphaeroides diphosphoryl lipid A inhibits interleukin-6 production in CD14-negative murine marrow stromal ST2 cells stimulated with lipopolysaccharide or paclitaxel (taxol) SO JOURNAL OF ENDOTOXIN RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; MONOCYTE DIFFERENTIATION ANTIGEN; RHODOPSEUDOMONAS-SPHAEROIDES; BINDING-PROTEIN; SOLUBLE CD14; BACTERIAL LIPOPOLYSACCHARIDE; NONTOXIC LIPOPOLYSACCHARIDE; TYROSINE PHOSPHORYLATION; ENDOTHELIAL-CELLS; FACTOR-ALPHA AB Paclitaxel (taxol), a microtubule stabilizer with anticancer activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages in vitro. Recent studies have shown that the Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA) inhibits both LPS- and paclitaxel-induced activation of murine macrophages, and have suggested that LPS, RsDPLA, and paclitaxel share the same receptor site on murine macrophages. To analyze this receptor site, the present study focused on the interactions between LPS, RsDPLA and paclitaxel in the activation of ST2 cells derived from murine bone marrow stroma. The ST2 cells did not express CD14 mRNA. The cells produced IL-6 molecules and expressed IL-6 mRNA in response to LPS, but did not produce TNF and nitric oxide. Paclitaxel induced IL-6 mRNA expression in ST2 cells. RsDPLA inhibited both LPS- and paclitaxel-induced IL-6 mRNA expression in a dose-dependent manner. These results suggest that LPS, RsDPLA, and paclitaxel are recognized by the same receptor complex on ST2 cells, and that the receptor functions without membrane CD14. C1 UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,MYCOBACTERIOL RES LAB,MADISON,WI. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI. OITA MED UNIV,DEPT PATHOL,OITA,JAPAN. RP Kirikae, T (reprint author), JICHI MED SCH,DEPT MICROBIOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. NR 56 TC 8 Z9 8 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0968-0519 J9 J ENDOTOXIN RES JI J. Endoxtin Res. PD APR PY 1997 VL 4 IS 2 BP 115 EP 122 PG 8 WC Biochemistry & Molecular Biology; Immunology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Immunology; Research & Experimental Medicine; Microbiology GA XF565 UT WOS:A1997XF56500005 ER PT J AU Collins, MM Barry, M Roberts, RG Oesterling, JE Fowler, FJ AF Collins, MM Barry, M Roberts, RG Oesterling, JE Fowler, FJ TI Diagnosis and treatment of benign prostatic hyperplasia - Practice patterns of primary care physicians SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the Society-of-General-Internal-Medicine CY MAY 02-04, 1996 CL WASHINGTON, DC SP Soc Gen Internal Med DE prostatic hyperplasia; primary care physicians; practice patterns; practice guideline ID CANCER; GUIDELINES; ANTIGEN AB OBJECTIVE: To define primary care physicians' (PCPs) practices in managing patients with benign prostatic hyperplasia (BPH), and to compare these practices to portions of the Agency for Health Care Policy and Research BPH guideline and urologists' practices. DESIGN: Mail survey. PARTICIPANTS: Nationwide random sample of PCPs and urologists, selected from the American Medical Association Registry. METHODS: Initial mailing, postcard reminder, second mailing, telephone reminder, final mailing. MAIN RESULTS: Primary care physicians (n = 444, response = 51%) reported seeing a median of 35 patients with BPH over the preceding year, in contrast to 240 for urologists (n = 394, response = 68%). Regarding tests recommended by the guideline, two thirds of PCPs reported rarely or never using the American Urological Association (AUA) symptom index, nearly all reported routinely performing digital rectal examinations, and many (66%) reported routinely ordering tests to determine the serum creatinine level, Although considered ''optional'' by the guideline, more than 90% of PCPs reported routinely ordering a prostate-specific antigen test, while infrequently using other optional tests. Regarding ''not recommended'' studies, a substantial minority reported selectively or routinely ordering intravenous pyelography (34%) and renal ultrasound (33%), while two thirds reported rarely or never ordering these tests. Eighty-six percent of PCPs reported prescribing medications for BPH over the preceding year; alpha blockers to a median of 12 patients, and finasteride to a median of 2. Variation in urology referral thresholds was suggested in responses to two patient scenarios. CONCLUSIONS: Primary care physicians are actively managing patients with BPH. Some of their diagnostic evaluations vary from the recommendations of a national guideline and urologists' practices. Referral thresholds appear to vary considerably. C1 MASSACHUSETTS GEN HOSP,MED SERV,DIV GEN MED,BOSTON,MA 02114. FU AHRQ HHS [HS 08397]; BHP HRSA HHS [5T32 PE11001-08] NR 27 TC 33 Z9 35 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD APR PY 1997 VL 12 IS 4 BP 224 EP 229 DI 10.1007/s11606-006-5044-2 PG 6 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA WU682 UT WOS:A1997WU68200004 PM 9127226 ER PT J AU Passman, LJ Garcia, RE Campbell, L Winter, E AF Passman, LJ Garcia, RE Campbell, L Winter, E TI Elderly veterans receiving care at a Veterans Affairs Medical Center while enrolled in Medicare-financed HMOs - Is the taxpayer paying twice? SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the Society-of-General-Internal-Medicine CY MAY 02-04, 1996 CL WASHINGTON, DC SP Soc Gen Internal Med DE veterans; elderly; Medicare; HMOs; health care financing AB Elderly veterans who visit our Veterans Affairs (VA) Medical Center primary care clinic often mention they are enrolled in HMOs. Approximately 20% of patients hospitalized at our facility report health insurance coverage. Of 1,000 hospitalizations during a 6-month period in which veterans reported insurance coverage, 337 involved elderly veterans. Of these 337 hospitalizations, 218 (65%) were for 174 veterans who stated they were enrolled in a Medicare-financed HMO. The VA's Medical Care Cost Recovery Program deemed only 46 (21%) of the hospitalizations billable and received reimbursement for 20 (9%). Thus, the VA is providing costly services already paid for by the Health Care Financing Administration under prepaid capitation contracts, and recovers minimal reimbursement from the HMOs. RP Passman, LJ (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED W111G,DIV GEN INTERNAL MED,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 7 TC 29 Z9 29 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD APR PY 1997 VL 12 IS 4 BP 247 EP 249 DI 10.1007/s11606-006-5048-y PG 3 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA WU682 UT WOS:A1997WU68200008 PM 9127230 ER PT J AU Lenderking, WR Wold, C Mayer, KH Goldstein, R Losina, N Seage, GR AF Lenderking, WR Wold, C Mayer, KH Goldstein, R Losina, N Seage, GR TI Childhood sexual abuse among homosexual men - Prevalence and association with unsafe sex SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE sexual abuse; HIV transmission; safe sex ID BISEXUAL MEN; CHILDREN; ADOLESCENTS; INFECTION AB Of 327 homosexual and bisexual men participating in an ongoing cohort study pertaining to risk factors for HIV infection who completed a survey regarding history of sexual abuse, 116 (35.5%) reported being sexually abused as children. Those abused were more likely to have more lifetime mate partners, to report more childhood stress, to have Lied in the past in order to have sex, and to have had unprotected receptive anal intercourse in the past 6 months (odds ratio 2.13; 95% confidence interval 1.15-3.95). Sexual abuse remained a significant predictor of unprotected receptive anal intercourse in a logistic model adjusting for potential confounding variables. RP Lenderking, WR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ROBERT B ANDREWS UNIT,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIAAA NIH HHS [R01AA9320-02]; PHS HHS [U64-CCU108309-02, U64/CCU100607-09] NR 20 TC 69 Z9 71 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD APR PY 1997 VL 12 IS 4 BP 250 EP 253 DI 10.1046/j.1525-1497.1997.012004250.x PG 4 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA WU682 UT WOS:A1997WU68200009 PM 9127231 ER PT J AU Schwarzschild, M Rordorf, G Bekken, K Buonanno, F Schmahmann, JD AF Schwarzschild, M Rordorf, G Bekken, K Buonanno, F Schmahmann, JD TI Normal-pressure hydrocephalus with misleading features of irreversible dementias: A case report SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID PREDICTIVE VALUE AB An 85-year-old man presented with the clinical triad (gait instability, dementia, and bladder and bowel incontinence), the ventriculomegaly, and the normal CSF pressure that characterize normal-pressure hydrocephalus (NPH). Diagnostic uncertainty was raised by an unusually rapid onset and a lack. of initial response to CSF tap tests. Additionally, periodic sharp waves on EEG suggested the possibility of Creutzfeldt-Jakob disease, and positron emission tomography (PET) demonstrated a pattern of cerebral hypometabolism typical of Alzheimer's disease. Nevertheless, the diagnosis of NPH was supported by delayed improvement following CSF tap tests, and it was confirmed by a dramatic clinical recovery after CSF shunting, resolution of the EEG and PET abnormalities, and a normal brain biopsy. NPH remains one of the few reversible causes of dementia, and the presence of its core features, regardless of rate of onset or ancillary test results, warrants careful consideration of therapeutic intervention. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD APR PY 1997 VL 10 IS 2 BP 51 EP 54 PG 4 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA XC899 UT WOS:A1997XC89900002 PM 9188018 ER PT J AU Carter, RH Doody, GM Bolen, JB Fearon, DT AF Carter, RH Doody, GM Bolen, JB Fearon, DT TI Membrane IgM-induced tyrosine phosphorylation of CD19 requires a CD19 domain that mediates association with components of the B cell antigen receptor complex SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SIGNAL-TRANSDUCTION MOLECULE; LYMPHOCYTES-B; T-CELL; PHOSPHATIDYLINOSITOL 3-KINASE; CYTOPLASMIC DOMAIN; CR2/CD19 COMPLEX; ACTIVATION; CD22; VAV; DIFFERENTIATION AB CD19 enhances membrane IgM (mIgM) signaling and is required for B lymphocyte responses to T-dependent Ags, CD19 is tyrosine phosphorylated when mIgM is ligated and binds SH2 domain-containing signaling proteins, We suggest that the basis for phosphorylation is the association of CD19 with Syk and other components of the mIgM complex, IgM, CD22, Ig-alpha, Ig-beta, and Syk were coimmunoprecipitated with CD19 from detergent lysates of B lymphocytes. The association was maintained with a chimeric form of CD19 containing only the transmembrane domain and the membrane proximal 17 amino acids of the cytoplasmic domain encoded by exon 6. This sequence is sufficient to mediate the association, as a synthetic peptide of the exon 6-encoded region adsorbs IgM and Syk, Deletion of the juxtamembrane 17 amino acids of the cytoplasmic domain encoded by CD19 exon 6 abolishes association of CD19 with the mIgM complex. Deletion of these amino acids, which contain no tyrosines, also reduces mIgM-induced tyrosine phosphorylation of the remainder of the CD19 cytoplasmic domain, Coligating this mutant CD19 to mIgM restores phosphorylation. Thus, a discrete region of the cytoplasmic domain regulates the tyrosine phosphorylation of CD19 in the activation of B cells by mIgM. C1 UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL. UNIV CAMBRIDGE,SCH CLIN MED,WELLCOME TRUST IMMUNOL UNIT,CAMBRIDGE CB2 1TN,ENGLAND. DNAX RES INST MOL & CELLULAR BIOL INC,PALO ALTO,CA 94304. RP Carter, RH (reprint author), UNIV ALABAMA,DEPT MED,409 LHRB,701 S 19TH ST,BIRMINGHAM,AL 35294, USA. FU Wellcome Trust NR 33 TC 65 Z9 66 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1997 VL 158 IS 7 BP 3062 EP 3069 PG 8 WC Immunology SC Immunology GA WQ643 UT WOS:A1997WQ64300005 PM 9120258 ER PT J AU Aranda, R Sydora, BC McAllister, PL Binder, SW Yang, HY Targan, SR Kronenberg, M AF Aranda, R Sydora, BC McAllister, PL Binder, SW Yang, HY Targan, SR Kronenberg, M TI Analysis of intestinal lymphocytes in mouse colitis mediated by transfer of CD4(+), CD45RB(high) T cells to SCID recipients SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INFLAMMATORY BOWEL-DISEASE; MUCOSAL IMMUNE-SYSTEM; INTRAEPITHELIAL LYMPHOCYTES; MONOCLONAL-ANTIBODY; MICE; INTERLEUKIN-8; CYTOKINES; INDUCE AB Transfer of specific T lymphocyte subsets isolated from the spleens of healthy donor mice into immunodeficient SCID mice leads to chronic intestinal inflammation with characteristics similar to those of human inflammatory bowel disease (IBD). CD4(+) CD45RB(high) cells cause disease, whereas CD4(+), CD45RB(low) and CD8(+) CD45RB(high) cells do not. Despite this difference, we demonstrate that all three T cell populations reconstitute the intraepithelial and lamina propria compartments of both small and large intestines of SCID recipients. Therefore, infiltration of lymphocytes alone is not sufficient for disease development. CD4(+) lymphocytes that have trafficked to the SCID intestine exhibit a phenotype characteristic of normal mucosal lymphocytes. This includes high expression of alpha(E) integrin and CD69, expression of CD8 alpha alpha homodimers in some of the intraepithelial lymphocytes, as well as low expression of CD62L and CD45RB. The phenotype of the infiltrating mucosal cells is indistinguishable, with respect to the cell surface markers tested, regardless of whether the starting donor population is CD45RB(high) or CD45RB(low). Severe inflammation is restricted primarily to the colon despite lymphocyte infiltration throughout the length of the intestine. This suggests that some property of the colon microenvironment contributes to inflammation. Consistent with this, transfer of CD4(+), CD45RB(high) cells to SCID mice that have significantly reduced numbers of enteric flora results in attenuation of the wasting and colitis. Fewer numbers of donor lymphocytes are recovered from the intraepithelial and lamina propria compartments of reduced flora SCID mice. We hypothesize that the ability of pathogenic cells to traffic to the intestine and mediate colitis may be driven by T cell reactivity to bacteria or bacterial products. C1 UNIV CALIF LOS ANGELES,INST MOL BIOL,LOS ANGELES,CA 90095. W LOS ANGELES VET AFFAIRS MED CTR,DEPT GASTROENTEROL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90095. MIDWAY HOSP MED CTR,LOS ANGELES,CA 90019. CEDARS SINAI MED CTR,DEPT MED,DIV MED GENET,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,DEPT PATHOL,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,CTR INFLAMMATORY BOWEL DIS,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,DIV GASTROENTEROL,LOS ANGELES,CA 90048. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NIDDK NIH HHS [P01 DK46763] NR 25 TC 229 Z9 234 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 APR 1 PY 1997 VL 158 IS 7 BP 3464 EP 3473 PG 10 WC Immunology SC Immunology GA WQ643 UT WOS:A1997WQ64300055 PM 9120308 ER PT J AU Pekary, AE Levin, SR Johnson, DG Berg, L Hershman, JM AF Pekary, AE Levin, SR Johnson, DG Berg, L Hershman, JM TI Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K+-ATPase in FRTL-5 rat thyroid cells SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH LA English DT Article ID BETA-SUBUNIT; RECEPTOR; PROTEIN; IODIDE; GENES; DNA; RNA AB We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process.((9)) TNF-alpha is only cytotoxic to aged (>40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. This cell line is, therefore, a convenient model for studies on the TSH-dependent and age-dependent inhibitory effects of these cytokines on epithelial cell growth, viability, and function. One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. In aged FRTL-5 cells, iodide uptake is only about 10% that of young control cells, Na+/K+-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. The following experiments quantitate the effects of TSH, aging, TNF-alpha and TGF-beta 1 on the expression and activity of Na+/K+-ATPase activity in FRTL-5 cells. Young (<20 passages) and aged (>40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. These treatments reduced the rate-limiting Na+/K+-ATPase beta 1 mRNA level and Na+/K+-ATPase activity in parallel in a dose-dependent and time-dependent fashion, Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K+-ATPase, We conclude that inhibition of Na+/K+-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. C1 W LOS ANGELES VET AFFAIRS MED CTR,DIABET RES LABS,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. RP Pekary, AE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL RES LABS,ENDOCRINOL & METAB SECT,LOS ANGELES,CA 90073, USA. NR 43 TC 15 Z9 16 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1079-9907 J9 J INTERF CYTOK RES JI J. Interferon Cytokine Res. PD APR PY 1997 VL 17 IS 4 BP 185 EP 195 DI 10.1089/jir.1997.17.185 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA WX550 UT WOS:A1997WX55000003 PM 9142647 ER PT J AU Riggs, DS Caulfield, MB AF Riggs, DS Caulfield, MB TI Expected consequences of male violence against their female dating partners SO JOURNAL OF INTERPERSONAL VIOLENCE LA English DT Article ID COURTSHIP VIOLENCE; AGGRESSION; STUDENTS; CONFLICT; FAMILY AB Ne examined the expected consequences of male college students to their perpetration of physical violence against their female dating partners and the association of these expected consequences to the actual use of violence in the men's current dating relationships. Using a measure of expected consequences adapted from an instrument used in an earlier study of dating violence (Breslin, Riggs, O'Leary, & Arias, 1990), we found significant differences in the expected consequences of violent and nonviolent men. Specifically, violent men were significantly more likely than nonviolent men to expect that violence would result in their winning the argument, whereas nonviolent men were more likely than violent men to believe that the use of violence would result in an end to the relationship. Expected consequences were also associated with the frequency/severity of self-reported aggressive behavior within the aggressive group. Theoretical and practical implications of these results are discussed. RP Riggs, DS (reprint author), BOSTON DVAMC,NATL CTR PTSD 116B2,150 S HUNTINGTON AVE,BOSTON,MA 02130, USA. NR 25 TC 16 Z9 16 U1 0 U2 5 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0886-2605 J9 J INTERPERS VIOLENCE JI J. Interpers. Violence PD APR PY 1997 VL 12 IS 2 BP 229 EP 240 DI 10.1177/088626097012002005 PG 12 WC Criminology & Penology; Family Studies; Psychology, Applied SC Criminology & Penology; Family Studies; Psychology GA WK933 UT WOS:A1997WK93300005 ER PT J AU Amano, S Takahara, K Gerecke, DR Nishiyama, T Lee, S Greenspan, DS Hogan, B Birk, DE Burgeson, RE AF Amano, S Takahara, K Gerecke, DR Nishiyama, T Lee, S Greenspan, DS Hogan, B Birk, DE Burgeson, RE TI The gamma-2 chain of laminin 5 is processed by BMP-1 and processing is essential to basement membrane assembly in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. SHISEIDO LIFE SCI RES CTR,YOKOHAMA,KANAGAWA,JAPAN. UNIV WISCONSIN,MADISON,WI. VANDERBILT UNIV,NASHVILLE,TN. TUFTS UNIV,SCH MED,BOSTON,MA 02111. RI Nishiyama, Toshio/C-5434-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 29 EP 29 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000050 ER PT J AU Gonzalez, S AlcarazMartinez, MV Diaz, F Kollias, N AF Gonzalez, S AlcarazMartinez, MV Diaz, F Kollias, N TI An extract of Polypodium leucotomos inhibits ultraviolet B photoaging in the skin of the hairless albino mouse. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. UNIV MALAGA,FAC MED,E-29071 MALAGA,SPAIN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 62 EP 62 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000087 ER PT J AU Torii, H Luster, AD Ozawa, H Takashima, A Granstein, RD AF Torii, H Luster, AD Ozawa, H Takashima, A Granstein, RD TI Eotaxin, a potent eosinophil chemotactic factor, is produced by epidermal cells. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,SW MED CTR,DEPT DERMATOL,DALLAS,TX. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. CORNELL UNIV MED COLL,DEPT DERMATOL,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 87 EP 87 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000109 ER PT J AU Detmar, M Brown, LF Schon, MP Fukumura, D Monsky, W Elicker, BM Nagy, JA Jain, RK AF Detmar, M Brown, LF Schon, MP Fukumura, D Monsky, W Elicker, BM Nagy, JA Jain, RK TI Overexpression of VPF/VEGF in the skin of transgenic mice leads to enhanced density of tortuous, hyperpermeable skin microvessels, and increased leucocyte rolling and adhesion. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 BETH ISRAEL DEACONESS MED CTR,DEPT PATHOL,BOSTON,MA. BETH ISRAEL DEACONESS MED CTR,DEPT DERMATOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT IMMUNOL & RHEUMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 137 EP 137 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000158 ER PT J AU Baciu, PC Goetinck, PF AF Baciu, PC Goetinck, PF TI Characterization of Syndecan-4 function during the formation and maintenance of cellular and extracellular matrix architecture. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 171 EP 171 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000193 ER PT J AU Gerecke, DR Olson, PF Koch, M Hudson, DL Champliaud, MF Burgeson, RE AF Gerecke, DR Olson, PF Koch, M Hudson, DL Champliaud, MF Burgeson, RE TI Complete primary structure and tissue specific distribution of two splice variants of human collagen XII. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 174 EP 174 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000197 ER PT J AU Hibino, T Ogo, M Takahashi, T Takeda, A Nakayama, Y Goetinck, PF AF Hibino, T Ogo, M Takahashi, T Takeda, A Nakayama, Y Goetinck, PF TI Suppression of apoptotic cell death by psoriastatin expressed in human fibroblasts. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 SHOWA UNIV,DEPT CLIN PATHOL,YOKOHAMA,KANAGAWA,JAPAN. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 182 EP 182 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000207 ER PT J AU Qureshi, AA Lerner, EA AF Qureshi, AA Lerner, EA TI Nitric oxide-induced B7-2 expression in murine macrophages. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 237 EP 237 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000259 ER PT J AU Avitahl, N Georgopoulos, K AF Avitahl, N Georgopoulos, K TI Ikaros proteins are important for lymphoid development and homeostasis SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA. HARVARD UNIV,SCH MED,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 264 EP 264 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000287 ER PT J AU Tyagi, S Bhol, K Natarajan, K LivirRallatos, C Foster, CS Ahmed, AR AF Tyagi, S Bhol, K Natarajan, K LivirRallatos, C Foster, CS Ahmed, AR TI Ocular cicatricial pemphigoid antigen: Partial sequence and biochemical characterization. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 311 EP 311 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000332 ER PT J AU Sugerman, P Bigby, M AF Sugerman, P Bigby, M TI Comparison of dermal and epidermal T cell migration and adhesion to keratinocytes. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 316 EP 316 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000340 ER PT J AU Lieb, LM Jorgensen, CM Morgan, JR Krueger, GG AF Lieb, LM Jorgensen, CM Morgan, JR Krueger, GG TI Delivery of transgenes to follicles of human scalp in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV UTAH,SCH MED,DEPT DERMATOL,SALT LAKE CITY,UT. HARVARD UNIV,SCH MED,SHRINERS BURNS INST,MASS GEN HOSP,SURG SERV,BOSTON,MA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 342 EP 342 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000365 ER PT J AU Jorgensen, CM Matsunami, N Morgan, JR Li, HL Petersen, MJ Krueger, GG AF Jorgensen, CM Matsunami, N Morgan, JR Li, HL Petersen, MJ Krueger, GG TI Immortalized human keratinocytes form a functional epidermis and express transgenes in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV UTAH,DEPT DERMATOL,SALT LAKE CITY,UT. UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,SHRINERS BURN INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 346 EP 346 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000370 ER PT J AU Albus, A Aoki, H Zervos, AS AF Albus, A Aoki, H Zervos, AS TI Role of MXI1 in keratinocyte growth and differentiation. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 401 EP 401 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000422 ER PT J AU Ouahes, N Amano, S Keene, D Burgeson, RE AF Ouahes, N Amano, S Keene, D Burgeson, RE TI Effect of BM-2 antibody on keratinocyte migration in an in vivo model of wound healing. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA. SHRINERS HOSP CRIPPLED CHILDREN,DEPT SURG,PORTLAND,OR. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 468 EP 468 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000491 ER PT J AU Dobens, L Raftery, L AF Dobens, L Raftery, L TI Genetic evidence that negative feedback draws a boundary between two cell fates patterned by a BMP growth factor gradient in Drosophila. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,DEPT DERMATOL,SCH MED,CAMBRIDGE,MA 02138. RI Raftery, Laurel/H-1406-2012 OI Raftery, Laurel/0000-0003-4797-4163 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 477 EP 477 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000499 ER PT J AU Moro, O Lipper, G Tajima, M Ohnuma, M Lerner, E AF Moro, O Lipper, G Tajima, M Ohnuma, M Lerner, E TI Maxadilan, the vasodilator peptide from sand flies, is a specific pituitary adenylate cyclase activating peptide type I receptor agonist. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 485 EP 485 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000506 ER PT J AU Tsoukas, MM Lin, GC Lee, MS Anderson, RR Kollias, N AF Tsoukas, MM Lin, GC Lee, MS Anderson, RR Kollias, N TI Predictive dosimetry for threshold phototoxicity in photodynamic therapy on normal skin: Red wavelengths produce more extensive damage than blue at equal threshold doses SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE action spectrum; laser; benzoporphyrin derivative monoacid ring A (BPD-MA); fluorescence spectroscopy ID BENZOPORPHYRIN DERIVATIVES; HEMATOPORPHYRIN; TUMOR; DEPENDENCE; PHOTOSENSITIZATION; MICE AB The goal of this investigation was to establish methodology to determine and prevent phototoxic responses of normal skin to photodynamic therapy (PDT). The drug used was a second-generation photosensitizer, benzoporphyrin derivative monoacid ring A (BPD-MA). The dependence of skin phototoxicity on drug dose (0.5-2.0 mg/kg), fluence (1.2-390 J/cm(2)), and wavelength (690 mn and 458 mn) was studied in the New Zealand albino rabbit in the first 5 h after injection, Skin responses were recorded for 2 wk after irradiation, Noninvasive measurements of drug fluorescence were made on unexposed skin sites during the first 5 h after drug injection, Immediate responses to PDT included erythema induced by 458 nm light and blanching induced by 690 nm light, Delayed reactions included edema on the day of exposure, purpura at 24 h, eschar by day 2 or 3, and scar by the end of follow-up, The threshold fluence for immediate responses correlated strongly with the threshold fluence for delayed reactions, The induction of threshold purpura on day I was a reliable index for skin phototoxicity that led to necrosis, The minimum purpura dose on day 1 after irradiation increased exponentially with the interval between drug injection and irradiation, independent of irradiation wavelength, for all drug doses. The action spectrum for threshold purpura mimics closely the absorption spectrum of BPD-MA, The in vivo drug fluorescence correlated with skin phototoxicity, thus allowing predictive dosimetry, This model system defines the safety Limits for skin phototoxicity of PDT with BPD-MA. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA 02114. NR 23 TC 15 Z9 16 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 501 EP 505 DI 10.1111/1523-1747.ep12289732 PG 5 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000016 PM 9077481 ER PT J AU Champliaud, MF Champliaud, D Albalat, R Baden, HP AF Champliaud, MF Champliaud, D Albalat, R Baden, HP TI The RNA-binding nuclear protein TLS appears to regulate mRNA synthesis during cornification of keratinocytes. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA. NYU,MED CTR,DEPT MED,NEW YORK,NY 10016. RI Albalat, Ricard/A-8379-2009 OI Albalat, Ricard/0000-0003-0282-9595 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 518 EP 518 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000543 ER PT J AU Qureshi, AA Lee, PK Lerner, EA AF Qureshi, AA Lee, PK Lerner, EA TI Nitric oxide is toxic for melanocytes. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 538 EP 538 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000562 ER PT J AU Bhol, K Tyagi, SR LivirRallatos, C Foster, CS Ahmed, AR AF Bhol, K Tyagi, SR LivirRallatos, C Foster, CS Ahmed, AR TI Characterization of oral pemphigoid antigen SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 589 EP 589 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000611 ER PT J AU Kurada, P Reichman, M Bae, E Lisi, S Tahaoglu, E White, K AF Kurada, P Reichman, M Bae, E Lisi, S Tahaoglu, E White, K TI New cell death genes and their role in skin and hair biology SO JOURNAL OF INVESTIGATIVE DERMATOLOGY 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 BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 687 EP 687 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000708 ER PT J AU Song, HK Goetinck, PF AF Song, HK Goetinck, PF TI FGF-2 signaling in the early development of cutaneous appendages SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 708 EP 708 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000730 ER PT J AU Werth, VP AF Werth, VP TI Dapsone as a glucocorticoid-sparing agent in pemphigus vulgaris. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV PENN,DEPT DERMATOL,PHILADELPHIA,PA 19104. PHILADELPHIA VA MED CTR,PHILADELPHIA,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 722 EP 722 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000746 ER PT J AU Carder, K Santhanam, U Gursky, R Misra, M Lehman, M Stiller, M Bartolone, J Drake, L AF Carder, K Santhanam, U Gursky, R Misra, M Lehman, M Stiller, M Bartolone, J Drake, L TI Effect of topical 8% glycolic and 8% L-lactic acid creams on collagen synthesis in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNILEVER RES LABS VLAARDINGEN,EDGEWATER,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 724 EP 724 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000747 ER PT J AU Gonzalez, S MartosRodriguez, A SantosAlvarez, I Kollias, N DelgadoBaeza, E AF Gonzalez, S MartosRodriguez, A SantosAlvarez, I Kollias, N DelgadoBaeza, E TI Topical retinol and all-trans retinoic acid act differently on apoptosis in the skin of the rhino mouse model. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. AUTONOMOUS UNIV MADRID,FAC MED,E-28049 MADRID,SPAIN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 735 EP 735 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000756 ER PT J AU Ibbotson, SH Lambert, CR Lynch, MC Moran, MN Kochevar, IE AF Ibbotson, SH Lambert, CR Lynch, MC Moran, MN Kochevar, IE TI Enhanced UVA-induced plasma membrane damage in the presence of benzoyl peroxide. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 762 EP 762 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000784 ER PT J AU Lee, S Kollias, N McAuliffe, DJ Flotte, TJ Doukas, AG AF Lee, S Kollias, N McAuliffe, DJ Flotte, TJ Doukas, AG TI Laser stress waves induce transient increase of the stratum corneum permeability: Implications for transdermal drug delivery. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 786 EP 786 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000808 ER PT J AU Stiller, M Bartolone, J Carder, K Wright, S Hawkins, S Drake, L AF Stiller, M Bartolone, J Carder, K Wright, S Hawkins, S Drake, L TI Efficacy of topical 8% L-lactic acid and 8% glycolic acid in ameliorating the roughness of photodamaged skin as determined by laser profilometric analysis of silicon rubber replicas. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNILEVER RES LABS VLAARDINGEN,EDGEWATER,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1997 VL 108 IS 4 BP 806 EP 806 PG 1 WC Dermatology SC Dermatology GA WP040 UT WOS:A1997WP04000830 ER PT J AU Yen, HH Zhang, YJ Penfold, S Rollins, BJ AF Yen, HH Zhang, YJ Penfold, S Rollins, BJ TI MCP-1-mediated chemotaxis requires activation of non-overlapping signal transduction pathways SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE chemokine; CCR2; ERK; PD 098059 ID PROTEIN-KINASE ACTIVATION; BETA-GAMMA-SUBUNITS; MAP KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; RECEPTOR; CHEMOATTRACTANT; WORTMANNIN; INHIBITOR; CELLS; RAS AB Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that attracts monocytes and T lymphocytes. Its receptor (CCR2) is a heptahelical G-protein-coupled receptor (GPCR) whose signal transduction pathways for chemotaxis have not been completely defined. Because other GPCRs stimulate the mitogen-activated protein kinase (MAPK) cascade, we examined this pathway's activity in response to MCP-1, MCP-1 induced rapid and transient activation of MAPK in human monocytes and in Chinese hamster ovary cells expressing CCR2B. This effect was largely insensitive to pertussis toxin and wortmannin, and was protein kinase C-dependent and protein tyrosine kinase-independent. PD 098059, an inhibitor of MEK activation, not only prevented MAPK activation but also inhibited MCP-1-induced chemotaxis. Because pertussis toxin and wortmannin also efficiently inhibit chemotaxis but do not completely inhibit MAPK activation, these data may define non-overlapping signal transduction pathways that all must be activated to produce chemokine-mediated chemotaxis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. FU NCI NIH HHS [CA53091] NR 25 TC 81 Z9 81 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD APR PY 1997 VL 61 IS 4 BP 529 EP 532 PG 4 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA WU025 UT WOS:A1997WU02500020 PM 9103241 ER PT J AU Worthington, JJ Pollack, MH Otto, MW Gould, RA Sabatino, SA Goldman, L Rosenbaum, JF Lee, TH AF Worthington, JJ Pollack, MH Otto, MW Gould, RA Sabatino, SA Goldman, L Rosenbaum, JF Lee, TH TI Panic disorder in emergency ward patients with chest pain SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article; Proceedings Paper CT 147th Annual Meeting of the American-Psychiatric-Association CY MAY 21-26, 1994 CL PHILADELPHIA, PA SP Amer Psychiat Assoc, NIMH, Dept Vet Affairs, Cooperat Studies Program, Med Res Serv ID PSYCHIATRIC-DISORDERS; PREVALENCE; DIAGNOSIS; LIFETIME; CARE; ROOM C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP Worthington, JJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ANXIET DISORDERS PROGRAM,WAC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. FU AHRQ HHS [HS06452] NR 17 TC 15 Z9 15 U1 4 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD APR PY 1997 VL 185 IS 4 BP 274 EP 276 DI 10.1097/00005053-199704000-00009 PG 3 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA WT040 UT WOS:A1997WT04000009 PM 9114814 ER PT J AU Priest, CA Borsook, D Pfaff, DW AF Priest, CA Borsook, D Pfaff, DW TI Estrogen and stress interact to regulate the hypothalamic expression of a human proenkephalin promoter-beta-galactosidase fusion gene in a site-specific and sex-specific manner SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article DE paraventricular nucleus; ventromedial hypothalamus; opioid; sex-difference; transgenic mice; reproductive behavior ID CORTICOTROPIN-RELEASING-FACTOR; PREPROENKEPHALIN MESSENGER-RNA; LUTEINIZING-HORMONE RELEASE; MESENCEPHALIC CENTRAL GRAY; CENTRAL NERVOUS-SYSTEM; FEMALE RATS; PARAVENTRICULAR NUCLEUS; VENTROMEDIAL HYPOTHALAMUS; INSITU HYBRIDIZATION; RIBONUCLEIC-ACID AB Gonadal steroids and physiological stressors affect the regulation of proenkephalin (PPE) gene expression in the paraventricular (PVN) and ventromedial (VMH) hypothalamic nuclei. To examine the effects of these modulators at the cellular level, the current study utilized a transgenic mouse line that expresses a human proenkephalin promoter/bacterial beta-galactosidase fusion gene (ENK-1). Previous studies have demonstrated that the regulatory sequences included in this transgene are sufficient to support appropriate transcriptional regulation of the reporter gene in the PVN of male ENK-1 mice in response to stress. The present experimental paradigm was designed to examine possible interactions of sex and circulating estrogen levels with the opioid responses to acute systemic stressors, an intraperitoneal injection of hypertonic (1.5 M) or isotonic (0.15 M) saline. Adult ENK-1 mice were gonadally intact, gonadectomized, or 21 days postpartum Forty-eight hours before perfusion, castrated males and ovariectomized females received either 10 mu g estradiol benzoate or oil vehicle and 4 animals per group received no further treatment. Six h before perfusion, remaining animals received a single intraperitoneal injection of either hypertonic or isotonic saline. Tissues were sectioned through the hypothalamus and processed for X-gal histochemistry, In the VMH of ovariectomized females that received isotonic saline, estrogen significantly elevated transgene expression. This effect was not seen in females that only received estrogen or in those that received the severe systemic stressor of an injection of hypertonic saline. Estrogen and stress did not interact to elevate transgene expression in the VMH of males. A different pattern of expression was observed in the PVN; injection of hypertonic saline induced transgene expression only in gonadally intact males and in castrated males given estrogen. These findings demonstrate that stress and estrogen have sex-specific and site-specific regulatory effects on the expression of a PPE promoter transgene in hypothalamic neurons. C1 ROCKEFELLER UNIV,NEUROBIOL & BEHAV LAB,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,LAB MOL & DEV NEUROSCI,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NIMHD NIH HHS [MD05751] NR 100 TC 17 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0953-8194 J9 J NEUROENDOCRINOL JI J. Neuroendocrinol. PD APR PY 1997 VL 9 IS 4 BP 317 EP 326 DI 10.1046/j.1365-2826.1997.00589.x PG 10 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA WV753 UT WOS:A1997WV75300009 PM 9147295 ER PT J AU McDermott, KL Raghupathi, R Fernandez, SC Saatman, KE Protter, AA Finklestein, SP Sinson, G Smith, DH McIntosh, TK AF McDermott, KL Raghupathi, R Fernandez, SC Saatman, KE Protter, AA Finklestein, SP Sinson, G Smith, DH McIntosh, TK TI Delayed administration of basic fibroblast growth factor (bFGF) attenuates cognitive dysfunction following parasagittal fluid percussion brain injury in the rat SO JOURNAL OF NEUROTRAUMA LA English DT Article DE basic fibroblast growth factor; cognition; fluid-percussion injury; neurotrophic factors; traumatic brain injury ID CEREBRAL BLOOD-FLOW; FIMBRIA FORNIX TRANSECTION; FACTOR PROMOTES SURVIVAL; CHOLINERGIC NEURONS; HEAD-INJURY; EXCITOTOXIC LESIONS; NERVE; ISCHEMIA; DEATH; HIPPOCAMPUS AB The present study evaluates the therapeutic effects of delayed administration of bFGF on cognitive dysfunction and histopathological damage following lateral fluid-percussion (FP) brain injury, Male Sprague-Dawley rats were trained to learn a visuospatial task in a Morris Water Maze (MWM) paradigm and then were anesthetized and subjected to either FP brain injury of moderate severity (2.5-2.8 atm, n = 32) or surgery without brain injury (n = 10), Twenty-four hours postinjury, an infusion cannula connected to a mini-osmotic pump was implanted into the area of maximal cortical injury to continuously infuse either bFGF (2.0 g) or vehicle for 7 days, Treatment with bFGF significantly attenuated posttraumatic memory dysfunction in the MWM at 8 days postinjury when compared to vehicle treatment (p < 0.05). The cortical lesion and significant cell loss in the ipsilateral CA3 region of the hippocampus, produced by FP injury, was not affected by bFGF treatment, However, immunohistochemical evaluation of glial fibrillary acidic protein revealed a trend toward increased astrocytosis in the injured cortex of bFGF-treated animals compared to vehicle-treated animals (p < 0.1). These results indicate that bFGF may be efficacious in attenuating cognitive dysfunction associated with traumatic brain injury. C1 UNIV PENN,DIV NEUROSURG,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,DEPT NEUROL,CNS GROWTH FACTOR RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. SCIOS NOVA INC,MT VIEW,CA 94043. RI smith, douglas/A-1321-2007 FU NIGMS NIH HHS [R01-GM34690]; NINDS NIH HHS [P01-NS08803, R01-NS26818] NR 66 TC 61 Z9 62 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0897-7151 J9 J NEUROTRAUM JI J. Neurotrauma PD APR PY 1997 VL 14 IS 4 BP 191 EP 200 DI 10.1089/neu.1997.14.191 PG 10 WC Critical Care Medicine; Clinical Neurology; Neurosciences SC General & Internal Medicine; Neurosciences & Neurology GA WY593 UT WOS:A1997WY59300002 PM 9151768 ER PT J AU Buerhaus, PI Clifford, J Erickson, JI Fay, MS Miller, JR Sporing, EM Weissman, GK AF Buerhaus, PI Clifford, J Erickson, JI Fay, MS Miller, JR Sporing, EM Weissman, GK TI Executive Nursing Leadership - Summary of the Harvard Nursing Research Institute's Follow-up Conference SO JOURNAL OF NURSING ADMINISTRATION LA English DT Article ID ACADEMIC MEDICAL-CENTERS; RAPID CHANGES AB A follow-up national invitational conference focused on the implications of managed care, challenges facing nurse executives in major teaching hospitals and academic health centers, and efforts to improve community health and nursing documentation. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,CAMBRIDGE,MA 02138. BETH ISRAEL MED CTR,NEW YORK,NY 10003. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. CHILDRENS HOSP,PATIENT SERV,BOSTON,MA 02115. PARTNERS HEALTHCARE SYST INC,PATIENT CARE SERV,BOSTON,MA. RP Buerhaus, PI (reprint author), HARVARD UNIV,NURSING RES INST,CAMBRIDGE,MA 02138, USA. NR 6 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-0443 J9 J NURS ADMIN JI J. Nurs. Adm. PD APR PY 1997 VL 27 IS 4 BP 12 EP 20 DI 10.1097/00005110-199704000-00006 PG 9 WC Nursing SC Nursing GA WT817 UT WOS:A1997WT81700005 PM 9107193 ER PT J AU Aurang, K Wang, J Lloyd, KCK AF Aurang, K Wang, J Lloyd, KCK TI Somatostatin inhibition of acid and histamine release by activation of somatostatin receptor subtype 2 receptors in rats SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID ENTEROCHROMAFFIN-LIKE CELLS; MONOCLONAL-ANTIBODY IMMUNONEUTRALIZATION; CANINE PARIETAL-CELLS; GASTRIC-ACID; FUNCTIONAL-CHARACTERIZATION; FUNDIC SOMATOSTATIN; ANESTHETIZED RATS; PRIMARY CULTURE; MUCOSAL CELLS; SECRETION AB Peptide analogs of somatostatin with relatively selective binding affinities for specific somatostatin receptor subtypes, including SMS-201-995 [somatostatin receptor subtype (sst)(2), sst(3) and sst(5)], NC-8-12 (sst(2)), BIM-23058 (sst(3)) and BIM-23052 (sst(5)), were administered i.v. to anesthetized rats to determine the somatostatin receptor subtypes involved in regulation of acid secretion stimulated by either pentagastrin (24 mu g/kg/hr), bethanechol (0.2 mg/kg/hr) or histamine (5 mg/kg/hr) and in regulation of histamine release stimulated by either pentagastrin or bethanecol. Somatostatin-14 (10 nmol/kg/hr) inhibited pentagastrin-stimulated and bethanecol-stimulated acid secretion to basal levels but inhibited histamine-stimulated secretion to just 68% of maximum. SMS-201-995 (10 nmol/kg/hr) inhibited acid secretion similarly to somatostatin-14, indicating that activation of sst(2), sst(3) and/or sst(5) receptors accounts for acid inhibition induced by somatostatin. NC-8-12 dose-dependently (0.1, 1, 10 and 100 nmol/kg/hr) inhibited acid secretion stimulated by pentagastrin and by bethanecol, but only the highest dose administered (100 nmol/kg/hr) blocked by half the acid response to histamine; BIM-23058 and BIM-23052 were significantly less effective. NC-8-12 (60 +/- 12% of maximum) and somatostatin-14 (50 +/- 14% of maximum) also blocked pentagastrin-stimulated histamine release, whereas BIM-23058 and BIM-23052 were ineffective. None of the agonists significantly reduced bethanecol-stimulated histamine release. These results indicate that somatostatin activation of sst(2) receptors is the principal physiological pathway for somatostatin-induced inhibition of gastric acid secretion stimulated by either pentagastrin, bethanecol or histamine and of pentagastrin-stimulated histamine release. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,MED RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,DEPT PHYSIOL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,SCH MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CURE VA,DIGEST DIS RES CTR,LOS ANGELES,CA 90073. FU NIDDK NIH HHS [DK41301, DK45752] NR 63 TC 26 Z9 26 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 APR PY 1997 VL 281 IS 1 BP 245 EP 252 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WU522 UT WOS:A1997WU52200031 PM 9103503 ER PT J AU Bunting, RW Selig, MK Dickersin, GR AF Bunting, RW Selig, MK Dickersin, GR TI Apoptotic cells in peripheral blood from patients with low serum cobalamin SO JOURNAL OF SUBMICROSCOPIC CYTOLOGY AND PATHOLOGY LA English DT Article DE apoptosis; cobalamin deficiency ID DEATH; MECHANISM; NEURONS; DISEASE AB Apoptotic leukocytes were found by using ultrastructural and light microscopic techniques to examine peripheral blood in ten of twelve patients with low serum cobalamin (vitamin B12) and rarely in normal controls. A total of 88 apoptotic cells (.14% of total leukocytes) were identified in all the patients. One patient also had apoptotic cells found on a routine blood smear. There was no correlation between the finding of these cells and nuclear hypersegmentation, serum cobalamin levels, serum intrinsic factor antibody serum methylmalonic acid and homocysteine or the Schilling test. Two patients, however, with the most se were vitamin deficiency did not have increased numbers of apoptotic cells suggesting that these patients had lost the ability to initiate the cell death program. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP Bunting, RW (reprint author), SPAULDING REHABIL HOSP,DEPT HEMATOL,125 NASHUA ST,BOSTON,MA 02114, USA. NR 20 TC 8 Z9 8 U1 0 U2 0 PU EDITRICE COMPOSITORI BOLOGNA PI BOLOGNA PA VIA STALINGRADO 97/2, I-40128 BOLOGNA, ITALY SN 1122-9497 J9 J SUBMICR CYTOL PATH JI J. Submicrosc. Cytol. Pathol. PD APR PY 1997 VL 29 IS 2 BP 223 EP 227 PG 5 WC Pathology SC Pathology GA WX126 UT WOS:A1997WX12600008 PM 9165716 ER PT J AU Elgadi, KM Souba, WW Bode, BP Abcouwer, SF AF Elgadi, KM Souba, WW Bode, BP Abcouwer, SF TI Hepatic glutaminase gene expression in the tumor-bearing rat SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Academic-Surgery CY NOV 13-16, 1996 CL CHICAGO, IL SP Assoc Acad Surg ID KIDNEY-TYPE GLUTAMINASE; AMINO-ACID-TRANSPORT; MESSENGER-RNA; UREA CYCLE; LIVER; METABOLISM; INSULIN; HEPATOCYTES; GLUCOSE; HUMANS AB Previous studies have documented an increase in hepatic plasma membrane glutamine transport in the tumor-bearing rat, but the effects of tumor burden on hepatic glutaminase expression have not been carefully studied. The purpose of this study was to examine the effects of tumor burden and food intake on hepatic glutaminase expression. Rats were implanted with syngeneic methylcholanthrene-induced fibrosarcoma tumor tissue; control rats were sham operated and pair-fed every 24 hr. Northern blotting was used to assay the effect of tumor burden and fasting on hepatic glutaminase mRNA levels, using beta-actin mRNA as a control. Hepatic glutaminase mRNA levels in livers of pair-fed controls were found to be 4-fold greater than levels in livers of tumor-bearing animals. Examination of food intake patterns in these animals indicated that pair-fed controls ate their allotted chow quickly while tumor-bearing rats ate small amounts throughout each 24 hr period. This observation suggested that the differences in glutaminase mRNA levels may be due to a period of fasting by pair-fed animals which was not experienced by the tumor-bearing group. Hepatic glutaminase mRNA levels rapidly increased in normal rats during acute fasting to levels 5.5-fold greater than fed animals. Glucose feeding and insulin injection rapidly reversed the effect of fasting on hepatic glutaminase mRNA levels in normal rats. Tumor-bearing rats also exhibited upregulation of hepatic glutaminase mRNA levels in response to fasting. Conclusions: (1) Tumor burden itself does not alter hepatic glutaminase expression, at least at the pre-translational level. Instead, differences in hepatic glutaminase mRNA content are due to differences in food intake patterns. (2) Hepatic glutaminase mRNA levels are rapidly upregulated in response to fasting, an effect which appears to be linked to a decrease in plasma insulin concentrations. Because tumor-bearing rats eat regularly over a 24 hr period (albeit in small increments), thereby maintaining the plasma insulin concentration, hepatic glutaminase mRNA may not rise as it does in pair-fed controls whose daily chow intake is complete within hours of food allocation. (3) This study indicates that differences in the timing of food intake between tumor-bearing rats and pair-fed controls can alter the expression of genes that are influenced by nutrient availability. These differences should be taken into account when designing studies which involve pair-feeding to control nutrient intake. (C) 1997 Academic Press. RP Elgadi, KM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. OI Abcouwer, Steven F/0000-0003-2580-1288 FU NCI NIH HHS [CA57690] NR 22 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1997 VL 69 IS 1 BP 33 EP 39 DI 10.1006/jsre.1997.5000 PG 7 WC Surgery SC Surgery GA XF539 UT WOS:A1997XF53900006 PM 9202643 ER PT J AU Ravicz, ME Rosowski, JJ AF Ravicz, ME Rosowski, JJ TI Sound-power collection by the auditory periphery of the Mongolian gerbil Meriones unguiculatus .3. Effect of variations in middle-ear volume SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID GUINEA-PIG; KANGAROO RAT; EXTERNAL-EAR; HEARING; CHINCHILLA; CAT; HETEROMYIDAE; FREQUENCY; IMPEDANCE; SYSTEMS AB The effects of variations in middle-ear cavity size on hearing sensitivity in the Mongolian gerbil are predicted by computing the effect on acoustic power input to the middle ear. Acoustic power collection from a diffuse sound field was computed from measurements of the middle-ear input impedance and external-ear radiation impedance and mathematical models of the middle and external ear presented in the first two papers of this series [J. Acoust. Sec. Am. 92, 157-177 (1992); J. Acoust. Sec. Am. 99, 3044-3063 (1996)]. A reduction in middle-ear cavity volume to 1/4 its normal value is predicted to cause a frequency-selective elevation in auditory threshold of as much as 12 dB, with the largest elevation occuring in the 1-2 kHz range. Greater reductions produce larger threshold elevations. Increases in cavity volume cause decreases in the predicted threshold of at most 12 dB. Threshold predictions for volumes equal to those of the smaller hamster and the larger kangaroo-rat middle-ear cavity volumes resemble threshold functions measured in those animals. Results are consistent with the idea that large middle-ear cavities evolved in gerbil to improve hearing sensitivity below 3 kHz and thereby improve the animal's chances for survival. (C) 1997 Acoustical Society of America. C1 MIT,ELECT RES LAB,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. RP Ravicz, ME (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [R01 DC00194, R01 DC000194] NR 66 TC 16 Z9 16 U1 0 U2 2 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD APR PY 1997 VL 101 IS 4 BP 2135 EP 2147 DI 10.1121/1.418275 PG 13 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA WV173 UT WOS:A1997WV17300039 PM 9104016 ER PT J AU Wilens, TE Spencer, TJ Biederman, J Schleifer, D AF Wilens, TE Spencer, TJ Biederman, J Schleifer, D TI Case study: Nefazodone for juvenile mood disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE pediatric; antidepressant; depression; mood disorders ID MAJOR DEPRESSION; PLASMA-LEVEL; CHILDREN; ADOLESCENTS; IMIPRAMINE; PLACEBO; NORTRIPTYLINE; DESIPRAMINE; PREVALENCE AB Objective: Despite the increasing recognition of juvenile mood disorders, few medications have been shown to be effective. Nefazodone is a novel antidepressant that remains untested in children. Seven cases are described, including four with bipolar depression, in which nefazodone was used for depression. Method: The authors systematically studied the response to nefazodone used naturalistically in seven treatment-refractory and very comorbid children and adolescents (mean age +/- SD, 12.4 +/- 3.1) with a juvenile mood disorder that was diagnosed clinically and confirmed by structured psychiatric interview. Response to treatment was evaluated retrospectively by an independent rater using the Clinical Global Impression (CGI) of severity and improvement of depression. Results: Children and adolescents received nefazodone for 13 (+/-8) weeks at a mean daily dose of 357 +/- 151 mg (3.4 mg/kg). Fifty-six percent of children and adolescents previously unresponsive to multiple medication trials manifested much to very much improvement as measured by the CGI. Two of four children with bipolar depression responded well to treatment, whereas the other two had mild manic activation. Overall, nefazodone was well tolerated, with adverse effects reported in only three subjects. Conclusion: Nefazodone appears to be a well-tolerated compound that may provide a treatment option for juveniles with mood disorders. Further controlled trials are warranted. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Wilens, TE (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,CHILD PSYCHIAT SERV,ACC 725,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-K2001175A02] NR 30 TC 19 Z9 19 U1 2 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD APR PY 1997 VL 36 IS 4 BP 481 EP 485 DI 10.1097/00004583-199704000-00010 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA WR090 UT WOS:A1997WR09000010 PM 9100422 ER PT J AU Mickelson, JK Blum, CM Geraci, JM AF Mickelson, JK Blum, CM Geraci, JM TI Acute myocardial infarction: Clinical characteristics, management and outcome in a metropolitan Veterans Affairs Medical Center teaching hospital SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; NON-Q-WAVE; ISCHEMIC-HEART-DISEASE; THROMBOLYTIC THERAPY; UNITED-STATES; CARDIOVASCULAR PROCEDURES; NATIONAL-REGISTRY; BLACK PERSONS; SURGERY; SURVIVAL AB Objectives. The influence of race and age on thrombolytic therapy, invasive cardiac procedures and outcomes was assessed in a Veterans Affairs teaching hospital. The influence of Q wave evolution on the use of invasive cardiac procedures and outcome was also assessed. Background. It is not well known how early revascularization procedures for acute myocardial infarction are delivered or influence survival in a Veterans Affairs patient population. Methods. From October 1993 to October 1995, all patients with myocardial infarction were identified by elevated creatine kinase, MB fraction (CK-MB) and one of the following: chest pain or shortness of breath during the preceding 24 h or electrocardiographic (EGG) abnormalities. Results. Racial groups were similar in terms of age, time to EGG, peak CK and length of hospital stay. Mortality increased with age (odds ratio [OR] 1.93, 95% confidence interval [CI] 1,33 to 2.81). A trend toward increased mortality occurred for race other than Caucasian. Patients meeting ECG criteria were given thrombolytic agents in 49% of cases, but age, comorbidity count and Hispanic race decreased the probability of thrombolytic use. Cardiac catheterization was performed more often after thrombolytic agents (OR 1.85, 95% CI 0.97 to 3.54), but less often in African-Americans (OR 0.59, 95% CI 0.35 to 1.02), older patients (OR 0.39, 95% CI 0.24 to 0.64) or patients with heart failure (OR 0.30, 95% CI 0.17 to 0.52). Patients evolving non-Q wave infarctions were older and had increased comorbidity counts and trends toward increased mortality. Angioplasty was chosen less for patients greater than or equal to 65 years old (p = 0.02); angioplasty and coronary artery bypass graft surgery were performed less in patients greater than or equal to 70 years old (p = 0.02). Patients treated invasively had lower mortality rates than those treated medically (p < 0.02). Conclusions. The use of thrombolytic agents and invasive treatment plans declined with age, and mortality increased with age. Trends toward increased mortality occurred with non-Q wave infarctions and race other than Caucasian. C1 BAYLOR COLL MED,DEPT MED,SECT CARDIOL & GEN INTERNAL MED,HOUSTON,TX 77030. RP Mickelson, JK (reprint author), HOUSTON VET AFFAIRS MED CTR,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 54 TC 33 Z9 33 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1997 VL 29 IS 5 BP 915 EP 925 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA WR446 UT WOS:A1997WR44600006 PM 9120176 ER PT J AU Cittadini, A Grossman, JD Napoli, R Katz, SE Stromer, H Smith, RJ Clark, R Morgan, JP Douglas, PS AF Cittadini, A Grossman, JD Napoli, R Katz, SE Stromer, H Smith, RJ Clark, R Morgan, JP Douglas, PS TI Growth hormone attenuates early left ventricular remodeling and improves cardiac function in rats with large myocardial infarction SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article; Proceedings Paper CT 45th Annual Scientific Session of the American-College-of-Cardiology Meeting CY MAR 24-28, 1996 CL ORLANDO, FL SP Amer Coll Cardiol ID FACTOR-I; HYPERTROPHY; METABOLISM; FAILURE; HEART; MASS; MODE AB Objectives. We sought to investigate the cardiac effects of growth hormone (GB) administration during the early phase of pathologic remodeling in a rat model of large myocardial infarction (MI). Background. Recent evidence suggests that exogenous administration of GH. evokes a hypertrophic response and increases left ventricular (LV) function in vivo in rats with normal or chronically failing hearts. We hypothesized that these effects would attenuate ventricular remodeling early after MI. Methods. Fifty-eight male rats underwent sham operation (n = 19) or had induced MI (n = 39). The day after the operation, the infarcted rats were randomized to receive 3 weeks of treatment with GH, 3 mg/kg body weight per day (n = 19) or placebo (n = 20). Echocardiography, catheterization and isolated whole heart preparations were used to define cardiac structure and function. Results. Growth hormone caused hypertrophy of the noninfarcted myocardium in a concentric pattern, as noted by higher echocardiographic relative wall thickness at 3 weeks and by morphometric histologic examination. Left ventricular dilation was reduced in the GH-treated versus placebo group (echocardiographic LV diastolic diameter to body weight ratio 2.9 +/- 0.1 vs. 3.5 +/- 0.2 cm/kg; p < 0.05). In vivo and in vitro cardiac function was improved after GH treatment. Despite elevated insulin-like growth factor-1 (IGF-1) serum levels in GH-treated rats, myocardial IGF-1 messenger ribonucleic acid was not different among the three groups, suggesting that an increase in its local expression does not appear necessary to yield the observed effects. Conclusions. These data demonstrate that early treatment of large MI with GH attenuates the early pathologic LV remodeling and improves LV function. (C)1997 by the American College of Cardiology. C1 BETH ISRAEL HOSP,DEPT MED,DIV CARDIOVASC,HARVARD THORNDIKE LAB,BOSTON,MA 02215. CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. GENENTECH INC,S SAN FRANCISCO,CA 94080. RI Cittadini, Antonio/I-8426-2012; OI Cittadini, Antonio/0000-0002-9905-9277; NAPOLI, Raffaele/0000-0002-3366-2321 FU NHLBI NIH HHS [HL-31117, HL-51307] NR 40 TC 115 Z9 116 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1997 VL 29 IS 5 BP 1109 EP 1116 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA WR446 UT WOS:A1997WR44600034 PM 9120168 ER PT J AU Ghusn, HF Teasdale, TA Jordan, D AF Ghusn, HF Teasdale, TA Jordan, D TI Continuity of do-not-resuscitate orders between hospital and nursing home settings SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ADVANCE DIRECTIVES; CARE AB OBJECTIVE: To determine the relationship between interinstitutional communication and continuity of advance directives from hospital to nursing home (NH) settings. DESIGN: Retrospective chart review of discharges to hospital affiliated or community NHs. SETTING: Teaching Veterans Affairs Hospital and affiliated and community nursing homes. MEASUREMENTS: Demographic characteristics, medical diagnoses, presence of advance directives, and documentation that relates to the topic. RESULTS: A total of 83 patients were discharged to either setting. Before discharge to a NH, the prevalence of chronic obstructive pulmonary disease and cancer was higher among those who had a DNR order. Overall, subsequent discussions about advance directives were equally common in NHs. Having a hospital discussion about advance directives or having a hospital DNR order were associated with a higher rate of advance directive discussions in NHs. Hospital DNR orders were continued for 93% and 41% of patients admitted to the hospital-affiliated NH compared with community NHs, respectively (P < .001). Specific communication of hospital DNR status to the receiving NH was associated with better continuity of DNR orders (49% vs 9%, P = .001). Factors that predicted continuity of DNR orders in logistic regression analysis correctly included hospital DNR status, communication of advance directives to the receiving NH, and NH advance directive discussions. CONCLUSIONS: There is higher continuation rate of DNR orders between the hospital under study and its affiliated NH than to community NHs despite a similar frequency of confirmation discussions. Completing advance directives before patients are discharged to NHs, communication of advance directives to the receiving NH, and follow-up discussions at the NH may improve the continuity of advance directives between hospitals and nursing homes. C1 HOUSTON VET AFFAIRS MED CTR,NURSING SERV,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. RP Ghusn, HF (reprint author), HOUSTON VET AFFAIRS MED CTR,GERIATR & EXTENDED CARE SERV 110,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 9 TC 15 Z9 15 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1997 VL 45 IS 4 BP 465 EP 469 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WT160 UT WOS:A1997WT16000011 PM 9100716 ER EF