FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Zarchin, N
Meilin, S
Kraut, A
Mendelman, A
Rifkind, J
Mayevsky, A
AF Zarchin, N
Meilin, S
Kraut, A
Mendelman, A
Rifkind, J
Mayevsky, A
TI Hemodynamic, metabolic, ionic and electrical changes during cerebral
ischemia in aged rats
SO NEUROSCIENCE LETTERS
LA English
DT Meeting Abstract
C1 Bar Ilan Univ, Dept Life Sci, Ramat Gan, Israel.
NIA, LCMB, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PY 1997
SU 48
BP S55
EP S55
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA ZB328
UT WOS:000072460000226
ER
PT J
AU Shankar, L
Ravindranath, V
Boyd, MR
Vistica, DT
Shankar, SK
AF Shankar, L
Ravindranath, V
Boyd, MR
Vistica, DT
Shankar, SK
TI Histological, histochemical and autoradiographic evidence of in vitro
neurotoxic effects of the novel antitumor agent,
9-methoxy-N-2-methylellipticinium acetate
SO NEUROTOXICOLOGY
LA English
DT Article
DE 9-methoxy-N-2-methylellipticinum acetate; ellipticines; brain;
neurotoxicity; brain slices
ID HUMAN BRAIN; CYTOTOXICITY
AB 9-Methoxy-N-2-methylellipticinium acetate (MMEA) exhibits selective cytotoxicity towards glial-derived human brain tumor cell lines comprising the U.S. National Cancer Institute preclinical drug screen. Neurotoxic potential of MMEA has been demonstrated in an in vitro model employing sagittal slices of rat brain. Histochemical staining of rat brain slices for lactate dehydrogenase (LDH) activity revealed decreased staining intensity following incubation with increasing concentrations of MMEA (0.1 - 100 mu M). Cytological evaluation of paraffin sections stained with Cresyl Fast Violet revealed neuronal damage delineated by cytoplasmic vacuolation, and distention and fraying of the plasma membrane. No glial or vascular pathology could be discerned. Autoradiography, following exposure to C-14-MMEA, revealed distinct labelling of the large neurons of the brain stem, neurons in the thalamus and pyramidal neurons of the hippocampus, indicating neuronal uptake of the drug. (C) 1997 Intox Press, Inc.
C1 NATL INST MENTAL HLTH & NEUROSCI,DEPT NEUROPATHOL,BANGALORE 560029,KARNATAKA,INDIA.
NATL INST MENTAL HLTH & NEUROSCI,DEPT NEUROCHEM,BANGALORE 560029,KARNATAKA,INDIA.
NCI,LAB DRUG DISCOVERY RES & DEV,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702.
NR 13
TC 1
Z9 1
U1 0
U2 0
PU INTOX PRESS INC
PI LITTLE ROCK
PA PO BOX 24865, LITTLE ROCK, AR 72221
SN 0161-813X
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PY 1997
VL 18
IS 1
BP 89
EP 95
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA XG646
UT WOS:A1997XG64600014
PM 9215991
ER
PT J
AU Sriram, K
Boyd, MR
Vistica, DT
Ravindranath, V
AF Sriram, K
Boyd, MR
Vistica, DT
Ravindranath, V
TI In vitro neurotoxicity of the antitumor agent
9-methoxy-N-2-methylellipticinium acetate (MMEA): Role of brain
cytochrome P-450
SO NEUROTOXICOLOGY
LA English
DT Article
DE 9-methoxy-N-2-methylellipticinium acetate; ellipticines; brain;
cytochrome P-450; neurotoxicity; brain slices
ID NADH-DEHYDROGENASE; INDUCED TOXICITY; DERIVATIVES; INVITRO;
CYTOTOXICITY; POTENTIATION; ELLIPTICINE; PROTECTION; INHIBITORS; BINDING
AB 9-Methoxy-N-2-methylellipticinium acetate (MMEA) is representative of a series of quaternized ellipticine derivatives that are selectively cytotoxic to human brain tumor cell lines derived from non-neuronal (glial) cells (Acton et al, 1994). In an attempt to determine whether MMEA may exhibit toxicity to normal brain cells, we have examined the effect of the drug, in vitro, using sagittal slices of rat brain. Incubation of rat brain slices in an artificial cerebrospinal fluid medium containing MMEA resulted in dose-dependent leakage of lactate dehydrogenase (LDH) into the surrounding medium. However, other subcellular marker enzymes such as Na+-K(+)ATPase (plasma membrane), cytochrome c oxidase, isocitrate dehydrogenase, NADH- dehydrogenase (mitochondrial), N-acetylglucosaminidase, acid phosphatase (lysosomal), glyceraldehyde-3-phosphate dehydrogenase and enolase (glycolytic enzymes) were unaffected even at the highest tested concentrations of MMEA (10 and 100 mu M). Preincubation of slices with reserpine (1 nM) or, dopamine or serotonin-specific reuptake inhibitors abolished MMEA-induced toxicity in brain slices. Pretreatment of slices with piperonyl butoxide and metyrapone, inhibitors of cytochrome P-450, also prevented the toxicity of MMEA. Further, brain slices prepared from phenobarbital-treated rats showed enhanced sensitivity to MMEA.
C1 NATL INST MENTAL HLTH & NEUROSCI,DEPT NEUROCHEM,BANGALORE 560029,KARNATAKA,INDIA.
NCI,LAB DRUG DISCOVERY RES & DEV,DEV THERAPEUT PROGRAM,NIH,FREDERICK,MD 21701.
NR 28
TC 3
Z9 3
U1 0
U2 1
PU INTOX PRESS INC
PI LITTLE ROCK
PA PO BOX 24865, LITTLE ROCK, AR 72221
SN 0161-813X
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PY 1997
VL 18
IS 1
BP 97
EP 104
PG 8
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA XG646
UT WOS:A1997XG64600015
PM 9215992
ER
PT J
AU Scortegagna, M
Hanbauer, I
AF Scortegagna, M
Hanbauer, I
TI The effect of lead exposure and serum deprivation on mesencephalic
primary cultures
SO NEUROTOXICOLOGY
LA English
DT Article
DE Pb-2 toxicity; mesencephalic primary cultures; glia; neurons; serum
deprivation
ID BLOOD-BRAIN-BARRIER; CALCIUM CHANNELS; METAL-IONS; RAT-BRAIN; TOXICITY;
CELLS; METALLOTHIONEIN; PROTEIN; NEURONS; ASTROCYTES
AB The effect of Pb2+ was studied in embryonic mesencephalic primary cultures that contain neurons and glia. Pb2+ exposure in absence of serum, damaged more efficaciously the cultured cells than Pb2+ exposure in presence of serum. In serum-free medium, Pb2+ elicited mainly necrosis and apoptosis in maximally 13 % of the cells in culture. The glial fibrillary acidic protein (GFAP) content was decreased by Pb2+ exposure in serum-containing medium. The abundance of GFAP was also decreased by serum deprivation that was augmented by the addition of 12.5 mu M Pb2+ in, serum-free medium. A 6h exposure to 6 mu M Pb2+ in serum-free medium also lowered the low affinity H-3-D-aspartate uptake. A 6h exposure of mesencephalic cells to 3-25 mu M Pb2+ in serum-free medium failed to alter the number of tyrosine hydroxylase-and calretinin-immunoreactive cells, whereas, 50 mu M Pb2+ obliterated both cell types. A 6h exposure of cells to 3 mu M Pb2+ in serum-free medium decreased H-3-dopamine uptake by 50 % and 12.5 mu M Pb2+ obliterated it. Addition of albumin to serum-free medium failed to prevent the Pb2+-elicited inhibition of [H-3]-dopamine uptake suggesting that the serum-afforded delay of cell death may not be due to a removal of reactive Pb2+ by protein/chelate formation but rather to the Pb2+-scavenging function of glial cells. Serum deprivation may exacerbate the Pb2+-induced neurotoxicity presumably by impairing the metal scavenging function of astrocytes. (C) 1997 Inter Press, Inc.
C1 NHLBI, LAB MOL IMMUNOL, BETHESDA, MD 20892 USA.
NR 30
TC 22
Z9 25
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0161-813X
EI 1872-9711
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PY 1997
VL 18
IS 2
BP 331
EP 339
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA XU979
UT WOS:A1997XU97900003
PM 9291483
ER
PT S
AU Alexander, NJ
Hecht, NB
AF Alexander, NJ
Hecht, NB
BE Coutifaris, C
Mastroianni, L
TI Male contraception: future possibilities
SO NEW HORIZONS IN REPRODUCTIVE MEDICINE
SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES
LA English
DT Proceedings Paper
CT IXth World Congress on Human Reproduction
CY MAY 28-JUN 02, 1996
CL PHILADELPHIA, PA
C1 NICHHD, Contracept Dev Branch, Populat Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Alexander, NJ (reprint author), NICHHD, Contracept Dev Branch, Populat Res Ctr, NIH, 6100 Execut Blvd,8B13G MSC 7510, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PARTHENON PUBLISHING GROUP LTD
PI LANCASTER
PA CASTERTON HALL, CARNFORTH, LANCASTER LA6 2LA, ENGLAND
SN 0969-2622
BN 1-85070-793-6
J9 I C S S
PY 1997
VL 12
BP 91
EP 97
PG 7
WC Andrology; Obstetrics & Gynecology; Reproductive Biology
SC Endocrinology & Metabolism; Obstetrics & Gynecology; Reproductive
Biology
GA BK07Y
UT WOS:000071091100013
ER
PT B
AU Bezrukov, SM
Vodyanoy, I
Pustovoit, MA
AF Bezrukov, SM
Vodyanoy, I
Pustovoit, MA
BE Claeys, C
Simoen, E
TI Noise-facilitated signal transduction in threshold-free non-dynamical
systems: Theory and experiment.
SO NOISE IN PHYSICAL SYSTEMS AND 1/F FLUCTUATIONS, PROCEEDINGS OF THE 14TH
INTERNATIONAL CONFERENCE
LA English
DT Proceedings Paper
CT 14th International Conference on Noise in Physical Systems and l/f
Fluctuations (ICNF 97)
CY JUL 14-18, 1997
CL LOUVAIN, BELGIUM
SP IMEC, European Lab Electr Noise, European Union Network Noise
AB We find stochastic resonance in a very general model - a random pulse train where the probability of pulse generation is exponentially dependent on an input which is composed of a sine-wave signal plus random noise. Thus, we demonstrate that SR is a fundamental property of a wide variety of 'kT-driven' systems ranging from semiconductor p-n junctions to modem mesoscopic electronic devices to voltage-dependent ion channels - 'elemental switches' of biological signal computing and sensing. Our results are supported by experiments with voltage-dependent ion channels and computer simulations.
C1 NIH, DCRT, Bethesda, MD 20892 USA.
RP Bezrukov, SM (reprint author), NIH, DCRT, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WORLD SCIENTIFIC PUBL CO PTE LTD
PI SINGAPORE
PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE
BN 981-02-3141-5
PY 1997
BP 369
EP 372
PG 4
WC Acoustics; Engineering, Electrical & Electronic; Physics, Applied
SC Acoustics; Engineering; Physics
GA BK26Y
UT WOS:000071639300081
ER
PT J
AU Choi, CW
Barker, WC
Buvat, I
Carrasquillo, JA
Bacharach, SL
AF Choi, CW
Barker, WC
Buvat, I
Carrasquillo, JA
Bacharach, SL
TI Implications of dual-energy-window (DEW) scatter correction inaccuracies
for In-111 quantitative geometric mean imaging
SO NUCLEAR MEDICINE COMMUNICATIONS
LA English
DT Article
ID SPECT QUANTIFICATION; MONOCLONAL-ANTIBODY; COMPENSATION; CANCER;
SCINTIGRAPHY; FRAGMENTS; CAMERA
AB There is increasing clinical interest in the use of quantitative imaging for radiopharmaceuticals labelled with In-111. Dual-energy-window (DEW) scatter correction is a frequently used component of planar geometric mean quantitative imaging, but it is known that the scatter multiplier k suffers from significant dependence on the characteristics of the scatter medium. Phantom studies with a variety of source geometries were carried out to determine the clinical impact of this dependence on the quantitative accuracy of tumour imaging carried out in conjunction with attenuation correction.
Spheres of various sizes (5-20 ml volumes) containing approximately 3.7 MBq (100 mu Ci) In-111 were imaged at a variety of depths (4.8-10.5 cm) within an elliptical water-filled phantom, as well as in air. Geometric mean emission images were acquired using a 20% photopeak window at 247 keV and a 10% scatter window at 205 keV. These emission images were corrected for attenuation using measured Tc-99(m) transmission data that were scaled to In-111 photon energies. Scatter correction was performed in two ways: (1) using the standard DEW method and (2) using a modified DEW method that takes into account benign scatter in the detector crystal.
Errors in the activity estimates ranged from -4% to +3% for method 1 in water, and -5% to +3% for method 2 in water. In air, method 1 ranged from -13% to -5%, and method 2 ranged from -10% to -1%. Method 1 was found to yield an accuracy equivalent to that of method 2, except in conditions of very low patient scatter, when the modified method behaved significantly better. We conclude that in a variety of realistic geometries, variations in scatter fraction as determined by the DEW scatter correction method combined with appropriate attenuation correction need not inhibit accurate absolute quantitation of spherical 'tumours' labelled with In-111 when using planar imaging.
C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892.
RI Carrasquillo, Jorge/E-7120-2010
NR 25
TC 3
Z9 3
U1 0
U2 0
PU CHAPMAN HALL LTD
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN
SN 0143-3636
J9 NUCL MED COMMUN
JI Nucl. Med. Commun.
PD JAN
PY 1997
VL 18
IS 1
BP 79
EP 86
DI 10.1097/00006231-199701000-00016
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA WJ116
UT WOS:A1997WJ11600016
PM 9061707
ER
PT J
AU Benson, DA
Boguski, MS
Lipman, DJ
Ostell, J
AF Benson, DA
Boguski, MS
Lipman, DJ
Ostell, J
TI GenBank
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
AB The GenBank sequence database incorporates DNA sequences from all available public sources, primarily through the direct submission of sequence data from authors and from large-scale sequencing projects, Data exchange with the EMBL Data Library and the DNA Data Bank of Japan helps ensure comprehensive coverage, GenBank continues to focus on quality control and annotation while expanding data coverage and retrieval services, An integrated retrieval system, known as Entrez, incorporates data from the major DNA and protein sequence databases, along with genome maps and protein structure information, MEDLINE abstracts from published articles describing the sequences are also included as an additional source of biological annotation, Sequence similarity searching is offered through the BLAST family of programs, All of NCBI's services are offered through the World Wide Web, In addition, there are specialized server/client versions as well as FTP and e-mail sewer access.
RP Benson, DA (reprint author), NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BLDG 38A,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA.
NR 9
TC 176
Z9 181
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN 1
PY 1997
VL 25
IS 1
BP 1
EP 6
DI 10.1093/nar/25.1.1
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD443
UT WOS:A1997WD44300001
PM 9016491
ER
PT J
AU Hainaut, P
Soussi, T
Shomer, B
Hollstein, M
Greenblatt, M
Hovig, E
Harris, CC
Montesano, R
AF Hainaut, P
Soussi, T
Shomer, B
Hollstein, M
Greenblatt, M
Hovig, E
Harris, CC
Montesano, R
TI Database of p53 gene somatic mutations in human tumors and cell lines:
Updated compilation and future prospects
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID BREAST CANCERS; SUPPRESSOR GENE; URANIUM MINERS; LUNG-CANCER; MUTANTS;
WOMEN; TRANSACTIVATION; ETIOLOGY; HOTSPOT; PATTERN
AB In recent years, there has been an exponential increase in the number of p53 mutations identified in human cancers, The p53 mutation database consists of a list of point mutations in the p53 gene of human tumors and cell lines, compiled from the published literature and made available through electronic media, The database is now maintained at the International Agency for Research on Cancer (IARC) and is updated twice a year, The current version contains records on 5091 published mutations and is expected to surpass the 6000 mark in the January 1997 release, The database is available in various formats through the European Bioinformatics Institute (EBI) ftp server at: ftp://ftp.ebi.ac.uk/pub/databases/p53/ or by request from IARC (p53database@iarc.fr) and will be searchable through the SRS system in the near future, This report provides a description of the criteria for inclusion of data and of the current formats, a summary of the relevance of p53 mutation analysis to clinical and biological questions, and a brief discussion of the prospects for future developments.
C1 INT AGCY RES CANC,F-69372 LYON 08,FRANCE.
INSERM,U301,F-75010 PARIS,FRANCE.
EUROPEAN MOL BIOL LAB,OUTSTN EUROPEAN BIOINFORMAT INST,CAMBRIDGE CB10 1SD,ENGLAND.
GERMAN CANC RES CTR,D-69120 HEIDELBERG,GERMANY.
UNIV VERMONT,COLL MED,BURLINGTON,VT 05405.
NORWEGIAN RADIUM HOSP,INST CANC RES,N-0310 OSLO,NORWAY.
NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892.
RI Hovig, Eivind/H-2474-2011; Hainaut, Pierre /B-6018-2012;
OI Hovig, Eivind/0000-0002-9103-1077; Hainaut, Pierre /0000-0002-1303-1610;
soussi, thierry/0000-0001-8184-3293
NR 27
TC 253
Z9 259
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN 1
PY 1997
VL 25
IS 1
BP 151
EP 157
DI 10.1093/nar/25.1.151
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD443
UT WOS:A1997WD44300037
PM 9016527
ER
PT J
AU Martinez, E
Moore, DD
Keller, E
Pearce, D
Robinson, V
MacDonald, PN
Simons, SS
Sanchez, E
Danielsen, M
AF Martinez, E
Moore, DD
Keller, E
Pearce, D
Robinson, V
MacDonald, PN
Simons, SS
Sanchez, E
Danielsen, M
TI The Nuclear Receptor Resource project
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
AB We have expanded the original Glucocorticoid Receptor Resource (GRR) database to include several individual resources as part of a larger project called the Nuclear Receptor Resource (NRR), In addition to the GRR, the NRR currently features the Thyroid Hormone Receptor Resource, the Androgen Receptor Resource, the Mineralocorticoid Receptor Resource, the Vitamin D Receptor Resource, and the Steroid Receptor Associated Proteins Resource, The goal of the NRR project is to provide a comprehensive resource for information on the nuclear receptor superfamily, and to provide a forum for the dissemination and discussion of both published and unpublished material on these proteins, Although the individual resources are managed from different servers, all the files are integrated and can be accessed through the project's Home Page, housed at http://nrr.georgetown.edu/nrr.html. In the near future, we hope to expand the project to contain information on other nuclear receptors and to better our electronic publication system, To accomplish this, we encourage the involvement of nuclear receptor investigators in the NRR.
C1 GEORGETOWN UNIV,SCH MED,DEPT BIOCHEM & MOL BIOL,WASHINGTON,DC 20007.
HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT MOL BIOL & GENET,BOSTON,MA 02114.
EASTERN VIRGINIA MED SCH,GLENNAN CTR,NORFOLK,VA 23507.
UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94110.
ST LOUIS UNIV,HLTH SCI CTR,DEPT PHARMACOL & PHYSIOL SCI,ST LOUIS,MO 63104.
NIDDK,STEROID HORMONES SECT,NIH,BETHESDA,MD 20892.
MED COLL OHIO,DEPT PHARMACOL,TOLEDO,OH 43699.
RI Danielsen, Mark/B-1606-2008
OI Danielsen, Mark/0000-0002-0923-9945
FU NIDDK NIH HHS [R01 DK43382]; PHS HHS [K04 02105]
NR 0
TC 8
Z9 8
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN 1
PY 1997
VL 25
IS 1
BP 163
EP 165
DI 10.1093/nar/25.1.163
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD443
UT WOS:A1997WD44300039
PM 9016529
ER
PT J
AU Baxevanis, AD
Landsman, D
AF Baxevanis, AD
Landsman, D
TI Histone and histone fold sequences and structures: A database
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ALIGNMENT; CHROMATIN; PROTEINS; TOOL; DNA
AB A database of aligned histone protein sequences has been constructed based on the results of homology searches of the major public sequence databases. In addition, sequences of proteins identified as containing the histone fold motif and structures of all known histone and histone fold proteins have been included in the current release. Database resources include information on conflicts between similar sequence entries in different source databases, multiple sequence alignments, and links to the Entrez integrated information retrieval system at the National Center for Biotechnology Information (NCBI). The database currently contains over 1000 protein sequences.
C1 NIH,COMPUTAT BIOL BRANCH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20894.
NIH,NATL CTR HUMAN GENOME RES,GENOME TECHNOL BRANCH,BETHESDA,MD 20892.
RI Landsman, David/C-5923-2009;
OI Landsman, David/0000-0002-9819-6675
NR 17
TC 10
Z9 10
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN 1
PY 1997
VL 25
IS 1
BP 272
EP 273
DI 10.1093/nar/25.1.272
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD443
UT WOS:A1997WD44300062
PM 9016552
ER
PT J
AU Tutonda, MG
Fain, HD
Buckheit, RW
Broom, AD
AF Tutonda, MG
Fain, HD
Buckheit, RW
Broom, AD
TI The role of hydrophobic versus hydrophilic base character in the
anti-HIV activity of purine-containing polyribonucleotides
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; STRANDED POLYRIBONUCLEOTIDES;
NUCLEOSIDES; INFECTION; THERAPY
AB In contrast to the highly amphiphilic poly(1-methyl-6-thioinosinic acid), a potent anti-HIV agent, poly(1-amino-6-thioinosinic acid) (PATI) lacks the unique melting behavior characteristic of the amphiphilic polymers and is completely devoid of anti-HIV activity. This is consistent with the hypothesis that amphiphilic character and the ability to form an ordered secondary structure in solution are prerequisites for potent anti-HIV activity of single-stranded polynucleotides.
C1 UNIV UTAH,COLL PHARM,DEPT MED CHEM,SALT LAKE CITY,UT 84112.
FREDERICK CANC RES & DEV CTR,SO RES INST,VIROL RES DIV,FREDERICK,MD 21701.
NR 15
TC 8
Z9 8
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 1-2
BP 173
EP 182
DI 10.1080/07328319708002531
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WL664
UT WOS:A1997WL66400016
ER
PT J
AU Eritja, R
Adam, V
Avino, A
Diaz, AR
Fabrega, C
Ferrer, E
Grotli, M
Garcia, RG
Hoffmann, M
Marquez, VE
Wiersma, M
AF Eritja, R
Adam, V
Avino, A
Diaz, AR
Fabrega, C
Ferrer, E
Grotli, M
Garcia, RG
Hoffmann, M
Marquez, VE
Wiersma, M
TI Preparation of oligonucleotides containing nonnatural base analogs.
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article
ID DNA; DERIVATIVES; NUCLEOSIDE
AB The preparation of oligonucleotides containing 5-amino-2'-deoxyuridine, 5-N-acetamido-2'-deoxyuridine, 5-aza-2'-deoxycytidine and N-2-substituted guanosine derivatives is described. In each case selection of the appropriate protective group, synthesis and deprotection conditions is discussed.
C1 NCI,NIH,BETHESDA,MD 20892.
RP Eritja, R (reprint author), EUROPEAN MOL BIOL LAB,MEYERHOFSTR 1,D-69117 HEIDELBERG,GERMANY.
RI Grotli, Morten/A-8735-2010; eritja, ramon/B-5613-2008; Avino,
Anna/N-5223-2015; Fabrega, MCarme/K-9847-2014
OI Grotli, Morten/0000-0002-0154-0151; eritja, ramon/0000-0001-5383-9334;
Avino, Anna/0000-0003-3047-738X; Fabrega, MCarme/0000-0003-3816-7634
NR 14
TC 2
Z9 2
U1 0
U2 3
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 5-6
BP 697
EP 702
DI 10.1080/07328319708002936
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA XP845
UT WOS:A1997XP84500026
ER
PT J
AU Agrawal, S
Jiang, ZW
Zhao, QY
Shaw, D
Sun, D
Saxinger, C
AF Agrawal, S
Jiang, ZW
Zhao, QY
Shaw, D
Sun, D
Saxinger, C
TI Mixed-backbone oligonucleotides containing phosphorothioate and
methylphosphonate linkages as second generation antisense
oligonucleotide
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID IMMUNODEFICIENCY-VIRUS TYPE-1; OLIGODEOXYNUCLEOTIDE PHOSPHOROTHIOATES;
PHARMACOKINETICS; REPLICATION; ACTIVATION; MICE; RNA
AB Antisense oligonucleotides are being studied as novel therapeutic agents. To further improve the properties of antisense oligonucleotides, we have synthesized phosphorothioate oligonucleotides containing methylphosphonate linkages at the 5'-end, the 3'-end, or in the center, and have evaluated the impact of these linkages on the biophysical properties, biological properties, and some of the safety parameters.
C1 UNIV ALABAMA,LURLEEN B WALLACE TUMOR INST,BIRMINGHAM,AL 35233.
NCI,DIV BASIC SCI,BETHESDA,MD 20892.
RP Agrawal, S (reprint author), HYBRIDON INC,1 INNOVAT DR,WORCESTER,MA 01605, USA.
NR 19
TC 7
Z9 7
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 927
EP 936
DI 10.1080/07328319708006109
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000006
ER
PT J
AU Jeong, LS
Bae, M
Chun, MW
Marquez, VE
AF Jeong, LS
Bae, M
Chun, MW
Marquez, VE
TI Synthesis and anti-HIV activity of carbocyclic ring-enlarged
4',1'a-methano oxetanocin analogues
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
AB Synthesis of carbocyclic ring-enlarged 4',1'a-methano oxetanocin analogues via completely regioselective opening of cyclic sulfites by sodium azide or purine bases is described.
C1 SEOUL NATL UNIV,COLL PHARM,SEOUL 151742,SOUTH KOREA.
NCI,DIV BASIC SCI,MED CHEM LAB,NIH,BETHESDA,MD 20892.
RP Jeong, LS (reprint author), EWHA WOMANS UNIV,COLL PHARM,MED CHEM LAB,SEOUL 120750,SOUTH KOREA.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1059
EP 1062
DI 10.1080/07328319708006132
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000029
ER
PT J
AU Eritja, R
Marquez, VE
Garcia, RG
AF Eritja, R
Marquez, VE
Garcia, RG
TI Synthesis and properties of oligonucleotides containing
5-aza-2'-deoxycytidine.
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID LABILE
AB The preparation of a protected derivative of 5-aza-2'-deoxycytidine carrying the 2-(p-nitrophenyl)ethyl group is described. The new derivative is useful for the preparation of oligonucleotides containing 5-aza-2'-deoxycytidine using a special methodology that avoids the use of ammonia.
C1 NCI,NIH,BETHESDA,MD 20892.
RP Eritja, R (reprint author), EUROPEAN MOL BIOL LAB,MEYERHOFSTR 1,D-69117 HEIDELBERG,GERMANY.
RI eritja, ramon/B-5613-2008
OI eritja, ramon/0000-0001-5383-9334
NR 8
TC 2
Z9 2
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1111
EP 1114
DI 10.1080/07328319708006144
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000041
ER
PT J
AU Cramer, H
Torrence, PF
AF Cramer, H
Torrence, PF
TI Synthesis of (2',5')-oligoadenylate antisense chimeras targeting steroid
5 alpha-reductase
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID 2-5A ANTISENSE; RNA TARGET
AB 2-5A antisense chimeras have been synthesized which target human steroid 5 alpha-reductase mRNA. To enhance the stability of the chimera towards degradative enzymes the terminal phosphodiester bond was isomerized from 3',5' to 3',3' and the 5'-phosphate group was thiolated.
C1 NIDDK,SECT BIOMED CHEM,MED CHEM LAB,NIH,BETHESDA,MD 20892.
NR 9
TC 0
Z9 0
U1 0
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1201
EP 1204
DI 10.1080/07328319708006157
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000054
ER
PT J
AU Player, MR
Maitra, R
Silverman, R
Torrence, PF
AF Player, MR
Maitra, R
Silverman, R
Torrence, PF
TI Targeting HIV mRNA for degradation: 2,5-A antisense chimeras as
potential chemotherapeutic agents for AIDS
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
AB We have identified a region within a 1 kb HIV gag RNA which can be ablated in vitro using a 2,5-A antisense chimera. The cleavage was specific and almost complete at a concentration of 100 nM chimera.
C1 NIDDKD,NIH,BETHESDA,MD 20892.
CLEVELAND CLIN RES FDN,CLEVELAND,OH 44195.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1221
EP 1222
DI 10.1080/07328319708006162
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000059
ER
PT J
AU Valette, G
Girardet, JL
Pompon, A
Perigaud, C
Gosselin, G
Korba, B
Hantz, O
Imbach, JL
AF Valette, G
Girardet, JL
Pompon, A
Perigaud, C
Gosselin, G
Korba, B
Hantz, O
Imbach, JL
TI The pronucleotide approach .3. Synthesis, anti-HBV activity and
stability studies of the bis(S-pivaloyl-2-thioethyl) phosphotriester
derivative of acyclovir
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID T-CELL CULTURE; INTRACELLULAR DELIVERY; 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE
AB The nucleoside analog Acyclovir (ACV) is used in the treatment of herpes simplex (HSV) and varicella-zoster (VZV) diseases. The possibility to extend the application field of ACV by using the bis[SATE] pronucleotide approach in order to deliver ACVMP inside the cell was investigated, And actually, the title compound has potent anti-hepatitis B activity in cell culture experiments. Here, we also report its synthesis and stability in various media.
C1 UNIV MONTPELLIER 2,CNRS,UMR USTL 5625,CHIM BIOORGAN LAB,F-34095 MONTPELLIER 5,FRANCE.
NIH,VIROL BRANCH,DMID,BETHESDA,MD 20892.
SIDA & RETROVIRUS HUMAINS,INSERM,U 271,UNITE RECH HEPATITES,F-69424 LYON 3,FRANCE.
NR 7
TC 6
Z9 6
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1331
EP 1335
DI 10.1080/07328319708006182
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000079
ER
PT J
AU Winter, H
Maeda, Y
Mitsuya, H
Zemlicka, J
AF Winter, H
Maeda, Y
Mitsuya, H
Zemlicka, J
TI Phosphodiester amidates of unsaturated nucleoside analogues as anti-HIV
agents
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID INTRACELLULAR DELIVERY; ABSOLUTE-CONFIGURATION; ENANTIOSELECTIVITY;
DERIVATIVES; PATHWAYS; ISODDA
AB Lipophilic phosphodiester L-alaninates of acyclic unsaturated nucleoside analogues 1d, 1e, 2d, 2e, 3d, 3e, 4d and 5d were prepared and their antiretroviral activity was examined in ATH8 cell culture infected with HIV-1. A possible mechanism of action of these analogues is discussed.
C1 WAYNE STATE UNIV,SCH MED,BARBARA ANN KARMANOS CANC INST,DETROIT,MI 48201.
NCI,EXPT RETROVIROL SECT,MED BRANCH,NIH,BETHESDA,MD 20892.
NR 11
TC 4
Z9 4
U1 0
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1341
EP 1345
DI 10.1080/07328319708006184
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000081
ER
PT J
AU Charubala, R
Maurinsh, J
Rosler, A
Melguizo, M
Jungmann, O
Gottlieb, M
Lehbauer, J
Hawkins, M
Pfleiderer, W
AF Charubala, R
Maurinsh, J
Rosler, A
Melguizo, M
Jungmann, O
Gottlieb, M
Lehbauer, J
Hawkins, M
Pfleiderer, W
TI Pteridine nucleosides new - New versatile building blocks in
oligonucleotide synthesis
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID LUMAZINE
AB Chemical syntheses of 1-(2-deoxy-beta-D-ribofuranosyl)lumazines and isopterins as well as 8-(2-deoxy-beta-D-ribofuranosyl)-4-amino-7(8H)pteridones and -isoxanthopterins have been developed to make the structural analogs of the naturally occurring 2'-deoxyribonucleosides in the pteridine series available. The corresponding phosphoramidites have been used in machine-aided solid-support syntheses leading to new types of fluorescence labeled oligonucleotides. The effects of the various fluorophors on duplex formation and as labels for enzyme reactions is demonstrated.
C1 NIH,BETHESDA,MD 20892.
RP Charubala, R (reprint author), UNIV KONSTANZ,FAK CHEM,POSTFACH 5560,D-78434 CONSTANCE,GERMANY.
RI Melguizo, Manuel/M-1273-2014
OI Melguizo, Manuel/0000-0002-2210-9547
NR 16
TC 12
Z9 12
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1369
EP 1378
DI 10.1080/07328319708006188
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000085
ER
PT J
AU Marquez, VE
Ezzitouni, A
Siddiqui, MA
Russ, P
Ikeda, H
George, C
AF Marquez, VE
Ezzitouni, A
Siddiqui, MA
Russ, P
Ikeda, H
George, C
TI Conformational analysis of nucleosides constructed on a
bicyclo[3.1.0]hexane template. Structure-antiviral activity analysis for
the northern and southern hemispheres of the pseudorotational cycle
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID CARBOCYCLIC THYMIDINE
AB A conformational analysis of carbocyclic nucleosides built on a rigid bicyclo[3.1.0]hexane template (1-4, Northern and 5-8 Southern) showed that the Northern conformation prefers an anti glycosyl torsion angle whereas the Southern conformation favors the syn range. Antiviral activity was mostly associated with the Northern conformers.
C1 USN,RES LAB,STRUCT MATTER LAB,WASHINGTON,DC 20375.
RP Marquez, VE (reprint author), NCI,MED CHEM LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892, USA.
NR 4
TC 11
Z9 11
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1431
EP 1434
DI 10.1080/07328319708006199
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000096
ER
PT J
AU Zhang, WF
Torrence, P
AF Zhang, WF
Torrence, P
TI The synthesis of 2-5A antisense chimeras with various non-nucleoside
components.
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
ID RNA
AB We have synthesized a series of 2-5A chimeras in which the nature of the oligoadenylate-antisense linkage and the length of the 2',5'-oligoadenylate were varied. In addition, a branched linker was introduced to relocate the 2',5'-oligoadenylate with respect to the antisense domain.
C1 NIDDKD,SECT BIOMED CHEM,MED CHEM LAB,NIH,BETHESDA,MD 20892.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1579
EP 1582
DI 10.1080/07328319708006234
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000131
ER
PT J
AU Xiao, W
Li, GY
Torrence, PF
Cirino, NM
Silverman, RH
AF Xiao, W
Li, GY
Torrence, PF
Cirino, NM
Silverman, RH
TI Inhibition of Respiratory Syncytial Virus by double termini-protected
2-5A antisense chimeras
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article; Proceedings Paper
CT XII International Round Table on Nucleosides, Nucleotides and their
Biological Applications - Making Drugs Out of Nucleosides and
Oligonucleotides
CY SEP 15-19, 1996
CL LA JOLLA, CA
AB Respiratory syncytial virus (RSV) replication was reduced by greater than 90% after treatment of infected human tracheal epithelial cell line, 9HTE, with double termini-protected 2-5 A antisense chimeras.
C1 NIDDK,SECT BIOMED CHEM,NIH,BETHESDA,MD 20892.
CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195.
NR 5
TC 2
Z9 2
U1 0
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 7-9
BP 1735
EP 1738
DI 10.1080/07328319708006266
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YF530
UT WOS:A1997YF53000163
ER
PT J
AU Buolamwini, JK
Barchi, JJ
AF Buolamwini, JK
Barchi, JJ
TI Solution NMR conformational analysis of the potent equilibrative
sensitive (ES) nucleoside transporter inhibitor,
S-(4-nitrobenzyl)mercaptopurine riboside (NBMPR)
SO NUCLEOSIDES & NUCLEOTIDES
LA English
DT Article
ID COUPLING-CONSTANTS; SUBSTITUENT ELECTRONEGATIVITIES; KARPLUS EQUATION;
SUGAR RING; PROTEIN; BINDING; ANALOGS
AB High resolution NMR analysis involving one-dimensional (1-D) H-1 and nuclear Overhauser (NOE) difference spectroscopy was applied to solutions of NBMPR in DMSO-d(6). Coupling constants were obtained at different temperatures between 285 and 353 K, and used to analyze the rotamer preferences about the C-4'-C-5' bond. The results revealed a rotamer distribution about the chi tortion angle that favors the high-anti range, a preponderance of the gamma(+) rotamer (at similar to 64%) with respect to the gamma torsion angle, and a higher population of the south (S) conformer, which was favored by as little as the 4% to as much as 31% over the north (N) conformer as calculated by the program PSEUROT 6.2. The high-anti glycosidic torsion orientation appears to be the major conformational difference between the solution structure of NBMPR determined in this study and the structure previously observed in the solid state.
C1 Univ Mississippi, Sch Pharm, Pharmaceut Sci Res Inst, Dept Med Chem, University, MS 38677 USA.
Univ Mississippi, Sch Pharm, Pharmaceut Sci Res Inst, Natl Ctr Dev Nat Prod, University, MS 38677 USA.
NCI, Med Chem Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA.
RP Buolamwini, JK (reprint author), Univ Mississippi, Sch Pharm, Pharmaceut Sci Res Inst, Dept Med Chem, University, MS 38677 USA.
RI Barchi Jr., Joseph/N-3784-2014
NR 19
TC 4
Z9 4
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0732-8311
J9 NUCLEOS NUCLEOT
JI Nucleosides Nucleotides
PY 1997
VL 16
IS 12
BP 2101
EP 2110
DI 10.1080/07328319708002561
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA YN745
UT WOS:000071202100002
ER
PT S
AU McCormick, KA
AF McCormick, KA
BE Gerdin, U
Tallberg, M
Wainwright, P
TI Improving nursing documentation to include outcomes of care in
computerized information systems
SO NURSING INFORMATICS: THE IMPACT OF NURSING KNOWLEDGE ON HEALTH CARE
INFORMATICS
SE STUDIES IN HEALTH TECHNOLOGY AND INFORMATICS
LA English
DT Proceedings Paper
CT 6th Triennial International Congress of IMIA-NI on Nursing Informatics -
The Impact of Nursing Knowledge on Health Care Informatics (NI 97)
CY 1997
CL STOCKHOLM, SWEDEN
SP Int Med Informat Assoc, Special Interest Grp Nursing Informat, No Nurses Federat, Swedish Nurses Assoc, Swedish Assoc Hlth Officers, Swedish Federat Cty Council, Stockholm Univ Coll Hlth Sci, Swedish Inst Hlth Serv Dev, S Stockholm Hlth Care Dist
AB Oftentimes when models of information systems are developed, outcomes are either left out or described as an end product of treatment alone. However, in research demonstrating outcomes, evaluating whether outcomes are achieved can best be accomplished when the outcomes are integrated into the entire care process. This paper describes a model for nursing to consider when integrating outcomes during several components of nursing care delivery, and several nursing domains for achieving outcome of care.
RP McCormick, KA (reprint author), AGCY HLTH CARE POLICY & RES,CTR INFORMAT TECHNOL,2101 E JEFFERSON ST,SUITE 602,ROCKVILLE,MD 20852, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU I O S PRESS
PI AMSTERDAM
PA VAN DIEMENSTRAAT 94, 1013 CN AMSTERDAM, NETHERLANDS
SN 0926-9630
BN 90-5199-362-5
J9 ST HEAL T
PY 1997
VL 46
BP 105
EP 110
PG 6
WC Medical Informatics; Nursing
SC Medical Informatics; Nursing
GA BJ94F
UT WOS:A1997BJ94F00018
PM 10175380
ER
PT J
AU Grady, P
AF Grady, P
TI NINR and the nursing research community: The next 10 years ... The next
century
SO NURSING OUTLOOK
LA English
DT News Item
RP Grady, P (reprint author), NIH,NINR,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0029-6554
J9 NURS OUTLOOK
JI Nurs. Outlook
PD JAN-FEB
PY 1997
VL 45
IS 1
BP 43
EP 43
DI 10.1016/S0029-6554(97)90059-2
PG 1
WC Nursing
SC Nursing
GA WJ887
UT WOS:A1997WJ88700010
PM 9139263
ER
PT J
AU Leidy, NK
Abbott, RD
Fedenko, KM
AF Leidy, NK
Abbott, RD
Fedenko, KM
TI Sensitivity and reproducibility of the dual-mode actigraph under
controlled levels of activity intensity
SO NURSING RESEARCH
LA English
DT Article; Proceedings Paper
CT Sigma Theta Tau 33rd Biennial Convention
CY NOV 05, 1995
CL DETROIT, MI
SP Sigma Theta Tau
ID PHYSICAL-ACTIVITY; PERCEIVED EXERTION; MOTOR-ACTIVITY; PLACEMENT;
DISEASE; DESIGN
AB The purpose of this study was to test the sensitivity and reproducibility of dual-made actigraphy as an objective measure of functional performance in healthy adults under controlled levels of activity intensity. Twenty subjects wore the instrument on the nondominant wrist while performing standardized tasks selected to represent day-to-day activities at three levels of intensity (five tasks in each level): light (1-2 metabolic equivalents), moderate (3-4 metabolic equivalents), and heavy (4-6 metabolic equivalents). Upon completion of each intensity level, subjects were asked to rate their level of exertion using Borg's 15-point rating of perceived exertion (RPE) scale. Eighteen subjects repeated the protocol within 7 days. Zero-crossing and time-above-threshold mades successfully differentiated between light and moderate and between light and heavy activity. Reproducibility correlation coefficients (r(s)) across activity levels were .80 and .66 for the two modes, respectively. Results suggest dual-mode actigraphy may be useful for the study of performance variation and structure in healthy and chronically ill individuals.
C1 NATL INST NURSING RES,LAB STUDY HUMAN RESPONSES HLTH & ILLNESS,NIH,BETHESDA,MD.
UNIV VIRGINIA,DEPT MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22903.
UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201.
NR 41
TC 17
Z9 17
U1 0
U2 1
PU AMER J NURSING CO
PI NEW YORK
PA 555 W 57TH ST, NEW YORK, NY 10019-2961
SN 0029-6562
J9 NURS RES
JI Nurs. Res.
PD JAN-FEB
PY 1997
VL 46
IS 1
BP 5
EP 11
DI 10.1097/00006199-199701000-00002
PG 7
WC Nursing
SC Nursing
GA WF263
UT WOS:A1997WF26300002
PM 9024418
ER
PT J
AU Morse, MA
Kresty, LA
Steele, VE
Kelloff, GJ
Boone, CW
Balentine, DA
Harbowy, ME
Stoner, GD
AF Morse, MA
Kresty, LA
Steele, VE
Kelloff, GJ
Boone, CW
Balentine, DA
Harbowy, ME
Stoner, GD
TI Effects of theaflavins on N-nitrosomethylbenzylamine-induced esophageal
tumorigenesis
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID PHENETHYL ISOTHIOCYANATE; DNA METHYLATION; ELLAGIC ACID; BLACK TEA;
RATS; CANCER; CONSUMPTION; INHIBITION; CHEMOPREVENTION; GREEN
AB The purpose of this experiment was to compare the inhibitory effects of the polyphenol fraction of black tea, theaflavins (TF), the polyphenol fraction of green tea, and (-)-epigallocatechin-3-gallate (EGCG) in the rat esophageal tumor model. The tea fractions were administered in the drinking water at concentrations of 360 and 1,200 ppm for two weeks before administration of the esophageal carcinogen N-nitrosomethylbenzylamine (NMBA). NMBA was administered subcutaneously in 10% dimethyl sulfoxide three times weekly for five weeks. Additional groups of rats received only vehicle and plain drinking water or vehicle and drinking water containing 1,200 ppm of each tea fraction. Twenty-five weeks after NMBA administration began, the experiment was terminated and esophagi were excised and scored for tumors. Rats that were not dosed with NMBA had no tumors. Rats treated with NMBA only had an esophageal tumor incidence of 100% and a multiplicity of 3.3 +/- 0.4 tumors/rat. The proportion of rats developing tumors was not significantly reduced by any of the four tea fractions at the concentrations tested. However, the 1,200 ppm concentrations of each tea fraction in the drinking water produced some reduction in esophageal tumor multiplicity, although only TF significantly reduced tumor multiplicity compared with rats treated with NMBA only. The rates of esophageal tumor formation were significantly reduced at 360 and 1,200 ppm by TF and EGCG.
C1 NCI,CHEMOPREVENT BRANCH,BETHESDA,MD 20892.
THOMAS J LIPTON TEA CO,ENGLEWOOD CLIFFS,NJ 07632.
RP Morse, MA (reprint author), OHIO STATE UNIV,SCH PUBL HLTH,DIV ENVIRONM HLTH SCI,CHRI 1148,300 W 10TH AVE,COLUMBUS,OH 43210, USA.
OI Harbowy, Matthew/0000-0003-4861-9411
FU NCI NIH HHS [N01-CN-25486-01]
NR 28
TC 42
Z9 45
U1 0
U2 2
PU LAWRENCE ERLBAUM ASSOC INC
PI MAHWAH
PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 1997
VL 29
IS 1
BP 7
EP 12
PG 6
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA YF603
UT WOS:A1997YF60300002
PM 9383778
ER
PT J
AU Fu, YM
Yu, ZX
Ferrans, VJ
Meadows, GG
AF Fu, YM
Yu, ZX
Ferrans, VJ
Meadows, GG
TI Tyrosine and phenylalanine restriction induces G0/G1 cell cycle arrest
in murine melanoma in vitro and in vivo
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID B-16 MELANOMA; NUCLEAR ANTIGEN; METASTATIC PHENOTYPE; MESSENGER-RNA;
GROWTH-FACTOR; INHIBITION; SELECTION; CANCER; PROLIFERATION; ENHANCEMENT
AB Tyr-Phe and Met limitation in vitro inhibited cell proliferation and proliferating cell nuclear antigen (PCNA) expression to a gl eater extent than serum limitation. Tyr-Phe and serum limitation arrested cells in the G0/GI phase; Met limitation blocked cells in the G0/GI and S phases. Tyr-Phe limitation progressively decreased cyclin D-1 expression to 30% of control within four days and did not affect expression of cyclin D-3 or cyclin-dependent kinase (CDK2, CDK4, and CDK5) expression. Met limitation decreased cyclin D-3 expression to 25% of control and CDK2 expression to 32% of control by Day 4 and did not affect expression of cyclin D-1, CDK4, and CDK5. Serum limitation inhibited cyclin D-1 and cyclin D-3 expression to 24% of control after four days and did not effect CDK expression. Expression of two CDK inhibitors, p21(WAF1/Cip1) and P27(Kip1), was not changed by amino acid or serum limitation. Dietary restriction of Tyr-Phe in mice bearing subcutaneous B16BL6 melanoma tumors decreased tumor growth rate compared with mice fed a normal diet. Tumors from Tyr-Phe-restricted mice exhibited decreased PCNA expression, G0/GI phase cell cycle arrest and reduced cyclin D-1 expression. These data indicate that decreased tumor growth in vivo associated with dietary restriction of Tyr and Phe is cell cycle specific.
C1 Washington State Univ, Coll Pharm, Dept Pharmaceut Sci, Pullman, WA 99164 USA.
Washington State Univ, Coll Pharm, Pharmacol & Toxicol Grad Program, Pullman, WA 99164 USA.
NHLBI, Pathol Sect, Bethesda, MD 20892 USA.
RP Meadows, GG (reprint author), Washington State Univ, Coll Pharm, Dept Pharmaceut Sci, Box 646510, Pullman, WA 99164 USA.
FU NCI NIH HHS [R01-CA-42465]
NR 34
TC 24
Z9 25
U1 1
U2 3
PU LAWRENCE ERLBAUM ASSOC INC
PI MAHWAH
PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 1997
VL 29
IS 2
BP 104
EP 113
PG 10
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA YM124
UT WOS:000071031100002
PM 9427972
ER
PT J
AU Breslow, RA
Subar, AF
Patterson, BH
Block, G
AF Breslow, RA
Subar, AF
Patterson, BH
Block, G
TI Trends in food intake: The 1987 and 1992 National Health Interview
Surveys
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID CANCER PREVENTION; QUESTIONNAIRE; RECORDS; WOMEN; VALIDATION; FREQUENCY
AB Tc, examine food intake trends in the US population, cross-sectional nationally representative food intake data were obtained from the 1987 and 1992 National Wealth Interview Survey Cancer control Supplements. In each of these years, approximately 10,000 respondents completed methodologically consistent food frequency questionnaires containing the same 57 food items. Between 1987 and 1992, the proportion of Americans consuming high-fat foods, including fried fish, fried chicken, bacon, eggs, whole milk, and butter, decreased. The proportion of Americans drinking alcoholic beverages also decreased: fewer drank wine and hard liquor in 1992. The proportion of fruit and vegetable consumers remained stable over time. These results are similar to those obtained from more detailed national surveys. National guidelines urge Americans to avoid intake of high-fat foods, increase consumption of fruits and vegetables, and practice moderation when drinking alcoholic beverages to prevent cancer and other chronic diseases. The direction of Americans' apparent changes in food usage between 1987 and 1992, evaluated using limited data from food frequency questionnaires, suggests greater behavioral changes in the direction of guidelines recommending avoidance of foods that may increase the risk of cancer than in the direction of guidelines recommending increased consumption of foods that may confer protection.
C1 UNIV CALIF BERKELEY,BERKELEY,CA 94720.
RP Breslow, RA (reprint author), NCI,EPN 313,BIOMETRY BRANCH,6130 EXECUT BLVD,BETHESDA,MD 20892, USA.
RI Block, Gladys/E-3304-2010
NR 32
TC 20
Z9 20
U1 1
U2 4
PU LAWRENCE ERLBAUM ASSOC INC
PI MAHWAH
PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 1997
VL 28
IS 1
BP 86
EP 92
PG 7
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA XE795
UT WOS:A1997XE79500013
PM 9200155
ER
PT J
AU Shoff, SM
Newcomb, PA
Longnecker, MP
AF Shoff, SM
Newcomb, PA
Longnecker, MP
TI Frequency of eating and risk of colorectal cancer in women
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID COLON-CANCER; DIETARY FACTORS; BREAST-CANCER; LARGE-BOWEL; WISCONSIN
AB Numerous dietary constituents have been extensively studied with regard to colorectal cancer risk, but food intake patterns have been studied less frequently. The purpose of these analyses was to describe associations between frequency of eating and colorectal cancer risk in women. Female Wisconsin residents aged 30-74 years with a diagnosis of colorectal cancer within two years were identified through the statewide tumor registry. Control subjects were randomly selected from lists of licensed drivers (<65 yrs old) and Medicare beneficiaries (65-74 yrs old). Meal and snack frequency was obtained on a subset of case (n = 189) and control (n = 322) subjects. Odds ratios and 95% confidence intervals (CIs) obtained from conditional logistic regression models were used to estimate multivariate-adjusted relative risks. Compared with women consuming three or four meat daily, women consuming one to two meals daily had an adjusted relative risk of 0.57 (95% CI = 0.34-0.94). Snacking frequency and frequency of meals + snacks were not associated with cancer risk. These results are consistent with other reports and suggest that meal frequency is associated with colorectal cancer risk.
C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706.
FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104.
NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709.
RP Shoff, SM (reprint author), UNIV WISCONSIN,CTR COMPREHENS CANC,MED SCI CTR,ROOM 47660,1300 UNIV AVE,MADISON,WI 53706, USA.
OI Longnecker, Matthew/0000-0001-6073-5322
FU NCI NIH HHS [R25CA-47785]
NR 16
TC 11
Z9 11
U1 0
U2 0
PU LAWRENCE ERLBAUM ASSOC INC
PI MAHWAH
PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PY 1997
VL 27
IS 1
BP 22
EP 25
PG 4
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA VX321
UT WOS:A1997VX32100003
PM 8970177
ER
PT S
AU Hibbeln, JR
Umhau, JC
George, DT
Salem, N
AF Hibbeln, JR
Umhau, JC
George, DT
Salem, N
BE Simopoulos, AP
Pavlou, KN
TI Do plasma polyunsaturates predict hostility and depression?
SO NUTRITION AND FITNESS: METABOLIC AND BEHAVIORAL ASPECTS IN HEALTH AND
DISEASE
SE World Review of Nutrition and Dietetics
LA English
DT Article; Proceedings Paper
CT 3rd International Conference on Nutrition and Fitness
CY MAY 24-27, 1996
CL ATHENS, GREECE
ID FATTY-ACID METABOLISM; CEREBROSPINAL-FLUID; SERUM-CHOLESTEROL;
5-HYDROXYINDOLEACETIC ACID; SOCIAL-BEHAVIOR; HUMAN CSF; SEROTONIN;
VIOLENT; DISEASE; MEN
RP Hibbeln, JR (reprint author), NIAAA, LAB MEMBRANE BIOCHEM & BIOPHYS, 12501 WASHINGTON AVE, ROCKVILLE, MD 20852 USA.
NR 69
TC 45
Z9 48
U1 1
U2 2
PU KARGER
PI BASEL
PA POSTFACH, CH-4009 BASEL, SWITZERLAND
SN 0084-2230
BN 3-8055-6474-0
J9 WORLD REV NUTR DIET
JI World Rev.Nutr.Diet.
PY 1997
VL 82
BP 175
EP 186
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA BJ41E
UT WOS:A1997BJ41E00012
PM 9270321
ER
PT S
AU Nolan, PJ
Knepper, MA
Packer, RK
AF Nolan, PJ
Knepper, MA
Packer, RK
BE ODonovan, DJ
Endou, H
Schoolwerth, AC
Tizianello, A
Walls, J
TI Role of adrenal steroids in stimulating ammonium excretion during acute
metabolic acidosis
SO NUTRITIONAL AND ACID-BASE ASPECTS OF AMINO ACID METABOLISM
SE CONTRIBUTIONS TO NEPHROLOGY
LA English
DT Article; Proceedings Paper
CT 7th International Ammoniagenesis Workshop
CY MAY 20-23, 1996
CL GALWAY, IRELAND
SP Gambro Ltd, Shire Pharm Ltd, Janssen Cilag Ltd, Pfizer Corp, Univ Kyorin, Sch Med, Tokyo, Bord Failte, Conf Bur Ireland, Univ Coll, Galway
ID 11-BETA-HYDROXYSTEROID DEHYDROGENASE; INNER MEDULLA; RAT;
CORTICOSTERONE; ACIDIFICATION; PURIFICATION; TRANSPORT; SEGMENTS;
NEPHRON; CELLS
C1 GEORGE WASHINGTON UNIV,DEPT BIOL SCI,WASHINGTON,DC 20052.
NHLBI,KIDNEY & ELECTROLYTE METAB LAB,NIH,BETHESDA,MD 20892.
NR 23
TC 1
Z9 1
U1 0
U2 0
PU KARGER
PI BASEL
PA POSTFACH, CH-4009 BASEL, SWITZERLAND
SN 0302-5144
BN 3-8055-6490-2
J9 CONTRIB NEPHROL
JI Contrib.Nephrol.
PY 1997
VL 121
BP 55
EP 61
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA BJ75M
UT WOS:A1997BJ75M00009
PM 9336698
ER
PT S
AU Tataranni, PA
Ravussin, E
AF Tataranni, PA
Ravussin, E
BE Anderson, GH
Rolls, BJ
Steffen, DG
TI Effect of fat intake on energy balance
SO NUTRITIONAL IMPLICATIONS OF MACRONUTRIENT SUBSTITUTES
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT Conference on Nutritional Implications of Macronutrient Substitutes
CY OCT 27-29, 1996
CL ARLINGTON, VA
SP New York Acad Sci, Int Life Sci Inst, N Amer Tech Comm Macronutrient Substitut
ID DIETARY-FAT; PIMA-INDIANS; WEIGHT-GAIN; INSULIN-RESISTANCE;
LIPOPROTEIN-LIPASE; OBESE SUBJECTS; CARBOHYDRATE; OXIDATION;
EXPENDITURE; HUMANS
RP Tataranni, PA (reprint author), NIDDKD, CLIN DIABET & NUTR SECT, NIH, 4212 N 16TH ST, ROOM 541-A, PHOENIX, AZ 85016 USA.
NR 48
TC 17
Z9 17
U1 1
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-084-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 819
BP 37
EP 43
DI 10.1111/j.1749-6632.1997.tb51797.x
PG 7
WC Food Science & Technology; Multidisciplinary Sciences; Nutrition &
Dietetics
SC Food Science & Technology; Science & Technology - Other Topics;
Nutrition & Dietetics
GA BH98L
UT WOS:A1997BH98L00005
PM 9186759
ER
PT S
AU Wickstrom, E
Tyson, FL
AF Wickstrom, E
Tyson, FL
BE Chadwick, DJ
Cardew, G
TI Differential oligonucleotide activity in cell culture versus mouse
models
SO OLIGONUCLEOTIDES AS THERAPEUTIC AGENTS
SE CIBA FOUNDATION SYMPOSIA
LA English
DT Article; Proceedings Paper
CT Symposium on Oligonucleotides as Therapeutic Agents
CY JAN 07-09, 1997
CL CIBA FDN, LONDON, ENGLAND
HO CIBA FDN
ID BREAST-CARCINOMA CELLS; ANTISENSE OLIGONUCLEOTIDES; NUDE-MICE; ONCOGENE
AMPLIFICATION; DOWN-REGULATION; OVARIAN-CANCER; EXPRESSION; DNA;
PHOSPHOROTHIOATE; INHIBITION
AB The usual course of drug discovery begins with the demonstration of compound activity in cells and, usually, a lower level of activity in animals. Successive rounds of drug design may result in a compound with sufficient activity in animals to justify clinical trials. The basic endpoints of therapeutic oligonucleotide experiments include target antigen reduction, target messenger reduction and inhibition of transformed cell proliferation or viral replication. However, one should expect oligonucleotides to exhibit pleiotropic behaviour, as do all other drugs. In an animal oligonucleotides will necessarily bind to and dissociate from all macromolecules encountered in the blood, in tissues, on cell surfaces and within cellular compartments. Contrary to expectations, oligonucleotides designed to be complementary to certain transcripts have sometimes been found moderately effective in cell-free extracts, more effective in cell culture and most effective in animal models. If greater potency against standard endpoints is reported in mouse models than was observed in cell culture, critical examination must consider alternate modes of action in animals that may not apply in cell culture. This counterintuitive paradox will be examined, based on studies of Ha-ras expression in bladder cancer, Ki-ras expression in pancreatic cancer, erbB2 expression in ovarian cancer and c-myc expression in B cell lymphoma.
C1 Thomas Jefferson Univ, Dept Microbiol & Immunol, Philadelphia, PA 19107 USA.
Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
RP Wickstrom, E (reprint author), Thomas Jefferson Univ, Dept Microbiol & Immunol, 1025 Walnut St, Philadelphia, PA 19107 USA.
FU NCI NIH HHS [CA42960, CA60139]
NR 41
TC 10
Z9 10
U1 0
U2 0
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND
SN 0300-5208
BN 0-471-97279-7
J9 CIBA F SYMP
PY 1997
VL 209
BP 124
EP 137
PG 14
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Medicine, General & Internal
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
General & Internal Medicine
GA BL63X
UT WOS:000076141500018
PM 9383573
ER
PT J
AU Ren, QF
VanGroeningen, CJ
Hardcastle, A
Aherne, GW
Geoffroy, F
Allegra, CJ
Johnston, PG
Grem, JL
AF Ren, QF
VanGroeningen, CJ
Hardcastle, A
Aherne, GW
Geoffroy, F
Allegra, CJ
Johnston, PG
Grem, JL
TI Determinants of cytotoxicity with prolonged exposure to fluorouracil in
human colon cancer cells
SO ONCOLOGY RESEARCH
LA English
DT Article
DE fluorouracil; DNA damage; thymidylate synthase; colon cancer
ID METASTATIC COLORECTAL-CARCINOMA; THYMIDYLATE SYNTHASE INHIBITION;
5-FLUOROURACIL CYTO-TOXICITY; MOUSE FM3A CELLS; CONTINUOUS-INFUSION;
HUMAN-BREAST; NUCLEAR-RNA; DNA-DAMAGE; LEUCOVORIN; RESISTANCE
AB To explore the determinants of cytotoxicity during prolonged exposure to pharmacologically relevant concentrations of 5-fluorouracil (FUra), we studied the effects of FUra at concentrations ranging from 0.1 to 1 mu M in HCT 116 and HT 29 colon cancer cells grown in the presence of physiologic levels of leucovorin. A 5- and 7-day exposure to 1 mu M FUra reduced cell growth to 46% and 20% of control in HT 29 cells and to 74% and 38% of control in HCT 116 cells. Concurrent exposure to thymidine (10 or 20 mu M) or uridine (1 mM) provided partial protection against FUra toxicity in HT 29 cells, but did not protect HCT 116 cells. After a 24-h exposure to 1 mu M [H-3]FUra, free 5-fluoro-2'-deoxyuridine-5'-monophosphate (FdUMP) and FUDP + FUTP levels were 0.7 and 144 pmol/10(6) cells in HT 29 cells, respectively, and 3.9 and 178 pmol/10(6) cells in HCT 116 cells. FdUMP and FUDP + FUTP pools increased by 5.7- and 2.0-fold in HT 29 cells and by 1.7- and 3.3-fold in HCT 116 cells over the next 48 h, but did not accumulate thereafter. After a 24-h exposure to 1 PM [H-3]FUra, FUra-RNA levels were 158 and 280 fmol/mu g in HT 29 and HCT 116 cells, respectively; FUra-RNA levels increased over time, and reached 700 and 1156 fmol/mu g at day 5. Concurrent exposure to 1 mM uridine for 72 h did not diminish [H-3]FUra-RNA incorporation. Upon removal of [H-3]FUra following a 24-h exposure, FUra-RNA levels remained relatively stable with 57-78% retained at 120 h. A low level of [H-3]FUra-DNA incorporation was detected in HT 29 cells. Thymidylate synthase (TS) catalytic activity in control cells was 2-fold higher in HCT 116 cells compared to HT 29 cells (47 vs. 23 pmol/min/mg). Total TS content increased 1.5- to 3-fold over control in both cell lines during FUra exposure, and ternary complex formation was evident for up to 96 h. dTTP pools were not depleted in FUra-treated cells, suggesting that residual TS catalytic activity was sufficient to maintain dTTP pools relative to demand. Surprisingly, the partial inhibition of TS was accompanied by a striking accumulation of immunoreactive ''dUMP'' pools in both lines; dUTP pools also increased 2- to 3-fold. In summary, the gradual and stable accumulation of FUra in RNA noted in both lines may account for the thymidine-insensitive component of FUra toxicity. Because dTTP pools were not appreciably diminished, the interference with nascent DNA chain elongation and induction of single-strand breaks in newly synthesized DNA in both cell lines may be due to misincorporation of deoxyuridine nucleotides.
C1 NATL NAVAL MED CTR, NCI, MED BRANCH, DEV THERAPEUT DEPT, DIV CLIN SCI, BETHESDA, MD 20889 USA.
NR 57
TC 16
Z9 16
U1 0
U2 0
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701
SN 0965-0407
J9 ONCOL RES
JI Oncol. Res.
PY 1997
VL 9
IS 2
BP 77
EP 88
PG 12
WC Oncology
SC Oncology
GA XA700
UT WOS:A1997XA70000005
PM 9167189
ER
PT J
AU Agbaria, R
Kelley, JA
Jackman, J
Viola, JJ
Ram, Z
Oldfield, E
Johns, DG
AF Agbaria, R
Kelley, JA
Jackman, J
Viola, JJ
Ram, Z
Oldfield, E
Johns, DG
TI Antiproliferative effects of cyclopentenyl cytosine (NSC 375575) in
human glioblastoma cells
SO ONCOLOGY RESEARCH
LA English
DT Article
DE cyclopentenyl cytosine; CTP synthase; glioblastoma; intracerebral
tumors; blood-brain barrier
ID TRIPHOSPHATE; PENETRATION; METABOLISM; ANTITUMOR; INFUSION; BRAIN
AB Cyclopentenyl cytosine (CPEC) exerts an antiproliferative effect against a wide variety of human and murine tumor lines, including a panel of human gliosarcoma and astrocytoma lines. This effect is produced primarily by the 5'-triphosphate metabolite CPEC-TP, an inhibitor of cytidine-5'-triphosphate (CTP) synthase (EC 6.3.4.2). Be cause previous studies with human glioma cell lines utilized cells in long-term tissue culture, we have undertaken to determine whether the activity of CPEC in such model systems is also demonstrable in freshly excised human glioblastoma cells. Glioma cells obtained at surgery and in log phase growth were exposed to the drug at levels ranging from 0.01 to 1 mu M for 24 h, and CPEC-TP and CTP levels were determined by HPLC. Dose-dependent accumulation of CPEC-TP was accompanied by a concomitant decrease in CTP pools, with 50% depletion of the latter being achieved at a CPEC lever of ca. 0.1 mu M. Human glioma cell proliferation was inhibited 50% by 24 h exposure to 0.07 mu M CPEC. Postexposure decay of CPEC-TP was slow, with a half-time of 30 h. DNA cytometry showed a dose-dependent shift in cell cycle distribution, with an accumulation of cells in S-phase. The pharmacological effects of CPEC on freshly excised glioblastoma cells are quantitatively similar to those seen in a range of established tissue culture lines, including human glioma, colon carcinoma, and MOLT-4 lymphoblasts, supporting the recommendation that the drug may be advantageous for the treatment of human glioblastoma.
C1 NCI,MED CHEM LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892.
NCI,MOL PHARMACOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892.
NINCDS,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892.
NR 20
TC 14
Z9 14
U1 0
U2 0
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701
SN 0965-0407
J9 ONCOL RES
JI Oncol. Res.
PY 1997
VL 9
IS 3
BP 111
EP 118
PG 8
WC Oncology
SC Oncology
GA XG611
UT WOS:A1997XG61100002
PM 9220496
ER
PT J
AU Varricchio, F
Husain, SR
Leland, P
Gill, P
Puri, RK
AF Varricchio, F
Husain, SR
Leland, P
Gill, P
Puri, RK
TI Interleukin-4 receptor expression in vivo on human AIDS-related Kaposi's
sarcoma
SO ONCOLOGY RESEARCH
LA English
DT Article
DE Kaposi's sarcoma; interleukin-1 receptors; immunohistochemistry; basic
fibroblast growth factor; S-100
ID RENAL-CELL-CARCINOMA; IMMUNODEFICIENCY-VIRUS TYPE-1; FIBROBLAST
GROWTH-FACTOR; ADHESION MOLECULE-1 ICAM-1; LONG-TERM CULTURE; TAT
PROTEIN; DIFFERENTIAL EXPRESSION; PSEUDOMONAS EXOTOXIN; CHIMERIC
PROTEIN; GENE-EXPRESSION
AB We have investigated the expression of interleukin-4 receptors (IL-4R) in acquired immunodeficiency syndrome (AIDS)-related Kaposi's Sarcoma (KS) in situ by immunohistochemistry. Frozen and fixed sections from five patch stage and two nodular stage KS lesions were stained with anti-IL-4R monoclonal antibody with similar results. Skin biopsies from the clinically apparent lesions and adjacent clinically uninvolved skin were also examined. We observed that individual KS cells lining the irregular vascular spaces were stained with anti-IL-4R antibody, although the degree of staining was variable. The epithelioid and oval cells appear to stain more than the spindle cells in plaque stages or nodular lesions. The sections from nonclinically involved skin also contained a few cells with features of KS, singly or in clusters that also stained for IL-4R. Skin sections from four normal donors did not stain with IL-4R antibody except for hair follicles, sweat glands, and faint staining of blood vessels. KS sections were also stained with antibodies to basic fibroblast growth factor (FGF), S100, fibronectin, and von Willebrand factor. KS lesions from clinically involved and uninvolved skin sections were positive for all four antibodies. Thus, the differences between KS lesion and clinically uninvolved skin adjacent to a KS lesion may be more quantitative than qualitative. The IL-4 receptors on KS cells were functional as IL-4 modulated intercellular adhesion molecule 1 (ICAM-1) on these cells. Taken together, our results suggest that AIDS-KS cells express eleveated levels of IL-4R compared to normal endothelial and skin cells and, thus, the receptors for IL-4 on KS may serve as an attractive target for anticancer therapy.
C1 US FDA, Dept Biostat & Epidemiol, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA.
US FDA, Lab Mol Tumor Biol, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA.
Univ So Calif, Sch Med, Dept Hematol, Los Angeles, CA USA.
RP Puri, RK (reprint author), US FDA, Lab Mol Tumor Biol, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res,NIH, HFM-530,Bldg 29B,Room 2NN10,29 Lincoln Dr MSC 455, Bethesda, MD 20892 USA.
EM PURI@A1.CBER.FDA.GOV
NR 63
TC 9
Z9 9
U1 0
U2 0
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 0965-0407
J9 ONCOL RES
JI Oncol. Res.
PY 1997
VL 9
IS 9
BP 495
EP 503
PG 9
WC Oncology
SC Oncology
GA YX637
UT WOS:000072061200006
PM 9495455
ER
PT J
AU Takahashi, N
Iwahori, A
Breitman, TR
Fukui, T
AF Takahashi, N
Iwahori, A
Breitman, TR
Fukui, T
TI Tunicamycin in combination with retinoic acid synergistically inhibits
cell growth while decreasing palmitoylation and enhancing retinoylation
of proteins in the human breast cancer cell line MCF-7
SO ONCOLOGY RESEARCH
LA English
DT Article
DE retinoylation; palmitoylation; tunicamycin; drug synergism; cell
division
ID ACUTE PROMYELOCYTIC LEUKEMIA; THERAPEUTIC ANTICANCER AGENTS; F9
TERATOCARCINOMA CELLS; BINDING-PROTEIN; CRABP-I; DIFFERENTIATION
THERAPY; NUCLEAR RECEPTORS; EXPRESSION; CARCINOMA; 17-BETA-ESTRADIOL
AB All-trans-Retinoic acid (RA) induces differentiation and inhibits growth of many tumor types. Whereas the RA nuclear receptors mediate genomic effects of RA, there also are many nongenomic effects that do not have defined mechanisms. Some nongenomic effects of RA may involve retinoylation (RA acylation), a posttranslational modification of proteins occurring in many eukaryotic cell lines including the human breast cancer cell line MCF-7. To gain further knowledge of the role(s) of retinoylation, we studied the effects of tunicamycin (TM), an inhibitor of both protein N-glycosylation and palmitoylation, on growth and retinoylation in MCF-7 cells. We found that RA or TM alone inhibited growth of MCF-7 cells. Combinations of RA and TM inhibited growth synergistically. TM increased retinoylation and decreased palmitoylation. These results suggest that increased retinoylation and decreased glycosylation and palmitoylation may play a role in the synergistic inhibition of cell growth by combinations of TM and RA in MCF-7 cells. Furthermore, our results suggest that combinations of TM and RA may have clinical utility.
C1 Hoshi Univ, Dept Hlth Chem, Shinagawa Ku, Tokyo 142, Japan.
NCI, Biol Chem Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA.
RP Takahashi, N (reprint author), Hoshi Univ, Dept Hlth Chem, Shinagawa Ku, 4-41 Ebara 2 Chome, Tokyo 142, Japan.
NR 46
TC 10
Z9 10
U1 0
U2 2
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 0965-0407
J9 ONCOL RES
JI Oncol. Res.
PY 1997
VL 9
IS 10
BP 527
EP 533
PG 7
WC Oncology
SC Oncology
GA YY230
UT WOS:000072126300002
PM 9507530
ER
PT J
AU Song, KM
Li, ZW
Seth, P
Cowan, KH
Sinha, BK
AF Song, KM
Li, ZW
Seth, P
Cowan, KH
Sinha, BK
TI Sensitization of cis-platinum by a recombinant adenovirus vector
expressing wild-type p53 gene in human ovarian carcinomas
SO ONCOLOGY RESEARCH
LA English
DT Article
DE cis-platinum; drug resistance; p53 gene; adenovirus; gene therapy;
ovarian carcinoma
ID PROGRAMMED CELL-DEATH; IN-VIVO; DRUG-RESISTANCE; CANCER-CELLS; CISPLATIN
RESISTANCE; POTENT INHIBITOR; LUNG-CANCER; APOPTOSIS; BCL-2; BAX
AB Mutations of the tumor suppressor wild-type p53 gene have been implicated in the development of resistance to anticancer drugs. We have examined the role of wild-type p53 in resistance to cis-diamminedichloroplatinum (II) (CDDP) in human ovarian cancer cells using a recombinant adenovirus containing human wild-type p53 cDNA (Adwtp53). In this study we used the human ovarian A2780 tumor cells (wtp53), which are sensitive to CDDP and A2780/CP tumor cells (nonfunctional/mutant p53) and are resistant to CDDP. Studies show that introduction of wtp53 protein via adenovirus gene transfer into A2780/CP cells significantly sensitized these cells to CDDP cytotoxicity, indicating wtp53 was involved in resistance to CDDP. We found that introduction of wtp53 protein also resulted in growth arrest of A2780/CP tumor cells whereas the parent A2780 cells were significantly less sensitive to Adwtp53. This synthesis of wtp53 protein induced by Adwtp53 in A2780/CP cells resulted in a significant increase in the expression of Bax protein without significantly effecting the expression of bcl2 protein, and induced a dose-dependent increase in the nucleosomal DNA fragmentation. The presence of CDDP further enhanced this apoptosis, causing a 30-fold sensitization of A2780/CP cells to CDDP. These results indicate that mutation of p53 protein in A2780/CP ovarian tumor cells resulted in the resistance to CDDP and that combinations of wtp53 gene and CDDP may result in sensitization of mutant p53-containing tumors to chemogenetherapy.
C1 NCI, Dev Therapeut Dept, Med Branch, Div Clin Sci,NIH, Bethesda, MD 20892 USA.
RP Sinha, BK (reprint author), NCI, Dev Therapeut Dept, Med Branch, Div Clin Sci,NIH, Bldg 10,Room 12C-210, Bethesda, MD 20892 USA.
EM bks@box-b.nih.gov
NR 40
TC 28
Z9 28
U1 0
U2 1
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 0965-0407
J9 ONCOL RES
JI Oncol. Res.
PY 1997
VL 9
IS 11-12
BP 603
EP 609
PG 7
WC Oncology
SC Oncology
GA ZF081
UT WOS:000072860700006
PM 9563008
ER
PT J
AU Nussenblatt, R
AF Nussenblatt, R
TI Use of laser flare photometry to assess and monitor inflammation in
uveitis - Discussion
SO OPHTHALMOLOGY
LA English
DT Editorial Material
RP Nussenblatt, R (reprint author), NEI,NIH,BETHESDA,MD 20892, USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0161-6420
J9 OPHTHALMOLOGY
JI Ophthalmology
PD JAN
PY 1997
VL 104
IS 1
BP 71
EP 72
PG 2
WC Ophthalmology
SC Ophthalmology
GA WE575
UT WOS:A1997WE57500022
ER
PT S
AU Zeffiro, TA
Eden, GF
Woods, RP
VanMeter, JW
AF Zeffiro, TA
Eden, GF
Woods, RP
VanMeter, JW
BE Villringer, A
Dirnagl, U
TI Intersubject analysis of fMRI data using spatial normalization
SO OPTICAL IMAGING OF BRAIN FUNCTION AND METABOLISM 2: PHYSIOLOGICAL BASIS
AND COMPARISON TO OTHER FUNCTIONAL NEUROIMAGING METHODS
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT International Symposium on Optical Imaging and Metabolism
CY MAY 01-02, 1995
CL BERLIN, GERMANY
SP Volkswagen Stift, Hertie Stift, Bayer, Fresenius, Hamamatsu Protonics, Sanofi Winthrop, IBM, Siemens AG
ID POSITRON-EMISSION TOMOGRAPHY; HUMAN VISUAL-CORTEX; HUMAN BRAIN; PET
IMAGES
C1 NIH, LAB DIAGNOST RADIOL RES, OD, BETHESDA, MD 20892 USA.
NIMH, SECT FUNCT BRAIN IMAGING, NIH, BETHESDA, MD 20892 USA.
UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA 90024 USA.
RP Zeffiro, TA (reprint author), SENSOR SYST INC, 103A CARPENTER DR, STERLING, VA 20163 USA.
NR 19
TC 4
Z9 4
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45585-4
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 413
BP 235
EP 240
PG 6
WC Medicine, Research & Experimental; Clinical Neurology; Neurosciences;
Radiology, Nuclear Medicine & Medical Imaging
SC Research & Experimental Medicine; Neurosciences & Neurology; Radiology,
Nuclear Medicine & Medical Imaging
GA BJ16K
UT WOS:A1997BJ16K00026
PM 9238505
ER
PT B
AU Gandjbakhche, AH
Chernomordik, V
Bonner, RF
Hebden, JC
Nossal, R
AF Gandjbakhche, AH
Chernomordik, V
Bonner, RF
Hebden, JC
Nossal, R
BE Chance, B
Alfano, RR
TI Use of time-dependent contrast functions to discriminate between the
scattering and absorption properties of abnormal regions hidden within a
tissue-like phantom
SO OPTICAL TOMOGRAPHY AND SPECTROSCOPY OF TISSUE: THEORY, INSTRUMENTATION,
MODEL, AND HUMAN STUDIES II, PROCEEDINGS OF
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on Optical Tomography and Spectroscopy of Tissue - Theory,
Instrumentation, Model, and Human Studies II
CY FEB 09-12, 1997
CL SAN JOSE, CA
SP Int Biomed Opt soc, Soc Photo Opt Instrumentat Engineers, Amer Soc Laser Med & Surg Inc
AB The success of time-resolved imaging of an abnormal site embedded in thick tissue may rely on one's ability to quantify the absorption coefficient of the target as a specific spectroscopic signature. This task is particularly complicated when the scattering properties of the target differ from those of the surrounding tissue. Using data obtained from time-resolved transillumination experiments of abnormally absorbing and differentially scattering objects embedded in a tissue-like phantom, we show how a new deconvolution algorithm enables us to quantify the optical properties of the target. The algorithm is based on a photon random walk theory that expresses different time-dependent point spread functions to calculate the diffusive and absorptive contrasts obtained in time-of-flight measurements.
RP Gandjbakhche, AH (reprint author), NIH,PHYS SCI LAB,DCRT,BETHESDA,MD 20892, USA.
RI Bonner, Robert/C-6783-2015
NR 0
TC 4
Z9 4
U1 0
U2 0
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2390-4
J9 P SOC PHOTO-OPT INS
PY 1997
VL 2979
BP 211
EP 218
DI 10.1117/12.280246
PG 8
WC Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical
Imaging
SC Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging
GA BJ71N
UT WOS:A1997BJ71N00024
ER
PT J
AU Luyten, FP
AF Luyten, FP
TI A scientific basis for the biologic regeneration of synovial joints
SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS
LA English
DT Article; Proceedings Paper
CT National-Institutes-of-Health Technology Assessment Conference on
Management of Temporomandibular Disorders
CY APR 29-MAY 01, 1996
CL BETHESDA, MD
SP NIH, NIDR, NIH Off Med Applicat Res, NIAMSD, NINDS, NINR, NIH Off Res Women Hlth
ID FACTOR-BETA SUPERFAMILY; PROTEIN; MEMBERS
AB Temporomandibular joint disorders represent a large group of conditions involving a local or more generalized musculoskeletal disease process. The disorders have many features and many causes and may result in limited or more severe damage of the joint associated tissues including the disks, the articular surface, the underlying bone, and the ligamentous structures. As our understanding of the molecular processes guiding skeletal tissue formation progresses, new opportunities arise in the field of skeletal tissue and joint repair. Reconstruction of the temporomandibular joint by means of scientifically designed approaches will revolutionize surgical treatment modalities.
RP Luyten, FP (reprint author), NIDR,DEV BIOL PROJECT,BONE RES BRANCH,NIH,BETHESDA,MD 20892, USA.
NR 11
TC 8
Z9 8
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 1079-2104
J9 ORAL SURG ORAL MED O
JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod.
PD JAN
PY 1997
VL 83
IS 1
BP 167
EP 169
DI 10.1016/S1079-2104(97)90109-8
PG 3
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA WD102
UT WOS:A1997WD10200034
PM 9007942
ER
PT J
AU Lipton, JA
AF Lipton, JA
TI Introduction: National institutes of health technology assessment
conference on management of temporomandibular disorders
SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND
ENDODONTOLOGY
LA English
DT Article
RP Lipton, JA (reprint author), NIDR, DIV EXTRAMURAL RES, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1079-2104
J9 ORAL SURG ORAL MED O
JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod.
PD JAN
PY 1997
VL 83
IS 1
BP 49
EP 50
PG 2
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA WD102
UT WOS:A1997WD10200015
ER
PT J
AU Dionne, RA
AF Dionne, RA
TI Pharmacologic treatments for temporomandibular disorders
SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND
ENDODONTOLOGY
LA English
DT Article; Proceedings Paper
CT National-Institutes-of-Health Technology Assessment Conference on
Management of Temporomandibular Disorders
CY APR 29-MAY 01, 1996
CL BETHESDA, MD
SP NIH, NIDR, NIH Off Med Applicat Res, NIAMSD, NINDS, NINR, NIH Off Res Women Hlth
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; CHRONIC NONMALIGNANT PAIN; LOW-DOSE
AMITRIPTYLINE; SPLINT THERAPY; FACIAL-PAIN; PLACEBO; DYSFUNCTION;
ANTIDEPRESSANTS; METAANALYSIS; MANAGEMENT
AB Drugs are widely used in the management of acute and chronic orofacial pain. Whereas the use of analgesics for acute orofacial pain is well documented through hundreds of controlled clinical trials, the use of a broad spectrum of drugs for chronic pain is based on very few studies. In the absence of data supporting a therapeutic benefit for a drug used chronically for pain, toxicity associated with the drug can still occur. It is critical, therefore, to assess the balance between therapeutic benefit and safety. This article reviews current evidence supporting the use of several drug classes for temporomandibular disorders (TMD) and identifies therapeutic controversies in need of further research.
C1 NIDR, NEUROBIOL & ANESTHESIOL BRANCH,NIH, CLIN PHARMACOL UNIT,DIV INTRAMURAL, BETHESDA, MD 20892 USA.
NR 55
TC 57
Z9 59
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1079-2104
J9 ORAL SURG ORAL MED O
JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod.
PD JAN
PY 1997
VL 83
IS 1
BP 134
EP 142
DI 10.1016/S1079-2104(97)90104-9
PG 9
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA WD102
UT WOS:A1997WD10200029
PM 9007937
ER
PT S
AU Rifkind, JM
Ajmani, RS
Heim, J
AF Rifkind, JM
Ajmani, RS
Heim, J
BE Harrison, DK
Delpy, DT
TI Impaired hemorheology in the aged associated with oxidative stress
SO OXYGEN TRANSPORT TO TISSUE XIX
SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
LA English
DT Article; Proceedings Paper
CT 24th Scientific Meeting of the
International-Society-on-Oxygen-Transport-to-Tissue
CY AUG, 1996
CL UNIV DUNDEE, DUNDEE, SCOTLAND
SP Int Soc Oxygen Transport Tissue, British Microcirculat Soc, Inst Phys & Engn Med, 6th World Congress Microcirculat, Alliance Pharm, Baxter Hlth Corp, Blood Substitutes Div, Dundee City Council, Dundee Teaching Hosp, Scottish Enterprise Tayside, Hamamatsu UK, Oxygen Sensors Inc, Pfizer UK, Pharmacia & Upjohn, Univ Dundee
HO UNIV DUNDEE
ID CORONARY HEART-DISEASE; PLASMA-FIBRINOGEN; HEMOGLOBIN; SUPEROXIDE;
INFARCTION; GENERATION; OXYGEN
C1 NIA, Cellular & Mol Biol Lab, Mol Dynam Sect, NIH, Baltimore, MD 21224 USA.
RP Rifkind, JM (reprint author), NIA, Cellular & Mol Biol Lab, Mol Dynam Sect, NIH, 4940 Eastern Ave, Baltimore, MD 21224 USA.
NR 22
TC 15
Z9 16
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45711-3
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 428
BP 7
EP 13
PG 7
WC Medicine, Research & Experimental; Physiology; Peripheral Vascular
Disease
SC Research & Experimental Medicine; Physiology; Cardiovascular System &
Cardiology
GA BK38E
UT WOS:000071952600002
PM 9500022
ER
PT S
AU Balagopalakrishna, C
Nirmala, R
Rifkind, JM
Chatterjee, S
AF Balagopalakrishna, C
Nirmala, R
Rifkind, JM
Chatterjee, S
BE Nemoto, EM
LaManna, JC
TI Modification of low density lipoproteins by erythrocytes and hemoglobin
under hypoxic conditions
SO OXYGEN TRANSPORT TO TISSUE XVIII
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT 23rd Annual Meeting of the
International-Society-on-Oxygen-Transport-to-Tissue - Oxygen Transport
to Tissue XVIII
CY AUG 23-27, 1995
CL PITTSBURGH, PA
SP Int Soc Oxygen Transport Tissue
ID SMOOTH-MUSCLE CELL; GROWTH; LDL
AB Oxidation of low density lipoprotein (LDL) has been implicated in atherogenesis. It has also been suggested that modification of LDL in the presence of endothelial and smooth muscle cells is associated with the production of superoxide. Red cells and hemoglobin have been shown to be a source for enhanced superoxide production under hypoxic conditions. We now show that incubation of LDL with both hemoglobin and erythrocytes under hypoxic conditions produces the increased Relative Electrophoretic Mobility (REM) associated with LDL oxidation. With hypoxic hemoglobin, this reaction is over within 10 minutes, appreciably faster than other in vitro methods for LDL oxidation. The increased REM was found to be associated with partial deoxygenation of hemoglobin indicative of appreciable oxygen utilization and a more hypoxic state. At later times, the modified LDL was found to produce enhanced hemoglobin oxidation. The resultant modified LDL was shown to have elevated TEARS indicative of LDL oxidation. In addition, it was found to induce smooth muscle cell proliferation which is one of the biological factors thought to be associated with atherogenesis. The relatively rapid LDL modification detected with hypoxic erythrocytes and hemoglobin suggest that even under in vivo conditions with the antioxidants present in plasma, oxidation may still occur in the circulation with the associated vascular damage occurring as the blood containing elevated levels of oxidized LDL leave the pulmonary circulation.
RP Balagopalakrishna, C (reprint author), NIA, CELLULAR & MOL BIOL LAB, NIH, 4940 EASTERN AVE, BALTIMORE, MD 21224 USA.
NR 14
TC 3
Z9 3
U1 0
U2 1
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45516-1
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 411
BP 337
EP 345
PG 9
WC Cell Biology; Medicine, Research & Experimental; Physiology
SC Cell Biology; Research & Experimental Medicine; Physiology
GA BJ31R
UT WOS:A1997BJ31R00042
PM 9269446
ER
PT B
AU Long, LR
Pillemer, SR
Goh, GH
Berman, LE
Neve, L
Thoma, GR
Premkuman, A
Ostchega, Y
Lawrence, RC
Altman, RD
Lane, NE
Scott, WW
AF Long, LR
Pillemer, SR
Goh, GH
Berman, LE
Neve, L
Thoma, GR
Premkuman, A
Ostchega, Y
Lawrence, RC
Altman, RD
Lane, NE
Scott, WW
BE Horii, SC
Blaine, GJ
TI A digital atlas for spinal x-rays
SO PACS DESIGN AND EVALUATION: ENGINEERING AND CLINICAL ISSUES - MEDICAL
IMAGING 1997
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on PACS Design and Evaluation - Engineering and Clinical
Issues, at the Medical Imaging 1997 Meeting
CY FEB 25-28, 1997
CL NEWPORT BEACH, CA
SP Soc Photo Opt Instrumentat Engineers, Amer Assoc Physicists Med, Amer Physiol Soc, US FDA, Ctr Devices & Radiol Hlth, Soc Imaging Sci & Technol, Natl Elect Manufacturers Assoc, Diagnost Imaging & Therapy Syst Div, Radiol Informat Syst Consortium, Radiol Soc N Amer, Soc Comp Applicat Radiol
DE atlas; digital; x-ray; osteoarthritis,; cervical spine; lumbar spine;
Internet; World Wide Web; NHANES; NLM; NIAMS; NCHS
AB At the National Library of Medicine (NLM) we are developing a digital atlas to serve as a reference tool for the interpretation of cervical and lumbar spine x-rays. The atlas contains representative images for four grades of severity for cervical/lumbar anterior osteophytes and disc space narrowing, and presence/absence for cervical subluxation and lumbar spondylolisthesis. A prototype version of the atlas has been built using images for which expert rheumatologist readers reached exact agreement in grading.
The atlas functionality includes the ability to display cervical and lumbar anatomy, display of single images or multiple simultaneous images, image processing functions, and capability to add user-defined images to the atlas. Images are selected for display by the user specifying feature and grade (example: ''anterior osteophytes, grade 2''). Currently, the atlas runs on a Sun SPARC workstation under the Solaris operating system.
The initial use of the atlas is to aid in reading a collection of 17,000 NHANES II digitized x-rays. The atlas may also be used as a general digital reference tool for the standardized interpretation of digital x-rays for osteoarthritis. We are investigating further development of the atlas to accommodate a wider set of Images, to operate on multiple platforms, and, to be accessible via the World Wide Web.
RP Long, LR (reprint author), NATL LIB MED,BETHESDA,MD 20894, USA.
NR 0
TC 7
Z9 7
U1 0
U2 0
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2446-3
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3035
BP 586
EP 594
DI 10.1117/12.274621
PG 9
WC Optics; Radiology, Nuclear Medicine & Medical Imaging
SC Optics; Radiology, Nuclear Medicine & Medical Imaging
GA BH98D
UT WOS:A1997BH98D00073
ER
PT J
AU Adams, MM
Herman, AA
Notzon, FC
AF Adams, MM
Herman, AA
Notzon, FC
TI International symposium on maternally-linked pregnancy outcomes -
Preface
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Editorial Material
C1 NICHHD,NIH,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892.
CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,OFF INT STAT,HYATTSVILLE,MD 20782.
RP Adams, MM (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV REPROD HLTH,WHO,ATLANTA,GA, USA.
NR 0
TC 25
Z9 25
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE
SN 0269-5022
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 1997
VL 11
SU 1
BP 1
EP 1
PG 1
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA WC570
UT WOS:A1997WC57000001
ER
PT J
AU McCarthy, BJ
Berendes, HW
AF McCarthy, BJ
Berendes, HW
TI Pregnancy outcome investigation for the 21st century - Commentary
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Editorial Material
C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,NIH,BETHESDA,MD 20892.
RP McCarthy, BJ (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV REPROD HLTH,WHO,ATLANTA,GA 30341, USA.
NR 3
TC 8
Z9 8
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE
SN 0269-5022
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 1997
VL 11
SU 1
BP 2
EP 4
PG 3
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA WC570
UT WOS:A1997WC57000002
PM 9018710
ER
PT J
AU Herman, AA
McCarthy, BJ
Bakewell, JM
Ward, RH
Mueller, BA
Maconochie, NE
Read, AW
Zadka, P
Skjaerven, R
AF Herman, AA
McCarthy, BJ
Bakewell, JM
Ward, RH
Mueller, BA
Maconochie, NE
Read, AW
Zadka, P
Skjaerven, R
TI Data linkage methods used in maternally-linked birth and infant death
surveillance data sets from the United States (Georgia, Missouri, Utah
and Washington State), Israel, Norway, Scotland and Western Australia
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article; Proceedings Paper
CT International Symposium on Maternally Linked Pregnancy Outcomes
CY SEP, 1995
CL ATLANTA, GA
ID PREGNANCY
AB In this paper we describe the methods used to link birth and infant mortality and morbidity surveillance data sets into sibships using deterministic or multistage probabilistic linkage methods. We describe nine linked data sets: four in the United States (Georgia, Missouri, Utah and Washington State), and four elsewhere (Scotland, Norway, Israel and Western Australia). Norway and Israel use deterministic methods to Link births and deaths into sibships. The deterministic linkage is usually dependent on the availability of national identification numbers. In both countries they assign these numbers at birth. Deterministic Linkage is usually highly successful, and the major problem is the validation of linkages. In the United States, Western Australia and UK linkage is multistage and probabilistic. This approach is usually dependent on the calculation linkage weights from sociodemographic variables. The success rates of probabilistic methods are above 80%. Maternally-linked perinatal data open new vistas for epidemiological research. Recurrence of poor perinatal outcomes is more appropriately studied using longitudinally-linked data sets. In addition, the emergence of risk factors and the recurrence of risk factors can be studied.
C1 CTR DIS CONTROL & PREVENT, NATL CTR CHRON DIS PREVENT & HLTH PROMOT, DIV REPROD HLTH, WHO, ATLANTA, GA USA.
MISSOURI DEPT HLTH, BUR HLTH DATA ANAL, JEFFERSON CITY, MO USA.
UNIV UTAH, DEPT HUMAN GENET, SALT LAKE CITY, UT USA.
UNIV WASHINGTON, DEPT EPIDEMIOL, SEATTLE, WA USA.
UNIV OXFORD, ICRF, CANC EPIDEMIOL UNIT, OXFORD, ENGLAND.
TVW TELETHON INST CHILD HLTH RES, PERTH, WA, AUSTRALIA.
CENT BUR STAT, HLTH DIV, JERUSALEM, ISRAEL.
UNIV BERGEN, MED INFORMAT & STAT SECT, BERGEN, NORWAY.
RP Herman, AA (reprint author), NICHHD, EPIDEMIOL BRANCH,DIV EPIDEMIOL STAT & PREVENT RES, NIH,BLDG 6100, ROOM 7803, BETHESDA, MD 20892 USA.
FU NICHD NIH HHS [N01-HD-0-2915, N01-HD-0-2916]; Wellcome Trust
NR 20
TC 106
Z9 107
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 1997
VL 11
SU 1
BP 5
EP 22
DI 10.1046/j.1365-3016.11.s1.11.x
PG 18
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA WC570
UT WOS:A1997WC57000003
PM 9018711
ER
PT J
AU Krulewitch, CJ
Herman, AA
Yu, KF
Johnson, YR
AF Krulewitch, CJ
Herman, AA
Yu, KF
Johnson, YR
TI Does changing paternity contribute to the risk of intrauterine growth
retardation?
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article; Proceedings Paper
CT International Symposium on Maternally Linked Pregnancy Outcomes
CY SEP, 1995
CL ATLANTA, GA
ID CHRONIC VILLITIS; PRE-ECLAMPSIA; PREECLAMPSIA; PREGNANCIES; PLACENTAE;
COMPLEX
AB An immune reaction initiated by paternal antigens may be necessary for healthy placental development, pregnancy maintenance and infant growth. An inadequate immune response may result in intrauterine growth retardation (IUGR). We hypothesised that a change in paternity may interfere with the immune response and cause poor placentation with resultant IUGR. Ln this paper we examine the risk of IUGR associated with changes in paternity. We used the Utah Successive Pregnancies Data Set that contains information on women across their pregnancies. We restricted the analysis to 141 817 women with two or three pregnancies. Women who did not have an IUGR infant in the previous pregnancy were at a 20-30% greater risk of developing IUGR if they had changed partners. Women who had a previous IUGR infant were at no increased risk for IUGR after a change in paternity. These results may point to an immune mechanism or may be as a result of residual confounding of unmeasured risk factors for IUGR. Further studies with data that contain more sociodemographic and biological risk factors for IUGR are necessary to exclude residual confounding.
C1 CTR DIS CONTROL & PREVENT,PREGNANCY & INFANT HLTH BRANCH,DIV REPROD HLTH,ATLANTA,GA.
NICHHD,NIH,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892.
NR 23
TC 8
Z9 8
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE
SN 0269-5022
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 1997
VL 11
SU 1
BP 41
EP 47
DI 10.1046/j.1365-3016.11.s1.7.x
PG 7
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA WC570
UT WOS:A1997WC57000006
PM 9018714
ER
PT J
AU Herman, AA
Yu, KF
AF Herman, AA
Yu, KF
TI Adolescent age at first pregnancy and subsequent obesity
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article; Proceedings Paper
CT International Symposium on Maternally Linked Pregnancy Outcomes
CY SEP, 1995
CL ATLANTA, GA
ID POSTPARTUM WEIGHT RETENTION; MATERNAL BODY-WEIGHT; RISK FACTOR; WOMEN
AB Adolescent pregnancy has been associated with subsequent obesity. This paper examines the patterns of obesity for second and third pregnancies among women who had their first singleton pregnancy as teenagers. We used maternally-linked data from 1978 to 1990 among 43 160 Missouri resident women. Age, parity, interpregnancy interval and prior body mass index were significantly associated with subsequent obesity among adolescents. Race, marital status and smoking had significant interactions with age. Among older women, being African-American and never having married was associated with an increased probability of obesity, and smoking had a greater effect on obesity at higher maternal age. Race and marital status did not have significant effects on obesity among younger women, The most important predictor of obesity was prior body mass index. Body mass index before the first pregnancy had a greater effect on subsequent obesity if the intervening interpregnancy weight gains were large. Excessive weight gain during pregnancy presents the health care provider with a dilemma. An increase in birthweight associated with high prenatal weight gains may diminish the risk of infant mortality and morbidity in an index pregnancy, but subsequent obesity may increase perinatal mortality rates, the rates of obstetric problems and neural tube defects.
C1 NICHHD,STAT BRANCH,DIV EPIDEMIOL STAT & PREVENT RES,NIH,BETHESDA,MD 20892.
RP Herman, AA (reprint author), NICHHD,EPIDEMIOL BRANCH,DIV EPIDEMIOL STAT & PREVENT RES,NIH,BLDG 6100,ROOM 7803,BETHESDA,MD 20892, USA.
NR 30
TC 31
Z9 31
U1 0
U2 1
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE
SN 0269-5022
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD JAN
PY 1997
VL 11
SU 1
BP 130
EP 141
DI 10.1046/j.1365-3016.11.s1.5.x
PG 12
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA WC570
UT WOS:A1997WC57000014
PM 9018722
ER
PT J
AU Cheever, AW
Lewis, FA
Wynn, TA
AF Cheever, AW
Lewis, FA
Wynn, TA
TI Schistosoma mansoni: Unisexual infections sensitize mice for granuloma
formation around intravenously injected eggs
SO PARASITOLOGY RESEARCH
LA English
DT Article
ID IDENTIFICATION; RESPONSES; ANTIBODY; ANTIGENS
AB Mice carrying unisexual infection with male or female Schistosoma mansoni for 9 weeks developed accelerated and augmented reactions to S. mansoni eggs injected intravenously. The size of circumoval granulomas observed in the lungs of unisexually infected mice did not differ significantly from the reactions seen in bisexually infected mice. Tissue eosinophilia in the granulomas was also augmented similarly over that in naive mice by unisexual or bisexual infection. The cross-reactivity between worm and egg antigens is relevant to the development of acute toxemic schistosomiasis mansoni and, perhaps, to the consideration of antigens to be used for vaccination against S. mansoni infection.
C1 BIOMED RES INST,ROCKVILLE,MD 20852.
RP Cheever, AW (reprint author), NIAID,PARASIT DIS LAB,NIH,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA.
RI Wynn, Thomas/C-2797-2011
NR 11
TC 22
Z9 23
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0044-3255
J9 PARASITOL RES
JI Parasitol. Res.
PD JAN
PY 1997
VL 83
IS 1
BP 57
EP 59
PG 3
WC Parasitology
SC Parasitology
GA VW842
UT WOS:A1997VW84200012
PM 9000235
ER
PT J
AU Quakyi, EK
Carter, PH
Tsai, CM
Marti, GE
AF Quakyi, EK
Carter, PH
Tsai, CM
Marti, GE
TI Immunization with meningococcal membrane-bound lipooligosaccharide
accelerates granulocyte recovery enhances lymphocyte proliferation in
myelosuppressed mice
SO PATHOBIOLOGY
LA English
DT Article
DE septic shock; myelosuppression; granulocytes; lipooligosaccharide;
meningococcus; cyclophosphamide; flow cytometry; interferon-gamma;
interleukin-6; interleukin-1 beta; interleukin-3; white blood cell lysis
ID COLONY-STIMULATING FACTOR; STEM-CELL FACTOR; MURINE HEMATOPOIETIC
PROGENITORS; INTERFERON-GAMMA; BONE-MARROW; INTERLEUKIN-6; IL-6;
CYCLOPHOSPHAMIDE; VACCINE; MECHANISMS
AB Protective effects of detergent-treated outer membrane vesicles (D-OMVs) prepared from the parent group B M986 strain and the nonencapsulated M986-NCV mutant in myelosuppressed mice were investigated in models of experimental septic shock. The effects of D-OMVs on expansion of the myeloid compartment, on spleen cell proliferation to mitogen stimulation, and on cytokines induced during this period were investigated. On 3 consecutive days, mice were injected with 1 mu g/kg of lipooligosaccharide (LOS) or lipopolysaccharide, or 75 mu g/kg D-OMV followed by a single dose of cyclophosphamide (200 mg/kg) 24 h later, Eight weeks after the last injection, animals were challenged with a combination of galactosamine (400 mg/kg) and live Neisseria meningitidis. More than 90% of control mice died within 24 h when challenged with 10(5) CFU of bacteria. Mice immunized with LOS or D-OMV were rendered neutropenic but were protected against bacterial challenge of at least 10(7) CFU. At different time intervals, peripheral blood samples were obtained to characterize changes in circulating blood cells. The rise in absolute granulocyte numbers occurred 24 h earlier with peak cell counts about 3 times higher than those seen in the placebo groups, Peripheral blood cells from D-OMV-treated animals expressed about twofold more Gr-1 antigen (myeloid surface cell marker) than placebo-treated controls. The proliferative responses to both B and T cells were reduced in all treatment groups due to the effects of cyclophosphamide. D-OMV treatment afforded the greatest protection for mitogen-activated lymphocytes from the lethal effects of cyclophosphamide and also enhanced T and B cell proliferation. Low IL-1 beta levels and increases in serum IL-6 were detected in all treatment groups. In contrast, significant IFN-gamma and IL-3 levels were only detected in D-OMV-treated groups. These results indicate that D-OMVs, which have reduced toxicity, have prophylactic potential in inducing specific cytokines that accelerate granulocyte recovery following cytoreductive therapy by promoting both proliferation and maturation of myeloid precursors as well as augmenting the immune system.
C1 US FDA,CTR BIOL EVALUAT & RES,DIV CELL & GENE THERAPIES,FLOW & IMAGE CYTOMETRY SECT,NIH,BETHESDA,MD 20892.
NR 49
TC 7
Z9 7
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1015-2008
J9 PATHOBIOLOGY
JI Pathobiology
PD JAN-FEB
PY 1997
VL 65
IS 1
BP 26
EP 38
DI 10.1159/000164100
PG 13
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA XE702
UT WOS:A1997XE70200003
PM 9200187
ER
PT J
AU Shaffer, DN
Mansmann, PT
AF Shaffer, DN
Mansmann, PT
TI Leukotriene inhibition and advances in the treatment of asthma: A
pharmacological review
SO PEDIATRIC ASTHMA ALLERGY & IMMUNOLOGY
LA English
DT Review
ID 5-LIPOXYGENASE
AB The optimal treatment of asthma remains problematic when considered by healthcare providers, Despite increasing knowledge regarding the pathophysiology of asthma and the role of inflammatory mediators, prevalence as well as morbidity and mortality rates continue to rise, Since the introduction of inhaled beta-agonists and inhaled corticosteroids in the 1980s, little has changed in the pharmacological armamentarium of treatment options, Recently, attention has focused on the pharmacological manipulation of leukotrienes as treatment modalities, Two leukotriene modifiers introduced in 1996 herald the first new pharmacological class of antiasthma medicines in the United States in 25 years, With the significant morbidity and mortality of asthma as well as cost in healthcare dollars and time lost from work, attention to these agents and their role in the treatment of asthma is warranted. The objective of this article is to review the pharmacology and clinical applications of this new class of drugs focusing specifically on the two recently introduced agents, zafirlukast and zileuton, Historical perspectives in the treatment of asthma and potential, future uses of leukotriene modifiers is also addressed.
C1 W Virginia Univ, Sch Med, Robert C Byrd Hlth Sci Ctr, Dept Med & Rheumatol, Morgantown, WV 26506 USA.
RP Shaffer, DN (reprint author), NHLBI, NIH, Bldg 10,Room 8C103, Bethesda, MD 20892 USA.
NR 18
TC 3
Z9 3
U1 0
U2 1
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 0883-1874
J9 PEDIATR ASTHMA ALLER
JI Pediatr. Asthma Allergy Immunol.
PY 1997
VL 11
IS 4
BP 171
EP 179
DI 10.1089/pai.1997.11.171
PG 9
WC Allergy; Immunology; Pediatrics; Respiratory System
SC Allergy; Immunology; Pediatrics; Respiratory System
GA YZ957
UT WOS:000072312200002
ER
PT J
AU Freifeld, A
Pizzo, P
AF Freifeld, A
Pizzo, P
TI Use of fluoroquinolones for empirical management of febrile neutropenia
in pediatric cancer patients
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE fluoroquinolones; febrile neutropenia; cancer; pediatric; empiric
treatment
ID INTRAVENOUS CIPROFLOXACIN; ANTIBIOTIC-THERAPY; RANDOMIZED TRIAL;
IMMUNOCOMPROMISED PATIENTS; PREDICTION RULE; FEVER; CEFTAZIDIME;
EPISODES; COMBINATION; MONOTHERAPY
AB Background. Empiric antibiotic therapy has become a standard of care far the febrile neutropenic patient. Many clinical trials over the previous three decades have demonstrated that a variety of antibiotic combinations and more recently potent antibiotic monotherapies may preserve the patient through the critical time of fever and neutropenia. Recently attempts have been made to identify ''low risk'' patients who may not require traditional, intensive, hospitalized intravenous antimicrobial therapy. Therefore the need for new treatment alternatives for the febrile neutropenic pediatric cancer patient in particular revolves around the desire for less complex regimens, agents with minimal toxicity and expense and the option of an oral formulation for outpatient management.
Objective. Fluoroquinolones, especially ciprofloxacin and ofloxacin, are examined in this paper as potential oral alternatives for managing the low risk neutropenic pediatric cancer patient population. Attention must be paid to their antibacterial spectra, however, and in some cases fluoroquinolones should be combined with a second agent for additional Gram-positive coverage.
Results, Several studies, including one ongoing trial at the National. Cancer Institute, have shown the potential benefits of oral fluoroquinolone therapy among low risk febrile neutropenic patients, joint complaints in children after ciprofloxacin therapy in the National Cancer Institute trial thus far have been minimal, reversible and felt to be unrelated to ciprofloxacin treatment.
Conclusion. The use of outpatient therapy, such as the fluoroquinolones, to manage febrile neutropenic episodes must be approached with caution and should be undertaken only in selected low risk patients.
RP Freifeld, A (reprint author), NCI,INFECT DIS SECT,NIH,BETHESDA,MD 20892, USA.
NR 29
TC 25
Z9 26
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD JAN
PY 1997
VL 16
IS 1
BP 140
EP 146
DI 10.1097/00006454-199701000-00039
PG 7
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA WC701
UT WOS:A1997WC70100035
PM 9002125
ER
PT J
AU Bendon, RW
FayePetersen, O
Pavlova, Z
Qureshi, F
Elder, N
Das, A
Hauth, J
McNellis, D
Mercer, B
Miodovnik, M
AF Bendon, RW
FayePetersen, O
Pavlova, Z
Qureshi, F
Elder, N
Das, A
Hauth, J
McNellis, D
Mercer, B
Miodovnik, M
TI Histologic features of chorioamnion membrane rupture: Development of
methodology
SO PEDIATRIC PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
DE placenta; premature rupture of membranes; preterm labor
ID PREMATURE RUPTURE; AGREEMENT; FLUID
AB This study developed a set of histologic features that will allow subclassification of placentas with preterm premature rupture of membranes. Placentas were obtained from patients participating in a multi-institutional NICHD Maternal-Fetal Medicine Unit Network study of antimicrobial therapy after preterm premature rupture of membranes. The rupture site was sampled by inking the open sac margin and rolling a membrane strip in four quadrants from the ink to the placental margin. Independently, four pathologists used a provisional feature list to score the slides from 15 placentas. A concordance analysis was performed on those results. With those results, the slides were reviewed concurrently to discover the source of disagreements and to revise the feature list. The sampling method frequently demonstrated a rupture site with histology distinct front timi of the remainder of the membranes. After review of the preliminary scoring results, 29 features of membrane histology present in preterm premature rupture could be objectively described with agreement among four pathologists. The feature list allows both novel and commonly recognized histologic features of fetal membranes to be recorded with objectivity. This list, with the described sampling technique, is presented as a tool for clinical correlation in studies of membrane rupture, especially in preterm, premature rupture.
C1 UNIV ALABAMA,BIRMINGHAM,AL.
UNIV SO CALIF,MED CTR,LOS ANGELES,CA.
WAYNE STATE UNIV,DETROIT,MI.
UNIV CINCINNATI,CINCINNATI,OH.
GEORGE WASHINGTON UNIV,WASHINGTON,DC.
NICHHD,MFMU NETWORK,BETHESDA,MD.
UNIV TENNESSEE,MEMPHIS,TN.
RP Bendon, RW (reprint author), KOSAIR CHILDRENS HOSP,DEPT PATHOL,231 E CHESTNUT ST,LOUISVILLE,KY 40232, USA.
FU NICHD NIH HHS [HD21414, HD21410, HD21434]
NR 23
TC 20
Z9 20
U1 0
U2 1
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 JAN-FEB
PY 1997
VL 17
IS 1
BP 27
EP 42
DI 10.1080/107710497175001
PG 16
WC Pathology; Pediatrics
SC Pathology; Pediatrics
GA WF268
UT WOS:A1997WF26800003
PM 9050058
ER
PT J
AU Seibel, NL
Walsh, TJ
AF Seibel, NL
Walsh, TJ
TI Pulmonary aspergillosis in immunocompromised children
SO PEDIATRIC PULMONOLOGY
LA English
DT Article; Proceedings Paper
CT 2nd International Congress on Pediatric Pulmonology (CIPP II)
CY JUN 02-05, 1996
CL NICE, FRANCE
ID BRONCHOALVEOLAR LAVAGE; DIAGNOSIS
C1 Childrens Natl Med Ctr, Dept Hematol Oncol, Washington, DC 20010 USA.
NCI, Pediat Branch, Infect Dis Sect, Mycol Unit, Bethesda, MD 20892 USA.
RP Seibel, NL (reprint author), Childrens Natl Med Ctr, Dept Hematol Oncol, 111 Michigan Ave NW, Washington, DC 20010 USA.
NR 9
TC 0
Z9 1
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 8755-6863
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PY 1997
SU 16
BP 61
EP 62
PG 2
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA YR008
UT WOS:000071447800032
PM 9443201
ER
PT J
AU Berlin, CM
McCarverMay, DG
Notterman, DA
Ward, RM
Weismann, DN
Wilson, GS
Wilson, JT
Weller, EB
Bennett, DR
Mulinare, J
Kaufman, P
Krough, C
Rieder, MJ
Troendle, G
Yaffe, SJ
Cote, CJ
Szefler, SJ
Blumer, JL
Frader, JE
Crain, LS
Moseley, KL
Nelson, RM
Porter, IH
Vizcarrondo, FE
Bowes, WA
Kazura, A
Krug, EF
Caniano, DA
Dressser, R
King, NMP
AF Berlin, CM
McCarverMay, DG
Notterman, DA
Ward, RM
Weismann, DN
Wilson, GS
Wilson, JT
Weller, EB
Bennett, DR
Mulinare, J
Kaufman, P
Krough, C
Rieder, MJ
Troendle, G
Yaffe, SJ
Cote, CJ
Szefler, SJ
Blumer, JL
Frader, JE
Crain, LS
Moseley, KL
Nelson, RM
Porter, IH
Vizcarrondo, FE
Bowes, WA
Kazura, A
Krug, EF
Caniano, DA
Dressser, R
King, NMP
TI Considerations related to the use of recombinant human growth hormone in
children
SO PEDIATRICS
LA English
DT Article
ID CONSTITUTIONAL SHORT STATURE; CREUTZFELDT-JAKOB DISEASE;
CHRONIC-RENAL-FAILURE; DEFICIENT CHILDREN; TURNER SYNDROME; THERAPY;
HYPOPITUITARISM; ADOLESCENTS; METABOLISM; SECRETION
AB Since 1985 molecular biology techniques have made possible the synthetic synthesis of pure human growth hormone in potentially unlimited amounts. With this increased availability, its use in patients other than children with growth hormone deficiency has been associated with clinical and ethical questions. This statement presents an analysis of the current status of the use of human growth hormone in children.
C1 AMER MED ASSOC,US PHARMACOPEIA,CHICAGO,IL.
AMER COLL OBSTETRICIANS & GYNECOLOGISTS,WASHINGTON,DC.
HLTH PROTECT BRANCH,OTTAWA,ON,CANADA.
US FDA,ROCKVILLE,MD 20857.
NIH,BETHESDA,MD.
AMER BOARD PEDIAT INC,CHAPEL HILL,NC.
RI Moseley, Kathryn/A-8859-2009; Frader, Joel/A-8610-2010
NR 71
TC 39
Z9 40
U1 0
U2 0
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD JAN
PY 1997
VL 99
IS 1
BP 122
EP 129
PG 8
WC Pediatrics
SC Pediatrics
GA WB350
UT WOS:A1997WB35000020
ER
PT J
AU Halsey, NA
Abramson, JS
Chesney, PJ
Fisher, MC
Gerber, MA
Gromisch, DS
Kohl, S
Marcy, SM
Murray, DL
Overturf, GD
Whitley, RJ
Yogev, R
AF Halsey, NA
Abramson, JS
Chesney, PJ
Fisher, MC
Gerber, MA
Gromisch, DS
Kohl, S
Marcy, SM
Murray, DL
Overturf, GD
Whitley, RJ
Yogev, R
TI Recommended childhood immunization schedule - United States,
January-December 1997
SO PEDIATRICS
LA English
DT Article
C1 US FDA,ROCKVILLE,MD 20857.
AMER THORAC SOC,NEW YORK,NY.
NIAID,BETHESDA,MD.
CTR DIS CONTROL & PREVENT,ATLANTA,GA 30333.
NR 1
TC 12
Z9 13
U1 0
U2 0
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD JAN
PY 1997
VL 99
IS 1
BP 136
EP 138
PG 3
WC Pediatrics
SC Pediatrics
GA WB350
UT WOS:A1997WB35000023
ER
PT J
AU Viswanathan, M
DeOliveira, AM
Johren, O
Saavedra, JM
AF Viswanathan, M
DeOliveira, AM
Johren, O
Saavedra, JM
TI Increased endothelin ETA receptor expression in rat carotid arteries
after balloon injury
SO PEPTIDES
LA English
DT Article
DE endothelin; endothelin receptor subtypes; growth; vascular smooth muscle
ID SMOOTH-MUSCLE CELLS; INDUCED NEOINTIMA FORMATION; ANGIOTENSIN-II;
DNA-SYNTHESIS; ANTAGONIST; PROLIFERATION; ANGIOPLASTY; ATHEROSCLEROSIS;
BINDING; BQ-123
AB Endothelins are vasoactive peptides and are believed to act as vascular smooth muscle mitogens. Vascular injury results in medial smooth muscle migration and proliferation with the formation of a neointima. Using quantitative autoradiography, we examined the expression of endothelin receptor subtypes ETA and ETB in the rat carotid artery 2, 8, and 16 days after balloon- catheter injury. At two and eight days after balloon catheterization, ETA receptor expression was significantly increased in the media of the injured vessel when compared to that in the media of the intact vessel. The enhanced expression of receptors returned to normal levels by 16 days after the injury. Neointimal cells also expressed ETA receptors at a lower lever than that expressed by the injured media 8 days after injury, and continued to express ETA receptors 16 days after the injury. ETB receptors were not detectable in the media or the neointima at any time after the injury. Our results suggest that ETA receptors may have a significant role in injury induced vascular smooth muscle proliferation and neointima formation. Published by Elsevier Science Inc.
RP Viswanathan, M (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,10 CTR DR MS 1514,BETHESDA,MD 20892, USA.
RI Johren, Olaf/G-6967-2011
NR 42
TC 12
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0196-9781
J9 PEPTIDES
JI Peptides
PY 1997
VL 18
IS 2
BP 247
EP 255
DI 10.1016/S0196-9781(96)00285-9
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA WX954
UT WOS:A1997WX95400011
PM 9149297
ER
PT J
AU Moody, TW
Miller, MJ
Martinez, A
Unsworth, E
Cuttitta, F
AF Moody, TW
Miller, MJ
Martinez, A
Unsworth, E
Cuttitta, F
TI Adrenomedullin binds with high affinity, elevates cyclic AMP, and
stimulates c-fos mRNA in C6 glioma cells
SO PEPTIDES
LA English
DT Article
DE adrenomedullin; cGRP; receptors; cAMP; proliferation
ID GENE-RELATED PEPTIDE; RAT ADRENOMEDULLIN; HUMAN TISSUE; CALCITONIN;
RECEPTOR; EXPRESSION; GROWTH; SITES; IDENTIFICATION; NEUROBLASTOMA
AB The effects of adrenomedul lin (ADM) on C6 glioma cells were investigated. [I-125]ADM bound with high affinity (K-d = 24 nM) to a single class of sites (B-max = 36,000/cell) in C6 cells. Specific [I-125]ADM binding was inhibited with high affinity by ADM (IC50 value of 10 nM) but not ADM(22-52) or pro-adrenomedullin N-terminal 20 peptide (PAMP). By RT-PCR, ADM receptors were detected in C6 cells. ADM elevated cAMP (ED50 value of 10 nM) whereas PAMP and ADM(22-52) did not. ADM stimulated transiently c-fos mRNA in a concentration-dependent manner. Monoclonal antibody G6, which neutralizes ADM, significantly inhibited C6 proliferation and decreased the ability of ADM to elevate c-fos mRNA. These data suggest that ADM is a regulatory peptide of C6 cells. (C) 1997 Elsevier Science Inc.
RP Moody, TW (reprint author), NCI, MED BRANCH,DEPT CELL & CANC BIOL,DIV CLIN SCI, BLDG KWC,RM 300, 9610 MED CTR DR, ROCKVILLE, MD 20850 USA.
RI Martinez, Alfredo/A-3077-2013
OI Martinez, Alfredo/0000-0003-4882-4044
NR 31
TC 29
Z9 29
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PY 1997
VL 18
IS 8
BP 1111
EP 1115
DI 10.1016/S0196-9781(97)00179-4
PG 5
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA YF797
UT WOS:A1997YF79700003
PM 9396050
ER
PT J
AU Wu, JY
Henins, KA
Gressens, P
Gozes, I
Fridkin, M
Brenneman, DE
Hill, JM
AF Wu, JY
Henins, KA
Gressens, P
Gozes, I
Fridkin, M
Brenneman, DE
Hill, JM
TI Neurobehavioral development of neonatal mice following blockade of VIP
during the early embryonic period
SO PEPTIDES
LA English
DT Article
DE vasoactive intestinal peptide; neurobehavioral development; VIP
antagonist; mouse embryos; developmental milestones; developmental
retardation
ID VASOACTIVE-INTESTINAL-PEPTIDE; CENTRAL-NERVOUS-SYSTEM; RAT-BRAIN;
INTRACELLULAR CALCIUM; FUNCTIONAL EXPRESSION; NEURONAL SURVIVAL;
CEREBRAL-CORTEX; BINDING-SITES; SLEEP FACTOR; RECEPTORS
AB Previous work has shown that blockade of VIP function in the early postimplantation embryo results in growth retardation and microcephaly. In the present work, the neurobehavioral development of neonatal mice was examined following treatment of dams with a VIP antagonist during this period. Inhibition of VIP functions during early embryogenesis impaired the performance of 5 of 10 developmental behaviors. These behaviors included developmental milestones (first appearance of ear twitch and eye opening) and complex motor behaviors (negative geotaxis, surface righting, and air righting). The retardation of neurobehavioral development produced by inhibition of VIP action indicates that this peptide is important to the progression of embryonic development. Published by Elsevier Science Inc.
C1 NICHHD, LDN, SECT DEV & MOL PHARMACOL, NIH, BETHESDA, MD 20892 USA.
HOP ROBERT DEBRE, SERV NEUROPEDIAT, F-75019 PARIS, FRANCE.
TEL AVIV UNIV, SACKLER SCH MED, DEPT CLIN BIOCHEM, IL-69978 TEL AVIV, ISRAEL.
WEIZMANN INST SCI, DEPT ORGAN CHEM, IL-76100 REHOVOT, ISRAEL.
NR 45
TC 40
Z9 41
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PY 1997
VL 18
IS 8
BP 1131
EP 1137
DI 10.1016/S0196-9781(97)00146-0
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA YF797
UT WOS:A1997YF79700006
PM 9396053
ER
PT B
AU Schmidt, PJ
Roca, CA
Rubinow, DR
AF Schmidt, PJ
Roca, CA
Rubinow, DR
BE Lobo, RA
TI Perimenopausal depression
SO PERIMENOPAUSE
SE SERONO SYMPOSIA, USA
LA English
DT Proceedings Paper
CT International Symposium on Perimenopause
CY NOV 17-20, 1995
CL PALM BEACH GARDENS, FL
SP Serono Symp USA Inc
RP Schmidt, PJ (reprint author), NIMH,SECT BEHAV ENDOCRINOL,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER-VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
BN 0-387-94967-4
J9 SERONO SYMP
PY 1997
BP 246
EP 254
PG 9
WC Endocrinology & Metabolism; Obstetrics & Gynecology
SC Endocrinology & Metabolism; Obstetrics & Gynecology
GA BJ84Q
UT WOS:A1997BJ84Q00018
ER
PT S
AU LaMontagne, JR
AF LaMontagne, JR
BE Brown, F
Greco, D
Mastrantonio, P
Salmaso, S
Wassilak, S
TI The United States research strategy on pertussis
SO PERTUSSIS VACCINE TRIALS
SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION
LA English
DT Article; Proceedings Paper
CT International Symposium on Pertussis Vaccine Trials
CY OCT 30, 1995-NOV 01, 1996
CL ROME, ITALY
SP Ist Super Sanita, WHO, Childrens Vaccine Initiat, NiAID, Int Federat Pharm Manufacturers Assoc, European Commiss COST STD Initiat, European Vaccine Res, Int Assoc Biol Standardizat
AB Wide-scale use of whole-cell Vaccines has led to good control of pertussis disease in the United States; however, this control has been achieved at the cost of common and uncommon adverse events of known frequencies. Agencies of the U.S. Public Health Service actively stimulated the development of new pertussis Vaccines by directly supporting basic and applied research and increasing interactions with industry and with health authorities in other countries. This international cooperation resulted in a better understanding of the pathogenesis of pertussis and in the final development and clinical testing of several candidate acellular pertussis vaccines.
RP LaMontagne, JR (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,NIH,3A18 SOLAR BLDG,BETHESDA,MD 20892, USA.
NR 6
TC 1
Z9 1
U1 0
U2 0
PU KARGER
PI BASEL
PA POSTFACH, CH-4009 BASEL, SWITZERLAND
SN 0301-5149
BN 3-8055-6481-3
J9 DEV BIOL STAND
JI Dev.Biol.Stand.
PY 1997
VL 89
BP 25
EP 28
PG 4
WC Biology; Biotechnology & Applied Microbiology
SC Life Sciences & Biomedicine - Other Topics; Biotechnology & Applied
Microbiology
GA BJ43T
UT WOS:A1997BJ43T00003
PM 9272332
ER
PT S
AU Blackwelder, WC
VanRaden, MJ
Deloria, MA
AF Blackwelder, WC
VanRaden, MJ
Deloria, MA
BE Brown, F
Greco, D
Mastrantonio, P
Salmaso, S
Wassilak, S
TI Estimation of pertussis vaccine efficacy in the presence of covariates
in three randomized trials
SO PERTUSSIS VACCINE TRIALS
SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION
LA English
DT Article; Proceedings Paper
CT International Symposium on Pertussis Vaccine Trials
CY OCT 30, 1995-NOV 01, 1996
CL ROME, ITALY
SP Ist Super Sanita, WHO, Childrens Vaccine Initiat, NiAID, Int Federat Pharm Manufacturers Assoc, European Commiss COST STD Initiat, European Vaccine Res, Int Assoc Biol Standardizat
DE acellular pertussis vaccines; efficacy; covariates; duration of
protection
AB We estimated efficacy of pertussis Vaccines in three randomized controlled trials with adjustment for several baseline covariates: presence of one or more other children in the household, sex of the study child, and geographical area. Adjusted and unadjusted efficacy estimates differed only trivially. We also assessed the association of efficacy with time since vaccination and background pertussis incidence. The acellular vaccines, except for the two-component vaccine in the Stockholm trial, appeared to maintain their efficacy during two years of follow-up. in contrast, efficacy of a whole-cell vaccine decreased significantly in both the Stockholm and Italian trials. The relationship between efficacy and background incidence was not consistent across studies and vaccines.
RP Blackwelder, WC (reprint author), NIAID,SOLAR BLDG,ROOM 3A03,BETHESDA,MD 20892, USA.
NR 6
TC 1
Z9 1
U1 0
U2 0
PU KARGER
PI BASEL
PA POSTFACH, CH-4009 BASEL, SWITZERLAND
SN 0301-5149
BN 3-8055-6481-3
J9 DEV BIOL STAND
JI Dev.Biol.Stand.
PY 1997
VL 89
BP 161
EP 166
PG 6
WC Biology; Biotechnology & Applied Microbiology
SC Life Sciences & Biomedicine - Other Topics; Biotechnology & Applied
Microbiology
GA BJ43T
UT WOS:A1997BJ43T00017
PM 9272346
ER
PT S
AU Schneerson, R
Robbins, JB
Taranger, J
Lagerard, T
Trollfors, B
AF Schneerson, R
Robbins, JB
Taranger, J
Lagerard, T
Trollfors, B
BE Brown, F
Greco, D
Mastrantonio, P
Salmaso, S
Wassilak, S
TI Examination of similarities between diphtheria and pertussis and their
toxoids provide insight into vaccine-induced protection to Bordetella
pertussis
SO PERTUSSIS VACCINE TRIALS
SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION
LA English
DT Article; Proceedings Paper
CT International Symposium on Pertussis Vaccine Trials
CY OCT 30, 1995-NOV 01, 1996
CL ROME, ITALY
SP Ist Super Sanita, WHO, Childrens Vaccine Initiat, NiAID, Int Federat Pharm Manufacturers Assoc, European Commiss COST STD Initiat, European Vaccine Res, Int Assoc Biol Standardizat
DE diphtheria toxoids; pertussis toxoids; vaccination
ID WHOOPING-COUGH; TOXIN; EPIDEMIOLOGY; IMMUNITY; EFFICACY; GENE
C1 NICHHD,NIH,BETHESDA,MD 20892.
NR 34
TC 2
Z9 2
U1 0
U2 0
PU KARGER
PI BASEL
PA POSTFACH, CH-4009 BASEL, SWITZERLAND
SN 0301-5149
BN 3-8055-6481-3
J9 DEV BIOL STAND
JI Dev.Biol.Stand.
PY 1997
VL 89
BP 321
EP 326
PG 6
WC Biology; Biotechnology & Applied Microbiology
SC Life Sciences & Biomedicine - Other Topics; Biotechnology & Applied
Microbiology
GA BJ43T
UT WOS:A1997BJ43T00037
PM 9272366
ER
PT J
AU He, XJ
Tse, CM
Donowitz, M
Alper, SL
Gabriel, SE
Baum, BJ
AF He, XJ
Tse, CM
Donowitz, M
Alper, SL
Gabriel, SE
Baum, BJ
TI Polarized distribution of key membrane transport proteins in the rat
submandibular gland
SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
LA English
DT Article
DE confocal microscopy; immunofluorescence; membrane proteins; salivary
secretion; salivary glands
ID SALIVARY-GLANDS; FLUID SECRETION; ION-TRANSPORT; MOLECULAR-CLONING;
WATER CHANNELS; ACINAR-CELLS; LOCALIZATION; DUCTS; IDENTIFICATION;
EPITHELIUM
AB Immunofluorescence labelling and confocal microscopy were employed to examine the polarized distribution of several membrane transport proteins believed to be essential for salivary secretion in the rat submandibular gland. The Na+/K+-ATPase, Na+/H+ exchanger isoform 1 (NHE1), and the secretory Na+/K+/2Cl(-) cotransporter isoform were all found in the basolateral membranes of acinar and intralobular duct cells. Anion exchanger isoform 2 (AE2) was found only in the basolateral membranes of acinar cells, while AE1 was absent from glandular epithelial cells. Aquaporin 5 was detected in the apical membranes of acinar cells, while the cystic fibrosis transmembrane conductance regulator was found only in apical membranes of intralobular duct cells. NHEs 2 and 3 were found in the apical membranes of both acinar and intralobular duct cells. Our results are generally consistent with the expected distribution of most transporters based on previous physiological and pharmacological experiments. However, the epical localization of NHEs 2 and 3, and the presence of the secretory isoform of the Na+/K+/2Cl(-) cotransporter in intralobular duct cells were not predicted.
C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,NIH,BETHESDA,MD 20892.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GASTROENTEROL,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,DIV GASTROENTEROL,BALTIMORE,MD 21205.
BETH ISRAEL HOSP,MOL MED UNIT,BOSTON,MA 02215.
BETH ISRAEL HOSP,RENAL UNIT,BOSTON,MA 02215.
UNIV N CAROLINA,CYST FIBROSIS RES & TREATMENT CTR,CHAPEL HILL,NC 27599.
NR 43
TC 121
Z9 123
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0031-6768
J9 PFLUG ARCH EUR J PHY
JI Pflugers Arch.
PD JAN
PY 1997
VL 433
IS 3
BP 260
EP 268
PG 9
WC Physiology
SC Physiology
GA WH693
UT WOS:A1997WH69300006
PM 9064641
ER
PT J
AU Gorlach, A
Roesler, J
Chanock, SJ
Curnutte, JT
AF Gorlach, A
Roesler, J
Chanock, SJ
Curnutte, JT
TI Identification of a pseudogene highly homologous to the NADPH oxidase
component p47phox.
SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
LA English
DT Meeting Abstract
C1 UNIV ZURICH IRCHEL, INST PHYSIOL, CH-8057 ZURICH, SWITZERLAND.
SCRIPPS RES INST, LA JOLLA, CA 92037 USA.
NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA.
TECH UNIV DRESDEN, KINDERKLIN, D-8027 DRESDEN, GERMANY.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0031-6768
J9 PFLUG ARCH EUR J PHY
JI Pflugers Arch.
PY 1997
VL 433
IS 6
SU S
BP O92
EP O92
PG 1
WC Physiology
SC Physiology
GA WV421
UT WOS:A1997WV42100091
ER
PT J
AU Long, RM
AF Long, RM
TI What is the NIGMS doing to help smooth out the irregularities in funding
for ongoing research programs that almost inevitably occur over time in
today's fiscal climate?
SO PHARMACEUTICAL RESEARCH
LA English
DT News Item
RP Long, RM (reprint author), NIGMS,PHARMACOL & PHYSIOL SCI BRANCH,DIV PHARMACOL PHYSIOL & BIOL CHEM,NIH,BETHESDA,MD, USA.
NR 0
TC 9
Z9 9
U1 0
U2 0
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0724-8741
J9 PHARMACEUT RES
JI Pharm. Res.
PD JAN
PY 1997
VL 14
IS 1
BP 1
EP 1
PG 1
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA WJ623
UT WOS:A1997WJ62300001
PM 9034213
ER
PT J
AU Witkin, JM
Acri, JB
Gleeson, S
Barrett, EJ
AF Witkin, JM
Acri, JB
Gleeson, S
Barrett, EJ
TI Blockade of behavioral effects of bretazenil by flumazenil and ZK 93,426
in pigeons
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE bretazenil; flumazenil; ZK 93,426; midazolam; punished behavior; drug
discrimination
ID BENZODIAZEPINE-RECEPTOR ANTAGONIST; DISCRIMINATIVE STIMULUS PROPERTIES;
AMINOBUTYRIC ACID(A) RECEPTOR; GABA-A RECEPTORS; RO 15-1788; DRUG
DISCRIMINATION; PARTIAL AGONISTS; PENTYLENETETRAZOLE-CUE; INTRINSIC
EFFICACIES; DIAZEPAM
AB Benzodiazepine receptor partial agonists manifest full efficacy in preclinical tests of anxiolytic drug action but do not fully reproduce the discriminative stimulus effects of benzodiazepine receptor full agonists in pigeons. The partial agonist, bretazenil, binds to both diazepam-sensitive and diazepam-insensitive GABA(A) receptors. Previous studies have suggested a role for each of these receptor populations in some behavioral effects of bretazenil in pigeons. A possible role for these receptor subtypes in the behavioral effects of bretazenil was further investigated through drug interaction studies with the benzodiazepine receptor antagonists, flumazenil and ZK 93,426. Whereas flumazenil binds with high affinity to both receptor isoforms, ZK 93,426 binds preferentially to diazepam-sensitive binding sites. Bretazenil markedly increased punished responding of pigeons without significantly affecting nonpunished responding. In pigeons discriminating the full benzodiazepine receptor agonist, midazolam, from saline, bretazenil produced only 60-75% maximal effect. Flumazenil and ZK 93,426 neither increased punished responding nor substituted for midazolam, but hose-dependently blocked the effects of bretazenil on punished responding. Flumazenil also dose-dependently blocked the effects of bretazenil in midazolam-discriminating pigeons, whereas ZK 93,426 only attenuated this effect. These results indicate that bretazenil's actions as a partial agonist at diazepam-sensitive benzodiazepine receptors mediate increases in unished responding and substitution for the discriminiative stimulus effects of midazolam in pigeons. The differences in the effects of flumazenil and ZK 93,426 on the discriminative stimulus effects of bretazenil suggest a potential contribution of diazepam-insensitive sites to this behavioral effect. Copyright (C) 1997 Elsevier Science Inc.
C1 UNIFORMED SERV UNIV HLTH SCI, DEPT PSYCHIAT, BETHESDA, MD 20814 USA.
RP Witkin, JM (reprint author), NIDA, ADDICT RES CTR, DRUG DEV GRP, NIH, POB 5180, BALTIMORE, MD 21224 USA.
NR 56
TC 4
Z9 4
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD JAN
PY 1997
VL 56
IS 1
BP 1
EP 7
DI 10.1016/S0091-3057(96)00120-7
PG 7
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA WA251
UT WOS:A1997WA25100001
PM 8981602
ER
PT J
AU Figg, WD
Pluda, JM
Lush, RM
Saville, MW
Wyvill, K
Reed, E
Yarchoan, R
AF Figg, WD
Pluda, JM
Lush, RM
Saville, MW
Wyvill, K
Reed, E
Yarchoan, R
TI The pharmacokinetics of TNP-470, a new angiogenesis inhibitor
SO PHARMACOTHERAPY
LA English
DT Article
ID ACQUIRED IMMUNODEFICIENCY SYNDROME; KAPOSIS-SARCOMA; TUMOR-GROWTH;
AGM-1470; FUMAGILLIN; CELLS; SURAMIN; GENE
AB Study Objective. To characterize the pharmacokinetic profile of TNP-470, a synthetic analog of fumagillin that is a potent inhibitor of angiogenesis and inhibits neovascularization in several solid tumor models.
Design. A dose-escalation phase I clinical trial.
Setting. The National Institutes of Health.
Patients. Patients with human immunodeficiency virus-associated Kaposi's sarcoma.
Interventions. The TNP-470 dosage was increased in 13 sequential cohorts using a modified Fibonacci escalation scheme (4.6, 9.3, 15.4, 23.2, and 43.1 mg/m(2)). The drug was administered as a 1-hour intravenous infusion. Serial blood samples were collected and assayed by reverse-phase highperformance liquid chromatography and the pharmacokinetics were characterized.
Measurements and Main Results. There was a linear relationship between the dose of TNP-470 and both area under the curve to infinity (AUC([inf])) and time to maximum concentration (C-max). The C-max ranged between 6.6 ng/ml at the lowest dosage (4.6 mg/m(2)) and 597.1 ng/ml at the highest dosage (43.1 mg/m(2)). The agent was rapidly cleared from the circulation with a short terminal half-life (0.88 +/- 2.5 hr), which is consistent with preclinical data. Peak plasma concentrations of AGM-1883, an active metabolite, ranged between 0.4 and 158.1 ng/ml.
Conclusion. Concentrations of TNP-470 that have in vitro activity were achievable in vivo. The drug was rapidly cleared from the circulation after a single 1-hour infusion. There was considerable interpatient variability in the clearance, but no evidence of saturable elimination. If more prolonged exposure is necessary for activity, administration of TNP-470 by continuous infusion may be suitable.
C1 NCI,DEV CHEMOTHERAPY SECT,INVEST DRUG BRANCH,CANC TREATMENT EVALUAT PROGRAM,NIH,BETHESDA,MD 20892.
NCI,RETROVIRAL DIS SECT,MED BRANCH,CLIN ONCOL PROGRAM,DIV CANC TREATMENT,NIH,BETHESDA,MD 20892.
RP Figg, WD (reprint author), NCI,CLIN PHARMACOL BRANCH,CLIN PHARMACOKINET SECT,CLIN ONCOL PROGRAM,NIH,BLDG 10,ROOM 5A01,BETHESDA,MD 20892, USA.
RI Figg Sr, William/M-2411-2016
NR 33
TC 51
Z9 53
U1 0
U2 2
PU PHARMACOTHERAPY PUBLICATIONS INC
PI BOSTON
PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111
SN 0277-0008
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD JAN-FEB
PY 1997
VL 17
IS 1
BP 91
EP 97
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA WD766
UT WOS:A1997WD76600008
PM 9017768
ER
PT J
AU Spouge, JL
AF Spouge, JL
TI Single-particle survival in parallel gated trapping
SO PHYSICAL REVIEW E
LA English
DT Article
ID DYNAMIC TRAP
AB Any chemical reaction A* + B --> C whose progress is modulated by another reaction of the form A* reversible arrow A is said to be gated. The gating reaction A* reversible arrow A represents a reversible fluctuation from a reactive state A* to an unreactive state A not reacting with B. Reversibly blocked chemical reactions, conformational fluctuations in proteins, and reactions occurring within biomembranes or involving biological molecules have all been studied recently in contexts related to gating. This article calculates certain trapping rates and mean survival times in the presence of a single gated trap. Unlike previous methods, the formalism in this paper is based directly on trapping rates and not on Green's functions. The trapping rate formalism leads quite naturally to explicit solutions for some recently developed (''parallel'') gating models, solutions that might be quite difficult to derive within a Green's-function formalism. These solutions give time-dependent rate coefficients for parallel gated chemical reactions.
RP Spouge, JL (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894, USA.
NR 16
TC 7
Z9 7
U1 0
U2 3
PU AMERICAN PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1063-651X
J9 PHYS REV E
JI Phys. Rev. E
PD JAN
PY 1997
VL 55
IS 1
BP 421
EP 425
DI 10.1103/PhysRevE.55.421
PN A
PG 5
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA WD545
UT WOS:A1997WD54500053
ER
PT S
AU Sherman, A
Smolen, P
AF Sherman, A
Smolen, P
BE Soria, B
TI Computer modeling of heterogeneous beta-cell populations
SO PHYSIOLOGY AND PATHOPHYSIOLOGY OF THE ISLETS OF LANGERHANS
SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
LA English
DT Article; Proceedings Paper
CT 1st International Meeting of the Pancreatic-Islet-Study-Group of the
European-Association-for-the-Study-of-Diabetes
CY NOV 25-28, 1994
CL ALICANTE, SPAIN
SP European Assoc Study Diabetes, Pancreat Islet Study Grp, Fundacion CAM, Generalitat Valenciana, Alicante City Council, Univ Alicante
ID ELECTRICAL-ACTIVITY; PANCREATIC-ISLETS; MOUSE; OSCILLATIONS; GLUCOSE;
LANGERHANS; CURRENTS; K+
C1 NIH, Math Res Branch, Bethesda, MD 20892 USA.
RP Sherman, A (reprint author), NIH, Math Res Branch, Bldg 10, Bethesda, MD 20892 USA.
NR 26
TC 2
Z9 2
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45702-4
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 426
BP 275
EP 284
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Medicine,
Research & Experimental; Pathology; Physiology
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Research &
Experimental Medicine; Pathology; Physiology
GA BK61Q
UT WOS:000072747900038
PM 9544285
ER
PT B
AU Bernard, M
Iuvone, PM
Cassone, VM
Roseboom, PH
Coon, SL
Klein, DC
AF Bernard, M
Iuvone, PM
Cassone, VM
Roseboom, PH
Coon, SL
Klein, DC
BE Webb, SM
PuigDomingo, M
Moller, M
Pevet, P
TI Chicken arylalkylamine N-acetyltransferase: Cloning and circadian
regulation in the pineal gland
SO PINEAL UPDATE: FROM MOLECULAR MECHANISMS TO CLINICAL IMPLICATIONS
LA English
DT Proceedings Paper
CT 7th Colloquium of the European-Pineal-Society
CY MAR 29-31, 1996
CL SITGES, SPAIN
SP European Pineal Soc
AB Serotonin N-acetyltransferase (arylalkylamine N-acetyltransferase, AA-NAT) drives the circadian rhythm in melatonin production in the pineal gland. We have cloned cDNA encoding chicken AA-NAT and have used this to determine that AA-NAT mRNA levels in the pineal gland exhibit a strong day/night rhythm with a peak at night. This rhythm persists in constant darkness (DD) and constant lighting (LL), indicating that it is controlled by a circadian oscillator. Exposure to LL damps the AA-NAT activity rhythm, but does not decrease the amplitude of the rhythm in AA-NAT mRNA. Further evidence that activity and mRNA levels are not necessarily related comes from the observation that an unexpected pulse of light rapidly decreases enzyme activity, but not the levels of the AA-NAT transcript. In LL, the peak in both AA-NAT mRNA and AA-NAT activity was delayed by similar to 6 hr. These findings indicate that a clock controls the rhythm in AA-NAT mRNA and that independent mechanisms appear to control the translation of changes in mRNA into changes in enzyme activity.
C1 NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bethesda, MD 20892 USA.
RP Klein, DC (reprint author), NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU P J D PUBLICATIONS LTD
PI WESTBURY
PA PO BOX 966, WESTBURY, NY 11590 USA
BN 0-915340-19-4
PY 1997
BP 29
EP 36
PG 4
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA BK42W
UT WOS:000072152700003
ER
PT B
AU Baler, RD
Klein, DC
AF Baler, RD
Klein, DC
BE Webb, SM
PuigDomingo, M
Moller, M
Pevet, P
TI Circadian regulation of transcription factor Fra-2 in the rat pineal
gland
SO PINEAL UPDATE: FROM MOLECULAR MECHANISMS TO CLINICAL IMPLICATIONS
LA English
DT Proceedings Paper
CT 7th Colloquium of the European-Pineal-Society
CY MAR 29-31, 1996
CL SITGES, SPAIN
SP European Pineal Soc
AB Fra-2 is a member of the FOS family of transcription factors. We found that expression of this gene and its protein product is regulated on a circadian basis in the pineal gland and that regulation involves an adrenergic --> cyclic AMP mechanism. Fra-2 may be an integral component of transduction in this and other tissues.
C1 NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bethesda, MD 20892 USA.
RP Klein, DC (reprint author), NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bldg 49,Room 5A38, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU P J D PUBLICATIONS LTD
PI WESTBURY
PA PO BOX 966, WESTBURY, NY 11590 USA
BN 0-915340-19-4
PY 1997
BP 37
EP 47
PG 3
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA BK42W
UT WOS:000072152700004
ER
PT S
AU Vande Woude, GF
Jeffers, M
Cortner, J
Alvord, G
Tsarfaty, I
Resau, J
AF Vande Woude, GF
Jeffers, M
Cortner, J
Alvord, G
Tsarfaty, I
Resau, J
BE Bock, GR
Goode, JA
TI Met-HGF/SF: tumorigenesis, invasion and metastasis
SO PLASMINOGEN-RELATED GROWTH FACTORS
SE CIBA FOUNDATION SYMPOSIA
LA English
DT Article; Proceedings Paper
CT Symposium on Plasminogen-Related Growth Factors
CY APR 08-10, 1997
CL CIBA FDN, LONDON, ENGLAND
HO CIBA FDN
ID HEPATOCYTE GROWTH-FACTOR; FACTOR SCATTER FACTOR; BETA-CATENIN; HER-2/NEU
AMPLIFICATION; PROTOONCOGENE PRODUCT; BREAST-CANCER; C127 CELLS;
RECEPTOR; EXPRESSION; TRANSFORMATION
AB Hepatocyte growth factor/scatter factor (HGF/SF) is synthesized by mesenchymal cells and is a paracrine effector of cells, predominantly epithelial, that express the Met tyrosine kinase-receptor. We have demonstrated that autocrine HGF/SF expression in mouse fibroblasts results in transformation and tumorigenesis. HGF/SF-treated cells expressing Met can respond in a variety of ways: mitogenically, by scattering (motility), and by forming branching tubules in gel matrices (branching morphogenesis). HGF/SF also induces in vitro invasiveness and is angiogenic ih in vivo assays. A human cell line and several mouse cell lines that we have constructed to express Met-HGF/SF in an autocrine fashion are tumorigenic, invasive and metastatic in athymic nude mice. Thus, the very complex process of invasion and metastasis can be mediated by a ligand-receptor signalling pathway, and the cell lines we have developed provide important model systems for identifying the signalling molecules that mediate these phenotypes: For example Met-HGF/SF signalling activates the urokinase plasminogen proteolysis network, thus coupling this signal transduction pathway to the proteases that mediate dissolution of the extracellular matrix. Branching morphogenesis, mediated by Met-HGF/SF signalling, is dependent on this process, as well as the formation of cell-cell junctions and interaction with the extracellular matrix. We have proposed a hypothesis for the role of Met and downstream signalling molecules in generating normal ducts and lumenal structures, as well as a model for how interruption of this signalling leads to abonormal malignant progression. Is Met involved in human cancer? Human sarcomas often inappropriately express Met, suggesting that it is an important oncogene in these cancers, and an increasing number of reports have implicated Met-HGF/SF signalling in a variety of human cancers.
C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA.
NCI, Frederick Canc Res & Dev Ctr, Data Management Syst, Frederick, MD 21702 USA.
Tel Aviv Univ, Sackler Sch Med, Dept Human Microbiol, IL-69978 Tel Aviv, Israel.
RP Vande Woude, GF (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, POB B, Frederick, MD 21702 USA.
NR 40
TC 99
Z9 100
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND
SN 0300-5208
BN 0-471-97456-0
J9 CIBA F SYMP
PY 1997
VL 212
BP 119
EP 132
PG 14
WC Biochemistry & Molecular Biology; Oncology; Medicine, General & Internal
SC Biochemistry & Molecular Biology; Oncology; General & Internal Medicine
GA BM64R
UT WOS:000079333200011
PM 9524767
ER
PT S
AU Leonard, EJ
AF Leonard, EJ
BE Bock, GR
Goode, JA
TI Biological aspects of macrophage-stimulating protein (MSP) and its
receptor
SO PLASMINOGEN-RELATED GROWTH FACTORS
SE CIBA FOUNDATION SYMPOSIA
LA English
DT Article; Proceedings Paper
CT Symposium on Plasminogen-Related Growth Factors
CY APR 08-10, 1997
CL CIBA FDN, LONDON, ENGLAND
HO CIBA FDN
ID HEPATOCYTE GROWTH-FACTOR; TYROSINE KINASE; MOLECULAR-CLONING;
GENE-PRODUCT; RON; STK; IDENTIFICATION; ACTIVATION; FAMILY; CHAIN
AB Macrophage-stimulating protein (MSP; also known as HGF-like protein [HGF1]) is a 78 kDa plasma protein that is secreted by the liver into the circulation as single-chain, biologically inactive pro-MSP. The presence of conserved triple disulfide loops (kringles) places pro-MSP in a family of coagulation system serine protease zymogens that are activated by proteolytic cleavage. Although pro-MSP has lost enzymic activity, it has retained the activation mechanism, in that proteolytic cleavage at a single site yields biologically active disulfide-linked ap-chain heterodimeric MSP. The MSP receptor is a transmembrane protein tyrosine kinase. MSP causes phosphorylation of the receptor cytoplasmic domain, association of phosphatidylinositol (PI)-3 kinase with the receptor, and phosphorylation of receptor-bound PI-3 kinase. Inhibition of PI-3 kinase by wortmannin prevents MSP action on cells. MSP stimulates motility of murine resident peritoneal macrophages. However, it does not act on exudate macrophages or blood monocytes, since these earlier maturational stages of the lineage do not express the receptor. MSP also stimulates keratinocyte cell lines, causing either chemotactic responses or increased cell numbers in culture. We suggest that pro-MSP diffuses into local tissue sites, where proteolytic cleavage to MSP results in stimulation of keratinocytes and macrophages. It possibly plays a role in tissue injury or wound healing.
C1 NCI, Immunol Lab, Frederick, MD 21702 USA.
RP Leonard, EJ (reprint author), NCI, Immunol Lab, Bldg 560,Room 12-71, Frederick, MD 21702 USA.
NR 29
TC 24
Z9 24
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND
SN 0300-5208
BN 0-471-97456-0
J9 CIBA F SYMP
PY 1997
VL 212
BP 183
EP 197
PG 15
WC Biochemistry & Molecular Biology; Oncology; Medicine, General & Internal
SC Biochemistry & Molecular Biology; Oncology; General & Internal Medicine
GA BM64R
UT WOS:000079333200016
PM 9524771
ER
PT S
AU Rosen, EM
Lamszus, K
Laterra, J
Polverini, PJ
Rubin, JS
Goldberg, ID
AF Rosen, EM
Lamszus, K
Laterra, J
Polverini, PJ
Rubin, JS
Goldberg, ID
BE Bock, GR
Goode, JA
TI HGF/SF in angiogenesis
SO PLASMINOGEN-RELATED GROWTH FACTORS
SE CIBA FOUNDATION SYMPOSIA
LA English
DT Article; Proceedings Paper
CT Symposium on Plasminogen-Related Growth Factors
CY APR 08-10, 1997
CL CIBA FDN, LONDON, ENGLAND
HO CIBA FDN
ID HEPATOCYTE GROWTH-FACTOR; INVASIVE BREAST-CARCINOMA; C-MET RECEPTOR;
SCATTER FACTOR; TUMOR ANGIOGENESIS; MOLECULAR-CLONING; EPITHELIAL-CELLS;
ENDOTHELIAL-CELLS; SEQUENCE-ANALYSIS; FACTOR EXPRESSION
AB Hepatocyte growth factor/scatter factor (HGF/SF) is a mesenchyme-derived cytokine that stimulates motility and invasiveness of epithelial and cancer cells. These responses are transduced through the c-met proto-oncogene product, a transmembrane tyrosine kinase that functions as the HGF/SF receptor. We have shown that HGF/SF is a potent angiogenic molecule and that its angiogenic activity is mediated primarily through direct actions on vascular endothelial cells. These include stimulation of cell migration, proliferation, protease production, invasion, and organization into capillary-like tubes. We further showed that HGF/SF is overexpressed in invasive human cancers, including breast cancer, relative to non-invasive cancers and benign conditions. In invasive breast cancers, the content of HGF/SF is strongly correlated with that of von Willebrand's factor, a marker of vascular endothelial cells. Furthermore, transfection of breast cancer and glioma cell lines with HGF/SF cDNA greatly enhanced the ability of these cells to grow as tumours in orthotopic sites in syngeneic or immunocompromized host animals. The increased growth rate of the HGF/SF-transfected cells was attributable, in part, to increased tumour angiogenesis. These findings suggest that HGF/SF may function as a tumour progression factor, in part by stimulating tumour cell invasiveness and in part by stimulating angiogenesis.
C1 Long Isl Jewish Med Ctr, Dept Radiat Oncol, New Hyde Pk, NY 11040 USA.
Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
Johns Hopkins Sch Med, Dept Oncol, Baltimore, MD USA.
Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD USA.
Kennedy Krieger Res Inst, Baltimore, MD USA.
Sch Dent, Dept Oral Pathol, Ann Arbor, MI 48109 USA.
NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA.
RP Rosen, EM (reprint author), Long Isl Jewish Med Ctr, Dept Radiat Oncol, 270-05 76th Ave, New Hyde Pk, NY 11040 USA.
FU NCI NIH HHS [CA-64869, CA-64416]
NR 58
TC 90
Z9 90
U1 0
U2 0
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND
SN 0300-5208
BN 0-471-97456-0
J9 CIBA F SYMP
PY 1997
VL 212
BP 215
EP 229
PG 15
WC Biochemistry & Molecular Biology; Oncology; Medicine, General & Internal
SC Biochemistry & Molecular Biology; Oncology; General & Internal Medicine
GA BM64R
UT WOS:000079333200018
PM 9524773
ER
PT S
AU Sherman, MR
Williams, LD
Saifer, MGP
French, JA
Kwak, LW
Oppenheim, JJ
AF Sherman, MR
Williams, LD
Saifer, MGP
French, JA
Kwak, LW
Oppenheim, JJ
BE Harris, JM
Zalipsky, S
TI Conjugation of high-molecular weight poly(ethylene glycol) to cytokines:
Granulocyte-macrophage colony-stimulating factors as model substrates
SO POLY(ETHYLENE GLYCOL): CHEMISTRY AND BIOLOGICAL APPLICATIONS
SE ACS Symposium Series
LA English
DT Review
CT Symposium on Poly(ethylene glycol) - Chemistry and Biological
Applications, at the 213th National Meeting of the
American-Chemical-Society
CY APR 13-17, 1997
CL SAN FRANCISCO, CA
SP Amer Chem Soc, Div Polym Chem
ID FACTOR GM-CSF; MODIFIED SUPEROXIDE-DISMUTASE; WATER-SOLUBLE POLYMERS;
TUMOR-NECROSIS-FACTOR; AMINO-ACID-SEQUENCE; POLYETHYLENE-GLYCOL;
HORSERADISH-PEROXIDASE; GLOMERULAR-FILTRATION; RECOMBINANT
INTERLEUKIN-2; CHEMICAL MODIFICATION
AB The ability of the small receptor-binding protein, recombinant murine granulocyte-macrophage colony-stimulating factor (GM-CSF), to increase the abundance of certain blood cell types in mice was enhanced markedly by covalent attachment of a single long strand of PEG (30-40 kDa). Potency was not increased further by coupling a second strand. Such conjugates can be synthesized efficiently by reaction of protein amino groups with PEG propionaldehydes in the presence of NaBH(3)CN or with PEG p-nitrophenyl carbonates. Both methods have been used to prepare recombinant human GM-CSF conjugates of predetermined composition, e.g. PEG(1)GM-CSF and PEG(2)GM-CSF, in high yield. These compounds, or analogous derivatives of other cytokines, purified by ion-exchange and size-exclusion chromatography, may be suitable candidates for pharmaceutical development.
C1 Mt View Pharmaceut Inc, Menlo Pk, CA 94025 USA.
NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
RP Sherman, MR (reprint author), Mt View Pharmaceut Inc, 871-L Ind Pk, Menlo Pk, CA 94025 USA.
NR 71
TC 22
Z9 22
U1 2
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 USA
SN 0097-6156
BN 0-8412-3537-6
J9 ACS SYM SER
JI ACS Symp. Ser.
PY 1997
VL 680
BP 155
EP 169
PG 15
WC Chemistry, Applied; Chemistry, Medicinal; Chemistry, Multidisciplinary;
Polymer Science
SC Chemistry; Pharmacology & Pharmacy; Polymer Science
GA BK03M
UT WOS:000070951700011
ER
PT J
AU Einolf, HJ
Gross, MA
Butch, ER
Lin, JM
Amin, S
Yagi, H
Jerina, DM
Baird, WM
AF Einolf, HJ
Gross, MA
Butch, ER
Lin, JM
Amin, S
Yagi, H
Jerina, DM
Baird, WM
TI Selective recognition of substituted chrysene-diol epoxide-2-DNA adducts
by antiserum prepared against DNA adducts of benzo[C]-phenanthrene-diol
epoxide-2
SO POLYCYCLIC AROMATIC COMPOUNDS
LA English
DT Article
DE immunodetection; benzo[c]phenanthrene-DNA adducts; substituted
chrysene-DNA adducts
ID ANTI-DIHYDRODIOL-EPOXIDES; SALMONELLA-TYPHIMURIUM; MOUSE SKIN; CHEMICAL
CARCINOGENESIS; AROMATIC-HYDROCARBONS; MAMMALIAN-CELLS; NEWBORN MICE;
REGION; MUTAGENICITY; BENZO(C)PHENANTHRENE
AB Polyclonal antiserum prepared against DNA that was modified with racemic benzo[c]phenanthrene-3,4-diol-1,2-epoxide-2 (B[c]PhDE-2; benzylic hydroxyl and epoxide oxygen trans) was characterized for specificity of antigen recognition. Previous studies have demonstrated that the antisera stereoselectively recognized B[c]PhDE-2-DNA and failed to recognize DNA modified with racemic benzo [c]phenanthrene-3,4-diol-1,2-epoxide-1 (B[c]PhDE-1-DNA, benzylic hydroxyl and epoxide oxygen cis), benzo[a]pyrene-7,8-diol-9, 10-epoxide-2-DNA (B[a]PDE-2-DNA) and 7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide-1-DNA (DMBADE-1-DNA). DNA samples modified by diol-epoxide-2 diastereomers of several hydrocarbons were tested in competitive ELISA assays utilizing B[c]PhDE-2-DNA (270 fmol adducts per well). DNA modified with racemic diol-epoxide-2 of various substituted chrysenes (including chrysene, benzo[g]chrysene (B[g]C), 6-methylchrysene (6-MeC), and 5-methychrysene (5-MeC), gave 50% inhibition of antisera binding at significantly higher concentrations (5 to 7-fold) than the parent B[c]PhDE-2-DNA or 5,6-diMeCDE-DNA. DNA modified with 5, 7-dimethylchryseneDE-2 (5,7-diMeCDE-2) and dibenzo[a,l]pyreneDE-2 (DB[a,l] PDE-2) required 20 and > 100-fold greater levels of adducts to give 50% inhibition. Results with B[c]Ph, 5,6-diMeC, chrysene, 6-MeC and 5-MeC diol epoxide-2-DNA indicate that substitution of a methyl group in the vicinity of the bay-region of the PAH-molecule had limited effects on antigen recognition by this antiserum. However, the addition of a ring or methyl group remote from the diol epoxide moiety, as in DB[a,l] PDE-2-DNA or 5,7-diMeCDE-2-DNA greatly decreased antigen recognition. The ability of this antiserum to recognize DNA adducts of a particular class of polycyclic aromatic hydrocarbons will be useful for studies of their contribution to the DNA-binding that results from exposure to complex environmental mixtures.
C1 PURDUE UNIV,DEPT MED CHEM & MOL PHARMACOL,W LAFAYETTE,IN 47907.
AMER HLTH FDN,NAYLOR DANA INST DIS PREVENT,VALHALLA,NY 10595.
NIDDK,NIH,BETHESDA,MD 20892.
NR 37
TC 0
Z9 0
U1 0
U2 0
PU GORDON BREACH SCI PUBL LTD
PI READING
PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL
SN 1040-6638
J9 POLYCYCL AROMAT COMP
JI Polycycl. Aromat. Compd.
PY 1997
VL 12
IS 2
BP 125
EP 138
DI 10.1080/10406639708233831
PG 14
WC Chemistry, Organic
SC Chemistry
GA XY369
UT WOS:A1997XY36900002
ER
PT S
AU Dosemeci, M
Rothman, N
Yin, SN
Li, GL
Linet, M
Wacholder, S
Chow, WH
Hayes, RB
AF Dosemeci, M
Rothman, N
Yin, SN
Li, GL
Linet, M
Wacholder, S
Chow, WH
Hayes, RB
BE Bingham, E
Rall, DP
TI Validation of benzene exposure assessment
SO PREVENTIVE STRATEGIES FOR LIVING IN A CHEMICAL WORLD: A SYMPOSIUM IN
HONOR OF IRVING J. SELIKOFF
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT International Symposium on Preventive Strategies for Living in a
Chemical World, Dedicated to the Memory of Irving J Selikoff
CY NOV 02-05, 1995
CL WASHINGTON, D.C.
SP Collegium Ramazzini
ID OCCUPATIONAL EXPOSURE; VALIDITY; COHORT; CHINA; INFORMATION; AGREEMENT;
CANCER
C1 NCI, Occupat Epidemiol Branch, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
Chinese Acad Prevent Med, Inst Occupat Med, Beijing 100050, Peoples R China.
RP Dosemeci, M (reprint author), NCI, Occupat Epidemiol Branch, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, 6130 Execut Blvd,Room 418, Rockville, MD 20852 USA.
NR 23
TC 5
Z9 5
U1 0
U2 1
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-074-3
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 837
BP 114
EP 121
DI 10.1111/j.1749-6632.1997.tb56868.x
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Multidisciplinary Sciences; Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Science & Technology - Other Topics; Toxicology
GA BK42P
UT WOS:000072113300007
PM 9472334
ER
PT S
AU Cocco, P
Blair, A
Congia, P
Saba, G
Ecca, AR
Palmas, C
AF Cocco, P
Blair, A
Congia, P
Saba, G
Ecca, AR
Palmas, C
BE Bingham, E
Rall, DP
TI Long-term health effects of the occupational exposure to DDT - A
preliminary report
SO PREVENTIVE STRATEGIES FOR LIVING IN A CHEMICAL WORLD: A SYMPOSIUM IN
HONOR OF IRVING J. SELIKOFF
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT International Symposium on Preventive Strategies for Living in a
Chemical World, Dedicated to the Memory of Irving J Selikoff
CY NOV 02-05, 1995
CL WASHINGTON, D.C.
SP Collegium Ramazzini
ID NON-HODGKINS-LYMPHOMA; ADIPOSE-TISSUE; BREAST-CANCER; ORGANOCHLORINE
RESIDUES; MULTIPLE-MYELOMA; RISK; MORTALITY; PESTICIDES; COHORT; IOWA
C1 Univ Cagliari, Ist Med Lavoro, Cagliari, Italy.
NCI, Occupat Studies Sect, Environm Epidemiol Branch, Bethesda, MD 20892 USA.
Univ Cagliari, Ist Parassitol, Cagliari, Italy.
RP Cocco, P (reprint author), Univ Cagliari, Inst Occupat Med, Via San Giorgio 12, I-09126 Cagliari, Italy.
EM coccop@pacs.unica.it
NR 35
TC 27
Z9 27
U1 0
U2 7
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-074-3
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 837
BP 246
EP 256
DI 10.1111/j.1749-6632.1997.tb56878.x
PG 11
WC Environmental Sciences; Public, Environmental & Occupational Health;
Multidisciplinary Sciences; Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Science & Technology - Other Topics; Toxicology
GA BK42P
UT WOS:000072113300017
PM 9472344
ER
PT B
AU Summers, RM
Selbie, WS
Popp, J
Holland, SM
Sneller, MC
Shelhamer, JH
AF Summers, RM
Selbie, WS
Popp, J
Holland, SM
Sneller, MC
Shelhamer, JH
BE Boom, H
Robinson, C
Rutten, W
Neuman, M
Wijkstra, H
TI Implicit modeling and virtual endoscopy of pulmonic cavities
SO PROCEEDINGS OF THE 18TH ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE
ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY, VOL 18, PTS 1-5
SE PROCEEDINGS OF THE ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE
ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY
LA English
DT Proceedings Paper
CT 18th Annual International Conference of IEEE
Engineering-in-Medicine-amd-Biology-Society
CY OCT 31-NOV 03, 1996
CL AMSTERDAM, NETHERLANDS
SP IEEE Engn Med & Biol Soc
AB Pulmonary cavities are a devastating consequence of severe pneumonia and other necrotizing pulmonary disorders. As part of a project to understand cavity formation and heating, we evaluated different techniques for determining the shape of the cavities.
The pulmonary cavities were segmented from helical computed tomography scans of the thorax. We parameterized the shape of the cavities using two implicit functions, an ellipsoid and a superquadric. The original cavities and the parameterized models of the cavities were then visualized using a virtual endoscopy system.
Both functions produced reasonable fits to the data. RMS errors were lower with the superquadric although the superquadric tended to deform inappropriately if a bronchial segment communicated with the cavity or if the top or bottom of the cavity was not capped. We found that fitting the cavity data to both ellipsoids and superquadrics provides straightforward estimation of the global shape.
C1 NIH, Ctr Clin, Dept Radiol, Bethesda, MD 20892 USA.
RP Summers, RM (reprint author), NIH, Ctr Clin, Dept Radiol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU IEEE
PI NEW YORK
PA 345 E 47TH ST, NEW YORK, NY 10017 USA
BN 0-7803-3812-X
J9 P IEEE EMBS
PY 1997
VL 18
BP 639
EP 640
PG 2
WC Engineering, Biomedical
SC Engineering
GA BK41A
UT WOS:000072079000312
ER
PT B
AU Metter, EJ
AF Metter, EJ
BE Boom, H
Robinson, C
Rutten, W
Neuman, M
Wijkstra, H
TI Prevention of physical frailty
SO PROCEEDINGS OF THE 18TH ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE
ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY, VOL 18, PTS 1-5
SE PROCEEDINGS OF THE ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE
ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY
LA English
DT Proceedings Paper
CT 18th Annual International Conference of IEEE
Engineering-in-Medicine-amd-Biology-Society
CY OCT 31-NOV 03, 1996
CL AMSTERDAM, NETHERLANDS
SP IEEE Engn Med & Biol Soc
AB Aging is associated with continuous changes in strength and physical functioning. Different factors contribute to these changes at different ages. For discussion purposes, it, is useful to identify 4 adult stages that lay the ground work for disability: (1) Early adulthood where maximal performance is reached, (2) Late early adulthood where earliest changes begin with slowing of reactions, (3) Middle age with slow declines in strength and coordination, and (4) Older age with more dramatic and greater functional changes. Preventive strategies can be applied at each stage including exercise, diet, health habits, injury prevention, environmental and social adjustments. Interventions can focus on the person or their environment, and should consider the unique needs of each life stage, particularly middle aged and elderly. They should be acceptable to the average individual who is not health conscious, and should stimulate motivation toward safer and healthier lifestyles.
C1 NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA.
RP Metter, EJ (reprint author), NIA, Gerontol Res Ctr, 4940 Eastern Ave, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU IEEE
PI NEW YORK
PA 345 E 47TH ST, NEW YORK, NY 10017 USA
BN 0-7803-3812-X
J9 P IEEE EMBS
PY 1997
VL 18
BP 2148
EP 2149
PG 2
WC Engineering, Biomedical
SC Engineering
GA BK41A
UT WOS:000072079001036
ER
PT S
AU Kidder, LH
Levin, IW
Lewis, EN
AF Kidder, LH
Levin, IW
Lewis, EN
GP IEEE
IEEE
TI Infrared spectroscopic imaging using focal plane arrays: Applications to
tissue analysis and histopathology
SO PROCEEDINGS OF THE 19TH ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE
ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY, VOL 19, PTS 1-6:
MAGNIFICENT MILESTONES AND EMERGING OPPORTUNITIES IN MEDICAL ENGINEERING
SE PROCEEDINGS OF ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE ENGINEERING
IN MEDICINE AND BIOLOGY SOCIETY
LA English
DT Proceedings Paper
CT International Conference of the IEEE
Engineering-in-Medicine-and-Biology-Society
CY OCT 30-NOV 02, 1997
CL CHICAGO, IL
SP IEEE Engn Med & Biol Soc, Natl Inst Hlth
DE infrared imaging; clinical diagnostic; pathology; FTIR spectroscopy;
microscopy
ID BRAIN-TISSUE; MICROSPECTROSCOPY; SILICONE; CANCERS
AB Infrared imaging spectroscopy has been used to investigate several biological systems. The imaging instrument is comprised of IR sensitive array detectors coupled with a step-scan interferometer and microscope. Each pixel on the array simultaneously measures an IR spectrum in frequency ranges that depend only on the type of array employed. As image contrast is provided solely by spatial variations in a sample's intrinsic chemistry, this technique enables researchers and clinicians to visualize a sample directly in terms of its chemical heterogeneities. We illustrate the capability and versatility of this technique for readily and non-invasively visualizing chemical complexity and for providing statistical data on sample heterogeneity. FT-IR spectroscopic imaging provides the means to better understand the molecular composition and architecture of biological materials, as well the ability to probe the biochemistry of diseased tissue states.
C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Kidder, LH (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 5,Room B1-38, Bethesda, MD 20892 USA.
NR 10
TC 0
Z9 0
U1 0
U2 1
PU IEEE
PI NEW YORK
PA 345 E 47TH ST, NEW YORK, NY 10017 USA
SN 1094-687X
BN 0-7803-4262-3
J9 P ANN INT IEEE EMBS
PY 1997
VL 19
BP 689
EP 692
PN 1-6
PG 4
WC Engineering, Biomedical
SC Engineering
GA BM91F
UT WOS:000080103400197
ER
PT J
AU ChoChung, YS
AF ChoChung, YS
TI Antisense DNA toward type I protein kinase a produces sustained
inhibition of tumor growth
SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS
LA English
DT Article
DE cancer growth arrest; differentiation
ID RI-ALPHA-SUBUNIT; MAMMARY EPITHELIAL-CELLS; CYCLIC-AMP ANALOGS;
ADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE; HL-60 LEUKEMIA-CELLS; AMINO-ACID
SEQUENCE; REGULATORY SUBUNIT; GENE-EXPRESSION; MESSENGER-RNA;
MOLECULAR-CLONING
AB Expression of the RI(alpha) subunit of type I cyclic AMP-dependent protein kinase (PKA) is increased in human cancer cell lines, in primary tumors, in cells after transformation, and in cells upon stimulation of growth. The sequence-specific inhibition of RI(alpha) gene expression by RI(alpha) antisense oligodeoxynucleotide results in the differentiation of leukemia cells and growth arrest of cancer cells of epithelial origin, A single-injection RI(alpha) antisense treatment in vivo also results in a reduction in RI(alpha) expression and inhibition of tumor growth. One injection was sufficient to inhibit tumor growth in mice for 2 weeks. The antisense DNA achieves this long-lasting effect by altering the balance between the production of PKA type I and a competitive molecule, PKA type II. Tumor cells behaved like untransformed cells by making less protein kinase type I. The RI(alpha) antisense, which produces a biochemical imprint for growth control, requires infrequent dosing to restrain neoplastic growth in vivo.
RP ChoChung, YS (reprint author), NCI,CELLULAR BIOCHEM SECT,TUMOR IMMUNOL & BIOL LAB,NIH,BLDG 10,ROOM 5B05,BETHESDA,MD 20892, USA.
NR 61
TC 4
Z9 4
U1 0
U2 0
PU BLACKWELL SCIENCE INC
PI MALDEN
PA 350 MAIN ST, MALDEN, MA 02148
SN 1081-650X
J9 P ASSOC AM PHYSICIAN
JI Proc. Assoc. Am. Phys.
PD JAN
PY 1997
VL 109
IS 1
BP 23
EP 32
PG 10
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA WD146
UT WOS:A1997WD14600003
PM 9010913
ER
PT B
AU Shi, YB
IshizuyaOka, A
AF Shi, YB
IshizuyaOka, A
BE Shi, YB
Shi, YF
Xu, YH
Scott, DW
TI Activation of matrix metalloproteinase genes during thyroid
hormone-induced apoptotic tissue remodeling
SO PROGRAMMED CELL DEATH
LA English
DT Proceedings Paper
CT 1996 International Symposium on Programmed Cell Death
CY SEP 08-12, 1996
CL CHINESE ACAD SCI, SHANGHAI SCI CTR, SHANGHAI, PEOPLES R CHINA
SP NICHHD, US, Amer Red Cross, Holland Lab, US, Natl Nat Sci Fdn China, Academia Sinica, Shanghai Inst Cell Biol, China, BASF Corp, US, Genetech Inc, US, Shanghai Huaxin High Biotechnol Inc, China, Amgen Ctr, US, Beckman, US, Boehringer Mannheim Corp, US, DNAX Res Inst Molec & Cell Biol, US, PharMingen, US, Promega Corp, US, Clontech Labs, US, Hoffmann La roche Inc, US, Life Technol Inc, US, New England Biolabs, US
HO CHINESE ACAD SCI, SHANGHAI SCI CTR
AB Programmed cell death or apoptosis is an essential process during amphibian metamorphosis, not only in the resorption of tadpole specific tissues but also in the remodeling of existing tissues and de novo development of adult ones. The control of metamorphosis by thyroid hormone has allowed the identification and characterization of a number of genes which are involved in this process. Among them are genes encoding matrix metalloproteinases (MMPs), which are capable of digesting various components of the extracellular matrix (ECM). Of particular interest is the MMP stromelysin-3. The gene is activated prior to larval cell death and its high levels of expression correlate with basal lamina (the ECM that separates epithelium and the mesenchyme) modification. These and other observations implicate that stromelysin-3 may participate in ECM remodeling, which in turn regulates cell fate during metamorphosis. In addition, our analyses of the expression of several other MMPs indicate multiple MMPs function, in a tissue-dependent manner, at various steps of organ transformation, some in the regulation of cell death, proliferation, and differentiation, while others in post-apoptotic ECM removal.
RP Shi, YB (reprint author), NICHHD,MOL EMBRYOL LAB,BLDG 18T,RM 101,BETHESDA,MD 20892, USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45680-X
PY 1997
BP 13
EP 26
PG 14
WC Cell Biology
SC Cell Biology
GA BJ94H
UT WOS:A1997BJ94H00002
ER
PT B
AU Sarin, A
Ebnet, K
Zacharchuk, CM
Henkart, PA
AF Sarin, A
Ebnet, K
Zacharchuk, CM
Henkart, PA
BE Shi, YB
Shi, YF
Xu, YH
Scott, DW
TI Caspase inhibitors as molecular probes of cell death
SO PROGRAMMED CELL DEATH
LA English
DT Proceedings Paper
CT 1996 International Symposium on Programmed Cell Death
CY SEP 08-12, 1996
CL CHINESE ACAD SCI, SHANGHAI SCI CTR, SHANGHAI, PEOPLES R CHINA
SP NICHHD, US, Amer Red Cross, Holland Lab, US, Natl Nat Sci Fdn China, Academia Sinica, Shanghai Inst Cell Biol, China, BASF Corp, US, Genetech Inc, US, Shanghai Huaxin High Biotechnol Inc, China, Amgen Ctr, US, Beckman, US, Boehringer Mannheim Corp, US, DNAX Res Inst Molec & Cell Biol, US, PharMingen, US, Promega Corp, US, Clontech Labs, US, Hoffmann La roche Inc, US, Life Technol Inc, US, New England Biolabs, US
HO CHINESE ACAD SCI, SHANGHAI SCI CTR
RP Sarin, A (reprint author), NCI,EXPT IMMUNOL BRANCH,NIH,BETHESDA,MD 20892, USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45680-X
PY 1997
BP 51
EP 62
PG 12
WC Cell Biology
SC Cell Biology
GA BJ94H
UT WOS:A1997BJ94H00006
ER
PT B
AU Bortner, CD
Hughes, FM
Cidlowski, JA
AF Bortner, CD
Hughes, FM
Cidlowski, JA
BE Shi, YB
Shi, YF
Xu, YH
Scott, DW
TI Cell volume regulation, ions, and apoptosis
SO PROGRAMMED CELL DEATH
LA English
DT Proceedings Paper
CT 1996 International Symposium on Programmed Cell Death
CY SEP 08-12, 1996
CL CHINESE ACAD SCI, SHANGHAI SCI CTR, SHANGHAI, PEOPLES R CHINA
SP NICHHD, US, Amer Red Cross, Holland Lab, US, Natl Nat Sci Fdn China, Academia Sinica, Shanghai Inst Cell Biol, China, BASF Corp, US, Genetech Inc, US, Shanghai Huaxin High Biotechnol Inc, China, Amgen Ctr, US, Beckman, US, Boehringer Mannheim Corp, US, DNAX Res Inst Molec & Cell Biol, US, PharMingen, US, Promega Corp, US, Clontech Labs, US, Hoffmann La roche Inc, US, Life Technol Inc, US, New England Biolabs, US
HO CHINESE ACAD SCI, SHANGHAI SCI CTR
C1 NIEHS,LAB SIGNAL TRANSDUCT,NIH,RES TRIANGLE PK,NC 27709.
RP Cidlowski, JA (reprint author), NIEHS,LAB SIGNAL TRANSDUCT,NIH,RES TRIANGLE PK,NC 27709, USA.
NR 0
TC 5
Z9 5
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45680-X
PY 1997
BP 63
EP 70
PG 8
WC Cell Biology
SC Cell Biology
GA BJ94H
UT WOS:A1997BJ94H00007
ER
PT B
AU Libutti, SK
Bartlett, DL
Alexander, HR
AF Libutti, SK
Bartlett, DL
Alexander, HR
BE Siewert, JR
Roder, JD
TI The treatment of peritoneal carcinomatosis using continuous hyperthermic
peritoneal perfusion
SO PROGRESS IN GASTRIC CANCER RESEARCH 1997: PROCEEDINGS OF THE 2ND
INTERNATIONAL GASTRIC CANCER CONGRESS
LA English
DT Proceedings Paper
CT 2nd International Gastric Cancer Congress
CY APR 27-30, 1997
CL MUNICH, GERMANY
SP Auto Suture Deutschland GmbH, Tonisvorst
AB Peritoneal carcinomatosis resulting from gastrointestinal malignancy has a very poor prognosis and can present a very difficult management dilemma. Patients can develop very bulky intraabdominal disease resulting in symptoms from the mass effect of the tumor such as obstruction, abdominal pain and problems related to intractable ascites. Standard therapies such as surgical debulking are often ineffective in managing symptoms or impacting on the course of the disease. Continuous hyperthermic peritoneal perfusion (CHPP) as an adjunct to surgical debulking has shown some promise in ameliorating symptoms and altering the natural history of the disease. We describe the status of several ongoing clinical trials utilizing CHPP with a variety of chemotherapeutic agents for the management or prevention of peritoneal carcinomatosis. Technical aspects of the procedure and perfusion circuit will be highlighted.
RP Libutti, SK (reprint author), NCI,SURG BRANCH,SURG METAB SECT,NIH,BETHESDA,MD 20892, USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU MONDUZZI EDITORE
PI 40128 BOLOGNA
PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY
BN 88-323-0427-9
PY 1997
BP 1371
EP 1377
PG 7
WC Oncology; Gastroenterology & Hepatology; Medicine, General & Internal;
Pathology; Surgery
SC Oncology; Gastroenterology & Hepatology; General & Internal Medicine;
Pathology; Surgery
GA BJ02Q
UT WOS:A1997BJ02Q00260
ER
PT J
AU Young, HA
Ghosh, P
AF Young, HA
Ghosh, P
TI Molecular regulation of cytokine gene expression: Interferon-gamma as a
model system
SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL. 56
SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY
LA English
DT Review
ID HUMAN T-CELLS; LARGE GRANULAR LYMPHOCYTES; TUMOR-BEARING MICE;
NF-KAPPA-B; IFN-GAMMA; MESSENGER-RNA; TYROSINE PHOSPHORYLATION;
STIMULATORY FACTOR; ACCESSORY CELLS; MOPC-315 TUMOR
C1 NCI, Frederick Canc Res & Dev Ctr, Cellular & Mol Immunol Sect, Div Basic Sci, Frederick, MD 21702 USA.
RP Young, HA (reprint author), NCI, Frederick Canc Res & Dev Ctr, Cellular & Mol Immunol Sect, Div Basic Sci, Frederick, MD 21702 USA.
NR 82
TC 28
Z9 28
U1 1
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0079-6603
J9 PROG NUCLEIC ACID RE
PY 1997
VL 56
BP 109
EP 127
DI 10.1016/S0079-6603(08)61004-1
PG 19
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BK74H
UT WOS:000073311000004
PM 9187053
ER
PT S
AU Chattoraj, DK
Schneider, TD
AF Chattoraj, DK
Schneider, TD
BE Moldave, K
TI Replication control of plasmid P1 and its host chromosome: The common
ground
SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 57
SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY
LA English
DT Review
ID MINI-F PLASMID; ESCHERICHIA-COLI CHROMOSOME; HEAT-SHOCK PROTEINS;
COPY-NUMBER CONTROL; COMPLETE NUCLEOTIDE-SEQUENCE; CELL DIVISION CYCLE;
REPE INITIATOR PROTEIN; REPEATED DNA-SEQUENCES; PARTITION PAR LOCUS;
INCP-ALPHA PLASMIDS
C1 NCI, FREDERICK CANC RES & DEV CTR, LAB MATH BIOL, FREDERICK, MD 21701 USA.
RP Chattoraj, DK (reprint author), NCI, BIOCHEM LAB, NIH, BETHESDA, MD 20892 USA.
OI Schneider, Thomas/0000-0002-9841-1531
NR 240
TC 28
Z9 28
U1 0
U2 2
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0079-6603
BN 0-12-540057-8
J9 PROG NUCLEIC ACID RE
JI Prog. Nucl. Res. Molec. Biol.
PY 1997
VL 57
BP 145
EP 186
DI 10.1016/S0079-6603(08)60280-9
PG 42
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ03W
UT WOS:A1997BJ03W00005
PM 9175433
ER
PT J
AU Angov, E
McBride, JS
Kaslow, DC
Ballou, WR
Diggs, CL
Lyon, JA
AF Angov, E
McBride, JS
Kaslow, DC
Ballou, WR
Diggs, CL
Lyon, JA
TI Structural analysis of refolded-recombinant Plasmodium falciparum MSP1
C-terminal fragment by using conformation-specific monoclonal
antibodies.
SO PROTEIN ENGINEERING
LA English
DT Meeting Abstract
ID SURFACE
C1 WRAIR,DEPT IMMUNOL,WASHINGTON,DC 20307.
UNIV EDINBURGH,DIV BIOL SCI,EDINBURGH EH9 3JT,MIDLOTHIAN,SCOTLAND.
US AGCY INT DEV,WASHINGTON,DC 20523.
NIAID,BETHESDA,MD 20892.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0269-2139
J9 PROTEIN ENG
JI Protein Eng.
PY 1997
VL 10
SU S
BP 21
EP 21
PG 1
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA XD832
UT WOS:A1997XD83200025
ER
PT J
AU Bychkova, VE
Ptitsyn, OB
AF Bychkova, VE
Ptitsyn, OB
TI Folding intermediates and genetic diseases
SO PROTEIN ENGINEERING
LA English
DT Meeting Abstract
ID TRANSMEMBRANE CONDUCTANCE REGULATOR; INTRACELLULAR-TRANSPORT; PROTEIN;
MUTATIONS; CELLS
C1 RUSSIAN ACAD SCI,INST PROT RES,PUSHCHINO 142292,RUSSIA.
NCI,LMMB,NIH,BETHESDA,MD 20892.
NR 27
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0269-2139
J9 PROTEIN ENG
JI Protein Eng.
PY 1997
VL 10
SU S
BP 23
EP 23
PG 1
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA XD832
UT WOS:A1997XD83200029
ER
PT J
AU Ptitsyn, O
Bychkova, V
Dujsekina, A
Rossi, GL
Fantuzzi, A
Uversky, V
Tiktopulo, E
Klenin, S
AF Ptitsyn, O
Bychkova, V
Dujsekina, A
Rossi, GL
Fantuzzi, A
Uversky, V
Tiktopulo, E
Klenin, S
TI Modeling of the molten globule state of proteins near membranes
SO PROTEIN ENGINEERING
LA English
DT Meeting Abstract
C1 NCI,LMMB,NIH,BETHESDA,MD 20892.
RI Uversky, Vladimir/F-4515-2011
OI Uversky, Vladimir/0000-0002-4037-5857
NR 6
TC 1
Z9 1
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0269-2139
J9 PROTEIN ENG
JI Protein Eng.
PY 1997
VL 10
SU S
BP 32
EP 32
PG 1
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA XD832
UT WOS:A1997XD83200048
ER
PT J
AU Tsai, CJ
Nussinov, R
AF Tsai, CJ
Nussinov, R
TI Hydrophobic folding units derived from dissimilar monomer structures and
their interactions
SO PROTEIN SCIENCE
LA English
DT Article
DE compactness; domain cutting; folding unit; hydrophobic core; protein
folding
ID GLOBULAR-PROTEINS; COMPACT UNITS; DOMAINS; IDENTIFICATION;
THERMODYNAMICS; ORGANIZATION; LOCATION; BARNASE
AB We have designed an automated procedure to cut a protein into compact hydrophobic folding units. The hydrophobic units are large enough to contain tertiary non-local interactions, reflecting potential nucleation sites during protein folding. The quality of a hydrophobic folding unit is evaluated by four criteria. The first two correspond to visual characterization of a structural domain, namely, compactness and extent of isolation. We use the definition of Zehfus and Rose (Zehfus MH, Rose GD, 1986, Biochemistry 25:335-340) to calculate the compactness of a cut protein unit. The isolation of a unit is based on the solvent accessible surface area (ASA) originally buried in the interior and exposed to the solvent after cutting. The third quantity is the hydrophobicity, equivalent to the fraction of the buried non-polar ASA with respect to the total non-polar ASA. The last criterion in the evaluation of a folding unit is the number of segments it includes. To conform with the rationale of obtaining hydrophobic units, which may relate to early folding events, the hydrophobic interactions are implicitly and explicitly applied in their generation and assessment. We follow Helm and Sander (Helm L, Sander C, 1994, Proteins 19:256-268) to reduce the multiple cutting-point problem to a one-dimensional search for all reasonable trial cuts. However, as here we focus on the hydrophobic cores, the contact matrix used to obtain the first non-trivial eigenvector contains only hydrophobic contacts, rather than all, hydrophobic and hydrophilic, interactions. This dataset of hydrophobic folding units, derived from structurally dissimilar single chain monomers, is particularly useful far investigations of the mechanism of protein folding. For cases where there are kinetic data, the one or more hydrophobic folding units generated for a protein correlate with the two or with the three-state folding process observed. We carry out extensive amino acid sequence order independent structural comparisons to generate a structurally non-redundant set of hydrophobic folding units for fold recognition and for statistical purposes.
C1 NCI,MATH BIOL LAB,FCRDC,SAIC,FREDERICK,MD 21702.
TEL AVIV UNIV,SACKLER INST MOL MED,IL-69978 TEL AVIV,ISRAEL.
FU NCI NIH HHS [1-CO-74102]
NR 44
TC 81
Z9 83
U1 0
U2 5
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD JAN
PY 1997
VL 6
IS 1
BP 24
EP 42
PG 19
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD201
UT WOS:A1997WD20100004
PM 9007974
ER
PT J
AU Tsai, CJ
Lin, SL
Wolfson, HJ
Nussinov, R
AF Tsai, CJ
Lin, SL
Wolfson, HJ
Nussinov, R
TI Studies of protein-protein interfaces: A statistical analysis of the
hydrophobic effect
SO PROTEIN SCIENCE
LA English
DT Article
DE hydrophobic effect; protein cores; protein folding; protein-protein
recognition; subunit interfaces
ID SURFACE HYDROPHOBICITY; RECOGNITION; COMPLEMENTARITY; DOCKING; MOTIFS
AB Data sets of 362 structurally nonredundant protein-protein interfaces and of 57 symmetry-related oligomeric interfaces have been used to explore whether the hydrophobic effect that guides protein folding is also the main driving force for protein-protein associations. The buried nonpolar surface area has been used to measure the hydrophobic effect. Our analysis indicates that, although the hydrophobic effect plays a dominant role in protein-protein binding, it is not as strong as that observed in the interior of protein monomers. Comparison of the interiors of the monomers with those of the interfaces reveals that, in general, the hydrophobic amino acids are more frequent in the interior of the monomers than in the interior of the protein-protein interfaces. On the other hand, a higher proportion of charged and polar residues are buried at the interfaces, suggesting that hydrogen bonds and ion pairs contribute more to the stability of protein binding than to that of protein folding. Moreover, comparison of the interior of the interfaces to protein surfaces indicates that the interfaces are poorer in polar/charged than the surfaces and are richer in hydrophobic residues. The interior of the interfaces appears to constitute a compromise between the stabilization contributed by the hydrophobic effect on the one hand and avoiding patches on the protein surfaces that are too hydrophobic on the other. Such patches would be unfavorable for the unassociated monomers in solution. We conclude that, although the types of interactions are similar between protein-protein interfaces and single-chain proteins overall, the contribution of the hydrophobic effect to protein-protein associations is not as strong as to protein folding. This implies that packing patterns and interatom, or interresidue, pairwise potential functions, derived from monomers, are not ideally suited to predicting and assessing ligand associations or design. These would perform adequately only in cases where the hydrophobic effect at the binding site is substantial.
C1 NCI,MATH BIOL LAB,FCRF,SAIC,FREDERICK,MD 21702.
TEL AVIV UNIV,SCH MATH SCI,DEPT COMP SCI,IL-69978 TEL AVIV,ISRAEL.
TEL AVIV UNIV,SACKLER INST MOL MED,IL-69978 TEL AVIV,ISRAEL.
RI Wolfson, Haim/A-1837-2011
FU NCI NIH HHS [1-CO-74102]
NR 24
TC 279
Z9 284
U1 4
U2 18
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD JAN
PY 1997
VL 6
IS 1
BP 53
EP 64
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WD201
UT WOS:A1997WD20100006
PM 9007976
ER
PT J
AU Moult, J
Hubbard, T
Bryant, SH
Fidelis, K
Pedersen, JT
AF Moult, J
Hubbard, T
Bryant, SH
Fidelis, K
Pedersen, JT
TI Critical assessment of methods of protein structure prediction (CASP):
Round II
SO PROTEINS-STRUCTURE FUNCTION AND GENETICS
LA English
DT Article
DE protein structure prediction; community-wide experiment; GASP
C1 Univ Maryland, Inst Biotechnol, Ctr Adv Res Biotechnol, Rockville, MD 20850 USA.
Natl Ctr Biotechnol Informat, Computat Branch, NIH, Bethesda, MD USA.
Univ Calif Lawrence Livermore Natl Lab, Biol & Biotechnol Res Program, Livermore, CA USA.
RP Moult, J (reprint author), Univ Maryland, Inst Biotechnol, Ctr Adv Res Biotechnol, 9600 Gudelsky Dr, Rockville, MD 20850 USA.
EM jmoult@carb.nist.gov
RI Hubbard, Tim/C-2567-2008
OI Hubbard, Tim/0000-0002-1767-9318
NR 9
TC 55
Z9 59
U1 2
U2 4
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PY 1997
SU 1
BP 2
EP 6
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA YW306
UT WOS:000071920700002
ER
PT J
AU Marchler-Bauer, A
Bryant, SH
AF Marchler-Bauer, A
Bryant, SH
TI Measures of threading specificity and accuracy
SO PROTEINS-STRUCTURE FUNCTION AND GENETICS
LA English
DT Article
DE fold recognition; protein threading
ID PROTEIN-STRUCTURE PREDICTION; DOMAIN
AB Threading predictions for CASP2 target proteins were compared to their true structures using a series of precisely defined measures of agreement, calculated in a fully automatic way, Fold recognition specificity was calculated as the proportion of a predictor's "bet" that was placed on previously known structures similar to the prediction target, as identified by a "jury" of well-tested structure-structure comparison methods, Values approaching 100% indicate that a prediction correctly identified the structural and/or evolutionary family to which a target belongs, Alignment specificity was calculated as the proportion of aligned residue pairs in the predicted target-to-known-structure alignment that also occur in the structure-structure alignments produced by the "jury" methods, Contact specificity was calculated as the proportion of nonlocal residue contacts in the molecular model implied by threading alignment, that also occur in the experimental structure. of the target, Alignment specificity and contact specificity measure the accuracy of a predicted 3-dimensional model, Values approaching 100% indicate that target residues have been assigned to the correct spatial locations and that the model is as accurate as possible for a threading prediction. (C) 1998 Wiley-Liss, Inc.
C1 Natl Ctr Biotechnol Informat, Computat Biol Branch, NIH, Bethesda, MD 20894 USA.
RP Marchler-Bauer, A (reprint author), Natl Ctr Biotechnol Informat, Computat Biol Branch, NIH, 8600 Rockville Pike, Bethesda, MD 20894 USA.
RI Marchler-Bauer, Aron/A-9681-2009;
OI Marchler-Bauer, Aron/0000-0003-1516-0712
NR 41
TC 16
Z9 16
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PY 1997
SU 1
BP 74
EP 82
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA YW306
UT WOS:000071920700011
ER
PT J
AU Marchler-Bauer, A
Levitt, M
Bryant, SH
AF Marchler-Bauer, A
Levitt, M
Bryant, SH
TI A retrospective analysis of CASP2 threading predictions
SO PROTEINS-STRUCTURE FUNCTION AND GENETICS
LA English
DT Article
DE fold recognition; protein threading
ID PROTEIN-STRUCTURE PREDICTION; FOLD RECOGNITION
AB Analysis of CASP2 protein threading results shows that the success rate of structure predictions varies widely among prediction targets, We set "critical" thresholds in fold recognition specificity and threading model accuracy at the points where "incorrect" CASP2 predictions just outnumber "correct" predictions. Using these thresholds we find that correct predictions were made for all of those targets and for only those targets where more than 50% of target residues may be superimposed on previously known structures, Three-fourths of these correct predictions were furthermore made for targets with greater than 12% residue identity in structural alignment, where characteristic sequence motifs are also present. Based on these observations we suggest that the sustained performance of threading methods is best characterized by counting the numbers of correct predictions for targets of increasing "difficulty" We suggest that target difficulty may be assigned, once the true structure of the target is known, according to the fraction of residues superimposable onto previously known structures and the fraction of identical residues in those structural alignments. (C) 1998 Wiley-Liss, Inc.
C1 Natl Ctr Biotechnol Informat, Computat Biol Branch, NIH, Bethesda, MD 20894 USA.
Stanford Univ Med, Dept Biol Struct, Beckman Labs Struct Biol, Stanford, CA USA.
RP Bryant, SH (reprint author), Natl Ctr Biotechnol Informat, Computat Biol Branch, NIH, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM bryant@ncbi.nlm.nih.gov
RI Marchler-Bauer, Aron/A-9681-2009; Levitt, Michael/E-4582-2012;
OI Levitt, Michael/0000-0002-8414-7397; Marchler-Bauer,
Aron/0000-0003-1516-0712
NR 19
TC 3
Z9 3
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PY 1997
SU 1
BP 83
EP 91
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA YW306
UT WOS:000071920700012
ER
PT J
AU Di Francesco, V
Geetha, V
Garnier, J
Munson, PJ
AF Di Francesco, V
Geetha, V
Garnier, J
Munson, PJ
TI Fold recognition using predicted secondary structure sequences and
hidden Markov models of protein folds
SO PROTEINS-STRUCTURE FUNCTION AND GENETICS
LA English
DT Article
DE protein structure prediction; hidden Markov models; fold recognition;
secondary structure
ID AMINO-ACID-SEQUENCE; EPIDERMOLYTIC TOXINS
AB We present an analysis of the blind predictions submitted to the fold recognition category for the second meeting on the Critical Assessment of techniques for protein Structure Prediction. Our method achieves fold recognition from predicted secondary structure sequences using hidden Markov models (HMMs) of protein folds, HMMs are trained only with experimentally derived secondary structure sequences of proteins having similar fold, therefore protein structures are described by the models at a remarkably simplified level. We submitted predictions for five target sequences, of which four were later found to be suitable for threading. Our approach correctly predicted the fold for three of them, For a fourth sequence the fold could have been correctly predicted if a better model for its structure was available, We conclude that we have additional evidence that secondary structure information represents an important factor for achieving fold recognition. (C) 1998 Wiley-Liss, Inc.
C1 NIH, Analyt Biostat Sect, Struct Biol Lab, Bethesda, MD USA.
NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Di Francesco, V (reprint author), Inst Genom Res, Rockville, MD 20850 USA.
EM valedf@tigr.org
NR 22
TC 17
Z9 19
U1 0
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PY 1997
SU 1
BP 123
EP 128
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA YW306
UT WOS:000071920700016
ER
PT S
AU Putnam, FW
Trickett, PK
AF Putnam, FW
Trickett, PK
BE Yehuda, R
McFarlane, AC
TI Psychobiological effects of sexual abuse - A longitudinal study
SO PSYCHOBIOLOGY OF POSTTRAUMATIC STRESS DISORDER
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT Conference on Psychobiology of Posttraumatic Stress Disorder
CY SEP 07-10, 1996
CL NEW YORK, NY
SP New York Acad Sci
ID POSTTRAUMATIC-STRESS-DISORDER; CHILDREN; FEMALES; IMPACT
C1 UNIV SO CALIF, DEPT PSYCHOL, LOS ANGELES, CA 90089 USA.
RP Putnam, FW (reprint author), NIMH, UDT, BEHAV ENDOCRINOL BRANCH, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA.
NR 31
TC 70
Z9 71
U1 0
U2 1
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-079-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 821
BP 150
EP 159
DI 10.1111/j.1749-6632.1997.tb48276.x
PG 10
WC Behavioral Sciences; Multidisciplinary Sciences; Psychiatry
SC Behavioral Sciences; Science & Technology - Other Topics; Psychiatry
GA BJ18D
UT WOS:A1997BJ18D00013
PM 9238201
ER
PT S
AU Post, RM
Weiss, SRB
Smith, M
Li, H
McCann, U
AF Post, RM
Weiss, SRB
Smith, M
Li, H
McCann, U
BE Yehuda, R
McFarlane, AC
TI Kindling versus quenching - Implications for the evolution and treatment
of posttraumatic stress disorder
SO PSYCHOBIOLOGY OF POSTTRAUMATIC STRESS DISORDER
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT Conference on Psychobiology of Posttraumatic Stress Disorder
CY SEP 07-10, 1996
CL NEW YORK, NY
SP New York Acad Sci
ID THYROTROPIN-RELEASING-HORMONE; RECURRENT AFFECTIVE-DISORDER; EXPRESSION;
MECHANISMS; DEPRESSION; TRH; SENSITIZATION; NEUROBIOLOGY; STIMULATION;
ACTIVATION
RP Post, RM (reprint author), NIMH, BIOL PSYCHIAT BRANCH,NIH,BLDG 10,ROOM 3N212, 10 CTR DR MSC 1272, BETHESDA, MD 20892 USA.
NR 50
TC 65
Z9 66
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-079-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 821
BP 285
EP 295
DI 10.1111/j.1749-6632.1997.tb48287.x
PG 11
WC Behavioral Sciences; Multidisciplinary Sciences; Psychiatry
SC Behavioral Sciences; Science & Technology - Other Topics; Psychiatry
GA BJ18D
UT WOS:A1997BJ18D00024
PM 9238212
ER
PT S
AU Hall, FS
Huang, S
Fong, G
AF Hall, FS
Huang, S
Fong, G
BE Yehuda, R
McFarlane, AC
TI Effects of isolation-rearing on acoustic startle and pre-pulse
inhibition in Wistar and Fawn Hooded rats
SO PSYCHOBIOLOGY OF POSTTRAUMATIC STRESS DISORDER
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT Conference on Psychobiology of Posttraumatic Stress Disorder
CY SEP 07-10, 1996
CL NEW YORK, NY
SP New York Acad Sci
RP Hall, FS (reprint author), NIAAA, CLIN STUDIES LAB,DICBR,NIH,BLDG 10, ROOM 3C-207, BETHESDA, MD 20892 USA.
RI Hall, Frank/C-3036-2013
OI Hall, Frank/0000-0002-0822-4063
NR 5
TC 27
Z9 27
U1 0
U2 0
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-079-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 821
BP 542
EP 544
DI 10.1111/j.1749-6632.1997.tb48325.x
PG 3
WC Behavioral Sciences; Multidisciplinary Sciences; Psychiatry
SC Behavioral Sciences; Science & Technology - Other Topics; Psychiatry
GA BJ18D
UT WOS:A1997BJ18D00062
PM 9238248
ER
PT J
AU Oren, DA
Giesen, HA
Wehr, TA
AF Oren, DA
Giesen, HA
Wehr, TA
TI Restoration of detectable melatonin after entrainment to a 24-hour
schedule in a 'free-running' man
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE hypernychthemeral; sleep; light; circadian rhythms; melatonin;
testosterone
ID SEASONAL AFFECTIVE-DISORDER; SLEEP PHASE SYNDROME; PINEAL-GLAND;
SECRETION; LIGHT; HORMONE; RHYTHM; TESTOSTERONE; REPLACEMENT; ADAPTATION
AB We evaluated a 37-year-old male with a non-24-h sleep-wake disorder. His environment gave him little exposure to bright light. Circadian profiles of temperature, melatonin, thyrotropin, cortisol and testosterone were obtained along with endocrine challenges of the thyroid, adrenal, growth hormone and gonadal axes. Multiple endocrine abnormalities were detected. Testosterone was low and nocturnal thyrotropin levels were erratic. Serum melatonin was undetectable throughout the day and night on multiple occasions, and responses to infusions of TRH, GnRH and GRF-44 were abnormal. Responses to CRH infusion were normal. The patient was successfully entrained to a 24-h schedule by daily exposure to 2500 lux light from 0700h to 0900h, avoidance of light (by wearing dark goggles) from 1800h to 2300h, and strict enforcement of a dark environment from 2300h to 0700h. After entrainment, a normal pattern of nocturnal melatonin secretion was found. GH response to GRF-44 also normalized, although abnormal responses to TRH and GnRH persisted. This case raises the possibility that a complex interaction of light exposure with the circadian system can reversibly suspend pineal gland secretion of melatonin indefinitely. It also suggests that circadian rhythm disorders be considered in the differential diagnosis of abnormal endocrine function. Published by Elsevier Science Ltd.
C1 YALE UNIV,SCH MED,DVA,W HAVEN,CT 06516.
NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892.
NR 43
TC 12
Z9 13
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD JAN
PY 1997
VL 22
IS 1
BP 39
EP 52
DI 10.1016/S0306-4530(96)00038-8
PG 14
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA WR191
UT WOS:A1997WR19100004
PM 9141150
ER
PT J
AU Shoaib, M
Schindler, CW
Goldberg, SR
AF Shoaib, M
Schindler, CW
Goldberg, SR
TI Nicotine self-administration in rats: Strain and nicotine pre-exposure
effects on acquisition
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE nicotine; reinforcement; intravenous self-administration; strain
differences; rat
ID LOCOMOTOR-ACTIVITY; TASTE-AVERSION; COCAINE; BEHAVIOR; INJECTIONS;
REINFORCEMENT; ADDICTION; SCHEDULE
AB Nicotine has been shown to maintain intravenous self-administration behaviour in humans and laboratory animals. However, factors critical in the initiation of nicotine self administration are not well defined. In particular genetic differences and effects of pre-exposure to nicotine have not been examined. Male Sprague-Dawley or Long-Evans rats were surgically prepared with indwelling jugular catheters and 3 days later received chronic injections of nicotine (0.4 mg/kg SC) or vehicle (saline, 1 ml/kg) for 7 days in their home cage. The next day, 2-h daily test sessions were initiated, during which rats were given the opportunity to nose-poke for nicotine infusions (0.015, 0.03 or 0.06 mg/kg per infusion) under a one-response fixed-ratio (FR-1) schedule of reinforcement with a 20-s time out after each infusion. One hole was defined as active while pokes in the other hole were recorded but had no scheduled consequence. The response requirement was increased progressively to five (FR-5) over successive sessions. Both saline- and nicotine-pretreated Sprague-Dawley rats showed a preference for the active hole, while only the saline-pretreated Long-Evans rats acquired the self-administration as defined by significant differences between responding in the active versus the inactive holes. The Fisher (F344) and Lewis inbred strains also failed to acquire self-administration of nicotine under these conditions. With Sprague-Dawley and Long-Evans rats that acquired the self-administration, and showed stable levels of maintained responding for nicotine, substituting saline for the nicotine or pretreating with mecamylamine (2.0 mg/kg SC) extinguished the behaviour. When dose per infusion was varied, an inverted U-shaped dose-response curve was obtained. These results support previous reports that nicotine can serve as a reinforcer in rodents and demonstrate that environmental factors such as prior nicotine exposure or genetic factors such as rat strain can affect acquisition of nicotine self-administration.
RP Shoaib, M (reprint author), NIDA,PRECLIN PHARMACOL LAB,ADDICT RES CTR,DIR,NIH,POB 5180,BALTIMORE,MD 21224, USA.
NR 27
TC 183
Z9 184
U1 0
U2 2
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD JAN
PY 1997
VL 129
IS 1
BP 35
EP 43
DI 10.1007/s002130050159
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA WE139
UT WOS:A1997WE13900005
PM 9122361
ER
PT J
AU Gwirtsman, HE
Blehar, MC
McCullough, JP
Kocsis, JH
Prien, RF
AF Gwirtsman, HE
Blehar, MC
McCullough, JP
Kocsis, JH
Prien, RF
TI Standardized assessment of dysthymia: Report of a National Institute of
Mental Health conference
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Editorial Material
DE diagnosis; questionnaires; psychological interview; treatment outcome
ID MAJOR DEPRESSION; SOCIOENVIRONMENTAL CHARACTERISTICS; DIAGNOSTIC
INTERVIEW; SOCIAL ADJUSTMENT; ONSET DYSTHYMIA; GENERAL HEALTH; DISORDER;
PERSONALITY; RELIABILITY; RATIONALE
C1 NIMH,ROCKVILLE,MD 20857.
VIRGINIA COMMONWEALTH UNIV,RICHMOND,VA.
CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021.
NR 48
TC 30
Z9 30
U1 3
U2 6
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 1
BP 3
EP 11
PG 9
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA WU646
UT WOS:A1997WU64600002
PM 9133745
ER
PT J
AU Arnold, LE
Hoagwood, K
Jensen, PS
Vitiello, B
AF Arnold, LE
Hoagwood, K
Jensen, PS
Vitiello, B
TI Toward clinically relevant clinical trials
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article
DE treatment; services; research; clinician; patient; algorithm
ID METHYLPHENIDATE; DISORDER; CHILDREN
AB This article grapples with two closely related tensions threatening the credibility and relevance of clinical trials to clinicians as well as patients and their families: (1) the tension between clinical flexibility and scientific standardization of protocol and (2) the tension between the need to ensure scientific integrity through a standard, pre-specified protocol and the need to increase compliance by involving patients and their families in goal setting and treatment planning. We propose four partial solutions: (1) relaxed exclusion criteria to maximize generalizability, using only those exclusion criteria essential to the treatment; (2) extensive use of clinical algorithms to incorporate clinical flexibility in a standardized way; (3) active involvement of therapists in decision-making, including cross-site clinical decision panels; and (4) active involvement of families through a goal-setting and treatment-planning session as the first step of treatment. Although we focus on clinical trials with children and adolescents, the principles and ideas may also apply to clinical trials with patients of any age.
This article summarizes and elaborates on presentations made by three of the authors at workshops on psychiatric clinical trials in children and adolescents at the May 1996 New Clinical Drug Evaulation Unit (NCDEU) meeting, The focus was on enhancing the clinical relevance of clinical trials-making the results useful and credible to practitioners and patients and their families.
C1 NIMH,CHILD & ADOLESCENT DISORDERS RES BRANCH,DIV CLIN & TREATMENT RES,ROCKVILLE,MD 20857.
OHIO STATE UNIV,COLUMBUS,OH 43210.
NIMH,SERV RES BRANCH,ROCKVILLE,MD 20857.
OI Jensen, Peter/0000-0003-2387-0650
NR 15
TC 6
Z9 6
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 1
BP 135
EP 142
PG 8
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA WU646
UT WOS:A1997WU64600022
PM 9133765
ER
PT J
AU Schmidt, PJ
Rubinow, DR
AF Schmidt, PJ
Rubinow, DR
TI Neuroregulatory role of gonadal steroids in humans
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article
ID HORMONE RECEPTORS; ACTIVATION
RP Schmidt, PJ (reprint author), NIMH,BEHAV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA.
NR 12
TC 21
Z9 21
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 2
BP 219
EP 220
PG 2
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XM243
UT WOS:A1997XM24300005
PM 9230633
ER
PT J
AU Schmidt, ME
Goldstein, DS
Schouten, JL
Matochik, JA
Kim, HG
Potter, WZ
AF Schmidt, ME
Goldstein, DS
Schouten, JL
Matochik, JA
Kim, HG
Potter, WZ
TI Acute alpha(2) blockade by idazoxan increases insulin and lowers plasma
glucose during positron emission tomography
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article
DE [F-18]-fluoro-deoxyglucose; alpha(2) adrenoceptor antagonist;
norepinephrine; imidazoline
ID ALPHA-2-ADRENOCEPTOR ANTAGONIST; HEALTHY-SUBJECTS; BINDING-SITES;
BLOOD-FLOW; ADRENOCEPTOR; METABOLISM; RELEASE; SECRETION;
CATECHOLAMINES; NOREPINEPHRINE
AB The sympathetic nervous system can modulate glucose levels through a variety of mechanisms, including inhibition of insulin release by alpha(2)-adrenergic receptors. Such effects could potentially confound measurements of brain glucose metabolism during studies of the central actions of sympathomimetic drugs. Plasma glucose, insulin, and sympathetic responses to alpha, blockade were measured following infusion of idazoxan, a selective alpha, antagonist, or placebo, in 33 healthy volunteers (idazoxan: n=23, placebo: n=10). These measures were compared with estimates of global brain metabolism obtained from positron emission tomography (PET) scans before and after the infusion. Glucose revels fell and fractional levels of insulin rose after idazoxan, compared with placebo. Relative increases in insulin correlated with increases in epinephrine after active drug. The increases in insulin are consistent with the hypothesized role of alpha(2)-adrenoceptors in regulating insulin release. Estimates of global brain glucose metabolism did not appear to be influenced by the modest changes in plasma glucose.
C1 NIH,CLIN PHARMACOL SECT,EXPT THERAPEUT BRANCH,BETHESDA,MD 20892.
NINCDS,CLIN NEUROCHEM SECT,CLIN NEUROSCI BRANCH,NIH,BETHESDA,MD 20892.
NIDA,BRAIN IMAGING SECT,NIH,BALTIMORE,MD.
RP Schmidt, ME (reprint author), ELI LILLY & CO,LILLY CORP CTR,LILLY RES LABS,893 DELAWARE ST,INDIANAPOLIS,IN 46285, USA.
RI Schmidt, Mark/I-5052-2016
OI Schmidt, Mark/0000-0003-3417-8977
NR 48
TC 5
Z9 5
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 2
BP 253
EP 259
PG 7
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XM243
UT WOS:A1997XM24300011
PM 9230639
ER
PT J
AU Lebowitz, BD
Pollock, BG
Schneider, LS
AF Lebowitz, BD
Pollock, BG
Schneider, LS
TI Estrogen in geriatric psychopharmacology
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article
ID OLDER WOMEN; REPLACEMENT THERAPY; ALZHEIMERS-DISEASE; RISK
C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260.
UNIV SO CALIF,LOS ANGELES,CA 90089.
RP Lebowitz, BD (reprint author), NIMH,MENTAL DISORDERS AGING RES BRANCH,DIV CLIN RES,5600 FISHERS LANE,ROOM 18-101,ROCKVILLE,MD 20857, USA.
NR 23
TC 1
Z9 1
U1 4
U2 4
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 2
BP 287
EP 288
PG 2
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XM243
UT WOS:A1997XM24300016
PM 9230644
ER
PT J
AU Rudorfer, MV
Goldstein, H
AF Rudorfer, MV
Goldstein, H
TI Research priorities in eating disorders
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Editorial Material
C1 NIMH,EATING DISORDER PROGRAM,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 317
EP 319
PG 3
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800001
ER
PT J
AU Grilo, CM
Devlin, MJ
Cachelin, FM
Yanovski, SZ
AF Grilo, CM
Devlin, MJ
Cachelin, FM
Yanovski, SZ
TI Report of the National Institutes of Health (NIH) Workshop on the
Development of Research Priorities in Eating Disorders
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Editorial Material
DE eating disorders; anorexia nervosa; bulimia nervosa; research; workshops
AB The National Institutes of Health (NIH) Workshop on the Development of Research Priorities in Eating Disorders was convened in New York on April 24 and 25, 1996. The goals of the workshop were (1) to identify important unanswered questions in the study and treatment of eating disorders, (2) to discuss potentially fruitful approaches to answering these questions through basic and clinical research, and (3) to assist the NIH and other funding agencies in assigning priorities for research on eating disorders. The program consisted of a series of brief presentations by moderators, each followed by facilitated discussion of the topic with members of the audience. Three reporters (CMG, MJD, FMC) took detailed notes of the proceedings, which have been incorporated into this article, A summary of this workshop is presented, along with recommendations for future research that were identified by workshop participants.
C1 NIDDKD,DIV DIGEST DIS & NUTR,NIH,BETHESDA,MD 20892.
YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT.
COLUMBIA UNIV COLL PHYS & SURG,NEW YORK STATE PSYCHIAT INST,OFF MENTAL HLTH,NEW YORK,NY 10032.
WESLEYAN UNIV,DEPT PSYCHOL,MIDDLETOWN,CT.
NR 3
TC 28
Z9 28
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 321
EP 333
PG 13
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800002
PM 9550875
ER
PT J
AU Kumra, S
Herion, D
Jacobsen, LK
Briguglia, C
Grothe, D
AF Kumra, S
Herion, D
Jacobsen, LK
Briguglia, C
Grothe, D
TI Risperidone-induced hepatotoxicity in pediatric patients
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Meeting Abstract
C1 NIH,DEPT CHILD PSYCHIAT,BETHESDA,MD 20892.
NIH,DEPT GASTROENTEROL,BETHESDA,MD 20892.
NIH,DEPT CLIN CTR PHARM,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 540
EP 540
PG 1
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800088
ER
PT J
AU Kumra, S
Jacobsen, LK
Lenane, M
Lee, PR
Smith, AK
Bedwell, J
Malanga, CJ
Rapoport, JL
AF Kumra, S
Jacobsen, LK
Lenane, M
Lee, PR
Smith, AK
Bedwell, J
Malanga, CJ
Rapoport, JL
TI Childhood-onset schizophrenia: An open-label trial of olanzapine
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Meeting Abstract
C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 541
EP 541
PG 1
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800089
ER
PT J
AU Malhotra, AK
Goldman, D
Buchanan, R
Pickar, D
Breier, A
AF Malhotra, AK
Goldman, D
Buchanan, R
Pickar, D
Breier, A
TI The antipsychotic efficacy of clozapine and NMDA receptor function:
Evidence from clinical and molecular studies
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NIAAA,ROCKVILLE,MD 20852.
MARYLAND PSYCHIAT RES CTR,CATONSVILLE,MD 21228.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 551
EP 551
PG 1
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800099
ER
PT J
AU Vitiello, B
Goodkin, K
Heaton, R
Rochon, J
Atkinson, H
Wilkie, F
Brown, S
Feaster, D
Goldschmidts, W
Stover, E
Koslow, S
AF Vitiello, B
Goodkin, K
Heaton, R
Rochon, J
Atkinson, H
Wilkie, F
Brown, S
Feaster, D
Goldschmidts, W
Stover, E
Koslow, S
TI Factors associated with HIV-related cognitive impairment
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Meeting Abstract
C1 NIMH,NIH,ROCKVILLE,MD 20857.
UNIV MIAMI,DEPT PSYCHIAT,MIAMI,FL 33152.
UNIV CALIF SAN DIEGO,DEPT PSYCHIAT,SAN DIEGO,CA 92103.
GEORGE WASHINGTON UNIV,CTR BIOSTAT,ROCKVILLE,MD.
RI Feaster, Daniel/I-6079-2013
NR 2
TC 0
Z9 0
U1 0
U2 1
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 3
BP 600
EP 600
PG 1
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA XZ328
UT WOS:A1997XZ32800148
ER
PT J
AU Hibbs, ED
Clarke, G
Hechtman, L
Abikoff, HB
Greenhill, LL
Jensen, PS
AF Hibbs, ED
Clarke, G
Hechtman, L
Abikoff, HB
Greenhill, LL
Jensen, PS
TI Manual development for the treatment of child and adolescent disorders
SO PSYCHOPHARMACOLOGY BULLETIN
LA English
DT Article; Proceedings Paper
CT 37th Annual Meeting of the National-Center-for-Drug-Evaluation
CY MAY 27-30, 1997
CL BOCA RATON, FLORIDA
SP Natl Ctr Drug Eval Unit, NIMH
DE manuals; treatment; child; adolescent; therapy
ID COGNITIVE THERAPY; PSYCHOTHERAPY; ISSUES; CARE
AB There has been a proliferation of treatment manuals in the past decade as part of an effort to operationalize treatment applications and standardize treatments across subjects, settings, and therapists. In this article we present the essential elements needed to develop manuals for the psychosocial and psychopharmacological treatments of child and adolescent disorders, using one modality or in multimodal treatment trials. We delineate how to integrate various treatment components for psychosocial and psychopharmacological manuals, as well as those for central conditions. We also examine the therapist variable as it concerns training and adherence to the structured or flexible scripted manuals. Finally, we discuss the advantages and disadvantages of manuals in terms of how they may affect outcome, recommending that treatments be both empirically grounded and clinically meaningful.
C1 NIMH, Child & Adolescent Treatment & Prevent Intervent, Rockville, MD 20857 USA.
Kaiser Permanente, Ctr Hlth Res, Portland, OR USA.
McGill Univ, Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada.
NYU, Med Ctr, New York, NY 10016 USA.
Columbia Univ, New York State Psychiat Inst, New York, NY USA.
RP Hibbs, ED (reprint author), NIMH, Child & Adolescent Treatment & Prevent Intervent, Rm 100-09,5600 Fishers Lane, Rockville, MD 20857 USA.
OI Jensen, Peter/0000-0003-2387-0650
NR 33
TC 11
Z9 12
U1 0
U2 5
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 USA
SN 0048-5764
J9 PSYCHOPHARMACOL BULL
JI Psychopharmacol. Bull.
PY 1997
VL 33
IS 4
BP 619
EP 629
PG 11
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA YZ164
UT WOS:000072226700002
PM 9493471
ER
PT J
AU Sheffield, D
Sheps, DS
Light, KC
Krantz, DS
Stone, PH
Raczynski, J
Kaufmann, PG
Forman, S
AF Sheffield, D
Sheps, DS
Light, KC
Krantz, DS
Stone, PH
Raczynski, J
Kaufmann, PG
Forman, S
TI Triggers of myocardial ischemia during daily life: Results from the
psychophysiological investigation of myocardial ischemia (pimi) study.
SO PSYCHOSOMATIC MEDICINE
LA English
DT Meeting Abstract
C1 UNIV N CAROLINA,CHAPEL HILL,NC 27515.
UNIFORMED SERV UNIV HLTH SCI,BRIGHAM & WOMENS HOSP,BOSTON,MA.
UNIV ALABAMA,TUSCALOOSA,AL 35487.
NHLBI,BETHESDA,MD.
MARYLAND MED RES INST,BALTIMORE,MD.
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 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD JAN-FEB
PY 1997
VL 59
IS 1
BP 92
EP 92
PG 1
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA WF121
UT WOS:A1997WF12100080
ER
PT J
AU Sheps, D
Krantz, D
Knatterud, GL
Burg, MM
Blumenthal, JA
Kaufmann, PG
AF Sheps, D
Krantz, D
Knatterud, GL
Burg, MM
Blumenthal, JA
Kaufmann, PG
TI Psychological Stress-Induced Ischemia
SO PSYCHOSOMATIC MEDICINE
LA English
DT Meeting Abstract
C1 MARYLAND MED RES INST,BALTIMORE,MD.
VET ADM MED CTR,W HAVEN,CT 06516.
DUKE UNIV,MED CTR,DURHAM,NC.
NHLBI,BETHESDA,MD 20892.
UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814.
UNIV N CAROLINA,CHAPEL HILL,NC.
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 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD JAN-FEB
PY 1997
VL 59
IS 1
BP 108
EP 108
PG 1
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA WF121
UT WOS:A1997WF12100147
ER
PT J
AU Schechter, AN
AF Schechter, AN
TI Sickle cell disease expenditures and outcomes
SO PUBLIC HEALTH REPORTS
LA English
DT Editorial Material
ID ANEMIA
RP NIDDKD, BIOL CHEM LAB,NIH,BLDG 10,ROOM 9N307,10 CTR DR, MSC 1822, BETHESDA, MD 20892 USA.
OI Schechter, Alan N/0000-0002-5235-9408
NR 9
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0033-3549
EI 1468-2877
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD JAN-FEB
PY 1997
VL 112
IS 1
BP 38
EP 39
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA WD994
UT WOS:A1997WD99400023
PM 9018286
ER
PT J
AU Davis, H
Moore, RM
Gergen, PJ
AF Davis, H
Moore, RM
Gergen, PJ
TI Cost of hospitalizations associated with sickle cell disease in the
United States
SO PUBLIC HEALTH REPORTS
LA English
DT Article
ID FREQUENCY
AB Objective. This study estimated the number and cost of hospitalizations associated with sickle cell disease in the United Slates.
Methods. To estimate the number of hospitalizations per year in the United States of people with sickle cell disease, the authors used data for the years 1989 through 1993 from national hospital discharge surveys conducted by the National Center for Health Statistics. The authors derived cost estimates using data from a 1992 national hospital discharge survey conducted by the Agency for Health Care Policy and Research and a 1992 survey of physicians conducted by the American Medical Association.
Results. During the year 1989 through 1993, there were on average an estimated 75,000 hospitalizations per year of children and adults with sickle cell disease. The average direct cost per hospitalization (in 1996 dollars) was estimated at $6300, for a total direct cost of $475 million per year. In 66% of hospital discharge records, government programs were listed as the expected principal source of payment.
Conclusions. The cost of hospitalizations associated with sickle cell disease is substantial, Because government programs pay most of this cost, further government-funded research to develop interventions that prevent complications of the disease has great potential for cost savings as well as for reducing the suffering of those afflicted with this painful genetic disorder. These national cost estimates contribute to an understanding of the impact of sickle cell disease and should be useful in establishing research priorities.
C1 US DEPT HHS,OFF SECRETARY,OFF INT & REFUGE HLTH,WASHINGTON,DC 20201.
NIAID,NIH,BETHESDA,MD.
NR 6
TC 55
Z9 55
U1 1
U2 4
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD JAN-FEB
PY 1997
VL 112
IS 1
BP 40
EP 43
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA WD994
UT WOS:A1997WD99400024
PM 9018287
ER
PT J
AU Davis, H
Gergen, PJ
Moore, RM
AF Davis, H
Gergen, PJ
Moore, RM
TI Geographic differences in mortality of young children with sickle cell
disease in the United States
SO PUBLIC HEALTH REPORTS
LA English
DT Article
ID ANEMIA; SURVIVAL
AB Objectives. Because geographic differences in health care have been found for many diseases, including those affecting children, there are probably geographic differences in the health care of young children with sickle. cell disease. Consequently, survival of young children with sickle cell disease might differ among geographic areas. This study's objective was to identify areas in the United States where young children with sickle cell disease are at especially high and low risk of dying.
Methods. Using U.S. death certificate data From 1968 through 1992, the authors calculated the mortality rates of 1- through 4-year-old black children with sickle cell disease for states, counties, and cities. Deaths from trauma, congenital anomalies, and perinatal conditions were excluded.
Results. From 1968 through 1980 and from 1981 through 1992, 1- through 4-year-old black children with sickle cell disease in Florida had a markedly higher risk of dying, and those in Pennsylvania had a markedly lower risk of dying, than the average 1- through 4-year-old black child with the disease in the United States, From 1981 through 1992, 1- through 4-year-old black children with sickle cell disease in Maryland had the lowest mortality rate in the nation, During the same time period, 1- through 4-year-old black children with sickle cell disease in five counties in Florida were at especially high risk while in Baltimore no young black children with the disease died, These geographic differences in mortality of black children with sickle cell disease greatly exceeded geographic differences in mortality of black children without the disease.
Conclusions. Marked differences exist across the United States in mortality of young black children with sickle cell disease. To improve survival for children with the disease in high mortality areas, evaluations should be made of the accessibility and quality of medical care, and of parents' health care seeking behavior and compliance with antibiotic prophylaxis, in addition, efforts should be made to understand and duplicate the success of treatment programs in low mortality areas.
C1 US DEPT HHS,OFF SECRETARY,OFF INT & REFUGEE HLTH,WASHINGTON,DC.
NIAID,NIH,BETHESDA,MD 20892.
NR 20
TC 24
Z9 24
U1 0
U2 2
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD JAN-FEB
PY 1997
VL 112
IS 1
BP 52
EP 58
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA WD994
UT WOS:A1997WD99400026
PM 9018289
ER
PT J
AU Wu, C
Brechbiel, MW
Gansow, OA
Kobayashi, H
Carrasquillo, J
Pastan, I
AF Wu, C
Brechbiel, MW
Gansow, OA
Kobayashi, H
Carrasquillo, J
Pastan, I
TI Stability of the four 2-(p-nitrobenzyl)-trans-CyDTPA Y-88 complexes
SO RADIOCHIMICA ACTA
LA English
DT Article; Proceedings Paper
CT Symposium on Radiochemistry and Radioimmunotherapy at the 212th National
Meeting of the American-Chemical-Society
CY AUG 25-29, 1996
CL ORLANDO, FLORIDA
SP Amer Chem Soc, Div Nucl Chem & Technol
DE yttrium; antibodies; radioimmunotherapy; chelates; stereochemistry
ID PARTICLE-MEDIATED RADIOIMMUNOTHERAPY; MONOCLONAL-ANTIBODIES;
BIODISTRIBUTION; LIGANDS; DTPA; B3
AB The unusual stereochemical influence on in vivo stability of the two C-Functionalized cyclohexyl diethylenetriamine-N,N,N',N ",N "-pentaacetic acid (CyDTPA) chelating agents, (CHX-A, CHX-B), recently reported warranted further investigation to determine why such differences in configuration produce such striking effects on the stability of the Yttrium complex. To this end, all four individual component stereoisomers of CHX-A and CHX-B were synthesized for a detailed investigation into their chelation chemistry. Results of transchelation measurements, serum stability studies, and in vivo femur deposition measurements with Y-88 indicate that the Y-88-CHX-A chelates are significantly more stable, in vitro and in vivo, than the Y-88-CHX-B complexes. Additionally, significant difference in vivo between the Y-88 complexes formed from the component enantiomeric ligands were observed.
C1 NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
NCI, Dept Nucl Med, CC, NIH, Bethesda, MD 20892 USA.
NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Brechbiel, MW (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Carrasquillo, Jorge/E-7120-2010;
OI Carrasquillo, Jorge/0000-0002-8513-5734
NR 13
TC 6
Z9 6
U1 0
U2 0
PU R OLDENBOURG VERLAG
PI MUNICH
PA LEKTORAT M/N, K BERBER-NERLINGER, POSTFACH 80 13 60, D-81613 MUNICH,
GERMANY
SN 0033-8230
J9 RADIOCHIM ACTA
JI Radiochim. Acta
PY 1997
VL 79
IS 2
BP 123
EP 126
PG 4
WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology
SC Chemistry; Nuclear Science & Technology
GA YW901
UT WOS:000071986100012
ER
PT J
AU Wu, CC
Brechbiel, MW
Gansow, OA
AF Wu, CC
Brechbiel, MW
Gansow, OA
TI An improved generator for the production of Bi-213 from Ac-225
SO RADIOCHIMICA ACTA
LA English
DT Article; Proceedings Paper
CT Symposium on Radiochemistry and Radioimmunotherapy at the 212th National
Meeting of the American-Chemical-Society
CY AUG 25-29, 1996
CL ORLANDO, FLORIDA
SP Amer Chem Soc, Div Nucl Chem & Technol
DE Ac-225; Bi-213; generator; radioimmunotherapy; actinide
ID RADIOIMMUNOTHERAPY; RADIONUCLIDES; SEPARATION; RA-224
AB An improved generator was developed using a silica-based extraction chromatographic resin, Eichrom Silica Actinide Resin (Eichrom, Darien, IL), for the production of the alpha-emitting radionuclide Bi-213 and to minimize radiolysis of the Ac-225/Bi-213 generator. Ac-225 was adsorbed and evenly distributed on the top two-thirds of the generator resin. Bi-213 was eluted quantitatively with 1.0 M HCl. Simultaneous elution of the generator, subsequent dilution and re-adsorption of Bi-213 onto an MP-50 column to concentrate the activity was performed by assembling the columns in series. Breakthrough of Ac-225 from the generator was <0.05%, and no Ac-225 was found when Bi-213 was eluted from the second column. Bi-213 obtained can be easily used to radiolabel appropriate protein chelating agent conjugates. Hypothetically, resin damage by alpha-radiolysis should be obviated by employing such a silica-based resin and by broad distribution of the Ac-225 on the column.
C1 NCI, Inorgan & Radioimmune Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Wu, CC (reprint author), NCI, Inorgan & Radioimmune Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
NR 14
TC 22
Z9 22
U1 3
U2 4
PU R OLDENBOURG VERLAG
PI MUNICH
PA LEKTORAT M/N, K BERBER-NERLINGER, POSTFACH 80 13 60, D-81613 MUNICH,
GERMANY
SN 0033-8230
J9 RADIOCHIM ACTA
JI Radiochim. Acta
PY 1997
VL 79
IS 2
BP 141
EP 144
PG 4
WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology
SC Chemistry; Nuclear Science & Technology
GA YW901
UT WOS:000071986100016
ER
PT J
AU Wolff, SD
Balaban, RS
AF Wolff, SD
Balaban, RS
TI Assessing contrast on MR images
SO RADIOLOGY
LA English
DT Article
DE magnetic resonance (MR), contrast enhancement; magnetic resonance (MR),
pulse sequences; special reports
ID FAST-SPIN-ECHO; 1.5 T; LIVER; ANGIOGRAPHY; SEQUENCE; LESIONS; NOISE
AB Magnetic resonance imaging pulse sequences are frequently judged by their ability to facilitate discrimination between pathologic and normal tissue. Objective analysis is usually based on signal intensity measurements. However, the literature shows disagreement as to how this analysis should be performed. The ability to visually differentiate two objects on the basis of signal intensity depends on the contrast-to-noise ratio (CNR). This parameter, however, can be calculated only by measuring the intensity of photons reaching the eye from two distinct objects and, hence, is display dependent. The signal difference-to-noise ratio (SDNR) is a display-independent parameter that reflects the contrast-generating ability of a pulse sequence. When comparing two imaging sequences, the SDNR is proportional to the CNR, assuming the images being compared are displayed so that corresponding regions have the same intensity (ie, photon fluxes). Because the SDNR is display independent, it should be the preferred parameter for assessing the contrast-generating ability of a pulse sequence. The value and limitations of these parameters are discussed.
RP Wolff, SD (reprint author), NHLBI,CARDIAC ENERGET LAB,NIH,BLDG 10,RM B1D161,10 CTR DR,MSC-1061,BETHESDA,MD 20892, USA.
RI Balaban, Robert/A-7459-2009
OI Balaban, Robert/0000-0003-4086-0948
NR 16
TC 64
Z9 65
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 JAN
PY 1997
VL 202
IS 1
BP 25
EP 29
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA WA401
UT WOS:A1997WA40100007
PM 8988186
ER
PT J
AU Bryan, RN
Wells, SW
Miller, TJ
Elster, AD
Jungreis, CA
Poirier, VC
Lind, BK
Manolio, TA
AF Bryan, RN
Wells, SW
Miller, TJ
Elster, AD
Jungreis, CA
Poirier, VC
Lind, BK
Manolio, TA
TI Infarctlike lesions in the brain: Prevalence and anatomic
characteristics at MR imaging of the elderly - Data from the
cardiovascular health study
SO RADIOLOGY
LA English
DT Article
DE brain, infarction; brain, MR
ID LACUNAR INFARCTION; AGING BRAIN; OLDER ADULTS; RISK-FACTORS; STROKE;
POPULATION; DISEASE; TOMOGRAPHY; REGISTRY; FEATURES
AB PURPOSE: To determine the prevalence and anatomic characteristics of infarctlike lesions seen on cranial magnetic resonance (MR) images.
MATERIALS AND METHODS: The study cohort consisted of 5,888 community-living individuals aged 65 years and older enrolled in a longitudinal, population-based study of cardiovascular disease. MR images were obtained from 3,658 participants and evaluated by trained readers. Lesion size, anatomic location, and signal intensity were recorded. Infarctlike lesion was defined as a nonmass, hyperintense region on spin-density- and T2- weighted images and, in cerebral white matter and brain stem, a hypointense region on n- weighted images.
RESULTS: Infarctlike lesions were depicted on MR images of 1,323 (36%) participants. Eighty-five percent (1,128 participants) had lesions 3 mm or larger in maximum dimension, although 70.9% (1,320 of 1,861) of these lesions were 10 mn or less. Lesion prevalence increased with age, especially with lesions 3 mm or larger, which increased from 22.1% (86 of 389) in the 65-69-year age group to 42.9% (88 of 205) in the over-85-year age group (P < .0001). Lesion prevalence was slightly greater in men (497 of 1,527 [32.5%]) than in women (631 of 2,131 [29.6%]), but did not differ between blacks and nonblacks. The deep nuclei were the most commonly affected anatomic sites, with 78.2% (1,451 of 1,856) of lesions. Lesions that involved the cerebrum and posterior fossa accounted for 11.7% (218 of 1,856) and 10.1% (187 of 1,856) of lesions, respectively.
CONCLUSION: If the lesions reported in this study indicate cerebrovascular disease, subclinical disease may be more prevalent than clinical disease, and the prevalence of disease may rise with age. Also, infarctlike lesions have a distinctive anatomic profile.
C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC.
PRESBYTERIAN UNIV HOSP,PITTSBURGH,PA 15213.
UNIV CALIF DAVIS,SACRAMENTO,CA 95817.
CARDIOVASC HLTH STUDY COORDINATING CTR,SEATTLE,WA.
NHLBI,NIH,BETHESDA,MD 20892.
RP Bryan, RN (reprint author), JOHNS HOPKINS MED INST,DIV NEURORADIOL,600 N WOLFE ST,BALTIMORE,MD 21287, USA.
RI Bryan, R. Nick/P-1661-2014
FU NHLBI NIH HHS [N01-HC-15103]
NR 34
TC 146
Z9 148
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 JAN
PY 1997
VL 202
IS 1
BP 47
EP 54
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA WA401
UT WOS:A1997WA40100013
PM 8988191
ER
PT J
AU Termanini, B
Gibril, F
Doppman, JL
Reynolds, JC
Stewart, CA
Sutliff, VE
Venzon, DJ
Jensen, RT
AF Termanini, B
Gibril, F
Doppman, JL
Reynolds, JC
Stewart, CA
Sutliff, VE
Venzon, DJ
Jensen, RT
TI Distinguishing small hepatic hemangiomas from vascular liver metastases
in gastrinoma: Use of a somatostatin-receptor scintigraphic agent
SO RADIOLOGY
LA English
DT Article
DE liver neoplasms; liver neoplasms, radionuclide studies; liver neoplasms,
secondary; radionuclide imaging, comparative studies
ID ZOLLINGER-ELLISON SYNDROME; PANCREATIC ENDOCRINE TUMORS; BLOOD-CELL
SPECT; DYNAMIC BOLUS CT; CAVERNOUS HEMANGIOMA; LONG-TERM; NEUROENDOCRINE
TUMORS; AGGRESSIVE RESECTION; MALIGNANT GASTRINOMA; COMPUTED-TOMOGRAPHY
AB PURPOSE: To compare somatostatin-receptor scintigraphy and conventional imaging modalities in the differentiation of small hepatic hemangiomas from small liver metastases in Zollinger-Ellison syndrome.
MATERIALS AND METHODS: Twenty-nine patients had hypervascular liver lesions smaller than 2 cm that could have been either metastases or hemangiomas. Fourteen patients had metastases, 14 had hemangiomas, and one had both. Scintigraphy was compared with computed tomography (CT), magnetic resonance (MR) imaging, and angiography for the correct identification of the lesions.
RESULTS: The hemangiomas and liver metastases both had a mean size of 1.3 cm. In the patients with hepatic hemangiomas, scintigraphy showed no lesions. CT, angiography, or MR imaging showed a lesion in 40%-93%. With metastases present, any liver lesion was detected in 93% with scintigraphy versus 20%-60% with another modality. Scintigraphy depicted liver metastases in 93% of patients, which was higher than the sensitivities of other modalities. The accuracy (96%) and positive (100%) and negative (93%) predictive values of scintigraphy for detecting liver metastases were superior to those of other modalities. There were 45 liver metastases and 31 hemangiomas; a per lesion analysis gave results similar to the per patient analysis results.
CONCLUSION: In Zollinger-Ellison syndrome, somatostatin-receptor scintigraphy provides an excellent diagnostic tool to differentiate small hepatic hemangiomas from small liver metastases.
C1 NIDDK,NIH,WARREN GRANT MAGNUSON CLIN CTR,DIGEST DIS BRANCH,BETHESDA,MD 20892.
NCI,NIH,WARREN GRANT MAGNUSON CLIN CTR,BIOSTAT DATA MANAGEMENT SECT,BETHESDA,MD 20892.
NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892.
NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892.
RI Venzon, David/B-3078-2008
NR 57
TC 35
Z9 35
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 JAN
PY 1997
VL 202
IS 1
BP 151
EP 158
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA WA401
UT WOS:A1997WA40100027
PM 8988205
ER
PT J
AU Amado, FML
Domingues, P
SantanaMarques, MG
FerrerCorreia, AJ
Tomer, KB
AF Amado, FML
Domingues, P
SantanaMarques, MG
FerrerCorreia, AJ
Tomer, KB
TI Discrimination effects and sensitivity variations in matrix-assisted
laser desorption/ionization
SO RAPID COMMUNICATIONS IN MASS SPECTROMETRY
LA English
DT Article; Proceedings Paper
CT 15th Annual Informal Meeting on Mass Spectrometry (IMMS)
CY MAY 12-16, 1997
CL SMOLENICE, SLOVAKIA
SP Italian Natl Council Res, Hungarian Acad Sci, Slovakian Acad Sci
ID IONIZATION MASS-SPECTROMETRY; DESORPTION; ACID; PROTEINS; IONS
AB In matrix-assisted laser desorption/ionization (MALDI) the analyte signal produced depends strongly on the analyte and on the sample preparation procedure. Comparing the results obtained with the dried-drop method with the results obtained,vith a homogeneous sample preparation procedure, discrimination effects, as web as sensitivity variations, are shown to be dependent on the molecular weight of the analysed compounds. The signal obtained in MALDI is shown to be dependent on the hydrophobicity and basicity of the analyte. With the dried-drop method, in particular, evidence of peripheral sample deposition of hydrophilic compounds is shown. These last effects are due to mass transfer caused by differences in surface activities during solvent evaporation, and are known as Marangoni effects. (C) 1997 by John Wiley & Sons, Ltd.
C1 NIEHS,LAB MOL BIOPHYS,RES TRIANGLE PK,NC 27709.
RP Amado, FML (reprint author), UNIV AVEIRO,DEPT CHEM,P-3800 AVEIRO,PORTUGAL.
RI Tomer, Kenneth/E-8018-2013; Domingues, Pedro/E-5202-2010; Amado,
Francisco/M-5337-2015
OI Domingues, Pedro/0000-0002-8060-7675; Amado,
Francisco/0000-0001-8256-1749
NR 26
TC 72
Z9 72
U1 0
U2 10
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0951-4198
J9 RAPID COMMUN MASS SP
JI Rapid Commun. Mass Spectrom.
PY 1997
VL 11
IS 12
BP 1347
EP 1352
DI 10.1002/(SICI)1097-0231(199708)11:12<1347::AID-RCM974>3.0.CO;2-8
PG 6
WC Chemistry, Analytical; Spectroscopy
SC Chemistry; Spectroscopy
GA XR697
UT WOS:A1997XR69700020
ER
PT B
AU Brawley, OW
Thompson, IM
AF Brawley, OW
Thompson, IM
BE Schroder, FH
TI Chemoprevention of prostate cancer and the prostate cancer prevention
trial
SO RECENT ADVANCES IN PROSTATE CANCER AND BPH
LA English
DT Proceedings Paper
CT IV Congress on Progress and Controversies in Oncological Urology (PACIOU
IV)
CY APR, 1996
CL ROTTERDAM, NETHERLANDS
RP Brawley, OW (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT & COMMUNITY ONCOL,BETHESDA,MD 20892, USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU PARTHENON PUBLISHING GROUP LTD
PI LANCASTER
PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA
BN 1-85070-784-7
PY 1997
BP 51
EP 59
PG 9
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA BH04Y
UT WOS:A1997BH04Y00006
ER
PT S
AU Sekiya, F
Morita, T
AF Sekiya, F
Morita, T
BE Takada, A
Collen, D
Gaffney, PJ
TI A new cascade theory of blood coagulation: Magnesium (II) is a crucial
constituent of the blood coagulation cascade
SO RECENT PROGRESS IN BLOOD COAGULATION AND FIBRINOLYSIS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT International Symposium on Clot Formation and Lysis, at the 74th Annual
Meeting of the Japanese-Society-of-Physiology
CY MAR 21-22, 1997
CL HAMAMATSU, JAPAN
SP Japanese Soc Physiol
C1 NHLBI, Lab Cell Signaling, NIH, Bethesda, MD 20892 USA.
RP Sekiya, F (reprint author), NHLBI, Lab Cell Signaling, NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-82602-5
J9 INT CONGR SER
PY 1997
VL 1129
BP 3
EP 7
PG 5
WC Hematology; Physiology
SC Hematology; Physiology
GA BK22F
UT WOS:000071570600001
ER
PT S
AU Klein, DC
Coon, SL
Roseboom, PH
Weller, JL
Bernard, M
Gastel, JA
Zatz, M
Iuvone, PM
Rodriguez, IR
Begay, V
Falcon, J
Cahill, GM
Cassone, VM
Baler, R
AF Klein, DC
Coon, SL
Roseboom, PH
Weller, JL
Bernard, M
Gastel, JA
Zatz, M
Iuvone, PM
Rodriguez, IR
Begay, V
Falcon, J
Cahill, GM
Cassone, VM
Baler, R
BE Conn, PM
TI The melatonin rhythm-generating enzyme: Molecular regulation of
serotonin N-acetyltransferase in the pineal gland
SO RECENT PROGRESS IN HORMONE RESEARCH, PROCEEDINGS OF THE 1996 CONFERENCE,
VOL 52
SE RECENT PROGRESS IN HORMONE RESEARCH
LA English
DT Article; Proceedings Paper
CT 52nd Meeting of Recent Progress on Hormone Research
CY 1996
CL STEVENSON, WASHINGTON
SP Endocrine Soc, Merck & Co Inc, Glaxo Wellcome Inc, Eli Lilly & Co
ID BETA-ADRENERGIC STIMULATION; PROTEIN KINASE-C; RAT PINEALOCYTES;
CIRCADIAN-RHYTHMS; INDOLE METABOLISM; CHICKEN RETINA; KAINIC ACID;
CELLS; EXPRESSION; LIGHT
AB A remarkably constant feature of vertebrate physiology is a daily rhythm of melatonin in the circulation which serves as the hormonal signal of the daily light/dark cycle: melatonin levels are always elevated at night. The biochemical basis of this hormonal rhythm is one of the enzymes involved in melatonin synthesis in the pineal gland-the melatonin rhythm-generating enzyme-serotonin N-acetyltransferase (arylalkylamine N-acetyltransferase, AA-NAT, E.C. 2.3.1.87). In all vertebrates, enzyme activity is high at night. This reflects the influences of internal circadian clocks and of light. The dynamics of this enzyme an remarkable. The magnitude of the nocturnal increase in enzyme activity ranges from 7- to 150-fold on a species-to-species basis among vertebrates. In all cases the nocturnal levels of AA-NAT activity decrease very rapidly following exposure to light. A major advance in the study of the molecular basis of these changes was the cloning of cDNA encoding the enzyme. This has resulted in rapid progress in our understanding of the biology and structure of AA-NAT and how it is regulated. Several constant features of this enzyme have become apparent, including structural features, tissue distribution, and a close association of enzyme activity and protein. However, some remarkable differences among species in the molecular mechanisms involved in regulating the enzyme have been discovered. In sheep, AA-NAT mRNA levels show relatively little change over a 24-hour period and changes in AA-NAT activity are primarily regulated at the protein level. In the rat, AA-NAT is also regulated at a protein level; however, in addition, AA-NAT mRNA levels exhibit a 150-fold rhythm, which reflects cyclic AMP-dependent regulation of expression of the AA-NAT gene. In the chicken, cyclic AMP acts primarily at the protein level and a rhythm in AA-NAT mRNA is driven by a noncyclic AMP-dependent mechanism linked to the clock within the pineal gland. Finally, in the trout, AA-NAT mRNA levels shoe little change and activity is regulated by light acting directly on the pineal gland. The variety of mechanisms that have evolved among vertebrates to achieve the same goal-a rhythm in melatonin-underlines the important role melatonin plays as the hormonal signal of environmental lighting in vertebrates.
C1 NICHHD, Sect Neuroendocrinol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA.
NIMH, Sect Biochem Pharmacol, Lab Cellular & Mol Regulat, NIH, Bethesda, MD 20892 USA.
Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
NEI, Retinal Cell & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
UFR Sci, Lab Neurobiol & Cellular Neuroendocrinol, Dept Neurosci, UMR CNRS 6558, F-86022 Poitiers, France.
Univ Houston, Dept Biol, Houston, TX 77204 USA.
Texas A&M Univ, Dept Biol, College Stn, TX 77843 USA.
RP Klein, DC (reprint author), NICHHD, Sect Neuroendocrinol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA.
RI FALCON, Jack/I-5302-2013
OI FALCON, Jack/0000-0002-7572-6581
FU NEI NIH HHS [EY-04864, R01 EY004864]
NR 72
TC 396
Z9 408
U1 3
U2 26
PU ENDOCRINE SOC
PI BETHESDA
PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4410 USA
SN 0079-9963
BN 1-879225-26-3
J9 RECENT PROG HORM RES
PY 1997
VL 52
BP 307
EP 358
PG 52
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA BK30S
UT WOS:000071740900013
PM 9238858
ER
PT J
AU Kapp, OH
Siemion, J
Eckelman, WC
Cohen, VI
Reba, RC
AF Kapp, OH
Siemion, J
Eckelman, WC
Cohen, VI
Reba, RC
TI Molecular modeling of the interaction of diagnostic radiopharmaceuticals
with receptor proteins - m2 antagonist binding to the muscarinic m2
subtype receptor
SO RECEPTORS & SIGNAL TRANSDUCTION
LA English
DT Review
DE muscarinic receptors; drug design; PET; SPECT; diagnostic
radiopharmaceuticals; molecular modeling; G-protein-linked receptors;
m2; antagonist
ID SITE-DIRECTED MUTAGENESIS; BETA-ADRENERGIC-RECEPTOR; IN-VIVO
SELECTIVITY; AMINO-ACID SUBSTITUTIONS; 3RD CYTOPLASMIC LOOP; COUPLED
RECEPTORS; LIGAND-BINDING; ACETYLCHOLINE-RECEPTORS; 3-DIMENSIONAL
MODELS; AUTORADIOGRAPHIC EVIDENCE
AB Models of the m2 muscarinic receptor have been built and acetylcholine and an antagonist of the quinuclidinylbenzilate family docked to the putative active site. We have incorporated aspects of homology, site-directed mutagenesis studies and structure-activity studies of specific lead compounds in the construction of our receptor models with a primary focus on the structure of the binding sites. We have observed a deep pocket binding of 5-BrQNT, suggesting a plausible explanation for the observation that agonists and antagonists do not bind competitively. The results of these computational studies are interpreted within the context of the observed in vitro results. Our goal is to assist in the development of subtype receptor selective radiopharmaceuticals for use in PET and SPECT.
C1 Univ Chicago, Dept Radiol, Chicago, IL 60637 USA.
Univ Chicago, Enrico Fermi Inst, Chicago, IL 60637 USA.
NIH, Bethesda, MD 20892 USA.
George Washington Univ, Med Ctr, Dept Radiol, Washington, DC 20037 USA.
NR 136
TC 1
Z9 1
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1052-8040
J9 RECEPT SIGNAL TRANS
JI Recept. Signal Transduct.
PY 1997
VL 7
IS 3
BP 177
EP 201
PG 25
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA YN149
UT WOS:000071138000005
PM 9440504
ER
PT J
AU Goyer, R
Eknoyan, G
DeBroe, ME
Buckalew, VM
Mutti, A
Porter, GA
Morin, JP
AF Goyer, R
Eknoyan, G
DeBroe, ME
Buckalew, VM
Mutti, A
Porter, GA
Morin, JP
TI Urinary biomarkers to detect significant effects of environmental and
occupational exposure to nephrotoxins .2. Nephrotoxins of significant
frequency and economic impact
SO RENAL FAILURE
LA English
DT Article; Proceedings Paper
CT Joint US/European Union Workshop on Urinary Biomarkers to Detect
Significant Effects of Environmental and Occupational Exposure to
Nephrotoxins
CY SEP 15-17, 1995
CL ATLANTA, GA
ID BALKAN ENDEMIC NEPHROPATHY; STAGE RENAL-FAILURE; ANALGESIC NEPHROPATHY;
HYDROCARBON EXPOSURE; ORGANIC-SOLVENTS; OCHRATOXIN-A; CHRONIC
GLOMERULONEPHRITIS; DIAGNOSTIC-CRITERIA; MODEL; RISK
RP Goyer, R (reprint author), NIEHS, OFF SENIOR SCI ADVISOR DIRECTOR, MAIL DROP WC05, POB 12233, RES TRIANGLE PK, NC 27709 USA.
RI Mutti, Antonio/C-1095-2011
OI Mutti, Antonio/0000-0003-2189-3808
NR 41
TC 1
Z9 1
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0886-022X
J9 RENAL FAILURE
JI Ren. Fail.
PY 1997
VL 19
IS 4
BP 523
EP 534
DI 10.3109/08860229709048689
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA XR747
UT WOS:A1997XR74700003
PM 9276902
ER
PT J
AU Giurgiovich, AJ
Anderson, LM
Jones, AB
Dove, LF
Moskal, TJ
Rice, JM
Olivero, OA
Poirier, MC
AF Giurgiovich, AJ
Anderson, LM
Jones, AB
Dove, LF
Moskal, TJ
Rice, JM
Olivero, OA
Poirier, MC
TI Transplacental cisplatin exposure induces persistent fetal mitochondrial
and genomic DNA damage in patas monkeys
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
DE fetal monkey; DNA adduct; cisplatin-DNA dissociation-enhanced lanthanide
fluoroimmunoassay; genomic DNA; mitochondrial DNA
ID EPITHELIAL OVARIAN-CARCINOMA; PREFERENTIAL BINDING; CHEMOTHERAPY;
PREGNANCY; ADDUCTS; SAMPLES; TISSUES; TUMORS; RATS
AB A previous attempt to model transplacental cisplatin exposure and genotoxicity employed several pregnant Erythrocebus patas monkeys; most of the animals were exposed near the end of gestation and cisplatin-DNA adduct analyses included only genomic DNA. Here, both genomic and mitochondrial DNA adduct formation have been determined in fetuses from two pregnant monkeys exposed at the end of the second trimester of gestation, Multiple fetal tissues were obtained after doses of 0.315 mg cisplatin/kg body weight (5.3 mg/m(2) total) on days 101 and 106 of gestation, Cesarean sections were performed 24 h after exposure and 27 d after exposure, Cisplatin genomic (g)-DNA adducts were observed in fetal adrenal, brain, heart, kidney, liver, skin, spleen, and thymus, When placentas from the two animals were divided into four concentric regions at increasing distances from the umbilical cord, and g-DNA was assayed, cisplatin DNA adduct levels were similar in all four regions, Mitochondrial (mt)-DNA adducts were higher than g-DNA adducts in maternal liver and fetal liver, brain and kidney, suggesting that the mitochondria may constitute a particular target for cisplatin genotoxicity. The study demonstrates significant fetal genotoxicity in g-DNA and mt-DNA of patas monkeys exposed to cisplatin in utero, suggesting that similarly exposed human fetuses may also sustain drug-induced DNA damage. (C) 1997 Elsevier Science Inc.
C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,NIH,BETHESDA,MD 20892.
NCI,COMPARAT CARCINOGENESIS LAB,FCRDC,FREDERICK,MD 21701.
BIOQUAL INC,ROCKVILLE,MD.
NR 22
TC 11
Z9 11
U1 1
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD JAN-FEB
PY 1997
VL 11
IS 1
BP 95
EP 100
DI 10.1016/S0890-6238(96)00201-8
PG 6
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA WK538
UT WOS:A1997WK53800011
PM 9138639
ER
PT J
AU Clegg, ED
Cook, JC
Chapin, RE
Foster, PMD
Foster, GP
AF Clegg, ED
Cook, JC
Chapin, RE
Foster, PMD
Foster, GP
TI Leydig cell hyperplasia and adenoma formation: Mechanisms and relevance
to humans
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
DE Leydig cell hyperplasia; adenoma formation; humans
ID ANDROGEN RECEPTOR ANTAGONIST; HUMAN CHORIONIC-GONADOTROPIN;
LUTEINIZING-HORMONE LEVELS; CHRONIC TOXICITY; 5-ALPHA-REDUCTASE
INHIBITOR; INHALATION TOXICITY; OXOLINIC ACID; GERM-CELL; MALE-RAT;
AMMONIUM PERFLUOROOCTANOATE
AB Leydig cell adenomas are observed frequently in studies evaluating the chronic toxicity of chemical agents in laboratory animals, Doubts have been raised about the relevance of such responses for human risk assessment, but the question of relevance has not been evaluated and presented in a comprehensive manner by a broad group of experts, This article reports the consensus conclusions from a workshop on rodent Leydig cell adenomas and human relevance. Five aspects of Leydig cell biology and toxicology were discussed: 1) control of Leydig cell proliferation; 2) mechanisms of toxicant-induced Leydig cell hyperplasia and tumorigenesis; 3) pathology of Leydig cell adenomas; 4) epidemiology of Leydig cell adenomas; and 5) risk assessment for Leydig cell tumorigens. Important research needs also were identified, Uncertainty exists about the true incidence of Leydig cell adenomas in men, although apparent incidence is rare and restricted primarily to white males, Also, surveillance databases for specific therapeutic agents as well as nicotine and lactose that have induced Leydig cell hyperplasia or adenoma in test species have detected no increased incidence in humans, Because uncertainties exist about the true incidence in humans, induction of Leydig cell adenomas in test species may be of concern under some conditions, Occurrence of Leydig cell hyperplasia alone in test species after lifetime exposure to a chemical does not constitute a cause for concern in a risk assessment for carcinogenic potential, but early occurrence may indicate a need for additional testing, Occurrence of Leydig cell adenomas in test species is of potential concern as both a carcinogenic and reproductive effect if the mode of induction and potential exposures cannot be ruled out as relevant for humans, The workgroup focused on seven hormonal modes of induction of which two, GnRH agonism and dopamine agonism, were considered not relevant to humans, Androgen receptor antagonism, 5 alpha-reductase inhibition, testosterone biosynthesis inhibition, aromatase inhibition, and estrogen agonism were considered to he relevant or potentially relevant, but quantitative differences may exist across species, with rodents being more sensitive, A margin of exposure (MOE; the ratio of the lowest exposure associated with toxicity to the human exposure level) approach should be used for compounds causing Leydig cell adenoma by a hormonal mode that is relevant to humans. For agents that are positive for mutagenicity, the decision regarding a MOE or linear extrapolation approach should be made on a case-by-case basis, In the absence of information about mode of induction, it is necessary to utilize default assumptions, including linear behavior below the observable range, All of the evidence should be weighed in the decision-making process. (C) 1997 Elsevier Science Inc.
C1 DUPONT CO INC,HASKELL LAB TOXICOL & IND MED,CENT RES & DEV,NEWARK,DE 19714.
NIEHS,RES TRIANGLE PK,NC 27709.
CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709.
PROCTER & GAMBLE CO,CINCINNATI,OH.
RP Clegg, ED (reprint author), US EPA,NATL CTR ENVIRONM ASSESSMENT,8623,401 M ST SW,WASHINGTON,DC 20460, USA.
OI Chapin, Robert/0000-0002-5997-1261
NR 170
TC 85
Z9 87
U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD JAN-FEB
PY 1997
VL 11
IS 1
BP 107
EP 121
DI 10.1016/S0890-6238(96)00203-1
PG 15
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA WK538
UT WOS:A1997WK53800013
PM 9138629
ER
PT S
AU Henderson, DK
AF Henderson, DK
BE Henderson, DK
Levy, SB
TI Confronting antimicrobial resistance - Historical perspectives
SO RESISTANT ORGANISMS: GLOBAL IMPACT ON CONTINUUM OF CARE
SE ROYAL SOCIETY OF MEDICINE INTERNATIONAL CONGRESS AND SYMPOSIUM SERIES
LA English
DT Proceedings Paper
CT Conference on Resistant Organisms - Global Impact on Continuum of Care
CY SEP 27, 1996
CL ROYAL SOC MED, LONDON, ENGLAND
SP 3M Hlth Care & Regent Med
HO ROYAL SOC MED
RP Henderson, DK (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,BLDG 10,ROOM 2C144,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON, ENGLAND W1M 8AE
SN 0142-2367
BN 1-85315-313-3
J9 ROY SOC MED INT CONG
PY 1997
VL 220
BP 1
EP 6
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA BJ07F
UT WOS:A1997BJ07F00001
ER
PT S
AU Lee, L
AF Lee, L
BE Henderson, DK
Levy, SB
TI Institutional care: Taking concepts into practice
SO RESISTANT ORGANISMS: GLOBAL IMPACT ON CONTINUUM OF CARE
SE ROYAL SOCIETY OF MEDICINE INTERNATIONAL CONGRESS AND SYMPOSIUM SERIES
LA English
DT Proceedings Paper
CT Conference on Resistant Organisms - Global Impact on Continuum of Care
CY SEP 27, 1996
CL ROYAL SOC MED, LONDON, ENGLAND
SP 3M Hlth Care & Regent Med
HO ROYAL SOC MED
RP Lee, L (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,BLDG 10,ROOM 2C144,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON, ENGLAND W1M 8AE
SN 0142-2367
BN 1-85315-313-3
J9 ROY SOC MED INT CONG
PY 1997
VL 220
BP 35
EP 41
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA BJ07F
UT WOS:A1997BJ07F00005
ER
PT S
AU Henderson, DK
AF Henderson, DK
BE Henderson, DK
Levy, SB
TI Implications for surgical practice
SO RESISTANT ORGANISMS: GLOBAL IMPACT ON CONTINUUM OF CARE
SE ROYAL SOCIETY OF MEDICINE INTERNATIONAL CONGRESS AND SYMPOSIUM SERIES
LA English
DT Proceedings Paper
CT Conference on Resistant Organisms - Global Impact on Continuum of Care
CY SEP 27, 1996
CL ROYAL SOC MED, LONDON, ENGLAND
SP 3M Hlth Care & Regent Med
HO ROYAL SOC MED
RP Henderson, DK (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,BLDG 10,ROOM 2C144,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON, ENGLAND W1M 8AE
SN 0142-2367
BN 1-85315-313-3
J9 ROY SOC MED INT CONG
PY 1997
VL 220
BP 43
EP 50
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA BJ07F
UT WOS:A1997BJ07F00006
ER
PT B
AU Berson, A
AF Berson, A
BE Thompson, DO
Chimenti, DE
TI Imaging structure and function in medicine and biology
SO REVIEW OF PROGRESS IN QUANTITATIVE NONDESTRUCTIVE EVALUATION, VOLS 16A
AND 16B
SE REVIEW OF PROGRESS IN QUANTITATIVE NONDESTRUCTIVE EVALUATION
LA English
DT Proceedings Paper
CT 23rd Symposium on Quantitative Nondestructive Evaluation
CY JUL 28-AUG 02, 1996
CL BRUNSWICK, ME
SP Iowa State Univ, Ctr NDE, Amer Soc Nondestruct Testing, US DOE, Ames Lab, FAA, NIST, Natl Sci Fdn, Ind Univ Cooperat Res Ctr Program
RP Berson, A (reprint author), NHLBI,NIH,6701 ROCKLEDGE DR,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45597-8
J9 REV PROG Q
PY 1997
VL 16
BP 1
EP 8
PN A&B
PG 8
WC Materials Science, Characterization & Testing
SC Materials Science
GA BJ03K
UT WOS:A1997BJ03K00001
ER
PT J
AU Lu, B
Figurov, A
AF Lu, B
Figurov, A
TI Role of neurotrophins in synapse development and plasticity
SO REVIEWS IN THE NEUROSCIENCES
LA English
DT Article
DE neurotrophins; NGF; BDNF; NT-3; NT-4/5; trk receptor tyrosine kinases;
neuromuscular junction; hippocampus; cortex; synapse; synaptogenesis;
transmitter release; plasticity
ID NERVE GROWTH-FACTOR; LONG-TERM POTENTIATION; DEVELOPING NEUROMUSCULAR
SYNAPSES; CULTURED HIPPOCAMPAL-NEURONS; MESSENGER-RNA EXPRESSION;
POSTNATAL RAT-BRAIN; VISUAL-CORTEX; TRANSMITTER RELEASE;
CORTICAL-NEURONS; LIMBIC SEIZURES
AB Neurotrophic factors are traditionally viewed as secretory proteins that regulate long-term survival and differentiation of neurons. The role of neurotrophic factors in the structural integrity of the nervous system makes them attractive candidates as therapeutic agents for neurodegenerative diseases, However, the fact that expression of many neurotrophic factors in the central nervous system is rapidly enhanced by neuronal activity suggests a new role for these factors in activity-dependent processes, such as synaptic development and plasticity. A series of recent studies has provided strong evidence for this novel function of neurotrophic factors, The neurotrophin family of proteins has been shown to acutely potentiate synaptic transmission at the neuromuscular junction and in the brain, These factors are also involved in the maturation of the neuromuscular synapses and in the development of synapses in the visual system. Gene targeting and experiments demonstrate that neurotrophic factor (BDNF) plays an important role in long-term potentiation (LTP), a cellular model for learning and memory. These findings have brought together two hotly pursued areas of neuroscience, namely, the function of neurotrophic factors and the mechanisms for synaptic plasticity. Continuous studies in this new field will help understand how synapses develop and function in the brain, and may have significant implications in treating learning disorders in both children and adults.
C1 NICHHD,DEV NEUROBIOL LAB,UNIT SYNAPSE DEV & PLAST,NIH,BETHESDA,MD 20892.
RI Lu, Bai/A-4018-2012
NR 78
TC 178
Z9 182
U1 0
U2 5
PU FREUND PUBLISHING HOUSE
PI LONDON
PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA
SN 0334-1763
J9 REV NEUROSCIENCE
JI Rev. Neurosci.
PD JAN-MAR
PY 1997
VL 8
IS 1
BP 1
EP 12
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA WZ054
UT WOS:A1997WZ05400001
PM 9402641
ER
PT J
AU Shore, D
Hsiao, JK
AF Shore, D
Hsiao, JK
TI At issue: Medication-free intervals and schizophrenia research -
Editors' introduction
SO SCHIZOPHRENIA BULLETIN
LA English
DT Editorial Material
RP Shore, D (reprint author), NIMH,DIV CLIN & TREATMENT RES,ROCKVILLE,MD 20857, USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 1
BP 1
EP 1
PG 1
WC Psychiatry
SC Psychiatry
GA WJ706
UT WOS:A1997WJ70600001
ER
PT J
AU Wyatt, RJ
AF Wyatt, RJ
TI Research in schizophrenia and the discontinuation of antipsychotic
medications
SO SCHIZOPHRENIA BULLETIN
LA English
DT Editorial Material
ID MAINTENANCE NEUROLEPTIC THERAPY; FOLLOW-UP; EARLY INTERVENTION; NATURAL
COURSE; WITHDRAWAL; PREDICTORS; PSYCHOSIS; EPISODES; DURATION; ILLNESS
AB This article, and the accompanying one by Dr. Carpenter, discuss the benefits and risks associated with taking patients with schizophrenia off medications for research purposes. This article reviews the concept that at least some forms of schizophrenia are progressive, Evidence for this view is provided by studies examining the impact of early intervention with antipsychotic medications on the long-term morbidity of schizophrenia, as well as the few studies examining the long-term risks of discontinuing antipsychotic medications in patients with schizophrenia. While there is evidence that early intervention improves the long-term course of the illness, it is not known whether withdrawal of antipsychotic medications increases long-term morbidity, This is an area where further information is needed for clinical practice and research.
RP Wyatt, RJ (reprint author), NIMH,NEUROPSYCHIAT RES HOSP,NEUROPSYCHIAT BRANCH,2700 MARTIN LUTHER KING,JR AVE,WASHINGTON,DC 20032, USA.
NR 45
TC 27
Z9 27
U1 0
U2 2
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 1
BP 3
EP 9
PG 7
WC Psychiatry
SC Psychiatry
GA WJ706
UT WOS:A1997WJ70600002
PM 9050108
ER
PT J
AU Weinberger, DR
AF Weinberger, DR
TI On localizing schizophrenic neuropathology
SO SCHIZOPHRENIA BULLETIN
LA English
DT Editorial Material
ID POSITRON EMISSION TOMOGRAPHY; MEDIODORSAL THALAMIC NUCLEUS;
ABNORMALITIES; DISTURBANCES; LOBE
AB Many brain regions and circuits have been implicated in the neuropathology of schizophrenia. Drs. Bogerts and Jones have reviewed the evidence that links the disorder to temporal limbic structures and to frontal-thalamic circuits, respectively. Each article is an important update on what we know about the relevance of these brain regions to schizophrenia, In addition, each article, in summarizing the accumulation of relevant research data, is a testament to the likelihood that these structures play a role in the disease. In light of their compelling arguments, this commentary emphasizes incompleteness in the data and inconsistencies in published findings. The principal weaknesses of the temporal limbic findings are that most have been reported in chronically ill patients and that the only qualitative finding of cytoarchitectural disorganization has not been replicated convincingly, Problems of replication also compromise the interpretation of neuropathological findings in prefrontal cortex and thalamus, Despite the loose ends, I agree with the conclusions of Drs, Bogerts and Jones that brain circuits involving thalamus, prefrontal, and temporolimbic cortices are involved in the basic biology of schizophrenia.
RP Weinberger, DR (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,NIH,WASHINGTON,DC 20032, USA.
NR 22
TC 27
Z9 27
U1 0
U2 0
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 3
BP 537
EP 540
PG 4
WC Psychiatry
SC Psychiatry
GA XR438
UT WOS:A1997XR43800022
PM 9327520
ER
PT J
AU Moldin, SO
Gottesman, II
AF Moldin, SO
Gottesman, II
TI At issue: Genes, experience, and chance in schizophrenia - Positioning
for the 21st century
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
ID BANTU-SPEAKING FAMILIES; SUSCEPTIBILITY LOCUS; LINKAGE ANALYSIS;
CHROMOSOME 6P; VULNERABILITY LOCUS; POTENTIAL LINKAGE; COMPLEX TRAITS;
NO EVIDENCE; FOLLOW-UP; DISEASE
AB Genetic factors make important contributions to the etiologies of schizophrenia. The mode of familial inheritance remains unknown, but it is highly likely that multiple genes and idiosyncratic environmental factors are involved. Rapidly evolving genetic technologies have been applied in the genetic analysis of schizophrenia, and several genomic regions have been posited as harboring susceptibility genes. Currently, the strongest evidence implicates chromosomes 6 and 8, but these linkages are not yet confirmed. In this article we discuss genetic risk factors, gene-environment interaction, the feasibility of genetic testing, psychiatric genetic counseling, and the dangers of genetic discrimination as they apply to schizophrenia. We also address and correct specific misconceptions about the genetics of schizophrenia held by many in the scientific community and in the media, and discuss a blueprint for future genetic research and informed dissemination of findings to the public and to lawmakers.
C1 GEORGETOWN UNIV,MED CTR,DEPT PSYCHIAT,WASHINGTON,DC 20057.
UNIV VIRGINIA,CHARLOTTESVILLE,VA 22903.
RP Moldin, SO (reprint author), NIMH,DIV BASIC & CLIN NEUROSCI RES,NIH,PARKLAWN BLDG,RM 10C-26,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA.
RI G, I/D-8042-2011
NR 89
TC 91
Z9 92
U1 3
U2 7
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 4
BP 547
EP 561
PG 15
WC Psychiatry
SC Psychiatry
GA YE793
UT WOS:A1997YE79300001
PM 9365994
ER
PT J
AU Egan, ME
Apud, J
Wyatt, RJ
AF Egan, ME
Apud, J
Wyatt, RJ
TI Treatment of tardive dyskinesia
SO SCHIZOPHRENIA BULLETIN
LA English
DT Review
ID LONG-TERM TREATMENT; VITAMIN-E TREATMENT; DOUBLE-BLIND;
SCHIZOPHRENIC-PATIENTS; PARKINSONS-DISEASE; MOVEMENT-DISORDERS;
FOLLOW-UP; RAT-BRAIN; NEUROLEPTIC WITHDRAWAL; RISK-FACTORS
AB Although the new generation of atypical antipsychotic agents could some day eliminate concerns about tardive dyskinesia (TD), this disorder remains a significant clinical problem for both patients and physicians. Fortunately, many, if not most, cases of TD are mild. For patients with mild to moderate TD, therapeutic efforts are primarily directed at minimizing neuroleptic exposure or, when possible, changing to atypical agents. Most cases of TD do not seem to progress, suggesting that the risk of remaining on typical neuroleptics is probably small. Patients with moderate to severe forms of TD present greater challenges. These patients frequently require medication to suppress their dyskinesias. A variety of suppressive agents have been tried with limited success. No treatment strategy has emerged that is clearly superior or even successful in most patients. Increasing doses of typical neuroleptics may be useful for short-term suppression; however, the long-term efficacy and risk of this strategy have not been studied carefully. Data on atypical neuroleptics are scant. Clozapine's short-term suppressive effects seem, at best, weak, but patients may improve with long-term treatment. Medications with relatively few side effects that may have suppressive efficacy for some patients include calcium channel blockers, adrenergic antagonists, and vitamin E. Gamma-amino-butyric acid agonists agents and dopamine depleters are frequently useful, but have troubling side effects of their own. A variety of other medications have been employed, but are not well studied. For patients with tardive dystonia, anticholinergic agents or botulinum toxin has been particularly effective. Efforts to understand the neurobiology of TD may shed light on this persistent clinical conundrum.
RP Egan, ME (reprint author), ST ELIZABETH HOSP,CTR NEUROSCI,NIMH,NEUROPSYCHIAT BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA.
NR 255
TC 106
Z9 106
U1 3
U2 5
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 4
BP 583
EP 609
PG 27
WC Psychiatry
SC Psychiatry
GA YE793
UT WOS:A1997YE79300004
PM 9365997
ER
PT J
AU Hyde, TM
Weinberger, DR
AF Hyde, TM
Weinberger, DR
TI Seizures and schizophrenia
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
ID TEMPORAL-LOBE EPILEPSY; 1ST UNPROVOKED SEIZURE; POSITRON-EMISSION
TOMOGRAPHY; INDUCED WATER-INTOXICATION; FOLLOW-UP; PSYCHIATRIC
MANIFESTATIONS; ANTIEPILEPTIC DRUGS; PSYCHOTROPIC-DRUGS; INVITRO
TECHNIQUE; RELATIVE RISK
AB Patients with epilepsy develop psychosis or schizophrenia at a rate exceeding that expected if the two disorders were independent. Similarly, patients with schizophrenia are more prone to seizures than the general population, This excess vulnerability may be conferred by the neuropathological substrate of schizophrenia itself or by the secondary effects of the illness, including exposure to psychotropic medications that lower the seizure threshold. Neuropathological investigations into the anatomic substrate of seizures in patients with psychosis or schizophrenia are consistent with the notion that there are neurodevelopmental abnormalities involving the mesial temporal lobe, Finally, clinical recommendations for the evaluation and pharmacological management of patients with schizophrenia who have one or more seizures are described.
RP Hyde, TM (reprint author), NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA.
NR 87
TC 53
Z9 53
U1 1
U2 2
PU US GOVERNMENT PRINTING OFFICE
PI WASHINGTON
PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PY 1997
VL 23
IS 4
BP 611
EP 622
PG 12
WC Psychiatry
SC Psychiatry
GA YE793
UT WOS:A1997YE79300005
PM 9365998
ER
PT B
AU Bulte, JWM
Brooks, RA
AF Bulte, JWM
Brooks, RA
BE Hafeli, U
Schutt, W
Teller, J
Zborowski, M
TI Magnetic nanoparticles as contrast agents for MR imaging - An overview
SO SCIENTIFIC AND CLINICAL APPLICATIONS OF MAGNETIC CARRIERS
LA English
DT Proceedings Paper
CT International Conference on Scientific and Clinical Applications of
Magnetic Carriers
CY SEP 05-07, 1996
CL ROSTOCK, GERMANY
AB Following a brief introduction to the basic concepts of relaxation and contrast enhancement in magnetic resonance imaging (MRI), this chapter presents an overview of the use of magnetic nanoparticles as contrast agents for MRI. It covers the basic principles of preparation and characterization, including variable-field relaxometry. II is shown how a detailed understanding of T1 and T2 relaxation by magnetic nanoparticles may aid further magnetopharmaceutical development. While this overview is far from complete because of the rapid recent developments in the field, an attempt is made to give an overview of current applications and future directions of magnetic nanoparticles as MR contrast agent.
RP Bulte, JWM (reprint author), NIH,LAB DIAGNOST RADIOL RES,10 CTR DR MSC 1074,BETHESDA,MD 20892, USA.
RI Bulte, Jeff/A-3240-2008
OI Bulte, Jeff/0000-0003-1202-1610
NR 0
TC 37
Z9 40
U1 0
U2 3
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45687-7
PY 1997
BP 527
EP 543
PG 17
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Pharmacology & Pharmacy
GA BJ32T
UT WOS:A1997BJ32T00040
ER
PT J
AU Herman, B
Iversen, L
AF Herman, B
Iversen, L
TI Strategies for treatment of opiate abuse
SO SEMINARS IN NEUROSCIENCE
LA English
DT Editorial Material
C1 NIDA, Rockville, MD USA.
Univ Oxford, Oxford OX1 3QT, England.
RP Herman, B (reprint author), NIDA, Rockville, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-5765
J9 SEMIN NEUROSCI
JI Semin. Neurosci.
PY 1997
VL 9
IS 3-4
BP 69
EP 69
DI 10.1006/smns.1997.0107
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA YP155
UT WOS:000071248200001
ER
PT J
AU Ernst, M
London, ED
AF Ernst, M
London, ED
TI Brain imaging studies of drug abuse: Therapeutic implications
SO SEMINARS IN NEUROSCIENCE
LA English
DT Article
DE brain imaging; human studies; positron emission tomography; substance
abuse; single photon emission computed tomography
ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; PRECIPITATED
MORPHINE-WITHDRAWAL; OPIATE RECEPTOR-BINDING; COCAINE POLYDRUG USERS;
GLUCOSE-METABOLISM; BUPRENORPHINE; SENSITIZATION; INHIBITION; DEPENDENCE
C1 NIDA, Brain Imaging Ctr, Baltimore, MD 21224 USA.
RP Ernst, M (reprint author), NIDA, Brain Imaging Ctr, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
NR 65
TC 6
Z9 6
U1 1
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-5765
J9 SEMIN NEUROSCI
JI Semin. Neurosci.
PY 1997
VL 9
IS 3-4
BP 120
EP 130
DI 10.1006/smns.1997.0112
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA YP155
UT WOS:000071248200006
ER
PT J
AU Herman, BH
O'Brien, CP
AF Herman, BH
O'Brien, CP
TI Clinical medications development for opiate addiction: Focus on
nonopioids and opioid antagonists for the amelioration of opiate
withdrawal symptoms and relapse prevention
SO SEMINARS IN NEUROSCIENCE
LA English
DT Review
ID NMDA RECEPTOR ANTAGONISTS; CCK-B RECEPTOR; OXIDE SYNTHASE INHIBITORS;
DOUBLE-BLIND; ALCOHOL DEPENDENCE; MORPHINE-TOLERANCE; HEROIN-ADDICTS;
ENKEPHALINASE INHIBITOR; NARCOTIC-ANTAGONISTS; GENERALIZED ANXIETY
C1 NIDA, Clin Trials Branch, Medicat Dev Div, NIH, Rockville, MD 20857 USA.
Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Herman, BH (reprint author), NIDA, Clin Trials Branch, Medicat Dev Div, NIH, 5600 Fishers Lane,Rm 11A55, Rockville, MD 20857 USA.
NR 125
TC 21
Z9 21
U1 0
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-5765
J9 SEMIN NEUROSCI
JI Semin. Neurosci.
PY 1997
VL 9
IS 3-4
BP 158
EP 172
DI 10.1006/smns.1997.0115
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA YP155
UT WOS:000071248200009
ER
PT J
AU Cote, LR
Azar, ST
AF Cote, LR
Azar, ST
TI Child age, parent and child gender, and domain differences in parents'
attributions and responses to children's outcomes
SO SEX ROLES
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the Eastern-Psychological-Association
CY APR 14-17, 1994
CL PROVIDENCE, RI
SP E Psychol Assoc
ID SOCIALIZATION; MOTHERS; PERCEPTIONS; ACHIEVEMENT; COMPETENCE; BEHAVIOR
AB The influence of children's age, and parents' and children's gender on parents' attributions and emotional and behavioral responses to their children's successful and unsuccessful social and academic outcomes, was investigated. Seventy-six dual-parent families (mothers and fathers) of fifth (n = 28), eighth (n = 23), and eleventh grade (n = 25) children participated The results of this study suggest that from fifth grade on, at least, the ways parents explain the causes of and respond to their children's social behavior and academic outcomes involves a complex interaction of children's age, children's gender parents' gender, domain, and outcome. Results are discussed in terms of children's socialization.
C1 CLARK UNIV,WORCESTER,MA 01610.
RP Cote, LR (reprint author), NICHHD,CHILD & FAMILY RES LAB,BLDG 31,ROOM B2B15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 27
TC 15
Z9 15
U1 0
U2 1
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0360-0025
J9 SEX ROLES
JI Sex Roles
PD JAN
PY 1997
VL 36
IS 1-2
BP 23
EP 50
DI 10.1007/BF02766237
PG 28
WC Psychology, Developmental; Psychology, Social; Women's Studies
SC Psychology; Women's Studies
GA WR788
UT WOS:A1997WR78800002
ER
PT J
AU Crowell, DH
Brooks, LJ
Colton, T
Corwin, MJ
Hoppenbrouwers, TT
Hunt, CE
Kapuniai, LE
Lister, G
Neuman, MR
Peucker, M
Ward, SLD
WeeseMayer, DE
Willinger, M
Baird, M
Hufford, D
Keens, TG
Martin, RJ
Ramanathan, R
Schafer, SC
Silvestri, JM
Tinsley, L
AF Crowell, DH
Brooks, LJ
Colton, T
Corwin, MJ
Hoppenbrouwers, TT
Hunt, CE
Kapuniai, LE
Lister, G
Neuman, MR
Peucker, M
Ward, SLD
WeeseMayer, DE
Willinger, M
Baird, M
Hufford, D
Keens, TG
Martin, RJ
Ramanathan, R
Schafer, SC
Silvestri, JM
Tinsley, L
TI Infant polysomnography: Reliability
SO SLEEP
LA English
DT Article
DE polysomnography; infant; reliability; scoring; SIDS
ID PRETERM INFANTS; SLEEP; TERM; AGES
AB Infant polysomnography (IPSG) is an increasingly important procedure for studying infants with sleep and breathing disorders. Since analyses of these IPSG data are subjective, an equally important issue is the reliability or strength of agreement among scorers (especially among experienced clinicians) of sleep parameters (SP) and sleep states (SS). One basic issue of this problem was examined by proposing and testing the hypothesis that infant SP and SS ratings can be reliably scored at substantial levels of agreement, that is, kappa (kappa) greater than or equal to 0.61.
In light of the importance of IPSG reliability in the collaborative home infant monitoring evaluation (CHIME) study, a reliability training and evaluation process was developed and implemented. The bases for training on SP and SS scoring were CHIME criteria that were modifications and supplements to Anders, Emde, and Parmelee (10). The kappa statistic was adopted as the method for evaluating reliability between and among scorers. Scorers were three experienced investigators and four trainees.
Inter- and intrarater reliabilities for SP codes and SSs were calculated for 408 randomly selected 30-second epochs of nocturnal IPSG recorded at five CHIME clinical sites from healthy full term (n = 5), preterm (n = 4), apnea of infancy (n = 2), and siblings of the sudden infant death syndrome (SIDS) (n = 4) enrolled subjects. Infant PSG data set 1 was scored by both experienced investigators and trained scorers and was used to asses initial inter-rater reliability. Infant PSG data set 2 was scored twice by the trained scorers and was used to reassess inter-rater reliability and to assess intrarater reliability. The kappa s for SS ranged from 0.45 to 0.58 for data set 1 and represented a moderate level of agreement. Therefore, rater disagreements were reviewed, and the scoring criteria were modified to clarify ambiguities. The kappa s and confidence intervals (CIs) computed for data set 2 yielded substantial inter-rater and intrarater agreements for the four trained scorers; for SS, the kappa = 0.68 and for SP the kappa s ranged from 0.62 to 0.76.
Acceptance of the hypothesis supports the conclusion that the IPSG is a reliable source of clinical and research data when supported by significant kappa s and CIs. Reliability can be maximized with strictly detailed scoring guidelines and training.
C1 RAINBOW BABIES & CHILDRENS HOSP,CLEVELAND,OH 44106.
BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA.
BOSTON UNIV,MED CTR,BOSTON,MA.
LAC & USC MED CTR,WOMENS & CHILDRENS HOSP,LOS ANGELES,CA.
MED COLL OHIO,TOLEDO,OH 43699.
YALE UNIV,NEW HAVEN,CT 06520.
CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106.
CHILDRENS HOSP LOS ANGELES,LOS ANGELES,CA 90027.
RUSH PRESBYTERIAN ST LUKES MED CTR,RUSH CHILDRENS HOSP,CHICAGO,IL 60612.
NICHD,CRMC,PREGNANCY & PERINATOL BRANCH,NIH,BETHESDA,MD 20892.
TOLEDO HOSP,TOLEDO,OH.
RP Crowell, DH (reprint author), UNIV HAWAII,KAPIOLANI MED CTR,1319 PUNAHOU ST,HONOLULU,HI 96826, USA.
FU NICHD NIH HHS [2 U10 HD28971, HD29067, HD29071]
NR 11
TC 38
Z9 39
U1 0
U2 1
PU AMER SLEEP DISORDERS ASSOC
PI ROCHESTER
PA 1610 14TH STREET NW SUITE 300, ROCHESTER, MN 55806
SN 0161-8105
J9 SLEEP
JI Sleep
PY 1997
VL 20
IS 7
BP 553
EP 560
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA XY817
UT WOS:A1997XY81700007
PM 9322271
ER
PT J
AU Quan, SF
Howard, BV
Iber, C
Kiley, JP
Nieto, FJ
O'Connor, GT
Rapoport, DM
Redline, S
Robbins, J
Samet, JM
Wahl, PW
AF Quan, SF
Howard, BV
Iber, C
Kiley, JP
Nieto, FJ
O'Connor, GT
Rapoport, DM
Redline, S
Robbins, J
Samet, JM
Wahl, PW
TI The sleep heart health study: Design, rationale, and methods
SO SLEEP
LA English
DT Article
DE sleep apnea; cardiovascular disease; epidemiology; risk factors
ID AMBULATORY BLOOD-PRESSURE; APNEA; PREVALENCE; POPULATION; EXPERIENCE;
MORTALITY; DISEASES
AB The Sleep Heart Health Study (SHHS) is a prospective cohort study designed to investigate obstructive sleep apnea (OSA) and other sleep-disordered breathing (SDB) as risk factors for the development of cardiovascular disease. The study is designed to enroll 6,600 adult participants aged 40 years and older who will undergo a home polysomnogram to assess the presence of OSA and other SDB. Participants in SHHS have been recruited from cohort studies in progress. Therefore, SHHS adds the assessment of OSA to the protocols of these studies and will use already collected data on the principal risk factors for cardiovascular disease as well as follow-up and outcome information pertaining to cardiovascular disease. Parent cohort studies and recruitment targets for these cohorts are the following: Atherosclerosis Risk in Communities Study (1,750 participants), Cardiovascular Health Study (1,350 participants), Framingham Heart Study (1,000 participants), Strong Heart Study (600 participants), New York Hypertension Cohorts (1,000 participants), and Tucson Epidemiologic Study of Airways Obstructive Diseases and the Health and Environment Study (900 participants). As part of the parent study follow-up procedures, participants will be surveyed at periodic intervals for the incidence and recurrence of cardiovascular disease events. The study provides sufficient statistical power for assessing OSA and other SDB as risk factors for major cardiovascular events, including myocardial infarction and stroke.
C1 Univ Arizona, Coll Med, Resp Sci Ctr, Tucson, AZ 85724 USA.
Univ Arizona, Coll Med, Dept Med, Tucson, AZ 85724 USA.
Medlant Res Inst, Washington, DC USA.
Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
NHLBI, Bethesda, MD 20892 USA.
Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
NYU, Dept Med, New York, NY 10016 USA.
Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
Univ Calif Davis, Dept Med, Davis, CA USA.
Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Quan, SF (reprint author), Univ Arizona, Coll Med, Resp Sci Ctr, 1501 N Campbell, Tucson, AZ 85724 USA.
OI O'Connor, George/0000-0002-6476-3926
FU NHLBI NIH HHS [U01 HL053938, U01HL53938, U01HL53940, U01HL53941]
NR 30
TC 342
Z9 349
U1 2
U2 8
PU AMER SLEEP DISORDERS ASSOC
PI ROCHESTER
PA 1610 14TH STREET NW SUITE 300, ROCHESTER, MN 55806 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PY 1997
VL 20
IS 12
BP 1077
EP 1085
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA YW402
UT WOS:000071931700002
PM 9493915
ER
PT J
AU Vissing, YM
Diament, J
AF Vissing, YM
Diament, J
TI Housing distress among high school students
SO SOCIAL WORK
LA English
DT Article
DE adolescents; homelessness; housing distress; school; youths
ID HOMELESS
AB The word ''homelessness'' is not a useful term to explain housing problems experienced by high school-aged youths. The term ''housing distress'' is preferable because it includes both teenagers who are homeless and those who are at risk of homelessness. Many teenagers feel that they have no place where they belong and seek alternative living arrangements for a variety of reasons. Housing distress is a problem for schools because students have difficulties achieving academic success when they have no consistent, safe place to live. To understand how much or how little housing distress is experienced by high school-aged youths, 3,676 high school-aged teenagers weve surveyed in nine communities along the seacoast of New Hampshire and southwestern Maine. Between 5 percent and 10 percent of the teenagers surveyed reported that they had been homeless sometime during the past year. Up to 20 percent of the high school students lived in arrangements that could be considered to be distressing and to put them at risk of becoming homeless.
C1 SALEM STATE COLL,DURHAM,NH 03824.
RP Vissing, YM (reprint author), NIMH,POB 547,DURHAM,NH 03824, USA.
NR 39
TC 2
Z9 2
U1 0
U2 0
PU NATL ASSOC SOCIAL WORKERS
PI WASHINGTON
PA 750 FIRST ST, NE, STE 700, WASHINGTON, DC 20002-4241
SN 0037-8046
J9 SOC WORK
JI Soc. Work
PD JAN
PY 1997
VL 42
IS 1
BP 31
EP 41
PG 11
WC Social Work
SC Social Work
GA WC785
UT WOS:A1997WC78500005
PM 9009887
ER
PT B
AU Nussenblatt, R
Gery, I
Shiloach, J
Ramaley, N
Weiner, H
Perry, C
Caspi, R
Ferris, F
Foster, S
Whitcup, S
AF Nussenblatt, R
Gery, I
Shiloach, J
Ramaley, N
Weiner, H
Perry, C
Caspi, R
Ferris, F
Foster, S
Whitcup, S
BE Suveges, I
Follmann, P
TI The use of the oral administration of retinal antigens in the treatment
of uveitis
SO SOE '97 - XI CONGRESS OF THE EUROPEAN SOCIETY OF OPHTHALMOLOGY, VOLS 1
AND 2
LA English
DT Proceedings Paper
CT XI Congress of the European-Society-of-Ophthalmology (SOE 97)
CY JUN 01-05, 1997
CL BUDAPEST, HUNGARY
SP European Soc Ophthalmol
AB The effect of the oral administration of retinal antigens to induce immunologic tolerance in patients with intermediate and posterior uveitis was evaluated. Patients received either Retinal S-antigen alone (n=10), Retinal S-antigen and a retinal mixture (n=10), retinal mixture alone (n=10), or placebo (n=15), given orally t.i.w. for eight weeks, then once a week for one year, and then monthly. An attempt was made to taper patients completely off their standard immunosuppressive therapy over an eight week period. Time to development of uveitis was not different between groups, but for the ability to totally discontinue immunosuppressive agents, there was a strong trend favoring the group receiving the purified S-antigen alone (p=0.08), white women in the S-antigen group fared even better when compared to the placebo group (p=0.01). No toxic effects attributable to any treatment were observed.
RP Nussenblatt, R (reprint author), NEI,IMMUNOL LAB,BLDG 10,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MONDUZZI EDITORE
PI 40128 BOLOGNA
PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY
BN 88-323-0601-8
PY 1997
BP 669
EP 672
PG 4
WC Ophthalmology
SC Ophthalmology
GA BJ48B
UT WOS:A1997BJ48B00122
ER
PT B
AU Chourpa, I
Riou, JF
Pommier, Y
Manfait, M
AF Chourpa, I
Riou, JF
Pommier, Y
Manfait, M
BE Carmona, P
Navarro, R
Hernanz, A
TI SERS and fluorescence study of the molecular interactions of
camptothecins with DNA and DNA topoisomerase I and in their ternary
cleavable complexes.
SO SPECTROSCOPY OF BIOLOGICAL MOLECULES: MODERN TRENDS
LA English
DT Proceedings Paper
CT 1997 European Conference on Spectroscopy of Biological Molecules (ECSBM)
CY 1997
CL MADRID, SPAIN
SP Univ Nacl Educ Distancia, Consejo Super Invest Cient, Spanish Minist Educ, Complutense Univ Madrid, Univ S Pable CEU, Reg Community Madrid, Embassy France, Spain, British Council, Deutsch Forsch Gemeinsch, Caja Ahorros Madrid
C1 UFR Pharm, Lab Spect Biomol, IFR 53, F-51096 Reims, France.
Rhone Poulenc Rorer, F-94403 Vitry Sur Seine, France.
NCI, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
RP Chourpa, I (reprint author), UFR Pharm, Lab Spect Biomol, IFR 53, 51 Rue Cognacq Jay, F-51096 Reims, France.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
BN 0-7923-4685-8
PY 1997
BP 361
EP 362
PG 2
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Chemistry, Physical; Spectroscopy
SC Biochemistry & Molecular Biology; Biophysics; Chemistry; Spectroscopy
GA BK55N
UT WOS:000072556800160
ER
PT S
AU Ludlow, CL
Siren, K
Zikria, M
AF Ludlow, CL
Siren, K
Zikria, M
BE Hulstijn, W
Peters, HFM
vanLieshout, PHH
TI Speech production learning in adults with chronic developmental
stuttering
SO SPEECH PRODUCTION: MOTOR CONTROL, BRAIN RESEARCH AND FLUENCY DISORDERS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT 3rd International Conference on Speech Motor Production and Fluency
Disorders
CY JUN 05-08, 1996
CL NIJMEGEN, NETHERLANDS
SP Univ Hosp Nijmegen, Inst Otorhinolaryngol, Dept Voice & Speech Pathol, Nijmegen Inst Cognit & Informat, Univ Nijmegen, Interfac Res Unit Language & Speech, Univ Hosp Nijmegen, Inst Med Psychol, Univ Congress Off
AB Speech learning for novel pseudowords was compared in adults who stutter and control subjects. Subjects performed 11 test recall trials which were interspersed with modeling practice trials for two novel pseudowords associated with meaningless idiographs. The number of phonemes correctly achieved on each of the 11 test trials were scored by the same listener. The adults who stuttered were impaired in their rate of learning as well as the overall accuracy of their word productions. The results suggest that the speech production learning is less efficient in those affected by chronic stuttering and may contribute to their less efficient and unstable speech production capabilities throughout adult life.
C1 NIDCD, NIH, Bethesda, MD 20892 USA.
RP Ludlow, CL (reprint author), NIDCD, NIH, 10 Ctr Dr MSC 1416,Room 5D38, Bethesda, MD 20892 USA.
NR 0
TC 14
Z9 14
U1 1
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-82460-X
J9 INT CONGR SER
PY 1997
VL 1146
BP 221
EP 230
PG 10
WC Behavioral Sciences; Neurosciences; Psychology
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA BK04T
UT WOS:000070984300019
ER
PT S
AU Braun, AR
Varga, M
Stager, S
Schulz, G
Selbie, S
Maisog, JM
Carson, RE
Ludlow, CL
AF Braun, AR
Varga, M
Stager, S
Schulz, G
Selbie, S
Maisog, JM
Carson, RE
Ludlow, CL
BE Hulstijn, W
Peters, HFM
vanLieshout, PHH
TI A typical lateralization of hemispheric activity in developmental
stuttering: An (H2O)-O-15 positron emission tomography study.
SO SPEECH PRODUCTION: MOTOR CONTROL, BRAIN RESEARCH AND FLUENCY DISORDERS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT 3rd International Conference on Speech Motor Production and Fluency
Disorders
CY JUN 05-08, 1996
CL NIJMEGEN, NETHERLANDS
SP Univ Hosp Nijmegen, Inst Otorhinolaryngol, Dept Voice & Speech Pathol, Nijmegen Inst Cognit & Informat, Univ Nijmegen, Interfac Res Unit Language & Speech, Univ Hosp Nijmegen, Inst Med Psychol, Univ Congress Off
AB Cerebral blood flow was measured with (H2O)-O-15 and positron emission tomography (PET) in order to assess dynamic brain function in adults who had stuttered since childhood. PET scans were performed during oral motor control tasks and speech tasks designed to evoke stuttering. Speech samples were acquired simultaneously and quantitatively compared with the PET images. Stuttering subjects differed markedly in the formulation and expression of language, failing to demonstrate left hemispheric lateralization typically observed in controls; instead, regional responses were either absent, bilateral, or lateralized to the right hemisphere. Covariance analyses indicated that activation of left hemispheric regions may be related to the production of stuttered speech, while activation of right hemispheric regions may represent compensatory processes associated with the production of fluent speech.
C1 NIDCD, NIH, Bethesda, MD 20892 USA.
RP Braun, AR (reprint author), NIDCD, NIH, 10 Ctr Dr MSC 1416,Room 5D38, Bethesda, MD 20892 USA.
RI Carson, Richard/H-3250-2011
OI Carson, Richard/0000-0002-9338-7966
NR 0
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-82460-X
J9 INT CONGR SER
PY 1997
VL 1146
BP 279
EP 292
PG 14
WC Behavioral Sciences; Neurosciences; Psychology
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA BK04T
UT WOS:000070984300023
ER
PT S
AU Stager, S
Calis, K
Grothe, D
Bloch, M
Turcasso, N
Ludlow, C
Braun, A
AF Stager, S
Calis, K
Grothe, D
Bloch, M
Turcasso, N
Ludlow, C
Braun, A
BE Hulstijn, W
Peters, HFM
vanLieshout, PHH
TI A double-blind trial of pimozide and paroxetine for stuttering
SO SPEECH PRODUCTION: MOTOR CONTROL, BRAIN RESEARCH AND FLUENCY DISORDERS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT 3rd International Conference on Speech Motor Production and Fluency
Disorders
CY JUN 05-08, 1996
CL NIJMEGEN, NETHERLANDS
SP Univ Hosp Nijmegen, Inst Otorhinolaryngol, Dept Voice & Speech Pathol, Nijmegen Inst Cognit & Informat, Univ Nijmegen, Interfac Res Unit Language & Speech, Univ Hosp Nijmegen, Inst Med Psychol, Univ Congress Off
AB A randomized double-blind, placebo-controlled crossover study was designed to examine the effects on fluency of a highly selective dopamine antagonist, pimozide, and a highly selective serotonin reuptake inhibitor, paroxetine, in adult persons who stutter. Eleven persons who stutter enrolled in this study but only a total of 6 individuals completed the pimozide phase, 6 the placebo phase, and 5 the paroxetine phase. This paper examined the following treatment outcome measures; self-perceptions of changes in fluency and factors to which they attributed these changes; comparison of self-ratings of fluency with objective measures of fluency; self-perceptions about changes in symptom severity, consistency of fluency, and measures of speech anxiety such as confidence in speaking, anxiety levels and satisfaction with speech; and reports from others noting fluency change. On pimozide, a positive clinical response was found for 4/6 individuals, and a negative clinical response for the other 2 individuals. Trends for significant differences between placebo and pimozide phases were found for percent of symptoms reported changed (p=0.03), percent of days where fluency change was attributed to medication (p=0.03); consistency of fluency (p=0.04); confidence in speaking (p=0.07), satisfaction with speech (p=0.08), anxiety while speaking (p=0.09) and level of fluency (p=0.1). Individuals randomized to the pimozide phase might have been more likely to report a change in fluency attributable to medication because they reported experiencing more side effects on pimozide than on paroxetine or placebo. No significant clinical response was found for paroxetine using any outcome measure, and significant side effects were experienced by 2 individuals while withdrawing from this medication.
C1 NIDCD, NIH, Bethesda, MD 20892 USA.
RP Stager, S (reprint author), NIDCD, NIH, 10 Ctr Dr,MSC 1416,Room 5D38, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-82460-X
J9 INT CONGR SER
PY 1997
VL 1146
BP 371
EP 378
PG 8
WC Behavioral Sciences; Neurosciences; Psychology
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA BK04T
UT WOS:000070984300031
ER
PT J
AU Farci, P
Bukh, J
Purcell, RH
AF Farci, P
Bukh, J
Purcell, RH
TI The quasispecies of hepatitis C virus and the host immune response
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
ID NON-B-HEPATITIS; ENVELOPE GLYCOPROTEIN GP70; POLYMERASE CHAIN-REACTION;
MAJOR GENETIC GROUPS; 5' NONCODING REGION; NON-A; HYPERVARIABLE REGION;
LIVER-DISEASE; SEQUENCE VARIATION; LONG-TERM
C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,NIH,BETHESDA,MD 20892.
RP Farci, P (reprint author), UNIV CAGLIARI,IST MED INTERNA,VIA SAN GIORGIO 12,I-09124 CAGLIARI,ITALY.
NR 146
TC 53
Z9 56
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 19
IS 1
BP 5
EP 26
DI 10.1007/BF00945022
PG 22
WC Immunology; Pathology
SC Immunology; Pathology
GA XL682
UT WOS:A1997XL68200002
PM 9266628
ER
PT J
AU Pantaleo, G
Fauci, AS
AF Pantaleo, G
Fauci, AS
TI Introduction: Recent advances in the pathogenesis of human
immunodeficiency virus infection
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Editorial Material
C1 NIAID,IMMUNOREGULAT LAB,NIH,BETHESDA,MD 20892.
RP Pantaleo, G (reprint author), CHU VAUDOIS,DIV INFECT DIS,DEPT MED,LAB AIDS IMMUNOPATHOGENESIS,CH-1011 LAUSANNE,SWITZERLAND.
RI Pantaleo, Giuseppe/K-6163-2016
NR 0
TC 4
Z9 4
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 18
IS 3
BP 253
EP 256
DI 10.1007/BF00813496
PG 4
WC Immunology; Pathology
SC Immunology; Pathology
GA WN668
UT WOS:A1997WN66800001
PM 9089947
ER
PT J
AU Pantaleo, G
Graziosi, C
Fauci, AS
AF Pantaleo, G
Graziosi, C
Fauci, AS
TI Virologic and immunologic events in primary HIV infection
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; FOLLICULAR DENDRITIC CELLS; LYMPHOID
ORGANS; GENETIC-VARIATION; TYPE-1 INFECTION; IMMUNE-RESPONSE; AIDS;
VIREMIA; PATHOGENESIS; PROGRESSION
C1 NIAID,IMMUNOREGULAT LAB,NIH,BETHESDA,MD 20892.
RP Pantaleo, G (reprint author), CHU VAUDOIS,DIV INFECT DIS,DEPT INTERNAL MED,LAB AIDS IMMUNOPATHOGENESIS,CH-1011 LAUSANNE,SWITZERLAND.
RI Pantaleo, Giuseppe/K-6163-2016
NR 47
TC 22
Z9 22
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 18
IS 3
BP 257
EP 266
DI 10.1007/BF00813497
PG 10
WC Immunology; Pathology
SC Immunology; Pathology
GA WN668
UT WOS:A1997WN66800002
PM 9089948
ER
PT J
AU Cohen, OJ
Pantaleo, G
Lam, GK
Fauci, AS
AF Cohen, OJ
Pantaleo, G
Lam, GK
Fauci, AS
TI Studies on lymphoid tissue from HIV-infected individuals: Implications
for the design of therapeutic strategies
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; FOLLICULAR DENDRITIC CELLS;
PLACEBO-CONTROLLED TRIAL; TYPE-1 INFECTION; CUBIC MILLIMETER;
T-LYMPHOCYTES; NITRIC-OXIDE; LYMPHADENOPATHY SYNDROME; DOUBLE-BLIND;
ZIDOVUDINE
AB Lymphoid tissue is a major reservoir of human immunodeficiency virus (HIV) infection in vivo. In addition, the lymphoid microenvironment provides a replicative advantage to the virus in that it provides a milieu of activated target cells that allows for efficient virus spread. The process of mobilization and activation of immune competent cells directed against the virus paradoxically contributes to the propagation of virus replication. Disruption of the lymphoid microenvironment during the progression of HIV disease is a poorly understood process, which may be of considerable importance pathogenically. Studies of lymph node biopsy samples taken 8 weeks apart from individuals who did not undergo any change in their therapeutic regimen (i.e., patients who either remained untreated or remained on their ongoing nucleoside analogue reverse transcriptase inhibitor monotherapy regimen) revealed little change in histopathology or viral load over the 8-week period. These results with successive lymph node biopsy samples taken from different sites indicate that an isolated lymph node biopsy accurately reflects the pathologic process associated with HIV infection and that this process diffusely involves the lymphoid system. Treatment with reverse transcriptase inhibitor monotherapy of patients in relatively early stage HIV disease had no detectable impact on the viral load in lymphoid tissue, suggesting the need to investigate more potent antiretroviral regimens during this stage of disease. Among patients with moderately advanced HIV disease, switching to combination therapy from a monotherapy regimen resulted in decreased viral replication in lymph nodes; this effect was associated with decreases in plasma viremia. Despite the fact that measures of viral replication decreased significantly, the net frequency of HIV-infected cells in peripheral blood and lymph nodes remained unchanged. Potent antiretroviral drug combinations may be capable of profound and long-term downregulation of plasma viremia. It will be essential to monitor the status of viral trapping, viral burden, and viral replication within lymphoid tissue during treatment with such drugs to determine accurately their true potential for impact on these key features of HIV pathogenesis.
RP Cohen, OJ (reprint author), NIAID,IMMUNOREGULAT LAB,NIH,10 CTR DR MSC 1876,BLDG 10,ROOM 11B13,BETHESDA,MD 20892, USA.
RI Pantaleo, Giuseppe/K-6163-2016
NR 67
TC 31
Z9 31
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 18
IS 3
BP 305
EP 322
DI 10.1007/BF00813500
PG 18
WC Immunology; Pathology
SC Immunology; Pathology
GA WN668
UT WOS:A1997WN66800005
PM 9089951
ER
PT J
AU Strober, W
Kelsall, BL
AF Strober, W
Kelsall, BL
TI Untitled - Introduction
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Editorial Material
RP Strober, W (reprint author), NIAID,MUCOSAL IMMUN SECT,CLIN INVEST LAB,NIH,BLDG 10,ROOM 11N 238,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 18
IS 4
BP 407
EP 408
DI 10.1007/BF00824049
PG 2
WC Immunology; Pathology
SC Immunology; Pathology
GA WW201
UT WOS:A1997WW20100001
ER
PT J
AU Kelsall, BL
Strober, W
AF Kelsall, BL
Strober, W
TI Dendritic cells of the gastrointestinal tract
SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Article
ID LANGERHANS CELLS; PEYERS-PATCHES; EPITHELIAL-CELLS; SMALL-INTESTINE;
MONOCLONAL-ANTIBODY; LYMPHOID-CELLS; LAMINA PROPRIA; MOUSE SPLEEN;
T-CELLS; ANTIGEN
RP Kelsall, BL (reprint author), NIAID, MUCOSAL IMMUN SECT,CLIN INVEST LAB,NIH,BLDG 10, ROOM 11N238, 9000 ROCKVILLE PIKE, BETHESDA, MD 20814 USA.
NR 56
TC 22
Z9 22
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-4325
J9 SPRINGER SEMIN IMMUN
JI Springer Semin. Immunopathol.
PY 1997
VL 18
IS 4
BP 409
EP 420
DI 10.1007/BF00824050
PG 12
WC Immunology; Pathology
SC Immunology; Pathology
GA WW201
UT WOS:A1997WW20100002
PM 9144862
ER
PT J
AU Orlic, D
Girard, LJ
Anderson, SM
Do, BKQ
Seidel, NE
Jordan, CT
Bodine, DM
AF Orlic, D
Girard, LJ
Anderson, SM
Do, BKQ
Seidel, NE
Jordan, CT
Bodine, DM
TI Transduction efficiency of cell lines and hematopoietic stem cells
correlates with retrovirus receptor mRNA levels
SO STEM CELLS
LA English
DT Article; Proceedings Paper
CT Symposium on Hematopoietic Stem Cells
CY 1996
CL HOHENZOLLERN CASTLE, MOUNT ZOLLERN, GERMANY
SP AMGEN
HO HOHENZOLLERN CASTLE
DE retrovirus; gene transfer; stem cells; bone marrow; cytokines; receptors
ID APE LEUKEMIA-VIRUS; MESSENGER-RNA; C-KIT; GENE; PURIFICATION; MOUSE
AB The low transduction efficiency of hematopoietic stem cells (HSC) using amphotropic retroviruses continues to plague gene therapy protocols. This low transduction efficiency may be related to a low level of amphotropic retrovirus binding to target cell receptors. We have assayed murine and human cell lines as well as primary bone marrow HSC populations for mRNA encoding retrovirus receptors. Total cellular RNA was amplified by reverse transcriptase-polymerase chain reaction and the level of ecotropic and amphotropic receptor mRNA was compared to the level of beta 2-microglobulin mRNA in the same cell populations. Cell lines that are easily transduced by ecotropic and amphotropic retroviruses have high levels of receptor mRNA. In studies using murine HSC-enriched populations obtained from bone marrow, we observed a high correlation between transduction efficiency and the level of ecotropic and amphotropic receptor mRNA. We predict from these findings that purification of monkey and human HSC populations with high levels of amphotropic receptor mRNA will enable us to obtain improved efficiency of gene transfer.
C1 SOMATIX THERAPY CORP, ALAMEDA, CA USA.
NATL HUMAN GENOME RES INST, LAB GENE TRANSFER, NIH, BETHESDA, MD USA.
NR 12
TC 17
Z9 17
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 23
EP 28
PG 6
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100008
PM 9368321
ER
PT J
AU Spangrude, GJ
Orlic, D
Griffin, JD
Moore, MAS
AF Spangrude, GJ
Orlic, D
Griffin, JD
Moore, MAS
TI Transduction efficiency of cell lines and hematopoietic stem cells
correlates with retrovirus receptor mRNA levels - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 NIH, LAB GENE TRANSFER, NCHGR, BETHESDA, MD 20892 USA.
DANA FARBER CANC INST, DIV HEMATOL MALIGNANCIES, BOSTON, MA 02115 USA.
SLOAN KETTERING INST CANC RES, NEW YORK, NY 10021 USA.
RP UNIV UTAH, SALT LAKE CITY, UT 84132 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 28
EP 29
PG 2
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100009
ER
PT J
AU Muszynski, KW
Ruscetti, FW
Gooya, JM
Linnekin, DM
Keller, JR
AF Muszynski, KW
Ruscetti, FW
Gooya, JM
Linnekin, DM
Keller, JR
TI Raf-1 protein is required for growth factor-induced proliferation of
primitive hematopoietic progenitors stimulated with synergistic
combinations of cytokines
SO STEM CELLS
LA English
DT Article
DE Raf-1; synergy; hematopoiesis; stem cells
ID STEM-CELL FACTOR; BONE-MARROW; FACTOR-I; ACTIVATION; KINASE;
PHOSPHORYLATION; DIFFERENTIATION; LINE; INTERLEUKIN-3
AB Raf-l is a serine/threonine kinase that has been identified as a component of growth factor-activated signal transduction pathways, and is required for growth factor-induced proliferation of leukemic cell lines and colony formation of hematopoietic progenitors stimulated,vith single colony-stimulating factors, which promote the growth of committed hematopoietic progenitor cells, However, it is known that the most primitive progenitors in the bone marrow require stimulation with multiple cytokines to promote cell growth, We have determined that c-raf antisense oligonucleotides inhibit the growth of murine lineage-negative progenitors stimulated with two-, three- and four-factor combinations of growth factors, including GM-CSF + interleukin (IL)-1, IL-3 + steel factor (SLF), IL-3 + IL-11 + SLF and IL-3 + IL-II + SLF + G-CSF, In addition, c-raf antisense oligonucleotides inhibit the synergistic response of the MO7e human progenitor cell line induced to proliferate with IL-3 + SLF (99%) or GM-CSF + SLF (99%), In contrast, c-paf antisense oligonucleotides only partially inhibited day 14 colony formation of CD34(+) human progenitors stimulated with IL-3 + SLF (50%) or GM-CSF + SLF (55%) but completely inhibited day 7 colony formation, However, pulsing CD34(+) cells with additional oligonucleotides on day 7 of the colony assay further inhibited day 14 colony formation (70%-80%), Furthermore, a comparison of the effect of c-raf antisense oligonucleotides on the synergistic response of normal human fetal liver cells in [H-3]thymidine incorporation assays and colony assays showed strong inhibition in short-term proliferation assays and partial inhibition in 14-day colony assays, Taken together, these results demonstrate that partial inhibition of colony formation of primitive human progenitors stimulated with multiple growth factors is a result of the length (14 days) of the human colony assay and does not represent a differential requirement of primitive progenitors for Raf-l, Thus Raf-l is required for the proliferation and differentiation of primitive hematopoietic progenitor cells stimulated with synergistic combinations of cytokines.
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,INTRAMURAL RES SUPPORT PROGRAM,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,LAB LEUKOCYTE BIOL,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-56000]
NR 36
TC 7
Z9 7
U1 0
U2 1
PU ALPHAMED PRESS
PI DAYTON
PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
IS 1
BP 63
EP 72
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA WE088
UT WOS:A1997WE08800009
PM 9007224
ER
PT J
AU Sharkis
Zanjani
Dunbar
Quesenberry
TorokStorb
AF Sharkis
Zanjani
Dunbar
Quesenberry
TorokStorb
TI Transplantation of hematopoietic stem cells in utero - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 VET ADM MED CTR, RENO, NV 89520 USA.
FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA.
NHLBI, HEMATOL BRANCH, NIH, BETHESDA, MD 20892 USA.
UNIV MASSACHUSETTS, MED CTR, CTR CANC, WORCESTER, MA 01605 USA.
RP JOHNS HOPKINS UNIV, CTR ONCOL, ROOM 2-127, 600 N WOLFE ST, BALTIMORE, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 93
EP 93
PG 1
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100023
ER
PT J
AU Licht, T
Herrmann, F
Gottesman, MM
Pastan, I
AF Licht, T
Herrmann, F
Gottesman, MM
Pastan, I
TI In vivo drug-selectable genes: A new concept in gene therapy
SO STEM CELLS
LA English
DT Review
DE chemotherapy; hematopoietic stem cells; multidrug resistance;
myelosuppression; P-glycoprotein; dihydrofolate reductase; transgenic
animals; retroviral vectors
ID MULTIDRUG-RESISTANCE GENE; HEMATOPOIETIC STEM-CELLS;
DIHYDROFOLATE-REDUCTASE GENE; GLUTATHIONE-S-TRANSFERASE; BONE-MARROW
CELLS; ADENOSINE-DEAMINASE GENE; ACUTE MYELOID-LEUKEMIA; LONG-TERM
PROTECTION; HUMAN MDR1 GENE; TRANSGENIC MICE
AB Chemoresistance genes, initially considered to be a major impediment to the successful treatment of cancer, may become useful tools for gene therapy of cancer and of genetically determined disorders, Various target cells are rendered resistant to anticancer drugs by transfer of chemoresistance genes encoding P-glycoprotein, the multidrug resistance-associated protein-transporter, dihydrofolate reductase, glutathione-S-transferase, O-6-alkylguanine DNA alkyltransferase, or aldehyde reductase. These genes can be used for selection in vivo because of the pharmacology and pharmacokinetics of their substrates, In contrast, several other selectable marker genes conferring resistance to substrates Like neomycin or hygromycin can only be utilized in tissue culture. Possible applications for chemoresistance genes include protection of bone marrow and other organs from adverse effects caused by the toxicity of chemotherapy. Strategies have also been developed to introduce and overexpress nonselectable genes in target cells by cotransduction with chemoresistance genes, Thereby expression of both transgenes can be increased following selection with drugs, Moreover, treatment with chemotherapeutic agents should restore transgene expression when or if expression levels decrease after several weeks or months, This approach may improve the efficacy of somatic gene therapy of hematopoietic disorders which is hampered by low or unstable gene expression in progenitor cells, In this article we review preclinical studies in tissue culture and animal models, and ongoing clinical trials on transfer of chemoresistance genes to hematopoietic precursor cells of cancer patients.
C1 NCI,CELL BIOL LAB,NIH,BETHESDA,MD 20892.
NCI,MOL BIOL LAB,NIH,BETHESDA,MD.
UNIV ULM,DEPT INTERNAL MED 3,D-7900 ULM,GERMANY.
NR 85
TC 32
Z9 32
U1 0
U2 0
PU ALPHAMED PRESS
PI DAYTON
PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
IS 2
BP 104
EP 111
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA WQ814
UT WOS:A1997WQ81400003
PM 9090786
ER
PT J
AU Dunbar, CE
Tisdale, J
Yu, JM
Soma, T
Zujewski, J
Bodine, D
Sellers, S
Cowan, K
Donahue, R
Emmons, R
AF Dunbar, CE
Tisdale, J
Yu, JM
Soma, T
Zujewski, J
Bodine, D
Sellers, S
Cowan, K
Donahue, R
Emmons, R
TI Transduction of hematopoietic stem cells in humans and in nonhuman
primates
SO STEM CELLS
LA English
DT Article; Proceedings Paper
CT Symposium on Hematopoietic Stem Cells
CY 1996
CL HOHENZOLLERN CASTLE, MOUNT ZOLLERN, GERMANY
SP AMGEN
HO HOHENZOLLERN CASTLE
DE hematopoiesis; retrovirus; gene therapy; gene transfer; stem cell;
transforming grow factor-beta; stem cell factor; autologous
transplantation
ID COLONY-STIMULATING FACTOR; CULTURE-INITIATING CELLS; BONE-MARROW;
PERIPHERAL-BLOOD; PROGENITOR CELLS; EX-VIVO; EXPANSION; GENE;
ENGRAFTMENT; INFUSION
AB Primitive hematopoietic progenitor and stem cells have been pursued as highly desirable targets for genetic therapy, Retroviral vectors have been used for the majority of preclinical and clinical studies directed at these cells; however, both preclinical and early clinical studies indicate that the gene transfer efficiency of the current generation of vectors using known transduction conditions into primate and human repopulating stem cells is too low to be of clinical utility in most situations. In this presentation I will summarize the status of our completed and ongoing clinical genetic marking trials, and describe our efforts in the laboratory and use of primate transplantation models to improve on these results.
RP NHLBI, HEMATOL BRANCH,HEMATOPOIESIS SECT,NCHGR,NIH, BLDG 10,ROOM 7C103, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA.
NR 15
TC 17
Z9 17
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 135
EP 139
PG 5
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100032
PM 9368333
ER
PT J
AU Spangrude
Dunbar
Hoffman
Moore
AF Spangrude
Dunbar
Hoffman
Moore
TI Transduction of hematopoietic stem cells in humans and in nonhuman
primates - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 NHLBI, HEMATOL BRANCH, NIH, BETHESDA, MD 20892 USA.
UNIV ILLINOIS, COLL MED, HEMATOL ONCOL SECT, CHICAGO, IL 60607 USA.
SLOAN KETTERING INST CANC RES, NEW YORK, NY 10021 USA.
RP UNIV UTAH, SALT LAKE CITY, UT 84132 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 139
EP 140
PG 2
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100033
ER
PT J
AU Zanjani
Kolb
Dunbar
Rammensee
TorokStorb
AF Zanjani
Kolb
Dunbar
Rammensee
TorokStorb
TI Hematopoietic transplantation: State of the art - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 UNIV MUNICH, KLINIKUM GROSSHADERN, MED KLIN 3, D-81377 MUNICH, GERMANY.
NHLBI, HEMATOL BRANCH, NIH, BETHESDA, MD 20892 USA.
FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA.
RP VET ADM MED CTR, 1000 LOCUST ST, RENO, NV 89520 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 158
EP 158
PG 1
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100036
ER
PT J
AU Hoffman
Brugger
Dunbar
AF Hoffman
Brugger
Dunbar
TI Purging of peripheral blood progenitor cell autografts and treatment of
minimal residual disease - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 UNIV TUBINGEN, D-72076 TUBINGEN, GERMANY.
NHLBI, HEMATOL BRANCH, NIH, BETHESDA, MD 20892 USA.
RP UNIV ILLINOIS, COLL MED,HEMATOL ONCOL SECT,ROOM 3150, MOL BIOL RES BLDG, 900 S ASHLAND AVE, CHICAGO, IL 60607 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 165
EP 165
PG 1
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100038
ER
PT J
AU Barrett, AJ
AF Barrett, AJ
TI Mechanisms of the graft-versus-leukemia reaction
SO STEM CELLS
LA English
DT Review
DE graft-versus-leukemia; graft-versus-host disease; bone marrow
transplantation; leukemia; immunogenicity; T cells
ID BONE-MARROW TRANSPLANTATION; CHRONIC MYELOID-LEUKEMIA; MINOR
HISTOCOMPATIBILITY ANTIGENS; CHRONIC MYELOGENOUS LEUKEMIA; CYTOTOXIC
LYMPHOCYTES-T; TUMOR NECROSIS FACTOR; HOST DISEASE; CELL CLONES;
HEMATOLOGIC RELAPSE; SCID MICE
AB It is now clear that the graft-versus-leukemia (GVL) effect which accompanies allogeneic bone marrow transplantation for hematological malignancies is a powerful therapeutic weapon which, if harnessed, could improve our ability to treat refractory malignant disorders. Advances in the understanding of the alloimmune response now provide a clearer picture of the mechanisms involved in the GVL reaction: the CD4(+) T cell plays a central role in the orchestration of leukemia cell killing. The immunogenicity of the leukemia is also a major factor determining the effectiveness of the GVL response. The characterization of antigens restricted to leukemia and hematopoietic tissues should make it eventually possible to produce specific and powerful antileukemic alloresponses in donor lymphocytes by adoptive immunotherapy or by vaccines.
RP Barrett, AJ (reprint author), NHLBI,BMT UNIT,HEMATOL BRANCH,NIH,BLDG 10,ROOM 7C 103,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 106
TC 67
Z9 71
U1 0
U2 2
PU ALPHAMED PRESS
PI DAYTON
PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
IS 4
BP 248
EP 258
PG 11
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA XM463
UT WOS:A1997XM46300001
PM 9253108
ER
PT J
AU Sharkis, SJ
Moore, MAS
Lansdorp, PM
Eaves, C
TorokStorb, B
Broxmeyer, HE
Adamson, JW
Spangrude, GJ
Griffin, JD
Papayannopoulou, T
Ogawa, M
Orlic, D
Kanz, L
AF Sharkis, SJ
Moore, MAS
Lansdorp, PM
Eaves, C
TorokStorb, B
Broxmeyer, HE
Adamson, JW
Spangrude, GJ
Griffin, JD
Papayannopoulou, T
Ogawa, M
Orlic, D
Kanz, L
TI Stem cell proliferation: Ex vivo and in vivo observations - Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 SLOAN KETTERING INST CANC RES, NEW YORK, NY 10021 USA.
TERRY FOX LAB, VANCOUVER, BC V5Z 1L3, CANADA.
FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA.
INDIANA UNIV, SCH MED, WALTHER ONCOL CTR, DEPT IMMUNOL & MICROBIOL, INDIANAPOLIS, IN 46202 USA.
NEW YORK BLOOD CTR, NEW YORK, NY 10021 USA.
UNIV UTAH, SALT LAKE CITY, UT USA.
DANA FARBER CANC INST, DIV HEMATOL MALIGNANCIES, BOSTON, MA 02115 USA.
UNIV WASHINGTON, SEATTLE, WA 98195 USA.
VET ADM MED CTR, CHARLESTON, SC 29401 USA.
NIH, NCHGR, LAB GENE TRANSFER, BETHESDA, MD 20892 USA.
UNIV TUBINGEN, DEPT HEMATOL, D-72076 TUBINGEN, GERMANY.
RP JOHNS HOPKINS UNIV, CTR ONCOL, 600 N WOLFE ST, BALTIMORE, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 248
EP 251
PG 4
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100057
ER
PT J
AU Nienhuis, A
Moore, MAS
Dick, JE
Stamatoyannopoulos, G
Lemischka, IR
TorokStorb, B
Spangrude, GJ
Papayannopoulou, T
Flugel, RM
Orlic, D
Broxmeyer, HE
Quesenberry, PJ
Sharkis, SJ
Lansdorp, PM
AF Nienhuis, A
Moore, MAS
Dick, JE
Stamatoyannopoulos, G
Lemischka, IR
TorokStorb, B
Spangrude, GJ
Papayannopoulou, T
Flugel, RM
Orlic, D
Broxmeyer, HE
Quesenberry, PJ
Sharkis, SJ
Lansdorp, PM
TI What are the current limitations for HSC transduction? How can we
overcome them? Discussion
SO STEM CELLS
LA English
DT Editorial Material
C1 SLOAN KETTERING INST CANC RES, NEW YORK, NY 10021 USA.
UNIV TORONTO, HOSP SICK CHILDREN, RES INST, DEPT GENET, TORONTO, ON M5G 1X8, CANADA.
UNIV WASHINGTON, DIV MED GENET, SEATTLE, WA 98195 USA.
PRINCETON UNIV, DEPT MOL BIOL, PRINCETON, NJ 08544 USA.
FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA.
UNIV UTAH, SALT LAKE CITY, UT 84132 USA.
DFKZ, INF 242, FORSCH SCHEWERPUNKT ANGEW TUMORVIROL, ABT RETROVIRALE GENEXPRESSION, D-69009 HEIDELBERG, GERMANY.
NIH, NCHGR, LAB GENE TRANSFER, BETHESDA, MD 20892 USA.
INDIANA UNIV, SCH MED, WALTHER ONCOL CTR, DEPT IMMUNOL & MICROBIOL, INDIANAPOLIS, IN 46202 USA.
UNIV MASSACHUSETTS, MED CTR, CTR CANC, WORCESTER, MA 01605 USA.
TERRY FOX LAB, VANCOUVER, BC V5Z 1L3, CANADA.
JOHNS HOPKINS UNIV, CTR ONCOL, BALTIMORE, MD 21287 USA.
RP ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, DIV EXPT HEMATOL, 332 N LAUDERDALE ST, MEMPHIS, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 255
EP 263
PG 9
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100058
PM 9368349
ER
PT J
AU Orlic, D
Sharkis, SJ
AF Orlic, D
Sharkis, SJ
TI The elusive stem cell: How close are we?
SO STEM CELLS
LA English
DT Editorial Material
C1 JOHNS HOPKINS UNIV, CTR ONCOL, BALTIMORE, MD 21287 USA.
RP NIH, LAB GENE TRANSFER,NCHGR,BLDG 49,ROOM 3A14, 49 CONVENT DR, MSC 4442, BETHESDA, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PY 1997
VL 15
SU 2
BP 283
EP 284
PG 2
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA YF081
UT WOS:A1997YF08100061
ER
PT J
AU Dufau, ML
Miyagawa, Y
Takada, S
Khanum, A
Miyagawa, H
Buczko, E
AF Dufau, ML
Miyagawa, Y
Takada, S
Khanum, A
Miyagawa, H
Buczko, E
TI Regulation of androgen synthesis: The late steroidogenic pathway
SO STEROIDS
LA English
DT Article; Proceedings Paper
CT 2nd International Symposium on Molecular Steroidogenesis
CY JUN 08-11, 1996
CL OFFICE CONTINUING MED EDUC, SAN FRANCISCO, CA
SP UCSF Dept Pediat
HO OFFICE CONTINUING MED EDUC
DE 17 beta-HSD; P450 17 alpha-hydroxylase; CYP17; P450c17; testosterone
ID SITE-DIRECTED MUTAGENESIS; 17-ALPHA-HYDROXYLASE/17,20 LYASE;
TRANSCRIPTIONAL REGULATION; CYTOCHROME P-45017-ALPHA; RAT P45017-ALPHA;
ACTIVE-SITE; GENE; CYP17; EXPRESSION; SEQUENCE
AB Studies of the regulation of androgen synthesis in steroidogenic cells have focused on both transcriptional and post-translational regulation of the proteins that catalyze these reactions: the P450c17 that catalyzed the production of DHEA or androstenedione in consecutive hydroxylase and lyase activities, and the 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) that catalyzes the conversion of androstenedione to testosterone. Our studies of the regulation of the CYP17 lyase activity at the molecular level have utilized species-and tissue-specific differences to identify target regulatory sequences. Adenovirus infection of rat CYP17 promoter/luciferase reporter gene constructs in primary cultures of rat adrenal and rat Leydig cells revealed a rat-specific domain between-1 and -108bp that cause inhibition of both basal and cAMP-induced CYP17 transcription in the adrenal, but not the Leydig cell. In contrast, similar promoter constructs from other species exhibited substantial cAMP-induced transcriptional activity in the rat adrenal. Mutagenesis of the conserved region of the rat and human proteins reveals significant differences in the amino acid domains required for hydroxylase and lyase activities within and between the two species, consistent with their differential regulation of lyase activity. The 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) reaction requires a viable glucose transporter system for optimal activity, and a high-energy phosphate was discovered to be the requisite product of glucose metabolism in 17 beta-HSD activation. These studies have provided insight into potential mechanisms of control of androgen synthesis in the late steroidogenic pathway, at the transcriptional and post-translational levels. (C) 1997 by Elsevier Science Inc.
RP Dufau, ML (reprint author), NICHHD,NIH,ENDOCRINOL & REPROD RES BRANCH,SECT MOL ENDOCRINOL,BETHESDA,MD 20892, USA.
NR 23
TC 12
Z9 14
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0039-128X
J9 STEROIDS
JI Steroids
PD JAN
PY 1997
VL 62
IS 1
BP 128
EP 132
DI 10.1016/S0039-128X(96)00171-7
PG 5
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA WF577
UT WOS:A1997WF57700021
PM 9029727
ER
PT B
AU Long, LR
Ostchega, Y
Goh, GH
Thoma, GR
AF Long, LR
Ostchega, Y
Goh, GH
Thoma, GR
BE Sethi, IK
Jain, RC
TI Distributed data collection for a database of radiological image
interpretations
SO STORAGE AND RETRIEVAL FOR IMAGE AND VIDEO DATABASES V
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on Storage and Retrieval for Image and Video Databases V
CY FEB 13-14, 1997
CL SAN JOSE, CA
SP Soc Imaging Sci & Technol, Soc Photo Opt Instrumentat Engineers
DE radiographs; digital xray; client/server; National Library of Medicine;
DBMS; Internet DBMS
AB The National Library of Medicine, in collaboration with the National Center for Health Statistics and the National Institute for Arthritis and Musculoskeletal and Skin Diseases, has built a system for collecting radiological interpretations for a large set of x-ray images acquired as part of the data gathered in the second National Health and Nutrition Examination Survey. This system is capable of delivering across the Internet 5- and 10-megabyte x-ray images to Sun workstations equipped with X Window based 2048x2560 image displays, for the purpose of having these images interpreted for the degree of presence of particular osteoarthritic conditions in the cervical and lumbar spines. The collected interpretations can then be stored in a database at the National Library of Medicine, under control of the Illustra DBMS. This system is a client/server database application which integrates (1) distributed server processing of client requests, (2) a customized image transmission method for faster Internet data delivery, (3) distributed client workstations with high resolution displays, image processing functions and an on-line digital atlas, and (4) relational database management of the collected data.
RP Long, LR (reprint author), NATL LIB MED,BETHESDA,MD 20209, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2433-1
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3022
BP 228
EP 237
DI 10.1117/12.263412
PG 2
WC Computer Science, Information Systems; Computer Science, Software
Engineering; Optics
SC Computer Science; Optics
GA BH07C
UT WOS:A1997BH07C00021
ER
PT S
AU Long, LR
Pillemer, SR
Lawrence, RC
Goh, GH
Neve, L
Thoma, GR
AF Long, LR
Pillemer, SR
Lawrence, RC
Goh, GH
Neve, L
Thoma, GR
BE Sethi, IK
Jain, RC
TI WebMIRS: Web-based Medical Information Retrieval System
SO STORAGE AND RETRIEVAL FOR IMAGE AND VIDEO DATABASES VI
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Storage and Retrieval for Image and Video Databases VI Conference
CY JAN 28-30, 1998
CL SAN JOSE, CA
SP Soc Photo Opt Instrumentat Engineers, Soc Imaging Sci & Technol
DE World Wide Web; biomedical; informatics; Internet; database; spine;
digital image; morphometry; x-ray image; image query by content; NHANES;
NLM
AB At the Lister Hill National Center for Biomedical Communications, a research and development division of the National Library of Medicine (NLM), we are developing a prototype multimedia database system to provide World Wide Web access to biomedical databases. WebMIRS (Web-based Medical Information Retrieval System) will allow access to databases containing text and images and will allow database query by standard SQL, by image content, or by a combination of the two. The system is being developed in the form of Java applets, which will communicate with the Informix DBMS on an NLM Sun workstation running the Solaris operating system. The system architecture will allow access from any hardware platform, which supports a Java-enabled Web browser, such as Netscape or Internet Explorer. Initial databases will include data from two national health surveys conducted by the National Center for Health Statistics (NCHS), and will include x-ray images from those surveys. In addition to describing in-house research in database access systems, this paper describes ongoing work toward querying by image content. Image content search capability will include capability to search for x-ray images similar to an input image with respect to vertebral morphometry used to characterize features such as fractures and disc space narrowing.
C1 Natl Lib Med, Bethesda, MD 20894 USA.
RP Long, LR (reprint author), Natl Lib Med, Bethesda, MD 20894 USA.
NR 0
TC 5
Z9 5
U1 0
U2 0
PU SPIE-INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA
SN 0277-786X
BN 0-8194-2752-7
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3312
BP 392
EP 403
DI 10.1117/12.298448
PG 12
WC Computer Science, Information Systems; Engineering, Electrical &
Electronic; Optics
SC Computer Science; Engineering; Optics
GA BK26B
UT WOS:000071633300035
ER
PT S
AU Garvey, MA
Swedo, SE
AF Garvey, MA
Swedo, SE
BE Horaud, T
Bouvet, A
Leclercq, R
deMontclos, H
Sicard, M
TI Sydenham's chorea - Clinical and therapeutic update
SO STREPTOCOCCI AND THE HOST
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT XIII Lancefield International Symposium on Streptococci and
Streptococcal Diseases
CY SEP 16-20, 1996
CL INST PASTEUR, PARIS, FRANCE
SP Inst Pasteur, Abbott Labs, Assoc Enseignement Odontol & Stomatol, bioMerieux, Bristol Meyers Squibb Co, CNRS, Federat European Microbiol Soc, Fdn Marcel Merieux, GenProbe, Grp Danone, Inst Sci Roussel, Int Lancefield Soc, Int Sci Fdn, Pasteur Merieux MSD, Pharmacia & Upjohn, Rhone Poulenc Rorer, Rhone Poulene Rorer, Ctr Rech Vitry Alfortville, France, Rhone Poulenc Rorer Bellon, France, Rhone Poulenc Rorer Specia, France, Sanofi Diagnost Pasteur, France, SmithKline Beecham Labs Pharm, France, Wyeth Ayerst, Lederle Int, US, Yamanouchi Pharm, Japan
HO INST PASTEUR
ID SYMPTOMS
RP Garvey, MA (reprint author), NIMH, CHILD PSYCHIAT BRANCH, BEHAV PEDIAT SECT, NIH, BLDG 10, BETHESDA, MD 20892 USA.
NR 17
TC 28
Z9 28
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45603-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 418
BP 115
EP 120
PG 6
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology
GA BJ94C
UT WOS:A1997BJ94C00028
PM 9331612
ER
PT S
AU Andersen, RN
Lunsford, RD
Kolenbrander, PE
AF Andersen, RN
Lunsford, RD
Kolenbrander, PE
BE Horaud, T
Bouvet, A
Leclercq, R
deMontclos, H
Sicard, M
TI Determination of the transcript size and start site of the putative sca
operon of Streptococcus gordonii ATCC 51656 (formerly strain PK488)
SO STREPTOCOCCI AND THE HOST
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT XIII Lancefield International Symposium on Streptococci and
Streptococcal Diseases
CY SEP 16-20, 1996
CL INST PASTEUR, PARIS, FRANCE
SP Inst Pasteur, Abbott Labs, Assoc Enseignement Odontol & Stomatol, bioMerieux, Bristol Meyers Squibb Co, CNRS, Federat European Microbiol Soc, Fdn Marcel Merieux, GenProbe, Grp Danone, Inst Sci Roussel, Int Lancefield Soc, Int Sci Fdn, Pasteur Merieux MSD, Pharmacia & Upjohn, Rhone Poulenc Rorer, Rhone Poulene Rorer, Ctr Rech Vitry Alfortville, France, Rhone Poulenc Rorer Bellon, France, Rhone Poulenc Rorer Specia, France, Sanofi Diagnost Pasteur, France, SmithKline Beecham Labs Pharm, France, Wyeth Ayerst, Lederle Int, US, Yamanouchi Pharm, Japan
HO INST PASTEUR
ID ACTINOMYCES-NAESLUNDII PK606; NUCLEOTIDE-SEQUENCE; ORAL STREPTOCOCCI;
COAGGREGATION; CLONING; ADHESIN; GENE
RP Andersen, RN (reprint author), NIDR, NIH, BLDG 30, ROOM 310, 30 CONVENT DR MSC 4350, BETHESDA, MD 20892 USA.
NR 9
TC 5
Z9 5
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45603-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 418
BP 657
EP 660
PG 4
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology
GA BJ94C
UT WOS:A1997BJ94C00153
PM 9331737
ER
PT S
AU Whittaker, CJ
Kolenbrander, PE
AF Whittaker, CJ
Kolenbrander, PE
BE Horaud, T
Bouvet, A
Leclercq, R
deMontclos, H
Sicard, M
TI Identification and further characterization of a locus coding for a
hypothetical 33.6-kDa protein involved in intrageneric coaggregation of
oral streptococci
SO STREPTOCOCCI AND THE HOST
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT XIII Lancefield International Symposium on Streptococci and
Streptococcal Diseases
CY SEP 16-20, 1996
CL INST PASTEUR, PARIS, FRANCE
SP Inst Pasteur, Abbott Labs, Assoc Enseignement Odontol & Stomatol, bioMerieux, Bristol Meyers Squibb Co, CNRS, Federat European Microbiol Soc, Fdn Marcel Merieux, GenProbe, Grp Danone, Inst Sci Roussel, Int Lancefield Soc, Int Sci Fdn, Pasteur Merieux MSD, Pharmacia & Upjohn, Rhone Poulenc Rorer, Rhone Poulene Rorer, Ctr Rech Vitry Alfortville, France, Rhone Poulenc Rorer Bellon, France, Rhone Poulenc Rorer Specia, France, Sanofi Diagnost Pasteur, France, SmithKline Beecham Labs Pharm, France, Wyeth Ayerst, Lederle Int, US, Yamanouchi Pharm, Japan
HO INST PASTEUR
ID CHALLIS
RP Whittaker, CJ (reprint author), NIDR, NIH, BLDG 30, ROOM 312, 30 CONVENT DR MSC 4350, BETHESDA, MD 20892 USA.
NR 3
TC 2
Z9 2
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45603-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 418
BP 695
EP 698
PG 4
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology
GA BJ94C
UT WOS:A1997BJ94C00162
PM 9331746
ER
PT S
AU Mittleman, BB
AF Mittleman, BB
BE Horaud, T
Bouvet, A
Leclercq, R
deMontclos, H
Sicard, M
TI Cytokine networks in Sydenham's chorea and pandas
SO STREPTOCOCCI AND THE HOST
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT XIII Lancefield International Symposium on Streptococci and
Streptococcal Diseases
CY SEP 16-20, 1996
CL INST PASTEUR, PARIS, FRANCE
SP Inst Pasteur, Abbott Labs, Assoc Enseignement Odontol & Stomatol, bioMerieux, Bristol Meyers Squibb Co, CNRS, Federat European Microbiol Soc, Fdn Marcel Merieux, GenProbe, Grp Danone, Inst Sci Roussel, Int Lancefield Soc, Int Sci Fdn, Pasteur Merieux MSD, Pharmacia & Upjohn, Rhone Poulenc Rorer, Rhone Poulene Rorer, Ctr Rech Vitry Alfortville, France, Rhone Poulenc Rorer Bellon, France, Rhone Poulenc Rorer Specia, France, Sanofi Diagnost Pasteur, France, SmithKline Beecham Labs Pharm, France, Wyeth Ayerst, Lederle Int, US, Yamanouchi Pharm, Japan
HO INST PASTEUR
ID DYSFUNCTION; CELLS
RP Mittleman, BB (reprint author), NIMH, CHILD PSYCHIAT BRANCH, BEHAV PEDIAT SECT, BLDG 10, ROOM 4N312, BETHESDA, MD 20892 USA.
NR 11
TC 10
Z9 10
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-45603-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 1997
VL 418
BP 933
EP 935
PG 3
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology
GA BJ94C
UT WOS:A1997BJ94C00219
PM 9331803
ER
PT J
AU Becker, KJ
McCarron, RM
Hallenbeck, JM
AF Becker, KJ
McCarron, RM
Hallenbeck, JM
TI Oral tolerance to myelin basic protein decreases stroke size
SO STROKE
LA English
DT Meeting Abstract
C1 NIH,STROKE BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 1997
VL 28
IS 1
BP 72
EP 72
PG 1
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA WB814
UT WOS:A1997WB81400123
ER
PT J
AU Bhardwaj, A
Kirsch, JR
Koehler, RC
London, ED
Traystman, RJ
AF Bhardwaj, A
Kirsch, JR
Koehler, RC
London, ED
Traystman, RJ
TI The sigma ligand (+)-pentazocine attenuates N-methyl-D-aspartate
enhanced striatal nitric oxide production in vivo
SO STROKE
LA English
DT Meeting Abstract
C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD.
NIDA,BALTIMORE,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 1997
VL 28
IS 1
BP 125
EP 125
PG 1
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA WB814
UT WOS:A1997WB81400176
ER
PT J
AU Yasuma, Y
McCarron, RM
Strasser, A
Spatz, M
AF Yasuma, Y
McCarron, RM
Strasser, A
Spatz, M
TI The role of ET receptors in postischemic cerebral hypoperfusion
SO STROKE
LA English
DT Meeting Abstract
C1 NINCDS,STROKE BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 1997
VL 28
IS 1
BP 135
EP 135
PG 1
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA WB814
UT WOS:A1997WB81400186
ER
PT J
AU Leshner, AI
AF Leshner, AI
TI Comments on ''Perspective on the integration of substance user needs
assessment and treatment planning,'' by William E. Ford
SO SUBSTANCE USE & MISUSE
LA English
DT Editorial Material
ID SERVICES; ABUSE
RP Leshner, AI (reprint author), NATL INST DRUG ABUSE,5600 FISHERS LANE,ROOM 10-05,ROCKVILLE,MD 20857, USA.
NR 13
TC 1
Z9 1
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 1082-6084
J9 SUBST USE MISUSE
JI Subst. Use Misuse
PY 1997
VL 32
IS 3
BP 351
EP 357
DI 10.3109/10826089709055855
PG 7
WC Substance Abuse; Psychiatry; Psychology
SC Substance Abuse; Psychiatry; Psychology
GA WK835
UT WOS:A1997WK83500008
ER
PT J
AU Gordis, E
AF Gordis, E
TI Comments on ''Perspective on the integration of substance user needs
assessment and treatment planning,'' by William E. Ford
SO SUBSTANCE USE & MISUSE
LA English
DT Editorial Material
RP Gordis, E (reprint author), NIAAA,6000 EXECUT BLVD,BETHESDA,MD 20892, USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 1082-6084
J9 SUBST USE MISUSE
JI Subst. Use Misuse
PY 1997
VL 32
IS 3
BP 359
EP 360
DI 10.3109/10826089709055856
PG 2
WC Substance Abuse; Psychiatry; Psychology
SC Substance Abuse; Psychiatry; Psychology
GA WK835
UT WOS:A1997WK83500009
ER
PT J
AU Leshner, AI
AF Leshner, AI
TI Understanding and preventing drug abuse
SO SUBSTANCE USE & MISUSE
LA English
DT Editorial Material
DE drug use; policy; etiology; prevention; treatment; psychopathology;
behavior problems
AB The National Institute on Drug Abuse (NIDA) is the lead Federal agency responsible for monitoring the nature and extent of drug abuse in the United States. NIDA engages in research on the etiology of drug use and supports state-of-the-art research to develop prevention and treatment methods. NIDA's etiology research has played a crucial role not only in helping to understand the origins and development of substance abuse, psychopathologies, and other mental health and behavioral problems, but also has contributed significantly to effective prevention and treatment.
RP Leshner, AI (reprint author), NIDA,5600 FISHERS LANE,PARKLAWN BLDG,ROOM 10-05,ROCKVILLE,MD 20857, USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 1082-6084
J9 SUBST USE MISUSE
JI Subst. Use Misuse
PY 1997
VL 32
IS 12-13
BP 1619
EP 1624
DI 10.3109/10826089709035554
PG 6
WC Substance Abuse; Psychiatry; Psychology
SC Substance Abuse; Psychiatry; Psychology
GA YF362
UT WOS:A1997YF36200001
ER
PT J
AU Liu, QY
Vautrin, J
Schaffner, AE
Ma, W
Barker, JL
AF Liu, QY
Vautrin, J
Schaffner, AE
Ma, W
Barker, JL
TI GABA induces GABAergic MSCs in cultured embryonic rat thalamic neurons
SO SYNAPSE
LA English
DT Article
DE GABA(A) receptors; thalamus; neurotransmission; neuronal development;
synapse
ID CA3 HIPPOCAMPAL-NEURONS; EARLY POSTNATAL LIFE; DORSAL HORN NEURONS;
SPINAL-CORD; EXCITATORY TRANSMITTER; GRANULE CELLS; VISUAL-CORTEX;
CURRENTS; GLYCINE; DEPOLARIZATION
AB Application of 0.1-10 mu M GABA in the vicinity of cultured embryonic rat thalamic neurons recorded with patch pipettes in the presence of 2 mu M TTX induced or increased the frequency of miniature synaptic currents (MSCs) that reversed polarity at the Cl- equilibrium potential. These MSCs were blocked by the GABA(A) receptor antagonist bicuculline and exhibited exponential decay kinetics that closely paralleled those estimated from fluctuation analysis of Cl- channels activated pharmacologically by applying 1-10 mu M GABA to the same cells. We conclude that the MSCs are mediated by GABA. Application of the GABA(A) receptor agonist muscimol activated Cl- current but failed to induce GABAergic MSCs while submicromolar concentrations of GABA evoked GABAergic MSCs but did not activate Cl- channels. The GABA(B) receptor agonist (-)baclofen did not mimic GABA in inducing MSCs. Induction of GABAergic MSCs by GABA required extracellular Ca2+. Verapamil and Co2+, which block voltage-dependent calcium channels, completely blocked GABA-induced MSCs independent of their effects on the direct activation of a Cl- current response. The results indicate that GABA can trigger GABAergic Cl--dependent MSCs in a Ca-o(2+)-dependent manner. The mechanism may involve a novel receptor and/or signal transduction pathway. (C) 1997 Wiley-Liss, Inc.*
RP Liu, QY (reprint author), NINCDS,NEUROPHYSIOL LAB,NIH,BLDG 36,RM 2C02,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 30
TC 5
Z9 5
U1 1
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0887-4476
J9 SYNAPSE
JI Synapse
PD JAN
PY 1997
VL 25
IS 1
BP 15
EP 23
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA VZ866
UT WOS:A1997VZ86600002
PM 8987143
ER
PT B
AU Chertova, E
Kane, BP
Coren, LV
Johnson, DG
Sowder, RC
Nower, P
CasasFinet, JR
Arthur, LO
Henderson, LE
AF Chertova, E
Kane, BP
Coren, LV
Johnson, DG
Sowder, RC
Nower, P
CasasFinet, JR
Arthur, LO
Henderson, LE
BE Marshak, DR
TI Reaction of HIV-1 NC p7 zinc fingers with electrophilic reagents
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP Chertova, E (reprint author), NCI,SAIC,FCRDC,FREDERICK,MD 21702, USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 231
EP 244
DI 10.1016/S1080-8914(97)80025-7
PG 14
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00022
ER
PT B
AU Alexandratos, J
Bujacz, G
Jaskolski, M
Wlodawer, A
Merkel, G
Katz, RA
Skalka, AM
AF Alexandratos, J
Bujacz, G
Jaskolski, M
Wlodawer, A
Merkel, G
Katz, RA
Skalka, AM
BE Marshak, DR
TI Crystal structure of avian sarcoma virus integrase with bound essential
cations
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP Alexandratos, J (reprint author), NCI,MACROMOL STRUCT LAB,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 417
EP 425
DI 10.1016/S1080-8914(97)80042-7
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00039
ER
PT B
AU SchalkHihi, C
Lubkowski, J
Zdanov, A
Wlodawer, A
Gustchina, A
Laco, GS
Elder, JH
AF SchalkHihi, C
Lubkowski, J
Zdanov, A
Wlodawer, A
Gustchina, A
Laco, GS
Elder, JH
BE Marshak, DR
TI Structure of the D30N active site mutant of FIV proteinase complexed
with a statine-based inhibitor
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP SchalkHihi, C (reprint author), NCI,MACROMOL STRUCT LAB,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 643
EP 654
DI 10.1016/S1080-8914(97)80064-6
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00061
ER
PT B
AU Geetha, V
Munson, PJ
AF Geetha, V
Munson, PJ
BE Marshak, DR
TI Analysis of linkers of regular secondary structures in proteins
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP Geetha, V (reprint author), NIH,ANALYT BIOSTAT SECT,STRUCT BIOL LAB,DCRT,BLDG 10,BETHESDA,MD 20892, USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 667
EP 677
DI 10.1016/S1080-8914(97)80066-X
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00063
ER
PT B
AU Thompson, PA
AF Thompson, PA
BE Marshak, DR
TI Laser temperature jump for the study of early events in protein folding
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP Thompson, PA (reprint author), NIDDK,PHYS CHEM LAB,NATL INST HLTH,BETHESDA,MD 20892, USA.
NR 0
TC 6
Z9 6
U1 0
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 735
EP 743
DI 10.1016/S1080-8914(97)80072-5
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00069
ER
PT B
AU Sergeev, YV
Hejtmancik, JF
AF Sergeev, YV
Hejtmancik, JF
BE Marshak, DR
TI A method for determining domain binding sites in proteins with swapped
domains: implications for beta A3- and beta B2-crystallins
SO TECHNIQUES IN PROTEIN CHEMISTRY VIII
SE TECHNIQUES IN PROTEIN CHEMISTRY (ACADEMIC PRESS INC)
LA English
DT Proceedings Paper
CT 10th Symposium of the Protein-Society
CY AUG 03-07, 1996
CL SAN JOSE, CA
SP Protein Soc, Aviv Instruments Inc, Beckman Instruments Inc, BioMolecular Technol Inc, BIOSYM Molec Simulat, Bristol Myers Squibb, Finnigan MAT, Fisons Instruments, Hewlett Packard Co, IntelliGenetics Inc, JASCO Inc, Kirin Brewery Co Ltd, Michrom BioResources Inc, Molec Simulat Inc, Perkin Elmer Corp, Appl Biosyst Div, PerSept Biosyst Inc, Pharm Biotech Inc, Rainin Instrument Co Inc, Schering Plough Res Inst, Shimadzu Sci Instruments Inc, Supelco Inc, VYDAC, Waters Corp, Wyatt Technol Corp, ZymoGenetics
RP Sergeev, YV (reprint author), NEI,NATL INST HLTH,BETHESDA,MD 20892, USA.
NR 0
TC 5
Z9 5
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
BN 0-12-473557-6
J9 TECH PROT CHEM
PY 1997
VL 8
BP 817
EP 826
DI 10.1016/S1080-8914(97)80079-8
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology
GA BJ32Y
UT WOS:A1997BJ32Y00076
ER
PT B
AU Altschul, SE
AF Altschul, SE
BE Suhai, S
TI Evaluating the statistical significance of multiple distinct local
alignments
SO THEORETICAL AND COMPUTATIONAL METHODS IN GENOME RESEARCH
LA English
DT Proceedings Paper
CT International Symposium on Theoretical and Computational Genome Research
CY MAR 24-27, 1996
CL HEIDELBERG, GERMANY
SP Commiss European Communities
AB A comparison of two sequences may uncover multiple regions of local similarity. While the significance of each local alignment may be evaluated independently, sometimes a combined assessment is appropriate. This paper discusses a variety of statistical and algorithmic issues that such an assessment presents.
RP Altschul, SE (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,NATL INST HLTH,BETHESDA,MD 20894, USA.
NR 0
TC 44
Z9 45
U1 0
U2 0
PU PLENUM PRESS DIV PLENUM PUBLISHING CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
BN 0-306-45503-X
PY 1997
BP 1
EP 14
PG 14
WC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology; Computer Science, Interdisciplinary Applications; Genetics
& Heredity
SC Biochemistry & Molecular Biology; Biophysics; Biotechnology & Applied
Microbiology; Computer Science; Genetics & Heredity
GA BJ19F
UT WOS:A1997BJ19F00001
ER
PT S
AU Talan, M
AF Talan, M
BE Blatteis, CM
TI Age-related changes in thermoregulation of mice
SO THERMOREGULATION: TENTH INTERNATIONAL SYMPOSIUM ON THE PHARMACOLOGY OF
THERMOREGULATION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 10th International Symposium on Thermoregulation
CY AUG 17-22, 1996
CL MEMPHIS, TENNESSEE
SP New York Acad Sci, Mini Mitter Co Inc, Data Sci Int, Augustine Med Inc, Int Sci Fdn, Int Union Physiol Sci, IUPS Commiss Thermal Physiol, Univ Tennessee, Memphis, Dept Physiol & Biophys
ID BROWN ADIPOSE-TISSUE; SYMPATHETIC NERVOUS ACTIVITY; UNCOUPLING PROTEIN;
C57BL/6J MICE; GDP BINDING; COLD STRESS; OLD RATS; THERMOGENESIS;
EXPRESSION
C1 NIA, Gerontol Res Ctr, Behav Sci Lab, Baltimore, MD 21224 USA.
RP Talan, M (reprint author), NIA, Gerontol Res Ctr, Behav Sci Lab, 4940 Eastern Ave, Baltimore, MD 21224 USA.
NR 21
TC 4
Z9 4
U1 0
U2 1
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-088-3
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 813
BP 95
EP 100
DI 10.1111/j.1749-6632.1997.tb51678.x
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA BM49A
UT WOS:000078895700014
PM 9100868
ER
PT J
AU Merryman, P
Tannenbaum, SH
Gralnick, HR
Yu, K
Arnold, WS
Alexander, HR
Fraker, D
Horne, MK
AF Merryman, P
Tannenbaum, SH
Gralnick, HR
Yu, K
Arnold, WS
Alexander, HR
Fraker, D
Horne, MK
TI Fibrinolytic and coagulant responses to regional limb perfusions of
tumor necrosis factor, interferon-gamma, and/or melphalan
SO THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
ID PLASMINOGEN-ACTIVATOR INHIBITOR; ENDOTHELIAL-CELLS; CARDIOPULMONARY
BYPASS; VASCULAR ENDOTHELIUM; CYTOKINE ACTIVATION; FACTOR INFUSIONS;
CARDIAC-SURGERY; PLASMA; PAI-1; DEGRADATION
AB Regional limb perfusion with antineoplastic agents stresses the local vasculature in a variety of ways. However, by monitoring the perfusates from limbs treated with melphalan alone or with melphalan plus tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma), we were able to distinguish the effect of the cytokines on the observed coagulant and fibrinolytic responses. We collected samples of effluent from a series of lower extremities that were perfused with the cytokines and/or melphalan as treatment for localized melanoma. Both regimens produced statistically significant evidence of coagulant and fibrinolytic activation. However, limbs receiving cytokines in addition to the melphalan responded with a sharper rise in tissue plasminogen activator (tPA) and plasmin (plasmin-antiplasmin complexes [PAP]) than limbs treated with melphalan alone. Evidence of thrombin formation (prothrombin fragment 1+2 [F1+2], thrombin-antithrombin complexes [TAT]) was also greater when the cytokines were included, although the response was delayed and less consistent than the fibrinolytic activation.
C1 NCI,HEMATOL SECT,DEPT CLIN PATHOL,WARREN G MAGNUSON CLIN CTR,NIH,BETHESDA,MD 20892.
NCI,SURG BRANCH,NIH,BETHESDA,MD 20892.
NR 29
TC 6
Z9 6
U1 0
U2 0
PU F K SCHATTAUER VERLAG GMBH
PI STUTTGART
PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY
SN 0340-6245
J9 THROMB HAEMOSTASIS
JI Thromb. Haemost.
PD JAN
PY 1997
VL 77
IS 1
BP 53
EP 56
PG 4
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA WE554
UT WOS:A1997WE55400010
PM 9031449
ER
PT J
AU Waalkes, MP
Rehm, S
Devor, DE
AF Waalkes, MP
Rehm, S
Devor, DE
TI The effects of continuous testosterone exposure on spontaneous and
cadmium-induced tumors in the male Fischer (F344/NCr) rat: Loss of
testicular response
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT 35th Annual Meeting of the Society-of-Toxicology
CY MAR 10-14, 1996
CL ANAHEIM, CA
SP Soc Toxicol
ID LEYDIG-CELL TUMORIGENESIS; MECHANISM; CHLORIDE; INVITRO; SYSTEM; CANCER
AB In the rodent testes, cadmium induces severe necrosis followed by chronic degeneration. Cadmium is also an effective testicular tumorigen, and a single dose produces a high incidence of Leydig cell tumors. The mechanism of tumor formation is unknown, but pituitary feedback, i.e., increased luteinizing hormone (LH) production due to low circulating androgen, has been implicated in causation of proliferative lesions within degenerate, hypofunctioning testes. Thus, the effects of androgen replacement on the testicular toxicity of cadmium in Fischer (F344/NCr) rats was studied. Groups (n = 50) of 10-week-old rats either received testosterone implants that approximate normal circulating levels in castrated rats or were left untreated. After 2 weeks of stabilization, rats were given either 20 mu mol CdCl2/kg, sc, weekly for the next 5 weeks (total dose 100 mu mol/kg) or saline for a total of four treatment groups (control, testosterone alone, testosterone + cadmium, or cadmium alone). Portions of each group were killed either 10 weeks after initiation of cadmium exposure (n = 10), for assessment of endocrine function, or over the next 2 years (n = 40), for assessment of testicular neoplastic lesions. At 10 weeks, cadmium reduced circulating testosterone in nonimplanted rats by nearly 80% and induced a marked weight loss of the testes (>70%) and sex accessory glands (reflected in a 50% reduction in prostate mass). Testosterone implantation restored circulating testosterone levels in cadmium-treated rats and prevented Cd-induced weight loss of the sex accessory glands but not of the testes. Over 2 years, cadmium alone induced a >84% incidence of Leydig cell neoplasia and a >97% incidence of chronic degeneration, both significant increases over control rates (60 and 0%, respectively). Testosterone implantation abolished both cadmium-induced and spontaneously occurring Leydig cell tumors but had no effect on cadmium-induced chronic testicular degeneration. Thus cadmium-induced hypofunction of the testes, and subsequent loss of circulating testesterone, appears to be a critical aspect in cadmium induction of tumors in the rat testes. (C) 1997 Academic Press.
RP Waalkes, MP (reprint author), NCI,INORGAN CARCINOGENESIS SECT,COMPARAT CARCINOGENESIS LAB,DIV BASIC SCI,FREDERICK,MD 21702, USA.
NR 36
TC 37
Z9 43
U1 1
U2 5
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JAN
PY 1997
VL 142
IS 1
BP 40
EP 46
DI 10.1006/taap.1996.8005
PG 7
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA WD570
UT WOS:A1997WD57000005
PM 9007032
ER
PT J
AU Valentine, WM
Amarnath, V
Graham, DG
Morgan, DL
Sills, RC
AF Valentine, WM
Amarnath, V
Graham, DG
Morgan, DL
Sills, RC
TI CS2-mediated cross-linking of erythrocyte spectrin and neurofilament
protein: Dose response and temporal relationship to the formation of
axonal swellings
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT 35th Annual Meeting of the Society-of-Toxicology
CY MAR 10-14, 1996
CL ANAHEIM, CA
SP Soc Toxicol
ID CARBON-DISULFIDE NEUROTOXICITY; 2,5-HEXANEDIONE INTOXICATION;
3,4-DIMETHYL SUBSTITUTION; PYRROLE FORMATION; NERVOUS-SYSTEM; EXPOSURE;
TRANSPORT; NEUROPATHY; RATS; DEGENERATION
AB Using model proteins, a mechanism for CS2-mediated covalent cross-linking of proteins has been demonstrated previously, The biologic importance of CS2-promoted protein cross-linking is apparent as a possible dosimeter of CS2 exposure and as a potential mechanism to account for the identical neuropathies produced by 2,5-hexanedione and CS2. The present investigation examines the utility of erythrocyte spectrin cross-linking as a biomarker of effect for inhalation exposure to CS2 and examines the ability of CS2 to cross-link neurofilament proteins, a potential neurotoxic target. Rats were exposed to CS2 via inhalation at control, 50-, 500-, and 800-ppm levels for 2, 4, 8, and 13 weeks and spectrin dimer formation was quantified using denaturing gel electrophoresis and densitometry. Neurofilament preparations were also obtained from spinal cords and examined for cross-linking using Western blotting methods, The results obtained for protein crosslinking were compared to morphologic changes in the cervical and lumbar spinal cord using light and electron microscopy. The spectrin dimer exhibited a cumulative dose response and was detectable at both the 50-ppm level employed that did not produce axonal swellings and prior to the development of axonal swellings for the 500- and 800-ppm levels used. Neurofilament protein cross-linking involved all three subunits and the temporal relationship of cross-linking was consistent with a contributing role in the development of axonal swellings. These results establish the sensitivity of spectrin cross-linking for evaluating inhalation exposures and extend the similarities observed for 2,5-hexanedione and CS2 in both clinical settings and in vitro models to their effects exerted on neurofilaments in the axon. (C) 1997 Academic Press.
C1 NIEHS,ENVIRONM TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709.
RP Valentine, WM (reprint author), VANDERBILT UNIV,MED CTR,DEPT PATHOL,NASHVILLE,TN 37232, USA.
FU NIEHS NIH HHS [ES02611, ES06387]
NR 50
TC 24
Z9 24
U1 0
U2 3
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JAN
PY 1997
VL 142
IS 1
BP 95
EP 105
DI 10.1006/taap.1996.8028
PG 11
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA WD570
UT WOS:A1997WD57000011
PM 9007038
ER
PT J
AU Shimada, H
Hochadel, JF
Waalkes, MP
AF Shimada, H
Hochadel, JF
Waalkes, MP
TI Progesterone pretreatment enhances cellular sensitivity to cadmium
despite a marked activation of the metallothionein gene
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
ID PRIMARY HEPATOCYTE CULTURES; BINDING PROTEIN; CYTO-TOXICITY; HEPATIC
METALLOTHIONEIN; INDUCED HEPATOTOXICITY; RE-EXAMINATION; LIVER-CELLS;
RAT-LIVER; GLUTATHIONE; RESISTANCE
AB Previously, we found that in vivo pretreatment with progesterone markedly increased cadmium lethality in rats, apparently by enhancing cadmium-induced hepatonecrosis. Therefore, the present study was designed to investigate this phenomenon at the molecular level in an in vitro system. TRL-1215 rat liver cells were exposed to various concentrations of progesterone (0, 1, 10, and 100 mu M) for 24 hr and subsequently exposed to cadmium (0, 1, 5, 10, and 50 mu M; as CdCl2) for an additional 24 hr. Although the levels of progesterone used were essentially nontoxic, progesterone pretreatment resulted in a concentration-dependent increase in sensitivity to cadmium as assessed by loss of mitochondrial enzyme activity (tetrazolium-based dye assay) and loss of cytosolic enzyme activity (glutamic oxaloacetic transaminase). The effects of progesterone treatment on intracellular levels of metallothionein (MT), an inducible metal-binding protein generally associated with cadmium tolerance, were also measured. Progesterone (100 mu M) alone increased MT levels 2.4-fold, while cadmium (10 mu M) alone resulted in a 7-fold increase over control. Progesterone pretreatment followed by cadmium exposure caused a marked, 16-fold induction in MT synthesis, a level of activity that has been associated with acquired tolerance to cadmium. In addition, progesterone pretreatment clearly induced transcription of the MT gene as evidenced by enhanced cadmium-induced accumulation of cellular MT mRNA. Progesterone pretreatment had no effect on the level of glutathione, a cellular thiol thought to be important in detoxication of cadmium prior to MT gene activation and MT protein accumulation, or on cellular accumulation of cadmium during the initial 3 hr of exposure to the metal. The proportion of total cellular cadmium bound to MT in cells pretreated with progesterone was greater than that in the cells treated with cadmium alone, indicating an enhanced sequestration of the metal by MT after pretreatment. These results indicate that progesterone, at nontoxic levels, markedly exacerbates cadmium toxicity at the cellular level in liver cells. This is in accord with the observed progesterone-induced enhancement of the hepatotoxic effects of cadmium in vivo. The observed facilitation of cytotoxicity is not based in altered toxicokinetics of cadmium and occurs despite a pronounced activation of the MT gene resulting in an enhanced sequestration of cadmium by MT. The mechanism by which progesterone enhances cadmium toxicity deserves further study. (C) 1997 Academic Press
C1 NCI,INORGAN CARCINOGENESIS SECT,COMPARAT CARCINOGENESIS LAB,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
NCI,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC FREDERICK,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
NR 58
TC 18
Z9 18
U1 1
U2 2
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD JAN
PY 1997
VL 142
IS 1
BP 178
EP 185
DI 10.1006/taap.1996.8008
PG 8
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA WD570
UT WOS:A1997WD57000020
PM 9007047
ER
PT J
AU Kanitz, MH
Li, EI
Schulte, PA
Anderson, NL
AF Kanitz, MH
Li, EI
Schulte, PA
Anderson, NL
TI Investigation of ornithine decarboxylase activity and two-dimensional
electrophoretic protein profile following exposure of T24 bladder
carcinoma cells to tumor promoter and carcinogen
SO TOXICOLOGY METHODS
LA English
DT Article
DE biomarker; bladder carcinogenesis; occupational exposure; ODC; 2D PAGE
ID GENE-EXPRESSION; URINARY-BLADDER; CANCER; RAT; INHIBITION; ADENOMAS;
SMOKING; GROWTH; MUCOSA; MICE
AB To develop appropriate screening tools for biomarkers of effects of exposure to occupational chemical insult. Changes were investigated in T24 human bladder carcinoma cell ornithine decarboxylase activity and protein profiles by quantitative two-dimensional polyacrylamide gel electrophoresis (2D PAGE), biochemical events potentially altered by an established human bladder carcinogen and tumor promoter. A unique chromatographic approach was used to demonstrate that in vitro exposure of T24 cells for 6 h to varying concentrations of the carcinogen 4-aminobiphenyl elevates enzyme activity 5.3- to 5.9-fold. As a second method to identify potential biomarkers of exposure, two-dimensional gel electrophoresis was used to compare the protein pattern of vehicle control-treated T24 to 4-aminobiphenyl or tumor promoter (12-o-tetradecanoylphorbol-13-acetate)-treated cells. Changes in abundance and modification of proteins are determined using the Kepler software package to analyze and compare gels across treatment groups. With this technology, protein markers are identified by significant alterations in spot density (mean ratio of Coomassie Blue intensity; p <.001, Student's t test) following T24 treatment with the carcinogen or the tumor promoter. Fifteen protein spots from a detectable pool of 542 demonstrate two-fold or greater changes in intensity. The results illustrate the potential of automated two-dimensional gel analysis for classifying different gel patterns, an approach that can be applied to patterns whose differences are obscured by the minor changes in spot intensity that arise between separate cell cultures. In addition to the ornithine decarboxylase assay, 2D PAGE offers much promise to evaluate potential biomarkers for occupational and environmental carcinogens. These results will be used to further develop NIOSH efforts in the molecular epidemiology of occupational bladder carcinogenesis.
C1 LARGE SCALE BIOL CORP,ROCKVILLE,MD.
NCI,BETHESDA,MD 20892.
RP Kanitz, MH (reprint author), NIOSH,TAFT LABS,MS-C-23,4676 COLUMBIA PKWY,CINCINNATI,OH 45226, USA.
NR 33
TC 1
Z9 1
U1 0
U2 0
PU TAYLOR & FRANCIS
PI BRISTOL
PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598
SN 1051-7235
J9 TOXICOL METHOD
JI Toxicol. Method.
PD JAN-MAR
PY 1997
VL 7
IS 1
BP 27
EP 41
PG 15
WC Toxicology
SC Toxicology
GA XC193
UT WOS:A1997XC19300004
ER
PT J
AU Klein, HG
Dodd, RY
Ness, PM
Fratantoni, JA
Nemo, GJ
AF Klein, HG
Dodd, RY
Ness, PM
Fratantoni, JA
Nemo, GJ
TI Current status of microbial contamination of blood components: Summary
of a conference
SO TRANSFUSION
LA English
DT Editorial Material
ID RNA GENE PROBE; BACTERIAL-CONTAMINATION; YERSINIA-ENTEROCOLITICA;
RED-CELLS; TRANSFUSION; IDENTIFICATION; PLATELETS; SURVEILLANCE;
SEPTICEMIA; SEPSIS
C1 AMER RED CROSS,JEROME H HOLLAND LAB,ROCKVILLE,MD.
US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL,BETHESDA,MD 20892.
NHLBI,DIV BLOOD DIS & RESOURCES,TRANSFUS MED SCI RES GRP,BETHESDA,MD 20892.
JOHNS HOPKINS UNIV HOSP,BLOOD BANK,BALTIMORE,MD 21287.
RP Klein, HG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BLDG 10,ROOM 1C711,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 22
TC 58
Z9 64
U1 0
U2 0
PU AMER ASSOC BLOOD BANKS
PI BETHESDA
PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749
SN 0041-1132
J9 TRANSFUSION
JI Transfusion
PD JAN
PY 1997
VL 37
IS 1
BP 95
EP 101
DI 10.1046/j.1537-2995.1997.37197176958.x
PG 7
WC Hematology
SC Hematology
GA WF548
UT WOS:A1997WF54800018
PM 9024497
ER
PT J
AU Blajchman, MA
Klein, HG
AF Blajchman, MA
Klein, HG
TI Looking back in anger: Retrospection in the face of a paradigm shift
SO TRANSFUSION MEDICINE REVIEWS
LA English
DT Editorial Material
ID TRANSFUSION; SYSTEM; SAFETY
C1 MCMASTER UNIV,DEPT MED,HAMILTON,ON L8N 3Z5,CANADA.
CANADIAN RED CROSS SOC,BLOOD SERV,HAMILTON,ON,CANADA.
NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892.
RP Blajchman, MA (reprint author), MCMASTER UNIV,DEPT PATHOL,1200 MAIN ST W,ROOM HSC 2N34,HAMILTON,ON L8N 3Z5,CANADA.
NR 19
TC 9
Z9 9
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0887-7963
J9 TRANSFUS MED REV
JI Transf. Med. Rev.
PD JAN
PY 1997
VL 11
IS 1
BP 1
EP 5
DI 10.1016/S0887-7963(97)80004-1
PG 5
WC Hematology
SC Hematology
GA WF980
UT WOS:A1997WF98000001
PM 9031485
ER
PT J
AU Hengen, PN
AF Hengen, PN
TI Methods and reagents - False positives from the yeast two-hybrid system
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Editorial Material
ID PROTEIN
RP Hengen, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA.
NR 9
TC 23
Z9 23
U1 0
U2 9
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 JAN
PY 1997
VL 22
IS 1
BP 33
EP 34
DI 10.1016/S0968-0004(96)30047-9
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WE017
UT WOS:A1997WE01700010
PM 9020590
ER
PT J
AU Hengen, PN
AF Hengen, PN
TI Internet newsgroups
SO TRENDS IN CELL BIOLOGY
LA English
DT Article
ID REAGENTS
RP Hengen, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,FREDERICK,MD 21702, USA.
NR 7
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB
SN 0962-8924
J9 TRENDS CELL BIOL
JI Trends Cell Biol.
PD JAN
PY 1997
VL 7
IS 1
BP 34
EP 35
DI 10.1016/S0962-8924(97)60045-8
PG 2
WC Cell Biology
SC Cell Biology
GA WE013
UT WOS:A1997WE01300008
ER
PT J
AU Clerici, M
Clivio, A
Shearer, GM
AF Clerici, M
Clivio, A
Shearer, GM
TI Resistance to HIV infection: The genes are only part of the solution
SO TRENDS IN MICROBIOLOGY
LA English
DT Editorial Material
ID RESPONSES; VIRUS
C1 UNIV MILAN,HL SACCO,PADIGL LITA,DIPARTIMENTO BIOL & GENET SCI MED,I-20157 MILAN,ITALY.
NCI,EXPT IMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
RP Clerici, M (reprint author), UNIV MILAN,HL SACCO,PADIGL LITA,CATTEDRA IMMUNOL,VIA GB GRASSI 74,I-20157 MILAN,ITALY.
OI CLIVIO, ALBERTO/0000-0002-1423-046X
NR 15
TC 6
Z9 9
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB
SN 0966-842X
J9 TRENDS MICROBIOL
JI Trends Microbiol.
PD JAN
PY 1997
VL 5
IS 1
BP 2
EP 4
DI 10.1016/S0966-842X(97)81762-3
PG 3
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA WE728
UT WOS:A1997WE72800003
PM 9025227
ER
PT J
AU Vanham, G
Toossi, Z
Hirsch, CS
Wallis, RS
Schwander, SK
Rich, EA
Ellner, JJ
AF Vanham, G
Toossi, Z
Hirsch, CS
Wallis, RS
Schwander, SK
Rich, EA
Ellner, JJ
TI Examining a paradox in the pathogenesis of human pulmonary tuberculosis:
immune activation and suppression/anergy
SO TUBERCLE AND LUNG DISEASE
LA English
DT Review
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-BETA;
CD4+ T-CELLS; INTERFERON-GAMMA PRODUCTION; HIV-INFECTED INDIVIDUALS;
ANTIGEN-PRESENTING CELL; MYCOBACTERIUM-TUBERCULOSIS; IFN-GAMMA; CYTOKINE
PRODUCTION
AB Protective immunity against Mycobacterium tuberculosis (MTB) in animal models is based on cell-mediated immunity (CMI), involving bi-directional interactions between T cells and cells of the monocyte/macrophage (MO/MA) lineage. Key factors include MO-derived interleukin (IL)-12 and tumor necrosis factor (TNF)-alpha as well as T cell derived IL-2 and interferon (IFN)-gamma. These cytokines appear particularly crucial in the induction of MA-mediated elimination of mycobacteria. Several lines of evidence indicate that similar mechanisms are operating in humans.
During active pulmonary tuberculosis (PTB), signs of both immune depression and immune activation are concomitantly present. Decreased tuberculin skin test reactivity in vivo and deficient IFN-gamma production by MTB-stimulated mononuclear cells in vitro are observed. On the other hand, the serum levels of several cytokines, including TNF, and other inflammatory mediators are increased and circulating MO and T cell show phenotypic and functional evidence of in vivo activation.
In this review, we will discuss the evidence for three models, which could explain this apparent paradox: 1. Stimulation of the T cell-suppressive function from MO/MA; 2. Intrinsic T cell refractoriness, possibly associated with tendency to apoptosis (programmed cell death), and 3. Compartmentalization and redistribution of immune responses to the site of disease.
The opportunistic behavior of MTB during human immunodeficiency virus (HIV) infection can be explained by suppression of type-1 responses at the level of antigen-presenting cells, CD4 T cells and effector macrophages. The ominous prognostic significance of intercurrent PTB during HIV infection seems primarily due to prolonged activation of HIV replication in macrophages.
Supportive immune therapy during PTB could aim at correcting the type-1 deficiency either by IFN-gamma inducers (e.g. IL-12, IL-18) or by neutralizing the suppressive cytokines transforming growth factor beta (TGF-P) and IL-10. Alternatively, inflammatory over-activity could be reduced by neutralizing TNF. Finally, anti-apoptotic therapies (e.g. IL-15) might be considered.
C1 Inst Trop Med, Dept Microbiol, Immunol Lab, B-2000 Antwerp, Belgium.
Case Western Reserve Univ Hosp, Dept Med, Div Infect Dis, Cleveland, OH 44106 USA.
Case Western Reserve Univ Hosp, Dept Med, Div Pulm & Crit Care Med, Cleveland, OH 44106 USA.
NIH, TB Res Unit, Bethesda, MD 20892 USA.
RP Vanham, G (reprint author), Inst Trop Med, Dept Microbiol, Immunol Lab, Nat Str 155, B-2000 Antwerp, Belgium.
EM gvanham@itg.be
RI Wallis, Robert/A-8018-2009
OI Wallis, Robert/0000-0001-6152-5183
NR 201
TC 52
Z9 56
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 0962-8479
J9 TUBERCLE LUNG DIS
JI Tubercle Lung Dis.
PY 1997
VL 78
IS 3-4
BP 145
EP 158
DI 10.1016/S0962-8479(97)90021-6
PG 14
WC Respiratory System
SC Respiratory System
GA ZT128
UT WOS:000074051300001
PM 9713647
ER
PT J
AU Jacobs, GG
Johnson, JL
Boom, WH
Wallis, RS
Whalen, CC
Ginsberg, AM
AF Jacobs, GG
Johnson, JL
Boom, WH
Wallis, RS
Whalen, CC
Ginsberg, AM
TI Tuberculosis vaccines: how close to human testing?
SO TUBERCLE AND LUNG DISEASE
LA English
DT Editorial Material
C1 NIAID, Div Microbiol & Infect Dis, Resp Dis Branch, NIH, Bethesda, MD 20892 USA.
Case Western Reserve Univ, Sch Med, Div Infect Dis, Cleveland, OH 44106 USA.
RP Jacobs, GG (reprint author), NIAID, Div Microbiol & Infect Dis, Resp Dis Branch, NIH, Solor Bldg,Rm 3A41,6003 Execut Blvd,MSC 7630, Bethesda, MD 20892 USA.
RI Wallis, Robert/A-8018-2009
OI Wallis, Robert/0000-0001-6152-5183
NR 0
TC 10
Z9 10
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 0962-8479
J9 TUBERCLE LUNG DIS
JI Tubercle Lung Dis.
PY 1997
VL 78
IS 3-4
BP 159
EP 169
DI 10.1016/S0962-8479(97)90022-8
PG 11
WC Respiratory System
SC Respiratory System
GA ZT128
UT WOS:000074051300002
PM 9713648
ER
PT J
AU Riley, WA
Evans, GW
Sharrett, AR
Burke, GL
Barnes, RW
AF Riley, WA
Evans, GW
Sharrett, AR
Burke, GL
Barnes, RW
TI Variation of common carotid artery elasticity with intimal-medial
thickness: The ARIC study
SO ULTRASOUND IN MEDICINE AND BIOLOGY
LA English
DT Article
DE arterial elasticity; distensibility; compliance; stiffness;
intimal-medial thickness; elastic modulus; ultrasonic imaging;
echo-tracking
ID B-MODE ULTRASOUND; ATHEROSCLEROTIC LESIONS; AORTIC COMPLIANCE; WALL;
DISTENSIBILITY; HYPERTENSION; PROGRESSION; STIFFNESS; MODULUS; RATIO
AB Atherosclerosis Risk in Communities (ARIC) study is a prospective investigation of the etiology and natural history of atherosclerosis and cardiovascular disease in four U.S. communities. The purpose of this work is to investigate the relationship between common carotid artery elasticity and intimal-medial thickness (IMT) in the four race-gender groups represented in the ARIC cohort. Noninvasive ultrasonic methods were used to measure IMT and the [systolic minus diastolic] diameter change (DC) of the left common carotid artery in 10,920 black and white, men and women between the ages of 45 and 64 y. The relationship between DC and IMT and IMT(2) was examined after adjustment of DC for age, height, diastolic diameter, diastolic blood pressure and linear and quadratic terms for pulse pressure. This adjusted value of DC was used as an index of elasticity of the common carotid artery in the ARIC cohort with larger values of adjusted DC implying a more elastic vessel. The general behavior of adjusted DC with increasing IMT was observed to be qualitatively similar in all four race-gender groups. Adjusted DC remained nearly constant or increased slightly for values of IMT between approximately 0.4 and 0.8 mm, up to approximately the 90th percentile of IMT, and then decreased above the 90th percentile of IMT. Common carotid artery elasticity, defined as adjusted DC, varies with increasing IMT in the ARIC cohort in a manner consistent with results from previous studies in animals and human subjects addressing the variation of several elasticity indices with atherosclerotic involvement and risk factor exposure in the aorta, and brachial and radial arteries. Our results suggest that thicker common carotid artery walls in middle-aged U.S. populations are no stiffer than thinner walls, except for the thickest 10% of arteries. Since the distal common carotid artery frequently contains atheromatous plaques in this population, the lack of change in stiffness, indeed, the reduction in stiffness per unit thickness, may reflect the various stages of early common carotid atherosclerosis most often found in this population. These are characterized more by destruction of arterial wall structural elements than by changes such as widespread or circumferential sclerosis, which would strengthen and stiffen the artery. (C) 1997 World Federation for Ultrasound in Medicine & Biology.
C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27157.
NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,NIH,BETHESDA,MD 20892.
RP Riley, WA (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT NEUROL,300 S HAWTHORNE RD,WINSTON SALEM,NC 27157, USA.
FU NHLBI NIH HHS [N01-HC-55015, N01-HC-55016, N01-HC-55018]
NR 27
TC 77
Z9 81
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0301-5629
J9 ULTRASOUND MED BIOL
JI Ultrasound Med. Biol.
PY 1997
VL 23
IS 2
BP 157
EP 164
DI 10.1016/S0301-5629(96)00211-6
PG 8
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA WT394
UT WOS:A1997WT39400001
PM 9140173
ER
PT J
AU Wagner, JR
Kleiner, DE
Walther, MM
Linehan, WM
AF Wagner, JR
Kleiner, DE
Walther, MM
Linehan, WM
TI Perirenal myelolipoma
SO UROLOGY
LA English
DT Article
ID RETROPERITONEAL
AB Extra-adrenal myelolipomas are rare, benign tumors composed of hematopoietic and adipose elements. Although these tumors can cause local symptoms or hemorrhage, they are generally asymptomatic. However, when discovered intraoperatively, they pose a diagnostic dilemma to the urologic surgeon. We present a case of perirenal extra-adrenal myelolipoma discovered intraoperatively in a patient with von Hippel-Lindau disease undergoing partial nephrectomy.
C1 NEI,UROL ONCOL SECT,SURG BRANCH,NIH,BETHESDA,MD 20892.
OI Kleiner, David/0000-0003-3442-4453
NR 10
TC 12
Z9 13
U1 0
U2 0
PU CAHNERS PUBL CO
PI NEW YORK
PA 249 WEST 17 STREET, NEW YORK, NY 10011
SN 0090-4295
J9 UROLOGY
JI UROLOGY
PD JAN
PY 1997
VL 49
IS 1
BP 128
EP 130
DI 10.1016/S0090-4295(97)00368-3
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA WC217
UT WOS:A1997WC21700033
PM 9000202
ER
PT S
AU Nieman, L
AF Nieman, L
BE Bulletti, C
deZiegler, D
Guller, S
Levitz, M
TI Antiprogestin action on the endometrium
SO UTERUS: ENDOMETRIUM AND MYOMETRIUM
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT 3rd International Conference on the Uterus - Endometrium and Myometrium
CY OCT 14-16, 1996
CL NYU MED CTR, NEW YORK, NY
SP Matria Hlth Care Inc, Schering AG, Takeda Italia Farmaceutici S p A, Upjohn Co, Wyeth Ayerst Int Inc, Wyeth Ayerst Labs, Wyeth S p A
HO NYU MED CTR
ID MENSTRUAL-CYCLE; LUTEAL-PHASE; MIFEPRISTONE RU-486; FOLLICULAR PHASE;
NORMAL WOMEN; LONG-TERM; RU486; PROGESTERONE; INHIBITION; MATURATION
AB A variety of synthetic steroidal compounds, including onapristone, lilopristone and mifepristone (RU 486), interact with the progesterone receptor and show antagonist properties in vivo.(1) Given the importance of progesterone to normal endometrial differentiation, one would predict that these agents have important endometrial effects during the luteal phase by blocking progesterone action. However, clinical studies have revealed a more complex spectrum of action. These competitive inhibitors of progesterone effects on transcription may have mixed agonist-antagonist properties related to the hormonal milieu and, like agonist compounds, the dose-response relationships seen with antiprogestins are tissue dependent. Thus, in addition to direct antagonism of progesterone action on the endometrium, antiprogestins may also alter endometrial function indirectly, by reducing gonadal steroid production. Evidence is also accumulating that some antiprogestins may interfere with estrogen action on the endometrium. This paper reviews endometrial effects of the best-studied antiprogestin, RU 486, in women and other primates. Emphasis is placed on morphologic and functional changes in the endometrium, as well as the ability to interrupt pregnancy or induce menstrual bleeding.
RU 486 is an orally active 19-norsteroid with glucocorticoid, androgen, and progesterone antagonist properties and little, if any, agonist activity; it does not react with the mineralocorticoid or estrogen receptor.(1,2). After oral administration to men or women, RU 486 has a prolonged half-life of about 20 hours, probably because of extensive binding to plasma proteins.(3) Although antiglucocorticoid effects are seen at single doses of > 5 mg/kg, antiprogestational activity is seen at smaller doses, in part allowing for exploitation of antiprogestin properties without clinical compromise of glucocorticoid status.(2)
RP Nieman, L (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, NIH, BETHESDA, MD 20892 USA.
NR 28
TC 1
Z9 1
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-105-7; 1-57331-104-9
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 1997
VL 828
BP 103
EP 107
DI 10.1111/j.1749-6632.1997.tb48527.x
PG 5
WC Multidisciplinary Sciences; Obstetrics & Gynecology; Reproductive
Biology
SC Science & Technology - Other Topics; Obstetrics & Gynecology;
Reproductive Biology
GA BJ68F
UT WOS:A1997BJ68F00009
PM 9329827
ER
PT S
AU Garrity, RR
Nara, PL
Lin, G
Johnson, S
AF Garrity, RR
Nara, PL
Lin, G
Johnson, S
BE Brown, F
Burton, D
Doherty, P
Mekalanos, J
Norrby, E
TI Genetic vaccination with naked HIV-1 RNA results in low-titer anti-gp120
response
SO VACCINES 97 - MOLECULAR APPROACHES TO THE CONTROL OF INFECTIOUS DISEASES
SE VACCINES (COLD SPRING HARBOR LABORATORY PRESS)
LA English
DT Proceedings Paper
CT 14th Annual Meeting on Modern Approaches to the Control of Infectious
Diseases
CY SEP 09-13, 1996
CL COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY
SP Pharmacia LKB Biotechnol, Alza Corp, Amgen Inc, BASF Biores Corp, Becton Dickinson & Co, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Hoechst Marion Roussel Inc, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Eli Lilly & Co, Merck Genome Res InstOncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Research Genet Inc, Sandoz Res Inst, Schering Plough Corp, Sumitomo Pharm Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC, Amer Cyanamid Co, Kirin Brewery, Monsanto Co, Pioneer Hi Bred Int Inc, Westvaco Corp
HO COLD SPRING HARBOR LAB
RP Garrity, RR (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRUS BIOL SECT,LTCB,FREDERICK,MD 21701, USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU COLD SPRING HARBOR LABORATORY PRESS
PI PLAINVIEW
PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500
SN 0899-4056
BN 0-87969-516-1
J9 VACCINES
PY 1997
BP 151
EP 156
PG 6
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology;
Virology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology;
Virology
GA BH99A
UT WOS:A1997BH99A00026
ER
PT S
AU Hirsch, VM
AdgerJohnson, D
Campbell, B
Goldstein, S
Brown, C
Elkins, WR
Montefiori, DC
AF Hirsch, VM
AdgerJohnson, D
Campbell, B
Goldstein, S
Brown, C
Elkins, WR
Montefiori, DC
BE Brown, F
Burton, D
Doherty, P
Mekalanos, J
Norrby, E
TI A molecularly cloned, pathogenic, neutralization-resistant simian
immunodeficiency virus, SIVsmE543-3
SO VACCINES 97 - MOLECULAR APPROACHES TO THE CONTROL OF INFECTIOUS DISEASES
SE VACCINES (COLD SPRING HARBOR LABORATORY PRESS)
LA English
DT Proceedings Paper
CT 14th Annual Meeting on Modern Approaches to the Control of Infectious
Diseases
CY SEP 09-13, 1996
CL COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY
SP Pharmacia LKB Biotechnol, Alza Corp, Amgen Inc, BASF Biores Corp, Becton Dickinson & Co, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Hoechst Marion Roussel Inc, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Eli Lilly & Co, Merck Genome Res InstOncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Research Genet Inc, Sandoz Res Inst, Schering Plough Corp, Sumitomo Pharm Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC, Amer Cyanamid Co, Kirin Brewery, Monsanto Co, Pioneer Hi Bred Int Inc, Westvaco Corp
HO COLD SPRING HARBOR LAB
RP Hirsch, VM (reprint author), NIAID,IMMUNOL VIRUSES SECT,LID,NIH,TWINBROOK 2 FACIL,ROCKVILLE,MD 20852, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU COLD SPRING HARBOR LABORATORY PRESS
PI PLAINVIEW
PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500
SN 0899-4056
BN 0-87969-516-1
J9 VACCINES
PY 1997
BP 285
EP 289
PG 5
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology;
Virology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology;
Virology
GA BH99A
UT WOS:A1997BH99A00048
ER
PT S
AU Glamann, J
Parren, P
Ditzel, H
Arnold, C
Kent, KA
Montefiori, D
Burton, D
Hirsch, VM
AF Glamann, J
Parren, P
Ditzel, H
Arnold, C
Kent, KA
Montefiori, D
Burton, D
Hirsch, VM
BE Brown, F
Burton, D
Doherty, P
Mekalanos, J
Norrby, E
TI Characterization of SIV envelope-specific fabs obtained by combinatorial
antibody cloning from a long-term, nonprogressor macaque
SO VACCINES 97 - MOLECULAR APPROACHES TO THE CONTROL OF INFECTIOUS DISEASES
SE VACCINES (COLD SPRING HARBOR LABORATORY PRESS)
LA English
DT Proceedings Paper
CT 14th Annual Meeting on Modern Approaches to the Control of Infectious
Diseases
CY SEP 09-13, 1996
CL COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY
SP Pharmacia LKB Biotechnol, Alza Corp, Amgen Inc, BASF Biores Corp, Becton Dickinson & Co, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Hoechst Marion Roussel Inc, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Eli Lilly & Co, Merck Genome Res InstOncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Research Genet Inc, Sandoz Res Inst, Schering Plough Corp, Sumitomo Pharm Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC, Amer Cyanamid Co, Kirin Brewery, Monsanto Co, Pioneer Hi Bred Int Inc, Westvaco Corp
HO COLD SPRING HARBOR LAB
RP Glamann, J (reprint author), NIAID,LID,NIH,TWINBROOK 2 FACIL,ROCKVILLE,MD 20852, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU COLD SPRING HARBOR LABORATORY PRESS
PI PLAINVIEW
PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500
SN 0899-4056
BN 0-87969-516-1
J9 VACCINES
PY 1997
BP 299
EP 303
PG 5
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology;
Virology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology;
Virology
GA BH99A
UT WOS:A1997BH99A00050
ER
PT S
AU Nara, PL
VanCott, TC
Birx, DL
AF Nara, PL
VanCott, TC
Birx, DL
BE Brown, F
Burton, D
Doherty, P
Mekalanos, J
Norrby, E
TI Evidence for a primary IgG response to the oligomeric form of gp160
during primary HIV-1 infection in both chimpanzees and humans
SO VACCINES 97 - MOLECULAR APPROACHES TO THE CONTROL OF INFECTIOUS DISEASES
SE VACCINES (COLD SPRING HARBOR LABORATORY PRESS)
LA English
DT Proceedings Paper
CT 14th Annual Meeting on Modern Approaches to the Control of Infectious
Diseases
CY SEP 09-13, 1996
CL COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY
SP Pharmacia LKB Biotechnol, Alza Corp, Amgen Inc, BASF Biores Corp, Becton Dickinson & Co, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Hoechst Marion Roussel Inc, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Eli Lilly & Co, Merck Genome Res InstOncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Research Genet Inc, Sandoz Res Inst, Schering Plough Corp, Sumitomo Pharm Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC, Amer Cyanamid Co, Kirin Brewery, Monsanto Co, Pioneer Hi Bred Int Inc, Westvaco Corp
HO COLD SPRING HARBOR LAB
RP Nara, PL (reprint author), NCI,FREDERICK CANC RES FACIL,VIRUS BIOL SECT,FREDERICK,MD 21701, USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU COLD SPRING HARBOR LABORATORY PRESS
PI PLAINVIEW
PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500
SN 0899-4056
BN 0-87969-516-1
J9 VACCINES
PY 1997
BP 331
EP 337
PG 7
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology;
Virology
SC Infectious Diseases; Research & Experimental Medicine; Microbiology;
Virology
GA BH99A
UT WOS:A1997BH99A00055
ER
PT J
AU Haynes, JS
Halbur, PG
Sirinarumitr, T
Paul, PS
Meng, XJ
Huffman, EL
AF Haynes, JS
Halbur, PG
Sirinarumitr, T
Paul, PS
Meng, XJ
Huffman, EL
TI Temporal and morphologic characterization of the distribution of porcine
reproductive and respiratory syndrome virus (PRRSV) by in situ
hybridization in pigs infected with isolates of PRRSV that differ in
virulence
SO VETERINARY PATHOLOGY
LA English
DT Article
DE in situ hybridization; interdigitating dendritic cells; lymphoid tissue;
macrophages; porcine reproductive and respiratory syndrome virus; swine
ID SWINE INFERTILITY; LELYSTAD VIRUS; ATCC VR-2332; ANTIGEN
AB Three groups of 5-week-old cesarian-derived, colostrum-deprived pigs were inoculated intranasally with either a high-virulence isolate (VR2385) or a low-virulence isolate (VR2431) of porcine reproductive and respiratory syndrome virus (PRRSV) or with uninfected cell culture and media. Formalin-fixed, paraffin-embedded tissues from pigs euthanatized at 10, 21, and 28 days post-inoculation were examined by in situ hybridization for PRRSV nucleic acid using a digoxigenin-labeled antisense RNA probe approximately 1,000 nucleotides in length. Alveolar macrophages were positive in the lungs of 9/9, 2/2, and 0/2 VR2385-inoculated pigs and 7/9, 1/2, and 2/3 VR2431-inoculated pigs at 10, 21, and 28 days post-inoculation, respectively. More positive cells were detected in lungs from VR2385-inoculated pigs compared to VR2431-inoculated pigs at 10 and 21 days post-inoculation. Positive cells within lymph nodes were tingible body macrophages in germinal centers and macrophages or interdigitating dendritic cells within the paracortical areas. VR2385 was detected in the tracheobronchial lymph node (TBLN) and mediastinal lymph node (MLN) of 7/9 and 9/9 pigs at 10 days post-inoculation, but was only detected in the TBLN of 1/2 and 0/2 pigs and in the MLN of 0/2 and 1/2 pigs at 21 and 28 days post-inoculation, respectively. In contrast, VR2431 was detected in the TBLN and MLN of 5/9 and 2/9 pigs at 10 days post-inoculation and in the TBLN of 0/2 and 1/3 pigs and in the MLN of 0/2 and 0/3 pigs at 21 and 28 days post-inoculation, respectively. There were more positive cells in TBLN and MLN in pigs inoculated with VR2385 at 10 days post-inoculation. Macrophages located at the epithelial-lymphoid interface of tonsilar crypts and within the paracortical areas were positive in tonsils of 9/9, 2/2, and 1/2 VR2385-inoculated pigs and 7/9, 1/2, and 1/3 VR2431-inoculated pigs at 10, 21, and 28 days post-inoculation, respectively. Positive cells in the thymic medulla were multinucleate and were only detected at 10 days post-inoculation in 2/9 VR2385-inoculated pigs and 4/9 VR2431-inoculated pigs. Positive cells within the spleen were few, spindle-shaped, located within smooth muscle trabecula, and only present at 10 days post-inoculation in 3/9 VR2385-inoculated pigs. We conclude that the tissue tropism and distribution of positive cells within tissues is similar for VR2385 and VR2431. However, tissues from more pigs and more cells within tissues were positive in pigs inoculated with VR2385 than VR2431 at 10 and 21 days post-inoculation. These findings indicate that the more virulent isolate VR2385 may replicate better in vivo than the less virulent isolate VR2431. This supports the hypothesis that an increased ability to replicate in vivo contributes to increased virulence of PRRSV.
C1 IOWA STATE UNIV,COLL VET MED,VET MED RES INST,AMES,IA 50011.
IOWA STATE UNIV,COLL VET MED,VET DIAGNOST LAB,AMES,IA 50011.
NIAID,NIH,BETHESDA,MD 20892.
RP Haynes, JS (reprint author), IOWA STATE UNIV,COLL VET MED,DEPT VET PATHOL,2718 VET MED BLDG,AMES,IA 50011, USA.
RI Meng, X.J./B-8769-2009
OI Meng, X.J./0000-0002-2739-1334
NR 12
TC 41
Z9 43
U1 0
U2 0
PU AMER COLL VET PATHOLOGIST
PI LAWRENCE
PA 810 EAST 10TH STREET, LAWRENCE, KS 66044
SN 0300-9858
J9 VET PATHOL
JI Vet. Pathol.
PD JAN
PY 1997
VL 34
IS 1
BP 39
EP 43
PG 5
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA WC748
UT WOS:A1997WC74800006
PM 9150544
ER
PT J
AU King, AD
Green, KY
AF King, AD
Green, KY
TI Sequence analysis of the gene encoding the capsid protein of the snow
mountain human calicivirus
SO VIRUS GENES
LA English
DT Article
DE SMV capsid; sequence analysis; calicivirus; gastroenteritis
ID ROUND-STRUCTURED VIRUSES; MOLECULAR CHARACTERIZATION; DIVERSITY
AB Snow Mountain virus (SMV) is the reference strain for serotype 3 as determined by immune electron microscopy of the human caliciviruses that are associated with epidemic gastroenteritis. In order to establish the genetic relationship of its capsid protein with those from other human caliciviriuses, the sequence of the open reading frame 2 (ORF2) encoding the SMV capsid protein was determined. The SMV ORF2 sequence was 1626 nucleotides in length and the deduced protein of 542 amino acids had a calculated molecular weight of 59.2 kD. The SMV capsid sequence showed approximately 48 and 77% amino acid sequence identity with the capsid proteins of the Norwalk (serotype 1) and Hawaii (serotype 2) human calicivirus reference strains, respectively, a finding consistent with its serotypic distinctiveness. Furthermore, the predicted amino acid sequence of the SMV capsid was found to share highest sequence identity (98%) with the Melksham human calicivirus in database searches.
C1 NIAID,INFECT DIS LAB,NIH,BETHESDA,MD 20892.
NR 8
TC 5
Z9 5
U1 0
U2 0
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0920-8569
J9 VIRUS GENES
JI Virus Genes
PY 1997
VL 15
IS 1
BP 5
EP 7
DI 10.1023/A:1007953126436
PG 3
WC Genetics & Heredity; Virology
SC Genetics & Heredity; Virology
GA YB480
UT WOS:A1997YB48000001
PM 9354262
ER
PT J
AU Tami, C
Kaplan, G
Piccone, ME
Palma, EL
AF Tami, C
Kaplan, G
Piccone, ME
Palma, EL
TI Nucleotide sequence of the P1 region of foot-and-mouth disease virus
strain O1 Caseros
SO VIRUS GENES
LA English
DT Article
DE picornavirus; foot-and-mouth disease virus; O1 Caseros P1 nucleotide
sequence
ID AMINO-ACID SUBSTITUTIONS; ANTIGENIC SITES; CAPSID PROTEINS; PROTECTION;
IDENTIFICATION; NEUTRALIZATION; HETEROGENEITY; RESPONSES; VARIANTS;
SURFACE
AB It has been shown that variation of antigenic site I in VP1 of foot-and-mouth disease virus (FMDV) plays an important role in the antigenic diversification of this virus. However, the O1 Campos strain is able to efficiently cross-protect cattle against the O1 Caseros strain, despite having a different sequence in the site I. In this paper we report and compare the P1 coding region for the capsid proteins of FMDV O1 Caseros and O1 Campos. The deduced amino acid sequence showed a total of 31 amino acid differences. Eight of them are located in surface-exposed loops that have been implicated in antigenic sites. This study should help to identify additional sites to be considered in the development of a new generation of FMDV vaccines.
C1 NIH,FDA GBER OVRR DVPP,BETHESDA,MD 20892.
INTA,CICV,INST BIOTECHNOL,MORON,BUENOS AIRES,ARGENTINA.
NR 30
TC 4
Z9 5
U1 0
U2 0
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0920-8569
J9 VIRUS GENES
JI Virus Genes
PY 1997
VL 14
IS 3
BP 255
EP 259
PG 5
WC Genetics & Heredity; Virology
SC Genetics & Heredity; Virology
GA XW592
UT WOS:A1997XW59200012
PM 9311571
ER
PT J
AU Levine, M
Rumsey, S
Wang, YH
AF Levine, M
Rumsey, S
Wang, YH
TI Principles involved in formulating recommendations for vitamin C intake:
A paradigm for water-soluble vitamins
SO VITAMINS AND COENZYMES, PT I
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID ASCORBIC-ACID TRANSPORT; HUMAN-NEUTROPHILS; ACCUMULATION; ABSORPTION;
DEPLETION; EXCRETION
RP Levine, M (reprint author), NIDDKD,MOL & CLIN NUTR SECT,NIH,BETHESDA,MD 20892, USA.
NR 44
TC 4
Z9 5
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 279
BP 43
EP 54
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ25G
UT WOS:A1997BJ25G00006
PM 9211256
ER
PT S
AU Fitzhugh, AL
Akee, RK
AF Fitzhugh, AL
Akee, RK
BE McCormick, DB
Suttie, JW
Wagner, C
TI Chemical synthesis of
(6S)-5-formyl-5,6,7,8-tetrahydropteroylpoly-gamma-L-glutamates
SO VITAMINS AND COENZYMES, PT K
SE Methods in Enzymology
LA English
DT Review
RP Fitzhugh, AL (reprint author), NCI, FREDERICK CANC RES & DEV CTR, SAIC FREDERICK, FREDERICK, MD 21702 USA.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182182-X
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 281
BP 88
EP 96
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ41A
UT WOS:A1997BJ41A00011
PM 9250971
ER
PT S
AU Milstien, S
AF Milstien, S
BE McCormick, DB
Suttie, JW
Wagner, C
TI Interconversion of 6- and 7-substituted tetrahydropterins via
enzyme-generated 4a-hydroxytetrahydropterin intermediates
SO VITAMINS AND COENZYMES, PT K
SE Methods in Enzymology
LA English
DT Review
ID 4A-CARBINOLAMINE DEHYDRATASE; PHENYLALANINE HYDROXYLATION; PTERINS;
COFACTOR
RP Milstien, S (reprint author), NIMH, LAB CELL & MOL REGULAT, NIH, BETHESDA, MD 20892 USA.
NR 10
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182182-X
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 281
BP 116
EP 123
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ41A
UT WOS:A1997BJ41A00014
PM 9250974
ER
PT S
AU Levine, M
Rumsey, SC
Wang, YH
Park, J
Kwon, O
Amano, N
AF Levine, M
Rumsey, SC
Wang, YH
Park, J
Kwon, O
Amano, N
BE McCormick, DB
Suttie, JW
Wagner, C
TI In situ kinetics: An approach to recommended intake of vitamin C
SO VITAMINS AND COENZYMES, PT K
SE Methods in Enzymology
LA English
DT Review
ID ASCORBIC-ACID TRANSPORT; LOW-DENSITY-LIPOPROTEIN; CHROMAFFIN GRANULES;
HUMAN-NEUTROPHILS; NOREPINEPHRINE BIOSYNTHESIS; INSITU KINETICS;
PLASMA-CONCENTRATIONS; ELECTRON-TRANSFER; BETA-CAROTENE; ELDERLY MEN
RP Levine, M (reprint author), NIDDKD, MOL & CLIN NUTR SECT, NIH, BETHESDA, MD 20892 USA.
NR 89
TC 8
Z9 8
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182182-X
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 281
BP 425
EP 437
PG 13
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ41A
UT WOS:A1997BJ41A00046
PM 9251006
ER
PT S
AU Ferrari, N
Vidali, G
Pfeffer, U
AF Ferrari, N
Vidali, G
Pfeffer, U
BE McCormick, DB
Suttie, JW
Wagner, C
TI Use of quantitative polymerase chain reaction to study retinoid receptor
expression
SO VITAMINS AND COENZYMES, PT L
SE Methods in Enzymology
LA English
DT Review
ID ACUTE PROMYELOCYTIC LEUKEMIA; REVERSE TRANSCRIPTION; RT-PCR; ENZYMATIC
AMPLIFICATION; DNA-POLYMERASE; RNA; ALPHA; BETA; DIAGNOSIS
RP Ferrari, N (reprint author), NATL CANC INST, ADV BIOTECHNOL CTR, MOL BIOL LAB, I-16132 GENOA, ITALY.
RI Pfeffer, Ulrich/J-7064-2016
OI Pfeffer, Ulrich/0000-0003-0872-4671
NR 20
TC 10
Z9 10
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182183-8
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 282
BP 48
EP 64
PG 17
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ75E
UT WOS:A1997BJ75E00005
PM 9330276
ER
PT S
AU Wojnowski, L
Zimmer, A
AF Wojnowski, L
Zimmer, A
BE McCormick, DB
Suttie, JW
Wagner, C
TI Use of transgenic mice to study activation of retinoic acid-responsive
promoters
SO VITAMINS AND COENZYMES, PT L
SE Methods in Enzymology
LA English
DT Review
ID BETA-GALACTOSIDASE; LACZ GENE; RECEPTORS; ELEMENT; IDENTIFICATION;
EXPRESSION; SEQUENCE; CELLS
RP Wojnowski, L (reprint author), NIMH, GENET SECT, NIH, BETHESDA, MD 20892 USA.
RI Zimmer, Andreas/B-8357-2009
NR 20
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182183-8
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 1997
VL 282
BP 77
EP 85
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BJ75E
UT WOS:A1997BJ75E00007
PM 9330278
ER
PT J
AU Snow, JB
AF Snow, JB
TI Research on hearing and balance - Current and future developments
SO VOLTA REVIEW
LA English
DT Article
ID MULTICHANNEL COCHLEAR IMPLANTS; SERUM ANTIBODIES; MENIERES-DISEASE;
CHILDREN; GENE; EXPRESSION; MUTATION; DEAFNESS; CELLS; AIDS
AB A multitude of disease genes causing hearing impairment have been located in the human genome, as have genes responsible for the normal development of the ear. Sensory cells of the inner ear have been demonstrated to regenerate in fish, birds, and even mammals. Substantial progress has been made in the development of vaccines to prevent otitis media. Hearing aids are now programmable, and cochlear implants continue to be improved with new sound processing strategies. Great progress has occurred in rehabilitation of individuals with balance disorders through the use of physical therapy.
C1 Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA.
NR 21
TC 0
Z9 0
U1 1
U2 1
PU ALEXANDER GRAHAM BELL ASSOC FOR THE DEAF
PI WASHINGTON
PA 3417 VOLTA PLACE NW, WASHINGTON, DC 20007 USA
SN 0042-8639
J9 VOLTA REV
JI Volta Rev.
PY 1997
VL 99
IS 5
BP 29
EP 42
PG 14
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 331FF
UT WOS:000088006100003
ER
PT B
AU Brigger, P
Unser, M
AF Brigger, P
Unser, M
BE Aldroubi, A
Laine, AF
Unser, MA
TI General discrete centered image pyramids
SO WAVELET APPLICATIONS IN SIGNAL AND IMAGE PROCESSING V
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on Wavelet Applications in Signal and Image Processing V
CY JUL 30-AUG 01, 1997
CL SAN DIEGO, CA
SP Soc Photo Opt Instrumentat Engineers
DE splines; multi-resolution decomposition; image pyramids; least squares
pyramids; centered pyramids
AB We present an improved type of image pyramid based on general approximation functions. The type of pyramid proposed maintains the good properties of symmetry and consistent boundary conditions of the Haar pyramid. Moreover, it is not restricted to a piece-wise constant image model, but allows the use of any generating sequence. The centered topology guarantees a clearly defined up-projection of labels and may be employed in applications for contour detection, object recognition and segmentation.
We start by introducing the general discrete framework for the design of least squares pyramids using the standard filtering and decimation tools based on arbitrary basis functions. Our design criterion is to minimize the l(2) norm of the approximation error. We then define the centered pyramid and give explicit filter coefficients for odd and even spline approximation functions. Finally, we compare the centered pyramid to the ordinary one and highlight some applications.
RP Brigger, P (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,NCRR,BLDG 13,ROOM 3N17,BETHESDA,MD 20892, USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2591-5
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3169
BP 212
EP 223
DI 10.1117/12.279688
PG 12
WC Engineering, Electrical & Electronic; Optics
SC Engineering; Optics
GA BJ98C
UT WOS:A1997BJ98C00020
ER
PT B
AU Thevenaz, P
Unser, M
AF Thevenaz, P
Unser, M
BE Aldroubi, A
Laine, AF
Unser, MA
TI Spline pyramids for inter-modal image registration using mutual
information
SO WAVELET APPLICATIONS IN SIGNAL AND IMAGE PROCESSING V
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on Wavelet Applications in Signal and Image Processing V
CY JUL 30-AUG 01, 1997
CL SAN DIEGO, CA
SP Soc Photo Opt Instrumentat Engineers
DE multiresolution; B-spline; Parzen window; Marquardt-Levenberg
AB We propose a new optimizer for multiresolution image registration. It is adapted to a criterion known as mutual information and is well suited to inter-modality. Our iteration strategy is inspired by the Marquardt-Levenberg algorithm, even though the underlying problem is not least-squares. We develop a framework based on a continuous polynomial spline representation of images. Together with the use of Parzen histogram estimates, it allows for closed-form expressions of the gradient and Hessian of the criterion. Tremendous simplifications result from the choice of Parzen windows satisfying the partition of unity, also based on B-splines. We use this framework to compute an image pyramid and to set our optimizer in a multiresolution context. We perform several experiments and show that it is particularly well adapted to a coarse-to-fine optimization strategy. We compare our approach to the popular Powell algorithm and conclude that our proposed optimizer is faster, at no cost in robustness or precision.
RP Thevenaz, P (reprint author), NIH,BEIP,NATL CTR RES RESOURCES,BETHESDA,MD 20892, USA.
NR 0
TC 29
Z9 29
U1 0
U2 0
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2591-5
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3169
BP 236
EP 247
DI 10.1117/12.292794
PG 12
WC Engineering, Electrical & Electronic; Optics
SC Engineering; Optics
GA BJ98C
UT WOS:A1997BJ98C00022
ER
PT B
AU Unser, M
AF Unser, M
BE Aldroubi, A
Laine, AF
Unser, MA
TI Ten good reasons for using spline wavelets
SO WAVELET APPLICATIONS IN SIGNAL AND IMAGE PROCESSING V
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
(SPIE)
LA English
DT Proceedings Paper
CT Conference on Wavelet Applications in Signal and Image Processing V
CY JUL 30-AUG 01, 1997
CL SAN DIEGO, CA
SP Soc Photo Opt Instrumentat Engineers
DE splines; wavelet basis; biorthogonal wavelets; regularity; smoothness;
time-frequency localization; approximation properties
AB The purpose of this note is to highlight some of the unique properties of spline wavelets. These wavelets can be classified in four categories: othogonal (Battle-Lemarie), semi-orthogonal (e.g., B-spline), shift-orthogonal, and biorthogonal (Cohen-Daubechies-Feauveau). Unlike most other wavelet bases, splines have explicit formulae in both the time and frequency domain, which greatly facilitates their manipulation. They allow for a progressive transition between the two extreme cases of a multiresolution: Haar's piecewise constant representation (spline of degree zero) versus Shannon's bandlimited model (which corresponds to a spline of infinite order). Spline wavelets are extremely regular and usually symmetric or anti-symmetric. They can be designed to have compact support and to achieve optimal time-frequency localization (B-spline wavelets). The underlying scaling functions are the B-splines, which are the shortest and most regular scaling functions of order L. Finally, splines have the best approximation properties among all known wavelets of a given order L. In other words, they are the best for approximating smooth functions.
RP Unser, M (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,ROOM 3N17,BETHESDA,MD 20892, USA.
NR 0
TC 46
Z9 47
U1 0
U2 3
PU SPIE - INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA PO BOX 10, BELLINGHAM, WA 98227-0010
BN 0-8194-2591-5
J9 P SOC PHOTO-OPT INS
PY 1997
VL 3169
BP 422
EP 431
DI 10.1117/12.292801
PG 10
WC Engineering, Electrical & Electronic; Optics
SC Engineering; Optics
GA BJ98C
UT WOS:A1997BJ98C00039
ER
PT B
AU Aldroubi, A
AF Aldroubi, A
BE DAttellis, CE
FernandezBerdaguer, EM
TI Oblique multiwavelet bases
SO WAVELET THEORY AND HARMONIC ANALYSIS IN APPLIED SCIENCES
SE APPLIED AND NUMERICAL HARMONIC ANALYSIS
LA English
DT Proceedings Paper
CT 1st Latin-American Conference on Mathematics in Industry and Medicine
CY NOV 27-DEC 01, 1995
CL BUENOS AIRES, ARGENTINA
RP Aldroubi, A (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIRKHAUSER BOSTON
PI CAMBRIDGE
PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139-2333
BN 0-8176-3953-5
J9 APPL NUM HARM ANAL
PY 1997
BP 73
EP 91
PG 19
WC Mathematics, Applied
SC Mathematics
GA BJ84R
UT WOS:A1997BJ84R00004
ER
PT J
AU Gerlach, KK
Marino, C
Weed, DL
Hoffman-Goetz, L
AF Gerlach, KK
Marino, C
Weed, DL
Hoffman-Goetz, L
TI Lack of colon cancer coverage in seven women's magazines
SO WOMEN & HEALTH
LA English
DT Article
ID COLORECTAL-CANCER; STATISTICS; RISK; MACRONUTRIENTS; SMOKING; HAZARDS;
MEDIA; FIBER
AB Women's magazines are an important source of health information. To evaluate the relevancy of articles in these publications to known disease risks, seven women's magazines were reviewed to assess their coverage of colon cancer, the third leading cause of cancer mortality in U.S. women. Specifically, the amount of coverage devoted to colon cancer as well as the presentation of issues in the prevention, risks, treatment, diagnosis and genetics of colon cancer were recorded. Twenty articles were published on colon cancer in these magazines during the years 1987-1995. Compared to five other cancers that also affect women, colon cancer was the focus of the fewest articles in the seven magazines analyzed.
C1 NCI, Prevent Oncol Branch, Bethesda, MD 20892 USA.
NCI, Canc Prevent & Control Fellowship Program, Bethesda, MD 20892 USA.
RP Weed, DL (reprint author), Execut Plaza S,Suite T-41,6130 Execut Blvd, Bethesda, MD 20892 USA.
NR 44
TC 23
Z9 23
U1 0
U2 0
PU HAWORTH PRESS INC
PI BINGHAMTON
PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA
SN 0363-0242
J9 WOMEN HEALTH
JI Women Health
PY 1997
VL 26
IS 2
BP 57
EP 68
PG 12
WC Public, Environmental & Occupational Health; Women's Studies
SC Public, Environmental & Occupational Health; Women's Studies
GA YU463
UT WOS:000071720400004
PM 9472955
ER
PT B
AU Korach, KS
Taki, M
Kimbro, KS
AF Korach, KS
Taki, M
Kimbro, KS
BE Paoletti, R
Crosignani, PG
Kenemans, P
Samsioe, G
Soma, MR
Jackson, AS
TI Rie effects of estrogen receptor gene disruption on bone
SO WOMEN'S HEALTH AND MENOPAUSE: RISK REDUCTION STRATEGIES
SE MEDICAL SCIENCE SYMPOSIA SERIES
LA English
DT Proceedings Paper
CT 2nd International Symposium on Womens Health in Menopause - Risk
Reduction Strategies
CY DEC 05-08, 1996
CL FLORENCE, ITALY
RP Korach, KS (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,RECEPTOR BIOL SECT,NIH,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 0
TC 7
Z9 7
U1 0
U2 0
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
BN 0-7923-4697-1
J9 MED SCI SYMP SER
PY 1997
VL 11
BP 69
EP 73
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA BJ79C
UT WOS:A1997BJ79C00010
ER
PT J
AU Leipe, DD
Tong, SM
Goggin, CL
Slemenda, SB
Pieniazek, NJ
Sogin, ML
AF Leipe, DD
Tong, SM
Goggin, CL
Slemenda, SB
Pieniazek, NJ
Sogin, ML
TI 16S-like rDNA sequences from Developayella elegans, Labyrinthuloides
haliotidis, and Proteromonas lacertae confirm that the stramenopiles are
a primarily heterotrophic group
SO EUROPEAN JOURNAL OF PROTISTOLOGY
LA English
DT Article
DE chromophytes; evolution; proteromonads; phylogeny; stramenopiles
ID RIBOSOMAL-RNA SEQUENCES; PHYLOGENETIC ANALYSIS; FLAGELLAR APPARATUS;
ALGAE; CLASSIFICATION; ULTRASTRUCTURE; REGIONS; TREES
AB A phylogenetic analysis of the S-16-like ribosomal RNA coding regions from Labyrinthuloides haliotidis, Developayella elegans, Proteromonas lacertae and other organisms corroborates morphological evidence that proteromonads and other eukaryotes with tripartite tubular hairs form a monophyletic group of organisms, the stramenopiles. Within the stramenopiles, the heterotrophic groups (proteromonads, Labyrinthulida, bicosoecids, Developayella and oomycetes) diverge before the radiation of the ''heterokont algae'', the autotrophic stramenopiles. The stramenopiles were initially ''protozoan'' but their ecological success is largely attributable to the late symbiotic acquisition of chloroplasts. The stramenopiles and other taxa with chlorophyll a+c containing chloroplasts (cryptomonads, dinoflagellates, and haptophytes) do not share a common autotrophic ancestor. These photosynthetic assemblages acquired their plastids independently.
C1 MARINE BIOL LAB, CTR MOL EVOLUT, WOODS HOLE, MA 02543 USA.
NATL LIB MED, NIH, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA.
UNIV SOUTHAMPTON, DEPT BIOL, SOUTHAMPTON SO16 7PX, HANTS, ENGLAND.
UNIV PRINCE EDWARD ISL, ATLANTIC VET COLL, CHARLOTTETOWN, PE C1A 4P3, CANADA.
CTR DIS CONTROL & PREVENT MS F13, ATLANTA, GA 30341 USA.
NR 55
TC 76
Z9 78
U1 1
U2 6
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0932-4739
EI 1618-0429
J9 EUR J PROTISTOL
JI Eur. J. Protistol.
PD DEC 31
PY 1996
VL 32
IS 4
BP 449
EP 458
PG 10
WC Microbiology
SC Microbiology
GA WG561
UT WOS:A1996WG56100004
ER
PT J
AU Park, YM
Yoo, YD
Paik, SY
Kim, BS
Tabor, E
AF Park, YM
Yoo, YD
Paik, SY
Kim, BS
Tabor, E
TI Mutation of tumor suppressor gene p53 in hepatocellular carcinomas from
Korea
SO EXPERIMENTAL AND MOLECULAR MEDICINE
LA English
DT Article
DE reverse transcription polymerase chain reaction; polymerase chain
reaction single strand conformation polymorphism; p53; tumor suppressor
gene; hepatocellular carcinoma
ID CHINA; HETEROGENEITY; ABERRATIONS; EXPRESSION; OCCUR
AB Mutation of the p53 gene in hepatocellular carcinoma has been recognized as one of the most important genetic alterations to occur during hepatocarcinogenesis. This study was performed to analyze the frequency and nature of p53 mutations in advanced hepatocellular carcinomas from Korea. Tissue samples were obtained by laparoscopic biopsy from 35 patients; adjacent nontumorous liver tissue was also obtained from 24 of them. Mutations of the p53 gene were identified in 11/35 (31%) of hepatocellular carcinomas, These included 7 missense mutations and 4 deletion mutations. Only one mutation was detected at codon 249, a ''hot spot'' at which mutations have been found frequently in hepatocellular carcinomas from some geographic areas; however, this was an A-to-T transversion at the first nucleotide, thus differing from commonly reported G-to-T transversion at the third nucleotide of codon 249 in hepatocellular carcinomas, Patients whose serum alkaline phosphatase levels were higher than the mean Value were more likely to have p53 mutations, compared to patients whose alkaline phosphatase levels were lower than the mean value [55% (6/11) vs. 21% (5/24)] (p<0.05). Thus, p53 mutations are found in many hepatocellular carcinomas in Korea. However, mutations commonly thought to be due to aflatoxin B-1 (G-to-T transversion at codon 249) were not found, suggesting that aflatoxin-B-1 does not play an important role in the etiology of hepatocellular carcinoma in Korea.
C1 NCI,NIH,BETHESDA,MD 20892.
CATHOLIC UNIV,SCH MED,KANGNAM ST MARYS HOSP,DEPT INTERNAL MED,SEOUL,SOUTH KOREA.
KOREAN CANC CTR HOSP,LAB EXPT THERAPEUT,SEOUL,SOUTH KOREA.
CATHOLIC UNIV,SCH MED,DEPT MICROBIOL,SEOUL,SOUTH KOREA.
US FDA,BETHESDA,MD 20014.
NR 26
TC 6
Z9 6
U1 1
U2 2
PU KOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY
PI SEOUL
PA #812 KOFST, 635-4 YOKSAM-DONG KANGNAM-GU, SEOUL 135-703, SOUTH KOREA
SN 1226-3613
J9 EXP MOL MED
JI Exp. Mol. Med.
PD DEC 31
PY 1996
VL 28
IS 4
BP 173
EP 179
PG 7
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA WC363
UT WOS:A1996WC36300004
ER
PT J
AU Lin, YJ
Bovetto, S
Carver, JM
Giordano, T
AF Lin, YJ
Bovetto, S
Carver, JM
Giordano, T
TI Cloning of the cDNA for the human NMDA receptor NR2C subunit and its
expression in the central nervous system and periphery
SO MOLECULAR BRAIN RESEARCH
LA English
DT Article
DE NMDA receptors; NR2C; distribution; cloning, in situ; human
ID D-ASPARTATE RECEPTORS; LONG-TERM POTENTIATION; GLUTAMATE-RECEPTOR;
MOLECULAR-CLONING; PHARMACOLOGICAL CHARACTERIZATION; SYNAPTIC
PLASTICITY; EPSILON-4 SUBUNIT; MESSENGER-RNAS; CLONED CDNAS; CHANNEL
AB Several overlapping cDNA clones containing 3995 nucleotides of the human 2C NMDA receptor subunit (NR2C) were isolated from human hippocampal and cerebellar cDNA libraries. The nucleic acid sequence of the overlapping cDNA clones displays 85% identity to that of rat NR2C. The predicted protein sequence is 1233 amino acids long and has 88% identity to the amino acid sequence of the rat NR2C. Northern blot analysis has demonstrated a wide distribution pattern of the NR2C transcript in the brain. While the predominant expression is in the cerebellum, as observed in the rat, readily detectable levels are present in the hippocampus, amygdala, caudate nucleus, corpus callosum, subthalamic nuclei and thalamus. NR2C was also detected in the heart, skeletal muscle and pancreas. Distribution of the mouse NR2C NMDA receptor subunit homologue was investigated in mouse brain by in situ hybridization histochemistry using exonic genomic probes. Expression of the transcript was principally in the cerebellum, but is also detected in the hippocampus, dentate gyrus, thalamic and subthalamic nuclei, vestibular nuclei and olfactory bulb. These results demonstrate a widespread expression pattern of the NR2C gene, both in the CNS and in the periphery.
C1 SYMPHONY PHARMACEUT INC,DEPT MOL BIOL,MALVERN,PA 19355.
NIDDK,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
NR 41
TC 28
Z9 29
U1 3
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0169-328X
J9 MOL BRAIN RES
JI Mol. Brain Res.
PD DEC 31
PY 1996
VL 43
IS 1-2
BP 57
EP 64
DI 10.1016/S0169-328X(96)00146-5
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA WD744
UT WOS:A1996WD74400007
ER
PT J
AU Soh, Y
Jeong, KS
AF Soh, Y
Jeong, KS
TI In vitro phosphorylation of purified transketolase by protein kinase C
SO MOLECULES AND CELLS
LA English
DT Article
ID WERNICKE-KORSAKOFF-SYNDROME; PURIFICATION; ABNORMALITY; ALCOHOLICS;
ENZYME
AB Catalytically active transketolase was purified from rat liver cytosolic fi action by more than 120-fold to near homogeneity by successive column chromatography using DEAE-Sephacel, hydroxylapatite and Mono P matrices. The purified transketolase was rapidly phosphorylated by protein kinase C (PKC) while it was minimally phosphorylated by cAMP-dependent protein kinase and casein kinase II. Phosphoamino acid analysis of the P-32-labeled enzyme revealed that only threonine residue was phosphorylated by PKC. The phosphorylated enzyme became less active (about 40%) than the non-phosphorylated counterpart. Our data suggest that transketolase can be phosphorylated by PKC, which could represent a new type of regulatory mechanism for transketolase.
C1 KIST,KOREA RES INST BIOSCI & BIOTECHNOL,TAEJON 305606,SOUTH KOREA.
RP Soh, Y (reprint author), NIAAA,NEUROGENET LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA.
NR 20
TC 1
Z9 1
U1 0
U2 0
PU KOREAN SOC MOLECULAR BIOLOGY
PI SEOUL
PA KOREA SCI TECHNOLOGY CENTER, ROOM 815, 635-4 YEOGSAM-DONG KANGNAM-GU,
SEOUL 135-703, SOUTH KOREA
SN 1016-8478
J9 MOL CELLS
JI Mol. Cells
PD DEC 31
PY 1996
VL 6
IS 6
BP 692
EP 696
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA WA011
UT WOS:A1996WA01100010
ER
PT J
AU Tonk, V
Schultz, RA
Christian, SL
Kubota, T
Ledbetter, DH
Wilson, GN
AF Tonk, V
Schultz, RA
Christian, SL
Kubota, T
Ledbetter, DH
Wilson, GN
TI Robertsonian (15q;15q) translocation in a child with Angelman syndrome:
Evidence of uniparental disomy
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE chromosome 15 translocations; Robertsonian translocation 15q15q;
Angelman syndrome; Prader-Willi syndrome; paternal uniparental disomy
AB A balanced Robertsonian translocation 45,XY,t(15q15q) was detected in a patient with mental retardation, microcephaly, and hypertonia. Deletion of the 15q11q13 region was unlikely based on fluorescence in situ hybridization studies that revealed hybridization of appropriate DNA probes to both arms of the Robertsonian chromosome. Inheritance of alleles from 13 highly polymorphic DNA markers on chromosome 15 showed paternal uniparental isodisomy. The clinical, cytogenetic, and molecular results are consistent with a diagnosis of Angelman syndrome. (C) 1996 Wiley-Liss, Inc.
C1 UNIV TEXAS,SW MED CTR,DEPT PEDIAT,DALLAS,TX 75235.
UNIV TEXAS,SW MED CTR,DEPT PATHOL,DALLAS,TX 75235.
UNIV TEXAS,SW MED CTR,MCDERMOTT CTR HUMAN GENET & DEV,DALLAS,TX 75235.
NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892.
NR 8
TC 13
Z9 14
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD DEC 30
PY 1996
VL 66
IS 4
BP 426
EP 428
DI 10.1002/(SICI)1096-8628(19961230)66:4<426::AID-AJMG7>3.0.CO;2-I
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA WA357
UT WOS:A1996WA35700007
PM 8989460
ER
PT J
AU Wyszynski, DF
Lewanda, AF
Beaty, TH
AF Wyszynski, DF
Lewanda, AF
Beaty, TH
TI Phenotypic discordance in a family with monozygotic twins and
non-syndromic cleft lip and palate
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Letter
ID GROWTH-FACTOR-ALPHA; MATERNAL CIGARETTE-SMOKING; AUTOSOMAL MAJOR LOCUS;
ORAL CLEFTS; CONGENITAL-MALFORMATIONS; OROFACIAL CLEFTS; FOLIC-ACID;
LINKAGE; PREGNANCY; GENE
C1 NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892.
CHILDRENS NATL MED CTR,DEPT MED GENET,WASHINGTON,DC 20010.
JOHNS HOPKINS UNIV HOSP,DEPT PEDIAT,BALTIMORE,MD 21287.
RP Wyszynski, DF (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,615 N WOLFE ST,BALTIMORE,MD 21205, USA.
FU NIDCR NIH HHS [D01-DE10293]
NR 40
TC 8
Z9 8
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD DEC 30
PY 1996
VL 66
IS 4
BP 468
EP 470
DI 10.1002/(SICI)1096-8628(19961230)66:4<468::AID-AJMG17>3.0.CO;2-S
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA WA357
UT WOS:A1996WA35700017
PM 8989470
ER
PT J
AU Chen, N
Chrambach, A
AF Chen, N
Chrambach, A
TI Improved resolution in the gel electrophoresis of proteins by a
periodically interrupted electric field
SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS
LA English
DT Article
DE protein; resolution; periodically interrupted electric field; field
strength; gel electrophoresis
ID AGAROSE GELS; DNA; SEPARATION; PARTICLES
AB The capability of the commercial gel electrophoresis apparatus with intermittent scanning of fluorescence (HPGE-1000, LabIntelligence) to provide time-dependent zone dispersion allows one to quantitate resolution. Using a model protein separation, that between phycoerythrin and fluorescein-labeled conalbumin, resolution was compared between separations conducted at a constant field strength of 80 V/cm and one conducted in 10-s pulses of the same field strength, interrupted periodically by 120 s in the absence of an electric field. Resolution was improved by a factor of two in the discontinuous application of the electric field compared to that obtained in its continuous application. Similarly, the intermittent application of 80 V/cm for 10 s, followed by 120-s pauses, gave rise to twice the resolution obtained from a continuous application of 7 V/cm.
C1 NICHHD,MACROMOL ANAL SECT,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892.
NR 21
TC 2
Z9 2
U1 2
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-022X
J9 J BIOCHEM BIOPH METH
JI J. Biochem. Biophys. Methods
PD DEC 30
PY 1996
VL 33
IS 3
BP 163
EP 170
DI 10.1016/S0165-022X(96)00021-8
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA WE643
UT WOS:A1996WE64300002
PM 9029260
ER
PT J
AU Wenner, P
Tsau, Y
Cohen, LB
ODonovan, MJ
Dan, Y
AF Wenner, P
Tsau, Y
Cohen, LB
ODonovan, MJ
Dan, Y
TI Voltage-sensitive dye recording using retrogradely transported dye in
the chicken spinal cord: Staining and signal characteristics
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE voltage-sensitive dye; optical recording; embryonic chick spinal cord;
multi-site recording; retrograde staining; dye vs electrode recording
ID SALAMANDER OLFACTORY-BULB; CENTRAL NERVOUS-SYSTEM; GILL-WITHDRAWAL
REFLEX; NEURONS; EMBRYO; MOTONEURONS; ORGANIZATION; ORIGIN; FURA-2;
SLICE
AB We describe a novel method for retrogradely labeling specific neuronal populations using voltage-sensitive dyes. Styryl dyes were injected into the Ventral roots of the isolated embryonic chick spinal cord. After waiting several hours, the dye labeled motoneurons and autonomic preganglionic neurons. Neuronal cell bodies, dendrites and axons were labeled; we presume that the dye traveled either by retrograde transport or by diffusion within the membrane of the axon to which the dyes were initially applied. Using either a photodiode array or a photomultiplier, fluorescence changes could be recorded from motoneurons following antidromic or synaptic activation. Several characteristics of the fluorescence changes were measured indicating that the signals did indeed reflect changes in the motoneuron membrane potential. The best labeling and optical signals were obtained using the relatively hydrophobic dyes di-8-ANEPPQ and di-12-ANEPEQ. In the great majority of cases these dyes responded with an increase in fluorescence of 1-3% (Delta F/F) in response to synaptic or antidromic depolarization of the motoneurons. We anticipate that these techniques should be useful in the mapping of activity patterns and connectivity in neural networks within a defined population of neurons.
C1 YALE UNIV,SCH MED,DEPT PHYSIOL,NEW HAVEN,CT 06510.
RP Wenner, P (reprint author), NIH,LAB NEURAL CONTROL,NINDS,BETHESDA,MD 20892, USA.
OI Wenner, Peter/0000-0002-7072-2194
FU NIGMS NIH HHS [GM35063]; NINDS NIH HHS [NS08437]
NR 28
TC 22
Z9 22
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD DEC 28
PY 1996
VL 70
IS 2
BP 111
EP 120
DI 10.1016/S0165-0270(96)00108-2
PG 10
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA WC979
UT WOS:A1996WC97900001
PM 9007750
ER
PT J
AU Tsau, Y
Wenner, P
ODonovan, MJ
Cohen, LB
Loew, LM
Wuskell, JP
AF Tsau, Y
Wenner, P
ODonovan, MJ
Cohen, LB
Loew, LM
Wuskell, JP
TI Dye screening and signal-to-noise ratio for retrogradely transported
voltage-sensitive dyes
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE voltage-sensitive dye; optical recording; embryonic chick spinal cord;
multi-site recording; retrograde staining; styryl dye; dye synthesis;
hydrophobic vs hydrophilic dye
ID CHARGE-SHIFT PROBES; SALAMANDER OLFACTORY-BULB; CENTRAL NERVOUS-SYSTEM;
MEMBRANE; FLUORESCENCE; NEURONS; AXONS
AB Using a novel method for retrogradely labeling specific neuronal populations, we tested different styryl dyes in attempt to find dyes whose staining would be specific, rapid, and lead to large activity dependent signals. The dyes were injected into the ventral roots of the isolated chick spinal cord from embryos at days E9-E12. The voltage-sensitive dye signals were recorded from synaptically activated motoneurons using a 464 element photodiode array. The best labeling and optical signals were obtained using the relatively hydrophobic dyes di-8-ANEPPQ and di-12-ANEPEQ. Over the 24 h period we examined, these dyes bound specifically to the cells with axons in the ventral roots. The dyes responded with an increase in fluorescence of 1-3% (Delta F/F) in response to synaptic depolarization of the motoneurons. The signal-to-noise ratio obtained in a single trial from a detector that received light from a 14 X 14 mu m(2) area of the motoneuron population was about 10:1. Nonetheless, signals on neighboring diodes were similar, suggesting that we were not detecting the activity of individual neurons. Retrograde labeling and optical recording with voltage-sensitive dyes provides a means for monitoring the activity of identified neurons in situations where microelectrode recordings are not feasible.
C1 YALE UNIV, SCH MED, DEPT PHYSIOL, NEW HAVEN, CT 06510 USA.
NIH, NEURAL CONTROL LAB, NINDS, BETHESDA, MD 20892 USA.
UNIV CONNECTICUT, CTR HLTH, DEPT PHYSIOL, FARMINGTON, CT 06032 USA.
MARINE BIOL LAB, WOODS HOLE, MA 02543 USA.
OI Loew, Leslie/0000-0002-1851-4646; Wenner, Peter/0000-0002-7072-2194
FU NIGMS NIH HHS [GM35063]; NINDS NIH HHS [NS08437]
NR 18
TC 33
Z9 34
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
EI 1872-678X
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD DEC 28
PY 1996
VL 70
IS 2
BP 121
EP 129
DI 10.1016/S0165-0270(96)00109-4
PG 9
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA WC979
UT WOS:A1996WC97900002
PM 9007751
ER
PT J
AU Mizzen, CA
Yang, XJ
Kokubo, T
Brownell, JE
Bannister, AJ
OwenHughes, T
Workman, J
Wang, L
Berger, SL
Kouzarides, T
Nakatani, Y
Allis, CD
AF Mizzen, CA
Yang, XJ
Kokubo, T
Brownell, JE
Bannister, AJ
OwenHughes, T
Workman, J
Wang, L
Berger, SL
Kouzarides, T
Nakatani, Y
Allis, CD
TI The TAF(II)250 subunit of TFIID has histone acetyltransferase activity
SO CELL
LA English
DT Article
ID RNA-POLYMERASE-II; TATA-BOX-BINDING; TRANSCRIPTION FACTOR; NUCLEOSOMAL
DNA; FACILITATED BINDING; ACETYLATION; CHROMATIN; GENE; ACTIVATION;
INITIATION
AB The transcription initiation factor TFIID is a multimeric protein complex composed of TATA box-binding protein (TBP) and many TBP-associated factors (TAF(II)s). TAF(II)s are important cofactors that mediate activated transcription by providing interaction sites for distinct activators. Here, we present evidence that human TAF(II)250 and its homologs in Drosophila and yeast have histone acetyltransferase (HAT) activity in vitro. HAT activity maps to the central, most conserved portion of dTAF(II)230 and yTAF(II)130. The HAT activity of dTAF(II)230 resembles that of yeast and human GCN5 in that it is specific for histones H3 and H4 in vitro. Our findings suggest that targeted histone acetylation at specific promoters by TAF(II)250 may be involved in mechanisms by which TFIID gains access to transcriptionally repressed chromatin.
C1 UNIV ROCHESTER, DEPT BIOL, ROCHESTER, NY 14627 USA.
NICHHD, LAB MOL GROWTH REGULAT, NIH, BETHESDA, MD 20892 USA.
UNIV CAMBRIDGE, WELLCOME CRC INST, CAMBRIDGE CB2 1QR, ENGLAND.
PENN STATE UNIV, DEPT BIOCHEM & MOL BIOL, UNIVERSITY PK, PA 16802 USA.
WISTAR INST ANAT & BIOL, PHILADELPHIA, PA 19104 USA.
NARA INST SCI & TECHNOL, NARA 63001, JAPAN.
OI Owen-Hughes, Tom/0000-0002-0618-8185
FU NIGMS NIH HHS [NIH-GM53512]; Wellcome Trust
NR 70
TC 578
Z9 585
U1 0
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD DEC 27
PY 1996
VL 87
IS 7
BP 1261
EP 1270
DI 10.1016/S0092-8674(00)81821-8
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA WA541
UT WOS:A1996WA54100014
PM 8980232
ER
PT J
AU Rice, PA
Yang, SW
Mizuuchi, K
NAsh, HA
AF Rice, PA
Yang, SW
Mizuuchi, K
NAsh, HA
TI Crystal structure of an IHF-DNA complex: A protein-induced DNA u-turn
SO CELL
LA English
DT Article
ID INTEGRATION HOST FACTOR; ESCHERICHIA-COLI; BINDING PROTEINS; ADENINE
TRACT; MINOR-GROOVE; HU PROTEIN; SITES; LATTICE; MUTANTS; RECOMBINATION
AB Integration host factor (IHF) is a small heterodimeric protein that specifically binds to DNA and functions as an architectural factor in many cellular processes in prokaryotes. Here, we report the crystal structure of IHF complexed with 35 bp of DNA. The DNA is wrapped around the protein and bent by >160 degrees, thus reversing the direction of the helix axis within a very short distance. Much of the bending occurs at two large kinks where the base stacking is interrupted by intercalation of a proline residue. IHF contacts the DNA exclusively via the phosphodiester backbone and the minor groove and relies heavily on indirect readout to recognize its binding sequence. One such readout involves a six-base A tract, providing evidence for the importance of a narrow minor groove.
C1 NIMH,MOL BIOL LAB,NIH,BETHESDA,MD 20892.
RP Rice, PA (reprint author), NIDDK,MOL BIOL LAB,NIH,BETHESDA,MD 20892, USA.
NR 66
TC 558
Z9 566
U1 2
U2 18
PU CELL PRESS
PI CAMBRIDGE
PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138
SN 0092-8674
J9 CELL
JI Cell
PD DEC 27
PY 1996
VL 87
IS 7
BP 1295
EP 1306
DI 10.1016/S0092-8674(00)81824-3
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA WA541
UT WOS:A1996WA54100017
PM 8980235
ER
PT J
AU Puzianowska-Kuznicka, M
Wong, JM
Kanamori, A
Shi, YB
AF Puzianowska-Kuznicka, M
Wong, JM
Kanamori, A
Shi, YB
TI Functional characterization of a mutant thyroid hormone receptor in
Xenopus laevis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RETINOIC ACID RECEPTORS; TRANSCRIPTIONAL ACTIVATION; AMPHIBIAN
METAMORPHOSIS; RESPONSE ELEMENTS; ONCOGENE PRODUCT; GENE-EXPRESSION;
DIRECT REPEATS; X RECEPTORS; BETA; REPRESSION
AB Thyroid hormone plays a causative role during frog metamorphosis, and its effect is mediated by thyroid hormone receptors (TRs), To investigate the function of Xenopus TRs, we have recently developed a thyroid hormone dependent in vivo transcription system by introducing TRs and RXRs (9-cis-retinoic acid receptors) into Xenopus oocytes. Interestingly, using this system, we have found that the TR alpha B cloned previously is defective in transcriptional activation compared with TR alpha A, In vitro DNA binding experiments show that TR alpha B . RXR heterodimers have drastically reduced affinity for a thyroid hormone response element, Site-directed mutagenesis shows that two of the seven amino acid residues that differ between TR alpha A and TR alpha B are responsible for the defect in TR alpha B function. These two residues affect the DNA binding by both TR . RXR heterodimers and TR homodimers, In contrast, heterodimer formation with RXRs is not affected as demonstrated by coimmunoprecipitation and dominant-transcriptional inhibition experiments, By cDNA and genomic DNA sequence analysis, we have demonstrated that the residues, which affect TR alpha B function when mutated, are identical between the wild type TR alpha B and TR alpha A, Thus, our experiments have discovered the first amphibian TR mutant, The DNA binding and transcription activation functions of the mutant are discussed in relation to the recently published TR crystal structure.
C1 NICHHD, MOL EMBRYOL LAB, NIH, BETHESDA, MD 20892 USA.
NATL RES INST AQUACULTURE, TAMAKI, MIE 51904, JAPAN.
NR 42
TC 9
Z9 9
U1 2
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 27
PY 1996
VL 271
IS 52
BP 33394
EP 33403
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WA713
UT WOS:A1996WA71300035
PM 8969201
ER
PT J
AU Pelton, JG
Torchia, DA
Remington, SJ
Murphy, KP
Meadow, ND
Roseman, S
AF Pelton, JG
Torchia, DA
Remington, SJ
Murphy, KP
Meadow, ND
Roseman, S
TI Structures of active site histidine mutants of IIIGlc, a major
signal-transducing protein in Escherichia coli - Effects on the
mechanism of regulation and phosphoryl transfer
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NUCLEAR MAGNETIC-RESONANCE; BACTERIAL PHOSPHOTRANSFERASE SYSTEM;
3-DIMENSIONAL NMR-SPECTROSCOPY; HYDROGEN-BONDING INTERACTIONS;
ALPHA-LYTIC PROTEASE; PHOSPHOCARRIER PROTEIN; BACILLUS-SUBTILIS; GLUCOSE
PERMEASE; IIA-DOMAIN; SUGAR-TRANSPORT
AB IIIGlc (also called IIA(Glc)), a major signal-transducing protein in Escherichia coli, is also a phosphorylcarrier in glucose uptake, The crystal and NMR structures of IIIGlc show that His(90), the phosphoryl acceptor, adjoins His(75) in the active site, Glutamine was substituted for His-, giving (IIIGlc)-I-H75Q and (IIIGlc)-I-H90Q, respectively (Presper, K. A., Wong, C.-Y., Liu, L., Meadow, N. D., and Roseman, S. (1989) Proc, Natl. Acad. Sci. U.S.A. 86, 4052-4055), but the mutants showed unexpected properties, (IIIGlc)-I-H90Q loses regulatory functions of IIIGlc, and the phosphoryltransfer rates between Hpr/(IIIGlc)-I-H75Q are 200-fold less than HPr/IIIGlc (Meadow, N. D., and Roseman, S. (1996) J. Biol. Chem. 271, 33440-33445), X-ray crystallography, differential scanning calorimetry, and NMR have now been used to determine the structures of the mutants (phospho-(IIIGlc)-I-H75Q was studied by NMR), The three methods gave completely consistent results. Except for the His to Gin substitutions, the only significant structural changes were in a few hydrogen bonds, (IIIGlc)-I-H90Q contains two structured water molecules (to Gln(90)), which could explain its inability to regulate glycerol kinase.
Phospho-IIIGlc contains a chymotrypsin like, hydrogen bond network (Thr(73)-His(75) -O(-)phosphoryl), whereas phospho-(IIIGlc)-I-H75Q contains only one bond (Gln(75)-O--phosphoryl), Hydrogen bonds play an essential role in a proposed mechanism for the phosphoryltransfer reaction.
C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218.
JOHNS HOPKINS UNIV,MCCOLLUM PRATT INST,BALTIMORE,MD 21218.
NIDR,BONE RES BRANCH,NIH,BETHESDA,MD 20892.
UNIV OREGON,DEPT PHYS,EUGENE,OR 97403.
UNIV IOWA,DEPT BIOCHEM,IOWA CITY,IA 52242.
FU NIGMS NIH HHS [GM38759, GM42618]
NR 63
TC 15
Z9 15
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 DEC 27
PY 1996
VL 271
IS 52
BP 33446
EP 33456
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WA713
UT WOS:A1996WA71300042
PM 8969208
ER
PT J
AU Simpson, PB
Russell, JT
AF Simpson, PB
Russell, JT
TI Mitochondria support inositol 1,4,5-trisphosphate-mediated Ca2+ waves in
cultured oligodendrocytes
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID INTRACELLULAR CALCIUM-CONCENTRATION; ENDOPLASMIC-RETICULUM;
PHOSPHOINOSITIDE HYDROLYSIS; RAT OLIGODENDROCYTES; ASTROCYTES; CELLS;
RECEPTORS; NEURONS; AGONIST; LOCALIZATION
AB We have examined the spatial and temporal nature of Ca2+ signals activated via the phosphoinositide pathway in oligodendrocytes and the cellular specializations underlying oligodendrocyte Ca2+ response characteristics. Cultured cortical oligodendrocytes were incubated with fluo 3 or fura 2, and digital video fluorescence microscopy was used to study the effect of methacholine on [Ca2+](i). Single peaks, oscillations, and steady-state plateau [Ca2+](i) elevations were evoked by increasing agonist concentration. The peaks and oscillations were found to be Ca2+ wave fronts, which propagate via distinct amplification regions in the cell where the kinetics of Ca2+ release (amplitude and rate of rise of response) are elevated. Staining with 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolecarbocyanine iodide (JC-1) and 3,3'-dihexyloxacarbocyanine iodide revealed that mitochondria are found in groups of three or more in oligodendrocyte processes and that the groups are distributed with considerable distance separating them. Cross-correlation analysis showed a high degree of correlation between sites where mitochondria are present and peaks in the amplitude and rate of rise of the Ca2+ response. Intramitochondrial Ca2+ concentration, measured using rhod 2, increased upon treatment with methacholine. Methacholine also evoked a rapid change in mitochondrial membrane potential as measured by the J-aggregate fluorescence of JC-1. Pretreatment with the mitochondrial inhibitors carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (1 mu M, 2 min) or antimycin (2 mu g/ml, 2 min) altered the methacholine-evoked Ca2+ response in most cells studied, responses being either markedly potentiated or inhibited. The results of this study demonstrate that stimulation of phosphoinositide-coupled muscarinic acetylcholinoceptors activates propagating Ca2+ wave fronts in oligodendrocytes and that the characteristics of these waves are dependent on mitochondrial location and function.
C1 NICHHD,LCMN,NIH,BETHESDA,MD 20892.
NR 46
TC 127
Z9 129
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 DEC 27
PY 1996
VL 271
IS 52
BP 33493
EP 33501
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WA713
UT WOS:A1996WA71300047
PM 8969213
ER
PT J
AU Sax, CM
Salamon, C
Kays, WT
Guo, J
Yu, FSX
Cuthbertson, RA
Piatigorsky, J
AF Sax, CM
Salamon, C
Kays, WT
Guo, J
Yu, FSX
Cuthbertson, RA
Piatigorsky, J
TI Transketolase is a major protein in the mouse cornea
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID WERNICKE-KORSAKOFF SYNDROME; ADENYLATE-CYCLASE ACTIVITY; LENS
CRYSTALLINS; ALDEHYDE DEHYDROGENASE; GLUTATHIONE-PEROXIDASE;
SUPEROXIDE-DISMUTASE; HUMAN-ERYTHROCYTES; EYE; EPITHELIUM; EXPRESSION
AB Earlier experiments in this laboratory identified a highly expressed 65-68-kDa protein in both mouse and human corneas (Cuthbertson, R. A., Tomarev, S. I., and Piatigorsky J. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 4004-4008). Here, we demonstrate that this protein is transketolase (TKT; EC 2.2.1.1), an enzyme in the nonoxidative branch of the pentose-phosphate pathway, based on peptide and cDNA isolation and sequence analysis of mouse cornea protein and RNA samples, respectively. While expressed at low levels in a number of tissues, the 2.1-kilobase TKT mRNA was expressed at a 50-fold higher level in the adult mouse cornea. The area of most abundant expression was localized to the cornea epithelial cell layer by in situ hybridization. Western blot analysis confirmed TKT protein abundance in the cornea and indicated that TKT may comprise as much as 10% of the total soluble protein of the adult mouse cornea. Soluble cornea extracts exhibited a correspondingly high level of TKT enzymatic activity. TKT expression increased progressively through cornea maturation, as shown by Northern blot, in situ hybridization, Western blot, and enzymatic analyses. TKT mRNA and protein were expressed at low levels in the cornea prior to eye opening, while markedly increased levels were observed after eye opening. Taken together, these observations suggest that TKT may be a cornea enzyme-crystallin, and suggest that the crystallin paradigm and concept of gene sharing, once thought to be restricted to the lens, apply to other transparent ocular tissues.
C1 HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA 02114.
RP Sax, CM (reprint author), NEI,MOL & DEV BIOL LAB,NIH,MSC 2730,BETHESDA,MD 20892, USA.
FU NEI NIH HHS [EY10869]
NR 71
TC 61
Z9 63
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 DEC 27
PY 1996
VL 271
IS 52
BP 33568
EP 33574
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WA713
UT WOS:A1996WA71300057
PM 8969223
ER
PT J
AU Zhang, SY
Coso, OA
Lee, CH
Gutkind, JS
Simonds, WF
AF Zhang, SY
Coso, OA
Lee, CH
Gutkind, JS
Simonds, WF
TI Selective activation of effector pathways by brain-specific G protein
beta(5)
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HETEROTRIMERIC G-PROTEINS; GAMMA-SUBUNITS; PHOSPHOLIPASE-C; SIGNALING
PATHWAY; KINASE ACTIVATION; ADENYLYL CYCLASE; ALPHA-SUBUNIT; BINDING;
STIMULATION; EXPRESSION
AB While multiple G protein beta and gamma subunit isoforms have been identified, the implications of this potential diversity of beta gamma heterodimers for signaling through beta gamma-regulated effector pathways remains unclear. Furthermore the molecular mechanism(s) by which the beta gamma complex modulates diverse mammalian effector molecules is unknown. Effector signaling by the structurally distinct brain-specific beta(5) subunit was assessed by transient cotransfection with gamma(2) in COS cells and compared with beta(1). Transfection of either beta(1) or beta(5) with gamma(2) stimulated the activity of cotransfected phospholipase C-beta(2) (PLC-beta(2)), as previously reported, In contrast, cotransfection of beta(1) but not beta(5) with gamma(2) stimulated the mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase (JNK) pathways even though the expression of beta(5) in COS cells was evident by immunoblotting. The G protein beta(5) expressed in transfected COS cells was properly folded as its pattern of stable C-terminal proteolytic fragments was identical to that of native brain beta(5). The inability of beta(5) to activate the MAPK and JNK pathways was not overcome by cotransfection with three additional G gamma isoforms. These results suggest it is the G beta subunit which determines the pattern of downstream signaling by the beta gamma complex and imply that the structural features of the beta gamma complex mediating effector regulation may differ among effectors.
C1 NIDDK,METAB RES BRANCH,BETHESDA,MD 20892.
NIDR,CELLULAR DEV & ONCOL LAB,MOL SIGNALLING UNIT,NIH,BETHESDA,MD 20892.
RI Gutkind, J. Silvio/A-1053-2009
NR 54
TC 74
Z9 74
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 27
PY 1996
VL 271
IS 52
BP 33575
EP 33579
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA WA713
UT WOS:A1996WA71300058
PM 8969224
ER
PT J
AU Rixe, O
Ortuzar, W
Alvarez, M
Parker, R
Reed, E
Paull, K
Fojo, T
AF Rixe, O
Ortuzar, W
Alvarez, M
Parker, R
Reed, E
Paull, K
Fojo, T
TI Oxaliplatin, tetraplatin, cisplatin, and carboplatin: Spectrum of
activity in drug-resistant cell lines and in the cell lines of the
National Cancer Institute's Anticancer Drug Screen panel
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE platinum; oxaliplatin; cisplatin; platinum resistance; drug screen; drug
discovery
ID OVARIAN-CARCINOMA XENOGRAFTS; ANTITUMOR-ACTIVITY; GLUTATHIONE DEPLETION;
CROSS-RESISTANCE; PLATINUM ANALOGS; AMPHOTERICIN-B; CYTO-TOXICITY;
PHASE-I; ACCUMULATION; CYTOTOXICITY
AB The present study was designed to explore the activity of platinum compounds in cisplatin-resistant cell lines, the unselected cell lines of the National Cancer Institute's Anticancer Drug Screen, and the potential for use in combination. The activities of four platinum compounds in cisplatin-resistant KB and A2780 cells were investigated. The cells were highly resistant to cisplatin and cross-resistant to carboplatin, but less than one tenth as resistant to oxaliplatin and tetraplatin. Cellular accumulation of all platinum compounds was decreased in both resistant cell lines. When the activities of cisplatin and oxaliplatin were evaluated in the National Cancer Institute's Anticancer Drug Screen, marked differences were observed. Evaluation of the activity profile using the COMPARE program revealed a different pattern for both agents: the cisplatin activity profile was similar to those of other diamine platinum compounds, alkylating agents including melphalan, and camptothecin analogs, whereas the activity profile of oxaliplatin resembled those of other ''dach'' (diaminocyclohexane) platinum compounds and of acridine derivatives. The sensitivity profiles are influenced by the target(s)/mechanism(s) of action and the mechanism(s) of resistance of a drug. The dissimilarity in profiles suggests that these two platinum compounds have a different target(s)/mechanism(s) of action, a different mechanism(s) of resistance, or most likely both. Studies evaluating combinations of cisplatin/oxaliplatin suggest that the activities of these two agents are at least additive and possibly synergistic. Oxaliplatin has a different spectrum of activity and low cross resistance to cisplatin and should be valuable in cisplatin refractory patients or in combination with cisplatin. Copyright (C) 1996 Elsevier Science Inc.
C1 NCI, NIH, DIV CLIN SCI, MED BRANCH, BETHESDA, MD 20892 USA.
HOP LA PITIE SALPETRIERE, MED ONCOL SERV, F-75651 PARIS, FRANCE.
NCI, NIH, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, BETHESDA, MD 20892 USA.
NR 48
TC 431
Z9 449
U1 6
U2 58
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD DEC 24
PY 1996
VL 52
IS 12
BP 1855
EP 1865
DI 10.1016/S0006-2952(97)81490-6
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA VV550
UT WOS:A1996VV55000007
PM 8951344
ER
PT J
AU Levine, RL
Mosoni, L
Berlett, BS
Stadtman, ER
AF Levine, RL
Mosoni, L
Berlett, BS
Stadtman, ER
TI Methionine residues as endogenous antioxidants in proteins
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID HUMAN ALPHA-1-PROTEINASE INHIBITOR; COLI GLUTAMINE-SYNTHETASE;
METAL-CATALYZED OXIDATION; ESCHERICHIA-COLI; SULFOXIDE FORMATION;
INACTIVATION; DISSOCIATION; PROTEOLYSIS; PROTEASE; ACID
AB Cysteine and methionine are the two sulfur-containing residues normally found in proteins, Cysteine residues function in the catalytic cycle of many enzymes, and they can form disulfide bonds that contribute to protein structure. In contrast, the specific functions of methionine residues are not known. We propose that methionine residues constitute an important antioxidant defense mechanism, A variety of oxidants react readily with methionine to farm methionine sulfoxide, and surface exposed methionine residues create an extremely high concentration of reactant, available as an efficient oxidant scavenger, Reduction back Po methionine by methionine sulfoxide reductases would allow the antioxidant system to function catalytically. The effect of hydrogen peroxide exposure upon glutamine synthetase from Escherichia coli was studied as an in vitro model system, Eight of the 16 methionine residues could he oxidized with little effect on catalytic activity of the enzyme, The oxidizable methionine residues were found to be relatively surface exposed, whereas the intact residues were generally buried within the core of the protein. Furthermore, the susceptible residues were physically arranged in an array that guarded the entrance to the active site.
RP Levine, RL (reprint author), NHLBI, BIOCHEM LAB, NIH, 3 CTR DR, MSC 0320, BETHESDA, MD 20892 USA.
RI Levine, Rodney/D-9885-2011
NR 28
TC 628
Z9 646
U1 2
U2 56
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 DEC 24
PY 1996
VL 93
IS 26
BP 15036
EP 15040
DI 10.1073/pnas.93.26.15036
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400010
PM 8986759
ER
PT J
AU Guimaraes, MJ
Peterson, D
Vicari, A
Cocks, BG
Copeland, NG
Gilbert, DJ
Jenkins, NA
Ferrick, DA
Kastelein, RA
Bazan, JF
Zlotnik, A
AF Guimaraes, MJ
Peterson, D
Vicari, A
Cocks, BG
Copeland, NG
Gilbert, DJ
Jenkins, NA
Ferrick, DA
Kastelein, RA
Bazan, JF
Zlotnik, A
TI Identification of a novel selD homolog from Eukaryotes, Bacteria, and
Archaea: Is there an autoregulatory mechanism in selenocysteine
metabolism?
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID 3' UNTRANSLATED REGION; SELENOPROTEIN SYNTHESIS; SECONDARY STRUCTURE;
SELENIUM DONOR; MESSENGER-RNA; GENE-PRODUCT; SEQUENCES; ENZYMES; CELLS;
MOUSE
AB Escherichia coli selenophosphate synthetase (SPS, the selD gene product) catalyzes the production of monoselenophosphate, the selenium donor compound required for synthesis of selenocysteine (Sec) and seleno-tRNAs. We report the molecular cloning of human kind mouse homologs of the selD gene, designated Sps2, which contains an in-frame TGA codon at a site corresponding to the enzyme's putative active site, These sequences allow the identification of selD gene homologs in the genomes of the bacterium Haemophilus influenzae and the archaeon Methanococcus jannaschii, which had been previously misinterpreted due to their in-frame TGA codon. Sps2 mRNA levels are elevated in organs previously implicated in the synthesis of selenoproteins and in active sites of blood cell development. In addition, we show that Sps2 mRNA is up-regulated upon activation of T lymphocytes and have mapped the Sps2 gene to mouse chromosome 7. Using the mouse gene isolated from the hematopoietic cell line FDCPmixA4, we devised a construct for protein expression that results in the insertion of a FLAG Lag sequence at the N terminus of the SPS2 protein, This strategy allowed us to document: the readthrough of the in-frame TGA codon and the incorporation of Se-75 into SPS2. These results suggest the existence of an autoregulatory mechanism involving the incorporation of Sec into SPS2 that might be relevant to blood cell biology. This mechanism is likely to have been present in ancient life forms and conserved in a variety of living organisms from all domains of life.
C1 DNAX RES INST MOL & CELLULAR BIOL INC, DEPT MOL BIOL, PALO ALTO, CA 94304 USA.
DNAX RES INST MOL & CELLULAR BIOL INC, DEPT IMMUNOL, PALO ALTO, CA 94304 USA.
NCI, ADV BIOSCI LABS, BASIC RES PROGRAM, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA.
LAWRENCE LIVERMORE NATL LAB, SCH VET MED, DEPT PATHOL MICROBIOL & IMMUNOL, DAVIS, CA 95616 USA.
RI Bazan, J. Fernando/B-4562-2010; Zlotnik, Albert/C-3791-2011
NR 42
TC 154
Z9 161
U1 2
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 24
PY 1996
VL 93
IS 26
BP 15086
EP 15091
DI 10.1073/pnas.93.26.15086
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400019
PM 8986768
ER
PT J
AU DeVries, L
Elenko, E
Hubler, L
Jones, TLZ
Farquhar, MG
AF DeVries, L
Elenko, E
Hubler, L
Jones, TLZ
Farquhar, MG
TI GAIP is membrane-anchored by palmitoylation and interacts with the
activated (GTP-bound) form of G alpha(i) subunits
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE G protein; regulator of G-protein signaling; GTPase-activating protein;
cysteine string
ID CYSTEINE-STRING PROTEIN; NIH 3T3 CELLS; ENDOPLASMIC-RETICULUM;
SIGNAL-TRANSDUCTION; CRYSTAL-STRUCTURE; ADENYLYL CYCLASE;
ESCHERICHIA-COLI; BETA-COP; GS-ALPHA; MUTATIONS
AB GAIP (G Alpha Interacting Protein) is a member of the recently described RGS (Regulators of G-protein Signaling) family that was isolated by interaction cloning with the heterotrimeric G-protein G alpha(i3) and was recently shown to be a GTPase-activating protein (GAP). In AtT-20 cells stably expressing GAIP, we found that GAIP is membrane-anchored and faces the cytoplasm, because it was not released by sodium carbonate treatment but was digested by proteinase K, When Cos cells were transiently transfected with GAIP and metabolically labeled with [S-35]methionine, two pools of GAIP-a soluble and a membrane-anchored pool-were found, Since the N terminus of GAIP contains a cysteine string motif and cysteine string proteins are heavily palmitoylated, we investigated the possibility that membrane-anchored GAIP might be palmitoylated, We found that after labeling with [H-3] palmitic acid, the membrane-anchored pool but not the soluble pool was palmitoylated, In the yeast two-hybrid system, GAIP was found to interact specifically with members of the G alpha(i) subfamily, G alpha(i1), G alpha(i2), G alpha(i3), G alpha(z), and G alpha(o), but not with members of other G alpha subfamilies, G alpha(s), G alpha(q), and G alpha(12/13). The C terminus of G alpha(i3) is important for binding because a 10-aa C-terminal truncation and a point mutant of G alpha(i3) showed significantly diminished interaction, GAIP interacted preferentially with the activated (GTP) form of G alpha(i3), which is in keeping with its GAP activity, We conclude that GAIP is a membrane-anchored GAP with a cysteine string motif, This motif, present in cysteine string proteins found on synaptic vesicles, pancreatic zymogen granules, and chromaffin granules, suggests GAIP's possible involvement in membrane trafficking.
C1 UNIV CALIF SAN DIEGO,DIV CELLULAR & MOL MED,LA JOLLA,CA 92093.
UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093.
NIDDK,METAB DIS BRANCH,NIH,BETHESDA,MD 20892.
FU NCI NIH HHS [CA58689, F32 CA066289]; NIDDK NIH HHS [R01 DK017780,
DK17780]; NIGMS NIH HHS [GM07752, T32 GM007752]
NR 56
TC 140
Z9 141
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 DEC 24
PY 1996
VL 93
IS 26
BP 15203
EP 15208
DI 10.1073/pnas.93.26.15203
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400040
PM 8986788
ER
PT J
AU Reiser, J
Harmison, G
KluepfelStahl, S
Brady, RO
Karlson, S
Schubert, M
AF Reiser, J
Harmison, G
KluepfelStahl, S
Brady, RO
Karlson, S
Schubert, M
TI Transduction of nondividing cells using pseudotyped defective high-titer
HIV type 1 particles
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene therapy; quiescent cells; human skin fibroblasts; CD34(+) cells;
cell cycle
ID HUMAN-IMMUNODEFICIENCY-VIRUS; VESICULAR STOMATITIS-VIRUS; EFFICIENT
GENE-TRANSFER; NUCLEAR-LOCALIZATION; MURINE RETROVIRUSES;
HUMAN-LYMPHOCYTES; AIDS VIRUS; INFECTION; VECTORS; EXPRESSION
AB The use of Moloney marine leukemia virus (Mo-MLV)-based vectors to deliver therapeutic genes into target cells is limited by their inability to transduce nondividing cells. To test the capacity of HIV-based vectors to deliver genes into nondividing cells, we have generated replication-defective HIV type 1 (HIV-1) reporter vectors carrying neomycin phosphotransferase or mouse heat stable antigen, replacing the HIV-1 sequences encoding gp160. These vectors also harbor inactive vpr, vpu, and nef coding regions, Pseudotyped HIV-1 particles carrying either the ecotropic or the amphotropic Mo-MLV envelope proteins or the vesicular stomatitis virus G protein were released after single or double transfections of either human 293T or monkey COS-7 cells with titers of up to 10(7) colony-forming units per milliliter, A simple ultrafiltration procedure resulted in an additional 10- to 20-fold concentration of the pseudotyped particles. These vectors along with Mo-MLV-based vectors were used to transduce primary human skin fibroblasts and human peripheral blood CD34(+) cells. The HIV-1 vector system was significantly more efficient than its Mo-MLV-based counterpart in transducing human skin fibroblasts arrested al the G(0)/G(1) stage of the cell. cycle by density-dependent inhibition of growth. Human CD34(+) cells were transduced efficiently using HIV-1 pseudotype particles without prior stimulation with cytokines.
C1 NATL INST NEUROL DISORDERS & STROKE,LAB MOL MED & NEUROSCI,MOL & VIRAL GENET SECT,NIH,BETHESDA,MD 20892.
RP Reiser, J (reprint author), NATL INST NEUROL DISORDERS & STROKE,DEV & METAB NEUROL BRANCH,MOL & MED GENET SECT,NIH,BLDG 10,BETHESDA,MD 20892, USA.
NR 56
TC 256
Z9 263
U1 0
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 DEC 24
PY 1996
VL 93
IS 26
BP 15266
EP 15271
DI 10.1073/pnas.93.26.15266
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400051
PM 8986799
ER
PT J
AU Moriuchi, H
Moriuchi, M
Combadiere, C
Murphy, PM
Fauci, AS
AF Moriuchi, H
Moriuchi, M
Combadiere, C
Murphy, PM
Fauci, AS
TI CD8(+) T-cell-derived soluble factor(s), but not beta-chemokines RANTES,
MIP-1 alpha, an MIP-1 beta, suppress HIV-1 replication in
monocyte/macrophages
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; MONONUCLEAR PHAGOCYTES; U1 CELLS;
MACROPHAGES; EXPRESSION; INFECTION; TYPE-1; INTERLEUKIN-6; LYMPHOCYTES;
MONOCYTES
AB It has been demonstrated that CD8(+) T cells produce a soluble factor(s) that suppresses human immunodeficiency virus (HIV) replication in CD4(+) T cells. The role of soluble factors in the suppression of HIV replication in monocyte/macrophages (M/M) has not been fully delineated. To investigate whether a CD8(+) T-cell-derived soluble factor(s) can also suppress HIV infection in the M/M system, primary macrophages were infected with the macrophage tropic HIV-1 strain Ba-L. CD8(+) T-cell-depleted peripheral blood mononuclear cells were also infected with HIV-1 IIIB or Ba-L. HIV expression from the chronically infected macrophage cell line U1 was also determined in the presence of CD8(+) T-cell supernatants or beta-chemokines. We demonstrate that: (i) CD8(+) T-cell supernatants did, but beta-chemokines did not, suppress HIV replication in the M/M system; (ii) antibodies to regulated on activation normal T-cell expressed and Secreted (RANTES), macrophage inflammatory protein 1 alpha (MIP-1 alpha) and MIP-1 beta did not, whereas antibodies to interleukin 10, interleukin 13, interferon alpha, or interferon gamma modestly reduced anti-HIV activity of the CD8(+) T-cell supernatants; and (iii) the CD8(+) T-cell supernatants did, but beta-chemokines did not, suppress HIV-1 IIIB replication in peripheral blood mononuclear cells as well as HIV expression in U1 cells. These results suggest that HIV-suppressor activity of CD8(+) T cells is a multifactorial phenomenon, and that RANTES, MIP-1 alpha, and MIP-1 beta do not account for the entire scope of CD8(+) T-cell-derived HIV-suppressor factors.
C1 NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892.
RP Moriuchi, H (reprint author), NIAID,IMMUNOREGULAT LAB,NIH,BLDG 10,ROOM 6A-11,10 CTR DR,MSC-1576,BETHESDA,MD 20892, USA.
RI Combadiere, Christophe/I-5639-2013
OI Combadiere, Christophe/0000-0002-1755-4531
NR 32
TC 141
Z9 142
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 24
PY 1996
VL 93
IS 26
BP 15341
EP 15345
DI 10.1073/pnas.93.26.15341
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400065
PM 8986813
ER
PT J
AU Farci, P
Shimoda, A
Wong, D
Cabezon, T
DeGioannis, D
Strazzera, A
Shimizu, Y
Shapiro, M
Alter, HJ
Purcell, RH
AF Farci, P
Shimoda, A
Wong, D
Cabezon, T
DeGioannis, D
Strazzera, A
Shimizu, Y
Shapiro, M
Alter, HJ
Purcell, RH
TI Prevention of hepatitis C virus infection in chimpanzees by hyperimmune
serum against the hypervariable region 1 of the envelope 2 protein
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID NON-B HEPATITIS; HUMORAL IMMUNE-RESPONSE; NON-A; GLYCOPROTEIN GP70;
GENETIC DRIFT; ANTIBODY; E2/NS1; GENOME; NEUTRALIZATION; PREVALENCE
AB The identification of the neutralization domains of hepatitis C virus (HCV) is essential for the development of an effective vaccine. sere, we show that the hypervariable region 1 (HVR1) of the envelope 2 (E2) protein is a critical neutralization domain of HCV. Neutralization of HCV in vitro was attempted with a rabbit hyperimmune serum raised against a homologous synthetic peptide derived from the HVR1 of the E2 protein, and the residual infectivity was evaluated by inoculation of HCV-seronegative chimpanzees. The source of HCV was plasma obtained from a patient (H) during the acute phase of posttransfusion non-A, non-B hepatitis, which hall been titered for infectivity in chimpanzees. The anti-HVR1 antiserum induced protection against homologous HCV infection in chimpanzees, but not against the emergence of neutralization escape mutants that were found to be already present in the complex viral quasispecies of the inoculum. The finding that HVR1 can elicit protective immunity opens new perspectives for the development of effective preventive strategies. However, the identification of the most variable region of HCV as a critical neutralization domain poses a major challenge for the development of a broadly reactive vaccine against HCV.
C1 SMITHKLINE BEECHAM BIOL,B-1330 RIXENSART,BELGIUM.
UNIV CAGLIARI,IST MED INTERNA,I-09124 CAGLIARI,ITALY.
UNIV TOKYO,DEPT BACTERIOL,TOKYO 113,JAPAN.
BIOEQUAL INC,ROCKVILLE,MD 20852.
NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892.
RP Farci, P (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,NIH,BLDG 7,ROOM 200,7 CTR DR,MSC 0740,BETHESDA,MD 20892, USA.
RI Cheng, Yushao/E-6256-2011
NR 37
TC 436
Z9 459
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 DEC 24
PY 1996
VL 93
IS 26
BP 15394
EP 15399
DI 10.1073/pnas.93.26.15394
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA WC204
UT WOS:A1996WC20400074
PM 8986822
ER
PT J
AU Steiner, H
Gerfen, CR
AF Steiner, H
Gerfen, CR
TI Dynorphin regulates D1 dopamine receptor-mediated responses in the
striatum: Relative contributions of pre- and postsynaptic mechanisms in
dorsal and ventral striatum demonstrated by altered immediate-early gene
induction
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE c-fos; zif 268; kappa receptor; opioid; gene expression
ID KAPPA-OPIOID RECEPTOR; IN-SITU HYBRIDIZATION; RAT NUCLEUS-ACCUMBENS;
FACTOR MESSENGER-RNAS; C-FOS EXPRESSION; STRIATONIGRAL DYNORPHIN;
DIFFERENTIALLY ALTERS; INSITU HYBRIDIZATION; SUBSTANTIA-NIGRA; OPIATE
AGONISTS
AB Dynorphin, an endogenous kappa opioid receptor ligand, acts in the striatum to regulate the response of striatonigral neurons to D1 dopamine receptor stimulation. We investigated the relative contributions of both presynaptic kappa receptors on dopamine terminals and postsynaptic kappa receptors on striatal neurons by analyzing opioid regulation of D1 effects in the absence of presynaptic kappa receptors, after B-hydroxydopamine depletion of striatal dopamine. D1-receptor-mediated immediate-early gene induction was measured by using in situ hybridization histochemistry. First, repeated treatment with the Dm-receptor agonist SKF-38393 (2 mg/kg/day, 3-14 days) was used to increase dynorphin levels in rats with dopamine depletions. In the nucleus accumbens, increased dynorphin expression was accompanied by reduced induction of the immediate-early genes c-fos and zif 268 by SKF-38393. In contrast, in dorsal/lateral aspects of the dopamine-depleted striatum, this Dm response was sustained despite a large increase in dynorphin expression, These results are consistent with a requirement of dopamine terminals (presynaptic kappa receptors) for the inhibitory action of dynorphin in the dorsal/lateral striatum, but not in the ventral striatum. Second, the kappa receptor agonist spiradoline (1-10 mg/kg) reduced c-fos and zif 268 induction by SKF-38393 (2.5 mg/kg) preferentially in ventral parts of the dopamine-depleted striatum, which contain higher levels of kappa receptor mRNA and binding. These results also indicate that postsynaptic kappa receptors contribute to the inhibition of the D1 response at least in the ventral striatum. Together, these results indicate that dynorphin in the striatum functions to regulate dopamine input to striatonigral neurons, acting at both pre- and postsynaptic sites, and that the relative contributions of these mechanisms differ between dorsal and ventral striatal regions. (C) 1996 Wiley-Liss, Inc.
C1 NIMH,LNP,BETHESDA,MD 20892.
NR 73
TC 60
Z9 61
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD DEC 23
PY 1996
VL 376
IS 4
BP 530
EP 541
DI 10.1002/(SICI)1096-9861(19961223)376:4<530::AID-CNE3>3.0.CO;2-2
PG 12
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA VZ433
UT WOS:A1996VZ43300003
PM 8978468
ER
PT J
AU Dunn, SE
Cullen, JM
AF Dunn, SE
Cullen, JM
TI Woodchuck p-glycoprotein found in virus-induced hepatocellular
carcinomas binds anticancer drugs
SO CANCER LETTERS
LA English
DT Article
DE multidrug resistance; viral carcinogenesis; liver; animal model;
p-glycoprotein
ID MULTIDRUG RESISTANCE; CANCER; DNA
AB Virally-induced hepatocellular carcinomas (HCC) are intrinsically resistant to cancer chemotherapy partly due to increased expression of p-glycoprotein (pgp). In this study, we determined that pgp expressed in woodchuck HCC had binding properties were similar to the drug resistant human pgp. Pgp drug binding properties were characterized by photoaffinity labeling with the calcium channel blocker [H-3]azidopine (AZD). AZD bound pgp in HCC but not in non-tumor liver samples, and binding was confirmed by competition with Adriamycin (IC50 = 10 mu M) and actinomycin D (IC50 = 1 mu M). In summary, WHV-induced HCC overexpress a pgp which binds anticancer drugs suggesting a common pathway for drug resistance.
C1 N CAROLINA STATE UNIV,COLL VET MED,DEPT MICROBIOL PATHOL & PARASITOL,RALEIGH,NC 27606.
RP Dunn, SE (reprint author), NIEHS,MOL CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709, USA.
NR 11
TC 4
Z9 4
U1 0
U2 2
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 20
PY 1996
VL 110
IS 1-2
BP 177
EP 180
DI 10.1016/S0304-3835(96)04488-6
PG 4
WC Oncology
SC Oncology
GA WD796
UT WOS:A1996WD79600025
PM 9018098
ER
PT J
AU Page, JE
Pataki, J
Harvey, RG
Dipple, A
AF Page, JE
Pataki, J
Harvey, RG
Dipple, A
TI Mutational specificity of the syn 1,2-dihydrodiol 3,4-epoxide of
5-methylchrysene
SO CANCER LETTERS
LA English
DT Article
DE mutational spectra; dihydrodiol epoxide; 5-methylchrysene
ID SHUTTLE VECTOR; NEWBORN MICE; TUMORIGENICITY; MUTAGENESIS; DIHYDRODIOL;
EPOXIDES
AB The mutational specificity of the syn dihydrodiol epoxide of 5-methylchrysene in the supF gene of the pSP189 vector was examined. Transversion mutations at GC pairs predominated with G --> T and G --> C changes accounting for 42 and 21% of total base change mutations. The types of mutations found reflect the previously determined chemical preference of this reactive species for reaction with deoxyguanosine residues in DNA.
C1 NCI, ABL BASIC RES PROGRAM, CHEM CARCINOGENESIS LAB, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA.
UNIV CHICAGO, BEN MAY INST, CHICAGO, IL 60637 USA.
NR 18
TC 5
Z9 6
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 20
PY 1996
VL 110
IS 1-2
BP 249
EP 252
DI 10.1016/S0304-3835(96)04506-5
PG 4
WC Oncology
SC Oncology
GA WD796
UT WOS:A1996WD79600036
PM 9018109
ER
PT J
AU George, A
Bannon, L
Sabsay, B
Dillon, JW
Malone, J
Veis, A
Jenkins, NA
Gilbert, DJ
Copeland, NG
AF George, A
Bannon, L
Sabsay, B
Dillon, JW
Malone, J
Veis, A
Jenkins, NA
Gilbert, DJ
Copeland, NG
TI The carboxyl-terminal domain of phosphophoryn contains unique extended
triplet amino acid repeat sequences forming ordered carboxyl-phosphate
interaction ridges that may be essential in the biomineralization
process
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BOVINE DENTIN PHOSPHOPHORYN; RAT INCISOR DENTIN; IMPERFECTA TYPE-II;
PHOSPHOPROTEIN; LOCALIZATION; PROTEINS; LOCUS; GENE; ORGANIZATION;
INDUCTION
AB Phosphophoryns (PPs), a family of Asp and Ser(P)-rich dentin proteins, are considered to be archetypal regulators of several aspects of extracellular matrix (ECM) biomineralization. We have cloned a rat incisor PP gene, Dmp2, from our odontoblast cDNA library and localized it to mouse chromosome 5q21 within 2 centimorgans of Dmp1, another tooth-specific ECM protein. The carboxyl-terminal region of Dmp2 protein (60 residue % Ser, 31 residue % Asp) is divided into two domains, one with unique repetitive blocks of [DSS](n,3 less than or equal to 14), the other with [SD](m = 2,3). Conformational analysis shows the phosphorylated form of the [DS*S*](n) repeats to have a unique structure with well defined ridges of phosphates and carboxyls available for counter ion binding. The [S*D](m) domains have different phosphate and carboxylate interaction edges and thus different calcium ion and apatite surface binding properties. These two domains and the colocalization of Dmp1 and Dmp2 genes at a position equivalent to the dentinogenesis imperfecta type II location on human 4q21 all suggest that the PPs are indeed involved in some aspect of ECM mineralization.
C1 NORTHWESTERN UNIV,CHICAGO,IL 60611.
NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,NIH,FREDERICK,MD 21702.
OI GEORGE, ANNE/0000-0002-9008-7642
FU NIDCR NIH HHS [DE 01374, DE 07201]
NR 32
TC 149
Z9 151
U1 0
U2 9
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 DEC 20
PY 1996
VL 271
IS 51
BP 32869
EP 32873
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VZ373
UT WOS:A1996VZ37300061
PM 8955126
ER
PT J
AU Lee, KP
Carlson, LM
Woodcock, JB
Ramachandra, N
Schultz, TL
Davis, TA
Lowe, JB
Thompson, CB
Larsen, RD
AF Lee, KP
Carlson, LM
Woodcock, JB
Ramachandra, N
Schultz, TL
Davis, TA
Lowe, JB
Thompson, CB
Larsen, RD
TI Molecular cloning and characterization of CFT1, a developmentally
regulated avian alpha(1,3)-fucosyltransferase gene
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SIALYL-LEWIS-X; HUMAN ALPHA(1,3)FUCOSYLTRANSFERASE GENE;
ELAM-1-DEPENDENT CELL-ADHESION; CARBOHYDRATE ANTIGEN;
FUCOSYL-TRANSFERASE; EMBRYONIC ANTIGEN; ALPHA(1,3)-FUCOSYL-TRANSFERASE
GENE; DIFFERENTIAL EXPRESSION; DETERMINES EXPRESSION;
MONOCLONAL-ANTIBODY
AB Although coordinate expression of carbohydrate epitopes during development is well described, mechanisms which regulate this expression remain largely unknown. In this study we demonstrate that developing chicken B cells express the Lewis(x) terminal oligosaccharide structure in a stage-specific manner. To examine regulation of this expression, we have cloned and expressed the chicken alpha(1,3)-fucosyltransferase gene involved in Lewis(x) biosynthesis, naming it chicken fucosyltransferase 1 (CFT1), CFT1 is characterized by a single long open reading frame of 356 amino acids encoding a type II transmembrane glycoprotein. The domain structure and predicted amino acid sequence are highly conserved between CFT1 and mammalian Fuc-TIV genes (52.8% and 46.3% identity to mouse and human respectively). In vitro CFT1 fucosyltransferase activity utilizes LacNAc > 3'sialyl-LacNAc accepters with almost no utilization of other neutral type II (lactose, 2-fucosyllactose), or type I (lacto-N-biose I) accepters, CFT1-transfected cells make cell surface Lewis(x) (COS-7) and Lewis(x) + VIM-2 structures (Chinese hamster ovary). CFT1 gene expression is tissue-specific and includes embryonic thymus and bursa. Furthermore, expression of the CFT1 gene and cell surface Lewis(x) structures are closely linked during B cell development. These findings reveal the evolutionary conservation between nonmammalian and mammalian alpha(1,3)-fucosyltransferase genes and demonstrate a role for fucosyltransferase gene regulation in the developmental expression of oligosaccharide structures.
C1 UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109.
NIAID,NIH,BETHESDA,MD 20892.
GLYCOMED INC,ALAMEDA,CA 94501.
UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109.
UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MOL GENET & CELL BIOL,CHICAGO,IL 60637.
UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MED,GWENN KNAPP CTR LUPUS & IMMUNOL RES,CHICAGO,IL 60637.
RP Lee, KP (reprint author), USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,RM 228,BLDG 18,8901 WISCONSIN AVE,BETHESDA,MD 20889, USA.
NR 61
TC 26
Z9 26
U1 1
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD DEC 20
PY 1996
VL 271
IS 51
BP 32960
EP 32967
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VZ373
UT WOS:A1996VZ37300074
PM 8955139
ER
PT J
AU Das, K
Ding, JP
Hsiou, Y
Clark, AD
Moereels, H
Koymans, L
Andries, K
Pauwels, R
Janssen, PAJ
Boyer, PL
Clark, P
Smith, RH
Smith, MBK
Michejda, CJ
Hughes, SH
Arnold, E
AF Das, K
Ding, JP
Hsiou, Y
Clark, AD
Moereels, H
Koymans, L
Andries, K
Pauwels, R
Janssen, PAJ
Boyer, PL
Clark, P
Smith, RH
Smith, MBK
Michejda, CJ
Hughes, SH
Arnold, E
TI Crystal structures of 8-Cl and 9-Cl TIBO complexed with wild-type HIV-1
RT and 8-Cl TIBO complexed with the Tyr181Cys HIV-1 RT drug-resistant
mutant
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE antiviral inhibitors; reverse transcriptase; drug resistance; protein
structure; drug design
ID HUMAN-IMMUNODEFICIENCY-VIRUS; REVERSE-TRANSCRIPTASE INHIBITORS;
NONNUCLEOSIDE INHIBITORS; MACROMOLECULAR STRUCTURES; ANGSTROM
RESOLUTION; MUTATIONS; MECHANISM; THERAPY; POTENT; DERIVATIVES
AB Human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) is an important target for chemotherapeutic agents used in the treatment of AIDS; the TIBO compounds are potent non-nucleoside inhibitors of HIV-1 RT (NNRTls). Crystal structures of HIV-1 RT complexed with 8-Cl TIBO (R86183, IC50 = 4.6 nM) and 9-Cl TIBO (R82913, IC50 = 33 nM) have been determined at 3.0 Angstrom resolution. Mutant HIV-1 RT, containing Cys in place of Tyr at position 181 (Tyr181Cys), is highly resistant to many NNRTIs and HIV-1 variants containing this mutation have been selected in both cell culture and clinical trials. We also report the crystal structure of Tyr181Cys HIV-1 RT in complex with 8-Cl TIBO (IC50 = 130 nM) determined at 3.2 Angstrom resolution. Averaging of the electron density maps computed for different HIV-1 RT/NNRTI complexes and from diffraction datasets obtained using a synchrotron source from frozen (-165 degrees C) and cooled (-10 degrees C) crystals of the same complex was employed to improve the quality of electron density maps and to reduce model bias. The overall locations and conformations of the bound inhibitors in the complexes containing wild-type HIV-1 RT and the two TIBO inhibitors are very similar, as are the overall shapes and volumes of the non-nucleoside inhibitor-binding pocket (NNIBP). The major differences between the two wild-type HIV-1 RT/TIBO complexes occur in the vicinity of the TIBO chlorine substituents and involve the polypeptide segments around the beta 5-beta 6 connecting loop (residues 95 to 105) and the beta 13-beta 14 hairpin (residues 235 and 236). In all known structures of HIV-1 RT/NNRTI complexes, including these two, the position of the beta 12-beta 13 hairpin or the ''primer grip'' is significantly displaced relative to the position in the structure of HIV-1 RT complexed with a double-stranded DNA and in unliganded HIV-1 RT structures. Since the primer grip helps to position the template-primer, this displacement suggests that binding of NNRTIs would affect the relative positions of the primer terminus and the polymerase active site. This could explain biochemical data showing that NNRTI binding to HIV-1 RT reduces efficiency of the chemical step of DNA polymerization, but does not prevent binding of either dNTPs or DNA.
When the structure of the Tyr181Cys mutant HIV-1 RT in complex with 8-Cl TIBO is compared with the corresponding structure containing wild-type HIV-1 RT, the overall conformations of Tyr181Cys and wild-type HIV-1 RT and of the 8-Cl TIBO inhibitors are very similar. Some positional changes in the polypeptide backbone of the beta 6-beta 10-beta 9 sheet containing residue 181 are observed when the Tyr181Cys and wild-type complexes are compared, particularly near residue Val179 of beta 9. In the p51 subunit, the Cys181 side-chain is oriented in a similar direction to the Tyr181 side-chain in the wild-type complex. However, the electron density corresponding to the sulfur of the Cys181 side-chain in the p66 subunit is very weak, indicating that the thiol group is disordered, presumably because there is no significant interaction with either 8-Cl TIBO or nearby amino acid residues. III the mutant complex, there are slight rearrangements of the side-chains of other amino acid residues in the NNIBP and of the flexible dimethylallyl group of 8-Cl TIBO; these conformational changes could potentially compensate for the interactions that were lost when the relatively large tyrosine at position 181 was replaced by a less bulky cysteine residue. In the corresponding wild-type complex, Tyr181 in the p66 subunit has significant interactions with the bound inhibitor and the position of the Tyr181 side-chain is well defined in both subunits. Apparently the Tyr181-->Cys mutation eliminates favorable contacts of the aromatic ring of the tyrosine and the bound inhibitor, reducing the stability of NNRTI binding. This is consistent with the observation that the Tyr181Cys mutant HIV-1 RT is more resistant to NNRTIs that have extensive interactions with the Tyr181 side-chain. This interpretation is supported by a recent biochemical study which found that an NNRTI dissociates from its complex with Tyr181Cys HIV-1 RT faster than it does from a complex with wild-type HIV-1 RT. (C) 1996 Academic Press Limited
C1 RUTGERS STATE UNIV,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854.
RUTGERS STATE UNIV,DEPT CHEM,PISCATAWAY,NJ 08854.
JANSSEN RES FDN,CTR MOL DESIGN,B-2350 VOSELAAR,BELGIUM.
JANSSEN RES FDN,B-2340 BEERSE,BELGIUM.
TIBOTEC,INST ANTIVIRAL RES,B-2650 EDEGEM,BELGIUM.
NCI,ABL BASIC RES PROGRAM,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701.
WESTERN MARYLAND COLL,DEPT CHEM,WESTMINSTER,MD 21157.
FU NIAID NIH HHS [AI 27690, AI 36144]
NR 61
TC 183
Z9 188
U1 1
U2 3
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD DEC 20
PY 1996
VL 264
IS 5
BP 1085
EP 1100
DI 10.1006/jmbi.1996.0698
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VZ951
UT WOS:A1996VZ95100018
PM 9000632
ER
PT J
AU Generoso, WM
Sega, GA
Lockhart, AM
Hughes, LA
Cain, KT
Cacheiro, NLA
Shelby, MD
AF Generoso, WM
Sega, GA
Lockhart, AM
Hughes, LA
Cain, KT
Cacheiro, NLA
Shelby, MD
TI Dominant lethal mutations, heritable translocations, and unscheduled DNA
synthesis induced in male mouse germ cells by glycidamide, a metabolite
of acrylamide
SO MUTATION RESEARCH-GENETIC TOXICOLOGY
LA English
DT Article
DE dominant lethal rest; heritable translocation test; UDS
ID HEMOGLOBIN ADDUCT FORMATION; MALE-MICE; LOCUS MUTATIONS; INDUCTION;
METHANESULFONATE; PROTAMINE; EXPOSURE; GENOTOXICITY; MUTAGENICITY;
ETHYLATION
AB The hypothesis that acrylamide induces dominant lethal mutations and heritable translocations in male mice, not through direct adduction, but by conversion to the reactive epoxide, glycidamide, was investigated. Three studies, namely, induction of dominant lethal mutations, heritable translocations, and unscheduled DNA synthesis in spermatids, which were conducted earlier in this laboratory for acrylamide, were also performed for glycidamide to determine its mutagenic properties and to compare responses. Results of these studies are consistent with the proposal that in vivo conversion to glycidamide is responsible for the mutagenicity of acrylamide in male mice.
C1 OAK RIDGE NATL LAB,DIV CHEM & ANALYT SCI,OAK RIDGE,TN 37831.
COMP SCI CORP,RES TRIANGLE PK,NC 27709.
NIEHS,RES TRIANGLE PK,NC 27709.
RP Generoso, WM (reprint author), OAK RIDGE NATL LAB,DIV BIOL,POB 2009,OAK RIDGE,TN 37831, USA.
FU NIEHS NIH HHS [YIO-ES-20085]
NR 29
TC 31
Z9 31
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-1218
J9 MUTAT RES-GENET TOX
JI Mutat. Res.-Genet. Toxicol.
PD DEC 20
PY 1996
VL 371
IS 3-4
BP 175
EP 183
DI 10.1016/S0165-1218(96)90106-8
PG 9
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA WC890
UT WOS:A1996WC89000004
PM 9008719
ER
PT J
AU TitenkoHolland, N
Levine, AJ
Smith, MT
Quintana, PJE
Boeniger, M
Hayes, R
Suruda, A
Schulte, P
AF TitenkoHolland, N
Levine, AJ
Smith, MT
Quintana, PJE
Boeniger, M
Hayes, R
Suruda, A
Schulte, P
TI Quantification of epithelial cell micronuclei by fluorescence in situ
hybridization (FISH) in mortuary science students exposed to
formaldehyde
SO MUTATION RESEARCH-GENETIC TOXICOLOGY
LA English
DT Article
DE exfoliated cell; mortuary science student; micronuclei; FISH;
formaldehyde
ID EXFOLIATED HUMAN-CELLS; OCCUPATIONAL EXPOSURE; GASEOUS FORMALDEHYDE;
LYMPHOCYTES; WORKERS; CANCER; CHROMOSOME; DAMAGE
AB A micronucleus assay employing fluorescence in situ hybridization (FISH) with a centromeric probe was used on specimens of exfoliated buccal and nasal cells collected from mortuary science students exposed to embalming fluid containing formaldehyde. FISH labeling allowed micronuclei (MN) containing a whole chromosome (centromere-positive, MN(+)) to be differentiated from those containing only chromosomal fragments (centromere-negative, MN(-)). Each student was sampled before and after the 90 day embalming class. We determined if an increase in MN frequency could be attributed to formaldehyde exposure and was specific to either MN(+) or MN(-). In buccal cells, total MN frequency was significantly increased from 0.6/1000 to 2/1000 (p = 0.007) following the course, whereas in nasal cells it was not (2 and 2.5/1000, respectively, p = 0.2). Cells with multiple MN were present only in samples taken after exposure to embalming fluid. Although the baseline frequency was higher for MN(+) in both buccal (0.4/1000 for MN(+) and 0.1/1000 for MN(-)) and nasal cells (1.2/1000 for MN(+) and 0.5/1000 for MN(-)), the increase in MN frequency was greater for MN(-), (9-fold, p = 0.005 for buccal cells; 2-fold, p = 0.03 for nasal cells) than for MN(+) (> 2-fold, p = 0.08 for buccal cells; no change, p = 0.31 for nasal cells) in both tissues, Thus, the primary mechanism of micronucleus formation appeared to be chromosome breakage, This finding is consistent with known clastogenic properties of formaldehyde, the component of embalming fluid most likely responsible for micronucleus induction.
C1 NIOSH,CINCINNATI,OH 45226.
NCI,ROCKVILLE,MD 20892.
RP TitenkoHolland, N (reprint author), UNIV CALIF BERKELEY,DIV ENVIRONM HLTH SCI,SCH PUBL HLTH,217 WARREN HALL,BERKELEY,CA 94720, USA.
FU NIEHS NIH HHS [P30 ES01896, P42-ES04705]
NR 34
TC 63
Z9 67
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-1218
J9 MUTAT RES-GENET TOX
JI Mutat. Res.-Genet. Toxicol.
PD DEC 20
PY 1996
VL 371
IS 3-4
BP 237
EP 248
DI 10.1016/S0165-1218(96)90112-3
PG 12
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA WC890
UT WOS:A1996WC89000010
PM 9008725
ER
PT J
AU Liechty, MC
Crosby, H
Murthy, A
Davis, LM
Caspary, WJ
Hozier, JC
AF Liechty, MC
Crosby, H
Murthy, A
Davis, LM
Caspary, WJ
Hozier, JC
TI Identification of a heteromorphic microsatellite within the thymidine
kinase gene in L5178Y mouse lymphoma cells
SO MUTATION RESEARCH-GENETIC TOXICOLOGY
LA English
DT Article
DE L5178Y mouse lymphoma cell; Tk1; microsatellite; loss of heterozygosity;
polymorphic probe
ID TK-/ MUTANTS; TRIFLUOROTHYMIDINE-RESISTANT; ASSAY SYSTEM; CYTOGENETIC
ANALYSIS; CHROMOSOME ANALYSIS; MAMMALIAN-CELLS; IN-SITU; MUTATIONS;
LOCUS; POLYMORPHISMS
AB The objective of this work is to identify a heteromorphism within the thymidine kinase (Tk1) gene which can be used to assay for allele loss by means of PCR. Intron F of mouse Tk1 contains two (CA), microsatellite sequences separated by 107 bp of non-repetitive sequence. We tested this region for heteromorphism in L5178Y mouse lymphoma cells. A PCR primer pair designated Agl1 yielded products of 396 and 194 bp from L5178Y tk(+/-) genomic DNA. The 194-bp product resulted from a secondary binding site between the two (CA), repeats for the forward Agl1 primer and was not produced from tk(-/-) mutants that had lost the functional Tk1(b) allele. Agl2 primers produced two PCR products of 523 and similar to 440 bp and Agl3 primers produced products of 579 and similar to 500 bp. In both these cases, the difference in product size was approximately equal, indicating that Intron F is similar to 80 bp shorter in the non-functional Tk1(a) allele than in Tk1(b). This heteromorphism forms the basis for an assay for allele loss by means of PCR. Agl1 and Agl3 primers yielded additional products of 91 and 274 bp, respectively, consistent with sizes expected from the mouse Tk1 pseudogenes (Tk1-ps), Our conclusions drawn from an analysis of 122 mutants for Tk1(b) loss using Agl2 primers agreed with previous analysis of the NcoI heteromorphism. Thus, a simple PCR-based analysis can identify Tk1(b) loss in the L5178Y mouse lymphoma cells.
C1 NIH,LAB ENVIRONM CARCINOGENESIS & MUTAGENESIS,RES TRIANGLE PK,NC 27709.
RP Liechty, MC (reprint author), APPL GENET LABS INC,1335 GATEWAY DR,SUITE 2001,MELBOURNE,FL 32901, USA.
NR 24
TC 12
Z9 15
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-1218
J9 MUTAT RES-GENET TOX
JI Mutat. Res.-Genet. Toxicol.
PD DEC 20
PY 1996
VL 371
IS 3-4
BP 265
EP 271
DI 10.1016/S0165-1218(96)90115-9
PG 7
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA WC890
UT WOS:A1996WC89000013
PM 9008728
ER
PT J
AU Rothman, RB
Ayestas, M
Baumann, MH
AF Rothman, RB
Ayestas, M
Baumann, MH
TI Phentermine pretreatment antagonizes the cocaine-induced rise in
mesolimbic dopamine
SO NEUROREPORT
LA English
DT Article
DE cocaine; fenfluramine; in vivo microdialysis; phentermine; treatment
agents
ID SUICIDAL-BEHAVIOR; WEIGHT CONTROL; SEROTONIN; RATS; MICRODIALYSIS;
WITHDRAWAL; DRUGS
AB COADMINISTRATION Of phentermine and fenfluramine has been used to treat cocaine dependence. Patients who relapse while receiving this treatment report diminished subjective effects of cocaine. Due to the importance of mesolimbic dopamine (DA) in mediating cocaine reinforcement, we hypothesized that phentermine might attenuate the effects of cocaine on DA transmission. We examined this proposal directly using in vivo microdialysis methods in the nucleus accumbens of awake rats. Rats were pretreated with saline or phentermine (1 mg kg(-1), i.v.) and then challenged with cocaine (3 mg kg(-1), i.v.). Phentermine alone caused a modest increase in DA, and phentermine pretreatment substantially reduced the cocaine-induced rise in extracellular DA. Phentermine did not alter the stimulatory effect of cocaine on 5-HT. Our findings suggest that phentermine may antagonize the subjective effects of cocaine in humans via a DA mechanism.
RP Rothman, RB (reprint author), NIDA,CLIN PSYCHOPHARMACOL SECT,DIR,NIH,5500 NATHAN SHOCK DR,BALTIMORE,MD 21224, USA.
NR 24
TC 14
Z9 14
U1 0
U2 0
PU RAPID SCIENCE PUBLISHERS
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH
SN 0959-4965
J9 NEUROREPORT
JI Neuroreport
PD DEC 20
PY 1996
VL 8
IS 1
BP 7
EP 9
DI 10.1097/00001756-199612200-00002
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA WX339
UT WOS:A1996WX33900003
PM 9051742
ER
PT J
AU Hokari, M
Wu, HQ
Schwarcz, R
Smith, QR
AF Hokari, M
Wu, HQ
Schwarcz, R
Smith, QR
TI Facilitated brain uptake of 4-chlorokynurenine and conversion to
7-chlorokynurenic acid
SO NEUROREPORT
LA English
DT Article
DE blood-brain barrier; 4-chlorokynurenine; excitotoxicity; glycine;
kynurenic acid; neurodegenerative disorders; NMDA; transport
ID NMDA RECEPTOR; GLYCINE SITE; TRANSPORT; ANTAGONISTS; BARRIER;
KYNURENINE; RAT
AB 7-CHLOROKYNURENIC acid (7-Cl-KYNA) and 5,7-dichlorokynurenic acid (5,7-Cl-2-KYNA) are of therapeutic interest as potent glycine/N-methyl-D-aspartate (NMDA) receptor antagonists, but are excluded from brain by the blood-brain barrier. We examined whether these compounds could be delivered to brain through their respective precursors, L-4-chlorokynurenine (4-Cl-KYN) and L-4,6-dichlorokynurenine (4,6-Cl-2-KYN), which are amino acids. 4-Cl-KYN was shown to be rapidly shuttled into the brain by the large neutral amino acid transporter of the blood-brain barrier (K-m = 105 +/- 14 mu M, V-max = 16.9 +/- 2.3 nmol min(-1) g(-1)) and to be converted intracerebrally to 7-Cl-KYNA. 4,6-Cl-2-KYN also expressed affinity for the transporter, but four-fold less than that of 4-Cl-KYN. In summary, the results show that because of their facilitated uptake 4-Cl-KYN and 4,6-Cl2KYN might be useful prodrugs for brain delivery of glycine-NMDA receptor antagonists.
C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
UNIV MARYLAND,SCH MED,MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228.
FU NINDS NIH HHS [NS 28236, NS 16102]
NR 14
TC 37
Z9 40
U1 0
U2 1
PU RAPID SCIENCE PUBLISHERS
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH
SN 0959-4965
J9 NEUROREPORT
JI Neuroreport
PD DEC 20
PY 1996
VL 8
IS 1
BP 15
EP 18
DI 10.1097/00001756-199612200-00004
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA WX339
UT WOS:A1996WX33900005
PM 9051744
ER
PT J
AU Chang, MCJ
Grange, E
Rabin, O
Bell, JM
Allen, DD
Rapaport, SI
AF Chang, MCJ
Grange, E
Rabin, O
Bell, JM
Allen, DD
Rapaport, SI
TI Lithium decreases turnover of arachidonate in several brain
phospholipids
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE lithium; arachidonate; palmitate; fatty acids; phospholipids;
phospholipase A(2); acyl-CoA; brain; rat; in vivo incorporation;
turnover; signal transduction
ID CEREBRAL-CORTEX; ACID RELEASE; CELLS; RAT; HIPPOCAMPUS; RECEPTORS; GTP
AB In vivo rates of incorporation and turnover of palmitate and arachidonate in brain phospholipids were measured in awake rats treated chronically with lithium, following intravenous infusion of radiolabeled palmitate and arachidonate, respectively. Chronic lithium, at a brain level considered to be therapeutic in humans, decreased turnover of arachidonate within brain phosphatidylinositol, phosphatidylcholine and phosphatidylethanolamine by up to 80% (P < 0.001). In contrast, lithium had a minimal effect on turnover of palmitate, causing only a 26% reduction in turnover in phosphatidylcholine (P < 0.01). These results suggest that a major therapeutic effect of lithium is to reduce turnover specifically of arachidonate, possibly by inhibiting phospholipase A(2) involved in signal transduction. The effect may be secondary to the known action of lithium on the phosphoinositide cycle, by inhibiting the activity of inositol monophosphatase. (C) 1996 Elsevier Science Ireland Ltd.
RP Chang, MCJ (reprint author), NIA, NEUROSCI LAB, NIH, 10 CTR DR, MSC 1582, BETHESDA, MD 20892 USA.
NR 20
TC 127
Z9 127
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD DEC 20
PY 1996
VL 220
IS 3
BP 171
EP 174
DI 10.1016/S0304-3940(96)13264-X
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA WB596
UT WOS:A1996WB59600007
PM 8994220
ER
PT J
AU Constantino, JN
Murphy, DL
AF Constantino, JN
Murphy, DL
TI Monoamine metabolites in 'leftover' newborn human cerebrospinal fluid -
A potential resource for biobehavioral research
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE 5-hydroxyindoleacetic acid; homovanillic acid;
3-methoxy-4-hydroxyphenylglycol; temperament; infancy; circadian rhythm;
twin studies
ID DISRUPTIVE BEHAVIOR DISORDERS; MACARTHUR LONGITUDINAL TWIN;
RHESUS-MONKEYS; 5-HYDROXYINDOLEACETIC ACID; AMINE METABOLITES;
HOMOVANILLIC-ACID; SEROTONIN; CHILDREN; CSF; AGGRESSION
AB Although variations in monoamine neurotransmission have been implicated in a Variety of psychopathologic outcomes in man, little is known about how monoamines influence or are affected by developmental processes early in childhood. In this study, assays for 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were obtained from 'leftover' cerebrospinal fluid (CSF) of 119 human newborns. The levels of these monoamine metabolites were in keeping with pre-existing 'normative' data from two small previously published studies. The levels were largely unaffected by variations in the infants' physiologic condition at the time of lumbar puncture, and exhibited evidence for circadian rhythms. Among 32 infants (8 neurologically normal, 24 neurologically compromised) for whom more than one CSF sample was obtained during the first year of life, the correlations between baseline and follow-up measurements for 5-HIAA and HVA were on the order of 0.75. Correlations between twins (four sets) were significantly higher than those between unrelated individuals for 5-HIAA and HVA. At 9-month follow-up, neurologically normal infants in the lower extreme 15% of the distribution for 5-HIAA exhibited a trend toward lower scores for sociability on the Colorado Childhood Temperament Inventory (maternal report) than their counterparts at the upper extreme of the 5-HIAA distribution. Leftover CSF is a readily available resource for measurements of monoamine metabolites (and possibly other CSF constituents) in population-based samples of human newborns. Copyright (C) 1996 Elsevier Science Ireland Ltd.
C1 UNIV WASHINGTON,SCH MED,DEPT PEDIAT,ST LOUIS,MO.
NIMH,CLIN SCI LAB,CTR CLIN,NIH,BETHESDA,MD 20892.
RP Constantino, JN (reprint author), WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,4940 CHILDRENS PL,ST LOUIS,MO 63110, USA.
NR 46
TC 16
Z9 16
U1 1
U2 1
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 DEC 20
PY 1996
VL 65
IS 3
BP 129
EP 142
DI 10.1016/S0165-1781(96)02976-9
PG 14
WC Psychiatry
SC Psychiatry
GA WF290
UT WOS:A1996WF29000001
PM 9029662
ER
PT J
AU McFarland, HF
AF McFarland, HF
TI Complexities in the treatment of autoimmune disease
SO SCIENCE
LA English
DT Editorial Material
ID GAMMA-INTERFERON; ENCEPHALOMYELITIS; RESPONSES; PROTEIN
RP McFarland, HF (reprint author), NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892, USA.
NR 13
TC 53
Z9 54
U1 0
U2 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD DEC 20
PY 1996
VL 274
IS 5295
BP 2037
EP 2038
DI 10.1126/science.274.5295.2037
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY974
UT WOS:A1996VY97400033
PM 8984662
ER
PT J
AU Cortez, D
Stoica, G
Pierce, JH
Pendergast, AM
AF Cortez, D
Stoica, G
Pierce, JH
Pendergast, AM
TI The BCR-ABL tyrosine kinase inhibits apoptosis by activating a
Ras-dependent signaling pathway
SO ONCOGENE
LA English
DT Article
DE BCR-ABL; apoptosis; Ras; tyrosine phosphorylation
ID HEMATOPOIETIC-CELLS; PC12 CELLS; TRANSFORMATION; DEATH; ONCOGENE;
PROLIFERATION; PROTEIN
AB BCR-ABL is a deregulated tyrosine kinase that is expressed in Philadelphia chromosome (Ph(1)) positive human leukemias, When expressed in hematopoietic cells, BCR-ABL causes cytokine independent proliferation, induces tumorigenic growth and prevents apoptosis in response to cytokine deprivation or DNA damage, One mechanism by which BCR-ABL signals in cells is by activating the small guanine nucleotide binding protein Ras, BCR-ABL-transformed cells have constitutively high levels of active, GTP-bound Ras, Here we use 32D cells that inducibly express a dominant negative Ras protein to define the Ras requirements in BCR-ABL-transformed cells, Dominant negative Ras inhibits BCR-ABL-mediated Ras activation, and induces cell death by an apoptotic mechanism, Therefore, BCR-ABL inhibits apoptosis through activation of a Ras-dependent signaling pathway.
C1 DUKE UNIV,MED CTR,DEPT MOL CANC BIOL,DURHAM,NC 27710.
DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710.
GEORGETOWN UNIV,SCH MED,DEPT BIOCHEM,WASHINGTON,DC 20007.
NIH,CELL & MOL BIOL LAB,BETHESDA,MD 20892.
FU NCI NIH HHS [CA61033]
NR 23
TC 122
Z9 126
U1 0
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC 19
PY 1996
VL 13
IS 12
BP 2589
EP 2594
PG 6
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA VZ654
UT WOS:A1996VZ65400008
PM 9000132
ER
PT J
AU Tayebi, N
Stern, H
Dymarskaia, I
Herman, J
Sidransky, E
AF Tayebi, N
Stern, H
Dymarskaia, I
Herman, J
Sidransky, E
TI 55-base pair deletion in certain patients with Gaucher disease
complicates screening for common Gaucher alleles
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Gaucher disease; glucocerebrosidase; pseudogene; deletion; genotyping
ID GLUCOCEREBROSIDASE GENE; MUTATIONS; PCR
AB Mutations in the glucocerebrosidase gene which result in Gaucher disease can originate from the highly homologous glucocerebrosidase pseudogene, A 55-bp deletion in exon 9, which corresponds to a 55-bp segment absent from the pseudogene, has been identified in patients with Gaucher disease, We have developed a simple polymerase chain reaction (PCR)-based method to detect this 55-bp deletion, and have found this mutation in 3 of 75 DNA samples (4%) collected from patients with Gaucher disease. Commonly used PCR-based screening methods for specific Gaucher mutations frequently make use of primers either within or surrounding the 55-bp gap to selectively distinguish the glucocerebrosidase gene from the pseudogene. However, if the 55-bp deletion in exon 9 occurs, primers will either fail to produce an amplification product or will produce a shortened product which will be falsely attributed to the pseudogene. This could lead to inaccurate genotyping and genetic counseling for some Gaucher patients and their families, We therefore recommend that laboratories using PCR-based screening techniques involving primers in this region initially determine whether this 55-bp sequence is present. (C) 1996 Wiley-Liss, Inc.
C1 NIMH,CLIN NEUROSCI BRANCH,NIH,BETHESDA,MD 20892.
GEORGE WASHINGTON UNIV,MED CTR,DEPT PEDIAT,WASHINGTON,DC 20037.
GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037.
CHILDRENS NATL MED CTR,DEPT LAB MED & MED GENET,WASHINGTON,DC 20010.
NR 20
TC 27
Z9 27
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD DEC 18
PY 1996
VL 66
IS 3
BP 316
EP 319
DI 10.1002/(SICI)1096-8628(19961218)66:3<316::AID-AJMG15>3.0.CO;2-P
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA WA048
UT WOS:A1996WA04800015
PM 8985494
ER
PT J
AU Henningfield, JE
Hariharan, M
Kozlowski, LT
AF Henningfield, JE
Hariharan, M
Kozlowski, LT
TI Nicotine content and health risks of cigars
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID CIGARETTES; SMOKERS
C1 UNIV MICHIGAN,SCH MED,DEPT PSYCHIAT,ANN ARBOR,MI.
PENN STATE UNIV,COLL HLTH & HUMAN DEV,DEPT BIOBEHAV HLTH,UNIVERSITY PK,PA 16802.
RP Henningfield, JE (reprint author), NATL INST DRUG ABUSE,INTRAMURAL RES PROGRAM,BALTIMORE,MD 21224, USA.
NR 12
TC 21
Z9 21
U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD DEC 18
PY 1996
VL 276
IS 23
BP 1857
EP 1858
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA VX522
UT WOS:A1996VX52200002
PM 8967995
ER
PT J
AU Tucker, KL
Mahnken, B
Wilson, PWF
Jacques, P
Selhub, J
AF Tucker, KL
Mahnken, B
Wilson, PWF
Jacques, P
Selhub, J
TI Folic acid fortification of the food supply - Potential benefits and
risks for the elderly population
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID COBALAMIN DEFICIENCY; PERNICIOUS-ANEMIA; PLASMA HOMOCYSTEINE; FOLATE;
HYPERHOMOCYSTEINEMIA; VITAMIN-B12; QUESTIONNAIRE; MACROCYTOSIS;
PREVALENCE; DIAGNOSIS
AB Objective.-To estimate the potential benefits and risks of food folic acid fortification for an elderly population, Benefits are expected through the improvement of folate and homocysteine status, but there is also a risk of masking or precipitating clinical manifestations related to vitamin B-12 deficiency with increasing exposure to folic acid.
Design.-Cross-sectional analysis, with projected change at various levels of folic acid fortification.
Setting.-Participants in the Framingham Heart Study original cohort.
Participants.-A total of 747 subjects aged 67 to 96 years who both completed usable food frequency questionnaires and had blood concentrations of B vitamins and homocysteine measured.
Main Outcome Measures.-Projected blood folate and homocysteine concentrations and combined high folate intake and low plasma vitamin B-12 concentration.
Results.-Percentages of this elderly population with folate intake below 400 mu g/d are projected to drop from 66% at baseline to 49% with 140 mu g of folate per 100 g of cereal-grain product, to 32% with 280 mu g, to 26% with 350 mu g, and to 11% with 700 mu g. Percentages with elevated homocysteine concentrations (>14 mu mol/L) are projected to drop from 26% at baseline to 21% with 140 mu g of folate per 100 g, to 17% with 280 mu g, to 16% with 350 mu g, and to 12% with 700 mu g. Without fortification, the prevalence of combined high folate intake (>1000 mu g/d) and low plasma vitamin B-12 concentration (<185 pmol/L [<250 pg/mL]) was 0.1%. This is projected to increase to 0.4% with folate fortification levels of 140 to 350 mu g/100 g and to 3.4% with 700 mu g.
Conclusion.-The evidence suggests that, at the level of 140 mu g/100 g of cereal-grain product mandated by the Food and Drug Administration, the benefits of folate fortification, through projected decreases in homocysteine level and heart disease risk, greatly outweigh the expected risks, However, quantification of the actual risks associated with vitamin B-12 deficiency remains elusive. Before higher levels of folio acid fortification are implemented, further research is needed to better understand the clinical course of various forms of Vitamin B-12 deficiency, to measure the potential effect of high folate intake on this course, and to identify cost-effective approaches to the identification and treatment of all forms of vitamin B-12 deficiency.
C1 NHLBI,FRAMINGHAM MASS HEART STUDY,BETHESDA,MD 20892.
RP Tucker, KL (reprint author), TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,711 WASHINGTON ST,BOSTON,MA 02111, USA.
RI Tucker, Katherine/A-4545-2010;
OI Tucker, Katherine/0000-0001-7640-662X
FU NHLBI NIH HHS [N01-HC-38038]
NR 48
TC 137
Z9 139
U1 1
U2 8
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 DEC 18
PY 1996
VL 276
IS 23
BP 1879
EP 1885
DI 10.1001/jama.276.23.1879
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA VX522
UT WOS:A1996VX52200035
PM 8968013
ER
PT J
AU Curb, JD
Pressel, SL
Cutler, JA
Savage, PJ
Applegate, WB
Black, H
Camel, G
Davis, BR
Frost, PH
Gonzalez, N
Guthrie, G
Oberman, A
Rutan, GH
Stamler, J
AF Curb, JD
Pressel, SL
Cutler, JA
Savage, PJ
Applegate, WB
Black, H
Camel, G
Davis, BR
Frost, PH
Gonzalez, N
Guthrie, G
Oberman, A
Rutan, GH
Stamler, J
TI Effect of diuretic-based antihypertensive treatment on cardiovascular
disease risk in older diabetic patients with isolated systolic
hypertension
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID EUROPEAN WORKING PARTY; HIGH BLOOD-PRESSURE; MORTALITY; MORBIDITY;
THERAPY; TRIAL
AB Objective.-To assess the effect of low-dose, diuretic-based antihypertensive treatment on major cardiovascular disease (CVD) event rates in older, non-insulin-treated diabetic patients with isolated systolic hypertension (ISH), compared with nondiabetic patients.
Design.-Double-blind, randomized, placebo-controlled trial: the Systolic Hypertension in the Elderly Program (SHEP).
Setting.-Multiple clinical and support centers in the United States.
Participants.-A total of 4736 men and women aged 60 years and older at baseline with ISH (systolic blood pressure [BP], greater than or equal to 160 mm Hg; diastolic BP, <90 mm Hg) al baseline, 583 non-insulin-dependent diabetic patients and 4149 nondiabetic patients (4 additional patients not so classifiable were randomized but not included in these analyses). Diabetes mellitus defined as physician diagnosis, taking oral hypoglycemic drugs, fasting glucose level of 7.8 mmol/L or more (greater than or equal to 140 mg/dL), or any combination of these characteristics.
Intervention.-The active treatment group received a low dose of chlorthalidone (12.5-25.0 mg/d) with a step-up to atenolol (25.0-50.0 mg/d) or reserpine (0.05-0.10 mg/d) if needed. The placebo group received placebo and any active antihypertensive drugs prescribed by patient's private physician for persistently high BP.
Main Outcome Measures.-The 5-year rates of major CVD events, nonfatal plus fatal stroke, nonfatal myocardial infarction (MI) and fatal coronary heart disease (CHD), major CHD events, and all-cause mortality.
Results.-The SHEP antihypertensive drug regimen lowered BP of both diabetic and nondiabetic patients, with few adverse effects. For both diabetic and nondiabetic patients, all outcome rates were lower for participants randomized to the active treatment group than for those randomized to the placebo group, Thus, 5-year major CVD rate was lower by 34% for active treatment compared with placebo, both for diabetic patients (95% confidence interval [CI], 6%-54%) and nondiabetic patients (95% CI, 21%-45%). Absolute risk reduction with active treatment compared with placebo was twice as great for diabetic vs nondiabetic patients (101/1000 vs 51/1000 randomized participants at the 5-year follow-up), reflecting the higher risk of diabetic patients.
Conclusion.-Low-dose diuretic-based (chlorthalidone) treatment is effective in preventing major CVD events, cerebral and cardiac, in both non-insulin-treated diabetic and nondiabetic cider patients with ISH.
C1 UNIV HAWAII,JOHN A BURNS SCH MED,HONOLULU,HI 96822.
UNIV TEXAS,SCH PUBL HLTH,HOUSTON,TX.
NHLBI,BETHESDA,MD 20892.
UNIV TENNESSEE,MEMPHIS,TN 38163.
RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612.
WASHINGTON UNIV,SCH MED,ST LOUIS,MO.
UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143.
UNIV MINNESOTA,MINNEAPOLIS,MN 55455.
UNIV KENTUCKY,LEXINGTON,KY.
UNIV ALABAMA,BIRMINGHAM,AL.
VET AFFAIRS MED CTR,MEMPHIS,TN.
NORTHWESTERN UNIV,CHICAGO,IL 60611.
SYSTOL HYPERTENS ELDERLY PROGRAM COORDINATING CTR,HOUSTON,TX 77030.
NR 20
TC 588
Z9 604
U1 3
U2 13
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 DEC 18
PY 1996
VL 276
IS 23
BP 1886
EP 1892
DI 10.1001/jama.276.23.1886
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA VX522
UT WOS:A1996VX52200036
PM 8968014
ER
PT J
AU Yanovski, SZ
Dietz, WH
Goodwin, NJ
Hill, JO
PiSunyer, FX
Rolls, B
Stern, J
Weinsier, RL
Wilson, GT
Wing, RR
Hoofnagle, JH
Everhart, JE
Hubbard, VS
AF Yanovski, SZ
Dietz, WH
Goodwin, NJ
Hill, JO
PiSunyer, FX
Rolls, B
Stern, J
Weinsier, RL
Wilson, GT
Wing, RR
Hoofnagle, JH
Everhart, JE
Hubbard, VS
TI Long-term pharmacotherapy in the management of obesity
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Review
ID FENFLURAMINE PLUS PHENTERMINE; CARDIOVASCULAR RISK-FACTORS; DOUBLE-BLIND
TRIAL; WEIGHT CONTROL; CALORIC RESTRICTION; BODY-WEIGHT; FOLLOW-UP;
DEXFENFLURAMINE TREATMENT; PULMONARY-HYPERTENSION; BEHAVIOR-MODIFICATION
AB Objectives.-To examine the rationale for long-term use of medications in the management of obesity, to provide an overview of published scientific information on their safety and efficacy, and to provide guidance to patients and practitioners regarding risks and benefits of treatment.
Data Sources.-Original reports and reviews obtained through electronic database searches on anorexiant drugs supplemented by a manual search of bibliographies.
Study Selection.-English-language articles that discussed the role of medications in the treatment of human obesity, and studies that evaluated their safety and efficacy for a minimum of 24 weeks.
Data Extraction.-Studies were reviewed by experts in the fields of nutrition, obesity, and eating disorders to evaluate study design and the validity of authors' conclusions.
Data Synthesis.-The long-term use of medications in the management of obesity is consistent with the current consensus that obesity responds poorly to short-term interventions. Net weight loss attributable to medication is modest, ranging from 2 to 10 kg, but patients taking active drug are more likely to lose 10% or more of initial body weight. Weight loss tends to reach a plateau by 6 months. Weight remains below baseline throughout treatment, although some studies show partial weight regain despite continued drug therapy. Most adverse effects are mild and self-limited, but rare serious outcomes have been reported.
Conclusions.-Pharmacotherapy for obesity, when combined with appropriate behavioral approaches to change diet and physical activity, helps some obese patients lose weight and maintain weight loss for at least 1 year. There is little justification for the short-term use of anorexiant medications, but few studies have evaluated their safety and efficacy for more than 1 year. Until more data are available, pharmacotherapy cannot be recommended for routine use in obese individuals, although it may be helpful in carefully selected patients.
C1 TUFTS UNIV,SCH MED,BOSTON,MA 02111.
HLTH WATCH INFORMAT & PROMOT SERV,NEW YORK,NY.
UNIV COLORADO,DENVER,CO 80202.
COLUMBIA UNIV,ST LUKES ROOSEVELT HOSP CTR,NEW YORK,NY.
PENN STATE UNIV,STATE COLL,PA 16804.
UNIV CALIF DAVIS,DAVIS,CA 95616.
UNIV ALABAMA,BIRMINGHAM,AL.
RUTGERS STATE UNIV,PISCATAWAY,NJ.
UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA.
NIDDK,DIV DIGEST DIS & NUTR,NIH,BETHESDA,MD.
NR 114
TC 163
Z9 163
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD DEC 18
PY 1996
VL 276
IS 23
BP 1907
EP 1915
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA VX522
UT WOS:A1996VX52200040
ER
PT J
AU LiWang, AC
Bax, A
AF LiWang, AC
Bax, A
TI Equilibrium protium/deuterium fractionation of backbone amides in
U-C-13/N-15 labeled human ubiquitin by triple resonance NMR
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID PROTEINS; SPECTRA; C-13
C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892.
NR 17
TC 42
Z9 42
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD DEC 18
PY 1996
VL 118
IS 50
BP 12864
EP 12865
DI 10.1021/ja9630553
PG 2
WC Chemistry, Multidisciplinary
SC Chemistry
GA VY900
UT WOS:A1996VY90000060
ER
PT J
AU Karp, JE
Smith, MA
AF Karp, JE
Smith, MA
TI Modifying risks of secondary leukemias: Is drug scheduling important?
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID ACUTE MYELOID-LEUKEMIA; CELL LUNG-CANCER; DNA-TOPOISOMERASE-II; HPRT
GENE; CHROMOSOME TRANSLOCATIONS; MALIGNANT TRANSFORMATION; RANDOMIZED
TRIAL; ETOPOSIDE; EPIPODOPHYLLOTOXINS; RECOMBINASE
C1 NCI,CLIN TRIALS EVALUAT PROGRAM,DIV CANC TREATMENT DIAG & CTR,BETHESDA,MD 20892.
RP Karp, JE (reprint author), UNIV MARYLAND,CTR CANC,22 S GREENE ST,RM S9D15,BALTIMORE,MD 21201, USA.
NR 36
TC 7
Z9 7
U1 0
U2 0
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 18
PY 1996
VL 88
IS 24
BP 1787
EP 1789
DI 10.1093/jnci/88.24.1787
PG 3
WC Oncology
SC Oncology
GA VY199
UT WOS:A1996VY19900001
PM 8961963
ER
PT J
AU Burke, TR
Ye, B
Yan, XJ
Wang, SM
Jia, ZC
Chen, L
Zhang, ZY
Barford, D
AF Burke, TR
Ye, B
Yan, XJ
Wang, SM
Jia, ZC
Chen, L
Zhang, ZY
Barford, D
TI Small molecule interactions with protein-tyrosine phosphatase PTP1B and
their use in inhibitor design
SO BIOCHEMISTRY
LA English
DT Article
ID SOLID-PHASE SYNTHESIS; O-PHOSPHOTYROSINE; NONHYDROLYZABLE MIMETICS;
N-BOC; POTENT; DERIVATIVES; ANALOGS; 1B; PHENYLALANINE; INACTIVATION
AB We have previously shown that a small peptide bearing the hydrolytically stable phosphotyrosyl (pTyr) mimetic, (difluorophosphonomethyl)phenylalanine (F(2)Pmp), is an extremely potent inhibitor of PTP1B, with an IC50 value of 100 nM [Burke, T. R., Kole, H. K., & Roller, P. P. (1994) Biochem. Biophys. Res. Commun. 204, 129-134]. We further demonstrated that removal of the peptide portion and incorporation of the difluorophosphonomethyl moiety onto a naphthalene ring system, but not a phenyl ring system, resulted in good inhibitory potency [Kole, H. K., Smyth, M. S., Russ, P. L., & Burke, T. R., Jr. (1995) Biochem. J. 311, 1025-1031]. In order to understand the structural basis for this inhibition, and to aid in the design of further analogs, we solved the X-ray structure of [1,1-difluoro-1-(2-naphthalenyl)-methyl]phosphonic acid (6) complexed within the catalytic site of PTP1B, solved to 2.3 Angstrom resolution. In addition to showing the manner in which the phosphonate group is held within the catalytic site, the X-ray structure also revealed extensive hydrophobic interactions with the naphthalene ring system, beyond that possible with an analog bearing a single phenyl ring. It is further evident that, of the two fluorine atoms, the pro-R alpha-fluorine interacts with the enzyme to a significantly greater degree than the pro-S alpha-fluorine, forming a hydrogen bond to Phe 182. On the basis of a computer-assisted molecular modeling analysis, it was determined that addition of a hydroxyl to the naphthyl 4-position, giving [1,1-difluoro-1-[2-(4-hydroxynaphthalenyl)] methyl]phosphonic acid (8), could potentially replace a water molecule situated in the PTP1B . 6 complex, thereby allowing new hydrogen-bonding interactions with Lys 120 and Tyr 46. Compound 8 was therefore prepared and found to exhibit a doubling of affinity (K-i = 94 mu M) relative to parent unsubstituted 6 (K-i = 179 mu M), supporting, in principle, the development of high-affinity ligands based on molecular modeling analysis of the enzyme-bound parent.
C1 UNIV OXFORD,MOL BIOPHYS LAB,OXFORD OX1 3QU,ENGLAND.
ALBERT EINSTEIN COLL MED,DEPT MOL PHARMACOL,BRONX,NY 10461.
RP Burke, TR (reprint author), NCI,MED CHEM LAB,DIV BASIC SCI,NIH,BLDG 37,ROOM 5C06,BETHESDA,MD 20892, USA.
RI Burke, Terrence/N-2601-2014
FU NIDDK NIH HHS [5P60 DK20541]; Wellcome Trust
NR 45
TC 118
Z9 120
U1 2
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD DEC 17
PY 1996
VL 35
IS 50
BP 15989
EP 15996
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VY897
UT WOS:A1996VY89700004
PM 8973169
ER
PT J
AU Arai, T
Jones, CR
Rapoport, SI
Weiss, SRB
AF Arai, T
Jones, CR
Rapoport, SI
Weiss, SRB
TI Evidence for membrane remodeling in ipsilateral thalamus and amygdala
following left amygdala-kindled seizures in awake rats
SO BRAIN RESEARCH
LA English
DT Article
DE kindling; amygdala; thalamus; fatty acid; palmitate; lipid;
deoxyglucose; brain; plasticity; seizure; phospholipid;
phosphatidylcholine; activation
ID CEREBRAL PALMITATE INCORPORATION; RADIOLABELED FATTY-ACIDS;
GLUCOSE-UTILIZATION; UNANESTHETIZED RATS; BRAIN INCORPORATION; PLASMA
PALMITATE; DENTATE GYRUS; MESSENGER-RNA; PHOSPHOLIPIDS;
NEUROPLASTICITIES
AB We examined regional cerebral metabolic rates for glucose (rCMR(glc)) and brain incorporation coefficients (k*) of each of three intravenously infused fatty acid radiotracers, [9,10-H-3]palmitate ([H-3]PAM), [1-C-14]arachidonate ([C-14]AA) and [1-C-14]docosahexaenoate ([C-14]DHA), in awake rats fully kindled by once-daily electrical stimulation of the left amygdala. Compared with sham-stimulated animals, rCMR(glc) was increased bilaterally during a seizure, particularly in midbrain-brain stem regions, thalamus and basolateral nucleus of the amygdala. At 24 h and 2 weeks after a seizure, there was no significant change in k* for either [C-14]AA or [C-14]DHA in any brain region, whereas k* for [H-3]PAM at 24 h was increased significantly (by 32-53%) ipsilateral to stimulation in regions of the amygdala and thalamus. Contralateral regions showed no significant change. Two weeks after a seizure, k* for [3H]PAM was increased in the ipsilateral lateral dorsal nucleus of the thalamus. These results argue for membrane remodeling involving phosphatidylcholine in the ipsilateral amygdala and thalamus at the completed phase of amygdala kindling. Remodeling may continue for up to 2 weeks after a seizure during the completed phase.
C1 NIMH,BIOL PSYCHIAT BRANCH,NIH,BETHESDA,MD 20892.
TOKYO MED & DENT UNIV,SCH MED,DEPT NEUROSURG,BUNKYO KU,TOKYO 113,JAPAN.
NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
NR 59
TC 5
Z9 5
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD DEC 16
PY 1996
VL 743
IS 1-2
BP 131
EP 140
DI 10.1016/S0006-8993(96)00854-2
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA WC373
UT WOS:A1996WC37300018
PM 9017240
ER
PT J
AU Pullia, D
DAmato, FR
Mele, A
Oliverio, A
Zocchi, A
Pavone, F
AF Pullia, D
DAmato, FR
Mele, A
Oliverio, A
Zocchi, A
Pavone, F
TI Time-related effects of stress on cholinergic sensitivity
SO BRAIN RESEARCH
LA English
DT Article
DE restraint; oxotremorine; locomotor activity; acetylcholine; muscarinic
receptor; prefrontal cortex; DBA/2 mice
ID ACUTE RESTRAINT STRESS; IMMOBILIZATION STRESS; LIFE EVENTS;
OXOTREMORINE; RATS; RECEPTORS; SUPERSENSITIVITY; HIPPOCAMPUS; TOLERANCE;
RESPONSES
AB The effect of the administration of the muscarinic cholinergic agonist oxotremorine on locomotor activity was investigated in DBA/2 mice subjected to chronic restraint stress of different durations (120 min daily for 10, 14 or 18 days). Oxotremorine induced a depressant effect on locomotion, which was reduced after 10 and 14 days of restraint, but not after a 18-day restraint stress. Acetylcholine (ACh) content was significantly reduced in prefrontal cortex after 10 and 14 days of stress but returned to control values after 18 days of restraint. No changes in ACh content were observed in nucleus accumbens and striatum. These results are discussed in terms of possible changes in muscarinic receptor sensitivity.
C1 CNR,IST PSICOBIOL & PSICOFARMACOL,I-00198 ROME,ITALY.
UNIV ROMA LA SAPIENZA,DIPARTIMENTO GENET & BIOL MOL,ROME,ITALY.
NIMH,BIOL PSYCHIAT BRANCH,NIH,BETHESDA,MD 20892.
OI Pavone, Flaminia/0000-0001-5189-2748; D'Amato,
Francesca/0000-0002-4577-4574
NR 25
TC 11
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD DEC 16
PY 1996
VL 743
IS 1-2
BP 333
EP 336
DI 10.1016/S0006-8993(96)00799-8
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA WC373
UT WOS:A1996WC37300042
PM 9017264
ER
PT J
AU Bezrukov, SM
Vodyanoy, I
Brutyan, RA
Kasianowicz, JJ
AF Bezrukov, SM
Vodyanoy, I
Brutyan, RA
Kasianowicz, JJ
TI Dynamics and free energy of polymers partitioning into a nanoscale pore
SO MACROMOLECULES
LA English
DT Article
ID PROBING ALAMETHICIN CHANNELS; WATER-SOLUBLE POLYMERS; SINGLE-ION
CHANNEL; ALPHA-TOXIN; STAPHYLOCOCCUS-AUREUS; VOLUME CHANGES;
PATCH-CLAMP; MEMBRANES; PROTEIN; DIFFUSION
AB Membrane-bound proteinaceous nanoscale pores allow us to simultaneously observe the thermodynamic and kinetic properties of differently sized polymers within their confines. We determine the dynamic partitioning of poly(ethylene glycol) (PEG) into the pore formed by Staphylococcus aureus alpha-toxin and evaluate the free energy of polymer confinement by measuring polymer-induced changes to the pore's ionic conductance. The free energy deduced from the partition coefficient has a sharper dependence on polymer length (or weight) than scaling theory predicts. Moreover, the polymer-induced conductance fluctuations show a striking nonmonotonic dependence on the polymer molecular weight. The movement of polymer inside the pore is characterized by a diffusion coefficient that is orders of magnitude smaller than that for polymer in the bulk aqueous solution, which suggests that PEG has an attractive interaction with the pore. Using an ad-hoc approach,we show that a simple molecular weight-dependent modification of the polymer's diffusion coefficient accounts for these results, but only qualitatively. Given that PEG associates with hydrophobic regions in proteins, we also conclude that, contrary to the conventional view of ion channels, the aqueous cavity of the alpha-toxin pore's interior is, to some extent, hydrophobic.
C1 ST PETERSBURG NUCL PHYS INST,GATCHINA 188350,RUSSIA.
ONR EUROPE,LONDON NW1 5TH,ENGLAND.
INST BIOTECHNOL,YEREVAN 375056,ARMENIA.
NIST,DIV BIOTECHNOL,GAITHERSBURG,MD 20899.
RP Bezrukov, SM (reprint author), NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA.
NR 44
TC 184
Z9 186
U1 2
U2 25
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0024-9297
J9 MACROMOLECULES
JI Macromolecules
PD DEC 16
PY 1996
VL 29
IS 26
BP 8517
EP 8522
DI 10.1021/ma960841j
PG 6
WC Polymer Science
SC Polymer Science
GA VY915
UT WOS:A1996VY91500034
ER
PT J
AU Oopik, AJ
Dorogy, M
Devereux, RB
Yeh, JL
Okin, PM
Lee, ET
Cowan, L
Fabsitz, RR
Howard, BV
Welty, TK
AF Oopik, AJ
Dorogy, M
Devereux, RB
Yeh, JL
Okin, PM
Lee, ET
Cowan, L
Fabsitz, RR
Howard, BV
Welty, TK
TI Major electrocardiographic abnormalities among American Indians aged 45
to 74 years (The Strong Heart Study)
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID CARDIOVASCULAR-DISEASE; PIMA-INDIANS; DIABETES-MELLITUS; HIGH
PREVALENCE; ROCHESTER; MINNESOTA; CRITERIA; HEALTH
AB As part of the Strong Heart Study assessment of prevalent cardiovascular disease in middle-aged to elderly American Indians, the prevalence of major Minnesota code electrocardiographic (ECG) abnormalities was assessed in 4,531 participants aged 45 to 74 years (59% women) in selected tribal communities in Arizona, South and North Dakota, and Oklahoma. The overall prevalence of major ECG abnormalities was lowest in Arizona participants, (e.g., definite ECG myocardial infarction in 0.3% vs 1.8% in the other centers), although nearly two thirds of them had diabetes. One or more major ECG abnormality occurred in progressively more women (10.4% to 21.2%) and men (13.3% to 32%) (both p <0.0001) from 45- to 54- to 55- to 64- and 65- to 74-year age groups, with the latter prevalence rates exceeding those in predominately white age peers in the Cardiovascular Health Study. Diabetes in women, but not in men, and hypertension in both genders showed positive associations with prevalence rates of major ECG abnormalities compatible with coronary artery disease or hypertensive cardiac hypertrophy. Hypercholesterolemia was not associated with ECG abnormalities except for definite myocardial infarction in women. In conclusion, major ECG abnormalities are common in middle-aged to elderly American Indians, consistent with recent documentation of higher cardiovascular mortality in this population than in similar-aged U.S. whites. (C) 1996 by Excerpta Medica, Inc.
C1 INDIAN HLTH SERV,ABERDEEN AREA,DENVER,CO.
FITZSIMONS ARMY MED CTR,DENVER,CO.
CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT MED,NEW YORK,NY 10021.
UNIV OKLAHOMA,CTR EPIDEMIOL RES,OKLAHOMA CITY,OK.
NHLBI,BETHESDA,MD 20892.
MEDLANT RES INST,WASHINGTON,DC.
FU NHLBI NIH HHS [U01-HL41652, U01-HL41642, U01-HL41654]
NR 28
TC 19
Z9 19
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 DEC 15
PY 1996
VL 78
IS 12
BP 1400
EP 1405
DI 10.1016/S0002-9149(96)00642-X
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA VX770
UT WOS:A1996VX77000013
PM 8970414
ER
PT J
AU Mathew, J
Davidson, S
Narra, L
Hafeez, T
Garg, R
AF Mathew, J
Davidson, S
Narra, L
Hafeez, T
Garg, R
TI Etiology and characteristics of congestive heart failure in blacks
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID VENTRICULAR DYSFUNCTION SOLVD; RISK
AB In this study of 301 black patients with congestive heart failure (CHF), systemic hypertension is the most common cause of CHF and is the primary etiology of CHF in 61%. Left ventricular hypertrophy is highly prevalent and is seen in 63% of the patients who had an echocardiogram.
C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,CLIN TRIALS BRANCH,BETHESDA,MD 20892.
RP Mathew, J (reprint author), COOK CTY HOSP,DIV ADULT CARDIOL,DEPT MED,1835 W HARRISON ST,CHICAGO,IL 60612, USA.
NR 13
TC 24
Z9 24
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 DEC 15
PY 1996
VL 78
IS 12
BP 1447
EP &
DI 10.1016/S0002-9149(96)00635-2
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA VX770
UT WOS:A1996VX77000025
PM 8970426
ER
PT J
AU Koley, AP
Buters, JTM
Robinson, RC
Markowitz, A
Friedman, FK
AF Koley, AP
Buters, JTM
Robinson, RC
Markowitz, A
Friedman, FK
TI Interaction of polycyclic aromatic hydrocarbons with human cytochrome
P450 1A1: A CO flash photolysis study
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE cytochrome P450; protein conformation; polycyclic aromatic hydrocarbons;
resorufins; kinetics
ID YEAST SACCHAROMYCES-CEREVISIAE; MICROSOMAL CYTOCHROME-P-450;
ENDOPLASMIC-RETICULUM; BINDING-KINETICS; EXPRESSION; BENZOPYRENE;
PURIFICATION; METABOLISM; ACTIVATION; OXIDATION
AB The kinetics of CO binding to human cytochrome P450 1A1 was used to probe the interaction of polycyclic aromatic hydrocarbons (PAHs) with the membrane-bound P450 expressed in baculovirus-infected SF9 insect cells. Biexponential kinetics was observed, indicating that P450 1A1 is composed of at least two kinetically distinguishable species. To define the substrate specificity of the individual species, we evaluated the effect of a series of PAHs of varying sizes and shapes on the CO binding kinetics of P450 1A1. The overall rate of CO binding was increased in the presence of the tricyclic PAHs phenanthrene and anthracene and the tetracyclic PAHs pyrene and 1,2-benzanthracene, but was decreased by the pentacyclic PAHs benzo[a]pyrene and 1,2:3,4-dibenzanthracene. A kinetic difference method was applied to kinetically define the individual P450 1A1 species. Two species differing in their PAH specificities were identified: a slowly reacting species sensitive to the smaller PAHs, and a rapidly reacting species responsive to larger PAHs. Upon PAH binding, CO binding to these species was accelerated and decelerated, respectively. The results furthermore suggest that the two species are interconvertable. In addition to PAHs, the interactions of P450 1A1 with 7-ethoxy- and 7-pentoxyresorufin were likewise examined for their effect on the CO binding kinetics. These compounds interacted with and decreased the rate of the rapidly and slowly reacting P450 1A1 species, respectively. The markedly variable effects of these PAHs and resorufins on the CO binding kinetics indicate differential modes of interaction with the two target P450 1A1 species, resulting in differential modulation of their conformations. These results demonstrate that multiple P450 1A1 species with distinct conformations and substrate recognition profiles coexist in a biological membrane and are resolvable using a rapid kinetic technique. (C) 1996 Academic Press, Inc.
C1 NCI,MOL CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892.
NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892.
RI Buters, Jeroen/G-5070-2011; Friedman, Fred/D-4208-2016
NR 32
TC 6
Z9 6
U1 1
U2 2
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD DEC 15
PY 1996
VL 336
IS 2
BP 261
EP 267
DI 10.1006/abbi.1996.0556
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA WA819
UT WOS:A1996WA81900008
PM 8954573
ER
PT J
AU Murphy, DL
Aulakh, C
MazzolaPomietto, P
Briggs, NC
AF Murphy, DL
Aulakh, C
MazzolaPomietto, P
Briggs, NC
TI Neuroendocrine responses to serotonergic agonists as indices of the
functional status of central serotonin neurotransmission in humans: A
preliminary comparative analysis of neuroendocrine endpoints versus
other endpoint measures
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article; Proceedings Paper
CT 3rd IUPHAR Satellite Meeting on Serotonin
CY JUL 30-AUG 03, 1994
CL CHICAGO, IL
DE cortisol; prolactin; serotonin; serotonin receptor; temperature;
anxiety; m-chlorophenylpiperazine
ID OBSESSIVE-COMPULSIVE DISORDER; TERM LITHIUM TREATMENT;
META-CHLOROPHENYLPIPERAZINE; PANIC DISORDER; M-CPP; RECEPTOR
HYPERSENSITIVITY; CLOMIPRAMINE TREATMENT; HEALTHY-SUBJECTS; FOOD-INTAKE;
HUMAN-BRAIN
AB The status of central serotonergic neurotransmission and of specific serotonin (5-HT) receptor subtype sensitivity has been inferred from neuroendocrine and other endpoint responses to serotonergic agents given to humans. The question of whether changes in neuroendocrine responsivity to the 5-HT2C partial agonist, meta-chlorophenylpiperazine (m-CPP), are accompanied by similar changes in other endpoints (temperature, behavior) is addressed in this brief review of published studies. These studies were selected based on the following criteria: (1) neuroendocrine (cortisol, prolactin increases) and at least one other endpoint (behavior and/or temperature increases) were measured in the same populations, and (2) statistically significant changes were observed after m-CPP in the healthy volunteer control or pre-long-term-treatment subjects. Parenthetically, in the 13 of 14 studies that reported both prolactin and cortisol responses, the results were congruent for the two neuroendocrine measures in 12 of the 13 (92%). However, neuroendocrine versus behavioral results were in agreement in fewer (7 of the 13) studies (54%). Neuroendocrine vs. temperature results were non-concordant in all 4 of the studies which included temperature measurements. These generally disparate findings suggest that these different endpoints may reflect brain serotonin neuroanatomic and receptor subsystem complexity and/or m-CPP's complex pharmacological properties. Thus, these neuroendocrine response measures cannot at this time be considered a general index of the other response measures, nor necessarily an index of the functional status of central serotonergic neurotransmission until this is established by more direct experimental investigations.
RP Murphy, DL (reprint author), NIMH, CLIN SCI LAB, BLDG 10, RM 3D41, 10 CTR DR MSC 1264, BETHESDA, MD 20892 USA.
NR 51
TC 21
Z9 21
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD DEC 15
PY 1996
VL 73
IS 1-2
BP 209
EP 214
PG 6
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA TP015
UT WOS:A1995TP01500038
PM 8788504
ER
PT J
AU Bonson, KR
Murphy, DL
AF Bonson, KR
Murphy, DL
TI Alterations in responses to LSD in humans associated with chronic
administration of tricyclic antidepressants, monoamine oxidase
inhibitors or lithium
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article; Proceedings Paper
CT 3rd IUPHAR Satellite Meeting on Serotonin
CY JUL 30-AUG 03, 1994
CL CHICAGO, IL
DE lithium; lysergic acid diethylamide; monoamine oxidase; tricyclic
antidepressant; chronic drug administration
ID LYSERGIC-ACID DIETHYLAMIDE; DOPAMINE-RECEPTORS; RAT-BRAIN; CHRONIC
IMIPRAMINE; SUPER-SENSITIVITY; AGONISTS; BINDING; 5-HT; HALLUCINOGENS;
HYPOTHESIS
AB This study sought to investigate possible interactions between antidepressant agents and lysergic acid diethylamide (LSD) in humans through the use of retrospective questionnaires. Ten subjects were identified who used LSD during chronic (3 weeks or longer) periods of antidepressant administration. These subjects were asked to describe the phenomenological effects of self-administered hallucinogens prior to and during antidepressant treatment; a structured, standardized questionnaire was used to evaluate LSD experiences. Chronic tricyclic antidepressant administration was associated with subjective increases in physical, hallucinatory and psychological responses to LSD. Similarly, subjects receiving lithium chronically also reported increases in their responses to LSD. In contrast, subjects who had been chronically taking an monoamine oxidase (MAO) inhibitor reported subjective decreases in the effects of LSD. This is similar to a previous report by our group of a decreased response to LSD in individuals who were chronically taking serotonin-selective antidepressants. These altered responses to LSD most likely involve differential changes in central serotonin and dopamine receptor systems and are consistent with other recent data suggesting that the clinical efficacy of different classes of antidepressants may not necessarily rely on a common mechanism of action in the brain.
RP Bonson, KR (reprint author), NIMH, CLIN SCI LAB, BLDG 10, ROOM 3D41, 10 CTR DR MSC 1264, BETHESDA, MD 20892 USA.
NR 41
TC 10
Z9 10
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD DEC 15
PY 1996
VL 73
IS 1-2
BP 229
EP 233
PG 5
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA TP015
UT WOS:A1995TP01500042
PM 8788508
ER
PT J
AU Yakel, JL
AF Yakel, JL
TI Desensitization of 5-HT3 receptors expressed in Xenopus oocytes:
Dependence on voltage and primary structure
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article; Proceedings Paper
CT 3rd IUPHAR Satellite Meeting on Serotonin
CY JUL 30-AUG 03, 1994
CL CHICAGO, IL
DE serotonin; ligand-gated ion channel; mutagenesis
ID CHANNEL
AB The wild-type and a mutant 5-HT3 receptor were expressed in Xenopus oocytes to further explore how the rate of onset of desensitization of the 5-HT3 receptor was dependent on membrane voltage and primary structure of the channel. The rapid application of serotonin (5-HT; 50 mu M) in a Ca2+-containing (1.8 mM) bathing solution elicited inward currents that decayed rapidly and with a biphasic time course in most cases. For oocytes expressing the wild-type 5-HT3 receptor and held at a potential of -90 mV, the value of the fast time constant of decay (tau(fast)) was 0.79+/-0.3 s (n=7), while tau(slow) was 16+/-3 s; the area of the decay phase contributed by tau(fast) (i.e., A(fast)) was 50+/-4% and A(slow) was 38+/-5%, with a remainder (i.e., non-desensitizing component) of 12%. The kinetics of the decay phase were strongly voltage-dependent. At a holding potential of -30 mV, the desensitization decay phase was now monophasic, with a time constant of 14.0+/-3.1 s (n=4). Mutating the leucine at position 286 of the wild-type 5-HT3 receptor to threonine (i.e., mutant L286T) resulted in desensitization kinetics that were biphasic at all membrane potentials tested and with a rate of decay that was not voltage dependent. Therefore, desensitization is a multifaceted and complex process, whose rate of onset depends in part to membrane voltage and primary structure of the ion channel.
RP Yakel, JL (reprint author), NIEHS, CELLULAR & MOLEC PHARMACOL LAB, POB 12233, 104 T W ALEXANDER DR, RES TRIANGLE PK, NC 27709 USA.
NR 8
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD DEC 15
PY 1996
VL 73
IS 1-2
BP 269
EP 272
PG 4
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA TP015
UT WOS:A1995TP01500050
PM 8788516
ER
PT J
AU Burnet, PWJ
Mefford, IN
Smith, CC
Gold, PW
Sternberg, EM
AF Burnet, PWJ
Mefford, IN
Smith, CC
Gold, PW
Sternberg, EM
TI Hippocampal 5-HT1A receptor binding site densities, 5-HT1A receptor
messenger ribonucleic acid abundance and serotonin levels parallel the
activity of the hypothalamo-pituitary-adrenal axis in rats
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article; Proceedings Paper
CT 3rd IUPHAR Satellite Meeting on Serotonin
CY JUL 30-AUG 03, 1994
CL CHICAGO, IL
DE adrenalectomy; 5-HT metabolism; 5-HT1A receptor density; 5-HT1A receptor
mRNA; rat strain differences; hippocampus; frontal cortex
ID LEWIS RATS; ARTHRITIS; CLONING; HORMONE; BRAIN
AB We have previously demonstrated that susceptibility of the Lewis rat to inflammatory disease, compared to the relatively resistant Fischer F344 rat, is related to a hyporesponsive hypothalamopituitary adrenal axis to inflammatory and other stress mediators. Since 5-HT and the 5HT(1A) receptor are important stimulators of this axis, we have investigated the levels of 5-HT1A receptor binding sites and encoding mRNA, 5-HT and 5-hydroxyindole acetic acid in various brain regions of Lewis, Harlan Sprague Dawley and Fischer F344 rats. Lewis rats expressed significantly less hippocampal and frontal cortical 5-HT1A receptor binding sites and mRNA than Harlan Sprague-Dawley and Fischer F344 rats. Adrenalectomy increased the number of 5HT(1A) receptor binding sites and mRNA expression in the hippocampus of all three strains. The levels of hippocampal 5-HT in Fischer F344 rats were significantly greater than levels detected in the same regions for the other two strains. Hypothalamic 5-HT and 5-hydroxyindole acetic acid levels in Harlan Sprague-Dawley rats were higher than the same area from the other two strains. Adrenalectomy increased the levels of 5-hydroxyindole acetic acid in the hypothalamus of all three strains. We conclude that hippocampal 5-HT1A receptor densities and 5-HT levels in the rat parallel the activity and responsiveness of the hypthalamopituitary-adrenal axis. We have published these data in an earlier report.
C1 RADCLIFFE INFIRM, NHS TRUST, DEPT NEUROPATHOL, OXFORD OX2 6HE, ENGLAND.
NIMH, CLIN NEUROENDOCRINOL BRANCH, UNIT NEUROENDOCRINE IMMUNOL & BEHAV, BETHESDA, MD 20892 USA.
NIMH, EXPTL THERAPEUT BRANCH, UNIT NEUROPHARMACOL, BETHESDA, MD 20892 USA.
RP Burnet, PWJ (reprint author), UNIV OXFORD, RADCLIFFE INFIRM, NHS TRUST, DEPT CLIN NEUROL, OXFORD OX2 6HE, ENGLAND.
NR 12
TC 20
Z9 20
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD DEC 15
PY 1996
VL 73
IS 1-2
BP 365
EP 368
PG 4
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA TP015
UT WOS:A1995TP01500067
PM 8788533
ER
PT J
AU Knable, MB
Hyde, TM
Murray, AM
Herman, MM
Kleinman, JE
AF Knable, MB
Hyde, TM
Murray, AM
Herman, MM
Kleinman, JE
TI A postmortem study of frontal cortical dopamine D1 receptors in
schizophrenics, psychiatric controls, and normal controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE schizophrenia; prefrontal cortex; cingulate cortex; dopamine; D1
receptors; [H-3]-SCH 23390
ID PRIMATE CEREBRAL-CORTEX; CHRONIC NEUROLEPTIC TREATMENT; PREFRONTAL
CORTEX; CINGULATE CORTEX; RAT STRIATUM; HALOPERIDOL; SYSTEM; BRAIN; D-1;
ABNORMALITIES
AB We tested the hypothesis that aberrant dopaminergic innervation in frontal and cingulate cortices of schizophrenic patients might be revealed by examining dopamine DI receptor density in these brain regions, A quantitative autoradiographic assay with [H-3]-SCH 23390 was performed with samples from schizophrenic patients, normal controls, neuroleptic-treated controls, and suicides, There was a significant elevation in specific binding of [H-3]-SCH 23390 in the intermediate layer of the prefrontal cortex from neuroleptic-treated controls (p = .05). Elevated [H-3]-SCH 23390 binding in several layers from prefrontal and cingulate cortex was observed in schizophrenic subjects, although these results did not reach statistical significance, When data from subjects who had received neuroleptics (schizophrenics and neuroleptic controls) were compared to subjects who had not received neuroleptics (normal controls and suicides), there was a significant elevation in receptor density in both the prefrontal (p = .05) and cingulate cortices (p = .03), These data suggest that elevated [H-3]-SCH 23390 binding in human prefrontal and cingulate cortices may occur with chronic neuroleptic treatment, although increased receptor density that may exist as a feature of psychotic illnesses cannot be excluded.
RP Knable, MB (reprint author), NIMH, INTRAMURAL RES PROGRAM, CLIN BRAIN DISORDERS BRANCH, 2700 MARTIN LUTHER KING JR AVE, WASHINGTON, DC 20032 USA.
NR 43
TC 32
Z9 32
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD DEC 15
PY 1996
VL 40
IS 12
BP 1191
EP 1199
DI 10.1016/S0006-3223(96)00116-3
PG 9
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VW938
UT WOS:A1996VW93800001
PM 8959283
ER
PT J
AU Jacobsen, LK
Hommer, DW
Hong, WL
Castellanos, FX
Frazier, JA
Giedd, JN
Rapoport, JL
AF Jacobsen, LK
Hommer, DW
Hong, WL
Castellanos, FX
Frazier, JA
Giedd, JN
Rapoport, JL
TI Blink rate in childhood-onset schizophrenia: Comparison with normal and
attention-deficit hyperactivity disorder controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE blink rate; schizophrenia; children; ADHD; eye tracking
ID SACCADIC EYE-MOVEMENTS; MONKEY SUPERIOR COLLICULUS; GABA-RELATED
SUBSTANCES; NIGRA PARS RETICULATA; SMOOTH-PURSUIT; NEUROLEPTIC
TREATMENT; TRACKING DYSFUNCTION; CHILDREN; RECEPTORS; DOPAMINE
AB Several lines of evidence have implicated central dopaminergic pathways in the modulation of blink rate. In the present study, blink rare during smooth pursuit was examined in 17 children with childhood-onset schizophrenia, on and off of clozapine, and compared to that of age-matched normal children and unmedicated children with attention-deficit hyperactivity disorder (ADHD). As has been observed in adolescent and adult schizophrenics, blink rate was significantly higher in schizophrenic children relative to normal and ADHD controls, Within the schizophrenic group, blink rate did not significantly change with the introduction of clozapine and was not related to clinical variables, Blink rate was positively correlated with deterioration in smooth pursuit in normal subjects. (C) 1996 Society of Biological Psychiatry
C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892.
ZENECA PHARMACEUT,CNS CLIN RES,WILMINGTON,DE.
RP Jacobsen, LK (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978
NR 55
TC 21
Z9 21
U1 3
U2 6
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 DEC 15
PY 1996
VL 40
IS 12
BP 1222
EP 1229
DI 10.1016/0006-3223(95)00625-7
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VW938
UT WOS:A1996VW93800005
PM 8959287
ER
PT J
AU Ozaki, N
Rosenthal, NE
Pesonen, U
Lappalainen, J
FeldmanNaim, S
Schwartz, PJ
Turner, EH
Goldman, D
AF Ozaki, N
Rosenthal, NE
Pesonen, U
Lappalainen, J
FeldmanNaim, S
Schwartz, PJ
Turner, EH
Goldman, D
TI Two naturally occurring amino acid substitutions of the 5-HT2A receptor:
Similar prevalence in patients with seasonal affective disorder and
controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE seasonal affective disorder; 5-HT2A; receptor; gene; polymorphism;
polymerase chain reaction; sequence
ID INCREASED SEROTONIN2; POINT MUTATIONS; GENE HTR2; BINDING; POLYMORPHISM;
RESPONSES
AB We screened the 5-HT2A receptor gene coding region in 50 patients with seasonal affective disorder (SAD) using a single strand conformational polymorphism analysis and estimated the frequencies of two synonymous and two non-synonymous substitutions we detected in 70 Centre d'Etude du Polymorphism Humain (CEPH) population controls and 62 normal controls, Both of the amino acid substitutions: Ala(447)-Val(447) and His(452)-Tyr(452), were located within the cytoplasmic, C-terminal tail of the receptor, Rarer allele frequencies in CEPH were 0.7% and 9.3% for Val(447) and Tyr(452), respectively. Allele frequencies of all four polymorphisms, including the two amino acid substitutions, were not significantly different in SAD patients as compared to CEPH and normal controls, Lack of association of Val(447) and Tyr(452) to SAD is consistent with observations showing normal 5-HT2A receptor Ca2+ response in platelets with this disorder, however, the two 5-HT2A amino acid substitutions may lead to differences in behavioral phenotypes. (C) 1996 Society of Biological Psychiatry
C1 NIAAA,NEUROGENET LAB,BETHESDA,MD.
RP Ozaki, N (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,ROOM 4S-239,10 CTR DR MSC 1390,BETHESDA,MD 20892, USA.
RI Turner, Erick/A-4848-2008; Ozaki, Norio/M-8908-2014; Goldman,
David/F-9772-2010
OI Turner, Erick/0000-0002-3522-3357; Ozaki, Norio/0000-0002-7360-4898;
Goldman, David/0000-0002-1724-5405
NR 27
TC 63
Z9 64
U1 0
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 DEC 15
PY 1996
VL 40
IS 12
BP 1267
EP 1272
DI 10.1016/0006-3223(95)00649-4
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VW938
UT WOS:A1996VW93800009
PM 8959291
ER
PT J
AU Adinoff, B
Kiser, JMC
Martin, PR
Linnoila, M
AF Adinoff, B
Kiser, JMC
Martin, PR
Linnoila, M
TI Response of dehydroepiandrosterone to corticotropin-releasing hormone
stimulation in alcohol-dependent subjects
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE alcoholism; corticotropin; hypothalamic-hypophyseal system; steroids
ID PLASMA DEHYDROEPIANDROSTERONE; SULFATE; INSULIN; MEN
C1 UNIV TEXAS,SW MED CTR,DEPT PSYCHIAT,DALLAS,TX 75230.
MED UNIV S CAROLINA,DEPT BIOMETRY & EPIDEMIOL,CHARLESTON,SC 29425.
VANDERBUILT SCH MED,DEPT PSYCHIAT,NASHVILLE,TN.
NIAAA,BETHESDA,MD.
RP Adinoff, B (reprint author), VET ADM MED CTR,4500 S LANCASTER,DALLAS,TX 75216, USA.
RI Martin, Peter/A-7738-2008
NR 15
TC 7
Z9 9
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 DEC 15
PY 1996
VL 40
IS 12
BP 1305
EP 1307
DI 10.1016/S0006-3223(96)00381-2
PG 3
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VW938
UT WOS:A1996VW93800016
PM 8959298
ER
PT J
AU Cumming, RC
Liu, JM
Youssoufian, H
Buchwald, M
AF Cumming, RC
Liu, JM
Youssoufian, H
Buchwald, M
TI Suppression of apoptosis in hematopoietic factor-dependent progenitor
cell lines by expression of the FAC gene
SO BLOOD
LA English
DT Article
ID ABNORMAL LYMPHOKINE PRODUCTION; DISEASE FANCONI-ANEMIA; GROUP-C; BCL-2
ONCOPROTEIN; STROMAL CELLS; PLASMA-CELLS; IN-VITRO; DEATH; GROWTH;
SURVIVAL
AB Fanconi anemia (FA) is a genetically heterogeneous, inherited blood disorder characterized by bone marrow failure, congenital malformations, and a predisposition to leukemias. Because FA cells are hypersensitive to DNA cross-linking agents and have chromosomal instability, FA has been viewed as a disorder of DNA repair, However, the exact cellular defect in FA cells has not been identified. Sequence analysis of the gene defective in group C patients (FAC) has shown no significant homologies to other known genes. The FAC protein has been localized to the cytoplasm, indicating that FAC may either play an indirect role in DMA repair or is involved in a different cellular pathway. Recent evidence has indicated that FA cells may be predisposed to apoptosis, especially after treatment with DNA cross-linking agents. The demonstration that genes can suppress apoptosis has been accomplished by overexpression of such genes in growth factor-dependent cell lines that die by apoptosis after factor withdrawal. Using retroviral-mediated gene transfer, we present evidence that expression of FAC in the hematopoietic factor-dependent progenitor cell lines 32D and MO7e can suppress apoptosis induced by growth factor withdrawal. Flow cytometry and morphologic analysis of propidium iodide stained cells showed significantly lower levels of apoptosis in FAC-retroviral transduced cells after growth factor deprivation. Expression of FAC in both cell lines promoted increased viability rather than proliferation, which is consistent with other apoptosis-inhibiting genes such as Bcl-2. These findings imply that FAC may act as a mediator of an apoptotic pathway initiated by growth factor withdrawal. Furthermore, the congenital malformations and hematologic abnormalities characterizing FA may be related to an increased predisposition of FA progenitor cells to undergo apoptosis, particularly in the absence of extracellular signals. (C) 1996 by The American Society of Hematology.
C1 HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO,ON M5G 1X8,CANADA.
UNIV TORONTO,DEPT MOL & MED GENET,TORONTO,ON,CANADA.
NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892.
BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115.
RI Cumming, Robert/G-2185-2010
FU NHLBI NIH HHS [HL52138]
NR 56
TC 70
Z9 70
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 DEC 15
PY 1996
VL 88
IS 12
BP 4558
EP 4567
PG 10
WC Hematology
SC Hematology
GA VZ305
UT WOS:A1996VZ30500017
PM 8977247
ER
PT J
AU Bridges, KR
Barabino, GD
Brugnara, C
Cho, MR
Christoph, GW
Dover, G
Ewenstein, BM
Golan, DE
Guttmann, CRG
Hofrichter, J
Mulkern, RV
Zhang, B
Eaton, WA
AF Bridges, KR
Barabino, GD
Brugnara, C
Cho, MR
Christoph, GW
Dover, G
Ewenstein, BM
Golan, DE
Guttmann, CRG
Hofrichter, J
Mulkern, RV
Zhang, B
Eaton, WA
TI A multiparameter analysis of sickle erythrocytes in patients undergoing
hydroxyurea therapy
SO BLOOD
LA English
DT Article
ID VASCULAR ENDOTHELIAL-CELLS; HEMOGLOBIN-F PRODUCTION; GLOBIN
GENE-CLUSTER; RED-BLOOD-CELLS; S GELATION; DELAY TIME; ANEMIA; DISEASE;
POLYMERIZATION; KINETICS
AB During 24 weeks of hydroxyurea treatment, we monitored red blood cell (RBC) parameters in three patients with sickle cell disease, including F-cell and F-reticulocyte profiles, distributions of delay times for intracellular polymerization, sickle erythrocyte adherence to human umbilical vein endothelial cells in a laminar flow chamber, RBC phthalate density profiles, mean corpuscular hemoglobin concentration and cation content, reticulocyte mean corpuscular hemoglobin concentration, H-1-nuclear magnetic resonance transverse relaxation rates of packed RBCs, and plasma membrane lateral and rotational mobilities of band 3 and glycophorins. Hydroxyurea increases the fraction of cells with sufficiently long delay times to escape the microcirculation before polymerization begins. Furthermore, high pretreatment adherence to human umbilical vein endothelial cells of sickle RBCs decreased to normal after only 2 weeks of hydroxyurea treatment, preceding the increase in fetal hemoglobin levels. The lower adhesion of sickle RBCs to endothelium would facilitate escape from the microcirculation before polymerization begins. Hydroxyurea shifted several biochemical and biophysical parameters of sickle erythrocytes toward values observed with hemoglobin SC disease, suggesting that hydroxyurea moderates sickle cell disease toward the milder, but still clinically significant, hemoglobin SC disease. The 50% reduction in sickle crises documented in the Multicenter Study of Hydroxyurea in Sickle Cell Disease is consistent with this degree of erythrocyte improvement. This is a US government work. There are no restrictions on its use.
C1 BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115.
CHILDRENS HOSP,DEPT PATHOL,BOSTON,MA.
CHILDRENS HOSP,DEPT LAB MED,BOSTON,MA.
CHILDRENS HOSP,DEPT RADIOL,BOSTON,MA.
MASSACHUSETTS GEN HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02114.
HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115.
HARVARD UNIV,SCH MED,DEPT MOL PHARMACOL,BOSTON,MA 02115.
HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115.
HARVARD UNIV,SCH MED,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA.
NORTHEASTERN UNIV,DEPT CHEM ENGN,BOSTON,MA 02115.
JOHNS HOPKINS UNIV HOSP,PEDIAT HEMATOL DIV,BALTIMORE,MD 21205.
NIDDK,CHEM PHYS LAB,NIH,BETHESDA,MD 20892.
RP Bridges, KR (reprint author), BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,DEPT MED,221 LONGWOOD AVE,LMRC 620,BOSTON,MA 02115, USA.
RI Brugnara, Carlo/A-8041-2010
OI Brugnara, Carlo/0000-0001-8192-8713
FU NHLBI NIH HHS [HL15157, HL28028, HL32854]
NR 48
TC 115
Z9 117
U1 0
U2 6
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 DEC 15
PY 1996
VL 88
IS 12
BP 4701
EP 4710
PG 10
WC Hematology
SC Hematology
GA VZ305
UT WOS:A1996VZ30500034
PM 8977264
ER
PT J
AU Hakim, F
Childs, R
Balow, J
Cowan, K
Zujewski, J
Gress, R
AF Hakim, F
Childs, R
Balow, J
Cowan, K
Zujewski, J
Gress, R
TI Development of paroxysmal nocturnal hemoglobinuria after chemotherapy
SO BLOOD
LA English
DT Letter
ID APLASTIC-ANEMIA; PATHOGENETIC LINK
RP Hakim, F (reprint author), NIDDK,NCI,BETHESDA,MD 20892, USA.
NR 7
TC 4
Z9 4
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 DEC 15
PY 1996
VL 88
IS 12
BP 4725
EP 4726
PG 2
WC Hematology
SC Hematology
GA VZ305
UT WOS:A1996VZ30500037
PM 8977267
ER
PT J
AU Henson, DE
AF Henson, DE
TI 25th Anniversary of the Signing of the National Cancer Act, December 23,
1971 - Introduction
SO CANCER
LA English
DT Editorial Material
RP Henson, DE (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,EPN BLDG,ROOM 305,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0008-543X
J9 CANCER
JI Cancer
PD DEC 15
PY 1996
VL 78
IS 12
BP 2582
EP 2583
PG 2
WC Oncology
SC Oncology
GA VW714
UT WOS:A1996VW71400019
PM 8952567
ER
PT J
AU Tisevich, DA
AF Tisevich, DA
TI Legislative history of the National Cancer Institute and the National
Cancer Program
SO CANCER
LA English
DT Article; Proceedings Paper
CT 25th Anniversary Meeting of the Signing of the National Cancer Act
CY JUN 10, 1996
CL WASHINGTON, DC
SP Amer Canc Soc
RP Tisevich, DA (reprint author), NCI,OFF LEGISLAT & CONGRESS ACTIV,BLDG 311,ROOM A11A21,31 CTR DR MSC 2590,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0008-543X
J9 CANCER
JI Cancer
PD DEC 15
PY 1996
VL 78
IS 12
BP 2620
EP 2621
DI 10.1002/(SICI)1097-0142(19961215)78:12<2620::AID-CNCR34>3.0.CO;2-W
PG 2
WC Oncology
SC Oncology
GA VW714
UT WOS:A1996VW71400032
PM 8952578
ER
PT J
AU Kohn, KW
AF Kohn, KW
TI Beyond DNA cross-linking: History and prospects of DNA-targeted cancer
treatment - Fifteenth Bruce F. Cain memorial award lecture
SO CANCER RESEARCH
LA English
DT Article
ID MOUSE LEUKEMIA-L1210 CELLS; TOPOISOMERASE-II CLEAVAGE; P53
TUMOR-SUPPRESSOR; DIFFERENTIAL CYTO-TOXICITY; L-PHENYLALANINE MUSTARD;
CARCINOMA HT-29 CELLS; SIMIAN VIRUS-40 DNA; HAMSTER OVARY CELLS; C-MYC
PROTOONCOGENE; DOUBLE-STRAND BREAK
AB The origin of cancer chemotherapy can be traced to the wartime discovery of the lymphotoxic action of nitrogen mustards, These and other bifunctional agents were later found to produce various types of DNA cross-links, and some of these agents continue to be mainstays of current therapy, The cellular pharmacology of these drugs was studied extensively during the 1970s and 1980s by means of DNA filter elution methodology. In the course of these investigations, DNA topoisomerases were discovered to be targets of anthracyclines and several other classes of anticancer drugs, DNA cross-linkers and topoisomerase blockers have generally similar cytotoxic mechanisms, which depend on DNA damage detection, DNA repair, cell cycle arrest, and cell death by apoptosis, The molecular control of these processes, involving oncogenes and tumor suppressor genes, is being revealed by current research, Cancer cells often have defects within these control systems, and these defects may confer selective sensitivity to appropriately designed drug therapy. Panels of human tumor cell lines may serve to link the molecular defects with specific drug sensitivities, Such correlations could guide the selection of drugs for therapy based on molecular diagnosis of individual tumors.
RP Kohn, KW (reprint author), NCI,MOL PHARMACOL LAB,DIV BASIC SCI,BETHESDA,MD 20892, USA.
NR 206
TC 78
Z9 79
U1 1
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 DEC 15
PY 1996
VL 56
IS 24
BP 5533
EP 5546
PG 14
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000002
PM 8971150
ER
PT J
AU Karp, JE
Chiarodo, A
Brawley, O
Kelloff, GJ
AF Karp, JE
Chiarodo, A
Brawley, O
Kelloff, GJ
TI Prostate cancer prevention: Investigational approaches and opportunities
SO CANCER RESEARCH
LA English
DT Review
ID ANDROGEN-RECEPTOR GENE; ENDOTHELIAL GROWTH-FACTOR; IN-SITU
HYBRIDIZATION; E-CADHERIN EXPRESSION; INTRAEPITHELIAL NEOPLASIA;
UNITED-STATES; BREAST-CANCER; INTEGRIN ALPHA(V)BETA(3); NUCLEOTIDE
EXCHANGE; TUMOR ANGIOGENESIS
C1 NCI,CHEMPREVENT BRANCH,DIV CANC PREVENT & CONTROL,NIH,ROCKVILLE,MD 20852.
NCI,ORGAN SYST PROGRAM,DIV CANC TREATMENT DIAG & CTR,NIH,ROCKVILLE,MD 20852.
NCI,COMMUNITY ONCOL BRANCH,DIV CANC PREVENT & CONTROL,NIH,ROCKVILLE,MD 20852.
NR 120
TC 38
Z9 38
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 1996
VL 56
IS 24
BP 5547
EP 5556
PG 10
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000003
PM 8971151
ER
PT J
AU Puri, RK
Hoon, DS
Leland, P
Snoy, P
Rand, RW
Pastan, I
Kreitman, RJ
AF Puri, RK
Hoon, DS
Leland, P
Snoy, P
Rand, RW
Pastan, I
Kreitman, RJ
TI Preclinical development of a recombinant toxin containing circularly
permuted interleukin 4 and truncated Pseudomonas exotoxin for therapy of
malignant astrocytoma
SO CANCER RESEARCH
LA English
DT Article
ID RENAL-CELL-CARCINOMA; TUMOR-NECROSIS-FACTOR; RECEPTOR GAMMA-CHAIN;
CHIMERIC PROTEIN; IL-4 RECEPTORS; HUMAN-MELANOMA; EXPRESSION; GROWTH;
INHIBITION; INTERFERON
AB Effective treatment is lacking for malignant glioblastoma/astrocytoma. We have identified interleukin-4 receptors (IL-4R) on human malignant astrocytoma. We demonstrate that 16 of 21 surgical samples of high-grade astrocytoma and glioblastoma but not normal brain tissues expressed IL-4R as assessed by reverse transcriptase PCR. We further demonstrate that human malignant astrocytoma cell lines express high-affinity IL-4R. Using a chimeric protein composed of circularly permuted IL-4 and a truncated form of Pseudomonas exotoxin A, we observed that this toxin (IL4(38-37)-PE38KDEL) is highly cytotoxic to IL-4R-bearing glioblastoma cells. Compared with a previously reported IL4-PE chimeric protein (IL-PE4E), IL4(38-37)-PE38KDEL bound with higher affinity and was 3-30-fold more cytotoxic to glioblastoma cell lines, Upon intrathecal administration in monkeys, high cerebrospinal fluid IL4(38-37)-PE38KDEL levels mere achieved using 2- and 6-mu g/kg doses without any central nervous system or other abnormalities. IL4(38-37)-PE38KDEL levels were not detectable in the serum of any monkey studied. When IL4(38-37)-PE38KDEL was injected into the right frontal cortex of rats, localized necrosis was observed at 1000-ng/ml doses but not at less than or equal to 100-ng/ml doses. We conclude that by localized administration, nontoxic levels of IL4(38-37)-PE38KDEL can be achieved, which may have significant cytotoxic activity against malignant astrocytoma.
C1 NIH,LAB MOL TUMOR BIOL,DIV VET SERV,CTR BIOL EVALUAT & RES,FOOD & DRUG ADM,BETHESDA,MD 20892.
ST JOHNS HOSP,JOHN WAYNE CANC INST,DIV MOL & CELLULAR IMMUNOL & NEUROONCOL,SANTA MONICA,CA 90404.
NCI,MOL BIOL LAB,DIV CANC BIOL DIAGNOSIS & CTR,NIH,BETHESDA,MD 20892.
RP Puri, RK (reprint author), NIH,LAB MOL TUMOR BIOL,DIV CELLULAR & GENE THERAPIES,CTR BIOL EVALUAT & RES,FOOD & DRUG ADM,BETHESDA,MD 20892, USA.
OI Hoon, Dave/0000-0003-1915-3683
NR 32
TC 91
Z9 95
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 DEC 15
PY 1996
VL 56
IS 24
BP 5631
EP 5637
PG 7
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000020
PM 8971168
ER
PT J
AU Siders, WM
Halloran, PJ
Fenton, RG
AF Siders, WM
Halloran, PJ
Fenton, RG
TI Transcriptional targeting of recombinant adenoviruses to human and
murine melanoma cells
SO CANCER RESEARCH
LA English
DT Article
ID THYMIDINE KINASE GENE; MOUSE TYROSINASE GENE; LUNG-CANCER CELLS;
TRANSGENIC MICE; CARCINOEMBRYONIC ANTIGEN; HEPATOCELLULAR-CARCINOMA;
MICROPHTHALMIA GENE; RETROVIRAL VECTORS; ENHANCER-PROMOTER; HUMAN-BREAST
AB One potential avenue for future cancer therapy involves the specific targeting of effector genes to cancer cells throughout the body, including distant metastatic sites. As a first step toward this goal, we tested the ability of the transcriptional regulatory elements of the human and mouse tyrosinase genes to promote high levels of pigment cell-specific transcription. A construct consisting of 209 hp of the human tyrosinase promoter linked to two enhancer elements was demonstrated to drive high-level, melanoma-specific expression of a beta-galactosidase (beta-gal) reporter gene in transient transfection assays, In studies of the murine tyrosinase promoter region, constructs containing up to 2500 bp of the 5' regulatory region were found to have very low transcriptional activity in murine melanoma cells, However, as with the human system, addition of two tandem repeats of an upstream enhancer element resulted in high levels of lineage-specific transcriptional activation, The murine tyrosinase promoter-enhancer expression cassette was introduced into the E1 region of a recombinant adenovirus to generate the virus AdmTyr-beta gal. This virus grows to high titer and maintains transcriptional specificity for pigment cell lineages, Strikingly, AdmTyF-beta gal is extremely active in human melanoma cells, in some cases exceeding the transcriptional activity of a cytomegalovirus promoter-driven recombinant beta-gal virus. Tissue specificity of gene expression is maintained, with very low levels observed in tumors and primary human cells derived from other lineages. These data provide evidence that it is possible to target human melanoma cells with great efficiency and specificity using high-titer recombinant adenovirus vectors.
C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CLIN SCI,FREDERICK,MD 21702.
RI Halloran, Philip/J-1390-2012
OI Halloran, Philip/0000-0003-1371-1947
FU NCI NIH HHS [N01-CO-74102]
NR 47
TC 67
Z9 71
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 DEC 15
PY 1996
VL 56
IS 24
BP 5638
EP 5646
PG 9
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000021
PM 8971169
ER
PT J
AU Reeves, ME
Royal, RE
Lam, JS
Rosenberg, SA
Hwu, P
AF Reeves, ME
Royal, RE
Lam, JS
Rosenberg, SA
Hwu, P
TI Retroviral transduction of human dendritic cells with a tumor-associated
antigen gene
SO CANCER RESEARCH
LA English
DT Article
ID INFILTRATING LYMPHOCYTES; STEM-CELLS; TNF-ALPHA; VIRUS; IDENTIFICATION;
PEPTIDES
AB Dendritic cells (DCs) are potent antigen-presenting cells that can activate quiescent T lymphocytes. When pulsed with tumor-associated antigen (TAA) peptide or protein, murine DCs can provide antitumor immunity. me reasoned that DCs retrovirally transduced with TAA genes might have important advantages over peptide- or protein-pulsed DCs, including long-term TAA presentation in pipe, and presentation of important but undefined epitopes. Therefore, we attempted to retrovirally transduce human DCs with a melanoma TAA gene (MART-1) and determine whether these transduced DCs could raise a specific antitumor response from quiescent autologous T lymphocytes. After retroviral transduction, human CD34(+) cells were differentiated into DCs in vitro using granulocyte macrophage colony-stimulating factor, tumor necrosis factor alpha, and stem cell factor, This method consistently yielded a population of DCs as analyzed by morphology phenotype, and MLR. Flow cytometric analysis revealed that 22-28% of cells expressing the DC phenotype also expressed a transduced marker gene. When DCs were transduced with the gene encoding MART-1, they stimulated much higher levels of cytokine release by MART-1-specific tumor-infiltrating lymphocytes than control DCs transduced with an irrelevant gene. In vitro stimulation using MART-1-transduced DCs but not control-transduced DCs raised specific antitumor CTLs from autologous quiescent T cells. These results provide evidence that human DCs can be retrovirally transduced with a TAA gene and that these transduced cells can raise a specific antitumor immune response in vitro, Transduced DCs may be useful for in vivo immunization against TAA.
C1 NCI, SURG BRANCH, NIH, BETHESDA, MD 20892 USA.
NR 28
TC 195
Z9 199
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD DEC 15
PY 1996
VL 56
IS 24
BP 5672
EP 5677
PG 6
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000026
PM 8971174
ER
PT J
AU Thompson, JS
Reese, KJ
DeBaun, MR
Perlman, EJ
Feinberg, AP
AF Thompson, JS
Reese, KJ
DeBaun, MR
Perlman, EJ
Feinberg, AP
TI Reduced expression of the cyclin-dependent kinase inhibitor gene
p57(KIP2) in Wilms' tumor
SO CANCER RESEARCH
LA English
DT Article
ID WIEDEMANN-BECKWITH SYNDROME; HUMAN CANCER; CHROMOSOME-11; H19;
RELAXATION; ANGELMAN; LOCUS
AB We have previously shown that the p57(KIP2) gene, which encodes a cyclin-dependent kinase inhibitor, undergoes genomic imprinting and lies within a 700-kb domain of imprinted genes on 11p15, including IGF2 and H19, Loss of heterozygosity and loss of imprinting (LOI) of this region are frequently observed in Wilms' tumor (WT) and other embryonal malignancies, Although LOI of p57(KIP2) was observed in some WTs (similar to 10%), allele-specific expression was preserved in most tumors examined, Because our initial studies were inconclusive concerning the absolute expression level of p57(KIP2) in WT, we developed a sensitive and quantitative RNase protection assay to determine if changes in p57(KIP2) expression play a role in WT. Expression of p57(KIP2) was found to he virtually absent in 21 of 21 WTs compared to matched normal kidney from the same patients, as well as compared to fetal kidney. We also examined p57(KIP2) expression in the normal kidney and tongue of patients with Beckwith-Wiedemann syndrome (BWS), which predisposes to WT and also involves LOI of IGF2 and H19, Although p57(KIP2) was undetectable in BWS tongue, similar results were also observed in postnatal non-BWS tongue samples. Most primary skin fibroblast cultures of BWS cell lines exhibited normal imprinting of p57(KIP2). However, one BWS patient did show LOI of p57(KIP2) in skin fibroblasts, Thus, p57(KIP2) is part of a domain of genes on 11p15 that show altered expression and, in some cases, altered imprinting in WT and BWS.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT MOL BIOL & GENET,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT ONCOL,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205.
NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892.
FU NCI NIH HHS [CA65145]
NR 28
TC 67
Z9 68
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 DEC 15
PY 1996
VL 56
IS 24
BP 5723
EP 5727
PG 5
WC Oncology
SC Oncology
GA VX880
UT WOS:A1996VX88000034
PM 8971182
ER
PT J
AU Wang, J
Hargrove, ME
Ting, CC
AF Wang, J
Hargrove, ME
Ting, CC
TI IL-2 and IL-4 mediate through two distinct kinase pathways for the
activation of alpha CD3-induced activated killer cells
SO CELLULAR IMMUNOLOGY
LA English
DT Article
ID STIMULATORY FACTOR-I; PROTEIN-TYROSINE KINASE; LYMPHOCYTE-T PRECURSORS;
SIGNAL-TRANSDUCTION; MONOCLONAL-ANTIBODY; ANTIGEN RECEPTOR; MYELOID
CELLS; JANUS KINASE; INTERLEUKIN-2; PHOSPHORYLATION
AB The present study has examined the role of IL-2 and IL-4 in the regulation of different kinase pathways for the generation of alpha CD3-induced activated killer cells, CD3-AK, It has previously been shown that the IL-2 promoted CD3-AK cell response is mediated through a PKC (protein kinase C)-dependent pathway, which is susceptible to PKC inhibitors and resistant to inhibitors of PTK (protein tyrosine kinase), and that IL-4 synergized with IL-2 to induce CD3-AK cells, However, the IL-4-promoted CDS-AK cell response was PKC-independent as assessed by its resistance to PKC inhibitors, These findings suggest a dichotomy in the pathways leading to CD3-AK cell generation, To further determine whether IL-4 mediated a different kinase pathway to activate the T cells, we studied its effect on protein tyrosine phosphorylation, IL-4 up-regulated protein tyrosine phosphorylation in CD3-AK cells in a dose-dependent fashion, and resulted in increased levels of a number of phosphorylated proteins, Of particular note was the increase of tyrosine phosphorylated p56(lck) and p59(fyn) in CD3-AK cells, The changes in global protein tyrosine phosphorylation were correlated with the up-regulation by IL-4 of CD3-AK cell cytolytic activity, and the production of granzyme A, alpha IL-4 specifically blocked all the effects which were induced by IL-4. The PTK inhibitor genistein inhibited the IL-4-augmented cytolytic activity of CD3-AK cells as well as the IL-4-induced augmentation of protein tyrosine phosphorylation to the basal level of CD3-AK cells cultured in IL-2 alone, Consistent with a dichotomy in pathways for IL-2- and IL-4-mediated CD3-AK generation, genistein had no effect on the generation of CDS-AK cells cultured in IL-2 alone, Thus while PKC is primarily involved in the generation of IL-2-promoted CD3-AK cells, PTK appears to be required for the regulation of IL-4-promoted CD3-AK response. (C) 1996 Academic Press, Inc.
C1 NCI,DIV BASIC SCI,LAB IMMUNE CELL BIOL,NIH,BETHESDA,MD 20892.
NR 43
TC 7
Z9 7
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0008-8749
J9 CELL IMMUNOL
JI Cell. Immunol.
PD DEC 15
PY 1996
VL 174
IS 2
BP 138
EP 146
DI 10.1006/cimm.1996.0303
PG 9
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA VZ377
UT WOS:A1996VZ37700004
PM 8954613
ER
PT J
AU Secord, EA
Rizzo, LV
Barroso, EWS
Umetsu, DT
Thorbecke, GJ
DeKruyff, RH
AF Secord, EA
Rizzo, LV
Barroso, EWS
Umetsu, DT
Thorbecke, GJ
DeKruyff, RH
TI Reconstitution of germinal center formation in nude mice with Th1 and
Th2 clones
SO CELLULAR IMMUNOLOGY
LA English
DT Article
ID CENTER B-CELLS; INDUCER T-CELLS; LEU 7+ CELLS; IMMUNE-RESPONSES;
FUNCTIONAL-HETEROGENEITY; LYMPHOID FOLLICLES; ANTIBODY-RESPONSES; CD40
LIGAND; IN-VIVO; MEMORY
AB We investigated the ability of hemocyanin (KLH)-specific cloned CD4(+) T cells expressing defined cytokine profiles to support germinal center (GC) formation in syngeneic athymic recipients in response to hapten-KLH challenge. Th1 clones producing IL-2 and IFN-gamma did not by themselves increase GC production above background, while Th2 cells producing IL-4 and IL-5 did. However, the combination of Th1 and Th2 cytokines was more effective than Th2 cytokines alone, suggesting a synergistic effect in this aspect of their help for B cells. In contrast to GC formation, antibody production could be induced with Th1 or Th2 clones given separately (Th1 clones inducing IgG2a, and Th2 clones inducing IgG1 and IgE). These results indicate that the T cell requirements for GC production are different from those for isotype switching and Ig secretion. It is postulated that the synergy between Th1 and Th2 cells in the induction of GC formation reflects the synergy between Th1 and Th2 cytokines, such as IFN-gamma and IL-5, in promotion of GC cell proliferation. (C) 1996 Academic Press, Inc.
C1 NYU,SCH MED,KAPLAN CANC CTR,NEW YORK,NY 10016.
NEI,IMMUNOL LAB,SECT IMMUNOREGULAT,BETHESDA,MD 20892.
STANFORD UNIV,DEPT PEDIAT,PALO ALTO,CA 94305.
RP Secord, EA (reprint author), NYU,SCH MED,DEPT PATHOL,NEW YORK,NY 10016, USA.
RI Rizzo, Luiz Vicente/B-4458-2009
FU NIA NIH HHS [AG-04980]
NR 62
TC 13
Z9 13
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0008-8749
J9 CELL IMMUNOL
JI Cell. Immunol.
PD DEC 15
PY 1996
VL 174
IS 2
BP 173
EP 179
DI 10.1006/cimm.1996.0307
PG 7
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA VZ377
UT WOS:A1996VZ37700008
PM 8954617
ER
PT J
AU Schott, ME
Wells, DT
Schlom, J
Abrams, SI
AF Schott, ME
Wells, DT
Schlom, J
Abrams, SI
TI Comparison of linear and branched peptide forms (MAPs) in the induction
of T helper responses to point-mutated ras immunogens
SO CELLULAR IMMUNOLOGY
LA English
DT Article
ID DEFINED SYNTHETIC VACCINE; MULTIPLE-ANTIGEN PEPTIDES; CELL RECOGNITION;
B-EPITOPE; DESIGN; LYMPHOCYTES; ANTIBODIES; PROTECTION; SYSTEM; HIV-1
AB The utility of multiple antigenic peptides (MAPs) for the induction of antibody and cellular immune responses in animal models has been demonstrated for a variety of peptide epitopes involved in human disease, However, little is known about immune responses to MAPs constructed with antigenic tumor epitopes, nor has peptide specificity in branched forms been addressed, A potentially important advantage of the MAP system over linear peptide immunogens for clinical applications is elimination of the need for a protein carrier with its associated toxicity and immunogenicity. Here, we examined cellular immune responses following in vivo administration of MAPs incorporating a 13-mer T helper epitope from point-mutated ras p21 (ras V12) and compared the potency of the responses to that of the linear peptide. The Gly --> Val mutation in position 12, which is associated with a range of human carcinomas, represents a useful system for evaluating the specificity of the immune response, In initial studies with the point-mutated Linear peptide epitope, optimal in vitro proliferation responses were obtained following sc administration of the peptide in a squalane-containing adjuvant formulation, Comparative immunization studies using point-mutated MAPs bearing two, four, or eight branches were administered either in saline or in adjuvant. These studies showed that adjuvant was required for the induction of cellular immune responses using both linear and all three forms of branched peptides, Moreover, there was no apparent advantage of using any of the MAPs vs linear peptide when equivalent mass amounts were administered, i.e., the intensity of the immune response was no greater using any of the branched structures compared to the linear form. Specificity of the in vivo responses for both the linear and the MAP immunogens was demonstrated by the higher stimulation indices observed in vitro in the presence of the mutant ras V12 vs the normal ras G12 linear peptide, No apparent cellular immune response to the MAP core structure itself was observed. However, a nonspecific response to the two-branched MAP2G12 structure was observed in some assays, the nature of which is unknown at this time, This work represents the first reported investigation of a cellular immune response using MAP immunogens incorporating a tumor-specific peptide epitope and demonstrates that linear peptides are as efficient as three different MAP structures in the generation of specific T cell responses.
C1 NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892.
NR 30
TC 12
Z9 13
U1 1
U2 2
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 DEC 15
PY 1996
VL 174
IS 2
BP 199
EP 209
DI 10.1006/cimm.1996.0310
PG 11
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA VZ377
UT WOS:A1996VZ37700011
PM 8954620
ER
PT J
AU Fukushima, PI
Phuong, KTN
OGrady, P
StetlerStevenson, M
AF Fukushima, PI
Phuong, KTN
OGrady, P
StetlerStevenson, M
TI Flow cytometric analysis of kappa and lambda light chain expression in
evaluation of specimens for B-cell neoplasia
SO CYTOMETRY
LA English
DT Article
DE light chain restriction; monoclonal B-cell detection; flow cytometry
ID NON-HODGKINS LYMPHOMA; IMMUNOGLOBULIN LIGHT; PERIPHERAL-BLOOD; CLONAL
EXCESS; ANTIBODIES; MYELOMA
AB Analysis of light chain expression is one of the most important determinations in flow cytometric immunophenotyping of patient specimens. Numerous technical factors, such as antibody choice and cytophilic antibody artifact, impact a laboratory's ability to perform this test. There have been conflicting reports concerning the efficacy of polyclonal versus monoclonal antibodies, as well as methods of circumventing cytophilic antibodies, indicating that a consensus has not been reached on optimal methods for light chain determination. The authors have investigated methods for light chain analysis in 104 normal donors and 366 patient specimens, comparing different anti-light chain antibodies as well as strategies for analysis of specimens with low numbers of monoclonal B cells, admired polyclonal B cells, or cytophilic antibodies. The patient specimens were either part of the initial diagnostic evaluation of patients with suspected lymphoma, or were performed for staging or assessment of treatment of patients with known B-cell neoplasia. No monoclonality was detected in control specimens, and there was no significant difference in staining with monoclonal verses polyclonal anti-light chain antibodies. In addition, cytophilic antibody did not obscure results in normal controls. Monoclonality was detected in 106 patient specimens, with 89 showing gross involvement with a predominant monoclonal B-cell process. However, in 43% of the grossly monoclonal specimens, there was failure to detect monoclonality with at least one light chain antibody set, with 8% of these cases showing failure with two anti-light chain sets. This indicates the importance of antibody choice in light chain analysis. Cytophilic antibody artifact in monoclonal specimens was easily overcome by appropriate antibody combinations, obviating the need for cytophilic antibody-shedding by incubation at 37 degrees C in fetal calf serum. In 27 patient specimens with low numbers of B cells or admired polyclonal B cells, a clonal search based on FSC and CD19 or CD20 expression was performed. In 17 of the 27 cases (63%), a small monoclonal population was detected among admired polyclonal B cells. The authors conclude that multiple strategies are necessary in flow cytometric analysis for B-cell monoclonality. (C) 1996 Wiley-Liss, Inc.*
C1 NCI,FLOW CYTOMETRY UNIT,PATHOL LAB,NIH,BETHESDA,MD 20892.
NR 18
TC 46
Z9 48
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 0196-4763
J9 CYTOMETRY
JI Cytometry
PD DEC 15
PY 1996
VL 26
IS 4
BP 243
EP 252
DI 10.1002/(SICI)1097-0320(19961215)26:4<243::AID-CYTO2>3.0.CO;2-D
PG 10
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA WB910
UT WOS:A1996WB91000002
PM 8979022
ER
PT J
AU Mardiney, M
Brown, MR
Fleisher, TA
AF Mardiney, M
Brown, MR
Fleisher, TA
TI Measurement of T-cell CD69 expression: A rapid and efficient means to
assess mitogen- or antigen-induced proliferative capacity in normals
SO CYTOMETRY
LA English
DT Article
DE CD69; H-3-thymidine; lymphocyte; mitogen; antigen
ID ACTIVATION ANTIGEN; LEU-23; INDUCTION; EA-1
AB We have analyzed the expression of the activation antigen CD69 on normal human T cells by flow cytometry following stimulation with mitogens and recall antigen. These data were compared to parallel studies assessing the proliferative response using the H-3-thymidine (H-3-TdR) incorporation assay. Three different mitogens (PHA, ConA, and CD2/CD2R) induced maximal expression of CD69 at 24 h, which remained stable throughout the 72 h culture period. The mitogen-stimulated cells initiated DNA synthesis as determined by the H-3-TdR assay (72 h) while nonstimulated cells failed to upregulate CD69 or incorporate H-3-TdR. We next compared T cell CD69 expression (n = 12) following stimulation with either CD2/CD2R (5 mu g/ml) or the recall antigen, tetanus toroid (1:1500). Cell proliferation was determined by the 3H-TdR assay at 72 h (CD2/CD2R) or 120 h (tetanus toxoid). Evaluation of CD69 expression at 6 h predicted CD2/CD2R but not tetanus responder status as defined by H-3-TdR incorporation. However, when 4 known tetanus responders (H-3-TdR) were evaluated over time, it was found that at 48 h the fluorescence intensity (of CD69) on tetanus-stimulated CD3(+) cells increased markedly compared with nonstimulated cells (range of increase 43-850%). One individual whose cells failed to respond to tetanus toroid (H-3-TdR and CD69) did respond normally to CD2/CD2R. These observations suggest that flow cytometric evaluation of T cell CD69 expression following mitogen (6 h) or antigen (48 h) stimulation may provide an accurate screen of T-cell responsiveness in normals. (C) 1996 Wiley-Liss, Inc.*
C1 NIH,SERV IMMUNOL,BETHESDA,MD 20892.
NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892.
NR 17
TC 75
Z9 85
U1 0
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PD DEC 15
PY 1996
VL 26
IS 4
BP 305
EP 310
DI 10.1002/(SICI)1097-0320(19961215)26:4<305::AID-CYTO11>3.0.CO;2-V
PG 6
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA WB910
UT WOS:A1996WB91000011
PM 8979031
ER
PT J
AU Wolfsberg, TG
White, JM
AF Wolfsberg, TG
White, JM
TI ADAMs in fertilization and development
SO DEVELOPMENTAL BIOLOGY
LA English
DT Review
ID SPERM-EGG FUSION; MDC PROTEIN FAMILY; DISINTEGRIN-LIKE; METALLOPROTEASE
DOMAIN; TRANSMEMBRANE PROTEIN; PLATELET-AGGREGATION; MEMBRANE-PROTEINS;
ALPHA-SUBUNIT; VENOM; CELL
C1 UNIV VIRGINIA,HLTH SCI CTR,DEPT CELL BIOL,CHARLOTTESVILLE,VA 22908.
RP Wolfsberg, TG (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894, USA.
FU NIGMS NIH HHS [GM48739]
NR 63
TC 202
Z9 212
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD DEC 15
PY 1996
VL 180
IS 2
BP 389
EP 401
DI 10.1006/dbio.1996.0313
PG 13
WC Developmental Biology
SC Developmental Biology
GA WA846
UT WOS:A1996WA84600002
PM 8954712
ER
PT J
AU Wray, S
Fueshko, SM
Kusano, K
Gainer, H
AF Wray, S
Fueshko, SM
Kusano, K
Gainer, H
TI GABAergic neurons in the embryonic olfactory pit/vomeronasal organ:
Maintenance of functional GABAergic synapses in olfactory explants
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
ID HORMONE-RELEASING HORMONE; GAMMA-AMINOBUTYRIC-ACID; GLUTAMATE
DECARBOXYLASES; GENE-EXPRESSION; NERVOUS-SYSTEM; MOUSE; GABA; CELLS;
CULTURES; SIGNALS
AB In previous work, we showed a robust gamma-aminobutyric acid (GABAergic) synaptic input onto embryonic luteinizing hormone-releasing hormone (LHRH) neurons maintained in olfactory explants. In this study, we identify GABAergic neurons in olfactory pit (OF) of embryonic mice in vivo and study, using patch-pipet whole-cell current and voltage clamp techniques, synaptic interactions of these neurons in explant cultures. In vivo, glutamate decarboxylase (GAD, the enzyme which synthesizes GABA) mRNA was first detected in nasal regions on Embryonic Day (E) 11.5. From E12.5 to E13.5, robust GAD expression was localized to cells primarily in the ventral aspect of the OF. GAD mRNA was not detected over dorsally located cells in olfactory sensory or respiratory epithelium. In addition, GAD mRNA was not observed in cells along olfactory axons. GAD mRNA was dramatically reduced in the OP/vomeronasal organ by E16.5. Using antibodies against both GABA and GAD, immunopositive axonal-like tracts were detected in the nasal septum on E12.5. GABAergic staining decreased by E13.5. To examine synaptic interactions of these GABAergic cells, embryonic olfactory explants were generated and maintained in serum-free media. As explants spread, neuron-like cells migrated into the periphery, sometimes forming ganglion-like clusters. Cells were recorded, marked intracellularly with Lucifer Yellow and postfixation, immunocytochemically examined. forty-six cells, typically multipolar, were GABAergic, had resting potentials around -50 mV, and exhibited spontaneous action potentials which were generated by spontaneous depolarizing GABAergic (GABA(A)) synaptic activity. OP neurons depolarized in response to GABA by increasing Cl- conductance. The biophysical properties of OF-derived GABAergic neurons were distinct from those reported for olfactory receptor neurons but similar to embryonic LHRH neurons. However, unlike LHRH neurons, GABAergic neurons did not migrate large distances in olfactory explants or appear to leave the olfactory pit in vivo. (C) 1996 Academic Press, Inc.
RP Wray, S (reprint author), NINCDS,NEUROCHEM LAB,NIH,BETHESDA,MD 20892, USA.
OI wray, susan/0000-0001-7670-3915
NR 33
TC 54
Z9 54
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 DEC 15
PY 1996
VL 180
IS 2
BP 631
EP 645
DI 10.1006/dbio.1996.0334
PG 15
WC Developmental Biology
SC Developmental Biology
GA WA846
UT WOS:A1996WA84600023
PM 8954733
ER
PT J
AU Johe, KK
Hazel, TG
Muller, T
DugichDjordjevic, MM
McKay, RDG
AF Johe, KK
Hazel, TG
Muller, T
DugichDjordjevic, MM
McKay, RDG
TI Single factors direct the differentiation of stem cells from the fetal
and adult central nervous system
SO GENES & DEVELOPMENT
LA English
DT Article
DE stem cells; neurons; glia
ID RAT CEREBRAL-CORTEX; REGION-SPECIFIC DIFFERENTIATION; FOREBRAIN
SUBVENTRICULAR ZONE; CLONALLY RELATED CELLS; GROWTH-FACTOR; PRECURSOR
CELL; DEVELOPMENTAL EXPRESSION; FUNCTIONAL-PROPERTIES;
HIPPOCAMPAL-NEURONS; COMMON PROGENITOR
AB Identifying the signals that regulate stem cell differentiation is fundamental to understanding cellular diversity in the brain. In this paper we identify factors that act in an instructive fashion to direct the differentiation of multipotential stem cells derived from the embryonic central nervous system (CNS). CNS stem cell clones differentiate to multiple fates: neurons, astrocytes, and oligodendrocytes. The differentiation of cells in a clone is influenced by extracellular signals: Platelet-derived growth factor (PDGF-AA, -AB, and -BB) supports neuronal differentiation. In contrast, ciliary neurotrophic factor and thyroid hormone T3 act instructively on stem cells to generate clones of astrocytes and oligodendrocytes, respectively. Adult stem cells had remarkably similar responses to these growth factors. These results support a simple model in which transient exposure to extrinsic factors acting through known pathways initiates fate decisions by multipotential CNS stem cells.
C1 NINCDS,MOL BIOL LAB,NIH,BETHESDA,MD 20892.
NR 58
TC 892
Z9 959
U1 3
U2 33
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 DEC 15
PY 1996
VL 10
IS 24
BP 3129
EP 3140
DI 10.1101/gad.10.24.3129
PG 12
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA WA909
UT WOS:A1996WA90900006
PM 8985182
ER
PT J
AU Miura, Y
Miyake, K
Yamashita, Y
Shimazu, R
Copeland, NG
Gilbert, DJ
Jenkins, NA
Inazawa, J
Abe, T
Kimoto, M
AF Miura, Y
Miyake, K
Yamashita, Y
Shimazu, R
Copeland, NG
Gilbert, DJ
Jenkins, NA
Inazawa, J
Abe, T
Kimoto, M
TI Molecular cloning of a human RP105 homologue and chromosomal
localization of the mouse and human RP105 genes (Ly64 and LY64)
SO GENOMICS
LA English
DT Article
ID LEUCINE-RICH REPEATS; B-CELL ACTIVATION; TRANSMEMBRANE PROTEIN; LINKAGE
MAP; DROSOPHILA; POLARITY; DOMAINS; TOLL
AB RP105 is a mouse B cell surface molecule that transmits a growth-promoting signal and is implicated in the life/death decision of B cells. RP105 has tandem repeats of a leucine-rich motif in the extracellular domain that is expected to be involved in protein-protein interactions. In the present study, a cDNA clone encoding the human homologue of RP105 was isolated. The amino acid sequence of human RP105 is highly homologous to that of mouse RP105 with 74% identity, and the leucine-rich repeats are well conserved. The expression of the human RP105 transcript was detected in some B cell lines, a histiocytic leukemia cell line, and peripheral blood leukocytes. We also determined the chromosomal locations of the mouse RP105 gene (Ly64 locus) and the human RP105 gene (LY64 locus). Interspecific mouse backcross analysis was used to map the Ly64 locus at the distal region of chromosome 13. The human LY64 locus was localized to 5q12 by fluorescence in situ hybridization, confirming the syntenic relationship between these regions of the mouse and human chromosomes. (C) 1996 Academic Press, Inc.
C1 SAGA MED SCH,DEPT IMMUNOL,SAGA 849,JAPAN.
NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702.
KYOTO PREFECTURAL UNIV MED,DEPT HYG,KYOTO 602,JAPAN.
NR 24
TC 32
Z9 33
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD DEC 15
PY 1996
VL 38
IS 3
BP 299
EP 304
DI 10.1006/geno.1996.0632
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA WB429
UT WOS:A1996WB42900008
PM 8975706
ER
PT J
AU Takai, S
Kozak, CA
Kitamura, K
Takeda, A
AF Takai, S
Kozak, CA
Kitamura, K
Takeda, A
TI Assignment of the CD45-AP gene to the centromeric end of mouse
chromosome 19 and human chromosome 11q13.1-q13.3
SO GENOMICS
LA English
DT Article
ID INSITU HYBRIDIZATION; PROTEIN; RECEPTOR; LOCALIZATION; ANTIGEN
AB CD45-AP is a recently identified phosphorylated protein that specifically associates with the leukocyte-specific transmembrane glycoprotein CD45. The gene for CD45-AP, Ptprcap (protein tyrosine phosphatase, receptor type c polypeptide associated protein), was mapped in mouse by typing the progeny of two multilocus crosses using the mouse CD45-AP cDNA as a Southern hybridization probe, The CD45-AP gene mapped to the centromeric region of Chr 19 proximal to the genes Fth, Cd5, and Pcna-rs. The gene for the human CD45-AP homologue, PTPRCAP, was localized to chromosome band 11q13.1-q13.3 by fluorescence in situ hybridization using human genomic CD45-AP DNA as a hybridization probe, The genetic mapping of the Ptprcap/PTPRCAP genes extends the previously defined synteny conservation of various genes that have been assigned to these regions of the mouse and the human chromosomes. (C) 1996 Academic Press, Inc.
C1 BROWN UNIV,ROGER WILLIAMS MED CTR,DEPT PATHOL,PROVIDENCE,RI 02908.
INT MED CTR JAPAN,DEPT GENET,RES INST,TOKYO 162,JAPAN.
NIAID,MOL MICROBIOL LAB,BETHESDA,MD 20892.
FU NIGMS NIH HHS [GM 48188]
NR 23
TC 3
Z9 3
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD DEC 15
PY 1996
VL 38
IS 3
BP 429
EP 431
DI 10.1006/geno.1996.0648
PG 3
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA WB429
UT WOS:A1996WB42900024
PM 8975722
ER
PT J
AU Farzadegan, H
Henrard, DR
Kleeberger, CA
Schrager, L
Kirby, AJ
Saah, AJ
Rinaldo, CR
OGorman, M
Detels, R
Taylor, E
Phair, JP
Margolick, JB
AF Farzadegan, H
Henrard, DR
Kleeberger, CA
Schrager, L
Kirby, AJ
Saah, AJ
Rinaldo, CR
OGorman, M
Detels, R
Taylor, E
Phair, JP
Margolick, JB
TI Virologic and serologic markers of rapid progression to AIDS after HIV-1
seroconversion
SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
LA English
DT Article
DE HIV-1; seroconversion; anti-gag immune response; progression; viral load
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DISEASE PROGRESSION; TYPE-1 INFECTION;
HOMOSEXUAL MEN; ANTIBODY; ANTIGEN; PLASMA; BLOOD; P24; RESPONSES
AB The association between early virologic and immunologic events after human immunodeficiency virus type 1 (HIV-1) infection and progression of HIV-1 infection to acquired immunodeficiency syndrome (AIDS) was studied among 59 homosexual men with documented time of seroconversion. Epidemiologic factors, such as number of lifetime sexual partners, history of sexually transmitted diseases, and other factors, also were studied. AII 17 seroconverters in the cohort who developed AIDS within 3 years (rapid progressors = RPs) were compared with 42 men without AIDS for at least 6 years seroconversion (nonrapid progressors = non-RPs). Plasma levels of HIV-1 RNA, p24 antigen, antibodies to HIV-1 structural genes, beta-2 microglobulin, neopterin, and interferon-alpha were measured at four time points: (a) the last seronegative visit, (b) the first seropositive visit, (c) the visit closest to AIDS (or the corresponding visit for the non-RPs) and (d) 6 years after seroconversion (for non-RPs). Up to seroconversion, the RPs had a significantly higher number of lifetime sexual partners than non-RPs (503 versus 171, respectively). At the first seropositive visit, RPs had significantly higher concentrations of plasma HIV-1 RNA (p < 0.01) and prevalence of p24 antigenemia (p < 0.001) and significantly lower levels of antibodies to the HIV-1 gag proteins p17 and p24 (p < 0.01-0.001) compared with non-RPs. These differences increased during follow-up visits. Antibodies to p66 and gp120 were significantly different only at the visit closest to AIDS (p < 0.001), as were beta-2 microglobulin and interferon alpha. These findings suggest that early virologic-immunologic events after HIV-1 infection may determine the rate of progression to AIDS. Anti-gag immune response may prevent rapid progression of HIV-1 disease and should be considered for future vaccine studies.
C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD.
JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MOL MICROBIOL & IMMUNOL,BALTIMORE,MD.
NIH,BETHESDA,MD 20892.
ABBOTT LABS,N CHICAGO,IL 60064.
UNIV PITTSBURGH,DEPT PATHOL,PITTSBURGH,PA.
UNIV PITTSBURGH,DEPT MICROBIOL,PITTSBURGH,PA.
NORTHWESTERN UNIV,SCH MED,DEPT PEDIAT,CHICAGO,IL 60611.
UNIV CALIF LOS ANGELES,DEPT EPIDEMIOL,LOS ANGELES,CA.
NORTHWESTERN UNIV,SCH MED,COMPREHENS AIDS CTR,CHICAGO,IL.
FU NIAID NIH HHS [U01-AI-35041, U01-AI-35039, U01-AI-35040]
NR 55
TC 32
Z9 32
U1 1
U2 2
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 DEC 15
PY 1996
VL 13
IS 5
BP 448
EP 455
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA VY574
UT WOS:A1996VY57400008
PM 8970472
ER
PT J
AU Kotake, S
Schumacher, HR
Wilder, RL
AF Kotake, S
Schumacher, HR
Wilder, RL
TI A simple nested RT-PCR method for quantitation of the relative amounts
of multiple cytokine mRNAs in small tissue samples
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE reverse transcriptase-polymerase chain reaction; synovium; cytokine;
mRNA; quantitation; needle biopsy
ID POLYMERASE CHAIN-REACTION; MESSENGER-RNA; THEORETICAL CONSIDERATIONS;
MONONUCLEAR-CELLS; VIRUS; EXPRESSION; RESPONSES; PRIMERS; GENE
AB It is difficult to quantitate cytokine mRNA profiles in small human tissue specimens obtained by a needle biopsy, even using standard RT-PCR methods, because the amount of mRNA in the specimens is very small. To address this problem, we developed highly sensitive, quantitative, nested RT-PCR techniques to evaluate the expression of multiple cytokine mRNAs in synovial specimens obtained by needle biopsy. To reduce effects of variation of initial RNA concentrations, cDNA from each target RNA sample was normalized, using a simplified competitive PCR method, to the levels of beta-actin cDNA. The first and the second (nested) PCR were performed in the same tube to prevent contamination. The number of PCR-product bands, evident on polyacrylamide gel electrophoresis, was used to quantitate the relative amounts of target cDNA. Using our methods, it was possible to evaluate, in a single synovial tissue specimen obtained by needle biopsy, the relative amounts of mRNAs for 10 cytokines (TNF-alpha, IL-1 beta, IL-2, IL-4, IL-6, IL-10, IL-12 p40, IL-13, IL-15, IFN-gamma) and CD3 delta chain. Our methods are particularly valuable if there are multiple target mRNAs, numerous samples, or if the amounts of mRNAs are limited. The methods are applicable to a wide variety of tissues and target mRNAs.
C1 NIAMSD,ARB,NIH,BETHESDA,MD 20892.
UNIV PENN,PHILADELPHIA,PA 19104.
NR 25
TC 39
Z9 39
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD DEC 15
PY 1996
VL 199
IS 2
BP 193
EP 203
DI 10.1016/S0022-1759(96)00184-6
PG 11
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA VZ015
UT WOS:A1996VZ01500011
PM 8982362
ER
PT J
AU Kanno, T
Siebenlist, U
AF Kanno, T
Siebenlist, U
TI Activation of nuclear factor-kappa B via T cell receptor requires a Raf
kinase and Ca2+ influx - Functional synergy between Raf and calcineurin
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PROTEIN-KINASE; CYCLOSPORINE-A; ANTIGEN RECEPTOR; LYMPHOCYTE-ACTIVATION;
SIGNAL-TRANSDUCTION; GENE-EXPRESSION; I TAX; CALCIUM; ALPHA;
PHOSPHORYLATION
AB Signals transduced via the TCR activate the transcription factor nuclear factor-kappa B (NF-kappa B), which, in turn, is critical to the transcriptional induction of many genes important for the proliferation and expression of a differentiated phenotype. Treatment of T cells with the protein kinase C activator PMA in combination with Ca2+ ionophores mimics this process, and the two agents are often substituted for TCR stimulation, bypassing the TCR. Here we identify intracellular signaling components involved in activation of NF-kappa B following TCR stimulation. TCR signaling was triggered by treating Jurkat T cells with PHA or anti-CD3 Abs, and NF-kappa B activation was monitored by electrophoretic mobility shift assays and/or by kappa B-dependent reporter assays. Contrary to the idea that protein kinase C is involved in TCR-mediated activation of NF-kappa B, high doses of staurosporine did not interfere with activation of NF-kappa B by PHA, while the same dose of staurosporine completely blocked activation by PMA. PHA-induced kappa B-dependent reporter activity was, however, effectively blocked by a dominant negative form of Raf-l, suggesting a critical role for a Raf kinase. The TCR-mediated activation of NF-kappa B was also dependent on a Ca2+ influx, because the Ca2+ channel blocker, SK&F 96365, as well as other agents that prevented the Ca2+ influx, inhibited NF-kappa B activation. Cotransfection of a constitutively active form of calcineurin largely substituted for the Ca2+ requirement and reversed the blockade by SK&F 96365. Consistent with these observations, coexpression of constitutively active forms of Raf-l and calcineurin synergistically induced kappa B-dependent reporter activity, suggesting a physiologically relevant functional interaction between the kinase and the phosphatase.
C1 NIAID,IMMUNOREGULAT LAB,NIH,BETHESDA,MD 20892.
KYOTO UNIV,INST VIRUS RES,DEPT VIRAL ONCOL,KYOTO 606,JAPAN.
NR 48
TC 73
Z9 74
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 DEC 15
PY 1996
VL 157
IS 12
BP 5277
EP 5283
PG 7
WC Immunology
SC Immunology
GA VX026
UT WOS:A1996VX02600009
PM 8955173
ER
PT J
AU Garboczi, DN
Utz, U
Ghosh, P
Seth, A
Kim, J
VanTienhoven, EAE
Biddison, WE
Wiley, DC
AF Garboczi, DN
Utz, U
Ghosh, P
Seth, A
Kim, J
VanTienhoven, EAE
Biddison, WE
Wiley, DC
TI Assembly, specific binding, and crystallization of a human TCR-alpha
beta with an antigenic tax peptide from human T lymphotropic virus type
1 and the class I MHC molecule HLA-A2
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CELL RECEPTOR FRAGMENTS; ESCHERICHIA-COLI; MONOCLONAL-ANTIBODY;
CRYSTAL-STRUCTURE; EXPRESSION; CHAIN; SECRETION; HETERODIMERS; PROTEINS;
RECOGNITION
AB T lymphocytes use TCR-alpha beta to bind and to recognize complexes of antigenic peptides bound to MHC proteins located at the surface of APCs, We have assembled and crystallized this intercellular complex of TCR/peptide/MHC from soluble human TCR-alpha beta and soluble peptide/HLA-A2 complexes. The soluble TCR-alpha beta binds specifically to its in vivo ligand, the complex of HLA-AZ, and a peptide from the Tax protein of human T lymphotropic virus type 1. The soluble TCR also binds in vitro to an altered peptide ligand, which appears to be a partial agonist in T cell assays as determined by its ability to elicit different cytolytic and lymphokine secretion responses, Heterodimerization and the antigenic specificity of the TCR do not require its interchain disulfide bond, transmembrane segments, or glycosylations, Crystals of the TCR/peptide/HLA-A2 complex diffract x-rays, providing the means to study in atomic detail the mechanism of Ag-specific cell-cell recognition between T cells and target cells.
C1 HARVARD UNIV,DEPT MOL & CELLULAR BIOL,CAMBRIDGE,MA 02138.
HARVARD UNIV,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02138.
CLIN RES INST MONTREAL,IMMUNOL LAB,MONTREAL,PQ H2W 1R7,CANADA.
NINCDS,MOL IMMUNOL SECT,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
CHILDRENS HOSP,HOWARD HUGHES MED INST,MOL MED LAB,BOSTON,MA 02115.
FU NICHD NIH HHS [HD-17461]
NR 48
TC 121
Z9 124
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 1996
VL 157
IS 12
BP 5403
EP 5410
PG 8
WC Immunology
SC Immunology
GA VX026
UT WOS:A1996VX02600024
PM 8955188
ER
PT J
AU Gray, JX
Haino, M
Roth, MJ
Maguire, JE
Jensen, PN
Yarme, A
StetlerStevenson, MA
Siebenlist, U
Kelly, K
AF Gray, JX
Haino, M
Roth, MJ
Maguire, JE
Jensen, PN
Yarme, A
StetlerStevenson, MA
Siebenlist, U
Kelly, K
TI CD97 is a processed, seven-transmembrane, heterodimeric receptor
associated with inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID EGF-LIKE DOMAIN; TYROSINE PHOSPHATASE; G-PROTEINS; LYMPHOCYTE
INTERACTIONS; EXTRACELLULAR DOMAIN; ADHESION MOLECULE; CALCIUM-BINDING;
MARFAN-SYNDROME; CELL-ADHESION; ACTIVATION
AB CD97 is a receptor that spans the membrane seven times, a defining feature of C protein-coupled receptors, CD97 is predominantly expressed in leukocytes, but the function and accurate protein structure of this receptor have not been described, We show here that CD97 has the novel property among C protein-coupled receptors characterized to date of being processed intracellularly in either the endoplasmic reticulum or early Golgi from a proprotein into a noncovalently associated two-subunit structure that becomes expressed on the cell surface and is composed of a large extracellular protein (CD97 alpha) and a seven-membrane spanning protein (CD97 beta), CD97 beta is part of an evolutionarily conserved subfamily of four proteins, including two Caenorhabditis elegans proteins of as yet unknown function, which is distinct from but most closely related to the glucagon receptor family, CD97 alpha exists in three alternatively spliced isoforms that contain between three and five epidermal growth factor (EGF)-like repeats that are related to the calcium binding EGF-like repeats in the microfibril protein fibrillin, Leukocytes strongly positive for CD97 are concentrated at sites of inflammation relative to CD97 expression in normal lymphoid tissues, Soluble CD97 alpha was found in body fluids from inflamed tissues, suggesting that a functional consequence of the CD97 heterodimeric structure is the stable existence of CD97 alpha in a cellfree form, CD97 appears to be a multifunctional protein that may play a signal transduction role associated with the establishment or development of an inflammatory process.
C1 NCI, PATHOL LAB, NIH, BETHESDA, MD 20892 USA.
NIAID, IMMUNOREGULAT LAB, NIH, BETHESDA, MD 20892 USA.
NR 40
TC 127
Z9 131
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 1996
VL 157
IS 12
BP 5438
EP 5447
PG 10
WC Immunology
SC Immunology
GA VX026
UT WOS:A1996VX02600028
PM 8955192
ER
PT J
AU Kim, PKM
Dutra, AS
Chandrasekharappa, SC
Puck, JM
AF Kim, PKM
Dutra, AS
Chandrasekharappa, SC
Puck, JM
TI Genomic structure and mapping of human FADD, an intracellular mediator
of lymphocyte apoptosis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID LYMPHOPROLIFERATIVE SYNDROME; BREAST-CANCER; DEATH DOMAIN; CYCLIN D1;
FAS; GENE; AMPLIFICATION; PROTEINS; REGION; INTERACTS
AB Fas-associated death domain protein (FADD)/MORT1 is a 23-kDa cytoplasmic protein containing a C-terminal death domain that interacts with the intracellular death domain of the Fas transmembrane receptor. Cross-linking of Fas mediates apoptosis in a variety of cells, primarily peripheral T lymphocytes, for which this pathway plays a major role in mature lymphocyte homeostasis, We report the characterization of the human FADD gene, which spans approximately 3.6 kb and contains two exons (286 and 341 bp) separated by a 2.0-kb intron, FADD was mapped to chromosome 11q13.3 by the independent techniques of PCR screening of somatic cell hybrid mapping panels and fluorescence in situ hybridization, In addition FADD was shown by fluorescence in situ hybridization to be amplified along with other 11q13.3 genes previously studied in the breast cancer cell line MDA-MB-134-VI, raising the possibility that overexpression of mutant FADD could contribute to poor prognosis and increased invasiveness of tumors, Its known role in apoptosis has made FADD a candidate susceptibility gene for autoimmune lymphoproliferative syndrome, Now that it has been colocalized in 11q13.3 with IDDM4, a diabetes susceptibility locus, alterations in FADD should also be considered as potential contributors to insulin-dependent familial diabetes. Elucidation of the map position and gene structure of FADD will make possible linkage and mutation analysis to study the role of this gene in human diseases.
C1 NIH,NATL CTR HUMAN GENOME RES,IMMUNOL GENET SECT,LAB GENE TRANSFER,BETHESDA,MD 20892.
NR 42
TC 30
Z9 33
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 15
PY 1996
VL 157
IS 12
BP 5461
EP 5466
PG 6
WC Immunology
SC Immunology
GA VX026
UT WOS:A1996VX02600031
PM 8955195
ER
PT J
AU GarciaZepeda, EA
Combadiere, C
Rothenberg, ME
Sarafi, MN
Lavigne, F
Hamid, Q
Murphy, PM
Luster, AD
AF GarciaZepeda, EA
Combadiere, C
Rothenberg, ME
Sarafi, MN
Lavigne, F
Hamid, Q
Murphy, PM
Luster, AD
TI Human monocyte chemoattractant protein (MCP)-4 is a novel CC chemokine
with activities on monocytes, eosinophils, and basophils induced in
allergic and nonallergic inflammation that signals through the CC
chemokine receptors (CCR)-2 and -3
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID FUNCTIONAL EXPRESSION; CHEMOTACTIC PROTEIN-1; MOLECULAR-CLONING;
ENDOTHELIAL-CELLS; MESSENGER-RNA; T-CELLS; GENE-EXPRESSION; CYTOKINE;
RANTES; MCP-2
AB The chemokines are a large family of cytokines that regulate the complex and precise recruitment of immune cells into inflammatory foci. To fully appreciate their role in the pathogenesis of human diseases, the entire spectrum of chemokines, their receptors, their cellular targets, and mechanisms of regulation need to be delineated. Using eotaxin as a probe, we isolated a cDNA for a novel human beta (or CC) chemokine that, based on its biological and structural features, we have named monocyte chemoattractant protein (MCP)-4. Purified recombinant MCP-4 protein was a potent chemoattractant for monocytes and eosinophils and stimulated histamine release from basophils. MCP-4 induced a calcium flux in HEK-293 cells transfected with the monocyte selective MCP-1 receptor (CCR-2B) and the eosinophil selective eotaxin receptor (CCR-3), but not in the more widely expressed CCR-1 or CCR-5. This novel chemokine is expressed in TNF-alpha and IL-1 activated epithelial and endothelial cells in vitro, and in the epithelial mucosa of patients with both Th2-type allergic and Th1-type nonallergic sinusitis. Furthermore, both IFN-gamma and IL-4, products of Th1 and Th2 cells, respectively, synergized with TNF-alpha and IL-1 in inducing MCP-4 mRNA accumulation, These properties of MCP-4 offer a molecular explanation for the observed accumulation of monocytes, eosinophils and basophils in both Th1- and Th2-type immune responses.
C1 MASSACHUSETTS GEN HOSP E,INFECT DIS UNIT,CHARLESTOWN,MA 02129.
HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129.
NIAID,HOST DEF LAB,BETHESDA,MD 20892.
HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115.
MCGILL UNIV,MEAKINS CHRISTIE LABS,DEPT PATHOL & MED,MONTREAL,PQ H3A 2T5,CANADA.
RI Combadiere, Christophe/I-5639-2013
OI Combadiere, Christophe/0000-0002-1755-4531
FU NCI NIH HHS [R01 CA69212-01]
NR 66
TC 215
Z9 218
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 DEC 15
PY 1996
VL 157
IS 12
BP 5613
EP 5626
PG 14
WC Immunology
SC Immunology
GA VX026
UT WOS:A1996VX02600050
PM 8955214
ER
PT J
AU Weiss, GH
Calabrese, PP
AF Weiss, GH
Calabrese, PP
TI Occupation times of a CTRW on a lattice with anomalous sites
SO PHYSICA A
LA English
DT Article
AB We develop formalism allowing us to derive results for the probability density of the occupation time of a set of sites on a lattice of a CTRW in which the pausing-time density on the set can differ from those on the remaining lattice sites. The problem is suggested by transillumination techniques used in optical imaging. Details are given for the case of a single site on the lattice and an anomalous pausing-time density. It is shown that if the random walk is transient (i.e., in three or more dimensions when the variance of a single jump is finite) the asymptotic density for the occupation time at the special point is a negative exponential. In one dimension the random walk is recurrent. Here it is shown that the occupation time scales as t(1/2). These results extend to finite numbers of anomalous points.
RP Weiss, GH (reprint author), NATL INST HLTH,BETHESDA,MD 20892, USA.
NR 14
TC 12
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-4371
J9 PHYSICA A
JI Physica A
PD DEC 15
PY 1996
VL 234
IS 1-2
BP 443
EP 454
DI 10.1016/S0378-4371(96)00362-7
PG 12
WC Physics, Multidisciplinary
SC Physics
GA WA080
UT WOS:A1996WA08000027
ER
PT J
AU Pinals, DA
Malhotra, AK
Missar, CD
Pickar, D
Breier, A
AF Pinals, DA
Malhotra, AK
Missar, CD
Pickar, D
Breier, A
TI Lack of gender differences in neuroleptic response in patients with
schizophrenia
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE gender; schizophrenia; neuroleptic treatment; sex differences
ID SEX; VARIABLES; AFTERCARE; ILLNESS; ONSET; DRUG; AGE
AB Objective: The authors sought to determine if there were gender differences in neuroleptic response in male and female patients with schizophrenia who were matched for clinical and demographic variables and participated in a double-blind trial of traditional antipsychotic drugs. Methods: 24 males (m) and 20 females (f) with schizophrenia or schizoaffective disorder who did not differ in clinical characteristics (age of onset, course of illness, prior hospitalizations, premorbid functioning) participated in an extended drug-free period followed by a neuroleptic trial under double-blind, placebo-controlled conditions. Results: Males and females showed significant improvement in total, positive and negative BPRS symptoms during neuroleptic treatment. However, there were no significant differences in treatment response between sexes. No sex differences were found in baseline drug-free symptomatology, neuroleptic dose or dosage by weight. Conclusions: There were no significant sex differences in neuroleptic treatment response in male and female patients well-matched for clinical, treatment and demographic characteristics. Methodological issues which distinguish this study from prior studies reporting gender differences in neuroleptic response are examined.
C1 NIMH,EXPT THERAPEUT BRANCH,NIH,BETHESDA,MD 20892.
NR 27
TC 28
Z9 28
U1 2
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC 15
PY 1996
VL 22
IS 3
BP 215
EP 222
DI 10.1016/S0920-9964(96)00067-9
PG 8
WC Psychiatry
SC Psychiatry
GA WA779
UT WOS:A1996WA77900004
PM 9000318
ER
PT J
AU Peell, GD
Green, JP
Elkashef, AM
Khandelwal, JK
Linnoila, M
Wyatt, RJ
Lawson, WB
Jaeger, AC
Kaufmann, CA
Kirch, DG
AF Peell, GD
Green, JP
Elkashef, AM
Khandelwal, JK
Linnoila, M
Wyatt, RJ
Lawson, WB
Jaeger, AC
Kaufmann, CA
Kirch, DG
TI The relationship between urine excretion and biogenic amines and their
metabolites in cerebrospinal fluid of schizophrenic patients (vol 19, pg
171, 1996)
SO SCHIZOPHRENIA RESEARCH
LA English
DT Correction, Addition
ID HISTAMINE METABOLITES; BRAIN
C1 ST ELIZABETH HOSP,NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032.
NIAAA,DIV INTRAMURAL CLIN & BIOL RES,BETHESDA,MD 20205.
RP Peell, GD (reprint author), CUNY MT SINAI SCH MED,DEPT PHARMACOL,BOX 1215,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC 15
PY 1996
VL 22
IS 3
BP 267
EP 267
DI 10.1016/S0920-9964(96)00073-4
PG 1
WC Psychiatry
SC Psychiatry
GA WA779
UT WOS:A1996WA77900011
ER
PT J
AU Peat, TS
Frank, EG
McDonald, JP
Levine, AS
Woodgate, R
Hendrickson, WA
AF Peat, TS
Frank, EG
McDonald, JP
Levine, AS
Woodgate, R
Hendrickson, WA
TI The UmuD' protein filament and its potential role in damage induced
mutagenesis
SO STRUCTURE
LA English
DT Article
DE filament structure; mutagenesis; self-cleavage reaction; SOS response;
X-ray crystallography
ID RECA-MEDIATED CLEAVAGE; DNA POLYMERASE-III; ESCHERICHIA-COLI; SOS
MUTAGENESIS; ANOMALOUS DIFFRACTION; STRUCTURAL BASIS; REPAIR; REPRESSOR;
MUTATIONS; DEFICIENT
AB Background: Damage induced 'SOS mutagenesis' may occur transiently as part of the global SOS response to DNA damage in bacteria, A key participant in this process is the UmuD protein, which is produced in an inactive form but converted to the active form, UmuD', by a RecA-mediated self-cleavage reaction. UmuD', together with UmuC and activated RecA (RecA*), enables the DNA polymerase III holoenzyme to replicate across chemical and UV induced lesions. The efficiency of this reaction depends on several intricate protein-protein interactions.
Results: Recent X-ray crystallographic analysis shows that in addition to forming molecular dimers, the N- and C-terminal tails of UmuD' extend from a globular beta structure to associate and produce crystallized filaments. We have investigated this phenomenon and find that these filaments appear to relate to biological activity. Higher order oligomers are found in solution with UmuD', but not with UmuD nor with a mutant of UmuD' lacking the extended N terminus. Deletion of the N terminus of UmuD' does not affect its ability to form molecular dimers but does severely compromise its ability to interact with a RecA-DNA filament and to participate in mutagenesis. Mutations in the C terminus of UmuD' result in both gain and loss of function for mutagenesis.
Conclusions: The activation of UmuD to UmuD' appears to cause a large conformational change in the protein which allows it to form oligomers in solution at physiologically relevant concentrations. Properties of these oligomers are consistent with the filament structures seen in crystals of UmuD'.
C1 COLUMBIA UNIV,DEPT BIOCHEM & MOL BIOPHYS,NEW YORK,NY 10032.
NICHHD,SECT DNA REPLICAT REPAIR & MUTAGENESIS,BETHESDA,MD 20892.
COLUMBIA UNIV,HOWARD HUGHES MED INST,NEW YORK,NY 10032.
RI Peat, Thomas/F-9817-2010
OI Peat, Thomas/0000-0002-6488-0831
NR 56
TC 32
Z9 32
U1 0
U2 0
PU CURRENT BIOLOGY LTD
PI LONDON
PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB
SN 0969-2126
J9 STRUCTURE
JI Structure
PD DEC 15
PY 1996
VL 4
IS 12
BP 1401
EP 1412
DI 10.1016/S0969-2126(96)00148-7
PG 12
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VY739
UT WOS:A1996VY73900004
PM 8994967
ER
PT J
AU Kocher, JP
Prevost, M
Wodak, SJ
Lee, B
AF Kocher, JP
Prevost, M
Wodak, SJ
Lee, B
TI Properties of the protein matrix revealed by the free energy of cavity
formation
SO STRUCTURE
LA English
DT Article
DE folding; hydrophobic interactions; sidechain packing; stability
ID PANCREATIC TRYPSIN-INHIBITOR; GLOBULAR-PROTEINS; BACTERIOPHAGE-T4
LYSOZYME; HYDROSTATIC-PRESSURE; POTENTIAL FUNCTIONS; INTERNAL CAVITIES;
MOLECULAR LIQUIDS; PACKING DEFECTS; BURIED WATERS; STABILITY
AB Background: The classical picture of the hydrophobic stabilization of proteins invokes a resemblance between the protein interior and nonpolar solvents, but the extent to which this is the case has often been questioned. The protein interior is believed to be at least as tightly packed as organic crystals, and was shown to have very low compressibility. There is also evidence that these properties are not uniform throughout the protein, and conflicting views exist on the nature of sidechain packing and on its influence on the properties of the protein.
Results: In order to probe the physical properties of the protein, the free energy associated with the formation of empty cavities has been evaluated for two proteins: barnase and T4 lysozyme. To this end, the likelihood of encountering such cavities was computed from room temperature molecular dynamics trajectories of these proteins in water. The free energy was evaluated in each protein taken as a whole and in submolecular regions. The computed free energies yielded information on the manner in which empty space is distributed in the system, while the latter undergoes thermal motion, a property hitherto not analyzed in heterogeneous media such as proteins. Our results showed that the free energy of cavity formation is higher in proteins than in both water and hexane, providing direct evidence that the native protein medium differs in fundamental ways from the two liquids. Furthermore, although the packing density was found to be higher in nonpolar regions of the protein than in polar ones, the free energy cost of forming atomic size cavities is significantly lower in nonpolar regions, implying that these regions contain larger chunks of empty space, thereby increasing the likelihood of containing atomic size packing defects. These larger empty spaces occur preferentially where buried hydrophobic sidechains belonging to secondary structures meet one another. These particular locations also appear to be more compressible than other parts of the core or surface of the protein.
Conclusions: The cavity free energy calculations described here provide a much more detailed physical picture of the protein matrix than volume and packing calculations. According to this picture, the packing of hydrophobic sidechains is tight in the interior of the protein, but far from uniform. In particular, the packing is tighter in regions where the backbone forms less regular hydrogen-bonding interactions than at interfaces between secondary structure elements, where such interactions are fully developed. This may have important implications on the role of sidechain packing in protein folding and stability.
C1 FREE UNIV BRUSSELS,UNITE CONFORMAT MACROMOL BIOL,B-1050 BRUSSELS,BELGIUM.
NCI,MOL BIOL LAB,NATL INST HLTH,BETHESDA,MD 20892.
NR 75
TC 52
Z9 52
U1 0
U2 5
PU CURRENT BIOLOGY LTD
PI LONDON
PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB
SN 0969-2126
J9 STRUCTURE
JI Structure
PD DEC 15
PY 1996
VL 4
IS 12
BP 1517
EP 1529
DI 10.1016/S0969-2126(96)00157-8
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VY739
UT WOS:A1996VY73900013
PM 8994976
ER
PT J
AU Tsai, WP
Conley, SR
Kung, HF
Garrity, RR
Nara, PL
AF Tsai, WP
Conley, SR
Kung, HF
Garrity, RR
Nara, PL
TI Preliminary in vitro growth cycle and transmission studies of HIV-1 in
an autologous primary cell assay of blood-derived macrophages and
peripheral blood mononuclear cells
SO VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 INFECTION; NEUTRALIZING ANTIBODY;
QUANTITATIVE-ANALYSIS; SOLUBLE CD4; TROPISM; PLASMA; PROTEINS;
GLYCOPROTEINS; PATHOGENESIS
AB Recent interest focused on the dynamics of HIV-1 replication in primary monocytes/macrophages and T-lymphocytes of the immune system, as well as the standardization of virological and immunological in vitro assays with primary isolates, provided the impetus for these studies. These types of studies have never been performed as they would occur in vivo, i.e., where the envelope of the virus and cell membranes of the two cell types of the same host origin. Therefore, the biological and physicochemical properties of an uncloned, primary dual-tropic isolate HIV-1(ADA) during the initial lag, log, and stationary phases of viral replication were studied in an autologous donor cell assay in peripheral blood mononuclear cells (PBMC) and blood monocyte-derived macrophages (MDM). Similar total numbers (10(9) virus particles/ml) were produced by both cell types during the stationary period. On a per cell per day basis, during peak stationary periods, 0.92 x 10(3) virions/day for MDMs and 5.31 x 10(3) virions/day for PBMCs were produced. Interestingly, virus replicating from MDMs during the log-growth phase demonstrated the greatest infectious fraction which was 3 logs greater than virus replicating in PBMCs. Despite constant virus particle production in MDMs, the infectious fraction was found to fall 3 to 4 lags over a In-day period. Due to an infectious fraction less than 1 (0.053 infectious unit/cell/24 hr), virus spread in PBMCs during the rapid log phase could only have occurred by cell-to-cell contact, whereas in MDMs with an infectious fraction of about one infectious particle (similar to 1/cell/24 hr), cell-free transmission could account for the observed results. Most of the MDMs (> 90%) became productively infected, whereas only 5-10% of the total PBMCs were found replicating virus. The period of peak stationary virus production (i.e., stationary phase) was at minimum 4 to 5 times longer in MDMs than PBMCs. Whereas the majority of p24, RT, and gp120 found to be associated with MDM-derived virions, no increased dissociation of these components was observed in PBMC-derived virions. The virion-associated gp120 was 3 to 4 times more stable on both PBMC- and MDM-derived virus (> 96 hr) and present at 10-25 times the concentration per virion than that observed for a T-cell-line-adapted laboratory strain of HIV-1 replicating in T-cell lines. These in vitro results suggest that important differences exist between MDMs and PBMCs with regard to the viral dynamics of infection and replication which should provide for a qualitative and quantitative basis to estimate virus replication on a per-cell basis for other known cellular targets of HIV-1. Studying the multiple biophysicochemical characteristics and viral replication dynamics as described herein provides an autologous in vitro model of additional quantifiable parameters for analysis and understanding of virus/host factor(s) and/or antivirals which influence them. (C) 1996 Academic Press, Inc.
C1 NCI,FREDERICK CANC RES & DEV CTR,DIV BASIC SCI,OFF DIRECTORS,DIRECTORS LAB,VIRUS BIOL SECT,FREDERICK,MD 21702.
SCI APPLICAT INT CORP,FREDERICK,MD 21702.
RP Tsai, WP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,LAB BIOCHEM PHYSIOL,DIV BASIC SCI,POB B,BLDG 560,ROOM 12-15,FREDERICK,MD 21702, USA.
NR 44
TC 30
Z9 30
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 0042-6822
J9 VIROLOGY
JI Virology
PD DEC 15
PY 1996
VL 226
IS 2
BP 205
EP 216
DI 10.1006/viro.1996.0648
PG 12
WC Virology
SC Virology
GA VZ463
UT WOS:A1996VZ46300008
PM 8955040
ER
PT J
AU Portis, JL
Fujisawa, R
McAtee, FJ
AF Portis, JL
Fujisawa, R
McAtee, FJ
TI The glycosylated gag protein of MuLV is a determinant of
neuroinvasiveness: Analysis of second site revertants of a mutant MuLV
lacking expression of this protein
SO VIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA-VIRUS; POLYPROTEIN PRECURSORS; INCUBATION PERIOD;
RETROVIRUS; SEQUENCE; DISEASE; TRANSLATION; INTERFERENCE; REPLICATION;
CELLS
AB Neuroinvasiveness is a property of all neurovirulent murine retroviruses, although the factors which facilitate infection of the CNS are not understood. We previously showed that mutant MuLV which lack expression of an accessory protein, glycosylated gag, had lost neurovirulence, indicating that this protein may be involved in promoting CNS infection, The mutations were located in the ''Kozak'' consensus sequence of the initiation codon for this protein. Here it is shown that shortly after inoculation of mice with one of these mutant viruses, revertants emerged which had regained expression or glycosylated gag and had also regained the neuroinvasiveness and neurovirulence exhibited by the wild-type virus. The phenotypic revertants retained the mutations in the ''Kozak'' consensus sequence but exhibited a G --> A mutation 12 codons downstream from the mutated start site, creating a new initiation codon and a glycosylated gag protein, which was truncated at its N-terminus. Using antibodies specific for glycosylated gag it is shown that the frequency of splenic infectious centers expressing revertant virus increased progressively during the 2 months following inoculation of mutant virus until greater than or equal to 50% of the virus-producing cells in the spleen expressed revertant virus; In contrast although phenotypic revertants were detectable at low frequency after cell-free passage in vitro in M. dunni fibroblasts, there was no evidence for selection. These results indicate that glycosylated gag facilitates virus spread within the spleen and to extra-splenic sites, such as the CNS, and suggest that the protein may function through its interaction with the host. (C) 1996 Academic Press, Inc.
RP Portis, JL (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,903 S 4TH ST,HAMILTON,MT 59840, USA.
NR 34
TC 16
Z9 16
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC 15
PY 1996
VL 226
IS 2
BP 384
EP 392
DI 10.1006/viro.1996.0666
PG 9
WC Virology
SC Virology
GA VZ463
UT WOS:A1996VZ46300026
PM 8955058
ER
PT J
AU Gvakharia, BO
Koonin, EK
Mathews, CK
AF Gvakharia, BO
Koonin, EK
Mathews, CK
TI Vaccinia virus G4L gene encodes a second glutaredoxin
SO VIROLOGY
LA English
DT Article
ID RIBONUCLEOTIDE REDUCTASE; THIOLTRANSFERASE GLUTAREDOXIN; THIOREDOXIN;
PROTEIN; SEQUENCE; ENZYME; ACID
AB Vaccinia virus (VV) was previously shown to encode a functional glutaredoxin, the product of the o21 gene, which is synthesized late in infection, after the onset of DNA replication. Here we report that an open reading frame in the VV genome designated as g41 encodes a protein that has sequence similarity to glutaredoxins and possesses thioltransferase and dehydroascorbate reductase activities. G4L protein in infected cells can be detected as early as 4 hr after infection and is constitutively expressed up to 24 hr postinfection. A protein homologous to G4L and retaining the predicted glutaredoxin active center is encoded by the recently sequenced Molluscum Contagiosum virus (MCV), whereas O2L protein is not conserved, suggesting that the glutaredoxin activity of G4L may be involved in replication of ail poxviruses. (C) 1996 Academic Press, Inc.
C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894.
RP Gvakharia, BO (reprint author), OREGON STATE UNIV,DEPT BIOCHEM & BIOPHYS,2011 AGR & LIFE SCI BLDG,CORVALLIS,OR 97331, USA.
FU NIGMS NIH HHS [GM 37508]
NR 25
TC 23
Z9 24
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0042-6822
J9 VIROLOGY
JI Virology
PD DEC 15
PY 1996
VL 226
IS 2
BP 408
EP 411
DI 10.1006/viro.1996.0669
PG 4
WC Virology
SC Virology
GA VZ463
UT WOS:A1996VZ46300029
PM 8955061
ER
PT J
AU Auvinen, A
AF Auvinen, A
TI Long cancer risk from indoor radon
SO LANCET
LA English
DT Letter
RP Auvinen, A (reprint author), NCI,RADIAT EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA.
OI Auvinen, Anssi/0000-0003-1125-4818
NR 2
TC 1
Z9 1
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 DEC 14
PY 1996
VL 348
IS 9042
BP 1662
EP 1663
DI 10.1016/S0140-6736(05)65732-7
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA VX876
UT WOS:A1996VX87600058
PM 8962013
ER
PT J
AU Bozzi, F
Bertuzzi, S
Strina, D
Giannetto, C
Vezzoni, P
Villa, A
AF Bozzi, F
Bertuzzi, S
Strina, D
Giannetto, C
Vezzoni, P
Villa, A
TI The exon-intron structure of human LHX1 gene
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID PROTEINS; MOTIF; HOMEODOMAIN; ELEGANS; DOMAIN
AB We have determined the genomic structure of the human LHX1 gene, a member of the LIM/homeobox (Lhx) gene family. The transcript is assembled from five exons, which are separated by introns ranging in size from 93 nt to 2.3 kb. The two LIM domains are entirely contained in the first and second exons, respectively, while the homeodomain is split into exons three and four. This structure closely parallels the organization of other mouse and human Lhx genes whose genomic Structure is known. An exception is the mouse and human isl1 genes, whose homeodomain does not contain introns. An intron at the same position also occurs in the Xlim1 gene as well as in other homeobox genes, such as evx1 and evx2, suggesting that this intron insertion represents an ancestral event, from which homeobox genes of different families originated. In this context, evolution of the Lhx gene family probably involved the shuffling of this intron-containing homeobox in the proximity of a LIM-only gene, while Islet genes were formed either by the shuffling of an intronless homeobox to the same LIM domain or, alternatively, by intron loss during their evolution. (C) 1996 Academic Press. Inc.
C1 NIHHD,NIH,LAB MAMMALIAN GENES & DEV,BETHESDA,MD 20892.
RP Bozzi, F (reprint author), CNR,IST TECNOL BIOMED AVANZATE,VIA AMPERE 56,I-20131 MILAN,ITALY.
OI Villa, Anna/0000-0003-4428-9013
NR 12
TC 8
Z9 8
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 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD DEC 13
PY 1996
VL 229
IS 2
BP 494
EP 497
DI 10.1006/bbrc.1996.1832
PG 4
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA VZ799
UT WOS:A1996VZ79900022
PM 8954926
ER
PT J
AU Mitton, KP
Kamiya, T
Tumminia, SJ
Russell, P
AF Mitton, KP
Kamiya, T
Tumminia, SJ
Russell, P
TI Cysteine protease activated by expression of HIV-1 protease in
transgenic mice - MIP26 (aquaporin-0) cleavage and cataract formation in
vivo and ex vivo
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CELL CHANNEL PROTEIN; LENS MEMBRANE; CALMODULIN; SEQUENCE; PERMEABILITY;
LIPOSOMES; COMPLEX; FAMILY; AIDS
AB Transgenic mice, homozygous for HIV-1 protease expression in the eye lens, display degradation of some lens crystallins and cytoskeletal proteins prior to cataract formation on postnatal days 23-25, Alterations to the internal lens hydration state also occur; therefore, the status of the aquaporin protein MIP26 was examined over postnatal days 16-25 to determine if it was altered during cataractogenesis. The MTP was identical in transgenic and control lenses until day 21. By postnatal day 25 (frank cataract), in the lenses obtained from transgenic animals, the 26-kDa band was absent and there was a concurrent increase in the proportion of MIP23, Immunoblotting demonstrated cleavage at the C terminus, Lenses were also maintained in an organ culture system to demonstrate that the cataractogenic process is inherent to the isolated lens and to determine the contribution of cysteine protease action, Organ culture experiments revealed a similar progression to nuclear cataract formation as seen in vivo. Two-dimensional gel analysis of the soluble lens crystallin fraction of organ cultured lenses revealed the same cleavage pattern as occurs in vivo, Organ culture of transgenic lenses with E64, a cysteine protease inhibitor, dramatically delayed cataractogenesis and prevented proteolytic cleavage of both MIP26 and crystallins, HIV-1 protease, while the trigger of cataract formation, does not appear to be the protease responsible for cleavage of MIP or lens crystallins. These results suggest that activation of endogenous cysteine protease activity is involved in the cleavage of these proteins and occurs downstream of HIV-1 protease action.
C1 KYOWA HAKKO KOGYO CO LTD,TOKYO 194,JAPAN.
RP Mitton, KP (reprint author), NEI,LAB MECHANISM OCULAR DIS,NIH,BLDG 6,RM 228,BETHESDA,MD 20892, USA.
NR 35
TC 13
Z9 13
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 DEC 13
PY 1996
VL 271
IS 50
BP 31803
EP 31806
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VY340
UT WOS:A1996VY34000011
PM 8943220
ER
PT J
AU Kosugi, S
Mori, T
Shenker, A
AF Kosugi, S
Mori, T
Shenker, A
TI The role of Asp(578) in maintaining the inactive conformation of the
human lutropin/choriogonadotropin receptor
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LUTEINIZING-HORMONE RECEPTOR; LIMITED PRECOCIOUS PUBERTY;
PROTEIN-COUPLED RECEPTOR; ACTIVATING POINT MUTATION; 2ND TRANSMEMBRANE
DOMAIN; CHORIOGONADOTROPIN RECEPTOR; CONSTITUTIVE ACTIVATION;
SIGNAL-TRANSDUCTION; BINDING; GENE
AB A constitutively activating mutation encoding Asp(578)-->Gly in transmembrane helix 6 of the lutropin/choriogonadotropin receptor (LHR) is the most common cause of gonadotropin-independent, male-limited precocious puberty. This mutant LHR produces a 4.5-fold increase in basal cAMP when expressed in COS-7 cells. To better understand the normal role of Asp(578) in the LHR we studied the effect of seven other amino acid substitutions at this position. No agonist binding or response was detected with the Asp(578)-->Pro mutant. Agonist binding affinity was unaffected by the other substitutions and estimated receptor concentrations ranged from 11 to 184% of wild type. Substitution of Asp(578) with Asn, a similarly sized, uncharged residue, did not produce agonist-independent activation. In contrast, replacement with Glu, Ser, or Leu caused 4.9-5.6-fold stimulation of basal cAMP. Substitution with Tyr (8.5-fold) or Phe (7.5-fold) had a greater activating effect. Only the Tyr, Phe, and Leu mutants showed constitutive activation of the inositol phosphate pathway. Our data suggest that it is the ability of the Asp(578) side chain to serve as a properly positioned hydrogen bond acceptor, rather than its negative charge, that is important for stabilizing the inactive state of the LHR. A bulky aromatic side chain at position 578 may further destabilize the inactive receptor conformation.
C1 KYOTO UNIV HOSP,SCH MED,DEPT LAB MED,SAKYO KU,KYOTO 60601,JAPAN.
NIDDK,METAB DIS BRANCH,NIH,BETHESDA,MD 20892.
CHILDRENS MEM HOSP,CHICAGO,IL 60614.
NORTHWESTERN UNIV,SCH MED,DEPT PEDIAT,DIV ENDOCRINOL,CHICAGO,IL 60614.
NR 34
TC 75
Z9 75
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 DEC 13
PY 1996
VL 271
IS 50
BP 31813
EP 31817
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VY340
UT WOS:A1996VY34000013
PM 8943222
ER
PT J
AU Wartmann, M
Cella, N
Hofer, P
Groner, B
Liu, XW
Hennighausen, L
Hynes, NE
AF Wartmann, M
Cella, N
Hofer, P
Groner, B
Liu, XW
Hennighausen, L
Hynes, NE
TI Lactogenic hormone activation of Stat5 and transcription of the
beta-casein gene in mammary epithelial cells is independent of p42 ERK2
mitogen-activated protein kinase activity
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; DNA-BINDING; MAP KINASE; SERINE PHOSPHORYLATION;
DEPENDENT ACTIVATION; PROLACTIN RECEPTOR; NUCLEAR FACTOR; FACTOR APRF;
EXPRESSION; TYROSINE
AB HC11 mammary epithelial cells have been used to characterize molecular events involved in the regulation of milk protein gene expression, Treatment of HC11 cells with the lactogenic hormones prolactin, insulin, and glucocorticoids results in transcription of the beta-casein gene, Prolactin induces a signaling event which involves tyrosine phosphorylation of the mammary gland factor, Stat5, a member of the family of signal transducers and activators of transcription (Stat). Here we show that HC11 cells express two Stat5 proteins, Stat5a and Stat5b. Phosphopeptide and phosphoamino acid analysis of Stat5a and Stat5b immunoprecipitated from phosphate-labeled HC11 cells revealed that both proteins were constitutively phosphorylated on serine, Lactogenic hormone treatment resulted in the appearance of a tyrosine-phosphorylated peptide in both Stat5 proteins, Consistent with this observation, a Western blot analysis of Stat5a and Stat5b showed that lactogenic hormones induced a rapid, transient increase in phosphotyrosine which paralleled the binding of Stat5 to its cognate recognition sequence in the beta-casein gene promoter, Lactogenic hormone treatment of the HC11 cells also led to a rapid activation of the mitogen activated protein (MAP) kinase pathway, We examined the role of this pathway in beta-casein transcription using a specific MAP kinase kinase inhibitor, PD98059, Concentrations of PD98059 which completely abrogated lactogen-induced MAP kinase activation did not affect the phosphorylation state of Stat5, its DNA binding activity, or transcriptional activation of a beta-casein reporter construct, This indicates that the MAP kinase pathway does not contribute to lactogenic hormone induction of the beta-casein gene.
C1 FRIEDRICH MIESCHER INST,CH-4002 BASEL,SWITZERLAND.
INST EXPT CANC RES,TUMOR BIOL CTR,D-79106 FREIBURG,GERMANY.
NIDDK,BIOCHEM & METAB LAB,NIH,BETHESDA,MD 20892.
RI Cella, Nathalie/A-3542-2012
OI Cella, Nathalie/0000-0001-6060-1076
NR 55
TC 99
Z9 99
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 DEC 13
PY 1996
VL 271
IS 50
BP 31863
EP 31868
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VY340
UT WOS:A1996VY34000020
PM 8943229
ER
PT J
AU Fuhrer, C
Hall, ZW
AF Fuhrer, C
Hall, ZW
TI Functional interaction of Src family kinases with the acetylcholine
receptor in C2 myotubes
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-TYROSINE KINASES; TORPEDO ELECTRIC ORGAN; SIGNAL-TRANSDUCTION;
DELTA-SUBUNIT; GROWTH-FACTOR; GENE-PRODUCT; MUSCLE-CELLS;
PHOSPHORYLATION; AGRIN; DYSTROPHIN
AB Tyrosine phosphorylation of the beta subunit of the acetylcholine receptor (AChR) has been postulated to play a role in AChR clustering during development of the neuromuscular junction. me have investigated the mechanism of this phosphorylation in mammalian C2 myotubes and report that the tyrosine kinase Src binds and phosphorylates glutathione S-transferase fusion proteins containing the N-terminal half of the cytoplasmic loop of the beta subunit. No binding occurs to the related kinases Fyn or Yes or to the corresponding regions from the gamma and delta subunits. Furthermore, AChRs affinity-isolated from C2 myotubes using alpha-bungarotoxin-Sepharose mere specifically associated with Src and Fyn and had tyrosine-phosphorylated beta subunits. We suggest that AChRs are initially phosphorylated by Src and subsequently bind Fyn in a phosphotyrosine-dependent manner. These interactions are likely to play an important role in construction of the specialized postsynaptic membrane during synaptogenesis.
C1 UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143.
NIMH,SECT SYNAPT MECHANISMS,CELL BIOL LAB,BETHESDA,MD 20892.
NR 55
TC 74
Z9 74
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 DEC 13
PY 1996
VL 271
IS 50
BP 32474
EP 32481
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VY340
UT WOS:A1996VY34000105
PM 8943314
ER
PT J
AU Radko, SP
Chrambach, A
AF Radko, SP
Chrambach, A
TI Electrophoresis in polymer solutions: Mechanisms of molecular sieving
SO JOURNAL OF PHYSICAL CHEMISTRY
LA English
DT Article
ID CONVEX FERGUSON PLOTS; GEL-ELECTROPHORESIS; UNCROSSLINKED
POLYACRYLAMIDE; DNA; MACROMOLECULES; SCATTERING; MOBILITY; MODEL
AB Passsage of rigid, ''spherical'' proteins in the range of 2-5 nm radius, R (40-500 kDa molecular weight), through semidilute solutions of a representative polymer, polyethylene glycol in the molecular weight range of (0.6-8) x 10(6), gives rise to a size dependent retardation (''molecular sieving'') analogous to that in a porous network composed of random planes. The average distance between those planes being equal to the screening length, xi, the retardation can be described by log(mu/mu(0)) = -(ARc(0.75)) where A is a constant dependent on solvent and type of monomer and c is the polymer concentration.
C1 NICHHD,THEORET & PHYS BIOL LAB,MACROMOL ANAL SECT,NIH,BETHESDA,MD 20892.
NR 25
TC 18
Z9 18
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-3654
J9 J PHYS CHEM-US
JI J. Phys. Chem.
PD DEC 12
PY 1996
VL 100
IS 50
BP 19461
EP 19465
DI 10.1021/jp9612339
PG 5
WC Chemistry, Physical
SC Chemistry
GA VX875
UT WOS:A1996VX87500040
ER
PT J
AU Fauci, AS
AF Fauci, AS
TI Host factors and the pathogenesis of HIV-induced disease
SO NATURE
LA English
DT Review
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; TYPE-1
INFECTION; IMMUNE-RESPONSE; FACTOR-ALPHA; PERIPHERAL-BLOOD; HOMOSEXUAL
MEN; CELL-LINE; IN-VIVO
AB The level of human immunodeficiency virus (HIV) replication in patients reflects a balance between stimulatory and inhibitory host factors (particularly endogenous cytokines). New information concerning the cellular co-receptors for HIV and the cellular tropism of different strains of virus will advance our understanding of HIV-induced pathogenesis and suggests new therapeutic and preventive strategies.
RP Fauci, AS (reprint author), NIAID,NIH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 113
TC 692
Z9 707
U1 0
U2 19
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF
SN 0028-0836
J9 NATURE
JI Nature
PD DEC 12
PY 1996
VL 384
IS 6609
BP 529
EP 534
DI 10.1038/384529a0
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VX769
UT WOS:A1996VX76900048
PM 8955267
ER
PT J
AU Flake, AW
Roncarolo, MG
Puck, JM
AlmeidaPorada, G
Evans, MI
Johnson, MP
Abella, EM
Harrison, DD
Zanjani, ED
AF Flake, AW
Roncarolo, MG
Puck, JM
AlmeidaPorada, G
Evans, MI
Johnson, MP
Abella, EM
Harrison, DD
Zanjani, ED
TI Treatment of X-linked severe combined immunodeficiency by in utero
transplantation of paternal bone marrow
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HEMATOPOIETIC STEM-CELLS; CHROMOSOME INACTIVATION; INUTERO
TRANSPLANTATION; CD34(+) CELLS; LYMPHOCYTES-T; SHEEP; ENGRAFTMENT;
CARRIERS; ONTOGENY; LINKAGE
C1 WAYNE STATE UNIV,DEPT PEDIAT SURG,DETROIT,MI.
WAYNE STATE UNIV,DEPT OBSTET & GYNECOL,CTR MOL MED & GENET,DETROIT,MI.
WAYNE STATE UNIV,DEPT PEDIAT,DETROIT,MI 48202.
DNAX RES INST MOL & CELLULAR BIOL INC,DEPT HUMAN IMMUNOL,PALO ALTO,CA 94304.
NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892.
UNIV NEVADA,VET AFFAIRS MED CTR,DEPT MED,RENO,NV 89557.
OI RONCAROLO, Maria Grazia/0000-0002-2193-9186
FU NHLBI NIH HHS [HL 52954, HL48378, HL49042-04]; Telethon [TGT06S01]
NR 42
TC 221
Z9 228
U1 0
U2 3
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 DEC 12
PY 1996
VL 335
IS 24
BP 1806
EP 1810
DI 10.1056/NEJM199612123352404
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA VW683
UT WOS:A1996VW68300004
PM 8943162
ER
PT J
AU Lockshin, MD
AF Lockshin, MD
TI Venous thromboembolism during pregnancy
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
RP Lockshin, MD (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD DEC 12
PY 1996
VL 335
IS 24
BP 1847
EP 1847
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA VW683
UT WOS:A1996VW68300026
PM 8965900
ER
PT J
AU Praseuth, D
Grigoriev, M
Guieysse, AL
Pritchard, LL
HarelBellan, A
Nielsen, PE
Helene, C
AF Praseuth, D
Grigoriev, M
Guieysse, AL
Pritchard, LL
HarelBellan, A
Nielsen, PE
Helene, C
TI Peptide nucleic acids directed to the promoter of the alpha-chain of the
interleukin-2 receptor
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
LA English
DT Article
DE peptide nucleic acid; interleukin 2 receptor; triple-helix; anti-gene
strategy; strand invasion; transcription regulation
ID THYMINE-SUBSTITUTED POLYAMIDE; STRAND-DISPLACEMENT; GENE-EXPRESSION;
DUPLEX DNA; PNA; SEQUENCE; BINDING; INHIBITION; ACTIVATION; BACKBONE
AB Two 10-mer oligopyrimidine peptide nucleic acids (PNAs) were designed to interfere with IL-2R alpha. promoter expression by binding to the regulatory sequences overlapping SRF and NF-kappa B transcription factor sites. Specific complexes were formed on each target sequence, and clearly involved(1) Hoogsteen hydrogen bonds as shown by experiments in which the purine strand of a single or double-stranded target was substituted with 7-deazadeoxyguanosine, (2) P-loop formation on double-helical DNA as evidenced by susceptibility to a single-strand-specific nuclease, When formed on a single-stranded DNA target, these highly stable complexes were responsible for efficient physical blockage of T7 DNA polymerase elongation on the template DNA containing the target oligopurine sequence, On a double-stranded target, these complexes only formed at low ionic strength and were slowly dissociated at physiological ionic strength (pH 6.5) with a t(1/2) of 6.5-7 h. The salt-dependent instability of preformed complexes on a plasmid target was probably the critical factor responsible for their lack of significant sequence-specific effect on IL-2R alpha promoter activity inside living cells.
C1 INST GUSTAVE ROUSSY, LAB BIOL TUMEURS HUMAINES, CNRS URA 1156, F-94805 VILLEJUIF, FRANCE.
NIKDD, GENET & BIOCHEM BRANCH, NIH, BETHESDA, MD 20892 USA.
INSERM U267 IMMUNOGENET ALLOGREFFES, F-94807 VILLEJUIF, FRANCE.
UNIV COPENHAGEN, PANUM INST, DEPT MED BIOCHEM & GENET, CTR BIOMOL RECOGNIT, DK-2200 COPENHAGEN N, DENMARK.
RP Praseuth, D (reprint author), MUSEUM NATL HIST NAT, BIOPHYS LAB, INSERM U201, CNRS URA 481, 43 RUE CUVIER, F-75231 PARIS 05, FRANCE.
RI Harel-Bellan, Annick/M-9795-2015;
OI Harel-Bellan, Annick/0000-0002-2339-153X
NR 29
TC 27
Z9 29
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-4781
J9 BBA-GENE STRUCT EXPR
JI Biochim. Biophys. Acta-Gene Struct. Expression
PD DEC 11
PY 1996
VL 1309
IS 3
BP 226
EP 238
DI 10.1016/S0167-4781(96)00146-7
PG 13
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA VX952
UT WOS:A1996VX95200012
PM 8982260
ER
PT J
AU Kafadar, K
Prorok, PC
AF Kafadar, K
Prorok, PC
TI Computer simulation of randomized cancer screening trials to compare
methods of estimating lead time and benefit time
SO COMPUTATIONAL STATISTICS & DATA ANALYSIS
LA English
DT Article
DE bivariate gamma density; catch-up point; disease progression model;
incidence rate; test sensitivity; sojourn time; survival time
ID DEPENDENT STOCHASTIC-MODEL; DISEASE STATE; LENGTH BIAS; LUNG
AB Screening studies provide information on lead time of the screening test (time by which diagnosis is advanced) and benefit (defined either as a reduction in overall mortality, or as the time by which survival has been extended by virtue of the screen), particularly when these studies are randomized trials. Several methods have been proposed to estimate average lead rime and average benefit time for the population which is offered screening. When applied to data from actual screening trials, the performance of these methods is uncertain, since the true averages are unknown. A simulated randomized screening trial offers flexibility in choosing the parameters of an actual trial, including distributions of preclinical and clinical disease, test sensitivity, actual benefit time, and correlation between any two of these parameters. By adjusting these parameters, we gain information on their joint effects on proposed estimators. This paper demonstrates this method of evaluation for estimators of average lead time and average benefit time and proposes avenues for generalizing these types of investigations.
C1 UNIV COLORADO,DEPT MATH,DENVER,CO 80217.
NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892.
NR 30
TC 9
Z9 9
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-9473
J9 COMPUT STAT DATA AN
JI Comput. Stat. Data Anal.
PD DEC 11
PY 1996
VL 23
IS 2
BP 263
EP 291
DI 10.1016/S0167-9473(96)00029-1
PG 29
WC Computer Science, Interdisciplinary Applications; Statistics &
Probability
SC Computer Science; Mathematics
GA VZ700
UT WOS:A1996VZ70000006
ER
PT J
AU Nonnenmacher, B
Kjaer, SK
Svare, EI
Scott, JD
Hubbert, NL
vandenBrule, AJC
Kirnbauer, R
Walboomers, JMM
Lowy, DR
Schiller, JT
AF Nonnenmacher, B
Kjaer, SK
Svare, EI
Scott, JD
Hubbert, NL
vandenBrule, AJC
Kirnbauer, R
Walboomers, JMM
Lowy, DR
Schiller, JT
TI Seroreactivity to HPV16 virus-like particles as a marker for cervical
cancer risk in high-risk populations
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID HUMAN PAPILLOMAVIRUS TYPE-16; POLYMERASE CHAIN-REACTION; HERPES-SIMPLEX
VIRUS; GREENLAND; DENMARK; SCRAPES; ANTIBODIES; GENOTYPES; INFECTION;
NEOPLASIA
AB Sexually transmitted genital human papillomavirus (HPV) infection, most often HPV 16, is considered the major etiologic determinant of cervical cancer. However, some studies have found relatively low prevalences of genital tract HPV DNA in some geographical areas, such as Greenland, that have high rates of cervical cancer. We sought to evaluate HPV 16 infection in high-risk cohorts using a serologic assay that assesses prior exposure as well as current infection and to compare the results with those obtained using a sensitive PCR-based HPV DNA assay. An ELISA based on HPV 16 virus-like particles was used to detect IgG serum antibodies in women attending sexually transmitted disease (STD) clinics in Nuuk, Greenland and Copenhagen, Denmark. Using a preassigned cut-off, 56% of Greenlandic and 41% of Danish women were seropositive (p=0.02). In Greenlandic women, there was a non-significant increase in seropositivity with age, and odds ratios for seropositivity were similar far women with more than 5 lifetime sex partners. Seropositivity in the Danish women, however, increased linearly with increases in these 2 factors, which are likely correlates of lifetime exposure to genital HPVs. In contrast, any genital HPV DNA (HPV16 specifically) was detected in 24% and 36% of Greenlandic and Danish women, respectively and was most frequently detected in women below 20. The finding that HPV DNA prevalences, unlike seroprevalences, tended to decrease with increased lifetime risk of infection, provides an explanation for the lack of correlation between HPV DNA prevalences and cervical cancer risk in previous studies of high-risk populations. (C) 1996 Wiley-Liss, Inc.
C1 NIH,CELLULAR ONCOL LAB,BETHESDA,MD 20892.
DANISH CANC SOC,DIV CANC EPIDEMIOL,COPENHAGEN,DENMARK.
FREE UNIV AMSTERDAM HOSP,DEPT PATHOL,AMSTERDAM,NETHERLANDS.
NR 21
TC 33
Z9 34
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 11
PY 1996
VL 68
IS 6
BP 704
EP 709
DI 10.1002/(SICI)1097-0215(19961211)68:6<704::AID-IJC3>3.0.CO;2-7
PG 6
WC Oncology
SC Oncology
GA WB320
UT WOS:A1996WB32000003
PM 8980170
ER
PT J
AU Biggar, RJ
Rosenberg, PS
Cote, T
AF Biggar, RJ
Rosenberg, PS
Cote, T
TI Kaposi's sarcoma and non-Hodgkin's lymphoma following the diagnosis of
aids
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HOMOSEXUAL MEN; DNA-SEQUENCES; RISK;
CANCER; INFECTION
AB We linked records of 83,434 AIDS cases reported to AIDS registries through 1990 to cancer registry records during times when overlap in registration existed. Of 8,496 Kaposi's-sarcoma (KS) cases meeting enrollment criteria, 1,045 occurred semesters 2 through 4 (6 through 23 months) after another AIDS-defining illness. KS risk in this period after AIDS declined steadily over the 1980s. Adjusting for age, gender, ethnic origin and calendar time period, we found the relative risk (RR) of KS to be 106,000 for homo/bisexual men with AIDS and 13,000 for other men with AIDS, Risk was highest for homo/bisexual men between 30 and 39 years old and among 20- to 29-year-old non-homo/bisexual men. The RR in black men was approximately half that reported in white men among home-bisexual men and others. Between the second and fourth semester after AIDS, the ratio of RR of KS to that of non-AIDS-related cancers increased 1.5-fold. In a similar analysis, there were 335 non-Hodgkin's lymphoma (NHL) cases in semesters 2 through 4 after AIDS. The overall risk was elevated 283-fold in homo/bisexual men and the RR ratio increased 1.8-fold between semester 2 and 4 after AIDS. In summary, the risk of KS following another AIDS-defining illness is strikingly high, more in white men than in black men, and the risks of KS and, especially, NHL appear to increase with time from AIDS. (C) 1996 Wiley-Liss, Inc.
C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892.
NCI,BIOSTAT BRANCH,BETHESDA,MD 20892.
NR 18
TC 80
Z9 81
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 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 11
PY 1996
VL 68
IS 6
BP 754
EP 758
PG 5
WC Oncology
SC Oncology
GA WB320
UT WOS:A1996WB32000012
PM 8980179
ER
PT J
AU Nelson, KB
AF Nelson, KB
TI Magnesium sulfate and risk of cerebral palsy in very low-birth-weight
infants
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID PREVENTION; BRAIN
RP Nelson, KB (reprint author), NIH,NEUROEPIDEMIOL BRANCH,7550 WISCONSIN AVE,ROOM 714 FB,BETHESDA,MD 20892, USA.
NR 17
TC 14
Z9 15
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD DEC 11
PY 1996
VL 276
IS 22
BP 1843
EP 1844
DI 10.1001/jama.276.22.1843
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA VV997
UT WOS:A1996VV99700037
PM 8946908
ER
PT J
AU Wang, YX
Freedberg, DI
Wingfield, PT
Stahl, SJ
Kaufman, JD
Kiso, Y
Bhat, TN
Erickson, JW
Torchia, DA
AF Wang, YX
Freedberg, DI
Wingfield, PT
Stahl, SJ
Kaufman, JD
Kiso, Y
Bhat, TN
Erickson, JW
Torchia, DA
TI Bound water molecules at the interface between the HIV-1 protease and a
potent inhibitor, KNI-272, determined by NMR
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID SPECTROSCOPY; HYDRATION
AB KNI-272 is a peptidomimetic transition state analog inhibitor, having very high specificity and binding affinity for the HIV-1 protease. In order to understand the interactions that enhance drug binding to the protease, we recorded 2D water/NOESY and water/ROESY spectra to identify water molecules that bind tightly to the protease/KNI-272 complex. Well-ordered water molecules are observed at the protease/inhibitor interface in the crystal structure of the complex that have short interproton distances to the Ile50/150, Ala28/128, and Asp29/129 amide protons. The cross peaks between these protein protons and water protons, observed in water/NOESY and water/ROESY spectra, provide strong evidence that these water molecules are present in the solution structure of the complex. Analysis of measured NOE and ROE cross relaxation rates indicates that, in solution, these water molecules have long residence times, at least 1 ns and possibly greater than 7 ns. The presence of long-lived hydration water molecules at the protein/inhibitor interface suggests that interactions involving these water molecules contribute to the potency of the inhibitor. Hence, consideration of the potential role of hydration water molecules in stabilizing protein/inhibitor structures could contribute to improved drug design and to a better understanding of the mechanisms of drug resistance.
C1 NIDR,STRUCT MOL BIOL UNIT,NIH,BETHESDA,MD 20892.
NIAMSD,PROT EXPRESS LAB,BETHESDA,MD 20892.
NCI,FREDERICK CANC RES & DEV CTR,STRUCT BIOCHEM PROGRAM,SAIC FREDERICK,FREDERICK,MD 21702.
KYOTO PHARMACEUT UNIV,YAMASHIMA KU,KYOTO 607,JAPAN.
NR 21
TC 47
Z9 48
U1 1
U2 2
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD DEC 11
PY 1996
VL 118
IS 49
BP 12287
EP 12290
DI 10.1021/ja962612i
PG 4
WC Chemistry, Multidisciplinary
SC Chemistry
GA VX654
UT WOS:A1996VX65400005
ER
PT J
AU Esteban, EN
Sherman, MP
Poiesz, BL
Marshak, RR
Waters, DJ
Ferrer, JF
AF Esteban, EN
Sherman, MP
Poiesz, BL
Marshak, RR
Waters, DJ
Ferrer, JF
TI Transmission of human T cell leukemia virus type I to sheep: Antibody
profile and detection of viral DNA sequences
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID TROPICAL SPASTIC PARAPARESIS; POLYMERASE CHAIN-REACTION; HTLV-I; GENE
AMPLIFICATION; INFECTION; RABBITS; LYMPHOCYTES; RETROVIRUS; MYELOPATHY;
LYMPHOMA
AB Lambs were inoculated intraperitoneally with either 1.8 x 10(7) live peripheral blood cells from an HTLV-I-infected person (five lambs) or with 8 x 10(7) live cells from the HTLV-I-producing cell lines MT-2 (four lambs) or C10 MJ (five lambs), Four control lambs were inoculated with minimal essential medium supplemented with fetal calf serum, The animals were monitored during a period of 24 months, Beginning at 5 to 12 months after inoculation, four of the five lambs inoculated with the fresh HTLV-I-infected peripheral blood cells began to develop detectable levels of antibodies to a recombinant HTLV-I gp21(env) antigen, as determined by an enzyme-linked immunoassay (ELISA). The anti-gp21 antibodies persisted for the remaining observation period, These antibodies were not detected in the sera from the other sheep, Absorption and blocking experiments demonstrated the specificity of the gp21 reactivity, This reactivity was also confirmed by Western blot (WB). With the exception of the serum of an MT-2-inoculated sheep that formed a weak band with p19 by WB, none of the sera of the four gp21-positive sheep or of the other experimental sheep reacted with other structural or regulatory HTLV-I proteins, as determined by ELISA, WB, and radioimmunoassay, PCR analyses demonstrated the presence of the HTLV-I provirus in peripheral blood leukocytes of the four sheep showing antibodies to gp21(env), The remaining sheep were negative, PCR analyses failed to detect BLV sequences in any of the experimental sheep, None of the sheep showed clinical abnormalities during the observation period, The potential value of the sheep model for studying atypical virus-host interactions in infected people is discussed.
C1 UNIV PENN, NEW BOLTON CTR, KENNETT SQ, PA 19348 USA.
SUNY HLTH SCI CTR, DEPT MED, SYRACUSE, NY 13210 USA.
FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA.
FU NHLBI NIH HHS [HB 67021]; NIAID NIH HHS [AI 27658]
NR 47
TC 3
Z9 3
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD DEC 10
PY 1996
VL 12
IS 18
BP 1717
EP 1724
DI 10.1089/aid.1996.12.1717
PG 8
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA VY708
UT WOS:A1996VY70800010
PM 8959249
ER
PT J
AU Shou, M
Gonzalez, FJ
Gelboin, HV
AF Shou, M
Gonzalez, FJ
Gelboin, HV
TI Stereoselective epoxidation and hydration at the K-region of polycyclic
aromatic hydrocarbons by cDNA-expressed cytochromes P450 1A1, 1A2, and
epoxide hydrolase
SO BIOCHEMISTRY
LA English
DT Article
ID PERFORMANCE LIQUID-CHROMATOGRAPHY; CHIRAL STATIONARY PHASES; LIVER
MICROSOMAL-ENZYMES; 5,6-EPOXIDE ENANTIOMERS; DIRECT SEPARATION; DIOL
ENANTIOMERS; VACCINIA VIRUS; ARENE OXIDES; METABOLISM; BENZOPYRENE
AB Stereoselective epoxidation by cytochrome P450s (P450s) and regioselective hydration by epoxide hydrolase determine the carcinogenic potency of some polycyclic aromatic hydrocarbons (PAHs). In this report, cDNA-expressed human and mouse P450s 1A1 and 1A2 and epoxide hydrolase were used to characterize the stereoselective epoxidation and regioselective hydration at the K-region of benz[a]anthracene (BA), 7,12-dimethylbenz[a]anthracene (DMBA), chrysene (CR), benzo[a]pyrene (B[a]P), dibenz[a,h]anthrancene (DB[a,h]A), and benzo[c]phenanthrene (B[c]Ph) by direct chiral stationary-phase HPLC (CSP-HPLC) analyses. Our results indicated that all P450 isoforms preferentially produced major K-region S,R-epoxides of BA (95-98%), DMBA (94-97%), B[a]P (91-96%), DB[a,h]A (94-98%), and B[c]Ph (87-92%), and major R,S-epoxide of CR (74-85%) in the presence of 3,3,3-trichloropropylene 1,2-oxide (TCPO), an inhibitor of epoxide hydrolase, suggesting that P450 enzymes exhibited the high stereoselectivity toward one of two stereoheterotopic faces of K-region double bond of the PAHs. Epoxide hydrolase either expressed from recombinant vaccinia virus or contained in human hepatoma G2 cells (HepG2) hydrated the C-O bond of epoxy-ring at the S-carbon of major metabolically-formed K-region epoxide enantiomers of BA, CR, DMBA, B[a]P, and DB[a,h]A to yield 80-98% dihydrodiols enriched in R,R-form and that at the R-carbon of B[c]Ph epoxide to yield 77-92% dihydrodiol enriched in S,S-form, suggesting that epoxide hydrolase was highly regioselective. The various enantiomeric components of dihydrodiol products in the metabolism of PAHs were apparently due to the combined effect of stereoselectivity of the P450s and regioselectivity of epoxide hydrolase. Our results provide a clear understanding of how these enzymes catalyze overall stereoselective metabolism at the K-region of the PAHs.
RP Shou, M (reprint author), NCI,MOL CARCINOGENESIS LAB,NATL INST HLTH,BLDG 37,ROOM 3E24,BETHESDA,MD 20892, USA.
NR 43
TC 64
Z9 65
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD DEC 10
PY 1996
VL 35
IS 49
BP 15807
EP 15813
DI 10.1021/bi962042z
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VX510
UT WOS:A1996VX51000023
PM 8961944
ER
PT J
AU Eurenius, KP
Chatfield, DC
Brooks, BR
Hodoscek, M
AF Eurenius, KP
Chatfield, DC
Brooks, BR
Hodoscek, M
TI Enzyme mechanisms with hybrid quantum and molecular mechanical
potentials .1. Theoretical considerations
SO INTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY
LA English
DT Article
ID FREE-ENERGY PERTURBATION; HYDROGEN-BONDED SYSTEMS; PROTON TRANSFERS;
AQUEOUS-SOLUTION; DYNAMICS SIMULATIONS; TRANSITION-STATES;
PHOSPHOLIPASE-A2; PHASE; ETHER; WATER
AB The application of hybrid quantum mechanical and molecular mechanical (QM/MM) potentials to the study of chemical reactions in enzymes is outlined. The discussion is general and addresses the difficulties encountered in an enzyme QM/MM study. First, general criteria for determining whether a particular enzyme is an appropriate candidate for a QM/MM approach are outlined. Methods for obtaining starting structures are detailed. The importance of choosing appropriate levels of ab initio or semiempirical theory is emphasized. Approaches for interfacing the QM and MM regions are briefly discussed, with greater detail given to describing our CHARMM-GAMESS interface. Techniques for partitioning the system into QM and MM regions are explored. Link atom placement, as distant from reacting atoms as possible within the confines of computational efficiency, is examined in some detail. Methods for determining reaction paths are also discussed. (C) 1996 John Wiley & Sons, Inc.
C1 NATL INST HLTH,DIV COMP RES & TECHNOL,STRUCT BIOL LAB,BETHESDA,MD 20892.
NATL INST CHEM,LJUBLJANA 61115,SLOVENIA.
NR 48
TC 161
Z9 161
U1 2
U2 10
PU JOHN WILEY & SONS INC
PI NEW YORK
PA 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7608
J9 INT J QUANTUM CHEM
JI Int. J. Quantum Chem.
PD DEC 10
PY 1996
VL 60
IS 6
BP 1189
EP 1200
DI 10.1002/(SICI)1097-461X(1996)60:6<1189::AID-QUA7>3.0.CO;2-W
PG 12
WC Chemistry, Physical; Mathematics, Interdisciplinary Applications;
Physics, Atomic, Molecular & Chemical
SC Chemistry; Mathematics; Physics
GA VU308
UT WOS:A1996VU30800008
ER
PT J
AU Frenking, G
Dapprich, S
Kohler, KF
Koch, W
Collins, JR
AF Frenking, G
Dapprich, S
Kohler, KF
Koch, W
Collins, JR
TI Structure and bonding of the remarkable donor-acceptor complexes XBeO
(X=NH3, NMe(3), CO, N-2, C2H2, C2H4, H-2, H2CO, O-2)
SO MOLECULAR PHYSICS
LA English
DT Article
ID MOLECULAR-ORBITAL METHODS; VALENCE BASIS-SETS; INFRARED-SPECTRA;
THEORETICAL PREDICTIONS; 2ND-ROW ELEMENTS; GROUND-STATE; SOLID ARGON;
CHEMISTRY; HELIUM; BEO
AB Quantum mechanical calculations at the MP4/6-311G(2df,2pd)//MP2/6-31G(d,p) level of theory are reported for the compounds XBeO with X = NH3 NMe(3), CO, N-2, C2H2, C2H4, H-2, H2CO and O-2. The calculations show that BeO is a very strong Lewis acid. The X-BeO bond strength is between D-e = 69.5 kcal mol(-1) for Me(3)NBeO and D-e = 11.2 kcal mol(-1) for pi-bonded N2BeO. The calculated bond strength for the yet unknown donor-acceptor complex Me(3)NBeO is significantly higher than the strongest experimentally known main-group donor-acceptor complex Me(3)NAlCl(3) (D-o = 47.5 kcal mol(-1)). Even the weak donor H-2 is bonded with D-e = 18.5 kcal mol(-1). The compounds O2BeO and its isomer berylliumozonide BeO3 should not be considered as donor-acceptor complexes. The results of the CDA method show that the donor-acceptor interactions in terms of orbital mixing are mainly described by the mixing of occupied orbitals of X with vacant orbitals of BeO, while the mixing of occupied orbitals of BeO with vacant orbitals of X is negligible. The topological analysis of the electronic charge distribution and the NBO partitioning scheme demonstrate that the X-BeO bonds have little or no covalent character; the bonds are caused by electrostatic attraction. The charge concentration at the donor atoms in the stronger bonded compounds is significantly deformed towards the beryllium atom.
C1 TECH UNIV BERLIN, INST ORGAN CHEM, D-10623 BERLIN, GERMANY.
NCI, FREDERICK, MD 21702 USA.
RP UNIV MARBURG, FACHBEREICH CHEM, HANS MEERWEIN STR, D-35032 MARBURG, GERMANY.
NR 43
TC 30
Z9 30
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0026-8976
EI 1362-3028
J9 MOL PHYS
JI Mol. Phys.
PD DEC 10
PY 1996
VL 89
IS 5
BP 1245
EP 1263
PG 19
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA VZ714
UT WOS:A1996VZ71400003
ER
PT J
AU Hill, TL
AF Hill, TL
TI Adsorption from a one-dimensional lattice gas and the
Brunauer-Emmett-Teller equation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Ising model; reference system; Gibbs excess adsorption; Gibbs integral
AB An exact treatment of adsorption from a one-dimensional lattice gas is used to eliminate and correct a well-known inconsistency in the Brunauer-Emmett-Teller (B.E.T.) equation-namely Gibbs excess adsorption is not taken into account and the Gibbs integral diverges at the transition point, However, neither model should be considered realistic for experimental adsorption systems.
RP Hill, TL (reprint author), NIDDKD,MOL BIOL LAB,NIH,BETHESDA,MD 20892, USA.
NR 9
TC 16
Z9 16
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 DEC 10
PY 1996
VL 93
IS 25
BP 14328
EP 14332
DI 10.1073/pnas.93.25.14328
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800027
PM 8962050
ER
PT J
AU Sweitzer, TD
Hanover, JA
AF Sweitzer, TD
Hanover, JA
TI Calmodulin activates nuclear protein import: A link between signal
transduction and nuclear transport
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID PERMEABILIZED MAMMALIAN-CELLS; ENDOPLASMIC-RETICULUM; PORE COMPLEX;
LOCALIZATION SIGNALS; BINDING-PROTEINS; IN-VITRO; CALCIUM;
IDENTIFICATION; SUBSTRATE; INTERACTS
AB In addition to the well-characterized GTP-dependent nuclear transport observed in permeabilized cells. we detected a mode of nuclear transport that was GTP-independent at elevated cytoplasmic calcium concentrations. Nuclear transport under these conditions was blocked by calmodulin inhibitors, Recombinant calmodulin restored ATP-dependent nuclear transport in the absence of cytosol. Calmodulin-dependent transport was inhibited by wheat germ agglutinin consistent with transport proceeding through nuclear pores, We propose that release of intracellular calcium stores upon cell activation inhibits GTP-dependent nuclear transport: the elevated cytosolic calcium then acts through calmodulin to stimulate the novel GTP-independent mode of import.
C1 NIDDKD,CELL BIOCHEM & BIOL LAB,NIH,BETHESDA,MD 20892.
NR 50
TC 69
Z9 69
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 DEC 10
PY 1996
VL 93
IS 25
BP 14574
EP 14579
DI 10.1073/pnas.93.25.14574
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800071
PM 8962094
ER
PT J
AU Iiri, T
Backlund, PS
Jones, TLZ
Wedegaertner, PB
Bourne, HR
AF Iiri, T
Backlund, PS
Jones, TLZ
Wedegaertner, PB
Bourne, HR
TI Reciprocal regulation of G(s alpha) by palmitate and the beta gamma
subunit
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE trimeric G proteins; lipid modification; membrane localization;
protein-protein interaction
ID PROTEIN ALPHA-SUBUNIT; GTP-BINDING PROTEIN; LIPID MODIFICATIONS;
MEMBRANE ATTACHMENT; SF9 CELLS; PALMITOYLATION; MYRISTOYLATION;
ACTIVATION; EXPRESSION; PURIFICATION
AB Hormonal activation of G(s), the stimulatory regulator of adenylyl cyclase, promotes dissociation of alpha(s) from G beta gamma, accelerates removal of covalently attached palmitate from the G alpha subunit, and triggers release of a fraction of alpha(s) from the plasma membrane into the cytosol. To elucidate relations among these three events, we assessed biochemical effects in vitro of attached palmitate on recombinant alpha(s) prepared from Sf9 cells. In comparison to the unpalmitoylated protein (obtained from cytosol of Sf9 cells, treated with a palmitoyl esterase, or expressed as a mutant protein lacking the site for palmitoylation), palmitoylated alpha(s) (from Sf9 membranes, 50% palmitoylated) was more hydrophobic, as indicated by partitioning into TX-114, and bound beta gamma with 5-fold higher affinity. beta gamma protected GDP-bound alpha(s), but not alpha(s) . GTP[gamma S], from depalmitoylation by a recombinant esterase. We conclude that beta gamma binding and palmitoylation reciprocally potentiate each other in promoting membrane attachment of at, and that dissociation of alpha(s) . GTP from beta gamma is likely to mediate receptor-induced alpha(s) depalmitoylation and translocation of the protein to cytosol in intact cells.
C1 UNIV CALIF SAN FRANCISCO,DEPT CELLULAR & MOL PHARMACOL,SAN FRANCISCO,CA 94143.
UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143.
UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,SAN FRANCISCO,CA 94143.
NIMH,LAB GEN & COMPARAT BIOCHEM,BETHESDA,MD 20892.
NIDDKD,METAB DIS BRANCH,NIH,BETHESDA,MD 20892.
THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,DEPT BIOCHEM & MOL PHARMACOL,PHILADELPHIA,PA 19107.
NR 37
TC 89
Z9 90
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 DEC 10
PY 1996
VL 93
IS 25
BP 14592
EP 14597
DI 10.1073/pnas.93.25.14592
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800074
PM 8962097
ER
PT J
AU Gueguen, M
Long, EO
AF Gueguen, M
Long, EO
TI Presentation of a cytosolic antigen by major histocompatibility complex
class II molecules requires a long-lived form of the antigen
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE antigen processing; HLA-DR; N-end rule; protein degradation; ubiquitin
ID NATURALLY PROCESSED PEPTIDES; RESTRICTED T-CELLS; HLA-DR MOLECULES; HEN
EGG LYSOZYME; ENHANCED DEGRADATION; RHEUMATOID-ARTHRITIS; VACCINIA
VIRUS; INFECTED CELLS; LYMPHOCYTES-T; MHC
AB Class I and class II molecules of the major histocompatibility complex present peptides to T cells, Class I molecules bind peptides that hare been generated in the cytosol by proteasomes and delivered into the endoplasmic reticulum by the transporter associated with antigen presentation, In contrast, class II molecules are very efficient in the presentation of antigens that have been internalized and processed in endosomal lysosomal compartments, In addition, class II molecules can present some cytosolic antigens by a TAP-independent pathway. To test whether this endogenous class II presentation pathway was linked to proteasome-mediated degradation of antigen in the cytosol, the N-end rule was utilized to produce two forms of the influenza virus matrix protein with different in vivo half-lives (10 min vs. 5 h) when expressed in human B cells, Whereas class I molecules presented both the short- and the long-lived matrix proteins, class II molecules presented exclusively the long-lived form of antigen, Thus, rapid degradation of matrix protein in the cytosol precluded its presentation by class II molecules, These data suggest that the turnover of long-lived cytosolic proteins, some of which is mediated by delivery into endosomal/lysosomal compartments, provides a mechanism for immune surveillance by CD4(+) T cells.
C1 NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852.
RI Long, Eric/G-5475-2011
OI Long, Eric/0000-0002-7793-3728
NR 47
TC 46
Z9 46
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 10
PY 1996
VL 93
IS 25
BP 14692
EP 14697
DI 10.1073/pnas.93.25.14692
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800093
PM 8962116
ER
PT J
AU Grossman, Z
Singer, A
AF Grossman, Z
Singer, A
TI Tuning of activation thresholds explains flexibility in the selection
and development of T cells in the thymus
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID POSITIVE SELECTION; RECEPTOR LIGAND; DIFFERENTIATION; PROLIFERATION;
SPECIFICITY; THYMOCYTES; LYMPHOCYTE; TOLERANCE; ANERGY; INVIVO
AB Immature CD4(+)CD8(+) thymocytes expressing T-cell antigen receptors (TCR) are selected by TCR-mediated recognition of peptides associated with major histocompatibility complex molecules on thymic stromal cells. Selection ensures reactivity of the mature cells to foreign antigens and tolerance to self Although much has been learned about tbe factors that determine whether a thymocyte with a given specificity will be positively or negatively selected, selection as an aspect of the developmental process as a whole is less well-understood. Here we invoke a model in which thymocytes tune their response characteristics individually and dynamically in the course of development, Cellular development and selection are driven by receptor-mediated metabolic perturbations. Perturbation is a measure of the net intracellular change induced by external stimulation, It results from the integration of several signals and countersignals over time and therefore depends on the environment and the maturation stage of the cell. Individual cell adaptation limits the range of perturbations. Such adaptation renders thymocytes less sensitive to the level of stimulation per se, but responsive to environmental changes in that level, This formulation begins to explain the mechanisms that link developmental and selection events to each other.
C1 NCI,EXPT IMMUNOL BRANCH,BETHESDA,MD 20892.
RP Grossman, Z (reprint author), TEL AVIV UNIV,SACKLER FAC MED,DEPT PHYSIOL & PHARMACOL,IL-69978 TEL AVIV,ISRAEL.
RI Grossman, Zvi/A-9643-2008
NR 26
TC 99
Z9 99
U1 0
U2 3
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD DEC 10
PY 1996
VL 93
IS 25
BP 14747
EP 14752
DI 10.1073/pnas.93.25.14747
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800103
PM 8962126
ER
PT J
AU Lorimer, IAJ
KepplerHafkemeyer, A
Beers, RA
Pegram, CN
Bigner, DD
Pastan, I
AF Lorimer, IAJ
KepplerHafkemeyer, A
Beers, RA
Pegram, CN
Bigner, DD
Pastan, I
TI Recombinant immunotoxins specific for a mutant epidermal growth factor
receptor: Targeting with a single chain antibody variable domain
isolated by phage display
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE EGFRvIII; glioblastoma; cancer therapy; Pseudomonas exotoxin A
ID HUMAN-BRAIN-TUMORS; PSEUDOMONAS EXOTOXIN; MONOCLONAL-ANTIBODY; LUNG
CARCINOMAS; EXPRESSION; FV; GLIOBLASTOMA; PROTEINS; GENE
AB EGFRvIII is a mutant epidermal growth factor receptor found in glioblastoma, and in carcinoma of the breast, ovary, and lung, The mutant receptor has a deletion in its extracellular domain that results in the formation of a new, tumor-specific extracellular sequence, Mice were immunized with a synthetic peptide corresponding to this sequence and purified EGFRvIII, A single chain antibody variable domain (scFv) phage display library of 8 x 10(6) members was made from the spleen of one immunized mouse. A scFv specific for EGFRvIII was isolated from this library by panning with successively decreasing amounts of synthetic peptide, This was used to make an immunotoxin by fusing the scFv DNA sequence to sequences coding for domains II and III of Pseudomonas exotoxin A. Purified immunotoxin had a K-d of 22 nM for peptide and a K-d of 11 nM for cell-surface EGFRvIII. The immunotoxin was very cytotoxic to cells expressing EGFRvIII, with an IC50 of 1 ng/ml (16 pM) on mouse fibroblasts transfected with EGFRvIII and an IC50 of 7-10 ng/ml (110-160 pM) on transfected glioblastoma cells, There was no cytotoxic activity at 1000 ng/ml on the untransfected parent glioblastoma cell line, The immunotoxin was completely stable upon incubation at 37 degrees C for 24 h in human serum, The combination of good affinity, cytotoxicity and stability make this immunotoxin a candidate for further preclinical evaluation.
C1 NCI,DIV BASIC SCI,MOL BIOL LAB,NIH,BETHESDA,MD 20892.
DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710.
NR 30
TC 107
Z9 109
U1 0
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 DEC 10
PY 1996
VL 93
IS 25
BP 14815
EP 14820
DI 10.1073/pnas.93.25.14815
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VY448
UT WOS:A1996VY44800115
PM 8962138
ER
PT J
AU Miller, M
Lubkowski, J
Rao, JKM
Danishefsky, AT
Omichinski, JG
Sakaguchi, K
Sakamoto, H
Appella, E
Gronenborn, AM
Clore, GM
AF Miller, M
Lubkowski, J
Rao, JKM
Danishefsky, AT
Omichinski, JG
Sakaguchi, K
Sakamoto, H
Appella, E
Gronenborn, AM
Clore, GM
TI The oligomerization domain of p53: Crystal structure of the trigonal
form
SO FEBS LETTERS
LA English
DT Article
DE p53; tumor suppressor; tetramerization domain; X-ray crystallography;
NMR; joint refinement
ID PROTEIN-STRUCTURE DETERMINATION; TUMOR-SUPPRESSOR; TRANSCRIPTIONAL
ACTIVATION; TETRAMERIZATION DOMAIN; DIRECT REFINEMENT; DNA-BINDING;
X-RAY; NMR; SEQUENCE; APOPTOSIS
AB The structure of the oligomerization domain of the p53 tumor suppressor protein was determined in the trigonal crystal form, using a refined NMR structure as a model. A synthetic peptide comprising residues 319-360 of human p53 crystallized in the space group P3(1)21. There is one biologically relevant tetrameric domain in the crystallographic asymmetric unit. The structure was refined jointly,vith NMR data, only the third such case (the previous examples being IL-1 beta (Shaanan, B., Gronenborn, A.M., Cohen, G.H., Gilliland, G.L., Veerapandian, B., Davies, D.R. and Clore, G.M. (1992) Science 257, 961-964 [1]) and BPTI (Schiffer, C., Huber, R., Wuthrich, K. and Van Gunsteren, W.F. (1994) J. Mol. Biol. 241, 588-599 [2])), to 2.5 Angstrom resolution with an R factor of 0.207. The distribution of tumor-derived mutations in the oligomerization region together with structural and biological data suggest a strategy for the design of antitumor therapeutics.
C1 UNIV MARYLAND,DEPT MED RES & TECHNOL,BALTIMORE,MD 21201.
NIDDKD,CHEM PHYS LAB,NIH,BETHESDA,MD 20892.
NCI,CELL BIOL LAB,NIH,BETHESDA,MD 20892.
RP Miller, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOL STRUCT LAB,FREDERICK,MD 21702, USA.
RI Clore, G. Marius/A-3511-2008; Sakamoto, Hiroshi/A-3181-2011; Miller,
Maria/I-1636-2013
OI Clore, G. Marius/0000-0003-3809-1027; Miller, Maria/0000-0003-0252-5348
NR 29
TC 30
Z9 30
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD DEC 9
PY 1996
VL 399
IS 1-2
BP 166
EP 170
DI 10.1016/S0014-5793(96)01231-8
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VY759
UT WOS:A1996VY75900037
PM 8980144
ER
PT J
AU Finegold, AA
Shatwell, KP
Segal, AW
Klausner, RD
Dancis, A
AF Finegold, AA
Shatwell, KP
Segal, AW
Klausner, RD
Dancis, A
TI Intramembrane bis-heme motif for transmembrane electron transport
conserved in a yeast iron reductase and the human NADPH oxidase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; SACCHAROMYCES-CEREVISIAE; CYTOCHROME-B;
FERRIC REDUCTASE; GENE; PHAGOCYTES; LOCATION; PROTEIN; SYSTEM
AB A plasma membrane iron reductase, required for cellular iron acquisition by Saccharomyces cerevisiae, and the human phagocytic NADPH oxidase, implicated in cellular defense, contain low potential plasma membrane b cytochromes that share elements of structure and function, Four critical histidine residues in the FRE1 protein of the iron reductase were identified by site-directed mutagenesis, Individual mutation of each histidine to alanine eliminated the entire heme spectrum without affecting expression of the apoprotein, documenting the specificity of the requirement for the histidine residues, These critical residues are predicted to coordinate a bis-heme structure between transmembrane domains of the FRE1 protein. The histidine residues are conserved in the related gp91(phox) protein of the NADPH oxidase of human granulocytes, predicting the sites of heme coordination in that protein complex, Similarly spaced histidine residues have also been implicated in heme binding by organelle b cytochromes with little overall sequence similarity to the plasma membrane b cytochromes. This bis-heme motif may play a role in transmembrane electron transport by distinct families of polytopic b cytochromes.
C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892.
UNIV LONDON UNIV COLL,SCH MED,DEPT MED,LONDON WC1E 6JJ,ENGLAND.
OI Segal, Anthony/0000-0001-7602-9043
FU Wellcome Trust
NR 27
TC 128
Z9 135
U1 0
U2 6
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 DEC 6
PY 1996
VL 271
IS 49
BP 31021
EP 31024
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VW686
UT WOS:A1996VW68600004
PM 8940093
ER
PT J
AU Vito, P
Wolozin, B
Ganjei, JK
Iwasaki, K
Lacana, E
DAdamio, L
AF Vito, P
Wolozin, B
Ganjei, JK
Iwasaki, K
Lacana, E
DAdamio, L
TI Requirement of the familial Alzheimer's disease gene PS2 for apoptosis -
Opposing effect of ALG-3
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID T-CELL HYBRIDOMAS; DNA FRAGMENTATION; CLONAL ELIMINATION; MISSENSE
MUTATIONS; SELF-TOLERANCE; ENTEROTOXIN-B; IN-SITU; DEATH; ACTIVATION;
ANTIGEN
AB ALG-3, a truncated mouse homologue of the chromosome I familial Alzheimer's disease gene PS2, rescues T hybridoma 3DO cells from T-cell receptor-induced apoptosis by inhibiting Fas ligand induction and Fas signaling, Here we show that ALG-3 transfected 3DO cells express a COOH-terminal PS2 polypeptide, Overexpression of PS2 in ALG-3 transfected 3DO cells reconstitutes sensitivity to receptor-induced cell death, suggesting that the artificial PS2 polypeptide functions as a dominant negative mutant of PS2, ALG-3 and antisense PS2 protect PC12 cells from glutamate-induced apoptosis but not from death induced by hydrogen peroxide or the free radical MPP(+). Thus, the PS2 gene is required for some forms of cell death in diverse cell types, and its function is opposed by ALG-3.
C1 NIAID,T CELL MOL BIOL UNIT,CELLULAR & MOL IMMUNOL LAB,NIH,BETHESDA,MD 20892.
NIMH,UNIV ALZHEIMER BIOL,CLIN SCI LAB,BETHESDA,MD 20892.
NR 32
TC 121
Z9 122
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 DEC 6
PY 1996
VL 271
IS 49
BP 31025
EP 31028
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VW686
UT WOS:A1996VW68600005
PM 8940094
ER
PT J
AU Kusk, P
John, S
Fragoso, G
Michelotti, J
Hager, GL
AF Kusk, P
John, S
Fragoso, G
Michelotti, J
Hager, GL
TI Characterization of an NF-1/CTF family member as a functional activator
of the mouse mammary tumor virus long terminal repeat 5' enhancer
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NUCLEAR FACTOR-I; TGGCA-BINDING PROTEIN; TRANSGENIC MICE;
DNA-REPLICATION; GLUCOCORTICOID REGULATION; TRANSCRIPTION FACTOR;
PROVIRAL ACTIVATION; RESPONSIVE ELEMENT; ONCOGENE INT-1; ADENOVIRUS DNA
AB The long terminal repeat of the mouse mammary tumor virus restricts virus expression primarily to the mammary epithelium. The extreme 5' end of the long terminal repeat contains an enhancer that has been associated with tissue-specific expression of the virus. A total of six functional cis-acting elements have been identified in the enhancer. Although proteins binding to these elements have been reported, only one has been identified; this factor, mp5, is identical or closely related to the transcription factor AP-2 (Mellentin-Michelotti, J., John, S., Pennie, W. D., Williams, T., and Hager, G. L. (1994) J. Biol. Chem. 269, 31983-31990). The other factors are hitherto unidentified and poorly described. We report here the characterization of another of the six elements, previously referred to as the F3 site (Mink, S., Hartig, E., Jennewein, P., Doppler, W., and Cato, A. C. (1992) Mol. Cell Biol, 12, 4906-4918), We show that the F3 binding activity and AP-2 act synergistically to enhance mouse mammary tumor virus-directed transcription, but only in the presence of glucocorticoid hormone, The F3 element has an NF-l-like half-site, but the activity recognizing this element has binding characteristics distinct from the NF-1/CTF family as well as the rest of the CCAAT-binding proteins. We conclude that the F3 activity represents a new member of the NF-1/CTF family.
C1 NCI,LAB RECEPTOR BIOL & GENE EXPRESS,BETHESDA,MD 20892.
NR 47
TC 18
Z9 18
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 DEC 6
PY 1996
VL 271
IS 49
BP 31269
EP 31276
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VW686
UT WOS:A1996VW68600042
PM 8940131
ER
PT J
AU Kole, HK
Liotta, AS
Kole, S
Roth, J
MontroseRafizadeh, C
Bernier, M
AF Kole, HK
Liotta, AS
Kole, S
Roth, J
MontroseRafizadeh, C
Bernier, M
TI A synthetic peptide derived from a COOH-terminal domain of the insulin
receptor specifically enhances insulin receptor signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-TYROSINE KINASE; SRC HOMOLOGY-2 DOMAINS; GROWTH-FACTOR RECEPTOR;
HAMSTER OVARY CELLS; BETA-SUBUNIT DOMAIN; FACTOR-I RECEPTORS;
PHOSPHATIDYLINOSITOL 3'-KINASE; C-TERMINUS; SUBSTRATE PHOSPHORYLATION;
AUTOPHOSPHORYLATION SITES
AB The role of the insulin receptor COOH-terminal domain in the regulation of insulin signal transduction was explored with a variety of synthetic peptides, One of the peptides, termed peptide HC, whose structure corresponds to residues 1293-1307 of the insulin proreceptor sequence, enhanced insulin-stimulated autophosphorylation of the insulin receptor in cell-free systems and in semipermeabilized Chinese hamster ovary (CHO) cells that had been transfected with an expression plasmid encoding the human insulin receptor (CHO/HIRc) at concentrations where there was no detectable effect on basal autophosphorylation levels or on receptor de phosphorylation, A lipophilic analogue of peptide HC, stearyl peptide HC, added to intact CHO/HIRc cells enhanced significantly insulin-stimulated insulin receptor autophosphorylation while having no effect on ligand-stimulated receptor phosphorylation in CHO cells overexpressing either the IGF-1 receptor or epidermal growth factor receptor, Addition of stearyl peptide HC to CHO/HIRc cells resulted in a 2.4 +/- 0.3-fold increase in the amount of insulin stimulated phosphatidylinositol 3-kinase detected in anti-IRS-1 immunoprecipitates and a 2.1 +/- 0.6-fold increase in the levels of tyrosine phosphorylation of mitogen-activated protein kinase in response to insulin, Finally, a derivative of peptide HC coupled to a biotin moiety was prepared and showed to bind with the beta-subunit of the wild-type insulin receptor and a truncated receptor that lacks 43 amino acids from its carboxyl terminus, However, there was little binding, if any, of the peptide with the IGF-1 receptors or the epidermal growth factor receptors, Taken together, our data demonstrate that a pentadecapeptide related to the carboxyl terminus of the insulin receptor binds to the insulin receptor beta-subunit and that this interaction may contribute to the increased receptor's intrinsic activity and signal transduction.
C1 NIA,GERONTOL RES CTR,DIABET SECT,LAB CLIN PHYSIOL,NIH,BALTIMORE,MD 21224.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD 21224.
OI Bernier, Michel/0000-0002-5948-368X
NR 52
TC 15
Z9 15
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 DEC 6
PY 1996
VL 271
IS 49
BP 31619
EP 31626
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VW686
UT WOS:A1996VW68600092
PM 8940181
ER
PT J
AU DavisSmyth, T
Duncan, RC
Zheng, T
Michelotti, G
Levens, D
AF DavisSmyth, T
Duncan, RC
Zheng, T
Michelotti, G
Levens, D
TI The far upstream element-binding proteins comprise an ancient family of
single-strand DNA-binding transactivators
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RICH ACTIVATION MOTIF; TRANSCRIPTION FACTOR; RNA-BINDING; C-MYC; FOS
PROTEINS; NUCLEIC-ACID; KH DOMAIN; REPLICATION; EXPRESSION; PROMOTER
AB The cloning and expression of two new human cDNAs encoding proteins highly related to the far upstream element-binding protein (FBP) are described, FBP, FBP2, and FBP3 comprise a family of single-strand DNA-binding proteins that possess all of the general features of more conventional transcription factors. The FBPs each bind sequence specifically to only one strand of the far upstream element (FUSE; originally identified upstream of c-myc), and each possesses potent activation domains when fused to the GAL4 DNA-binding domain and assayed by transient transfection. Typical of transcription factors, the proteins are most highly related in their central, DNA-binding domains, but extensive homology is also shared within the tyrosine-rich, carboxyl-terminal activation domains. Comparison with Gen Bank sequences revealed a fourth FBP family member encoded by Caenorhabditis elegans chromosome III, illustrating the high degree of homology in this evolutionarily ancient and conserved family.
C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892.
RI Levens, David/C-9216-2009; Duncan, Robert/I-8168-2015
OI Levens, David/0000-0002-7616-922X; Duncan, Robert/0000-0001-8409-2501
NR 41
TC 98
Z9 101
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 DEC 6
PY 1996
VL 271
IS 49
BP 31679
EP 31687
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VW686
UT WOS:A1996VW68600100
PM 8940189
ER
PT J
AU Lee, J
Lewin, NE
Acs, P
Blumberg, PM
Marquez, VE
AF Lee, J
Lewin, NE
Acs, P
Blumberg, PM
Marquez, VE
TI Conformationally constrained analogues of diacylglycerol .13. Protein
kinase C ligands based on templates derived from
2,3-dideoxy-L-erythro(threo)-hexono-1,4-lactone and 2-deoxyapiolactone
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID ACTIVATION; SPECIFICITY; RECEPTOR; LACTONES; BINDING; FAMILY
AB In the present investigation, the last two possible modes of generating conformationally semirigid diacylglycerol (DAG) analogues embedded into five-membered ring lactones as templates III and IV are investigated. The first two templates studied in previous investigations corresponded to 2-deoxyribonolactone (template I) and 4,4-disubstituted gamma-butyrolactone (template II), with the latter producing potent protein kinase C (PK-C) ligands with low nanomolar binding affinities. The templates reported in this work correspond to 2,3-dideoxy-L-erythro- or -threo-hexono-1,4-lactone (template III) and 2-deoxyapiolactone (template IV). Compounds constructed with the dideoxy-L-erythro- or -threo-hexono-1,4-lactone template were synthesized stereospecifically from tri-O-acetyl-L-glucal and L-galactono-1,4-lactone, respectively. Compounds constructed with the 2-deoxyapiolactone template were synthesized stereoselectively from di-O-isopropylidene-alpha-D-apiose. Inhibition of the binding of [H-3]phorbol-12,13-dibutyrate to PK-C alpha showed that only the threo-isomer, 5-O-tetradecanoyl-2,3-dideoxy-L-threo-hexono-1,4-lactone (2) was a good PK-C ligand (K-i = 1 mu M). The rest of the ligands had poorer affinities with K-i values between 10 and 28 mu M. With these results, the order of importance of five-membered ring lactones as competent templates for the construction of semirigid DAG surrogates with effective PK-C binding affinity can be established as II much greater than I similar to III > IV.
C1 NIH,NATL CANC INST,MED CHEM LAB,DIV BASIC SCI,BETHESDA,MD 20892.
NIH,NATL CANC INST,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,DIV BASIC SCI,BETHESDA,MD 20892.
NR 23
TC 11
Z9 11
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD DEC 6
PY 1996
VL 39
IS 25
BP 4912
EP 4919
DI 10.1021/jm960525v
PG 8
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA VX863
UT WOS:A1996VX86300007
PM 8960550
ER
PT J
AU Houlihan, WJ
Boja, JW
Parrino, VA
Kopajtic, TA
Kuhar, MJ
AF Houlihan, WJ
Boja, JW
Parrino, VA
Kopajtic, TA
Kuhar, MJ
TI Halogenated mazindol analogs as potential inhibitors of the cocaine
binding site at the dopamine transporter
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID NONHUMAN-PRIMATES; GROWTH-HORMONE; RHESUS-MONKEYS; RAT-BRAIN; ABUSE;
AMPHETAMINE; SEROTONIN; POTENCIES; STRIATUM; BEHAVIOR
AB A series of halogenated (F, Cl, Br, I), pyrimido and diazepino homologs of mazindol were prepared and evaluated for their ability to displace [H-3]WIN 35,428 binding and to inhibit uptake of [H-3]dopamine (DA) in rat striatal tissue. All of the compounds except for the 2'-chloro (6) and 2'-bromo (16) analogs of mazindol displaced [H-3]WIN 35,428 binding and inhibited [H-3]DA uptake more effectively than (R)-cocaine. Structure-activity studies indicated that best inhibition of [H-3]WIN 35,428 binding occurred in the imidazo series with compounds containing one or two Cl or Br atoms in the 3'- or 4'-position of the free phenyl group. Replacement of the imidazo ring by a pyrimido or diazepino ring enhanced binding inhibition. The most potent inhibitors of [H-3]WIN 35,428 binding and [H-3]DA uptake were 6-(3'-chlorophenyl)-2,3,4,6-tetrahydropyrimido[2,1-a]isoindol-6-ol (23; IC50 1.0 nM; 8x mazindol) and 7-(3',4'-dichlorophenyl)-2,3,4,5-tetrahydro-7H-diazepino[2,1-a]isoindol-7-ol (28; IC50 0.26 nM; 32x mazindol), respectively. No significant differences was found between binding and uptake inhibition. Mazindol and the pyrimido and diazepino homologs 24 and 27 showed a selectivity for the DA uptake over the serotonin (5-HT) uptake site of 5-, 250-, and 465-fold, respectively, and displayed weak or no affinity for a variety of neurotransmitter receptor sites.
C1 SANDOZ INC,RES INST,E HANOVER,NJ 07936.
NIDA,ADDICT RES CTR,BALTIMORE,MD 21224.
RP Houlihan, WJ (reprint author), DREW UNIV,CHARLES A DANA RES INST,HALL SCI,ROOM 331,MADISON,NJ 07940, USA.
FU NIDA NIH HHS [5RO3DA 08516-02]
NR 76
TC 26
Z9 26
U1 4
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD DEC 6
PY 1996
VL 39
IS 25
BP 4935
EP 4941
DI 10.1021/jm960288w
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA VX863
UT WOS:A1996VX86300010
PM 8960553
ER
PT J
AU Kaphalia, BS
Ghanayem, BI
Ansari, GAS
AF Kaphalia, BS
Ghanayem, BI
Ansari, GAS
TI Nonoxidative metabolism of 2-butoxyethanol via fatty acid conjugation in
Fischer 344 rats
SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH
LA English
DT Article
ID GLYCOL MONOBUTYL ETHER; BUTOXYACETIC ACID; MAJOR METABOLITE; INHALATION;
TOXICITY; 2-CHLOROETHANOL; SOLVENTS; HUMANS
AB Nonoxidative metabolism of ethylene glycol monobutyl ether (2-butoxyethanol or BE) via fatty acid conjugation was studied in the liver of Fischer 344 male rats following a single oral administration of 500 mg/kg body weight [ethyl-1,2-C-14]BE (70 mu Ci/kg). Animals were killed 2 h after the treatment, hepatic lipids extracted, and the neutral lipids were separated using solid-phase extraction. The neutral lipid fraction was subjected to preparative thin-layer chromatography, and the esters corresponding to the relative flow of authentic fatty acid 2-butoxyethyl esters were recovered and analyzed by reversed-phase high-performance liquid chromatography (HPLC) using methanol-water (37:3, v/v) as solvent. Approximately 85% of the C-14 label present in the ester fraction was coeluted at retention times corresponding to the different fatty acid 2-butoxyethyl ester standards. The radioactive fractions were analyzed by electron impact mass spectrometry. Molecular ion peaks and fragmentation patterns similar to that of 16:0, 18:0, 18:1, 18:2, and 20:4 fatty acid 2-butoxyethyl ester standards were detected in the corresponding radioactive HPLC fractions. Fatty acid ethyl ester synthase (FAEES), purified from the rat liver microsomal fraction, was also found to catalyze the formation of 18:1 fatty acid 2-butoxyethyl ester. These studies demonstrate that BE is metabolized nonoxidatively via conjugation with long-chain fatty acids, and the formation of these esters appears to be catalyzed by the enzyme(s) involved in fatty acid conjugation of xenobiotic alcohols. However, the biological significance of BE conjugation with fatty acids remains to be investigated.
C1 NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709.
RP Kaphalia, BS (reprint author), UNIV TEXAS,MED BRANCH,DEPT PATHOL,GALVESTON,TX 77555, USA.
FU NIEHS NIH HHS [ES 04815]
NR 30
TC 9
Z9 10
U1 1
U2 5
PU TAYLOR & FRANCIS
PI BRISTOL
PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598
SN 0098-4108
J9 J TOXICOL ENV HEALTH
JI J. Toxicol. Environ. Health
PD DEC 6
PY 1996
VL 49
IS 5
BP 463
EP 479
DI 10.1080/009841096160691
PG 17
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA VX941
UT WOS:A1996VX94100002
PM 8968408
ER
PT J
AU Eaton, WA
Henry, ER
Hofrichter, J
AF Eaton, WA
Henry, ER
Hofrichter, J
TI Nanosecond crystallographic snapshots of protein structural changes
SO SCIENCE
LA English
DT Editorial Material
ID CARBON-MONOXIDE; HEME-PROTEINS; CONFORMATIONAL-CHANGES;
MOLECULAR-DYNAMICS; SINGLE-CRYSTALS; LIGAND-BINDING; HEMOGLOBIN;
MYOGLOBIN; SPECTROSCOPY; REACTIVITY
RP Eaton, WA (reprint author), NIDDKD,CHEM PHYS LAB,NIH,BLDG 5,BETHESDA,MD 20892, USA.
RI Henry, Eric/J-3414-2013
OI Henry, Eric/0000-0002-5648-8696
NR 31
TC 10
Z9 10
U1 1
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 DEC 6
PY 1996
VL 274
IS 5293
BP 1631
EP 1632
DI 10.1126/science.274.5293.1631
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VW712
UT WOS:A1996VW71200038
PM 8984630
ER
PT J
AU Wolozin, B
Iwasaki, K
Vito, P
Ganjei, JK
Lacana, E
Sunderland, T
Zhao, BY
Kusiak, JW
Wasco, V
DAdamio, L
AF Wolozin, B
Iwasaki, K
Vito, P
Ganjei, JK
Lacana, E
Sunderland, T
Zhao, BY
Kusiak, JW
Wasco, V
DAdamio, L
TI Participation of Presenilin 2 in apoptosis: Enhanced basal activity
conferred by an Alzheimer mutation
SO SCIENCE
LA English
DT Article
ID AMYLOID PRECURSOR PROTEIN; PROGRAMMED CELL-DEATH; MISSENSE MUTATIONS;
ENDOTHELIAL-CELLS; DISEASE; GENE; ACTIVATION
AB Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells, The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved, A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity, This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic a familial Alzheimer's disease.
C1 NIMH,UNIT ALZHEIMER BIOL,CLIN SCI LAB,BETHESDA,MD 20892.
NIAID,T CELL MOL BIOL UNIT,CELLULAR & MOL IMMUNOL LAB,BETHESDA,MD 20892.
NIA,MOL NEUROBIOL UNIT,BALTIMORE,MD 21224.
NINCDS,CELLULAR NEUROBIOL BRANCH,GERONTOL RES CTR,BALTIMORE,MD 21224.
HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP E,DEPT NEUROL,GENET & AGING UNIT,CHARLESTOWN,MA 02139.
NIH,T CELL MOL BIOL UNIT,CELLULAR & MOL IMMUNOL LAB,BETHESDA,MD 20892.
NR 28
TC 389
Z9 394
U1 2
U2 6
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD DEC 6
PY 1996
VL 274
IS 5293
BP 1710
EP 1713
DI 10.1126/science.274.5293.1710
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VW712
UT WOS:A1996VW71200060
PM 8939861
ER
PT J
AU Schneider, TD
Mastronarde, DN
AF Schneider, TD
Mastronarde, DN
TI Fast multiple alignment of ungapped DNA sequences using information
theory and a relaxation method
SO DISCRETE APPLIED MATHEMATICS
LA English
DT Article
ID BINDING-SITES; MOLECULAR MACHINES; PROTEIN; LOGOS
AB An information theory based multiple alignment (''Malign'') method was used to align the DNA binding sequences of the OxyR and Fis proteins, whose sequence conservation is so spread out that it is difficult to identify the sites. In the algorithm described here, the information content of the sequences is used as a unique global criterion for the quality of the alignment. The algorithm uses look-up tables to avoid recalculating computationally expensive functions such as the logarithm. Because there are no arbitrary constants and because the results are reported in absolute units (bits), the best alignment can be chosen without ambiguity. Starting from randomly selected alignments, a hill-climbing algorithm can track through the immense space of s(n) combinations where s is the number of sequences and n is the number of positions possible for each sequence. Instead of producing a single alignment, the algorithm is fast enough that one can afford to use many start points and to classify the solutions. Good convergence is indicated by the presence of a single well-populated solution class having higher information content than other classes. The existence of several distinct classes for the Fis protein indicates that those binding sites have self-similar features.
C1 UNIV COLORADO,DEPT MOL CELLULAR & DEV BIOL,BOULDER,CO 80309.
RP Schneider, TD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,POB B,FREDERICK,MD 21702, USA.
OI Schneider, Thomas/0000-0002-9841-1531
FU Intramural NIH HHS [Z01 BC008396-20]; NIGMS NIH HHS [R01 GM028755]
NR 23
TC 27
Z9 28
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-218X
J9 DISCRETE APPL MATH
JI Discret Appl. Math.
PD DEC 5
PY 1996
VL 71
IS 1-3
BP 259
EP 268
DI 10.1016/S0166-218X(96)00068-6
PG 10
WC Mathematics, Applied
SC Mathematics
GA VX698
UT WOS:A1996VX69800016
PM 19953199
ER
PT J
AU VonLubitz, DKJE
Lin, RCS
Paul, IA
Beenhakker, M
Boyd, M
Bischofberger, N
Jacobson, KA
AF VonLubitz, DKJE
Lin, RCS
Paul, IA
Beenhakker, M
Boyd, M
Bischofberger, N
Jacobson, KA
TI Postischemic administration of adenosine amine congener (ADAC): Analysis
of recovery in gerbils
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE ischemia, treatment; adenosine; memory; MAP2 (microtubule-associated
protein 2); (gerbil)
ID MICROTUBULE-ASSOCIATED PROTEIN-2; CEREBRAL-ISCHEMIA; FOREBRAIN ISCHEMIA;
BRAIN; RAT; TEMPERATURE; DEGRADATION; RECEPTORS; AGONIST; INJURY
AB Although adenosine receptor-based treatment of cerebral ischemia and other neurodegenerative disorders has been frequently advocated, cardiovascular side effects and an uncertain therapeutic time window of such treatment have constituted major obstacles to clinical implementation. Therefore, we have investigated the neuroprotective effects of the adenosine A, receptor agonist adenosine amine congener (ADAC) injected after either 5 or 10 min ischemia at 100 mu g/kg. When the drug was administered at either 6 or 12 h following 5 min forebrain ischemia, all animals were still alive on the 14th day after the occlusion. In both ADAC treated groups neuronal survival was approximately 85% vs. 50% in controls. Administration of a single dose of ADAC at times 15 min to 12 h after 10 min ischemia resulted in a significant improvement of survival in animals injected either at 15 or 30 min, or at 1, 2, or 3 h after the insult. In all 10 min ischemia groups, administration of ADAC resulted in a significant protection of neuronal morphology and preservation of microtubule associated protein 2 (MAP-2). However, postischemic Morris' water maze tests revealed full preservation of spatial memory and learning ability in animals injected at 6 h. On the other hand, the performance of gerbils treated at 12 h postischemia was indistinguishable from that of the controls. Administration of ADAC at 100 mu g/kg in non-ischemic animals did not result in bradycardia, hypotension, or hypothermia. The data indicate that when ADAC is used postischemically, the most optimal level of protection is obtained when drugs are given at 30 min to 6 h after the insult. Although the mechanisms involved in neuroprotective effects of adenosine A(1) receptor agonists require further studies, the present results demonstrate the feasibility of their clinical applications.
C1 MED COLL PENN & HAHNEMANN UNIV, DEPT ANAT & NEUROBIOL, PHILADELPHIA, PA 19102 USA.
UNIV MISSISSIPPI, DEPT PSYCHIAT & HUMAN BEHAV, JACKSON, MS 39216 USA.
GILEAD SCI INC, FOSTER CITY, CA 94404 USA.
RP VonLubitz, DKJE (reprint author), NIDDK, MOL RECOGNIT SECT, NIH, BLDG 8, ROOM 1A15, BETHESDA, MD 20892 USA.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999]
NR 44
TC 37
Z9 38
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD DEC 5
PY 1996
VL 316
IS 2-3
BP 171
EP 179
DI 10.1016/S0014-2999(96)00667-X
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA VZ903
UT WOS:A1996VZ90300007
PM 8982684
ER
PT J
AU Bonifacino, JS
AF Bonifacino, JS
TI Reversal of fortune for nascent proteins
SO NATURE
LA English
DT Editorial Material
ID PROTEASOME; CFTR
RP Bonifacino, JS (reprint author), NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892, USA.
OI Bonifacino, Juan S./0000-0002-5673-6370
NR 13
TC 39
Z9 39
U1 0
U2 0
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF
SN 0028-0836
J9 NATURE
JI Nature
PD DEC 5
PY 1996
VL 384
IS 6608
BP 405
EP 406
DI 10.1038/384405a0
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA VW687
UT WOS:A1996VW68700029
PM 8945460
ER
PT J
AU Kost, RG
Straus, SE
AF Kost, RG
Straus, SE
TI Treatment of postherpetic neuralgia - Reply
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
RP Kost, RG (reprint author), NIAID,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD DEC 5
PY 1996
VL 335
IS 23
BP 1769
EP 1769
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA VW795
UT WOS:A1996VW79500023
ER
PT J
AU Todd, MC
Xiang, RH
Garcia, DK
Kerbacher, KE
Moore, SL
Hensel, CH
Liu, P
Siciliano, MJ
Kok, K
vandenBerg, A
Veldhuis, P
Buys, CHCM
Killary, AM
Naylor, SL
AF Todd, MC
Xiang, RH
Garcia, DK
Kerbacher, KE
Moore, SL
Hensel, CH
Liu, P
Siciliano, MJ
Kok, K
vandenBerg, A
Veldhuis, P
Buys, CHCM
Killary, AM
Naylor, SL
TI An 80 Kb P1 clone from chromosome 3p21.3 suppresses tumor growth in vivo
SO ONCOGENE
LA English
DT Article
DE tumor suppressor gene; small cell lung cancer; human chromosome 3;
positional cloning; homozygous deletion
ID CELL LUNG-CANCER; POLYMERASE CHAIN-REACTION; SHORT ARM; HOMOZYGOUS
DELETION; DNA-SEQUENCE; ALLELIC LOSS; OVARIAN-CANCER; CARCINOMA; LINE;
GENE
AB High frequencies of allelic loss on the short arm of chromosome 3 in small cell lung cancer (SCLC) and a number of other tumors suggest the existence of a tumor suppressor gene(s) within the deleted regions. Two small cell lung cancer lines, NCI H740 and GLC20, have been described which have homozygous deletions in the region 3p21.3. The deleted region overlaps with a 2 Mb fragment of human DNA present in the interspecies hybrid HA(3)BB9F, that suppresses tumor formation by mouse A9 fibrosarcoma cells. Human sequences from this cell hybrid were isolated using inter Alu PCR. From this starting point, a P1 contig was developed for the region of 450 Kb that is common to the homozygous deletions seen in the SCLC lines NCI H740 and GLC20 and is also present in HA(3)BB9F, the suppressed A9 hybrid. Individual P1 clones were assayed for their ability to suppress the tumorigenicity of the mouse fibrosarcoma cell line A9 as assayed by injection of transfected A9 cells into athymic nude mice. The introduction of one of the P1 clones into A9 cells resulted in suppression of tumor growth whereas two other P1 clones from the contig failed to suppress tumor formation in athymic nude mice. These data functionally delimit a tumor suppressor locus to a region of 80 kb within a P1 clone at 3p21.3.
C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284.
NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892.
MD ANDERSON CANC INST,DEPT MOL GENET,HOUSTON,TX 77030.
MD ANDERSON CANC INST,DEPT LAB MED,HOUSTON,TX 77030.
UNIV GRONINGEN,DEPT MED GENET,GRONINGEN,NETHERLANDS.
RI Liu, Paul/A-7976-2012; van den Berg, Anke/H-1718-2011; todd,
martin/I-4143-2015
OI Liu, Paul/0000-0002-6779-025X;
FU NCI NIH HHS [CA54174, CA56626]; PHS HHS [H600470]
NR 56
TC 49
Z9 50
U1 0
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC 5
PY 1996
VL 13
IS 11
BP 2387
EP 2396
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA VX108
UT WOS:A1996VX10800011
PM 8957080
ER
PT J
AU Wong, ML
Khatri, P
Licinio, J
Esposito, A
Gold, PW
AF Wong, ML
Khatri, P
Licinio, J
Esposito, A
Gold, PW
TI Identification of hypothalamic transcripts upregulated by
antidepressants
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID CORTICOTROPIN-RELEASING HORMONE; MESSENGER-RNA; THERAPEUTIC
IMPLICATIONS; TYROSINE-HYDROXYLASE; RAT-BRAIN; DEPRESSION; DISPLAY
AB Identification of quantitative changes in gene expression that occur in the brain after antidepressant treatment can yield novel molecular markers that may be useful in the diagnosis and treatment of major depression. Using a modification of the differential display polymerase chain reaction, we describe the isolation of two transcripts that are differentially expressed in the brain after an 8-week course of antidepressant administration, compared to saline-treated control animals. (C) 1996 Academic Press, Inc.
RP Wong, ML (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,NIH,BETHESDA,MD 20892, USA.
RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013
OI Licinio, Julio/0000-0001-6905-5884
NR 9
TC 17
Z9 18
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 DEC 4
PY 1996
VL 229
IS 1
BP 275
EP 279
DI 10.1006/bbrc.1996.1792
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA VX982
UT WOS:A1996VX98200046
PM 8954118
ER
PT J
AU Quinn, TC
Gaydos, C
Shepherd, M
Bobo, L
Hook, EW
Viscidi, R
Rompalo, A
AF Quinn, TC
Gaydos, C
Shepherd, M
Bobo, L
Hook, EW
Viscidi, R
Rompalo, A
TI Epidemiologic and microbiologic correlates of Chlamydia trachomatis
infection in sexual partnerships
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID POLYMERASE CHAIN-REACTION; PELVIC INFLAMMATORY DISEASE; FIRST-VOID
URINE; REACTION ASSAY; MONOCLONAL-ANTIBODIES; NEISSERIA-GONORRHOEAE;
ENZYME-IMMUNOASSAY; ASYMPTOMATIC MEN; DIAGNOSIS; WOMEN
AB Objectives.-To determine the frequency of Chlamydia trachomatis genital infection within sexual partnerships using highly sensitive polymerase chain reaction (PCR) amplification and to identify the variables that might modify transmission.
Design.-Cross-sectional study of sexual partnerships comparing in vitro culture and PCR amplification for C trachomatis.
Setting.-Two outpatient sexually transmitted disease clinics.
Participants.-Four hundred ninety-four people in sexual partnerships attending sexually transmitted disease clinics.
Main Outcome Measure.-Genital infection with C trachomatis.
Methods.-DNA sequencing was performed to examine specific genotypes within and between partnerships. Cross-sectional analysis was performed to determine characteristics associated with concordance or discordance of infection with partnerships.
Results.-Cultures were positive for C trachomatis in 8.5% of males and 12.9% of females (P=.03), Using PCR, more infections were identified both in males (14.2%) and in females (15.8%), and the difference in infection rates analyzed by sex was no longer significant. In 20.4% of 494 couples, at least 1 partner had PCR results positive for C trachomatis, with a concordant infection rate of 10.7%, significantly higher than the 5.5% concordant infection rate demonstrable by culture (P<.01). Male-female and female-male transmission frequencies were equal (68%). The nucleotide sequences of the major outer membrane protein gene products were identical and unique for each of 15 culture-negative, PCR-positive concordant partnerships. In concordant infections, factors associated with infection in female partners were age less than 20 years, more than 1 partner in the past 6 months, and cervical ectopy greater than 25%.
Conclusions.-Using PCR, the frequency of chlamydia transmission by infected males and females was nearly identical. The high rate of concordant infection, high frequency of infection among asymptomatic individuals, and high frequency of transmission regardless of sex underscore the importance of routine screening for chlamydia in both males and females, along with provision of treatment to all sexual partners of chlamydia-infected individuals.
C1 NIAID, NIH, BETHESDA, MD 20892 USA.
BALTIMORE CITY DEPT HLTH, BALTIMORE, MD USA.
RP Quinn, TC (reprint author), JOHNS HOPKINS UNIV, DIV INFECT DIS, DEPT MED, ROSS 1159, 720 RUTLAND AVE, BALTIMORE, MD 21205 USA.
RI Gaydos, Charlotte/E-9937-2010; Quinn, Thomas/A-2494-2010
FU NIAID NIH HHS [5R01 AI27727-03, 5R01 AI29508-02]
NR 41
TC 146
Z9 147
U1 0
U2 4
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 DEC 4
PY 1996
VL 276
IS 21
BP 1737
EP 1742
DI 10.1001/jama.276.21.1737
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA VV566
UT WOS:A1996VV56600031
PM 8940322
ER
PT J
AU Weed, DL
Kramer, BS
AF Weed, DL
Kramer, BS
TI Induced abortion, bias, and breast cancer: Why epidemiology hasn't
reached its limit
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID RISK; WOMEN
C1 GEORGETOWN UNIV,KENNEDY INST ETH,WASHINGTON,DC 20057.
RP Weed, DL (reprint author), NCI,PREVENT ONCOL BRANCH,DIV CANC PREVENT & CONTROL,NIH,EXECUT PLAZA S,RM T-41,BETHESDA,MD 20892, USA.
NR 29
TC 17
Z9 17
U1 0
U2 1
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 4
PY 1996
VL 88
IS 23
BP 1698
EP 1700
DI 10.1093/jnci/88.23.1698
PG 3
WC Oncology
SC Oncology
GA VV998
UT WOS:A1996VV99800001
PM 8943995
ER
PT J
AU Lee, JH
Miele, ME
Hicks, DJ
Phillips, KK
Trent, JM
Weissman, BE
Welch, DR
AF Lee, JH
Miele, ME
Hicks, DJ
Phillips, KK
Trent, JM
Weissman, BE
Welch, DR
TI KiSS-1, a novel human malignant melanoma metastasis-suppressor gene
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID SH3 DOMAINS; DIFFERENTIAL DISPLAY; SIGNAL-TRANSDUCTION; CANCER
METASTASIS; SUBTRACTIVE HYBRIDIZATION; MESSENGER-RNAS; CELL-LINES;
CHROMOSOME-6; TUMORIGENICITY; PROTEINS
AB Background: Microcell-mediated transfer of chromosome 6 into human C8161 and MelJuSo melanoma cells suppresses their ability to metastasize by at least 95% without affecting their tumorigenicity. This observation demonstrates that the ability to metastasize is a phenotype distinct from tumor formation and suggests that tumorigenic cells acquire metastatic capability only after accumulating additional genetic defects. These results also imply that mutations of genes on chromosome 6 are among those late genetic changes responsible for metastatic potential. They further suggest that a melanoma metastasis-suppressor gene(s) is encoded on chromosome 6 or is regulated by genes on chromosome 6. Purpose: Our objective was to identify the gene(s) responsible for the suppression of metastasis in chromosome 6/melanoma cell hybrids. Methods: A modified subtractive hybridization technique was used to compare the expression of messenger RNAs (mRNAs), via an analysis of complementary DNAs (cDNAs), in metastatic cells (C8161 or MelJuSo) and nonmetastatic hybrid clones (neo6/C8161 or neo6/MelJuSo). Results: A novel cDNA, designated KiSS-1, was isolated from malignant melanoma cells that had been suppressed for metastatic potential by the introduction of human chromosome 6. Northern blot analyses comparing mRNAs from a panel of human melanoma cells revealed that KiSS-1 mRNA expression occurred only in nonmetastatic melanoma cells. Expression of this mRNA in normal heart, brain, liver, lung, and skeletal muscle was undetectable by northern blot analysis. Weak expression was found in the kidney and pancreas, but the highest expression was observed in the placenta. The KiSS-1 cDNA encodes a predominantly hydrophilic, 164 amino acid protein with a polyproline-rich domain indicative of an SH3 ligand (binds to the homology 3 domain of the oncoprotein Src) and a putative protein-kinase C-alpha phosphorylation site. Transfection of a full-length KiSS-1 cDNA into C8161 melanoma cells suppressed metastasis in an expression-dependent manner. Conclusions: These data strongly suggest that KiSS-1 expression may suppress the metastatic potential of malignant melanoma cells, implications: KiSS-1 may be a useful marker for distinguishing metastatic melanomas from nonmetastatic melanomas.
C1 PENN STATE UNIV,COLL MED,DEPT EXPT PATHOL C7810,JAKE GITTLEN CANC RES INST,HERSHEY,PA 17033.
UNIV N CAROLINA,DEPT PATHOL,LINEBERGER CANC CTR,CHAPEL HILL,NC.
NIH,NATL CTR HUMAN GENOME RES,DIV INTRAMURAL RES,BETHESDA,MD 20892.
RI Welch, Danny/B-7310-2009
OI Welch, Danny/0000-0002-1951-4947
FU NCI NIH HHS [CA44470, CA62168]
NR 45
TC 503
Z9 585
U1 3
U2 18
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 4
PY 1996
VL 88
IS 23
BP 1731
EP 1737
DI 10.1093/jnci/88.23.1731
PG 7
WC Oncology
SC Oncology
GA VV998
UT WOS:A1996VV99800013
PM 8944003
ER
PT J
AU Shopland, DR
Hartman, AM
Gibson, JT
Mueller, MD
Kessler, LG
Lynn, WR
AF Shopland, DR
Hartman, AM
Gibson, JT
Mueller, MD
Kessler, LG
Lynn, WR
TI Cigarette smoking among US adults by state and region: Estimates from
the current population survey
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID UNITED-STATES; PREVALENCE; CANCER
AB Background: Cigarette smoking is responsible for at least one third of all cancer deaths annually in the United States. Few sources exist in the peer-reviewed literature documenting state and regional differences in smoking behavior, despite the fact that cancer prevention and control efforts are increasingly being implemented below the national level. Purpose: Our goals were to determine smoking prevalence rates among men and women, by region, and for each of the 50 states and the District of Columbia from census survey data collected in 1992 and 1993 and to compare these rates with rates determined in 1985. Methods: Every month, the U.S. Bureau of the Census collects labor force statistics on more than 100 000 individuals on its Current Population Survey (CPS). For the September 1992, January 1993, and May 1993 CPS, the National Cancer Institute sponsored a 40-item Tobacco Use Supplement. The definition of a current smoker changed slightly between 1985 and 1992-1993. For the 1985 CPS, individuals were considered current smokers if they had smoked 100 cigarettes in their lifetime and were smoking at the time of interview; for the 1992-1993 CPS, current smokers included anyone who had smoked 100 cigarettes and was currently smoking every day or just an some days. We calculated current smoking rates (every day and some days combined) based on more than a quarter million adults (n = 266 988) interviewed in 1992-1993. Results: Substantial geographic variation exists in rates of current cigarette use among adults within the United States. In general, adults in the southern United States have higher rates of smoking and adults in the western states have lower rates of smoking than adults in the rest of the country, although differences in smoking behavior between men and women and among various racial and ethnic populations strongly influence these patterns. Only two states, Kentucky and West Virginia, exhibited adult smoking rates (men and women combined) of 30% or higher in 1992-1993; in contrast, in 1985, such rates were reported from 20 states. The only states in which the prevalence was below 20% in 1992-1993 were Utah (17.1%) and California (19.5%). Rates approaching 20% were reported from New Jersey (20.7%), Massachusetts (21.5%), and Nebraska, New York, and Hawaii (22.0% each) in 1992-1993. Rhode Island experienced the greatest relative decline in smoking prevalence from 1985 to 1992-1993, with a calculated relative change of -30.7% (based on a change in rate from 33.5% to 23.2%), followed by Delaware (-25.9%), the of Columbia and New Jersey (-23.9% each), Connecticut (-23.2%), California (-22.9%), Alaska (-22.8%), Georgia (-22.6%), Massachusetts (-22.1%), and New York (-22.0%). Conclusions: Smoking rates are not uniform in the United States but vary considerably from state to state, even within the same region of the country. The CPS is the only mechanism currently capable of simultaneously monitoring smoking trends nationally, regionally, and on a state-by-state basis.
C1 IMS INC,SILVER SPRING,MD.
ROW SCI INC,ROCKVILLE,MD.
RP Shopland, DR (reprint author), NCI,DIV CANC PREVENT & CONTROL,NIH,EXECUT PLAZA N,RM 241,BETHESDA,MD 20892, USA.
NR 21
TC 71
Z9 72
U1 1
U2 3
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC 4
PY 1996
VL 88
IS 23
BP 1748
EP 1758
DI 10.1093/jnci/88.23.1748
PG 11
WC Oncology
SC Oncology
GA VV998
UT WOS:A1996VV99800015
PM 8944005
ER
PT J
AU Calvert, RJ
Buzard, GS
Anisimov, VN
Rice, JM
AF Calvert, RJ
Buzard, GS
Anisimov, VN
Rice, JM
TI K-ras codon 12 and 61 point mutations in bromodeoxyuridine- and
N-nitrosomethylurea-induced rat renal mesenchymal tumors
SO CANCER LETTERS
LA English
DT Article
DE K-ras; bromodeoxyuridine; N-nitrosomethylurea; renal mesenchymal tumors;
polymerase chain reaction
ID MAMMARY-GLANDS; ONCOGENES; ACTIVATION; CELLS; GENE; CARCINOGENESIS;
MUTAGENESIS; METHYLUREA
AB The mutagenic thymidine analog bromodeoxyuridine (BrdUrd) may incorrectly incorporate opposite deoxyguanine in DNA, then pair with deoxyadenosine during subsequent replication. It appears to preferentially target the 3'-G of 5'-NGGN-3' sequences in mammalian cells in culture to induce G --> A transitions. Ras genes should therefore be vulnerable to activation by mutation at glycine codons 12 (GGT) and/or 13 (GGC) by misincorporation of BrdUrd. There is limited evidence that BrdUrd may be carcinogenic or co-carcinogenic in rats: three renal mesenchymal tumors, a tumor known to be associated with activating mutations in the c-K-ras-2 oncogene, were reported in 87 rats treated with BrdUrd alone, while N-nitrosomethylurea (NMU) alone or MMU + BrdUrd resulted in incidences of 12/52 and 26/76, respectively, against a zero incidence in untreated rats. We analyzed renal mesenchymal tumors from rats treated with BrdUrd for mutations in K-ras exons 1 and 2 and compared the prevalence and spectrum of mutations with those found in comparable tumors induced with NMU. DNAs from 22 paraffin-embedded renal mesenchymal tumors from rats treated 12-15 months earlier with BrdUrd (three specimens) or NMU (11 specimens) or both agents sequentially (eight specimens) were amplified by PCR. The base sequence of codons 12-13 and 59-63 of K-ras was determined by the dideoxynucleotide method. Sequencing results were confirmed by allele-specific oligonucleotide hybridization. Two of three tumors that appeared in rats given BrdUrd alone contained both a codon 12 GGT --> GAT transition and a codon 61 CAA --> CTA transversion. One tumor induced by NMU alone also showed a codon 12 GGT --> GAT mutation, while only wild type sequence could be demonstrated in the codon 12-13 region in the remaining ten such tumors. Three NMU-induced tumors also showed codon 61 CAA --> CTA mutations, while the remaining tumors had wild type sequence. While the GGT --> GAT transitions identified in tumors from BrdUrd-treated rats are consistent with BrdUrd mutagenesis by misincorporation, the co-occurrence of CAA --> CTA transversions, the overall low prevalence of mutations, and the lack of any difference in mutation spectrum between tumors induced by NMU and those that occurred in BrdUrd-treated rats suggests that in both groups the mutations that did occur did not result from a direct effect of either agent.
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
NN PETROV ONCOL RES INST,ST PETERSBURG,RUSSIA.
NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702.
RP Calvert, RJ (reprint author), US FDA,OFF SPECIAL NUTRIT,MOD-1,HFS-452,8301 MUIRKIRK RD,LAUREL,MD 20708, USA.
NR 22
TC 4
Z9 4
U1 2
U2 2
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 3
PY 1996
VL 109
IS 1-2
BP 1
EP 7
DI 10.1016/S0304-3835(96)04350-9
PG 7
WC Oncology
SC Oncology
GA VZ698
UT WOS:A1996VZ69800001
PM 9020896
ER
PT J
AU Cysyk, RL
Chisena, CA
Hyman, R
Monks, A
AF Cysyk, RL
Chisena, CA
Hyman, R
Monks, A
TI Tiazofurin enhances the anabolism and toxicity of 5-fluorouracil
SO CANCER LETTERS
LA English
DT Article
DE tiazofurin; 5-fluorouracil; 5-phosphoribosyl-1-pyrophosphate (PRPP);
pyrimidines
ID 2-BETA-D-RIBOFURANOSYLTHIAZOLE-4-CARBOXAMIDE NSC 286193; CULTURED L1210
CELLS; N-(PHOSPHONACETYL)-L-ASPARTIC ACID; MECHANISM; MURINE; LEUKEMIA;
CONVERSION; CARCINOMA; ACIVICIN
AB Tiazofurin, a clinically active anticancer agent, is undergoing additional clinical testing in combination with other agents. We found that tiazofurin is an effective biochemical modulator of 5-fluorouracil anabolism. Pretreatment of cultured L1210 cells with tiazofurin at concentrations of 1-100 mu M results in an increase in the rate of conversion of 5-fluorouracil to phosphorylated metabolites. Concentrations of tiazofurin effective in increasing 5-fluorouracil anabolism cause a corresponding increase in the 5-phosphoribosyl-1-pyrophosphate pool. Studies in mice show that tiazofurin increases the lethal toxicity of 5-fluorouracil and increases the antitumor effectiveness of low doses of 5-fluorouracil; however, the combination is not more effective than an optimal dose of 5-fluorouracil given alone. These results indicate that caution should be exercised in the concurrent use of tiazofurin with other drugs, particularly 5-fluorouracil, that require 5-phosphoribosyl-1-pyrophosphate for activation or that are affected by a decrease in pyrimidine nucleotide synthesis.
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD.
RP Cysyk, RL (reprint author), NCI,DIV BASIC SCI,MED CHEM LAB,BLDG 37,ROOM 5E18,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA.
NR 22
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 3
PY 1996
VL 109
IS 1-2
BP 49
EP 55
DI 10.1016/S0304-3835(96)04416-3
PG 7
WC Oncology
SC Oncology
GA VZ698
UT WOS:A1996VZ69800007
PM 9020902
ER
PT J
AU Yu, FL
Cahill, JM
Lipinski, LJ
Dipple, A
AF Yu, FL
Cahill, JM
Lipinski, LJ
Dipple, A
TI Effect of aflatoxin B-1-8,9-epoxide-DNA adducts on transcription of a
supF gene fragment
SO CANCER LETTERS
LA English
DT Article
DE transcription; aflatoxin; carcinogen
ID RNA-POLYMERASE; DNA; BINDING; RAT; ELONGATION; CYTOSINE; INVITRO;
GUANINE; LESIONS; ADENINE
AB A linearized template, obtained from the vector pGEM-3Zf(+) containing a supF gene fragment, was treated with aflatoxin B-1-8,9-epoxide (AFB(1) epoxide) and transcription in vitro was then studied. The template functions of both strands of the supF gene were similarly inhibited as shown by transcription with both T7 and SP6 RNA polymerases. This inhibition was dose-dependent and affected the elongation step more extensively than the initiation step. Gel electrophoretic analysis of RNA formed by T7 RNA polymerase indicated that template treated with different AFB1 epoxide doses yielded the same three major truncated RNA fragments. Sequence analysis showed that these major sites of RNA truncation occurred in the vicinity of adjacent guanine residues in the template.
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702.
UNIV ILLINOIS,COLL MED,DEPT BIOMED SCI,ROCKFORD,IL 61107.
FU NCI NIH HHS [NC-CO-46000]
NR 28
TC 10
Z9 10
U1 0
U2 1
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 3
PY 1996
VL 109
IS 1-2
BP 77
EP 83
DI 10.1016/S0304-3835(96)04423-0
PG 7
WC Oncology
SC Oncology
GA VZ698
UT WOS:A1996VZ69800010
PM 9020905
ER
PT J
AU Lazutka, JR
Neel, JV
Major, EO
Dedonyte, V
Mierauskine, J
Slapsyte, G
Kesminiene, A
AF Lazutka, JR
Neel, JV
Major, EO
Dedonyte, V
Mierauskine, J
Slapsyte, G
Kesminiene, A
TI High titers of antibodies to two human polyomaviruses, JCV and BKV,
correlate with increased frequency of chromosomal damage in human
lymphocytes
SO CANCER LETTERS
LA English
DT Article
DE chromosome aberrations; rogue cells; JC virus; BK virus; p53
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; CHERNOBYL ACCIDENT; HUMAN
BRAIN; VIRUS; ABERRATIONS; CELLS; PATHOGENESIS; PERSISTENCE;
ONCOGENESIS; FIBROBLASTS
AB Associations of antibody titers to the JC and BK human polyoma viruses and the frequency of chromosome aberrations (CA) in human peripheral blood lymphocytes were studied. Study group consisted of 33 workers occupationally exposed to low doses of ionizing radiation and 11 control persons. There were no statistically significant differences in the JC and BK virus titer values between two groups of donors. It was found that JC and BK virus titers explained approximately 6% of total inter-individual variation in CA frequency. Such factors as alcohol abuse, age and, in this special group, exposure to ionizing radiation explained an additional 53% of the total variation in CA frequency. In six clean-up workers and one control, rogue cells (cells with multiple chromosome-type aberrations) were found. The incidence of rogue cells correlated significantly with JC and BK virus titers as well as a history of recent acute respiratory disease.
C1 UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109.
NINCDS,MOL MED & VIROL SECT,LAB MOL MED & NEUROSCI,NIH,BETHESDA,MD 20892.
LITHUANIAN CHERNOBYL MED CTR,LT-2001 VILNIUS,LITHUANIA.
RP Lazutka, JR (reprint author), VILNIUS STATE UNIV,DEPT BOT & GENET,21 CIURLIONIS ST,LT-2009 VILNIUS,LITHUANIA.
NR 28
TC 30
Z9 32
U1 1
U2 1
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD DEC 3
PY 1996
VL 109
IS 1-2
BP 177
EP 183
DI 10.1016/S0304-3835(96)04448-5
PG 7
WC Oncology
SC Oncology
GA VZ698
UT WOS:A1996VZ69800023
PM 9020918
ER
PT J
AU Kubota, T
Sutcliffe, JS
Aradhya, S
GillessenKaesbach, G
Christian, SL
Horsthemke, B
Beaudet, AL
Ledbetter, DH
AF Kubota, T
Sutcliffe, JS
Aradhya, S
GillessenKaesbach, G
Christian, SL
Horsthemke, B
Beaudet, AL
Ledbetter, DH
TI Validation studies of SNRPN methylation as a diagnostic test for
Prader-Willi syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Prader-Willi syndrome; DNA methylation; SNRPN; genomic imprinting
ID DNA METHYLATION; ANGELMAN SYNDROMES; MOLECULAR DIAGNOSIS; REGION;
15Q11-Q13; IMPRINT; DEFINE; PARENT
AB Prader-Willi syndrome (PWS) is caused by absence of a paternal contribution of the chromosome region 15q11-q13, resulting from paternal deletions, maternal uniparental disomy, or rare imprinting mutations. Laboratory diagnosis is currently performed using fluorescence in situ hybridization (FISH), DNA polymorphism (microsatellite) analysis, or DNA methylation analysis at locus PW71 (D15S63). We examined another parent-of-origin-specific DNA methylation assay at exon ex of the small nuclear ribonucleoprotein-associated polypeptide N gene (SNRPN) in patients referred with clinical suspicion of PWS or Angelman syndrome (AS). These included 30 PWS and 17 AS patients with known deletion or uniparental disomy status, and a larger cohort of patients (n = 512) suspected of PWS who had been analyzed previously for their methylation status at the PW71 locus. Results of SNRPN methylation were consistent with known deletion or uniparental disomy (UPD) status as determined by other molecular methods in all 47 cases of PWS and AS. In the larger cohort of possible PWS patients, SNRPN results were consistent with clinical diagnosis by examination and with PW71 methylation results in all cases. These data provide support for the use of SNRPN methylation as a diagnostic method. Because methylation analysis can detect all three major classes of genetic defects associated with PWS (deletion, UPD, or imprinting mutations), methylation analysis with either PW71 or SNRPN is an efficient primary screening test to rule out a diagnosis of PWS. Only patients with an abnormal methylation result require further diagnostic investigation by FISH or DNA polymorphism analysis to distinguish among the three classes for accurate genetic counseling and recurrence-risk assessment. (C) 1996 Wiley-Liss, Inc.
C1 NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892.
UNIV ESSEN GESAMTHSCH KLINIKUM,INST HUMAN GENET,D-4300 ESSEN,GERMANY.
BAYLOR COLL MED,DEPT MOL & HUMAN GENET,HOUSTON,TX 77030.
BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030.
RI Sutcliffe, James/C-1348-2012
OI Sutcliffe, James/0000-0001-5200-6007
NR 19
TC 61
Z9 63
U1 2
U2 8
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD DEC 2
PY 1996
VL 66
IS 1
BP 77
EP 80
DI 10.1002/(SICI)1096-8628(19961202)66:1<77::AID-AJMG18>3.0.CO;2-N
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA VV306
UT WOS:A1996VV30600018
PM 8957518
ER
PT J
AU Kustova, Y
Sei, Y
Goping, G
Basile, AS
AF Kustova, Y
Sei, Y
Goping, G
Basile, AS
TI Gliosis in the LP-BM5 murine leukemia virus-infected mouse: An animal
model of retrovirus-induced dementia
SO BRAIN RESEARCH
LA English
DT Article
DE astrocyte; microglia; mouse; LP-BM5 virus; dementia; AIDS
ID CENTRAL-NERVOUS-SYSTEM; HUMAN-IMMUNODEFICIENCY-VIRUS; QUINOLINIC ACID;
BRAIN; MICROGLIA; MACROPHAGES; ASTROCYTES; DISEASE; AIDS; CYTOKINES
AB Mice infected with the LP-BM5 murine leukemia virus (MuLV) mixture develop severe immunosuppression, neurotransmitter abnormalities and cognitive impairments in the absence of significant viral or macrophage invasion of the CNS. The time-course of the changes in glial activation have been characterized in an effort to understand the cellular basis of the neurobehavioral abnormalities observed in these mice. Glial activation was determined by measuring the relative changes in F4/80 protein and GFAP immunoreactivity using immunoblots. Augmented F4/80 expression preceded that of GFAP, with global elevations of 4-6-fold at 3 weeks, sustained for up to 12 weeks after inoculation. GFAP immunoreactivity increased 2-fold only in the cerebral cortex and striatum 5 weeks postinfection, declining to control levels by 12 weeks. Immunohistochemistry revealed significant increases in microglial size and staining intensity in the cortex, corpus callosum and striatum, with the development of a unique population of highly ramified, intensely stained microglia and microglial nodules in the corpus callosum and striatum. No evidence of ameboid microglia was found. Astrocyte size and degree of ramification was increased in the hippocampus, cortex, striatum and corpus callosum. Thus, microgliosis is an early event in LP-BM5 infection, preceding astrocytosis, neurotransmitter loss, and development of cognitive deficits. Activated microglia may secrete neurotoxins leading to the neurochemical alterations and cognitive deficits observed in these mice. Because gliosis and microglial nodule formation are hallmarks of HIV-1 encephalopathy, LP-BM5 MuLV-infected C57/B16 mice may afford insights into the mechanisms contributing to the early stages of this syndrome.
C1 NIDDK,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
NIDDK,CELL BIOL & GENET LAB,NIH,BETHESDA,MD 20892.
NR 45
TC 16
Z9 16
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD DEC 2
PY 1996
VL 742
IS 1-2
BP 271
EP 282
DI 10.1016/S0006-8993(96)01014-1
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA WC372
UT WOS:A1996WC37200032
PM 9117405
ER
PT J
AU Bujacz, G
Alexandratos, J
ZhouLiu, Q
ClementMella, C
Wlodawer, A
AF Bujacz, G
Alexandratos, J
ZhouLiu, Q
ClementMella, C
Wlodawer, A
TI The catalytic domain of human immunodeficiency virus integrase: Ordered
active site in the F185H mutant
SO FEBS LETTERS
LA English
DT Article
DE integrase; active site; disorder; metal binding
ID DNA-BINDING; RETROVIRAL INTEGRATION; HIV-1 INTEGRASE; PROTEIN;
IDENTIFICATION
AB We solved the structure and traced the complete active site of the catalytic domain of the human immunodeficiency virus type 1 integrase (HIV-1 IN) with the F185H mutation, The only previously available crystal structure, the F185K mutant of this domain, lacks one of the catalytically important residues, E152, located in a stretch of 12 disordered residues [Dyda et al, (1994) Science 266, 1981-1986], It is clear, however, that the active site of HIV-1 IN observed in either structure cannot correspond to that of the functional enzyme, since the cluster of three conserved carboxylic acids does not create a proper metal-binding site. The conformation of the loop was compared with two different conformations found in the catalytic domain of the related avian sarcoma virus integrase [Bujacz et al. (1995) J. Mol. Biol. 253, 333-346]. Flexibility of the active site region of integrases may be required in order for the enzyme to assume a functional conformation in the presence of substrate and/or cofactors.
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOL STRUCT LAB,FREDERICK,MD 21702.
TECH UNIV LODZ,FAC FOOD CHEM & BIOTECHNOL,PL-90924 LODZ,POLAND.
RHONE POULENC RORER SA,SERV BIOCHIM,F-94403 VITRY SUR SEINE,FRANCE.
NR 16
TC 99
Z9 101
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 DEC 2
PY 1996
VL 398
IS 2-3
BP 175
EP 178
DI 10.1016/S0014-5793(96)01236-7
PG 4
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VX781
UT WOS:A1996VX78100010
PM 8977101
ER
PT J
AU Watts, JD
Brabb, T
Bures, EJ
Wange, RL
Samelson, LE
Aebersold, R
AF Watts, JD
Brabb, T
Bures, EJ
Wange, RL
Samelson, LE
Aebersold, R
TI Identification and characterization of a substrate specific for the T
cell protein tyrosine kinase ZAP-70
SO FEBS LETTERS
LA English
DT Article
DE tyrosine kinase; T cell; band 3 protein; ZAP-70; Lck; Itk
ID SEVERE COMBINED IMMUNODEFICIENCY; HUMAN ERYTHROCYTE BAND-3; IONIZATION
MASS-SPECTROMETRY; TANDEM SH2 DOMAINS; ANTIGEN RECEPTOR;
SIGNAL-TRANSDUCTION; ZETA-CHAIN; PHOSPHORYLATION; LYMPHOCYTE; ACTIVATION
AB ZAP-70 is a protein tyrosine kinase (PTK) that plays a critical role in T cell activation, To study the role of ZAP-70 catalytic activity in this process, a substrate capable of distinguishing between the activities of ZAP-70 and other PTKs would be useful, especially since it has recently been shown that ZAP-70 interacts with another T cell PTK, Lck, We have thus identified a site of phosphorylation on the cytoplasmic fragment of the erythrocyte band 3 protein that is recognized by ZAP-70, but not Lck, A synthetic peptide based on this site has been demonstrated to be a good in vitro substrate for ZAP-70 and a poor substrate for the T cell PTKs Lck and Itk. This peptide molecule should thus prove useful to many investigators working in the field of T cell activation.
C1 NICHHD,NIH,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892.
RP Watts, JD (reprint author), UNIV WASHINGTON,DEPT MOL BIOTECHNOL,BOX 357730,SEATTLE,WA 98195, USA.
FU NCRR NIH HHS [RR07019]
NR 38
TC 10
Z9 10
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD DEC 2
PY 1996
VL 398
IS 2-3
BP 217
EP 222
DI 10.1016/S0014-5793(96)01241-0
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VX781
UT WOS:A1996VX78100019
PM 8977110
ER
PT J
AU Kessel, M
Wu, WF
Gottesman, S
Kocsis, E
Steven, AC
Maurizi, MR
AF Kessel, M
Wu, WF
Gottesman, S
Kocsis, E
Steven, AC
Maurizi, MR
TI Six-fold rotational symmetry of ClpQ, the E-coli homolog of the 20S
proteasome, and its ATP-dependent activator, ClpY
SO FEBS LETTERS
LA English
DT Article
DE Clp protease; HslU/HsiV; ATP-dependent protease; proteasome; rotational
symmetry; image analysis
ID ESCHERICHIA-COLI; ELECTRON-MICROSCOPY; THERMOPLASMA-ACIDOPHILUM;
CRYSTAL-STRUCTURE; PROTEIN; SEQUENCE; ORGANIZATION; RESOLUTION;
BACTERIAL; SUBSTRATE
AB ClpQ (HslV) is a homolog of the beta-subunits of the 20S proteasome. In E. coli, it is expressed from an operon that also encodes ClpY (HsIU), an ATPase homologous to the protease chaperone, ClpX. ClpQ (subunit M(r) 19 000) and ClpY (subunit M(r) 49 000) were purified separately as oligomeric proteins with molecular weights of similar to 220 000 and similar to 350 000, respectively, estimated by gel filtration. Mixtures of ClpY and ClpQ displayed ATP-dependent proteolytic activity against casein, and a complex of the two proteins was isolated by gel filtration in the presence of ATP. Image processing of negatively stained electron micrographs revealed strong six-fold rotational symmetry for both ClpY and ClpQ, suggesting that the subunits of both proteins are arranged in hexagonal rings. The molecular weight of ClpQ combined with its symmetry is consistent with a double hexameric ring, whereas the data on ClpY suggest only one such ring. The symmetry mismatch previously observed between hexameric ClpA and heptameric ClpP in the related ClpAP protease is apparently not reproduced in the symmetry-matched ClpYQ system.
C1 NIAMSD,STRUCT BIOL LAB,BETHESDA,MD 20892.
NCI,NIH,CELL BIOL LAB,BETHESDA,MD 20892.
NCI,NIH,MOL BIOL LAB,BETHESDA,MD 20892.
HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT MEMBRANE & ULTRASTRUCT RES,IL-91010 JERUSALEM,ISRAEL.
OI WU, WHI-FIN/0000-0002-9526-6287
NR 32
TC 89
Z9 91
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD DEC 2
PY 1996
VL 398
IS 2-3
BP 274
EP 278
DI 10.1016/S0014-5793(96)01261-6
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VX781
UT WOS:A1996VX78100031
PM 8977122
ER
PT J
AU Gronenborn, AM
Frank, MK
Clore, GM
AF Gronenborn, AM
Frank, MK
Clore, GM
TI Core mutants of the immunoglobulin binding domain of streptococcal
protein G: Stability and structural integrity
SO FEBS LETTERS
LA English
DT Article
DE protein G; B1 domain; core mutant; library; protein design; structure;
stability
ID AMINO-ACIDS; HYDROPHOBIC CORE; NMR-SPECTROSCOPY; FOLDED PROTEINS;
PACKING; DESIGN; LIBRARIES; HAIRPIN
AB A library of core mutants of the GB1 domain of streptococcal protein G was created, and the structure and stability of selected members was assessed by H-1-N-15 heteronuclear correlation NMR spectroscopy and fluorescence. All mutants comprised changes in beta-sheet residues, with sidechains at positions 5 (Leu), 7 (Leu), 52 (Phe) and 54 (Val) forming the beta-sheet side of the sheet-helix core interface. A solvent exposed position Ile-6 was chosen as a control. Randomization of bases at codon positions 1 and 3 with thymine at position 2 introduces five possible hydrophobic amino acids, namely Leu, Val, Ile, Phe, and Met. The distribution of encoded amino acids at all five positions is approximately as expected theoretically and indicates that no major bias was introduced towards particular residues. The overall structural integrity of several mutants, as assessed by NMR, ranges from very close to wild type to fully unfolded. Interestingly, the stability of the mutants is not strictly correlated with the number of changes or residue volume.
C1 UNIV MARYLAND,INST PHYS SCI & TECHNOL,CHEM PHYS GRAD PROGRAM,COLLEGE PK,MD 20742.
RP Gronenborn, AM (reprint author), NIDDK,NIH,CHEM PHYS LAB,BLDG 5,BETHESDA,MD 20892, USA.
RI Clore, G. Marius/A-3511-2008
OI Clore, G. Marius/0000-0003-3809-1027
NR 32
TC 21
Z9 21
U1 0
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD DEC 2
PY 1996
VL 398
IS 2-3
BP 312
EP 316
DI 10.1016/S0014-5793(96)01262-8
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA VX781
UT WOS:A1996VX78100038
PM 8977129
ER
PT J
AU VanBockstaele, EJ
Colago, EEO
Moriwaki, A
Uhl, GR
AF VanBockstaele, EJ
Colago, EEO
Moriwaki, A
Uhl, GR
TI Mu-opioid receptor is located on the plasma membrane of dendrites that
receive asymmetric synapses from axon terminals containing
leucine-enkephalin in the rat nucleus locus coeruleus
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE norepinephrine; drug abuse; enkephalin; opiates; morphine
ID OPIATE WITHDRAWAL; ADENYLATE-CYCLASE; IMMUNOREACTIVE TERMINALS;
CATECHOLAMINE AFFERENTS; CHRONIC MORPHINE; BRAIN; NEURONS; CERULEUS;
ULTRASTRUCTURE; LOCALIZATION
AB We have recently shown, by using immunoelectron microscopy, that the mu-opioid receptor (mu OR) is prominently distributed within noradrenergic perikarya and dendrites of the nucleus locus coeruleus (LC), many of which receive excitatory-type (i.e., asymmetric) synaptic contacts from unlabeled axon terminals. To characterize further the neurotransmitter present in these afferent terminals, we examined in the present study the ultrastructural localization of an antipeptide sequence unique to the mu OR in sections that were also dually labeled for the opioid peptide leucine-enkephalin (L-ENK). Immunogold-silver labeling for mu OR was localized to extrasynaptic portions of the plasma membranes of perikarya and dendrites. The mu OR-labeled dendrites were usually postsynaptic to axon terminals containing heterogeneous types of synaptic vesicles and forming asymmetric synaptic specializations characteristic of excitatory-type synapses. The majority of these were immunolabeled for the endogenous opioid peptide L-ENK. Some mu OR-labeled dendrites received synaptic contacts from unlabeled axon terminals in fields containing L-ENK immunoreactivity. In such cases, the mu OR-labeled dendrites were in proximity to L-ENK axon terminals that contained intense peroxidase labeling within large dense core vesicles along the perimeter of the axoplasm. These results indicate that L-ENK may be released by exocytosis from the dense core vesicles and diffuse within the extracellular space to reach mu OR sites on the postsynaptic dendrite or dendrites of other neighboring neurons. The present study also reveals that unlabeled terminals apposed to mu OR-labeled dendrites may contain other opioid peptides, such as methionine-enkephalin. These data demonstrate several sites where endogenous opioid peptides may interact with mu OR receptive sites in the LC and may provide an anatomical substrate for the LC's involvement in mechanisms of opiate dependence and withdrawal. (C) 1996 Wiley-Liss, Inc.
C1 CORNELL UNIV,COLL MED,DEPT NEUROL & NEUROSCI,NEW YORK,NY 10021.
NIDA,ADDICT RES CTR,DIV INTRAMURAL RES PROGRAM,BALTIMORE,MD 21224.
FU NIDA NIH HHS [R29 DA09082]; PHS HHS [18974]
NR 48
TC 29
Z9 30
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD DEC 2
PY 1996
VL 376
IS 1
BP 65
EP 74
DI 10.1002/(SICI)1096-9861(19961202)376:1<65::AID-CNE4>3.0.CO;2-M
PG 10
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA VU885
UT WOS:A1996VU88500004
PM 8946284
ER
PT J
AU Hof, PR
Ungerleider, LG
Webster, MJ
Gattass, R
Adams, MM
Sailstad, CA
Morrison, JH
AF Hof, PR
Ungerleider, LG
Webster, MJ
Gattass, R
Adams, MM
Sailstad, CA
Morrison, JH
TI Neurofilament protein is differentially distributed in subpopulations of
corticocortical projection neurons in the macaque monkey visual pathways
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE corticocortical projections; cytoskeleton; feedforward and feedback
projections; occipitoparietal and occipitotemporal pathways; primate
visual system
ID SUPERIOR TEMPORAL SULCUS; ALZHEIMERS-DISEASE; PYRAMIDAL NEURONS;
RHESUS-MONKEY; CORTICAL CONNECTIONS; QUANTITATIVE-ANALYSIS;
MONOCLONAL-ANTIBODY; EXTRASTRIATE CORTEX; AREA V2; TOPOGRAPHIC
ORGANIZATION
AB Previous studies of the primate cerebral cortex have shown that neurofilament protein is present in pyramidal neuron subpopulations displaying specific regional and laminar distribution patterns. In order to characterize further the neurochemical phenotype of the neurons furnishing feedforward and feedback pathways in the visual cortex of the macaque monkey, we performed an analysis of the distribution of neurofilament protein in corticocortical projection neurons in areas V1, V2, V3, V3A, V4, and MT. Injections of the retrogradely transported dyes Fast Blue and Diamidino Yellow were placed within areas V4 and MT, or in areas V1 and V2, in 14 adult rhesus monkeys, and the brains of these animals were processed for immunohistochemistry with an antibody to nonphosphorylated epitopes of the medium and heavy molecular weight subunits of the neurofilament protein. Overall, there was a higher proportion of neurons projecting from areas V1, V2, V3, and V3A to area MT that were neurofilament protein-immunoreactive (57-100%), than to area V4 (25-36%). Tn contrast, feedback projections from areas MT, V4, and V3 exhibited a more consistent proportion of neurofilament protein-containing neurons (70-80%), regardless of their target areas (V1 or V2). In addition, the vast majority of feedback neurons projecting to areas V1 and V2 were located in layers V and V1 in areas V4 and MT, while they were observed in both supragranular and infragranular layers in area V3. The laminar distribution of feedforward projecting neurons was heterogeneous. In area V1, Meynert and layer IVB cells were found to project to area MT, while neurons projecting to area V4 were particularly dense in layer III within the foveal representation. In area V2, almost all neurons projecting to areas MT or V4 were located in layer III, whereas they were found in both layers II-III and V-VI in areas V3 and V3A. These results suggest that neurofilament protein identifies particular subpopulations of corticocortically projecting neurons with distinct regional and laminar distribution in the monkey visual system. It is possible that the preferential distribution of neurofilament protein within feedforward connections to area MT and all feedback projections is related to other distinctive properties of these corticocortical projection neurons. (C) 1996 Wiley-Liss, Inc.
C1 CUNY MT SINAI SCH MED,LABS NEUROBIOL AGING,NEW YORK,NY 10029.
CUNY MT SINAI SCH MED,DEPT GERIATR & ADULT DEV,NEW YORK,NY 10029.
CUNY MT SINAI SCH MED,DEPT OPHTHALMOL,NEW YORK,NY 10029.
NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892.
NIMH,CTR NEUROSCI,STANLEY FDN RES PROGRAM,WASHINGTON,DC 20032.
FED UNIV RIO DE JANEIRO,INST BIOFIS CARLOS CHAGAS FILHO,DEPT NEUROBIOL,BR-21941900 RIO JANEIRO,BRAZIL.
RP Hof, PR (reprint author), CUNY MT SINAI SCH MED,FISHBERG RES CTR NEUROBIOL,BOX 1065,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA.
RI Morrison, John/F-9229-2012
FU NIA NIH HHS [AG06647]; NIMH NIH HHS [MH DA52154]
NR 94
TC 83
Z9 83
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD DEC 2
PY 1996
VL 376
IS 1
BP 112
EP 127
PG 16
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA VU885
UT WOS:A1996VU88500007
PM 8946287
ER
PT J
AU Taffe, BG
Larminat, F
Laval, J
Croteau, DL
Anson, RM
Bohr, VA
AF Taffe, BG
Larminat, F
Laval, J
Croteau, DL
Anson, RM
Bohr, VA
TI Gene-specific nuclear and mitochondrial repair of formamidopyrimidine
DNA glycosylase-sensitive sites in Chinese hamster ovary cells
SO MUTATION RESEARCH-DNA REPAIR
LA English
DT Article
DE oxidative DNA damage; DNA repair; mitochondrial DNA; gene-specific
repair; 8-oxodeoxyguanosine; 8-hydroxydeoxyguanosine; DNA adduct;
Chinese hamster ovary (CHO)
ID DIHYDROFOLATE-REDUCTASE GENE; OXIDATIVE DAMAGE; ESCHERICHIA-COLI;
PYRIMIDINE DIMERS; ACRIDINE-ORANGE; FREE SYSTEMS; DHFR GENE;
8-HYDROXYGUANINE; AGENTS; CANCER
AB This study examines the capacity of a mammalian cell to repair, at the gene level, DNA base lesions generated by photoactivation of acridine orange. Chinese hamster ovary fibroblasts were exposed to acridine orange and visible light, and gene-specific DNA repair was measured in the dihydrofolate reductase (DHFR) gene and in the mitochondrial genome. DNA lesions were recognized by Escherichia coli formamidopyrimidine-DNA glycosylase (FPG) which removes predominantly 8-oxodG and the corresponding formamidopyrimidine ring opened bases, and subsequently cleaves the DNA at the resulting apurinic site, FPG-recognized DNA lesions increased linearly with increasing photo-activation of AO, while cell survival was not affected by light alone and was negligibly affected by preincubation with AO in the dark. The frequency of induction of FPG-sensitive DNA damage by photoactivation of AO was similar in the transcribed and non-transcribed nuclear DNA as well as in the mitochondrial DNA. FPG-sensitive sites in the DHFR gene were repaired quickly, with 84% of adducts repaired within 4 h. The lesion frequency, kinetics and percent of repair of non-transcribed genomic DNA did not differ significantly from repair in the active DHFR gene up to 1 h postexposure. At late time points, transcribed DNA was repaired faster than the non-transcribed DNA. Mitochondrial DNA was efficiently repaired, at a rate similar to that in the active nuclear DNA.
C1 CNRS,LAB PHARMACOL & TOXICOL FONDAMENTALES,TOULOUSE,FRANCE.
INST GUSTAVE ROUSSY,VILLEJUIF,FRANCE.
NIA,GENET MOL LAB,NIH,BALTIMORE,MD.
WAYNE STATE UNIV,DETROIT,MI 48202.
NR 50
TC 61
Z9 62
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0921-8777
J9 MUTAT RES-DNA REPAIR
JI Mutat. Res.-DNA Repair
PD DEC 2
PY 1996
VL 364
IS 3
BP 183
EP 192
DI 10.1016/S0921-8777(96)00031-6
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA VW254
UT WOS:A1996VW25400005
PM 8960130
ER
PT J
AU Wakayama, I
Nerurkar, VR
Strong, MJ
Garruto, RM
AF Wakayama, I
Nerurkar, VR
Strong, MJ
Garruto, RM
TI Comparative study of chronic aluminum-induced neurofilamentous
aggregates with intracytoplasmic inclusions of amyotrophic lateral
sclerosis
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
DE immunocytochemistry; Bunina body; spheroid; neurofilament; animal model
ID MOTOR-NEURON DISEASE; ANTERIOR HORN CELLS; SPINAL MUSCULAR-ATROPHY;
BODY-LIKE INCLUSIONS; NEUROFIBRILLARY CHANGES; HYALINE INCLUSIONS;
PARKINSONISM-DEMENTIA; ANIMAL-MODEL; PATHOGENESIS; UBIQUITIN
AB Amyotrophic lateral sclerosis (ALS) is characterized neuropathologically by chromatolysis, Bunina bodies, hyaline inclusions, skein-like inclusions and axonal spheroids, Aluminum, a known neurotoxin, is the cause of dialysis encephalopathy and is considered to be a causative agent in high incidence foci of ALS in the western Pacific. We have developed an experimental model of motor neuron degeneration in New Zealand white rabbits using chronic low-dose intracisternal administration of aluminum and compared the clinical and neuropathological changes to those of human ALS. Aluminum-inoculated rabbits developed progressive hyperreflexia, hypertonia, limb splaying, gait impairment, muscle wasting, hindlimb paralysis and impaired tonic immobility responses without overt encephalopathic features over a 14-month period. Examination of spinal cords from these animals demonstrated the frequent occurrence and progressive development of anterior horn cell lesions that included small, round, argentophilic perikaryal inclusions similar to hyaline inclusions seen in human ALS. Other inclusions were more condensed and eosinophilic, while still others had neurofibrillary tangle-like morphologies. Axonal spheroids and neuritic thickenings were also prominent and were identical to those seen in human ALS, We believe that the similar and progressive development of neuropathological changes observed in the chronic aluminum-intoxication model, compared to hu man ALS, warrants further study to aid in understanding the cellular and molecular mechanisms of human motor neuron disease.
C1 NINCDS,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
KANSAI COLL ORIENTAL MED,RES CTR NEUROL DIS,KUMATORI,OSAKA,JAPAN.
NINCDS,CENT NERVOUS SYST STUDIES LAB,NIH,BETHESDA,MD 20892.
JOHN P ROBARTS RES INST,NEURODEGENERAT DIS RES GRP,LONDON,ON N6A 5A5,CANADA.
RI Strong, Michael/H-9689-2012
NR 68
TC 31
Z9 32
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0001-6322
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD DEC
PY 1996
VL 92
IS 6
BP 545
EP 554
PG 10
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA VW431
UT WOS:A1996VW43100002
PM 8960311
ER
PT J
AU Dawson, D
AF Dawson, D
TI Gender differences in the risk of alcohol dependence: United States,
1992
SO ADDICTION
LA English
DT Article
ID PROBLEM DRINKING; INTOXICATION; ADOLESCENCE; CONSUMPTION; PREVALENCE;
STABILITY; WOMEN; MEN
AB Data from a representative sample of US adults revealed that 24% of male life-time drinkers and 15% of female life-time drinkers met the DSM-IV criteria for life-time alcohol dependence, i.e. dependence during the year preceding interview or in any 12-month period prior to that year. The median interval from first drink to onset of dependence was 3.6 years for men and 3.0 years for women. After using survival techniques to adjust for potential gender differences in the exposure to risk of developing alcohol dependence, the cumulative conditional probability of having experienced onset of dependence was 35.1% for men and 24.6% for women. The conditional probability of onset of dependence was equal for men and women in the first year after initiation of drinking, about 30% higher for men in the period 1-4 years after the first drink, and about 45% higher for men thereafter. After using proportional hazard; models to adjust for the effects of age cohort, race and ethnicity, family history of alcoholism and age at first drink, these period-specific risk ratios remained virtually unchanged. Including a measure of average daily ethanol intake during periods of heaviest consumption rendered most of the gender differences statistically insignificant, revealing a slight excess risk of female dependence within the first year after initiation of drinking among the heaviest drinkers and leaving an excess male risk of dependence mostly among individuals with average daily intakes of less than one ounce of ethanol. The results suggest that different frequencies of binge drinking might help to account for these remaining gender differences and that men's and women's relative risk of developing alcohol dependence may vary as a function of life cycle stage, with men's excess risk greatest in the college/young adult years.
C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20852.
NR 36
TC 33
Z9 33
U1 0
U2 2
PU CARFAX PUBL CO
PI ABINGDON
PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE
SN 0965-2140
J9 ADDICTION
JI Addiction
PD DEC
PY 1996
VL 91
IS 12
BP 1831
EP 1842
DI 10.1111/j.1360-0443.1996.tb03812.x
PG 12
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA WB702
UT WOS:A1996WB70200014
PM 8997764
ER
PT J
AU Allen, J
Loman, C
Miller, WR
AF Allen, J
Loman, C
Miller, WR
TI Perspectives on precipitants of relapse
SO ADDICTION
LA English
DT Editorial Material
C1 UNIV NEW MEXICO,DEPT PSYCHOL,ALBUQUERQUE,NM 87131.
RP Allen, J (reprint author), NIAAA,NIH,SUITE 500,6000 EXECUT BLVD,WILLCO BLDG,BETHESDA,MD 20892, USA.
NR 0
TC 4
Z9 4
U1 0
U2 2
PU CARFAX PUBL CO
PI ABINGDON
PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE
SN 0965-2140
J9 ADDICTION
JI Addiction
PD DEC
PY 1996
VL 91
SU S
BP S3
EP S4
DI 10.1111/j.1360-0443.1996.tb02322.x
PG 2
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA WC567
UT WOS:A1996WC56700001
ER
PT J
AU Longabaugh, R
Rubin, A
Stout, RL
Zywiak, WH
Lowman, C
AF Longabaugh, R
Rubin, A
Stout, RL
Zywiak, WH
Lowman, C
TI The reliability of Marlatt's taxonomy for classifying relapses
SO ADDICTION
LA English
DT Article
ID MALE ALCOHOLICS; CUE REACTIVITY; SITUATIONS; DRINKING; EXPOSURE
AB Marlatt's focus on the relapse situation has had a major impact upon research and clinical practice in treating addictions. One component of his work was the development of a taxonomy for classifying precipitants of relapse. This taxonomy has been incorporated into the nomenclature of clinicians and clinical researchers as part of an explanatory framework for understanding relapses. Despite the taxonomy's influence it has never been examined for the reliability of its use across research studies. The present study compared the reliability of independent classifications of 149 relapse episodes by trained raters at three research laboratories. Despite considerable across-laboratory training, reliability was found to be inconsistent for research purposes. It is concluded that comparability of results based on Marlatt's relapse taxonomy across independent studies must be subject to question, and assumptions necessary for the aggregation of a Knowledge base are not supported. Recommendations are offered for improving the reliability of the taxonomy and the methods used to collect taxonomy data. More generally, questions regarding the value of the specific relapse categories, as well as the overall taxonomy, are raised.
C1 RES INST ADDICT,BUFFALO,NY 14203.
NIAAA,ROCKVILLE,MD 20852.
RP Longabaugh, R (reprint author), BROWN UNIV,CTR ALCOHOL & ADDICT STUDIES,SCH MED,BOX G,PROVIDENCE,RI 02912, USA.
FU ADAMHA HHS [ADM 281-91-0011]
NR 28
TC 20
Z9 20
U1 0
U2 0
PU CARFAX PUBL CO
PI ABINGDON
PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE
SN 0965-2140
J9 ADDICTION
JI Addiction
PD DEC
PY 1996
VL 91
SU S
BP S73
EP S88
DI 10.1111/j.1360-0443.1996.tb02328.x
PG 16
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA WC567
UT WOS:A1996WC56700007
PM 8997782
ER
PT J
AU Lowman, C
Allen, J
Stout, RL
Connors, GJ
Longabaugh, R
Maisto, SA
Miller, WR
Rubin, A
Waldron, D
Westerberg, VS
Zywiak, WH
AF Lowman, C
Allen, J
Stout, RL
Connors, GJ
Longabaugh, R
Maisto, SA
Miller, WR
Rubin, A
Waldron, D
Westerberg, VS
Zywiak, WH
TI Replication and extension of Marlatt's taxonomy of relapse precipitants:
Overview of procedures and results
SO ADDICTION
LA English
DT Article
ID COPING BEHAVIORS; ALCOHOLICS
AB The Relapse Replication and Extension Project (RREP) was a multisite study to replicate and extend Marlatt's taxonomy of relapse precipitants. In addition to replicating Marlatt's original taxonomic system, three independent research teams utilized prospective designs to identify additional predictors of relapse and developed and evaluated two alternative systems for assessing high risk relapse situations. This overview describes the replication methodology, summarizes seven RREP studies completed by the three research groups, and discusses five cross-cutting conclusions emerging from the studies. These conclusions are: (1) reliability of Marlatt's taxonomic system was variable both within and across the three research sites; (2) Marlatt's taxonomic system showed little predictive validity in analyses that used pretreatment relapse data to predict post-treatment relapse, but there are important unresolved issues; (3) an alternative taxonomy provided little more predictive validity than the original taxonomy even though it measured more dimensions of relapse situations and provided greater analytic flexibility; (4) the Reasons for Drinking Questionnaire appeared to be a successful psychometric transformation of Marlatt's taxonomy, one which did demonstrate predictive validity; and (5) Marlatt's taxonomy was based on a time-intensive model of relapse prediction whereas RREP prospective analyses represented time-extensive models of relapse prediction. Coping responses are noted to be effective predictors of relapse under both models.
C1 BROWN UNIV,CTR ALCOHOL & ADDICT STUDIES,PROVIDENCE,RI 02912.
RP Lowman, C (reprint author), NIAAA,NIH,WILCO BLDG,SUITE 505,6000 EXECUT BLVD,BETHESDA,MD 20892, USA.
FU ADAMHA HHS [ADM 281-91 0006, ADM 281-91 0007, ADM 281-91-0011]
NR 51
TC 56
Z9 57
U1 0
U2 9
PU CARFAX PUBL CO
PI ABINGDON
PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE
SN 0965-2140
J9 ADDICTION
JI Addiction
PD DEC
PY 1996
VL 91
SU S
BP S51
EP S71
DI 10.1111/j.1360-0443.1996.tb02327.x
PG 21
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA WC567
UT WOS:A1996WC56700006
PM 8997781
ER
PT J
AU Lauermann, V
Peden, K
Boeke, JD
AF Lauermann, V
Peden, K
Boeke, JD
TI Alternative tRNA primers for HIV
SO AIDS
LA English
DT Letter
ID IMMUNODEFICIENCY-VIRUS TYPE-1; TRANSFER-RNA; NUCLEOTIDE-SEQUENCE;
RHESUS-MONKEYS; BINDING-SITE; AIDS VIRUS; RETROTRANSPOSITION; DEFECT;
TY1
C1 US FDA,CTR BIOL EVALUAT & RES,LAB RETROVIRUS RES,BETHESDA,MD 20892.
JOHNS HOPKINS UNIV,SCH MED,DEPT MOL BIOL & GENET,BALTIMORE,MD 21205.
RP Lauermann, V (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS BASIC RES PROGRAM,FREDERICK,MD 21702, USA.
NR 19
TC 2
Z9 2
U1 0
U2 0
PU RAPID SCIENCE PUBLISHERS
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH
SN 0269-9370
J9 AIDS
JI Aids
PD DEC
PY 1996
VL 10
IS 14
BP 1738
EP 1740
PG 3
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA VY172
UT WOS:A1996VY17200021
PM 8970697
ER
PT J
AU Yanovski, JA
Yanovski, SZ
Filmer, KM
Hubbard, VS
Avila, N
Lewis, B
Reynolds, JC
Flood, M
AF Yanovski, JA
Yanovski, SZ
Filmer, KM
Hubbard, VS
Avila, N
Lewis, B
Reynolds, JC
Flood, M
TI Differences in body composition of black and white girls
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE visceral adipose tissue; race; blacks; whites; magnetic resonance
imaging; dual-energy X-ray absorptiometry; anthropometry; bioelectrical
impedance analysis
ID MASS INDEX; BIOELECTRIC IMPEDANCE; CHILDREN; FAT; OBESITY; WOMEN;
HEALTH; ALDOSTERONE; GREATER; ADULTS
AB Adults have racial differences in body composition that may modulate risks resulting from obesity. Although black and white children have been shown previously to have differences in bone mineral density and subcutaneous body fat, differences in visceral adipose tissue have not been evaluated. We studied 20 black and 20 white normal-weight girls aged 7-10 y, who were matched for weight, body mass index (BMI), bone age, chronological age, Tanner breast stage, and socioeconomic status. Each underwent anthropometric measurements, bioelectrical impedance analysis, dual-energy X-ray absorptiometry (DXA), and abdominal magnetic resonance imaging (MRI) for determination of total (TAT), visceral (VAT), and subcutaneous (SAT) adipose tissue. Serum lipids and fasting and 2-h oral-glucose-tolerance test (OGTT) glucose and insulin concentrations were also measured. There were no differences between groups in absolute waist circumference or waist-to-hip ratio, but waist-to-thigh ratio was smaller in black than in white girls. Black girls had greater bone mineral density and less TAT, VAT, and SAT than whites. VAT was not significantly correlated with any measure of insulin, or with serum lipids. However, both basal and 2-h OGTT serum insulin were significantly correlated with SAT as assessed by MRI in black girls (r(2) = 0.46 for basal insulin, P = 0.001; r(2) = 0.31 for 2-h insulin, P = 0.01) but not in white girls (r(2) < 0.05, for basal and 2-h insulin, NS). We conclude that there are significant racial differences in body composition and differences in the strength of association between abdominal adipose tissue depots and insulin sensitivity in black and white girls.
C1 NIDDK, DIV DIGEST DIS & NUTR, NIH, BETHESDA, MD USA.
RP Yanovski, JA (reprint author), NICHHD, WARREN GRANT MAGNUSON CLIN CTR, DEV ENDOCRINOL BRANCH,NIH,MSC 1862,BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA.
NR 39
TC 105
Z9 106
U1 0
U2 2
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD DEC
PY 1996
VL 64
IS 6
BP 833
EP 839
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA VU814
UT WOS:A1996VU81400001
PM 8942404
ER
PT J
AU Dorgan, JF
Judd, JT
Longcope, C
Brown, C
Schatzkin, A
Clevidence, BA
Campbell, WS
Nair, PP
Franz, C
Kahle, L
Taylor, PR
AF Dorgan, JF
Judd, JT
Longcope, C
Brown, C
Schatzkin, A
Clevidence, BA
Campbell, WS
Nair, PP
Franz, C
Kahle, L
Taylor, PR
TI Effects of dietary fat and fiber on plasma and urine androgens and
estrogens in men: A controlled feeding study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE diet; dietary fats; dietary fiber; estrogen; androgens
ID HORMONE-BINDING GLOBULIN; PROSTATE-CANCER RISK; SERUM SEX-HORMONES; FREE
TESTOSTERONE; ADULT MEN; WOMEN; VEGETARIAN; INTERRELATIONSHIPS;
CONSUMPTION; ESTRADIOL
AB We conducted a controlled feeding study to evaluate the effects of fat and fiber consumption on plasma and urine sex hormones in men. The study had a crossover design and included 43 healthy men aged 19-56 y. Men were initially randomly assigned to either a low-fat, high-fiber or high-fat, low-fiber diet for 10 wk and after a 2-wk washout period crossed over to the other diet. The energy content of diets was varied to maintain constant body weight but averaged approximate to 13.3 MJ (3170 kcal)/d on both diets. The low-fat diet provided 18.8% of energy from fat with a ratio of polyunsaturated to saturated fat (P:S) of 1.3, whereas the high-fat diet provided 41.0% of energy from fat with a P:S of 0.6. Total dietary fiber consumption from the low- and high-fat diets averaged 4.6 and 2.0 g . MJ(-1) . d(-1), respectively. Mean plasma concentrations of total and sex-hormone-binding-globulin (SHBG)-bound testosterone were 13% and 15% higher, respectively, on the high-fat, low-fiber diet and the difference from the low-fat, high-fiber diet was significant for the SHBG-bound fraction (P = 0.04). Men's daily urinary excretion of testosterone also was 13% higher with the high-fat, low-fiber diet than with the low-fat, high-fiber diet (P = 0.01). Conversely, their urinary excretion of estradiol and estrone and their 2-hydroxy metabolites were 12-28% lower with the high-fat, low-fiber diet (P less than or equal to 0.01). Results of this study suggest that diet may alter endogenous sex hormone metabolism in men.
C1 ARS,DIET & HUMAN PERFORMANCE LAB,USDA,BELTSVILLE,MD.
UNIV MASSACHUSETTS,SCH MED,DEPT OBSTET & GYNECOL,WORCESTER,MA.
UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA.
INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD.
RP Dorgan, JF (reprint author), NCI,DIV CANC PREVENT & CONTROL,CPSA,EXECUT PLAZA N,ROOM 211,6130 EXECUT BLVD,BETHESDA,MD 20892, USA.
RI Perez , Claudio Alejandro/F-8310-2010
OI Perez , Claudio Alejandro/0000-0001-9688-184X
NR 45
TC 110
Z9 113
U1 0
U2 7
PU AMER SOC CLIN NUTRITION INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD DEC
PY 1996
VL 64
IS 6
BP 850
EP 855
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA VU814
UT WOS:A1996VU81400004
PM 8942407
ER
PT J
AU Witte, JS
Longnecker, MP
Bird, CL
Lee, ER
Frankl, HD
Haile, RW
AF Witte, JS
Longnecker, MP
Bird, CL
Lee, ER
Frankl, HD
Haile, RW
TI Relation of vegetable, fruit, and grain consumption to colorectal
adenomatous polyps
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE case-control studies; cereals; colonic neoplasms; diet; fruit; garlic;
vegetables
ID COLON-CANCER; ANTIOXIDANT VITAMINS; DIETARY; EPIDEMIOLOGY; FOOD; RISK;
PREVENTION; QUESTIONNAIRE; RECURRENCE; HEALTH
AB Previous studies suggest that colorectal cancer risk decreases with higher intake of vegetables, fruits, and grains. Few studies, however, have examined these factors in relation to occurrence of colorectal polyps. The authors used case-control data from 488 matched pairs to evaluate associations of vegetables, fruits, and grains with polyps. Subjects were southern Californians aged 50-74 years who had a sigmoidoscopy in 1991-1993. Diet in the year before sigmoidoscopy was measured with a food frequency questionnaire. Frequent consumption of vegetables, fruits, and grains was associated with decreased polyp prevalence. Specifically, the adjusted odds ratio comparing the highest with the lowest quintile of intake for vegetables was 0.47 (95% confidence interval (CI) 0.29-0.76), for fruits was 0.65 (95% CI 0.40-1.05), and for grains was 0.55 (95% CI 0.33-0.91). The authors also found inverse associations for high carotenoid vegetables, cruciferae, high vitamin C fruits, garlic, and tofu (or soybeans). After further adjusting for potentially anticarcinogenic constituents of these foods, high carotenoid vegetables, cruciferous vegetables, garlic, and tofu (or soybeans) remained inversely associated with polyps. These findings support the hypothesis that high intake of vegetables, fruits, or grains decreases the risk of polyps and suggest that any protective effects might reflect unmeasured constituents in these foods.
C1 NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC.
UNIV SO CALIF,SCH MED,DEPT PREVENT MED,LOS ANGELES,CA 90033.
KAISER PERMANENTE MED CTR,DIV GASTROENTEROL BELLFLOWER,LOS ANGELES,CA 90034.
KAISER PERMANENTE MED CTR,DIV GASTROENTEROL SUNSET,LOS ANGELES,CA 90034.
RP Witte, JS (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,METROHLTH MED CTR,DEPT EPIDEMIOL & BIOSTAT,2500 METROHLTH DR,CLEVELAND,OH 44109, USA.
OI Longnecker, Matthew/0000-0001-6073-5322
FU NCI NIH HHS [CA 09142, CA 51923]
NR 37
TC 118
Z9 119
U1 0
U2 6
PU AMER J EPIDEMIOLOGY
PI BALTIMORE
PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 1996
VL 144
IS 11
BP 1015
EP 1025
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA VV535
UT WOS:A1996VV53500002
PM 8942431
ER
PT J
AU Klebanoff, MA
Clemens, JD
Read, JS
AF Klebanoff, MA
Clemens, JD
Read, JS
TI Maternal smoking during pregnancy and childhood cancer
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE carcinogens; cohort studies; neoplasms; pregnancy; smoking
ID PARENTS SMOKING; RISK; EXPOSURE
AB The association between maternal smoking during pregnancy and childhood cancer was investigated using prospectively collected data from 54,795 liveborn children in the Collaborative Perinatal Project (1959-1966). Cases of cancer had a histologic diagnosis and/or a compatible clinical course. There were 51 children with cancer, for a cumulative incidence of cancer of 1.1 per 1,000 by 96 months of age. Maternal smoking was determined al each prenatal visit; 52% of mothers reported smoking at one or more visits. By age 8 years, cancer had occurred in 1.4 per 1,000 children whose mothers did not smoke during pregnancy, compared with 0.9 per 1,000 children whose mothers smoked (p = 0.15 by log rank test); the hazard ratio was 0.67 (95% confidence interval (CI) 0.38-1.17). There was no dose-response effect of smoking compared with nonsmokers (hazard ratio for one to 10 cigarettes/day = 0.45, more than 10 cigarettes/day = 0.83). The hazard ratio for leukemia among children whose mothers smoked was 0.82 (95% CI 0.31-2.11); the hazard ratio for cancers other than leukemia was 0.60 (95% CI 0.30-1.20). Adjustment did not change the hazard ratio substantially. Although the relatively small number of cases precluded extensive study of individual types of cancer, the authors conclude that maternal smoking during pregnancy is not associated with an increased risk of childhood cancer in this cohort.
RP Klebanoff, MA (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,NIH,6100 BLDG,ROOM 7B03,BETHESDA,MD 20892, USA.
NR 22
TC 39
Z9 40
U1 0
U2 0
PU AMER J EPIDEMIOLOGY
PI BALTIMORE
PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 1996
VL 144
IS 11
BP 1028
EP 1033
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA VV535
UT WOS:A1996VV53500004
PM 8942433
ER
PT J
AU Szklo, M
Cerhan, J
DiezRoux, AV
Chambless, L
Cooper, L
Folsom, AR
Fried, LP
Knopman, D
Nieto, FJ
AF Szklo, M
Cerhan, J
DiezRoux, AV
Chambless, L
Cooper, L
Folsom, AR
Fried, LP
Knopman, D
Nieto, FJ
TI Estrogen replacement therapy and cognitive functioning in the
atherosclerosis risk in communities (ARIC) study
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE cognition; cognition disorders; estrogen replacement therapy; menopause;
women's health
ID DENDRITIC SPINE DENSITY; RAT PREOPTIC AREA; ALZHEIMERS-DISEASE; BASAL
FOREBRAIN; OLDER PERSONS; FEMALE RATS; WOMEN; POPULATION; RECEPTORS;
MORTALITY
AB The association of estrogen replacement therapy (ERT) with cognitive functioning was assessed in 6,110 women aged 48-67 years participating in the Atherosclerosis Risk in Communities (ARIC) study, a multicenter longitudinal investigation. ERI was evaluated in relation to results of three cognitive tests (the Delayed Word Recall (DWR) Test, the Digit Symbol Subtest of the Wechsler Adult Intelligence Scale-Revised (DSS/WAIS-R), and the Word Fluency (WF) Test) using data from the first follow-up visit of the cohort (1990-1992). No consistent associations were seen between ERT and either the DWR test or the DSS/WAIS-R after adjusting for age, education, and additional covariates previously found to be associated with cognitive function scores. Among surgically menopausal women aged 48-57 years, adjusted mean WF scores were slightly greater in ERT current users (mean WF 35.9) than in never users (mean WF 33.5) (p < 0.02); and within current users, adjusted WF scores increased with duration of ERT use. However, the finding that ERT was associated with a slightly higher level of performance on only one of three measures offers little support for the hypothesis that ERT has a major protective effect on cognitive function in women less than 68 years of age. The generalizability of these findings to older women who are more likely to experience cognitive decline and who may be using ERT for longer periods of time is limited by the relatively young age of the cohort.
C1 UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242.
UNIV N CAROLINA,SCH PUBL HLTH,DEPT BIOSTAT,COLLABORAT STUDIES COORDINATING CTR,CHAPEL HILL,NC.
NHLBI,NIH,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892.
UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455.
JOHNS HOPKINS MED INST,WELCH CTR PREVENT EPIDEMIOL & CLIN RES,BALTIMORE,MD 21205.
UNIV MINNESOTA,DEPT NEUROL,MINNEAPOLIS,MN 55455.
RP Szklo, M (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,605 N WOLFE ST,BALTIMORE,MD 21205, USA.
FU NHLBI NIH HHS [N01-HC-55015, N01-HC-55016, N01-HC-55018]
NR 46
TC 60
Z9 61
U1 1
U2 1
PU AMER J EPIDEMIOLOGY
PI BALTIMORE
PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 1996
VL 144
IS 11
BP 1048
EP 1057
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA VV535
UT WOS:A1996VV53500007
PM 8942436
ER
PT J
AU Ioannidis, JPA
Cappelleri, JC
Schmid, CH
Lau, J
AF Ioannidis, JPA
Cappelleri, JC
Schmid, CH
Lau, J
TI Impact of epidemic and individual heterogeneity on the population
distribution of disease progression rates - An example from patient
populations in trials of human immunodeficiency virus infection
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE HIV; latency; models; statistical; randomized controlled trials; study
design; survival
ID PLACEBO-CONTROLLED TRIAL; PNEUMOCYSTIS-CARINII PNEUMONIA; DEFERRED
ZIDOVUDINE THERAPY; AIDS-RELATED COMPLEX; CUBIC MILLIMETER; HIV-1
INFECTION; UNITED-STATES; DOUBLE-BLIND; CLINICAL-TRIALS; NATURAL-HISTORY
AB Patients at the same stage of a chronic disease may have had different rates of disease progression. The authors developed a mathematical modeling approach that allows reconstructing and comparing populations in terms of the disease progression rates of their participants when the disease onset and progression rates are unknown for individual patients. Human immunodeficiency virus 1 infection was used as an example. Both published and hypothetical models were used to describe the human immunodeficiency virus 1 epidemic (epidemic heterogeneity) and incubation and survival functions for different disease stages (individual heterogeneity). Reconstructions of populations with late disease (e.g., acquired immunodeficiency syndrome patients) show a marked predominance of rapid progressors, unless the incidence of new infections has been decreasing for a long time. Rapid progressors would also predominate in populations of acute seroconverters, unless diagnosis is based on repeated serologic screening rather than symptoms. Populations of patients who have not progressed beyond an early stage of the disease (e.g., patients with CD4 cell counts >500/mu l) tend to overrepresent slow progressors, especially if the epidemic has been decreasing for a long time. With this approach, one can assess whether the target population of a clinical trial is comparable with other patient populations at different places and times. Epidemic and individual diversity may even affect trial results if patients with different progression rates experience different benefits from a treatment. By modeling the targeted populations in trials of early versus deferred antiretroviral treatment, the authors observed larger treatment benefits in trials in which rapid progressors probably predominated, compared with trials of slow progressors.
C1 TUFTS UNIV NEW ENGLAND MED CTR,DIV CLIN CARE RES,BOSTON,MA.
TUFTS UNIV NEW ENGLAND MED CTR,BIOSTAT RES CTR,BOSTON,MA.
TUFTS UNIV,SCH MED,BOSTON,MA 02111.
RP Ioannidis, JPA (reprint author), NIAID,NIH,HIV RES BRANCH,THERAPEUT RES PROGRAM,SOLAR BLDG,ROOM 2C15,6003 EXECUT BLVD,BETHESDA,MD 20892, USA.
RI Ioannidis, John/G-9836-2011;
OI Schmid, Christopher/0000-0002-0855-5313
FU AHRQ HHS [R01 HS 07782]; NIAID NIH HHS [T32 AI07389]
NR 50
TC 25
Z9 25
U1 0
U2 0
PU AMER J EPIDEMIOLOGY
PI BALTIMORE
PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD DEC 1
PY 1996
VL 144
IS 11
BP 1074
EP 1085
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA VV535
UT WOS:A1996VV53500011
PM 8942440
ER
PT J
AU Martinez, RA
Mulsant, BH
Meyers, BS
Lebowitz, BD
AF Martinez, RA
Mulsant, BH
Meyers, BS
Lebowitz, BD
TI Delusional and psychotic depression in late life - Clinical research
needs
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
ID ELECTROCONVULSIVE-THERAPY; FOLLOW-UP; MEDICATION RESISTANCE;
AFFECTIVE-DISORDERS; MAJOR DEPRESSION; OLD-AGE; SUICIDE; UNIPOLAR;
MELANCHOLIA; LEUKOENCEPHALOPATHY
AB Psychotic depression in younger patients has been associated with an increased rate of suicide, refractoriness to somatic treatment, and overall poor prognosis. However, the public health and scientific significance of this disorder in older patients has received limited attention in the past two decades; the topic was excluded from the 1991 NIH Consensus Development Conference on the Diagnosis and Treatment of Depression in Late Life. To address this obvious need in the field, a special work-group of recognized experts met in a special NIMH workshop to review and discuss clinical issues and key research questions. This is a report of that workshop's proceedings.
C1 NIMH,MENTAL DISORDERS AGING RES BRANCH,ROCKVILLE,MD 20857.
NR 59
TC 13
Z9 13
U1 0
U2 0
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD WIN
PY 1996
VL 4
IS 1
BP 77
EP 84
PG 8
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA TL531
UT WOS:A1996TL53100009
ER
PT J
AU Williams, S
Linardic, C
Wilson, O
Comp, P
Gralnick, HR
AF Williams, S
Linardic, C
Wilson, O
Comp, P
Gralnick, HR
TI Acquired hypoprothrombinemia: Effects of Danazol(R) treatment
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
DE hypoprothrombinemia; lupus anticoagulant; discoid lupus erythematosus;
Danazol(R); factor II; factor IX; factor X; protein C; protein S
ID SYSTEMIC LUPUS-ERYTHEMATOSUS; PROTHROMBIN; ANTICOAGULANT; ANTIBODIES;
MECHANISM; ASSAY
AB The lupus anticoagulant may be accompanied by an acquired factor II deficiency and bleeding. We report on a patient with a lupus anticoagulant and factor II (FII) deficiency responsive to Danazol(R). Acquired hypoprothrombinemia (FII) with the lupus anticoagulant (LA) may be accompanied by a hemorrhagic diathesis. A 64-year-old male with discoid lupus erythematosis bled after an intestinal polypectomy. His FII level was 18%, and his FII antigen level was 20%. Danazol(R) (D) (600 mg per day) administration was associated with a rise in FII activity and antigen to 50% within 10 days. The patient underwent abdominal surgery. We studied the effect(s) of D on the FII level and on other coagulation factors in this patient. The patient's plasma FII antigen had a single precipitin are compared to the two peaks of normal plasma on counterimmunoelectrophoresis with Ca++. The samples pre- and during D therapy had the same positively charged are as normal samples, although they were quantitatively different. Neuraminidase treatment demonstrated a decrease in the positively charged migration of normal and the patient's FII antigen. Affinity chromatography of normal and patient plasma on a Sepharose protein A column revealed FII antigen present in the patient's bound fraction. The relative percentages of bound FII before and during D treatment were similar. During D therapy, levels of FIX and X rose 50-100%, and protein C rose 20-25%, while free protein S did not change. D is an effective therapy for acquired FII deficiency associated with LA. D does not affect the binding of Ig to FII, but D raises FII levels by increasing synthesis of the FII protein. (C) 1996 Wiley-Liss, Inc.
C1 NIH,DEPT CLIN HEMATOL,BETHESDA,MD 20892.
UNIV OKLAHOMA,OKLAHOMA CITY,OK.
NR 12
TC 11
Z9 11
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 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD DEC
PY 1996
VL 53
IS 4
BP 272
EP 276
DI 10.1002/(SICI)1096-8652(199612)53:4<272::AID-AJH14>3.0.CO;2-E
PG 5
WC Hematology
SC Hematology
GA VV478
UT WOS:A1996VV47800014
PM 8948670
ER
PT J
AU Zheng, CJ
Byers, B
AF Zheng, CJ
Byers, B
TI Implications of the oocyte-selection hypothesis: A response
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Letter
ID MATERNAL-AGE; MITOTIC ERRORS; TRISOMY-21
C1 UNIV WASHINGTON,DEPT GENET,SEATTLE,WA 98195.
RP Zheng, CJ (reprint author), NIDCD,EPIDEMIOL STAT & DATA SYST BRANCH,NIH,6120 EXECUT BLVD EPS 432,BETHESDA,MD 20892, USA.
NR 10
TC 3
Z9 3
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD DEC
PY 1996
VL 59
IS 6
BP 1397
EP 1398
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA VV315
UT WOS:A1996VV31500029
ER
PT J
AU Sparks, SM
AF Sparks, SM
TI Use of the Internet for infection control and epidemiology
SO AMERICAN JOURNAL OF INFECTION CONTROL
LA English
DT Article
AB Infection control professionals are taking advantage of the Internet for the rapid transmission and distribution of information that includes sounds, still and motion images, and text to their peers, colleagues, patients, and the public. This article provides some background information on the Internet and examples of some electronic resources and offers suggestions of additional applications of the Internet for infection control and epidemiology.
RP Sparks, SM (reprint author), NATL LIB MED,DIV EXTRAMURAL PROGRAMS,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA.
NR 0
TC 5
Z9 5
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0196-6553
J9 AM J INFECT CONTROL
JI Am. J. Infect. Control
PD DEC
PY 1996
VL 24
IS 6
BP 435
EP 439
DI 10.1016/S0196-6553(96)90037-1
PG 5
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA VY556
UT WOS:A1996VY55600004
PM 8974169
ER
PT J
AU Buckalew, VM
Berg, RL
Wang, SR
Porush, JG
Rauch, S
Schulman, G
AF Buckalew, VM
Berg, RL
Wang, SR
Porush, JG
Rauch, S
Schulman, G
TI Prevalence of hypertension in 1,795 subjects with chronic renal disease:
The modification of diet in renal disease study baseline cohort
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE hypertension; chronic renal disease; risk factors
ID POLYCYSTIC KIDNEY-DISEASE; BLOOD-PRESSURE; CHRONIC GLOMERULONEPHRITIS;
WEIGHT-LOSS; BODY-MASS; FAILURE; SENSITIVITY; SODIUM; INSUFFICIENCY;
PROGRESSION
AB The Modification of Diet in Renal Disease Study was a multicenter trial of the effect of protein restriction and strict blood pressure control on the progression rate of chronic renal failure of multiple causes. At the first baseline visit, 1,795 screened patients with renal disease had blood pressure measured, antihypertensive medications recorded, glomerular filtration rate (GFR) determined by I-125-iothalamate clearance, a nutritional assessment, and a 24-hour urine collection to determine sodium and potassium levels, A total of 1,494 patients in this cohort were classified as hypertensive (83%) and the remainder (301 patients) as nonhypertensive. Ninety-one percent of the hypertensive subjects were on treatment, 54% being controlled to a blood pressure of less than or equal to 140/90 mm Hg, To better understand the factors that contribute to the development of hypertension in chronic renal disease, some determinants of the prevalence of hypertension in this cohort were investigated, Compared with normotensive subjects, hypertensive patients were older (51.2 +/- 12.7 years v 46.6 +/- 13.1 years [mean +/- SD]), had a higher body mass index (BMI; 27.5 +/- 4.7 kg/m(2) v 25.4 +/- 4.2 kg/m(2)), and had a lower GFR (37.8 +/- 19.6 ml/min/1.73 m(2) v 50.1 +/- 25 mL/min/1.73 m(2)). All these differences were significant (P < 0.01). The prevalence of hypertension was significantly higher for men than for women (86% v 80%; P = 0.001), and for blacks than for whites (93% v 81%; P < 0.001). The prevalence of hypertension was higher in subjects with glomerular disease than in those with tubulointerstitial disease (85% v 62.6%; P < 0.001), The prevalence of hypertension varied inversely with GFR (from 66% at a GFR of 83 mL/min/1.73 m(2) to 95% at a GFR of 12 ml/min/1.73 m(2)). The prevalence of hypertension varied directly with BMI (from 70% with a BMI at the 10th percentile to 94% with a BMI at the 97th percentile), This relationship was independent of GFR. Multiple logistic regression analysis showed five predictors in decreasing order of significance as determined by chi-square values: GFR, 83.2; BMI, 36.7; black race, 19.9; increasing age, 14.5 (all P < 0.001); and male gender, 5.1 (P = 0.024). Salt intake was not a determinant of blood pressure status, These results confirm previous reports indicating that hypertension in renal disease is determined by the level of renal function, For the first time, three factors known to predict blood pressure levels in populations with normal renal function were also shown to be determinants of blood pressure in renal disease: BMI, black race, and age, In addition, the data suggest that hypertension is inadequately treated in more than half of patients with chronic renal disease in the United States. (C) 1996 by the National Kidney Foundation, Inc.
C1 NIDDK,NIH,BETHESDA,MD.
NR 44
TC 139
Z9 141
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD DEC
PY 1996
VL 28
IS 6
BP 811
EP 821
DI 10.1016/S0272-6386(96)90380-7
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA VX333
UT WOS:A1996VX33300004
PM 8957032
ER
PT J
AU Goldenberg, RL
DuBard, MB
Cliver, SP
Nelson, KG
Blankson, K
Ramey, SL
Herman, A
AF Goldenberg, RL
DuBard, MB
Cliver, SP
Nelson, KG
Blankson, K
Ramey, SL
Herman, A
TI Pregnancy outcome and intelligence at age five years
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE preterm birth; growth restriction; intelligence
ID LOW-BIRTH-WEIGHT; FETAL GROWTH-RETARDATION; MENTAL-RETARDATION;
GESTATIONAL-AGE; INFANTS; CHILDREN; TERM; METAANALYSIS; PREVALENCE;
PRETERM
AB OBJECTIVE: Our purpose was to determine the influence of being small for gestational age at term and being preterm <34 weeks on cognitive functioning at age 5 years.
STUDY DESIGN: Five hundred forty-six children of black low-income mothers, nearly all at risk for being small for gestational age, followed up prenatally with early ultrasonographic gestational age dating, were classified as either term appropriate for gestational age, term small for gestational age, or preterm at <34 weeks. At a mean of 5.5 +/- 0.5 years, a Wechsler Preschool and Primary Scale of Intelligence-Revised intelligence quotient test was administered. An intelligence quotient <70 was used to define mental retardation. Univariate and multivariate analyses adjusted for maternal age, smoking, education and language skills, home environment, and child gender and preschool attendance were performed.
RESULTS: Term small-for-gestational-age and preterm infants at <34 weeks had 4 and 6 point intelligence quotient reductions compared with term appropriate-for-gestational-age infants. In the regression analyses these differences in intelligence quotient remained significant after confounders were adjusted. High maternal receptive language level (8 points), a positive home environment (5 points), and attendance at preschool (5 points) were each significantly associated with an increase in intelligence quotient.
CONCLUSION: Both term small-for-gestational-age infants and those born at <34 weeks had a significantly lower mean intelligence quotient, and small-for-gestational-age infants had an increased risk of mental retardation at age 5 years. Higher maternal language skills, a positive home environment, and attendance at preschool each were associated with an increase in the mean intelligence quotient of 5 to 7 points.
C1 UNIV ALABAMA,DEPT OBSTET & GYNECOL,BIRMINGHAM,AL 35294.
UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL 35294.
NICHHD,NIH,BETHESDA,MD 20892.
RP Goldenberg, RL (reprint author), UNIV ALABAMA,CTR OBSTET RES,BIRMINGHAM,AL 35294, USA.
FU BHP HRSA HHS [DHHS-282-92-0055]; NICHD NIH HHS [N01-HD-42811]; PHS HHS
[PRP-90-11]
NR 25
TC 56
Z9 56
U1 4
U2 6
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 1996
VL 175
IS 6
BP 1511
EP 1515
DI 10.1016/S0002-9378(96)70099-6
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA WA641
UT WOS:A1996WA64100029
PM 8987934
ER
PT J
AU Alexander, M
Salgaller, ML
Celis, E
Sette, A
Barnes, WA
Rosenberg, SA
Steller, MA
AF Alexander, M
Salgaller, ML
Celis, E
Sette, A
Barnes, WA
Rosenberg, SA
Steller, MA
TI Generation of tumor-specific cytolytic T lymphocytes from peripheral
blood of cervical cancer patients by in vitro stimulation with a
synthetic human papillomavirus type 16 E7 epitope
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE human papillomavirus; vaccine; peptide epitopes; cervical cancer;
cytolytic T lymphocytes
ID CARCINOMA CELL-LINES; INFILTRATING LYMPHOCYTES; CTL EPITOPES; IN-VIVO;
HLA-A; IDENTIFICATION; SEQUENCES; PEPTIDES; E6; EXPRESSION
AB OBJECTIVE: Approximately 90% of squamous carcinomas of the cervix harbor the human papillomavirus and type 16 has been detected in nearly 50% of cases. Recent studies in mice have shown that the human papillomavirus type 16 E7 oncoprotein contains peptide epitopes that are processed and presented in association with a major histocompatibility antigen for recognition by cytolytic T lymphocytes. We investigated whether an epitope from human papillomavirus type 16 E7 could be used to generate specific human cytolytic T lymphocytes in patients with cervical carcinoma.
STUDY DESIGN: After radiation therapy, three patients with antigen HLA-A2 and with locally advanced cervical cancer underwent leukapheresis, Epitope-specific cytolytic T lymphocytes were generated from the peripheral blood mononuclear cells by in vitro stimulation with autologous peripheral blood mononuclear cells pulsed with a human papillomavirus type 16 E7, HLA-A2-restricted, synthetic peptide, E7(11-20) (YMLDLQPETT).
RESULTS: In two patients cytolytic T lymphocytes were capable of E7(11-20)-specific, HLA-A2-restricted cytolysis of the peptide-pulsed, HLA-matched, T2 target cell line. Cytolytic T lymphocytes from one of these patients also demonstrated specific cytolysis against the HLA-A2(+), HPV-16(+) CaSki cervical cancer cell line but did not lyse either HLA-A2(+), HPV-16(-) MS-751 cells or HLA-A2(-), HPV-16(-) HT-3 cells.
CONCLUSIONS: These experiments demonstrate that novel cytolytic T lymphocytes that recognize a human papillomavirus type 16 E7 epitope can be generated by using the peripheral blood mononuclear cells from irradiated patients with cervical cancer. In addition, because CaSki cells were specifically lysed by the cytolytic T lymphocytes, these data indicate that the peptide E7(11-20) is endogenously processed and presented on the cell surface of the CaSki cells. The demonstration of epitope-specific lysis of cytolytic T lymphocytes of HPV-16(+) cervical cancer cells supports further efforts to develop human papillomavirus peptide-based vaccines or antigen-specific adoptive immunotherapy for the prevention and treatment of cervical carcinoma.
C1 NCI,SURG BRANCH,BETHESDA,MD 20892.
GEORGETOWN UNIV,MED CTR,DIV GYNECOL ONCOL,WASHINGTON,DC 20007.
CYTEL CORP,SAN DIEGO,CA 92121.
NR 25
TC 65
Z9 68
U1 0
U2 6
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 1996
VL 175
IS 6
BP 1586
EP 1593
DI 10.1016/S0002-9378(96)70110-2
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA WA641
UT WOS:A1996WA64100040
PM 8987945
ER
PT J
AU Han, DP
Vine, AK
Blodi, BA
Elner, SG
Johnson, MW
Jessup, LM
Khanderia, S
Pierson, CL
Willis, J
McIver, F
Stanley, S
Sneed, SR
Capone, A
Aaberg, TM
Lim, JI
Sternberg, P
Coffman, DS
Moore, CN
Gardner, SK
Nolte, FS
Fremstad, A
Gibbs, D
Gilman, J
Swords, R
Aguilar, HE
Meredith, TA
Lakhanpal, V
Christian, FD
Hood, MA
Schwalbe, RS
Billings, EE
Buie, W
Mallonee, JJ
Millar, MA
Verbeek, S
Campochiaro, PA
Palardy, CB
Reynolds, L
Dick, JD
Cain, D
DAmico, DJ
Frederick, AR
Morley, MG
Pesavento, RD
Puliafito, CA
Topping, TM
Finn, SM
Raymond, LA
Baker, AS
Paton, B
Evans, C
Napoli, J
Kiernan, C
Makris, K
McInnes, T
Reidy, WT
White, R
Garfinkel, RA
Pilkerton, AR
Frantz, RA
Abernathy, GB
Barbaccia, JG
Ensey, HR
Ormes, CA
Park, CH
Caplan, J
Russel, K
Toma, R
Packo, KH
deBustros, S
Flood, TP
Glazer, L
DeAlba, M
Evanich, E
Montwill, MA
Rothman, JJ
Ruderman, G
Beard, M
Landau, W
Shen, MH
Gordon, M
Graff, S
Kwiatkowski, K
Pappas, L
Bryant, D
Doherty, D
Morini, F
Arredondo, L
Garretson, BR
Gerena, C
Hunt, M
Kinnaird, SM
Neri, T
Rice, TA
Novak, MA
Rwe, PS
Jamieson, S
Newberry, D
Rech, GR
Dul, MJ
Kinser, L
Strozewski, K
ClarkRath, S
DeLisio, M
Dempsey, DL
Kukula, D
PinterSmith, A
Rowe, PS
SmithBrewer, S
Ludwig, T
Chambers, RB
Davidorf, FH
Taylor, CS
Hale, KN
Buesching, WJ
Chaudhuri, C
Cover, NJ
Shortlidge, GR
Keating, MJ
Savage, SJ
Andrzejewska, P
Cornetet, S
Milliron, JD
Richmond, R
Schneider, L
Weisenberger, D
Cantrill, HL
Ramsay, RC
Brallier, AB
Johnson, TP
Rossing, EE
Knauth, KA
Monahan, MM
Oestreich, NW
Clark, KF
Glennen, AM
Yarian, DL
Green, SN
Leff, SR
Masciulli, L
Lucido, MM
Ludwig, EJ
Marano, CL
Peters, L
Joho, K
Volkert, DC
Andersen, F
Coffey, D
Schlosser, A
Honeywell, A
Mames, RN
Driebe, WT
Stern, GA
Francis, A
Zam, ZS
Cooper, R
Gaskins, D
Shamis, DJ
Willingham, M
Barker, K
Rosa, H
Friedman, SM
Gardner, TW
Blankenship, GW
Coyle, CJ
Bero, CJ
Halas, C
Schick, S
Walker, J
Cunningham, D
Lambert, HM
Clogston, PS
Frady, PM
Gardner, SN
Osato, MS
Carr, L
Shigley, J
Lopez, PF
Chong, LP
Frambach, DA
Cisneros, L
Padilla, M
Yee, EM
Nakamura, T
Walonker, AF
Morales, R
Nichols, T
Huete, ME
Liggett, PE
Ober, RR
QuillenThomas, B
Williams, M
Barr, CC
Bloom, SM
Greene, PJ
Whittington, GK
Martin, ME
Watson, G
JenkinsCurry, B
Gilkey, LA
Huelsman, S
Burton, TC
Mieler, WF
Pulido, JS
Reeser, FH
Newman, JL
Werner, KA
Pisarzewicz, PJ
Reinerio, NA
Walloch, MLK
Wilmer, Z
Laabs, J
Picchiottino, R
Phillips, J
Wipplinger, W
Abrams, GW
Jurkiewicz, DT
Leet, ML
Mandel, P
Metzger, K
Suchla, L
Zarling, D
Balles, MW
Ryan, EH
Knobloch, WH
Cook, SM
Luke, DG
Ferrieri, P
Schiminsky, NM
Genia, A
Philiph, DA
Stinson, EK
Wright, LM
McMichael, WC
Mielke, SJ
Ponwith, LJ
Pavan, PR
Pautler, SE
Coats, ML
Kirk, NM
Millard, SM
Castellano, FC
Edwards, CR
Marquardt, A
McCormack, AJ
McCormick, MT
Renshaw, B
Restuccia, A
Campbell, M
Christopher, N
Garrett, LS
Halkias, DG
Hothersall, K
MIckler, K
Minnick, TS
Burr, C
Saxon, W
Arcacha, MA
Carlton, S
Edison, SK
Mallis, MJ
Sayers, TL
Sudds, TW
Tiberia, RJ
Wolabaugh, S
Bradford, RH
Parke, DW
Wolf, TC
Shofner, JM
Tobey, LE
Jensen, HG
Sanchez, D
Shofner, J
Burris, R
Drake, KK
Grissom, KR
Rowsey, JJ
Wilkinson, CP
Brown, GC
Benson, WE
Federman, JL
Lucier, AC
Maguire, JI
Sarin, LK
Shakin, EP
Sivalingam, A
Tasman, W
Vander, JF
Ward, N
Weisbecker, CA
Agnew, CL
Lambert, R
Tomer, T
Carlson, K
Franchine, G
Serfass, MS
Doft, BH
Bergren, RL
Lobes, LA
Olsen, KR
Rinkoff, JS
Metz, DJ
Leonard, MN
Karenchak, LM
Kowalski, RP
Wellman, LA
Wilcox, LA
Campbell, AF
Steinberg, DR
Vagstad, GL
Flook, KA
Good, MM
Keenen, BJ
Mellinger, KA
Margherio, RR
Cox, MS
Murphy, PL
Trese, MT
Werner, JC
Williams, GA
Manatrey, PE
Prote, JL
Lucarotti, R
Martin, S
Band, J
Bostic, G
Cumming, K
Mitchell, B
Regan, VS
Bridges, C
Cox, S
Houston, G
Johnson, J
Streasik, P
Wood, B
Blumenkranz, MS
Cayo, L
Kaye, V
Valenzuela, CL
Orgel, IK
Poliner, LS
Tornambe, PE
Cannon, SV
Nielsen, JL
Carlson, A
Chan, P
Drake, L
Grim, M
Peterson, C
Borg, LA
Gillyatt, J
Beyer, C
Hammer, ME
Grizzard, WS
Shannon, TL
Traynom, JR
Collado, MJ
McManus, DW
Sweeney, DE
Adams, DH
Watson, TT
Antworth, MV
Araos, JG
Greenwald, MA
Habib, M
Myers, SK
Ockers, KM
Thibodeau, JA
Watkins, B
Nelsen, PT
Rosenthal, JG
Mintz, FV
Biedenbach, M
Leonardy, NJ
Lawniczak, SM
Bork, C
Hageage, G
Hunter, EB
Marshall, MJ
Roman, P
Hill, R
HOfbauer, T
Lemanowicz, J
Cupples, HP
Guzman, GI
Brodeur, RJ
Yee, D
Delaha, EC
Geyer, SL
Slovis, S
Shields, WJ
Lauber, S
Michelitsch, K
Barza, M
Kassoff, A
Watling, S
Wilson, LA
Buehler, JC
McVay, J
Kelsey, SF
Wisniewski, SR
Podobinski, GK
Sillett, RL
Groer, S
Avery, B
Belle, SH
Boles, J
Henry, L
Shema, SJ
TitusErnstoff, L
Davis, M
Magli, YL
Hubbard, L
Thomas, S
Everett, DF
Mowery, R
Davis, K
Azen, S
Covey, P
McCuen, B
Packer, A
Robbin, J
AF Han, DP
Vine, AK
Blodi, BA
Elner, SG
Johnson, MW
Jessup, LM
Khanderia, S
Pierson, CL
Willis, J
McIver, F
Stanley, S
Sneed, SR
Capone, A
Aaberg, TM
Lim, JI
Sternberg, P
Coffman, DS
Moore, CN
Gardner, SK
Nolte, FS
Fremstad, A
Gibbs, D
Gilman, J
Swords, R
Aguilar, HE
Meredith, TA
Lakhanpal, V
Christian, FD
Hood, MA
Schwalbe, RS
Billings, EE
Buie, W
Mallonee, JJ
Millar, MA
Verbeek, S
Campochiaro, PA
Palardy, CB
Reynolds, L
Dick, JD
Cain, D
DAmico, DJ
Frederick, AR
Morley, MG
Pesavento, RD
Puliafito, CA
Topping, TM
Finn, SM
Raymond, LA
Baker, AS
Paton, B
Evans, C
Napoli, J
Kiernan, C
Makris, K
McInnes, T
Reidy, WT
White, R
Garfinkel, RA
Pilkerton, AR
Frantz, RA
Abernathy, GB
Barbaccia, JG
Ensey, HR
Ormes, CA
Park, CH
Caplan, J
Russel, K
Toma, R
Packo, KH
deBustros, S
Flood, TP
Glazer, L
DeAlba, M
Evanich, E
Montwill, MA
Rothman, JJ
Ruderman, G
Beard, M
Landau, W
Shen, MH
Gordon, M
Graff, S
Kwiatkowski, K
Pappas, L
Bryant, D
Doherty, D
Morini, F
Arredondo, L
Garretson, BR
Gerena, C
Hunt, M
Kinnaird, SM
Neri, T
Rice, TA
Novak, MA
Rwe, PS
Jamieson, S
Newberry, D
Rech, GR
Dul, MJ
Kinser, L
Strozewski, K
ClarkRath, S
DeLisio, M
Dempsey, DL
Kukula, D
PinterSmith, A
Rowe, PS
SmithBrewer, S
Ludwig, T
Chambers, RB
Davidorf, FH
Taylor, CS
Hale, KN
Buesching, WJ
Chaudhuri, C
Cover, NJ
Shortlidge, GR
Keating, MJ
Savage, SJ
Andrzejewska, P
Cornetet, S
Milliron, JD
Richmond, R
Schneider, L
Weisenberger, D
Cantrill, HL
Ramsay, RC
Brallier, AB
Johnson, TP
Rossing, EE
Knauth, KA
Monahan, MM
Oestreich, NW
Clark, KF
Glennen, AM
Yarian, DL
Green, SN
Leff, SR
Masciulli, L
Lucido, MM
Ludwig, EJ
Marano, CL
Peters, L
Joho, K
Volkert, DC
Andersen, F
Coffey, D
Schlosser, A
Honeywell, A
Mames, RN
Driebe, WT
Stern, GA
Francis, A
Zam, ZS
Cooper, R
Gaskins, D
Shamis, DJ
Willingham, M
Barker, K
Rosa, H
Friedman, SM
Gardner, TW
Blankenship, GW
Coyle, CJ
Bero, CJ
Halas, C
Schick, S
Walker, J
Cunningham, D
Lambert, HM
Clogston, PS
Frady, PM
Gardner, SN
Osato, MS
Carr, L
Shigley, J
Lopez, PF
Chong, LP
Frambach, DA
Cisneros, L
Padilla, M
Yee, EM
Nakamura, T
Walonker, AF
Morales, R
Nichols, T
Huete, ME
Liggett, PE
Ober, RR
QuillenThomas, B
Williams, M
Barr, CC
Bloom, SM
Greene, PJ
Whittington, GK
Martin, ME
Watson, G
JenkinsCurry, B
Gilkey, LA
Huelsman, S
Burton, TC
Mieler, WF
Pulido, JS
Reeser, FH
Newman, JL
Werner, KA
Pisarzewicz, PJ
Reinerio, NA
Walloch, MLK
Wilmer, Z
Laabs, J
Picchiottino, R
Phillips, J
Wipplinger, W
Abrams, GW
Jurkiewicz, DT
Leet, ML
Mandel, P
Metzger, K
Suchla, L
Zarling, D
Balles, MW
Ryan, EH
Knobloch, WH
Cook, SM
Luke, DG
Ferrieri, P
Schiminsky, NM
Genia, A
Philiph, DA
Stinson, EK
Wright, LM
McMichael, WC
Mielke, SJ
Ponwith, LJ
Pavan, PR
Pautler, SE
Coats, ML
Kirk, NM
Millard, SM
Castellano, FC
Edwards, CR
Marquardt, A
McCormack, AJ
McCormick, MT
Renshaw, B
Restuccia, A
Campbell, M
Christopher, N
Garrett, LS
Halkias, DG
Hothersall, K
MIckler, K
Minnick, TS
Burr, C
Saxon, W
Arcacha, MA
Carlton, S
Edison, SK
Mallis, MJ
Sayers, TL
Sudds, TW
Tiberia, RJ
Wolabaugh, S
Bradford, RH
Parke, DW
Wolf, TC
Shofner, JM
Tobey, LE
Jensen, HG
Sanchez, D
Shofner, J
Burris, R
Drake, KK
Grissom, KR
Rowsey, JJ
Wilkinson, CP
Brown, GC
Benson, WE
Federman, JL
Lucier, AC
Maguire, JI
Sarin, LK
Shakin, EP
Sivalingam, A
Tasman, W
Vander, JF
Ward, N
Weisbecker, CA
Agnew, CL
Lambert, R
Tomer, T
Carlson, K
Franchine, G
Serfass, MS
Doft, BH
Bergren, RL
Lobes, LA
Olsen, KR
Rinkoff, JS
Metz, DJ
Leonard, MN
Karenchak, LM
Kowalski, RP
Wellman, LA
Wilcox, LA
Campbell, AF
Steinberg, DR
Vagstad, GL
Flook, KA
Good, MM
Keenen, BJ
Mellinger, KA
Margherio, RR
Cox, MS
Murphy, PL
Trese, MT
Werner, JC
Williams, GA
Manatrey, PE
Prote, JL
Lucarotti, R
Martin, S
Band, J
Bostic, G
Cumming, K
Mitchell, B
Regan, VS
Bridges, C
Cox, S
Houston, G
Johnson, J
Streasik, P
Wood, B
Blumenkranz, MS
Cayo, L
Kaye, V
Valenzuela, CL
Orgel, IK
Poliner, LS
Tornambe, PE
Cannon, SV
Nielsen, JL
Carlson, A
Chan, P
Drake, L
Grim, M
Peterson, C
Borg, LA
Gillyatt, J
Beyer, C
Hammer, ME
Grizzard, WS
Shannon, TL
Traynom, JR
Collado, MJ
McManus, DW
Sweeney, DE
Adams, DH
Watson, TT
Antworth, MV
Araos, JG
Greenwald, MA
Habib, M
Myers, SK
Ockers, KM
Thibodeau, JA
Watkins, B
Nelsen, PT
Rosenthal, JG
Mintz, FV
Biedenbach, M
Leonardy, NJ
Lawniczak, SM
Bork, C
Hageage, G
Hunter, EB
Marshall, MJ
Roman, P
Hill, R
HOfbauer, T
Lemanowicz, J
Cupples, HP
Guzman, GI
Brodeur, RJ
Yee, D
Delaha, EC
Geyer, SL
Slovis, S
Shields, WJ
Lauber, S
Michelitsch, K
Barza, M
Kassoff, A
Watling, S
Wilson, LA
Buehler, JC
McVay, J
Kelsey, SF
Wisniewski, SR
Podobinski, GK
Sillett, RL
Groer, S
Avery, B
Belle, SH
Boles, J
Henry, L
Shema, SJ
TitusErnstoff, L
Davis, M
Magli, YL
Hubbard, L
Thomas, S
Everett, DF
Mowery, R
Davis, K
Azen, S
Covey, P
McCuen, B
Packer, A
Robbin, J
TI Microbiologic factors and visual outcome in the endophthalmitis
vitrectomy study
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID STAPHYLOCOCCUS-EPIDERMIDIS ENDOPHTHALMITIS; COAGULASE-NEGATIVE
STAPHYLOCOCCI; INFECTIOUS ENDOPHTHALMITIS; MANAGEMENT; SPECTRUM
AB PURPOSE: To evaluate the relationship between microbiologic factors, effect of treatment, and visual outcome in the Endophthalmitis Vitrectomy Study.
METHODS: Four hundred twenty patients were enrolled in the Endophthalmitis Vitrectomy Study between February 1990 and January 1994. Of these, 394 completed 9 to 12 months of follow-up. Patients presented with features of bacterial endophthalmitis within 6 weeks of cataract extraction or secondary intraocular lens implantation. The relations between visual outcome and the identity of infecting species, gram stain results, antibiotic susceptibilities, and presence of vitrectomy cassette growth were examined.
RESULTS: Rates of achieving final visual acuity of 20/100 or better for the more common isolates were as follows: gram-positive, coagulase-negative micrococci, 84%; Staphylococcus aureus, 50%; streptococci, 30%; enterococci, 14%; and gram-negative organisms, 56%. A positive gram stain or infection with species other than gram-positive, coagulase-negative micrococci were significantly associated with poorer visual outcome (P <.001 for species group comparisons). However, presenting visual acuity was more powerful than microbiologic factors in predicting visual outcome and favorable response to vitrectomy. Bacterial growth from the vitrectomy cassette specimen had prognostic significance equivalent to growth from other intraocular sources.
CONCLUSIONS: Visual prognosis was strongly associated with the type of infecting organism and gram stain positivity. However, visual acuity at initial presentation appeared to be more useful than microbiologic factors in predicting visual outcome and judging the value of immediate vitrectomy in acute bacterial endophthalmitis after cataract surgery.
C1 UNIV MICHIGAN,ANN ARBOR,MI 48109.
EMORY EYE CTR,ATLANTA,GA.
UNIV MARYLAND,EYE ASSOCIATES,BALTIMORE,MD 21201.
JOHNS HOPKINS UNIV,BALTIMORE,MD.
MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114.
RETINA GRP WASHINGTON,CHEVY CHASE,MD.
RUSH UNIV,INGALLS HOSP,CHICAGO,IL 60612.
RETINA ASSOCIATES CLEVELAND INC,CLEVELAND,OH.
OHIO STATE UNIV,COLUMBUS,OH 43210.
UNIV MINNESOTA,EDINA,MN.
RETINA VITREOUS CTR PA,EDISON,NJ.
UNIV FLORIDA,GAINESVILLE,FL.
PENN STATE UNIV,HERSHEY,PA 17033.
BAYLOR COLL MED,HOUSTON,TX 77030.
UNIV SO CALIF,LOS ANGELES,CA.
UNIV LOUISVILLE,KENTUCKY LIONS EYE RES INST,LOUISVILLE,KY 40292.
MED COLL WISCONSIN,MILWAUKEE,WI 53226.
UNIV MINNESOTA,MINNEAPOLIS,MN 55455.
UNIV S FLORIDA,TAMPA,FL.
DEAN A MCGEE EYE INST,OKLAHOMA CITY,OK.
THOMAS JEFFERSON UNIV,WILLS EYE HOSP,PHILADELPHIA,PA 19107.
RETINA VITREOUS CONSULTANTS,PITTSBURGH,PA.
ASSOCIATED RETINAL CONSULTANTS,ROYAL OAK,MI.
RETINA CONSULTANTS,SAN DIEGO,CA.
UNIV S FLORIDA,TAMPA,FL.
RETINA CONSULTANTS NE OHIO,TOLEDO,OH.
RETINA VITREOUS ASSOCIATES INC,TOLEDO,OH.
GEORGETOWN UNIV,WASHINGTON,DC.
UNIV PITTSBURGH,PITTSBURGH,PA.
UNIV WISCONSIN,MADISON,WI.
NEI,PROGRAM OFF,BETHESDA,MD 20892.
WASHINGTON UNIV,SAFETY & DATA MONITORING COMM,ST LOUIS,MO.
UNIV SO CALIF,SAFETY & DATA MONITORING COMM,LOS ANGELES,CA 90089.
CARNEGIE MELLON UNIV,SAFETY & DATA MONITORING COMM,PITTSBURGH,PA 15213.
DUKE UNIV,CTR EYE,SAFETY & DATA MONITORING COMM,DURHAM,NC.
UNIV ILLINOIS,SAFETY & DATA MONITORING COMM,CHICAGO,IL 60680.
NIH,SAFETY & DATA MONITORING COMM,BETHESDA,MD 20892.
UNIV PITTSBURGH,SAFETY & DATA MONITORING COMM,PITTSBURGH,PA.
UNIV WISCONSIN,SAFETY & DATA MONITORING COMM,MADISON,WI 53706.
RI Rice, Treva/D-1385-2009
NR 23
TC 119
Z9 125
U1 0
U2 9
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 DEC
PY 1996
VL 122
IS 6
BP 830
EP 846
PG 17
WC Ophthalmology
SC Ophthalmology
GA VW758
UT WOS:A1996VW75800009
ER
PT J
AU Kupfer, C
AF Kupfer, C
TI The expanded role of randomized clinical trials
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Editorial Material
RP Kupfer, C (reprint author), NEI,NIH,BLDG 31,ROOM 6A03,31 CTR DR,MSC 2510,BETHESDA,MD 20892, USA.
NR 0
TC 10
Z9 10
U1 0
U2 1
PU OPHTHALMIC PUBL CO
PI CHICAGO
PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD DEC
PY 1996
VL 122
IS 6
BP 883
EP 885
PG 3
WC Ophthalmology
SC Ophthalmology
GA VW758
UT WOS:A1996VW75800015
PM 8956644
ER
PT J
AU Whitcup, SM
Iwata, F
Podgor, MJ
Valle, D
Sran, PK
KaiserKupfer, MI
AF Whitcup, SM
Iwata, F
Podgor, MJ
Valle, D
Sran, PK
KaiserKupfer, MI
TI Association of thyroid disease with retinitis pigmentosa and gyrate
atrophy
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
AB PURPOSE: To compare the prevalence of thyroid disease in patients with retinitis pigmentosa, in patients with gyrate atrophy of the choroid and retina, and in patients with no history of ocular disease.
METHOD: Forty four patients with retinitis pig mentosa, 34 patients with gyrate atrophy, and 30 normal control patients with no ocular disease were evaluated in a case control study for the presence of thyroid disease.
RESULTS: Thyroid disease was diagnosed in six of 44 patients with retinitis pigmentosa and seven of 34 patients with gyrate atrophy but in only one of 30 control patients. Compared with control patients, the odds ratio for the occurrence of thyroid disease was 6.2 for patients with retinitis pigmentosa and 12.7 for patients with gyrate atrophy.
CONCLUSION: These data suggest an increased occurrence of thyroid disease in patients with retinitis pigmentosa and gyrate atrophy.
C1 JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,GENET LAB,BALTIMORE,MD 21218.
RP Whitcup, SM (reprint author), NEI,NIH,10 CTR DR,BLDG 10,RM 10N 202,BETHESDA,MD 20892, USA.
NR 4
TC 2
Z9 2
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 DEC
PY 1996
VL 122
IS 6
BP 903
EP 905
PG 3
WC Ophthalmology
SC Ophthalmology
GA VW758
UT WOS:A1996VW75800026
PM 8956655
ER
PT J
AU Lubensky, IA
Gnarra, JR
Bertheau, P
Walther, MM
Linehan, WM
Zhuang, ZP
AF Lubensky, IA
Gnarra, JR
Bertheau, P
Walther, MM
Linehan, WM
Zhuang, ZP
TI Allelic deletions of the VHL gene detected in multiple microscopic clear
cell renal lesions in von Hippel Lindau disease patients
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; CARCINOMA; CHROMOSOME-3; PATHOLOGY; MUTATIONS;
SURGERY; REGION
AB Patients with von Hippel-Lindau (VHL) disease develop a spectrum of bilateral clear-cell renal lesions including cysts and renal cell carcinomas (RCCs). VHL gene deletions have been previously reported in VHL-associated macroscopic RCC. Although histological analysis suggests that microscopic cystic lesions in the VHL patients may represent precursors of the RCC, there is at present no direct molecular evidence of their relationship. To investigate the relationship between cystic lesions and RCC, 26 microdissected archival renal lesions from two VHL disease patients were studied for loss of heterozygosity at the VHL gene locus using polymerase chain reaction single-strand conformation polymorphism analysis. The renal lesions included 2 benign cysts, 5 atypical cysts, 5 microscopic RCCs in situ, 5 cysts lined by a single layer of cells, in which RCCs in situ were developing, and 2 microscopic and 7 macroscopic RCCs. Except for a single benign cyst, 25 of 26 renal lesions showed nonrandom allelic loss of the VHL gene. In either of the 2 patients, the same VHL allele was deleted in all of the lesions tested, indicating loss of the wild-type allele and retention of the inherited, mutated VHL allele. The results suggest that all clear-cell lesions in the VHL kidney represent neoplasms and that the loss of the VHL gene occurs early in their development. Atypical and benign cysts most likely represent the initial phenotype in malignant transformation to the RCC.
C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892.
NCI,SURG BRANCH,NIH,BETHESDA,MD 20892.
HOP ST LOUIS,ANAT PATHOL LAB,PARIS,FRANCE.
NR 21
TC 150
Z9 155
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 DEC
PY 1996
VL 149
IS 6
BP 2089
EP 2094
PG 6
WC Pathology
SC Pathology
GA VW787
UT WOS:A1996VW78700027
PM 8952541
ER
PT J
AU Wang, W
Merrill, MJ
Borchardt, RT
AF Wang, W
Merrill, MJ
Borchardt, RT
TI Vascular endothelial growth factor affects permeability of brain
microvessel endothelial cells in vitro
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE vascular permeability factor; blood-brain barrier; brain tumor
ID TYROSINE KINASE; TUMOR ANGIOGENESIS; BINDING-SITES; HUMAN GLIOMAS; MODEL
SYSTEM; RAT-TISSUES; BARRIER; EXPRESSION; RECEPTOR; VEGF
AB Vascular endothelial growth factor (VEGF), which stimulates endothelial cell growth and induces hyperpermeability of the microvasculature, plays an important role in normal and tumor-vasculature development and tumor edema generation. In this study, we investigated the effect of VEGF on the permeability of cultured bovine brain microvessel endothelial cells (BMECs), an in vitro blood-brain barrier (BBB) model. We found that addition of purified VEGF to both the apical and basolateral sides of the BMEC monolayers increased the permeability of the monolayer to [C-14]sucrose (similar to 3-fold). A more significant increase in permeability was observed when VEGF was applied to the basolateral side of the monolayer (3-fold) than to the apical side (1.5-fold). The permeability-increasing activity of VEGF on the BMEC monolayers is both dose and time dependent. The VEGF-induced permeability increase in BMECs requires a long incubation time with VEGF, and the effect is durable. These results suggest that this cell culture system may be useful for exploring the role of VEGF in regulating the permeability of the BBB, for studying the mechanism of the permeability-increasing effect of VEGF on the endothelial cells, and for evaluating the strategies to regulate the activity of VEGF.
C1 UNIV KANSAS, DEPT PHARMACEUT CHEM, SIMONS RES LABS, LAWRENCE, KS 66047 USA.
NINCDS, SURG NEUROL BRANCH, NIH, BETHESDA, MD 20892 USA.
NR 39
TC 95
Z9 97
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 DEC
PY 1996
VL 271
IS 6
BP C1973
EP C1980
PG 8
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA WA681
UT WOS:A1996WA68100023
ER
PT J
AU Shamburek, RD
Zech, LA
Cooper, PS
Vandenbroek, JM
Schwartz, CC
AF Shamburek, RD
Zech, LA
Cooper, PS
Vandenbroek, JM
Schwartz, CC
TI Disappearance of two major phosphatidylcholines from plasma is
predominantly via LCAT and hepatic lipase
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE cholesteryl ester; lecithin-cholesterol acyltransferase; bile acid;
compartmental model; lysophosphatidylcholine
ID LECITHIN-CHOLESTEROL ACYLTRANSFERASE; PERFORMANCE LIQUID-CHROMATOGRAPHY;
HIGH-DENSITY LIPOPROTEIN; BILIARY PHOSPHATIDYLCHOLINES; RAT-LIVER;
ESTERS; SPECIFICITY; METABOLISM; ACID; DEFICIENCY
AB Metabolism of 1-stearoyl-2-arachidonyl-phosphatidylcholine (SAPC), a major phosphatidylcholine (PC) species in rat plasma, was compared with 1-palmitoyl-2-linoleoyl-PC (PLPC) metabolism. High-density lipoproteins containing SAPC and PLPC tracers labeled in the sn-2 fatty acid with H-3 and C-14 isotopes, respectively, were administered. The rats were depleted of endogenous bile acids and infused via the ileum with individual bile acids that ranged widely in hydrophobicity. The half-lives for SAPC and PLPC in plasma were 48 and 57 min, respectively. Most of the H-3 activity that disappeared from plasma at 1 h was found in the liver in 1-palmitoyl-2-arachidonyl-PC, SAPC, and 1-oleoyl-2-arachidonyl-PC, indicating phospholipase A(1) hydrolysis of plasma SAPC forming 2-arachidonyl-lysophosphatidylcholine, which was reacylated in the liver. Plasma PLPC also underwent phospholipase A(1) hydrolysis, as reported previously. The fraction of H-3 dose that accumulated in plasma cholesteryl arachidonate was two- to threefold higher than the fraction of C-14 dose in cholesteryl linoleate. Multicompartmental models for SAPC and PLPC were developed that included lysophosphatidylcholines and cholesteryl esters. Bile acids did not influence plasma PC metabolism. Lecithin-cholesterol acyltransferase and phospholipase A(1) (hepatic lipase) hydrolysis accounted for greater than or equal to 90% of the SAPC and PLPC that disappeared from plasma; SAPC and PLPC are comparable as substrates for hepatic lipase, but SAPC is preferred by lecithin-cholesterol acyltransferase.
C1 VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT MED, DIV GASTROENTEROL, RICHMOND, VA 23298 USA.
NHLBI, NIH, BETHESDA, MD 20892 USA.
NR 30
TC 10
Z9 10
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD DEC
PY 1996
VL 271
IS 6
BP E1073
EP E1082
PG 10
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA WA522
UT WOS:A1996WA52200018
ER
PT J
AU Bonner, JC
Badgett, A
Lindroos, PM
Coin, PG
AF Bonner, JC
Badgett, A
Lindroos, PM
Coin, PG
TI Basic fibroblast growth factor induces expression of the PDGF
receptor-alpha on human bronchial smooth muscle cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE smooth muscle cell hyperplasia; asthma; platelet-derived growth factor;
receptor upregulation; inflammatory cytokines
ID CHAIN MESSENGER-RNA; ALVEOLAR MACROPHAGES; SIGNAL TRANSDUCTION;
UP-REGULATION; IN-VITRO; ASTHMA; BETA; PROLIFERATION; GENE; FIBROSIS
AB Bronchial smooth muscle cell (SMC) hyperplasia is a key feature in the pathology of asthma. Platelet-derived growth factor (PDGF) isoforms are SMC mitogens. We investigated the effect of basic fibroblast growth factor (bFGF), transforming growth factor-beta 1 (TGF-beta 1), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) on the PDGF receptor system on human bronchial SMC from three different donors. bFGF induced gene expression of the PDGF alpha-receptor (PDGF-R alpha) approximately threefold without altering the PDGF beta-receptor (PDGF-R beta). IL-1 beta and TNF-alpha did not affect the PDGF receptor system. TGF-beta 1 downregulated PDGF-R alpha mRNA similar to 60% without changing PDGF-R beta mRNA levels. Receptor assays showed that bFGF increased the [I-125]PDGF-AA binding site approximately twofold, whereas TGF-beta 1 reduced [I-125]PDGF-AA binding similar to 60%. TGF-beta 1, but not latent TGF-beta 1, counteracted the bFGF-induced increase in [I-125]PDGF-AA binding. PDGF-AA-stimulated tyrosine phosphorylation on the PDGF-R alpha was enhanced after treatment with bFGF. bFGF pretreatment enhanced the mitogenic response of SMC to PDGF-AA and PDGF-AB. These findings suggest that upregulation of the PDGF-R alpha by bFGF could contribute to SMC hyperplasia during chronic airway inflammation in asthma.
C1 VET AFFAIRS MED CTR, DURHAM, NC 27705 USA.
RP Bonner, JC (reprint author), NIEHS, PULM PATHOBIOL LAB, AIRWAY INFLAMMAT SECT, MAILDROP D2-02, POB 12233, RES TRIANGLE PK, NC 27709 USA.
NR 35
TC 40
Z9 41
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD DEC
PY 1996
VL 271
IS 6
BP L880
EP L888
PG 9
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA VZ650
UT WOS:A1996VZ65000002
PM 8997257
ER
PT J
AU Guzman, K
Gray, TE
Yoon, JH
Nettesheim, P
AF Guzman, K
Gray, TE
Yoon, JH
Nettesheim, P
TI Quantitation of mucin RNA by PCR reveals induction of both MUC2 and
MUC5AC mRNA levels by retinoids
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE reverse transcriptase polymerase chain reaction; vitamin A; retinoic
acid; retinol; tracheobronchial
ID POLYMERASE CHAIN-REACTION; EPITHELIAL-CELLS; MESSENGER-RNA; VITAMIN-A;
GENE-EXPRESSION; IN-VITRO; AMPLIFICATION; TITRATION; CLONING; CDNA
AB The polydispersity of most human secretory mucin messages has made them difficult to detect specifically and quantitatively, impeding the evaluation of the relative expression of the various mucin genes and their role in normal and pathological conditions. For this reason, we developed competitive reverse transcriptase-polymerase chain reaction (PCR) methods to measure the airway mucins MUC2 and MUC5AC. Oligonucleotide pairs were designed that specifically detect MUC2 and MUC5AC, as demonstrated by the size and sequence of the PCR product and the expected tissue distribution. The mucin oligonucleotide primers were used to synthesize internal competitive standards, called MIMIC. Using this assay, the relative expression of these messages was analyzed in retinoid-replete or -deprived cultures of normal human tracheobronchial epithelial (NHTBE) cells. Retinoid deficiency induces squamous metaplasia in vivo and in vitro. Consistent with these observations and in contrast to a previous report, retinoid-deprived cultures produced at least an order of magnitude less MUC2 and MUC5AC message than retinoid-replete cultures. In summary, this paper describes methodology that can be applied to the specific and quantitative measurement of mucin messages and demonstrates that, in NHTBE cells, the level of MUC2 and MUC5AC mRNA is increased by retinoids.
RP Guzman, K (reprint author), NIEHS, PULM PATHOBIOL LAB, POB 12233, LPP, MD D2-03, RES TRIANGLE PK, NC 27709 USA.
RI Yoon, Joo-Heon/E-5781-2016
NR 24
TC 49
Z9 50
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD DEC
PY 1996
VL 271
IS 6
BP L1023
EP L1028
PG 6
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA VZ650
UT WOS:A1996VZ65000019
ER
PT J
AU Klein, SL
Taymans, SE
DeVries, AC
Nelson, RJ
AF Klein, SL
Taymans, SE
DeVries, AC
Nelson, RJ
TI Cellular immunity is not compromised by high serum corticosterone
concentrations in prairie voles
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE arvicoline rodent; house mouse; adrenal; spleen; immunology
ID HORMONE-BINDING GLOBULIN; GLUCOCORTICOID RECEPTOR;
LYMPHOCYTE-PROLIFERATION; CORTISOL; RESISTANCE; INHIBITION;
INTERLEUKIN-1; DISEASE; MOUSE; RATS
AB Glucocorticoids compromise immune function in glucocorticoid-sensitive species (e.g., mice), but these immunosuppressive effects may be reduced in glucocorticoid-resistant species. Prairie voles (Microtus ochrogaster) have been characterized as glucocorticoid-resistant to their high circulating levels of corticosterone. Because glucocorticoid-sensitive species display suppressed lymphocyte proliferation in response to elevated blood glucocorticoid levels, proliferative values were hypothesized to be reduced in house mice (Mus musculus) compared with prairie voles. Prairie voles exhibited significantly higher splenocyte proliferative responses to the T cell mitogen, Concanavalin A, despite having higher basal total and free serum corticosterone levels than mice. Neither total nor free serum corticosterone correlated with proliferative responses from either species. These data provide further evidence for glucocorticoid resistance in prairie voles and suggest that the interactions between the hypothalamic-pituitary-adrenal axis and the immune system in prairie voles may differ from those in mice or other glucocorticoid-sensitive species. Therefore, prairie voles may serve as a valuable animal model for the syndrome of glucocorticoid resistance in humans and the role of glucocorticoids in conditions characterized by a hyperactive immune system.
C1 JOHNS HOPKINS UNIV, DEPT POPULAT DYNAM, BALTIMORE, MD 21218 USA.
NICHHD, DEV ENDOCRINOL BRANCH, NIH, BETHESDA, MD 20892 USA.
RP Klein, SL (reprint author), JOHNS HOPKINS UNIV, DEPT PSYCHOL, BEHAV NEUROENDOCRINOL GRP, BALTIMORE, MD 21218 USA.
NR 41
TC 14
Z9 14
U1 1
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD DEC
PY 1996
VL 271
IS 6
BP R1608
EP R1613
PG 6
WC Physiology
SC Physiology
GA WB876
UT WOS:A1996WB87600020
ER
PT J
AU Stonestreet, BS
Patlak, CS
Pettigrew, KD
Reilly, CB
Cserr, HF
AF Stonestreet, BS
Patlak, CS
Pettigrew, KD
Reilly, CB
Cserr, HF
TI Ontogeny of blood-brain barrier function in ovine fetuses, lambs, and
adults
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE brain; blood-brain barrier permeability; sheep; alpha-aminoisobutyric
acid
ID ALPHA-AMINOISOBUTYRIC-ACID; CARDIOPULMONARY-RESUSCITATION; TRANSPORT;
RAT; ELECTROLYTES; PERMEABILITY; CAPILLARIES; INTEGRITY; CORTEX; GROWTH
AB The ontogeny of regional blood-brain barrier function was quantified with the rate constant for influx (K-i) across the blood-brain barrier with the small molecular weight synthetic, inert hydrophilic amino acid alpha-aminoisobutyric acid (AIB) in chronically instrumented early (87 days of gestation, 60% of gestation) and late (137 days of gestation, 90% of gestation) gestation fetal, newborn (3 days of age), older (24 days of age), and adult (3 years of age) sheep. The K-i was significantly (P < 0.05) lower int he brain regions of the adult sheep and in most brain regions of newborn and older lambs compared with fetuses at 60 and 90% of gestation. The K-i exhibited regional brain heterogeneity (P < 0.05) in the five groups. The patterns of regional heterogeneity were accentuated (P < 0.05) in the younger groups. We conclude that ontogenic decreases in blood-brain barrier permeability are observed in ovine fetuses from 60% of gestation of maturity in the adult.
C1 BROWN UNIV, SCH MED, DEPT PEDIAT, PROVIDENCE, RI 02905 USA.
SUNY STONY BROOK, DEPT SURG, STONY BROOK, NY 11794 USA.
NIMH, DIV EPIDEMIOL & SERV RES, BETHESDA, MD 20892 USA.
RP Stonestreet, BS (reprint author), BROWN UNIV, WOMEN & INFANTS HOSP,SCH MED,DEPT PEDIAT, SECT PHYSIOL, 101 DUDLEY ST, PROVIDENCE, RI 02905 USA.
NR 35
TC 71
Z9 71
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD DEC
PY 1996
VL 271
IS 6
BP R1594
EP R1601
PG 8
WC Physiology
SC Physiology
GA WB876
UT WOS:A1996WB87600018
ER
PT J
AU Masereeuw, R
Russel, FGM
Miller, DS
AF Masereeuw, R
Russel, FGM
Miller, DS
TI Multiple pathways of organic anion secretion in renal proximal tubule
revealed by confocal microscopy
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE fluorescein; killifish; methotrexate; sodium-independent transport;
sulforhodamine 101; image analysis
ID FLUORESCEIN TRANSPORT; CANALICULAR MEMBRANE; MULTIDRUG-RESISTANCE;
METHOTREXATE; INHIBITION; CELLS; MECHANISMS; INVITRO; MONKEY; RAT
AB Previous studies with p-aminohippurate (PAH) and fluorescein (FL) have shown that cellular uptake and tubular secretion of organic anions is driven by indirect coupling to sodium. Here we used killifish proximal tubules and laser-scanning confocal microscopy to study the transport of a larger organic anion, fluorescein-methotrexate (FL-MTX, mol mass 923 Da). When tubules were incubated in medium containing 2 mu M FL-MTX, dye accumulated in both cells and tubular lumens. At steady state, luminal fluorescence was 4-5 times higher than cellular fluorescence. Ouabain (0.1 mM) did not affect cellular or luminal fluorescence, and replacement of medium sodium by N-methylglucamine had only a modest effect; preincubation with glutarate had no effect. KCN did not affect cellular uptake but abolished secretion into the lumen. Uptake and secretion of FL-MTX were inhibited by micromolar concentrations of other organic anions (MTX, folate, probenecid, bromocresol green, bromosulfophthalein), but 1 mM PAH had a relatively small effect. FL-MTX secretion into the lumen was inhibited by leukotriene C-4, cyclosporine A, and verapamil, none of which affected FL transport. Thus a substantial component of FL-MTX secretion is Na independent and ouabain insensitive. Both the basolateral and luminal steps in the Na-independent pathway differ from those usually associated with FL and PAH secretion.
C1 NIEHS, PHARMACOL & CHEM LAB, NIH, INTRACELLULAR REGULAT SECT, RES TRIANGLE PK, NC 27709 USA.
UNIV NIJMEGEN, FAC MED SCI, DEPT PHARMACOL, NL-6500 HB NIJMEGEN, NETHERLANDS.
RI Russel, Frans/B-3184-2014; Masereeuw, Roos/N-3582-2014
OI Russel, Frans/0000-0002-7959-2314;
NR 29
TC 59
Z9 59
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0363-6127
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Fluid Electrolyte Physiol.
PD DEC
PY 1996
VL 271
IS 6
BP F1173
EP F1182
PG 10
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA WA678
UT WOS:A1996WA67800009
ER
PT J
AU Bertolino, A
Nawroz, S
Mattay, VS
Barnett, AS
Duyn, JH
Moonen, CTW
Frank, JA
Tedeschi, G
Weinberger, DR
AF Bertolino, A
Nawroz, S
Mattay, VS
Barnett, AS
Duyn, JH
Moonen, CTW
Frank, JA
Tedeschi, G
Weinberger, DR
TI Regionally specific pattern of neurochemical pathology in schizophrenia
as assessed by multislice proton magnetic resonance spectroscopic
imaging
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID TEMPORAL-LOBE EPILEPSY; HUMAN BRAIN; IN-VIVO; CORTEX; ABNORMALITIES;
HIPPOCAMPUS; METABOLITES; CHOLINE
AB Objective: Several single-voxel proton magnetic resonance spectroscopy (H-1-MAS) studies of patients with schizophrenia have found evidence of reductions of N-acetyl-aspartate (NAA) concentrations in the temporal lobes. Multislice proton magnetic resonance spectroscopy imaging (H-1-MRSI) permits simultaneous acquisition and mapping of NAA, choline-containing compounds (CHO), and creatine/phosphocreatine (CRE) signal intensities from multiple whole brain slices consisting of 1.4-ml single-volume elements. We have used H-1-MRSI to assess the regional specificity of previously reported changes of metabolite signal intensities in schizophrenia. Hippocampal volume was also measured to test the relationship between H-1-MRSI findings and tissue volume in this region. Method: Ratios of areas under the metabolite peaks of she proton spectra were determined (i.e., NAA/CRE, NAA/CHO, CHO/CRE) for multiple cortical and subcortical regions in 10 inpatients with schizophrenia. Results: Patients showed significant reductions of NAA/CRE and NAA/CHO bilaterally in the hippocampal region and in the dorsolateral prefrontal cortex. There were no significant changes in CHO/CRE or in NAA ratios in any other area sampled. No significant correlation was found between metabolite ratios in the hippocampal region and its volume. Conclusions: NAA-relative signal intensity reductions in schizophrenia appear to be remarkably localized, involving primarily she hippocampal region and the dorsolateral prefrontal cortex, two regions implicated prominently in the pathophysiology of this disorder.
C1 NIMH, ST ELIZABETHS HOSP,CTR NEUROSCI, INTRAMURAL RES PROGRAMS,CLIN BRAIN DISORDERS BRAN, WASHINGTON, DC 20032 USA.
NINCDS, NEUROIMAGING BRANCH, BETHESDA, MD 20892 USA.
NIH, LAB DIAGNOST RADIOL RES, BETHESDA, MD 20892 USA.
NIH, OFF DIRECTOR, BETHESDA, MD 20892 USA.
NIH, IN VIVO NMR CTR, BETHESDA, MD 20892 USA.
RI Duyn, Jozef/F-2483-2010; Moonen, Chrit/K-4434-2016; Bertolino,
Alessandro/O-6352-2016
OI Moonen, Chrit/0000-0001-5593-3121; Bertolino,
Alessandro/0000-0002-1251-1380
NR 55
TC 222
Z9 224
U1 1
U2 5
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD DEC
PY 1996
VL 153
IS 12
BP 1554
EP 1563
PG 10
WC Psychiatry
SC Psychiatry
GA VV491
UT WOS:A1996VV49100009
PM 8942451
ER
PT J
AU Pickar, D
Su, TP
Weinberger, DR
Coppola, R
Malhotra, AK
Knable, MB
Lee, KS
Gorey, J
Bartko, JJ
Breier, A
Hsiao, J
AF Pickar, D
Su, TP
Weinberger, DR
Coppola, R
Malhotra, AK
Knable, MB
Lee, KS
Gorey, J
Bartko, JJ
Breier, A
Hsiao, J
TI Individual variation in D-2 dopamine receptor occupancy in
clozapine-treated patients
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID POSITRON EMISSION TOMOGRAPHY; FREE SCHIZOPHRENIC-PATIENTS; PLASMA
HOMOVANILLIC-ACID; I-123 IBZM; CLINICAL-RESPONSE; ATYPICAL NEUROLEPTICS;
ANTIPSYCHOTIC-DRUGS; IMAGING AGENT; BASAL GANGLIA; HUMAN-BRAIN
AB Objective: The objectives of this study were 1) to pursue the question of clozapine's striatal D-2 occupancy in relation to its clinical effectiveness; 2) to investigate the relation between schizophrenic symptoms, clozapine blood levels, and estimated D-2 occupancy during clinically stable and unstable conditions; and 3) to eh amine long-term stability in D-2 occupancy. Method: Specific binding of the D-2 radioligand [I-123]benzamide [I-123]IBZM) was studied with single photon emission computed tomography in 13 patients with schizophrenia when they were clinically stable during chronic clozapine treatment, after clozapine dose reduction of greater than or equal to 50%, and in a subgroup (N=7) after restabilization on clozapine regimens. Clozapine's estimated D-2 occupancy was based on comparison with values from drug-free normal subjects. Results: A wide range of estimated D-2 occupancies (18% to greater than or equal to 80%) were associated with sustained, favorable response to clozapine without correlation with residual symptoms. Clonzapine blood levels were negatively related to [(123)]IBZM specific binding. Acute dose reduction was associated with predicted worsening in positive and negative symptoms and increases in [I-123]IBZM specific binding. Independent of clozapine blood level, patients with more symptoms showed lower [I-123]IBZM specific binding, consistent with competition of endogenous dopamine for D-2 binding sites in patients with greater symptoms. Restabilization on clozapine regimens produced D-2 Occupancies closely correlated with baseline values. Conclusions: There was no evidence for a critical degree of D-2 occupancy required to sustain clozapine's therapeutic effects across subjects. Simple linear regression was the best-fit model for clozapine's D-2 occupancy. Longitudinal follow-up suggests stability over time of D-2 occupancy in relation to dose and clinical response within individual patients.
C1 NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032.
RP Pickar, D (reprint author), NIMH,EXPT THERAPEUT BRANCH,BLDG 10,RM 4N212,BETHESDA,MD 20892, USA.
NR 55
TC 51
Z9 52
U1 0
U2 0
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 DEC
PY 1996
VL 153
IS 12
BP 1571
EP 1578
PG 8
WC Psychiatry
SC Psychiatry
GA VV491
UT WOS:A1996VV49100011
PM 8942453
ER
PT J
AU Turino, GM
Barker, AF
Brantly, ML
Cohen, AB
Connelly, RP
Crystal, RG
Eden, E
Schluchter, MD
Stoller, JK
AF Turino, GM
Barker, AF
Brantly, ML
Cohen, AB
Connelly, RP
Crystal, RG
Eden, E
Schluchter, MD
Stoller, JK
TI Clinical features of individuals with PI(*)SL phenotype of
alpha(1)-antitrypsin deficiency
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
ID BRITISH-THORACIC-ASSOCIATION; PI-TYPE-SZ; ALPHA1-ANTITRYPSIN
AB This report describes the clinical characteristics of a group of 59 individuals with the PI*SZ phenotype and alpha(1)-antitrypsin (alpha(1)-AT) deficiency, identified during recruitment of a registry for subjects with severe alpha(1)-antitrypsin deficiency, Currently, 1,129 individuals with levels of alpha(1)-AT of 11 mu M or below have been enrolled in this registry. individuals with the SZ phenotype whose alpha(1)-AT levels are at or below 11 mu M will be followed in the registry; those whose levels exceeded 11 mu M had baseline studies and are included in this report. Baseline pulmonary function tests included spirometry before and after an inhaled bronchodilator, diffusing capacity for carbon monoxide (DL(CO)), and chest roentgenograms. Among nonsmokers, subjects with the 52 phenotype demonstrated airflow obstruction less frequently than those with with the-ZZ phenotype. Among ex- and current smokers, the frequency and severity: of airflow obstruction was similar between Sf and 22 subjects. individuals with the 52 phenotype reported respiratory symptoms less frequently than did ZZ subjects. Overall, airflow obstruction was less common and milder among PI*SZ than PI*ZZ subjects. Cigarette smoking correlated more strongly with airflow obstruction among PI*SZ than PI*ZZ subjects. These observations indicate that in smokers, the PI*SZ phenotype confers a significant risk of the development of chronic obstructive pulmonary disease (COPD). Of itself, except in rare instances in nonsmoking individuals, the PI*SZ phenotype may confer little or no added risk of developing COPD.
C1 OREGON HLTH SCI UNIV,DEPT PULM & CRIT CARE MED,PORTLAND,OR 97201.
NHLBI,PULM CRIT CARE MED BRANCH,NIH,BETHESDA,MD 20892.
UNIV TEXAS,CTR HLTH,DEPT MED,TYLER,TX 75710.
CLEVELAND CLIN FDN,DEPT BIOSTAT & EPIDEMIOL,CLEVELAND,OH 44195.
CLEVELAND CLIN FDN,DEPT PULM & CRIT CARE MED,CLEVELAND,OH 44195.
CORNELL UNIV,NEW YORK HOSP,MED CTR,DIV PULM & CRIT CARE MED,NEW YORK,NY.
RP Turino, GM (reprint author), COLUMBIA UNIV COLL PHYS & SURG,ST LUKES ROOSEVELT HOSP CTR,DEPT MED,1000 10TH AVE,NEW YORK,NY 10019, USA.
FU NHLBI NIH HHS [N01-HR-86036]
NR 15
TC 93
Z9 100
U1 0
U2 2
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 DEC
PY 1996
VL 154
IS 6
BP 1718
EP 1725
PG 8
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA VY202
UT WOS:A1996VY20200023
PM 8970361
ER
PT J
AU Paakko, P
Kirby, M
duBois, RM
Gillissen, A
Ferrans, VJ
Crystal, RG
AF Paakko, P
Kirby, M
duBois, RM
Gillissen, A
Ferrans, VJ
Crystal, RG
TI Activated neutrophilis secrete stored alpha(1)-antitrypsin
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
ID ALPHA-1-ANTITRYPSIN GENE; HUMAN-MONOCYTES; ELASTASE GENE; EXPRESSION;
MYELOPEROXIDASE; IMMUNOGOLD; INHIBITOR; CELLS
AB Neutrophil elastase (NE), a potent serine protease, is stored in primary granules of neutrophils and released following neutrophil activation. Alpha-1-antitrypsin (alpha(1)-AT), the major inhibitor of NE, is synthesized by mature neutrophils. In the context of the maintenance of tissue homeostasis, we hypothesized that neutrophils may be able to store alpha(1)-AT, thus having it available for release concordantly with NE. Immunofluorescence and quantitative flow-cytometric studies of neutrophils and monocytes labeled with fluorescein-conjugated alpha(1)-AT-anti body demonstrated larger amounts of cytoplasmic alpha(1)-AT in neutrophils than in monocytes. [S-35]methionine-labeling and anti-alpha(1)-AT immunoprecipitation analysis showed that although both neutrophils and monocytes synthesize alpha(1)-AT, the proportion of newly synthesized intracellular alpha(1)-AT was much higher in neutrophils than in monocytes. Flowcytometric analysis showed that in the presence of surface stimulation with cytochalasin B followed by formyl-methionyleucyIphenylalanine (fMLP), mean intracellular alpha(1)-AT was decreased in stimulated neutrophils compared with that in resting cells, suggesting that the stored alpha(1)-AT was rapidly released following surface triggering. Evaluation of surface-stimulated neutrophils by [S-35]methionine labeling and anti-alpha(1)-AT immunoprecipitation demonstrated increased secretion of alpha(1)-AT compared with that of resting neutrophils, with some of the secreted alpha(1)-AT capable of forming complexes with NE. Thus, neutrophils respond to surface stimulation not only by secreting NE but also by secreting its inhibitor, alpha(1)-AT, suggesting that these cells have an inherent mechanism for damping the local effects of NE, their most powerful proteolytic enzyme.
C1 NHLBI,PATHOL SECT,BETHESDA,MD 20892.
NHLBI,PULM BRANCH,BETHESDA,MD 20892.
UNIV OULU,DEPT PATHOL,OULU,FINLAND.
NR 32
TC 36
Z9 36
U1 0
U2 1
PU AMER LUNG ASSOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC
PY 1996
VL 154
IS 6
BP 1829
EP 1833
PG 5
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA VY202
UT WOS:A1996VY20200039
PM 8970377
ER
PT J
AU Weinmann, GG
Hyatt, R
AF Weinmann, GG
Hyatt, R
TI Evaluation and research in lung volume reduction surgery
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Editorial Material
ID OBSTRUCTIVE PULMONARY-DISEASE; EMPHYSEMA; SMOKERS; PRESSURE
C1 MAYO CLIN,DEPT MED,ROCHESTER,MN.
RP Weinmann, GG (reprint author), NHLBI,DIV LUNG DIS,NIH,MSC7952,BETHESDA,MD 20892, USA.
NR 21
TC 34
Z9 35
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 DEC
PY 1996
VL 154
IS 6
BP 1913
EP 1918
PG 6
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA VY202
UT WOS:A1996VY20200048
PM 8970386
ER
PT J
AU Simeonova, PP
Luster, MI
AF Simeonova, PP
Luster, MI
TI Asbestos induction of nuclear transcription factors and interleukin 8
gene regulation
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
ID NF-KAPPA-B; IDIOPATHIC PULMONARY FIBROSIS; TRACHEAL EPITHELIAL-CELLS;
BRONCHOALVEOLAR LAVAGE; CROCIDOLITE ASBESTOS; ALVEOLAR MACROPHAGES;
INFLAMMATORY CYTOKINES; RAT LUNG; EXPRESSION; ACTIVATION
AB Proinflammatory cytokines and chemotactic peptides are strongly implicated as mediators of the pathophysiologic responses of asbestosis and other chronic inflammatory lung diseases. Recent studies in our laboratory have demonstrated that asbestos fibers stimulate lung epithelial cells to produce interleukin-8 (IL-8), the major neutrophil chemoattractant in the lung. The mechanisms by which asbestos regulates IL-8 expression were studied using the pulmonary type II-like epithelial cell line A549. Membrane permeable hydroxyl scavengers inhibited asbestos induced IL-8 expression. Using A549 cells transfected with the -546 IL-8 construct linked to a chloramphenicol acetyl transferase reporter gene, we have shown that these antioxidants directly inhibited asbestos-stimulated IL-8 promoter-dependent transcription. Asbestos fibers as well as reactive oxygen species generating systems hypoxanthine-xanthine oxidase and hydrogen peroxide stimulated DNA binding activity to the regulatory elements in the IL-8 promoter, binding sites of nuclear factor (NF)-kappa B- and NF-IL-6-like transcription factors. Asbestos-inducible DNA binding activity was partially inhibited by tetramethylthiourea, a hydroxyl radical scavenger. IL-8 secretion was also suppressed by staurosporine, an inhibitor of protein kinase C, and by inhibitors of tyrosine kinase such as herbimycin A and genistein. The suppression paralleled the effect of these inhibitors on asbestos-induced DNA binding to the NF-kappa B- and NF-IL-6-like binding sites of the IL-8 promoter. Taken together, the results suggest that asbestos-induced redox changes and phosphorylation events, mediated by staurosporine-sensitive and tyrosine kinase(s), activate nuclear proteins which recognize the NF-kappa B/NF-IL-6 binding sites of the IL-8 promoter and contribute to the regulation of IL-8 gene expression.
C1 NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,RES TRIANGLE PK,NC 27709.
RP Simeonova, PP (reprint author), NIOSH,HELD,TOXICOL & MOL BIOL BRANCH,1095 WILLOWDALE RD,MORGANTOWN,WV 26505, USA.
NR 42
TC 73
Z9 76
U1 0
U2 1
PU AMER LUNG ASSOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD DEC
PY 1996
VL 15
IS 6
BP 787
EP 795
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA VY402
UT WOS:A1996VY40200013
PM 8969274
ER
PT J
AU Chow, CK
McCarthy, JS
Neafie, R
Cooper, RI
Limpuangthip, T
Limpuangthip, P
Nutman, TB
AF Chow, CK
McCarthy, JS
Neafie, R
Cooper, RI
Limpuangthip, T
Limpuangthip, P
Nutman, TB
TI Mammography of lymphatic filariasis
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
C1 NIAID,PARASIT DIS LAB,NIH,BETHESDA,MD 20892.
WASHINGTON ADVENTIST HOSP,DEPT RADIOL,TAKOMA PK,MD 20812.
WASHINGTON ADVENTIST HOSP,DEPT SURG,TAKOMA PK,MD 20812.
WASHINGTON ADVENTIST HOSP,DEPT INTERNAL MED,INFECT DIS BRANCH,TAKOMA PK,MD 20812.
RP Chow, CK (reprint author), NIH,DEPT DIAGNOST RADIOL,WARREN G MAGNUSON CLIN CTR,BLDG 10,RM 1C-660,10 CTR DR MSC 1182,BETHESDA,MD 20892, USA.
NR 6
TC 6
Z9 6
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 DEC
PY 1996
VL 167
IS 6
BP 1425
EP 1426
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA VW769
UT WOS:A1996VW76900015
PM 8956571
ER
PT J
AU Kingma, DW
Shad, A
Tsokos, M
Fest, T
Otsuki, T
Frekko, K
Werner, E
Werner, A
Magrath, I
Raffeld, M
Jaffe, ES
AF Kingma, DW
Shad, A
Tsokos, M
Fest, T
Otsuki, T
Frekko, K
Werner, E
Werner, A
Magrath, I
Raffeld, M
Jaffe, ES
TI Epstein-Barr virus (EBV)-associated smooth-muscle tumor arising in a
post-transplant patient treated successfully for two PT-EBV-associated
large-cell lymphomas - Case report
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
ID LATENT MEMBRANE-PROTEIN; LYMPHOPROLIFERATIVE DISORDERS;
HODGKINS-DISEASE; KAPOSIS-SARCOMA; DNA-SEQUENCES; NASOPHARYNGEAL
CARCINOMA; AIDS; GENE; IDENTIFICATION; EXPRESSION
AB The association of Epstein-Barr virus (EBV) with smooth-muscle tumors was recently reported in the setting of acquired immunodeficiency syndrome (AIDS) and post-transplantation. We report a case of an EBV-associated smooth-muscle tumor arising in a post-transplant (PT) patient who previously was treated successfully for two EBV-associated PT large-cell lymphomas. A 4-year-old girl required cardiac transplantation for dilated cardiomyopathy when she was aged 23 months. Her PT regimen included cyclosporine, azothiaprine, and diltiazem. At 16 months PT, she presented with anemia, guaiac-positive stools, and an abdominal mass diagnosed as diffuse large-cell lymphoma of B-cell phenotype. Immunosuppressive therapy was reduced, and interferon and i.v. immunoglobulin were initiated. She rapidly developed signs of rejection, and a cardiac biopsy was performed, revealing grade IIIB rejection. Subsequently, immunosuppressive therapy increased. At 23 months PT, a biopsy was done of a large pelvic mass that was diagnosed as immunoblastic large-cell lymphoma After treatment with chemotherapy and retinoic acid, the size of the mass markedly decreased. Follow-up computed tomography scan revealed multiple liver nodules. A needle biopsy of the liver showed a smooth-muscle tumor of indeterminate grade. Both the lymphomas and the smooth-muscle tumor contained EBV within >95% of tumor cells by Epstein-Barr (EBER1) in situ hybridization, were of strain type A by Epstein-Barr nuclear antigen-2 (EBNA-2) polymerase chain reaction (PCR) and contained an identical 30 base-pair deletion (amino acids 346-355) of the latent membrane protein (LMP)-1 oncogene by PCR analysis. Notably, the initial large-cell lymphoma and the subsequent immunoblastic lymphoma each contained a unique p53 mutation, suggesting that they were distinct. These data suggest that the same virus contributed to the pathogenesis of both the malignant lymphomas and the smooth-muscle tumor.
C1 NCI,LYMPHOMA BIOL SECT,PEDIAT BRANCH,DIV CANC TREATMENT,NIH,BETHESDA,MD 20892.
EASTERN VIRGINIA MED SCH,CHILDRENS HOSP KINGS DAUGHTERS,NORFOLK,VA 23501.
RP Kingma, DW (reprint author), NCI,HEMATOPATHOL SECT,PATHOL LAB,DIV CANC BIOL DIAG & CTR,NIH,BLDG 10,ROOM 2N110,BETHESDA,MD 20892, USA.
NR 33
TC 47
Z9 48
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 DEC
PY 1996
VL 20
IS 12
BP 1511
EP 1519
DI 10.1097/00000478-199612000-00011
PG 9
WC Pathology; Surgery
SC Pathology; Surgery
GA VV544
UT WOS:A1996VV54400011
PM 8944045
ER
PT J
AU Contoreggi, C
Cheskin, LJ
Lange, WR
AF Contoreggi, C
Cheskin, LJ
Lange, WR
TI Acute hepatitis after clozapine administration
SO AMERICAN JOURNAL ON ADDICTIONS
LA English
DT Article
ID HEPATOTOXICITY; GLUTATHIONE; ALCOHOLICS
AB The authors present a case report of a cocaine abuser who developed acute hepatitis and an extrapyramidal reaction after administration of clozapine, a novel dopamine antagonist. Previous clinical experience with clozapine is reviewed. Both clozapine and cocaine undergo hepatic metabolism, increasing the potential for hepatotoxicity in selected patients. The authors also review hepatic metabolism of biogenic amines, their central nervous system effects, and the pharmacologic effects of clozapine and other abused substances on bioamine metabolism. Substance abusers' high susceptibility to hepatotoxicity highlights the need for careful monitoring for this form of liver dysfunction when administering clozapine.
RP Contoreggi, C (reprint author), NIDA,NIH,INTRAMURAL RES PROGRAM,POB 5180,BALTIMORE,MD 21224, USA.
NR 29
TC 16
Z9 16
U1 1
U2 1
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 1055-0496
J9 AM J ADDICTION
JI Am. J. Addict.
PD WIN
PY 1996
VL 5
IS 1
BP 5
EP 11
PG 7
WC Substance Abuse
SC Substance Abuse
GA TV374
UT WOS:A1996TV37400001
ER
PT J
AU ElHachimi, KH
Cervenakova, L
Brown, P
Goldfarb, LG
Rubenstein, R
Gajdusek, DC
Foncin, JF
AF ElHachimi, KH
Cervenakova, L
Brown, P
Goldfarb, LG
Rubenstein, R
Gajdusek, DC
Foncin, JF
TI Mixed features of Alzheimer disease and Creutzfeldt-Jakob disease in a
family with a presenilin 1 mutation in chromosome 14
SO AMYLOID-INTERNATIONAL JOURNAL OF EXPERIMENTAL AND CLINICAL INVESTIGATION
LA English
DT Article; Proceedings Paper
CT World-Federation-of-Neurology-Research-Group-on-Dementia Meeting
CY APR 18-19, 1995
CL MARRAKECH, MOROCCO
SP World Federat Neurol Res Grp Dementia
DE presenilin; Alzheimer disease; Creutzfeldt-Jakob disease; AD3 gene; PRNP
gene; amyloid; prion
ID STRAUSSLER-SCHEINKER DISEASE; AMYLOID PRECURSOR PROTEIN; PAIRED HELICAL
FILAMENTS; NEUROFIBRILLARY TANGLES; MISSENSE MUTATIONS; PLAQUES; GENE;
INDIANA; DEMENTIA; COEXISTENCE
AB Alzheimer disease and Creutzfeldt-Jakob disease are both characterized by the onset in late-middle age of progressive dementia with a fatal outcome, and a degenerative neuropathology with neuronal loss and amyloid deposition. Whereas early studies underlined clinico-pathologic and genetic similarities between the two diseases, the more recent discovery of pathogenic mutations in genes on different chromosomes producing chemically distinct amyloids has emphasized their differences. We here describe a family with clinico-pathologic features of both diseases, including substantial cerebral deposition of both beta A4 and PrP amyloid proteins, in which the pathogenesis is linked to a mutation in codon 163 of the presenilin 1 (S182, AD3) gene on chromosome 14.
C1 NINCDS,CNS STUDIES LAB,NIH,BETHESDA,MD 20892.
NINCDS,LAB MOL & CELLULAR NEUROBIOL 3,NIH,BETHESDA,MD 20892.
EPHE,LAB NEUROHISTOL,F-75006 PARIS,FRANCE.
HOP LA PITIE SALPETRIERE,U106 INSERM,PARIS,FRANCE.
INST BASIC RES DEV DISABIL,STATEN ISL,NY.
NR 63
TC 17
Z9 17
U1 1
U2 1
PU PARTHENON PUBLISHING GROUP
PI CARNFORTH LANCASHIRE
PA CASTERTON HALL, CARNFORTH LANCASHIRE, ENGLAND LA6 2LA
SN 1350-6129
J9 AMYLOID
JI Amyloid-Int. J. Exp. Clin. Investig.
PD DEC
PY 1996
VL 3
IS 4
BP 223
EP 233
DI 10.3109/13506129609014369
PG 11
WC Biochemistry & Molecular Biology; Medicine, General & Internal;
Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; General & Internal Medicine; Research
& Experimental Medicine
GA VZ041
UT WOS:A1996VZ04100001
ER
PT J
AU Chan, KC
Muschik, CM
Issaq, HJ
Garvey, KJ
Generlette, PL
AF Chan, KC
Muschik, CM
Issaq, HJ
Garvey, KJ
Generlette, PL
TI High-speed screening of polymerase chain reaction products by capillary
electrophoresis
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
ID DNA FRAGMENTS; LIQUID-CHROMATOGRAPHY; ZONE ELECTROPHORESIS;
OLIGONUCLEOTIDES; SEPARATION; MUTATION
AB In an effort to develop capillary electrophoresis (CE) for high-throughput polymerase chain reaction (PCR) molecular diagnostics, a method was developed to rapidly screen small PCR products of similar molecular weights. The assay of interest required the separation of two PCR products (375 and 400 bp) in an assay of TGF-beta(1) knockout mice to determine the genotype of neonates. Using a commercially available CE instrument, the two PCR products were separated in 12 min with a replaceable gel buffer, a 20-cm effective length DB-17 capillary, and 185 V/cm field strength. With the coinjection of a 20-bp ladder, the sizes of the PCR products were determined hom the electropherogram without using a calibration plot and curve-fitting program. Faster separation was obtained using the combination of a short effective length capillary and high field strength. The two PCR products were separated in 82 s with a 7-cm effective length capillary and 556 V/cm. A 60% buffer further reduced the separation time in about a minute. This high-speed separation, with minimum postrun data processing, is highly desirable for the high-throughput screening of PCR products using a single-capillary CE system. (C) 1996 Academic Press, Inc.
C1 NCI, RECOMBINANT DNA LAB, SAIC FREDERICK, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA.
RP Chan, KC (reprint author), NCI, CHEM SYNTH & ANAL LAB, SAIC FREDERICK, FREDERICK CANC RES & DEV CTR, POB B, FREDERICK, MD 21702 USA.
NR 25
TC 22
Z9 22
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD DEC 1
PY 1996
VL 243
IS 1
BP 133
EP 139
DI 10.1006/abio.1996.0491
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA VX622
UT WOS:A1996VX62200017
PM 8954535
ER
PT J
AU Berlin, W
Sauer, B
AF Berlin, W
Sauer, B
TI In situ color detection of alpha-L-arabinofuranosidase, a
''no-background'' reporter gene, with
5-bromo-3-indolyl-alpha-L-arabinofuranoside
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
ID SEQUENCE
AB We describe the synthesis and use of 5-bromo-3-indolyl-alpha-L-arabinofuranoside (5-BI-ara) for the detection of alpha-L-arabinofuranosidase in bacterial colonies. Since the product of 5-BI-ara hydrolysis is an intensely colored indigo precipitate, it is a useful substrate for in situ detection of alpha-L-arabinofuranosidase activity. Here we show that colonies of an Escherichia coli strain expressing a recombinant alpha-L-arabinofuranosidase gene from Streptomyces lividans are readily identified by visual inspection on bacterial plates containing 5-BI-ara. Use of 5-BI-ara should facilitate the detection of endogenous alpha-L-arabinofuranosidase activity in a variety of microorganisms. In addition, since alpha-L-arabinofuranosidase activity is not commonly found in a large number of bacteria, yeast, and animal cells, 5-BI-ara will be useful in exploring the use of genes coding for alpha-L-arabinofuranosidase as gene expression reporters in heterologous systems. (C) 1996 Academic Press, Inc.
C1 NIDDKD,NIH,BETHESDA,MD 20892.
NR 11
TC 10
Z9 10
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD DEC 1
PY 1996
VL 243
IS 1
BP 171
EP 175
DI 10.1006/abio.1996.0497
PG 5
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA VX622
UT WOS:A1996VX62200023
PM 8954541
ER
PT J
AU Stover, ES
Goldschmidts, WL
Grau, LE
Mitnick, L
Pequegnat, W
Rausch, DM
Vitiello, B
AF Stover, ES
Goldschmidts, WL
Grau, LE
Mitnick, L
Pequegnat, W
Rausch, DM
Vitiello, B
TI Perspectives from the National Institute of Mental Health: Preventing or
living with AIDS
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
ID HIV SEROPREVALENCE; CONDOM-USE; INTERVENTION; PREVALENCE; REDUCTION;
INFECTION
AB This article provides a succinct overview of the history and current and future research priorities of the office on AIDS at the National Institute of Mental Health (NIMH). Throughout its history and currently, the Office on AIDS has encouraged and supported research on primary prevention of human immunodeficiency virus (HIV) transmission, effects of HIV disease on the central nervous system, and coping with the sequelae of infection. Future directions for the NIMH include the dissemination of research findings to the community, investigation of mechanisms for involving and retaining participants in large-scale vaccine trials, and continued attention to the prevention of HIV transmission through behavior change.
C1 NIMH,OFF AIDS,ROCKVILLE,MD 20857.
NR 14
TC 0
Z9 0
U1 0
U2 0
PU SOC BEHAVIORAL MEDICINE
PI ROCKVILLE
PA 103 S ADAMS ST, ROCKVILLE, MD 20850
SN 0883-6612
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD WIN
PY 1996
VL 18
IS 1
BP 58
EP 60
DI 10.1007/BF02903940
PG 3
WC Psychology, Multidisciplinary
SC Psychology
GA UY096
UT WOS:A1996UY09600008
PM 24203644
ER
PT J
AU Masur, H
Shelhamer, JH
AF Masur, H
Shelhamer, JH
TI Outpatient management of HIV-related pneumonia - In response
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Letter
ID IMMUNODEFICIENCY-VIRUS INFECTION; PNEUMOCYSTIS-CARINII PNEUMONIA;
TUBERCULOSIS
RP Masur, H (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572
SN 0003-4819
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD DEC 1
PY 1996
VL 125
IS 11
BP 938
EP 939
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA VV541
UT WOS:A1996VV54100017
ER
PT J
AU Grassi, G
Marini, JC
AF Grassi, G
Marini, JC
TI Ribozymes: Structure, function and potential therapy for dominant
genetic disorders
SO ANNALS OF MEDICINE
LA English
DT Review
DE genetic diseases; mRNA suppression; ribozymes
ID FIBROBLAST GROWTH-FACTOR; HEPATITIS-DELTA-VIRUS; SELF-CLEAVAGE REACTION;
OSTEOGENESIS IMPERFECTA; HAMMERHEAD RIBOZYMES; CROUZON-SYNDROME;
MARFAN-SYNDROME; RNA ENZYME; MEDIATED CLEAVAGE; MESSENGER-RNA
AB Some dominant genetic disorders, viral processes and neoplastic disorders base their pathogenicity on the production of protein or proteins that negatively affect cellular metabolism or environment. Thus, the inhibition of the synthesis of those proteins should prevent the biological damage. A promising approach to decreasing the level of the abnormal protein(s) is represented by specific interference with gene expression at the level of mRNA. The specific suppression of the expression of an mRNA can be achieved by using ribozymes. Ribozymes are RNA molecules able to break and form covalent bonds within a nucleic acid molecule. These molecules, with even greater potential advantages than antisense oligodeoxynucleotides, are able to bind specifically and cleave an mRNA substrate. There are advantages to using ribozymes instead of antisense oligodeoxynucleotides. Ribozymes can inactivate the target RNA without relying on the host cell's machinery and they have the capacity to cleave more than one copy of the target RNA by dissociating from the cleavage products and binding to another target molecule. Most of the studies performed to date have described the use of ribozymes as therapeutic agents for viral and cancer diseases. However, some dominant genetic disorders may also benefit from this approach. This is the case for some connective tissue disorders such as osteogenesis imperfecta, Marfan syndrome and the craniosynostotic syndromes.
C1 NICHHD,SECT CONNECT TISSUE DISORDERS,HERITABLE DISORDERS BRANCH,BETHESDA,MD 20892.
NR 117
TC 18
Z9 19
U1 1
U2 4
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE
SN 0785-3890
J9 ANN MED
JI Ann. Med.
PD DEC
PY 1996
VL 28
IS 6
BP 499
EP 510
DI 10.3109/07853899608999114
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA WC061
UT WOS:A1996WC06100005
PM 9017109
ER
PT J
AU Jacobs, JY
Gallelli, JF
AF Jacobs, JY
Gallelli, JF
TI Evaluation of antineoplastic drug package inserts from different
countries
SO ANNALS OF PHARMACOTHERAPY
LA English
DT Letter
C1 NIH,WARREN G MAGNUSON CLIN CTR,OFF DIRECTOR,BETHESDA,MD 20892.
RP Jacobs, JY (reprint author), HADASSAH MED ORG,KIRYAT HADASSAH,IL-91120 JERUSALEM,ISRAEL.
NR 6
TC 0
Z9 0
U1 0
U2 1
PU HARVEY WHITNEY BOOKS CO
PI CINCINNATI
PA PO BOX 42696, CINCINNATI, OH 45242
SN 1060-0280
J9 ANN PHARMACOTHER
JI Ann. Pharmacother.
PD DEC
PY 1996
VL 30
IS 12
BP 1496
EP 1498
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA VX904
UT WOS:A1996VX90400023
PM 8968467
ER
PT J
AU Xiao, W
Player, MR
Li, GY
Zhang, WT
Lesiak, K
Torrence, PF
AF Xiao, W
Player, MR
Li, GY
Zhang, WT
Lesiak, K
Torrence, PF
TI Synthesis and characterization of composite nucleic acids containing
2',5'-oligoriboadenylate linked to antisense DNA
SO ANTISENSE & NUCLEIC ACID DRUG DEVELOPMENT
LA English
DT Article
ID 2-5A ANTISENSE; RNA TARGET; CHIMERAS
AB Composite nucleic acids, known as 2-5A antisense chimeras, cause the 2-5A-dependent ribonuclease (RNase L) to catalyze the specific cleavage of RNA in cell free systems and in intact cells. Such 2-5A antisense chimeras are 5'-monophosphorylated, 2',5'-linked oligoadenylates covalently attached to antisense 3',5'-oligodeoxyribonucleotides by means of a linker containing two residues of 1,4-butanediol phosphate. Here we report a fully automated synthesis of 2-5A antisense chimeras on a solid support using phosphoramidite methodology with specific coupling time modifications and their subsequent purification by reverse-phase ion-pair and anion exchange HPLC, Purified 2-5A antisense chimeras were characterized by [H-1]NMR and [P-31]NMR, MALDIMS, and capillary gel electrophoresis, The synthetic 2',5'-linked oligoadenylate showed no phosphodiester isomerization to 3',5' during or after synthesis, In addition, we have developed facile methodologies to characterize the chimeras using digestion with various hydrolytic enzymes including snake venom phosphodiesterase I and nuclease P1. Finally, Maxam-Gilbert chemical sequencing protocols have been developed to confirm the entire sequence of these chimeric oligonucleotides.
C1 NIDDK,SECT BIOMED CHEM,MED CHEM LAB,NIH,BETHESDA,MD 20892.
NR 21
TC 23
Z9 23
U1 0
U2 2
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1087-2906
J9 ANTISENSE NUCLEIC A
JI Antisense Nucleic Acid Drug Dev.
PD WIN
PY 1996
VL 6
IS 4
BP 247
EP 258
DI 10.1089/oli.1.1996.6.247
PG 12
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Research & Experimental Medicine
GA WC495
UT WOS:A1996WC49500002
PM 9012860
ER
PT J
AU Tobin, GJ
Ennis, WH
Clanton, DJ
Gonda, MA
AF Tobin, GJ
Ennis, WH
Clanton, DJ
Gonda, MA
TI Inhibition of bovine immunodeficiency virus by anti-HIV-1 compounds in a
cell culture-based assay
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE bovine immunodeficiency virus; human immunodeficiency virus type 1; cell
culture-based inhibition assay; antiviral compounds
ID BIOLOGICALLY-ACTIVE PROVIRUSES; HIV PROTEASE INHIBITOR;
REVERSE-TRANSCRIPTASE; VISNA VIRUS; MOLECULAR-CLONING; POTENT INHIBITOR;
2',3'-DIDEOXYNUCLEOSIDES; REPLICATION; INFECTION; TYPE-1
AB The bovine immunodeficiency virus (BIV) and human immunodeficiency virus types 1 and 2 (HIV-1 and -2) are members of the lentivirus genus of retroviruses. Although DNA sequences of these viruses have diverged considerably, the BIV genome organization, function of structural and regulatory genes, and replication cycle are very similar to that of HIV-1, making BIV a potentially useful model to study compounds with anti-HIV-l activity. A cell culture-based antiviral assay was developed to test compounds for inhibition of BIV replication. The assay uses an embryonic rabbit epithelial (EREp) cell line that is highly sensitive to BIV infection and cytopathology. The 50% effective concentrations (EC(50)) at which the virus was inhibited in EREp cells were determined for 13 nucleoside analog, non-nucleoside, tumor-suppressive, or membrane-surface inhibitory compounds. The nucleoside analogs (3'-azido-2',3'-dideoxythymidine, 2',3'-dideoxyinosine and 2',3'-dideoxycytosine), surface-membrane inhibitors (dextran sulfate, hypericin, Chicago Sky Blue and quinobene), the nucleoside reductase inhibitor (hydroxyurea), and a tumor-suppressive phorbol ester (prostratin) inhibited BIV with EC(50) values similar to those derived in HIV-1 lymphocyte (CD4(+))-based assays. BIV was markedly more resistant to inhibition with HIV-I-specific non-nucleoside reverse transcriptase inhibitors (NNRTIs) (thiazolobenzimidazole, oxathiin carboxanilide and thiocarbamate) than was HIV-1, which parallels results with NNRTIs in HIV-2 assays.
C1 NCI,FREDERICK CANC RES & DEV CTR,AIDS DRUG SCREENING & DEV LAB,SAIC FREDERICK,FREDERICK,MD 21702.
RP Tobin, GJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,LAB CELL & MOL STRUCT,SAIC FREDERICK,FREDERICK,MD 21702, USA.
NR 51
TC 13
Z9 14
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD DEC
PY 1996
VL 33
IS 1
BP 21
EP 31
DI 10.1016/S0166-3542(96)00990-4
PG 11
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA VV545
UT WOS:A1996VV54500003
PM 8955850
ER
PT J
AU Halliday, SM
LackmanSmith, C
Bader, JP
Rice, WG
Clanton, DJ
Zalkow, LH
Buckheit, RW
AF Halliday, SM
LackmanSmith, C
Bader, JP
Rice, WG
Clanton, DJ
Zalkow, LH
Buckheit, RW
TI Inhibition of human immunodeficiency virus replication by the sulfonated
stilbene dye resobene
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE human immunodeficiency virus; resobene; antiviral
ID ANTI-HIV AGENT; REVERSE-TRANSCRIPTASE ACTIVITY; PRINCIPAL NEUTRALIZING
DOMAIN; SOLUBLE CD4; ENVELOPE GLYCOPROTEINS; DEXTRAN SULFATE;
CELL-LINES; TYPE-1; ENHANCEMENT; BINDING
AB The anti-HIV sulfonated dye, resobene, was found to be a potent inhibitor of the attachment of HIV to target cells, the fusion of envelope- and CD4-expressing cells, and the cell-to-cell transmission of virus. Resobene inhibited the infection of phenotypically distinct, established human cell lines and fresh human peripheral blood lymphocytes and macrophages by laboratory-derived isolates of human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2), and a panel of biologically diverse primary clinical isolates, including syncytium-inducing and non-syncytium-inducing viruses and strains representative of the various virus clades found worldwide. The compound was also active against all drug-resistant virus isolates tested. Cell-based and biochemical mechanism of action studies demonstrated that the compound inhibits the attachment of infectious virus and fusion of virus-infected cells to uninfected target cells by binding to the cationic V3 loop of the envelope glycoprotein. Resobene effectively inhibited the infection of cell populations which do and do not express cell surface CD4. Resobene prevented infection of the cervical epithelial cell line ME180, suggesting the compound may effectively act as a topical microbicide to prevent the sexual transmission of HIV.
C1 SO RES INST,FREDERICK RES CTR,VIROL RES GRP,FREDERICK,MD 21701.
NCI,DIV CANC TREATMENT DIAG & CTR,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
NCI,FREDERICK CANC RES & DEV CTR,SAIC,LAB ANTIVIRAL DRUG MECH,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,SAIC,ANTIAIDS VIRUS DURG SCREENING LAB,FREDERICK,MD 21702.
GEORGIA INST TECHNOL,SCH CHEM & BIOCHEM,ATLANTA,GA 30332.
FU NCI NIH HHS [N01-CM-37818]
NR 32
TC 14
Z9 15
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD DEC
PY 1996
VL 33
IS 1
BP 41
EP 53
DI 10.1016/S0166-3542(96)00994-1
PG 13
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA VV545
UT WOS:A1996VV54500005
PM 8955852
ER
PT J
AU Mahmoodian, F
Gosiewska, A
Peterkofsky, B
AF Mahmoodian, F
Gosiewska, A
Peterkofsky, B
TI Regulation and properties of bone alkaline phosphatase during vitamin C
deficiency in guinea pigs
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE alkaline phosphatase; osteocalcin; collagen; ascorbic acid; bone
ID HUMAN-SKIN FIBROBLASTS; COLLAGEN-SYNTHESIS; MESSENGER-RNA;
ASCORBIC-ACID; OSTEO-SARCOMA; SINGLE GENE; I COLLAGEN; RAT; EXPRESSION;
KIDNEY
AB The precise physiological role of alkaline phosphatase is unknown, although evidence suggests it is involved in bone mineralization. Previous studies showed that serum and bone alkaline phosphatase activity is decreased during vitamin C deficiency. Some effects of scurvy, such as inhibition of collagen synthesis, are related to weight loss and subsequent induction of insulin-like growth factor binding proteins and they can be duplicated in fasted guinea pigs receiving vitamin C, We found that decreased alkaline phosphatase activity in bone and serum during scurvy was not completely due to the ''fasting effect'' and that the decrease in serum was due to loss of bone isoenzyme activity, There also was a decrease in immunoreactive enzyme protein and alkaline phosphatase mRNA concentrations in bone of scorbutic animals, indicating that synthesis of the enzyme was inhibited, Sialylation and addition of the glycosylphosphatidylinositol anchor to the enzyme in bone tissue were not affected by scurvy, The concentration of mRNA for osteocalcin, a bone-specific marker, also fell during scurvy and to a much greater extent than either alkaline phosphatase or type I collagen mRNAs, while osteopontin mRNA concentrations increased. These results differ from the reported role of ascorbic acid on the pattern of expression of these proteins during differentiation of osteoblasts in culture. The decreased expression of collagen, alkaline phosphatase, and osteocalcin could explain the defects in bone caused by scurvy. (C) 1996 Academic Press, Inc.
C1 NCI, BIOCHEM LAB, BETHESDA, MD 20892 USA.
NR 49
TC 25
Z9 25
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD DEC 1
PY 1996
VL 336
IS 1
BP 86
EP 96
DI 10.1006/abbi.1996.0535
PG 11
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA VW848
UT WOS:A1996VW84800011
PM 8951038
ER
PT J
AU Blauvelt, A
AF Blauvelt, A
TI Hepatitis C virus and human immunodeficiency virus infection can alter
porphyrin metabolism and lead to porphyria cutanea tarda
SO ARCHIVES OF DERMATOLOGY
LA English
DT Editorial Material
ID NON-B-HEPATITIS; NON-A; LIVER-DISEASE; UNITED-STATES; ASSOCIATION;
ANTIBODIES; PHOTOSENSITIVITY; MANIFESTATIONS; HIV
RP Blauvelt, A (reprint author), NCI,DERMATOL BRANCH,BLDG 10,ROOM 12N238,10 CTR DR MSC 1908,BETHESDA,MD 20892, USA.
NR 34
TC 14
Z9 14
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD DEC
PY 1996
VL 132
IS 12
BP 1503
EP 1504
DI 10.1001/archderm.132.12.1503
PG 2
WC Dermatology
SC Dermatology
GA VX641
UT WOS:A1996VX64100016
PM 8961882
ER
PT J
AU Kumra, S
Frazier, JA
Jacobsen, LK
McKenna, K
Gordon, CT
Lenane, MC
Hamburger, SD
Smith, AK
Albus, KE
AlaghbandRad, J
Rapoport, JL
AF Kumra, S
Frazier, JA
Jacobsen, LK
McKenna, K
Gordon, CT
Lenane, MC
Hamburger, SD
Smith, AK
Albus, KE
AlaghbandRad, J
Rapoport, JL
TI Childhood-onset schizophrenia - A double-blind clozapine-haloperidol
comparison
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID TARDIVE-DYSKINESIA; INDUCED AGRANULOCYTOSIS; WEIGHT-GAIN; OPEN TRIAL;
ADOLESCENTS; CHILDREN; SEIZURES; PROGRESS; PATIENT; AGENTS
AB Background: Childhood-onset schizophrenia is a rare bur severe form of the disorder that is often treatment-refractory. In this study, the efficacy and adverse effects of clozapine and haloperidol were compared for children and adolescents with early-onset schizophrenia.
Methods: Twenty-one patients (mean [+/-SD] age, 14.0 +/- 2.3 years) with onset of Diagnostic an Statistical Manual of Mental Disorders, Revised Third Edition-defined schizophrenia that began by age 12 years and who had been nonresponsive to typical neuroleptics participated in the study. Patients were randomized to a 6-week double-blind parallel comparison of clozapine mean [+/-SD] final dose, 176 +/- 149 mg/d), or haloperidol, (16 +/- 8 mg/d).
Results: Clozapine was superior to haloperidol on ail measures of psychosis (P = .04-.002). Positive and negative symptoms of schizophrenia improved. However, neutropenia and seizures were major concerns. To date, one third of the group has discontinued using clozapine.
Conclusions: Clozapine has striking superiority for positive and negative symptoms in treatment-refractory childhood-onset schizophrenia. However, due to possibly increased toxic effects in this pediatric population, close monitoring for adverse events is essential.
C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115.
NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611.
UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201.
RP Kumra, S (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 68
TC 248
Z9 251
U1 3
U2 10
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD DEC
PY 1996
VL 53
IS 12
BP 1090
EP 1097
PG 8
WC Psychiatry
SC Psychiatry
GA VX336
UT WOS:A1996VX33600002
PM 8956674
ER
PT J
AU Ferris, FL
Murphy, RP
AF Ferris, FL
Murphy, RP
TI The peril of the pilot study
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Editorial Material
ID MACULAR DEGENERATION
RP Ferris, FL (reprint author), NEI,BLDG 31,ROOM 6A52,30 CTR DR,BETHESDA,MD 20892, USA.
NR 10
TC 6
Z9 6
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 DEC
PY 1996
VL 114
IS 12
BP 1506
EP 1507
PG 2
WC Ophthalmology
SC Ophthalmology
GA VX337
UT WOS:A1996VX33700009
PM 8953984
ER
PT J
AU Hammond, EH
Henson, DE
Farrow, G
Friedell, GH
Gospodarowicz, M
Heney, NM
Herr, H
Lerner, S
Montie, JE
Murphy, W
Platz, C
Prout, GR
Shipley, WU
Torti, F
True, LD
vonEschenbach, AC
Coppock, DL
Cunningham, MP
Farrow, GM
Gorstein, F
Hutter, RVP
Min, KW
Nash, G
Nielsen, ML
Page, DL
Rabson, AS
Ruby, SG
Scholosnagle, D
Schwartz, IS
Scully, RE
Seiffert, J
Smoron, GL
Travers, H
Webb, JH
Weiss, LL
Wick, MR
AF Hammond, EH
Henson, DE
Farrow, G
Friedell, GH
Gospodarowicz, M
Heney, NM
Herr, H
Lerner, S
Montie, JE
Murphy, W
Platz, C
Prout, GR
Shipley, WU
Torti, F
True, LD
vonEschenbach, AC
Coppock, DL
Cunningham, MP
Farrow, GM
Gorstein, F
Hutter, RVP
Min, KW
Nash, G
Nielsen, ML
Page, DL
Rabson, AS
Ruby, SG
Scholosnagle, D
Schwartz, IS
Scully, RE
Seiffert, J
Smoron, GL
Travers, H
Webb, JH
Weiss, LL
Wick, MR
TI Practice protocol for the examination of specimens removed from patients
with carcinoma of the urinary bladder, ureter, renal pelvis, and urethra
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID OF-AMERICAN-PATHOLOGISTS; SURGICAL PATHOLOGY; PROGNOSTIC FACTORS;
CANCER-COMMITTEE; OVEREXPRESSION; CHECKLISTS
AB This article details a practice protocol for the examination and reporting of specimens removed from patients with carcinoma of the urinary bladder, ureter, renal pelvis, or urethra. It was created by a multidisciplinary task force of pathologists and oncologists established by the Cancer Committee of the College of American Pathologists. Documentation for the protocol was obtained from the previously published protocol, the medical literature, personal experience, and consultation with colleagues. After creation and review by the task force, the protocol was sent to 1000 randomly selected practicing pathologists as a survey. Their comments and suggestions were addressed in the final version. The protocol was approved by the Board of Governors of the College of American Pathologists.
C1 UNIV UTAH,SCH MED,SALT LAKE CITY,UT.
NCI,EARLY DETECT BRANCH,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892.
RP Hammond, EH (reprint author), LATTER DAY ST HOSP,DEPT PATHOL,8TH AVE & C ST,SALT LAKE CITY,UT 84143, USA.
NR 25
TC 12
Z9 12
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 DEC
PY 1996
VL 120
IS 12
BP 1103
EP 1110
PG 8
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA WQ053
UT WOS:A1996WQ05300007
PM 15456174
ER
PT J
AU Ryu, JH
Song, BJ
Hong, S
Huh, JW
AF Ryu, JH
Song, BJ
Hong, S
Huh, JW
TI Purification and acetylation of protein X subunit of pyruvate
dehydrogenase complex (PDC) from bovine kidney
SO ARCHIVES OF PHARMACAL RESEARCH
LA English
DT Article
DE protein X; pyruvate dehydrogenase; purification; acetylation
ID SACCHAROMYCES-CEREVISIAE; COMPONENT-X; KINASE; HEART; GENE
AB Protein X is one of the subunits of pyruvate dehydrogenase complex. The biological role of this protein has not been fully elucidated, mainly because of the difficulty in its dissociation from the tightly bound dihydrolipoamide acetyltransferase-protein X subcomplex. We have found that the detachment of protein X from acetyltransferase subunit can be easily accomplished by the cycles of freezing and thawing process. Several lines of evidence including sodium dodecyl sulfate-polyacrylamide gel electrophoresis, N-terminal amino acid sequence analysis and acetylation with [2-C-14] pyruvate confirmed that the purified protein is protein X. The purified intact form of protein X was acetylated by [2-C-14] pyruvate in the presence of pyruvate dehydrogenase subunit. The acetylation efficiency of this protein was lower than that of acetyltransferase and was not affected by the presence of acetyltransferase.
C1 NIAAA, NEUROGENET LAB, ROCKVILLE, MD 20852 USA.
SUNGKYUNKWAN UNIV, DEPT GENET ENGN, SUWON 440746, SOUTH KOREA.
KOREA GREEN CROSS CORP, CENT RES INST, YONGIN KUN 449900, SOUTH KOREA.
RP SOOKMYUNG WOMENS UNIV, COLL PHARM, YONGSAN KU, CHUNGNA DONG 2 KA, SEOUL 140742, SOUTH KOREA.
NR 13
TC 1
Z9 1
U1 0
U2 0
PU PHARMACEUTICAL SOC KOREA
PI SEOUL
PA 1489-3 SUHCHO-DONG, SUHCHO-KU, SEOUL 137-071, SOUTH KOREA
SN 0253-6269
EI 1976-3786
J9 ARCH PHARM RES
JI Arch. Pharm. Res.
PD DEC
PY 1996
VL 19
IS 6
BP 502
EP 506
DI 10.1007/BF02986019
PG 5
WC Chemistry, Medicinal; Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA WA527
UT WOS:A1996WA52700013
ER
PT J
AU Curb, JD
Masaki, K
Rodriguez, BL
Abbott, RD
Burchfiel, CM
Chen, RD
Petrovitch, H
Sharp, D
Yano, K
AF Curb, JD
Masaki, K
Rodriguez, BL
Abbott, RD
Burchfiel, CM
Chen, RD
Petrovitch, H
Sharp, D
Yano, K
TI Peripheral artery disease and cardiovascular risk factors in the elderly
- The Honolulu Heart Program
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE elderly; peripheral artery disease; risk factor
ID BLOOD-PRESSURE INDEX; INTERMITTENT CLAUDICATION; WOMEN; MEN;
ATHEROSCLEROSIS; POPULATION; MORTALITY; HAWAII
AB Peripheral vascular disease as measured by the ankle/brachial blood pressure index (ABI) is associated with increased risk of mortality and morbidity. Few sources of data on the relationship of risk factors to ABI are available for the elderly, especially those >80 years of age, and minority populations. ABI measurements from the Honolulu Heart Program's fourth reexamination of 3450 ambulatory, elderly Japanese American men indicate that the prevalence of an abnormal ABI, defined as a ratio of <0.9, was 13.6%, increasing from 8.0% in those 71 to 74 years of age to 27.4% in those 85 to 93 years. Associations that were U or J shaped were present for a number of risk factors (higher rates of abnormality [ABI<0.9] in those in the lowest and highest risk factor quintiles) in a cross-sectional analysis. Risk factors measured at baseline were also predictive of an abnormal ABI 25 years later, even after adjustment for multiple risk factors. The odds ratio (OR) for an ABI<0.9 at the 80th percentile of cholesterol compared with that at the 20th percentile was 1.4; the OR for 1-hour postload glucose was 1.3, and for alcohol intake 1.2. The OR associated with hypertension was 1.8 and that for smoking, 2.9 (P<.05 for all ORs). These findings are consistent with ABI being a marker for generalized atherosclerotic disease in old and very old Japanese American men.
C1 UNIV HAWAII MANOA,JOHN A BURNS SCH MED,DEPT MED,DIV CLIN EPIDEMIOL,HONOLULU,HI 96822.
UNIV HAWAII MANOA,JOHN A BURNS SCH MED,DEPT MED,DIV GERIATR MED,HONOLULU,HI 96822.
KUAKINI MED CTR,HONOLULU HEART PROGRAM,HONOLULU,HI.
NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892.
UNIV VIRGINIA,SCH MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22908.
FU NHLBI NIH HHS [N01-HC-05102]
NR 18
TC 62
Z9 66
U1 0
U2 0
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 1079-5642
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD DEC
PY 1996
VL 16
IS 12
BP 1495
EP 1500
PG 6
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA WA769
UT WOS:A1996WA76900012
PM 8977454
ER
PT J
AU Pras, E
Schumacher, HR
Kastner, DL
Wilder, RL
AF Pras, E
Schumacher, HR
Kastner, DL
Wilder, RL
TI Lack of evidence of mycobacteria in synovial tissue from patients with
rheumatoid arthritis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID LYMPHOCYTES-T; RATS; DNA
C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104.
NIAMSD,BETHESDA,MD.
RP Pras, E (reprint author), CHAIM SHEBA MED CTR,IL-52621 TEL HASHOMER,ISRAEL.
NR 8
TC 12
Z9 12
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0004-3591
J9 ARTHRITIS RHEUM
JI Arthritis Rheum.
PD DEC
PY 1996
VL 39
IS 12
BP 2080
EP 2081
DI 10.1002/art.1780391221
PG 2
WC Rheumatology
SC Rheumatology
GA VX901
UT WOS:A1996VX90100020
PM 8961916
ER
PT J
AU Jensen, RT
AF Jensen, RT
TI Gastrinoma
SO BAILLIERES CLINICAL GASTROENTEROLOGY
LA English
DT Review
ID ZOLLINGER-ELLISON-SYNDROME; MULTIPLE ENDOCRINE NEOPLASIA;
ISLET-CELL-CARCINOMA; SOMATOSTATIN-RECEPTOR SCINTIGRAPHY; HEPATIC
ARTERIAL CHEMOEMBOLIZATION; HUMAN GASTROINTESTINAL TISSUES;
HELICOBACTER-PYLORI INFECTION; LONG-TERM TREATMENT; NEUROENDOCRINE
TUMORS; PANCREATIC TUMORS
RP Jensen, RT (reprint author), NIDDKD,DIGEST DIS BRANCH,NIH,BLDG 10,ROOM 9C-103,10 CTR DR,MSC 1804,BETHESDA,MD 20891, USA.
NR 205
TC 24
Z9 24
U1 0
U2 0
PU BAILLIERE TINDALL
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 0950-3528
J9 BAILLIERE CLIN GASTR
JI Baillieres Clin. Gastroenterol.
PD DEC
PY 1996
VL 10
IS 4
BP 603
EP 643
DI 10.1016/S0950-3528(96)90016-0
PG 41
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA WQ741
UT WOS:A1996WQ74100005
PM 9113315
ER
PT J
AU Horak, ID
Kremer, AB
Magrath, IT
AF Horak, ID
Kremer, AB
Magrath, IT
TI Management of histologically aggressive lymphomas with a high risk of
CNS disease
SO BAILLIERES CLINICAL HAEMATOLOGY
LA English
DT Article
ID T-CELL LEUKEMIA; NERVOUS-SYSTEM LYMPHOMA;
ACQUIRED-IMMUNODEFICIENCY-SYNDROME; BONE-MARROW TRANSPLANTATION;
NON-HODGKINS LYMPHOMAS; LYMPHOBLASTIC LYMPHOMA; BURKITTS-LYMPHOMA;
RADIATION-THERAPY; INTERFERON-ALFA; ANTI-TAC
C1 NCI,LYMPHOMA BIOL SECT,PEDIAT BRANCH,NIH,BETHESDA,MD 20892.
RP Horak, ID (reprint author), JANSSEN RES FDN,1125 TRENTON HARBOURTEN RD,TITUSVILLE,NJ 08650, USA.
NR 60
TC 1
Z9 1
U1 0
U2 0
PU BAILLIERE TINDALL
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 0950-3536
J9 BAILLIERE CLIN HAEM
JI Baillieres Clin. Haematol.
PD DEC
PY 1996
VL 9
IS 4
BP 707
EP 726
DI 10.1016/S0950-3536(96)80050-3
PG 20
WC Hematology
SC Hematology
GA WM275
UT WOS:A1996WM27500006
PM 9138614
ER
PT J
AU Hyman, SE
AF Hyman, SE
TI Addiction: Taking the brain seriously
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
AB Heyman's target article is an analytical tour de force, but it makes too hard a distinction between voluntary and riven behavior. It is more fruitful to think about brain and behavior as shifting, interacting ''agents,'' represented by multiple neural circuits. This has the virtue of better connecting behavioral analysis with wet neuroscience.
C1 NIMH,ROCKVILLE,MD 20857.
RP Hyman, SE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,LAB MOL & DEV NEUROSCI,BOSTON,MA 02114, USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0140-525X
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD DEC
PY 1996
VL 19
IS 4
BP 582
EP &
PG 0
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA WY849
UT WOS:A1996WY84900012
ER
PT J
AU Lamb, ME
AF Lamb, ME
TI What is selected in group selection?
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
AB Misunderstandings often develop when scientists from different backgrounds use the same words (e.g., ''selection'') when they mean different things by them. Theorists must therefore choose and define their terms carefully. In addition, proponents of ''new'' theories need to demonstrate empirically that theirs are more powerful than the existing theories they wish to supplant. Wilson & Sober have not yet done this.
RP Lamb, ME (reprint author), NICHHD,BETHESDA,MD 20814, USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0140-525X
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD DEC
PY 1996
VL 19
IS 4
BP 779
EP &
PG 0
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA WY849
UT WOS:A1996WY84900102
ER
PT J
AU Westergaard, GC
AF Westergaard, GC
TI The lithic technology of Cebus apella and its implications for brain
evolution and the preconditions of language in Homo habilis
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
ID CAPUCHIN MONKEYS; HANDEDNESS; MANIPULATION
AB Wilkins & Wakefield (1995) provide a thoughtful contribution to our understanding of language origins. In this commentary I attempt to define the relationship between object-manipulation and primate brain function further by reviewing research on aimed throwing and the production and use of stone tools by tufted capuchin monkeys (Cebus apella). I propose that examining the relation between brain function and object-manipulating in Cebus will provide insight into the preconditions of language in our hominid ancestors.
C1 NIH,ANIM CTR,POOLESVILLE,MD 20837.
RP Westergaard, GC (reprint author), NICHHD,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837, USA.
NR 21
TC 1
Z9 1
U1 1
U2 3
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0140-525X
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD DEC
PY 1996
VL 19
IS 4
BP 792
EP &
PG 0
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA WY849
UT WOS:A1996WY84900109
ER
PT J
AU Murray, EA
Wise, SP
AF Murray, EA
Wise, SP
TI Role of the hippocampus plus subjacent cortex but not amygdala in
visuomotor conditional learning in rhesus monkeys
SO BEHAVIORAL NEUROSCIENCE
LA English
DT Article
ID PREMOTOR CORTEX; FORNIX TRANSECTION; MEMORY SYSTEM; ASSOCIATION;
LESIONS; REWARD; DISCONNECTION; DEFICITS; MOVEMENT; OBJECTS
AB Rhesus monkeys were trained to learn a large series of visuomotor conditional associations, each involving the arbitrary coupling of a visual stimulus with 1 of 3 potentially correct forelimb movements. The monkeys then received bilateral aspiration lesions of either the amygdala plus subjacent cortex or the hippocampus plus subjacent cortex. Hippocampal but not amygdala removals significantly retarded the learning of new visuomotor associations. Neither lesion affected retention. The findings argue against a general role for the amygdala in associating information across modalities, construed broadly to include motor information. By contrast, the finding that the hippocampal formation and its subjacent cortex play a role in learning new sensorimotor associations supports the view that this region participates in the long-term storage of associative information or in the recall of recently acquired information.
C1 NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD.
RP Murray, EA (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892, USA.
OI Murray, Elisabeth/0000-0003-1450-1642
NR 34
TC 61
Z9 62
U1 0
U2 0
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242
SN 0735-7044
J9 BEHAV NEUROSCI
JI Behav. Neurosci.
PD DEC
PY 1996
VL 110
IS 6
BP 1261
EP 1270
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA WA174
UT WOS:A1996WA17400005
PM 8986330
ER
PT J
AU Stratakis, CA
Orban, Z
Burns, AL
Vottero, A
Mitsiades, CS
Marx, SJ
Abbassi, V
Chrousos, GP
AF Stratakis, CA
Orban, Z
Burns, AL
Vottero, A
Mitsiades, CS
Marx, SJ
Abbassi, V
Chrousos, GP
TI Dideoxyfingerprinting (ddF) analysis of the type X collagen gene
(COL10A1) and identification of a novel mutation (S671P) in a kindred
with schmid metaphyseal chondrodysplasia
SO BIOCHEMICAL AND MOLECULAR MEDICINE
LA English
DT Article
ID DOMAIN; RESISTANCE
AB Schmid metaphyseal chondrodysplasia (SMCD; MIM 156500) is an autosomal dominant disorder of the skeleton that is manifested in early childhood by short stature, coxa vara, and a waddling gait. Patients with SMCD have mutations in the gene that codes for the alpha-1 chain of collagen X (COL10A1); however, mutation analysis of this gene is hampered by its size. We studied a family with SMCD: the mother, a 36-year-old woman with a height of 149 cm, had mild bilateral coxa vara. Her two sons presented with short stature, bowed legs, and coxa vara in early childhood. DNA was extracted from peripheral lymphocytes from the three patients and subjected to PCR amplification by COL10A1 gene-specific primers. In addition to single-strand conformational polymorphism (SSCP) analysis of the COL10A1 gene, we used a novel method, dideoxy fingerprinting (ddF). The genetic defect in this family was found to be a previously unreported missense mutation (T-to-C transition) at nucleotide 2011. This change resulted in a Ser-to-Pro substitution at position 671 of the carboxy-terminus of the COL10A1 protein. In addition, the two boys, but not the mother, were found to carry a trinucleotide (CCC) deletion at position 2048 of the 3' untranslated region, a polymorphism of the COL10A1 gene, We conclude that ddF can be used in the analysis of the COL10A1 gene along with SSCP. The S671P substitution is novel, but located in the same region with the other reported COL10A1 mutations, con firming type X collagen as the locus for this disease.
C1 NIDDKD,GENET & ENDOCRINOL SECT,METAB DIS BRANCH,NIH,BETHESDA,MD 20892.
GEORGETOWN UNIV,CHILDRENS MED CTR,DEPT PEDIAT,DIV PEDIAT ENDOCRINOL,WASHINGTON,DC 20007.
RP Stratakis, CA (reprint author), NICHHD,SECT PEDIAT ENDOCRINOL,DEV ENDOCRINOL BRANCH,NIH,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA.
NR 17
TC 7
Z9 8
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 1077-3150
J9 BIOCHEM MOL MED
JI Biochem. Mol. Med.
PD DEC
PY 1996
VL 59
IS 2
BP 112
EP 117
DI 10.1006/bmme.1996.0075
PG 6
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA WD515
UT WOS:A1996WD51500004
PM 8986632
ER
PT J
AU Timmers, KI
Clark, AE
OmatsuKanbe, M
Whiteheart, SW
Bennett, MK
Holman, GD
Cushman, SW
AF Timmers, KI
Clark, AE
OmatsuKanbe, M
Whiteheart, SW
Bennett, MK
Holman, GD
Cushman, SW
TI Identification of SNAP receptors in rat adipose cell membrane fractions
and in SNARE complexes co-immunoprecipitated with epitope-tagged
N-ethylmaleimide-sensitive fusion protein
SO BIOCHEMICAL JOURNAL
LA English
DT Article
ID INSULIN-STIMULATED TRANSLOCATION; GLUCOSE-TRANSPORTER ISOFORM; SYNAPTIC
VESICLE DOCKING; PLASMA-MEMBRANE; SUBCELLULAR TRAFFICKING; POTENTIAL
MECHANISM; 3T3-L1 ADIPOCYTES; GLUT4; LOCALIZATION; SYNTAXIN
AB The vesicle-associated membrane proteins [VAMPs; vesicle SNAP receptors (v-SNAREs)] present on GLUT4-enriched vesicles prepared from rat adipose cells [Cain, Trimble and Lienhard (1992) J. Biol. Chem. 267, 11681-11684] have been identified as synaptobrevin 2 (VAMP 2) and cellubrevin (VAMP 3) by using isoform-specific antisera. Additional antisera identify syntaxins 2 and 4 as the predominant target membrane SNAP receptors (t-SNAREs) in the plasma membranes (PM), with syntaxin 3 at one-twentieth the level. Syntaxins 2 and 4 are enriched 5-10-fold in PM compared with low-density microsomes (LDM). Insulin treatment results in an 11-fold increase in immunodetectable GLUT4 in PM and smaller (approx, 2-fold) increases in VAMP 2 and VAMP 3, whereas the subcellular distributions of the syntaxins are not altered by insulin treatment. To determine which of the SNAP receptors (SNAREs) in PM might participate in SNARE complexes with proteins from GLUT4 vesicles, complexes were immunoprecipitated with anti-myc antibody from solubilized membranes after the addition of myc-epitope-tagged N-ethylmaleimide-sensitive fusion protein (NSF) and recombinant alpha-soluble NSF attachment protein (alpha-SNAP). These complexes contain VAMPs 2 and 3 and syntaxin 4, but not syntaxins 2 or 3. Complex formation requires ATP and is disrupted by ATP hydrolysis. When all membrane fractions are prepared from basal cells, few or no VAMPs and no syntaxin 4 are immunoprecipitated in SNARE complexes obtained from LDM alone (or from immunoisolated GLUT4 vesicles). The content of syntaxin 4 depends on the presence of PM, and participation of VAMPs 2 and 3 is enhanced 4-6-fold by the addition of solubilized GLUT4 vesicles to PM. The latter increase is greater than can be explained by the 2-fold higher levels of VAMPs added to the reaction mixture. When all membrane fractions are prepared from insulin-stimulated cells, SNARE complexes formed from PM alone contain similar levels of syntaxin 4 but 5-6-fold higher levels of VAMPs 2 and 3 compared with PM alone from basal cells. Addition of GLUT4 Vesicle proteins to PM from insulin-treated cells results in a further 2-fold increase in VAMP 2 recovered in SNARE complexes, Therefore the VAMPs in PM of insulin-treated but not basal cells, and in GLUT4-vesicles from cells in either condition, are in a form that readily forms a SNARE complex with PM t-SNAREs and NSF. Insulin seems to activate PM and/or GLUT4 vesicles so as to increase the efficiency of SNARE complex formation.
C1 NIDDKD,EXPT DIABET METAB & NUTR SECT,DIABET BRANCH,NIH,BETHESDA,MD 20892.
UNIV BATH,SCH BIOL & BIOCHEM,BATH BA2 7AY,AVON,ENGLAND.
UNIV KENTUCKY,ALBERT B CHANDLER MED CTR,DEPT BIOCHEM,LEXINGTON,KY 40536.
UNIV CALIF BERKELEY,DEPT MOL & CELL BIOL,BERKELEY,CA 94720.
OI Whiteheart, Sidney/0000-0001-5577-0473
FU NHLBI NIH HHS [R01 HL056652]
NR 32
TC 53
Z9 55
U1 0
U2 0
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD DEC 1
PY 1996
VL 320
BP 429
EP 436
PN 2
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VX989
UT WOS:A1996VX98900011
PM 8973549
ER
PT J
AU Heyes, MP
Achim, CL
Wiley, CA
Major, EO
Saito, K
Markey, SP
AF Heyes, MP
Achim, CL
Wiley, CA
Major, EO
Saito, K
Markey, SP
TI Human microglia convert L-tryptophan into the neurotoxin quinolinic acid
SO BIOCHEMICAL JOURNAL
LA English
DT Article
ID KYNURENINE PATHWAY METABOLISM; CEREBROSPINAL-FLUID; NEUROACTIVE
KYNURENINES; NEUROLOGICAL DISEASE; IMMUNE ACTIVATION; BRAIN; MECHANISM;
4-CHLORO-3-HYDROXYANTHRANILATE; 6-CHLOROTRYPTOPHAN; ASTROCYTES
AB Immune activation leads to accumulations of the neurotoxin and kynurenine pathway metabolite quinolinic acid within the central nervous system of human patients. Whereas macrophages can convert L-tryptophan to quinolinic acid, it is not known whether human brain microglia can synthesize quinolinic acid. Human microglia, peripheral blood macrophages and cultures of human fetal brain cells (astrocytes and neurons) were incubated with [C-13(6)]L-tryptophan in the absence or presence of interferon gamma. [C-13(6)]Quinolinic acid was identified and quantified by gas chromatography and electron-capture negative-chemical ionization mass spectrometry. Both L-kynurenine and [C-13(6)]quinolinic acid were produced by unstimulated cultures of microglia and macrophages. Interferon gamma, an inducer of indoleamine 2,3-dioxygenase, increased the accumulation of L-kynurenine by all three cell types (to more than 40 mu M). Whereas large quantities of [C-13(6)]quinolinic acid were produced by microglia and macrophages (to 438 and 1410 nM respectively), minute quantities of [C-13(6)]quinolinic acid were produced in human fetal brain cultures (not more than 2 nM). Activated microglia and macrophage infiltrates into the brain might be an important source of accelerated conversion of L-tryptophan into quinolinic acid within the central nervous system in inflammatory diseases.
C1 PRESBYTERIAN UNIV HOSP,DIV NEUROPATHOL,PITTSBURGH,PA 15213.
NINCDS,VIRAL & MOL PATHOGENESIS LAB,BETHESDA,MD 20892.
RP Heyes, MP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 20
TC 200
Z9 201
U1 1
U2 7
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD DEC 1
PY 1996
VL 320
BP 595
EP 597
PN 2
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VX989
UT WOS:A1996VX98900034
PM 8973572
ER
PT J
AU Higley, JD
Mehlman, PT
Poland, RE
Taub, DM
Vickers, J
Suomi, SJ
Linnoila, M
AF Higley, JD
Mehlman, PT
Poland, RE
Taub, DM
Vickers, J
Suomi, SJ
Linnoila, M
TI CSF testosterone and 5-HIAA correlate with different types of aggressive
behaviors
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE nonhuman primate; aggression; serotonin; impulsivity; cerebrospinal
fluid testosterone
ID CEREBROSPINAL-FLUID MONOAMINE; 5-HYDROXYINDOLEACETIC ACID; PERSONALITY
DIMENSIONS; AMINE METABOLITES; PLASMA TESTOSTERONE; HOMOVANILLIC-ACID;
VIOLENT OFFENDERS; IMPULSE CONTROL; FIRE SETTERS; NEUROENDOCRINE
FINDINGS
AB We studied the potential roles of testosterone and serotonin in various forms of aggressive and violent behaviors by measuring each biochemical and behavior in free-ranging adolescent male nonhuman primates. Our results showed that (1) CSF free testosterone concentrations were positively correlated with overall aggressiveness, but not with measures of impulsivity. (2) CSF 5-HIAA concentrations were negatively correlated with impulsive behavior, and severe, unrestrained aggression, but not with overall rates of aggression, High rates of impulsive behavior were positively correlated with severe, unrestrained aggression, but not overall rates of aggression. (3) Dimensional analyses showed that while subjects with low CSF 5-HIAA exhibited high rates of aggression, high CSF testosterone further augmented rates and intensity of aggression in subjects with low CSF 5-HIAA. We conclude that high CSF free testosterone concentrations are associated with competitive aggression, while low CSF 5-HIAA concentrations are associated with severe aggression which results from impaired impulse control, and perseverance. (C) 1996 Society of Biological Psychiatry
C1 NIAAA, CLIN STUDIES LAB, DICBR, BETHESDA, MD 20892 USA.
LAB ANIM BREEDERS & SERV, YEMASSEE, SC USA.
HARBOR UCLA MED CTR, DIV BIOL PSYCHIAT, TORRANCE, CA 90509 USA.
US FDA, WASHINGTON, DC 20204 USA.
RP Higley, JD (reprint author), NICHHD, COMPARAT ETHOL LAB,NIH,ANIM CTR,BLDG 112, POB 529, POOLESVILLE, MD 20837 USA.
NR 67
TC 219
Z9 221
U1 2
U2 26
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD DEC 1
PY 1996
VL 40
IS 11
BP 1067
EP 1082
DI 10.1016/S0006-3223(95)00675-3
PG 16
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VT527
UT WOS:A1996VT52700001
PM 8931909
ER
PT J
AU Jacobsen, LK
Hong, WL
Hommer, DW
Hamburger, SD
Castellanos, FX
Frazier, JA
Giedd, JN
Gordon, CT
Karp, BI
McKenna, K
Rapoport, JL
AF Jacobsen, LK
Hong, WL
Hommer, DW
Hamburger, SD
Castellanos, FX
Frazier, JA
Giedd, JN
Gordon, CT
Karp, BI
McKenna, K
Rapoport, JL
TI Smooth pursuit eye movements in childhood-onset schizophrenia:
Comparison with attention-deficit hyperactivity disorder and normal
controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE eye tracking; schizophrenia children; ADHD; saccade
ID TRACKING DYSFUNCTION; ANTIPSYCHOTIC MEDICATIONS; QUANTITATIVE-ANALYSIS;
SACCADIC INTRUSIONS; TARDIVE-DYSKINESIA; NEGATIVE SYMPTOMS; PERFORMANCE;
ABNORMALITIES; CHILDREN; NEUROLEPTICS
AB Abnormalities of the smooth pursuit eye movements of adults with schizophrenia have been well described. We examined smooth pursuit eye movements in schizophrenic children, contrasting them with normal and attention-deficit hyperactivity disorder (ADHD) subjects, to determine whether there is continuity of eye movement dysfunction between childhood- and adult-onset forms of schizophrenia. Seventeen schizophrenic children with onset of illness by age 12, 18 ADHD children, and 22 normal children were studied while engaged in a smooth pursuit eye tracking task. Eye tracking variables were compared across the three groups. Schizophrenic children exhibited significantly greater smooth pursuit impairments than either normal or ADHD subjects. Within the schizophrenic group, there were no significant relationships between eye tracking variables and clinical variables, or ventricular/brain ratio. Childhood-onset schizophrenia is associated with a similar pattern of smooth pursuit abnormalities to that seen in later-onset schizophrenia. (C) 1996 Society of Biological Psychiatry
C1 ZENECA PHARMACEUT,CNS CLIN RES,WILMINGTON,DE.
NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892.
UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201.
NINCDS,OFF CLIN DIRECTOR,BETHESDA,MD 20892.
NORTHWESTERN UNIV,SCH MED,CHICAGO,IL.
RP Jacobsen, LK (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978
NR 72
TC 52
Z9 54
U1 3
U2 6
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 DEC 1
PY 1996
VL 40
IS 11
BP 1144
EP 1154
DI 10.1016/S0006-3223(95)00630-3
PG 11
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA VT527
UT WOS:A1996VT52700010
PM 8931918
ER
PT J
AU Fissore, RA
He, CL
VandeWoude, GF
AF Fissore, RA
He, CL
VandeWoude, GF
TI Potential role of mitogen-activated protein kinase during meiosis
resumption in bovine oocytes
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
ID MATURATION-PROMOTING FACTOR; GERMINAL VESICLE BREAKDOWN;
SERINE-THREONINE KINASE; EPIDERMAL GROWTH-FACTOR; XENOPUS EGG EXTRACTS;
MAP KINASE; MOUSE OOCYTES; MEIOTIC MATURATION; M-PHASE; CYTOPLASMIC
MATURATION
AB During meiotic maturation, numerous cytoplasmic and nuclear events take place that prepare the oocytes for fertilization. These changes are initiated by an increase in the activity of several kinases, most notably maturation-promoting factor, also called histone H1 kinase. Another kinase, mitogen-activated protein (MAP) kinase, is also stimulated during this period. In this study, we investigated the role of MAP kinase in bovine oocyte maturation. First, the kinetics of activation of histone H1 and MAP kinases during maturation were assessed simultaneously by evaluating their catalytic activities in vitro. We found that they are activated at approximately the same time, around germinal vesicle breakdown (GVBD). Then, at approximately 15 h of maturation, the activity of H1 kinase temporarily decreases, whereas MAP kinase remains high through the metaphase II stage. Second, the activation and catalytic activity of MAP kinase was directly evaluated by Western blotting and by an in-gel kinase assay. We determined that MAP kinase becomes activated and exhibits a decreased mobility through SDS-polyacrylamide gels, and that its catalytic activity increases as maturation progresses. In our system, most of the MAP kinase activity can be attributed to p42(MAPK2). Third, the activation pathway of MAP kinase was explored. In Xenopus oocytes, MAP kinase is activated by a kinase cascade that includes several upstream activators; one of them is the product of the proto-oncogene mos. In bovine oocytes, injection of Mos RNA elicited a rapid and maximal activation of MAP kinase that resulted in accelerated resumption of meiosis and GVBD. These results were thought to be mediated by an overexpression of a kinase-active Mos product because injection of a kinase-inactive Mos RNA failed to activate MAP kinase. Together, these results suggest a role for MAP kinase during the initiation and progression of meiosis in bovine oocytes. The data also suggest the presence of an MAP kinase-activating cascade that can be initiated by the Mos protein.
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702.
RP Fissore, RA (reprint author), UNIV MASSACHUSETTS,DEPT VET & ANIM SCI,AMHERST,MA 01003, USA.
NR 78
TC 131
Z9 138
U1 0
U2 1
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PD DEC
PY 1996
VL 55
IS 6
BP 1261
EP 1270
DI 10.1095/biolreprod55.6.1261
PG 10
WC Reproductive Biology
SC Reproductive Biology
GA VU778
UT WOS:A1996VU77800010
PM 8949882
ER
PT J
AU Shih, JH
Louis, TA
AF Shih, JH
Louis, TA
TI Tests of independence for bivariate survival data
SO BIOMETRICS
LA English
DT Article
DE bivariate failure times; covariance; cross ratio; martingale residuals
ID CENSORED-DATA; RANK-TESTS; ASSOCIATION; DISTRIBUTIONS; MODEL
AB We propose two test statistics based on the covariance process of the martingale residuals for testing independence of bivariate survival data. The first test statistic takes the supremum over time of the absolute value of the covariance process, and the second test statistic is a time-weighted summary of the process. We derive asymptotic properties of the two test statistics under the null hypothesis of independence. In addition, we derive the asymptotic distribution of the weighted test and construct optimal weights for contiguous alternatives to independence. Through simulations, we compare the performance of the proposed tests and the inner product of the Savage scores statistics of Clayton and Cuzick (1985, Journal of the Royal Statistical Society, Series A 148, 82-108). These demonstrate that the supremum test is generally more powerful with comparatively little power loss relative to their test when Clayton's family alternative holds, and the weighted test is more powerful when the weight is appropriately chosen.
C1 UNIV MINNESOTA,DIV BIOSTAT,MINNEAPOLIS,MN 55455.
RP Shih, JH (reprint author), NHLBI,OFF BIOSTAT RES,BLDG 10,BETHESDA,MD 20892, USA.
NR 17
TC 12
Z9 12
U1 0
U2 1
PU INTERNATIONAL BIOMETRIC SOC
PI WASHINGTON
PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910
SN 0006-341X
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 1996
VL 52
IS 4
BP 1440
EP 1449
DI 10.2307/2532857
PG 10
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA VX804
UT WOS:A1996VX80400025
PM 8962462
ER
PT J
AU Choi, D
Stables, JP
Kohn, H
AF Choi, D
Stables, JP
Kohn, H
TI The anticonvulsant activities of functionalized N-benzyl
2-acetamidoacetamides. The importance of the 2-acetamido substituent
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
ID DRUG DEVELOPMENT PROGRAM; BENZYLACETAMIDE DERIVATIVES; ACID-DERIVATIVES;
AMINO-ACIDS; COMPLEXES; SERIES
AB Recent studies have demonstrated that substituted N-benzyl 2-acetamidoacetamides provide significant protection against maximal electroshock (MES)-induced seizures in mice and rats. In this study, we investigated whether the 2-acetamido moiety was necessary for anticonvulsant activity. Ten derivatives of the known anticonvulsant, N-benzyl 2-acetamido-2-phenyl acetamide were prepared in which the 2-acetamido group was replaced by hydrogen, methyl, oxygen, and halogen substituents. Evaluation of these compounds in the MES-induced seizure test demonstrated that both the hydroxy and the methoxy compounds provided full protection against MES-induced seizures in mice given ip at 100 mg/kg. Moreover, evaluation of the individual stereoisomers for the hydroxy compound showed that the principal activity resided in the (R)-isomer. These findings demonstrated that the 2-acetamido substituent is important but not obligatory for the prevention of MES-induced seizures. Further supporting evidence was provided by comparing the pharmacological activities of N-benzyl 2,3-dimethoxypropionamide with N-benzyl 2-acetamido-3-methoxypropionamide. The ED(50) value for the former in the MES test was 30 mg/kg (ip), which compared favorably with phenobarbital (ED(50) = 22 mg/kg), but the ED(50) value for N-benzyl 2-acetamido-3-methoxypropionamide was 8.3 mg/kg. Copyright (C) 1996 Elsevier Science Ltd
C1 UNIV HOUSTON, DEPT CHEM, HOUSTON, TX 77204 USA.
NINCDS, EPILEPSY BRANCH, NIH, BETHESDA, MD 20892 USA.
NR 33
TC 16
Z9 16
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD DEC
PY 1996
VL 4
IS 12
BP 2105
EP 2114
DI 10.1016/S0968-0896(96)00225-8
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA WE007
UT WOS:A1996WE00700008
PM 9022975
ER
PT J
AU Hiddemann, W
Longo, DL
Coiffier, B
Fisher, RI
Cabanillas, F
Cavalli, F
Nadler, LM
DeVita, VT
Lister, TA
Armitage, JO
AF Hiddemann, W
Longo, DL
Coiffier, B
Fisher, RI
Cabanillas, F
Cavalli, F
Nadler, LM
DeVita, VT
Lister, TA
Armitage, JO
TI Lymphoma classification - The gap between biology and clinical
management is closing
SO BLOOD
LA English
DT Editorial Material
ID MANTLE CELL LYMPHOMA; NEOPLASMS
C1 UNIV GOTTINGEN,DEPT HEMATOL ONCOL,D-3400 GOTTINGEN,GERMANY.
NIA,GERONTOL RES CTR,BALTIMORE,MD 21224.
CTR HOSP LYON SUD,DEPT HEMATOL,F-69310 PIERRE BENITE,FRANCE.
LOYOLA UNIV,CTR CANC,DIV HEMATOL ONCOL,MAYWOOD,IL 60153.
MD ANDERSON CANC CTR,DEPT HEMATOL,HOUSTON,TX 77030.
OSPED SAN GIOVANNI BELLINZONA,DIV ONCOL,BELLINZONA,SWITZERLAND.
DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115.
YALE UNIV,CTR CANC,NEW HAVEN,CT.
ST BARTHOLOMEWS HOSP,DEPT MED ONCOL,LONDON,ENGLAND.
UNIV NEBRASKA,DEPT INTERNAL MED,OMAHA,NE.
NR 15
TC 109
Z9 115
U1 1
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD DEC 1
PY 1996
VL 88
IS 11
BP 4085
EP 4089
PG 5
WC Hematology
SC Hematology
GA VV152
UT WOS:A1996VV15200001
PM 8943841
ER
PT J
AU Grzegorzewski, KJ
Komschlies, KL
Franco, JL
Ruscetti, FW
Keller, JR
Wiltrout, RH
AF Grzegorzewski, KJ
Komschlies, KL
Franco, JL
Ruscetti, FW
Keller, JR
Wiltrout, RH
TI Quantitative and cell-cycle differences in progenitor cells mobilized by
recombinant human interleukin-7 and recombinant human granulocyte
colony-stimulating factor
SO BLOOD
LA English
DT Article
ID BLOOD STEM-CELLS; PERIPHERAL-BLOOD; BONE-MARROW; HEMATOLOGICAL RECOVERY;
SUPPORTIVE CARE; RHG-CSF; IN-VIVO; MICE; TRANSPLANTATION; MYELOPOIESIS
AB Administration of recombinant human interleukin-7 (rhIL-7) to mice increases the exportation of myeloid progenitors (colony-forming unit [CFU]-c and CFU-granulocyte erythroid megakaryocyte macrophage [CFU-GEMM]) from the bone marrow (BM) to peripheral organs, including blood, and also increases the number of primitive progenitor and stem cells in the peripheral blood (PB). We now report that combined treatment of mice with rhIL-7 and recombinant human granulocyte-colony stimulating factor (rhG-CSF) stimulates a twofold to 10-fold increase in the total number of PB CFU-c, and a twofold to fivefold increase in the total number of PB CFU-spleen at day 8 (CFU-S-8) over the increase stimulated by rhIL-7 or rhG-CSF alone. In addition, the quality of mobilized cells with trilineage, long-term marrow-repopulating activity is maintained or increased in mice treated with rhIL-7 and rhG-CSF compared with rhIL-7 or rhG-CSF alone. These differences in mobilizing efficiency suggest qualitative differences in the mechanisms by which rhIL-7 and rhG-CSF mobilize progenitor cells. In fact, the functional status of progenitor cells mobilized by rhIL-7 differs from that of cells mobilized by rhG-CSF in that the incidence of actively cycling (S-phase) progenitors obtained from the PB is about 20-fold higher for rhIL-7-treated mice than for mice treated with rhG-CSF. These results suggest the use of rhIL-7-mobilized progenitor/stem cells for gene-modification and tracking studies, and highlight different functions and rates of repopulation after reconstitution with PB leukocytes obtained from mice treated with rhIL-7 versus rhG-CSF.
C1 SAIC FREDERICK,INTRAMURAL RES SUPPORT PROGRAM,FREDERICK,MD.
RP Grzegorzewski, KJ (reprint author), NCI,EXPT IMMUNOL LAB,LAB LEUKOCYTE BIOL,DIV BASIC SCI,FREDERICK CANC RES & DEV CTR,BLDG 560,FREDERICK,MD 21702, USA.
NR 34
TC 7
Z9 7
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 DEC 1
PY 1996
VL 88
IS 11
BP 4139
EP 4148
PG 10
WC Hematology
SC Hematology
GA VV152
UT WOS:A1996VV15200008
PM 8943848
ER
PT J
AU Donahue, RE
Byrne, ER
Thomas, TE
Kirby, MR
Agricola, BA
Sellers, SE
Gaudernack, G
Karlsson, S
Lansdorp, PM
AF Donahue, RE
Byrne, ER
Thomas, TE
Kirby, MR
Agricola, BA
Sellers, SE
Gaudernack, G
Karlsson, S
Lansdorp, PM
TI Transplantation and gene transfer of the human glucocerebrosidase gene
into immunoselected primate CD34(+)Thy-1(+) cells
SO BLOOD
LA English
DT Article
ID NATURAL-KILLER-CELLS; HEMATOPOIETIC PROGENITOR CELLS; CD34+
MARROW-CELLS; IN-VIVO EXPRESSION; BONE-MARROW; NONHUMAN-PRIMATES; HOST
RANGES; T-CELLS; GENERATION; LYMPHOMA
AB In an attempt to improve our gene transfer efficiency into hematopoietic stem cells and to evaluate the capacity of immunoselected CD34(+)Thy-1(+)(CDw90) cells to reconstitute hematopoiesis following myeloablation, bone marrow (BM) transplantation was performed using autologous, immunoselected CD34(+)Thy-1(+)cells in rhesus macaques. BM samples were positively selected for cells that express CD34, further subdivided using high gradient immunomagnetic selection for cells that express Thy-1, and transduced using a 7-day supernatant transduction protocol with a replication-defective retroviral vector that contained the human glucocerebrosidase (GC) gene. Circulating leukocytes were evaluated using a semiquantitative polymerase chain reaction (PCR) assay for the human GC gene, with the longest surviving animal evaluated at day 558. Provirus was detected at all time points in both CD20(+) B cells and CD2(+) dim T cells, but long-term gene transfer was not observed in the granulocyte population. The CD2(+) dim population was phenotypically identified as being CD8(+) natural killer cells. By day 302 and day 330, both the CD2(+) bright and dim cell populations and sorted CD4(+) and CD8(+) cells had detectable provirus. Vector-derived GC mRNA was detected by reverse transcriptase (RT)-PCR analysis as far out as day 588. Thus, CD34(+)Thy-1(+) cells isolated using high gradient magnetic separation techniques can engraft, be transduced with a replication-defective retroviral vector, and contribute to CD20(+) B lymphocytes, CD8(+) T lymphocytes, and CD4(+) T lymphocytes; making them a suitable cell population to target for gene therapies involving lymphocytes. (C) 1996 by The American Society of Hematology.
C1 TERRY FOX LAB,VANCOUVER,BC,CANADA.
NORWEGIAN RADIUM HOSP,OSLO,NORWAY.
NINCDS,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892.
RP Donahue, RE (reprint author), NHLBI,HEMATOL BRANCH,5 RES COURT,ROCKVILLE,MD 20850, USA.
NR 26
TC 21
Z9 21
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 DEC 1
PY 1996
VL 88
IS 11
BP 4166
EP 4172
PG 7
WC Hematology
SC Hematology
GA VV152
UT WOS:A1996VV15200011
PM 8943851
ER
PT J
AU Cooke, CB
Krenacs, L
StetlerStevenson, M
Greiner, TC
Raffeld, M
Kingma, DW
Abruzzo, L
Frantz, C
Kaviani, M
Jaffe, ES
AF Cooke, CB
Krenacs, L
StetlerStevenson, M
Greiner, TC
Raffeld, M
Kingma, DW
Abruzzo, L
Frantz, C
Kaviani, M
Jaffe, ES
TI Hepatosplenic T-cell lymphoma: A distinct clinicopathologic entity of
cytotoxic gamma delta T-Cell origin
SO BLOOD
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; EPSTEIN-BARR-VIRUS; HEMOPHAGOCYTIC
SYNDROME; SUBCUTANEOUS TISSUE; GENE REARRANGEMENTS; EXPRESSION; LINEAGE;
RECEPTORS; DISEASE; LOCALIZATION
AB We identified eight cases of T-cell lymphoma with evidence of a gamma delta phenotype over a 13-year period. Seven of these cases conformed to a distinct clinicopathologic entity of hepatosplenic gamma delta T-cell lymphoma. Nearly all of these patients were young adult males (five of seven), with a median age at presentation of 20 years. They presented with marked hepatosplenomegaly, without lymphadenopathy or significant peripheral blood lymphocytosis. Thrombocytopenia was seen in all patients, and five of seven were mildly anemic. The clinical course was aggressive, and despite multiagent chemotherapy, the median survival duration was less than 1 year. The morphologic findings were uniform; a monomorphic population of medium-sized lymphoid cells with moderately clumped chromatin and a rim of pale cytoplasm infiltrated the sinusoids of the spleen, liver, and bone marrow. The cells had a characteristic immunophenotype: CD2(+), CD3(+), CD4(-), CD5(-), CD7(+), CD16(+), CD57(-), CD25(-), T-cell receptor (TCR)delta(+), beta F1(-). CD8 was positive in four of seven cases tested, and CD56 was positive in five of six. All cases expressed the cytotoxic granule-associated protein, TlA1, but perforin was detected in only one case. All cases with assessable DNA had a TCR gamma gene rearrangement, and lacked Epstein-Barr virus sequences. Isochromosome 7q was identified in two cases with cytogenetic information. The one case of cutaneous gamma delta T-cell lymphoma differed in its clinical manifestations, histologic appearance, and immunophenotype. We conclude that hepatosplenic gamma delta T-cell lymphoma is a distinct clinicopathologic entity derived from cytotoxic gamma delta T cells, and should be distinguished from other lymphomas of T-cell and natural-killer cell (NK)-like T-cell derivation. This is a US government work. There are no restrictions on its use.
C1 NCI,DIV CLIN SCI,PATHOL LAB,HEMATOPATHOL SECT,NIH,BETHESDA,MD 20892.
DC GEN HOSP,WASHINGTON,DC.
UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201.
RI Krenacs, Laszlo/L-8063-2014
OI Krenacs, Laszlo/0000-0001-6541-3031
NR 47
TC 224
Z9 234
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 DEC 1
PY 1996
VL 88
IS 11
BP 4265
EP 4274
PG 10
WC Hematology
SC Hematology
GA VV152
UT WOS:A1996VV15200023
PM 8943863
ER
PT J
AU Rosenthal, J
Thurman, GW
Cusack, N
Peterson, VM
Malech, HL
Ambruso, DR
AF Rosenthal, J
Thurman, GW
Cusack, N
Peterson, VM
Malech, HL
Ambruso, DR
TI Neutrophils from patients after burn injury express a deficiency of the
oxidase components p47-phox and p67-phox
SO BLOOD
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; COLONY-STIMULATING FACTOR; CELL-FREE
SYSTEM; ADENINE-DINUCLEOTIDE PHOSPHATE; SEVERE THERMAL-INJURY; PROTEIN
KINASE-C; NADPH OXIDASE; RESPIRATORY BURST; POLYMORPHONUCLEAR
LEUKOCYTES; MYELOPEROXIDASE DEFICIENCY
AB Infection is a major cause of morbidity and mortality in patients after thermal injury. This predisposition to infections is related, in part, to abnormal polymorphonuclear leukocyte (PMN) function and a diminished respiratory burst. To evaluate the biochemical basis for the defective respiratory burst after major burns, the status of the oxidase enzyme system and its components was investigated. PMNs were isolated from 24 patients with 12% to 62% burns. Oxidase activity of intact PMNs, measured as superoxide anion (O-2(-)) generation or oxygen consumption, was decreased in burn compared with healthy controls. Subcellular fractions from patient PMNs generated less O-2(-) in the sodium dodecyl sulfate cell-free system, and this was related to a diminished contribution by cytosol but not by plasma membrane. Subsequently, cytosol was separated with CM-Sepharose, yielding two fractions; one contained the p47-phox and p67-phox (47/67 mix) and the other contained the remaining cytosolic components (run through [RT]). Although the contribution to oxidase activity made by RT from patient cytosol was similar to that of control, the activity of p47/67 mix from PMNs of burn patients was deficient. Quantitative assays using an immunoautoradiographic technique showed a consistent, but significant decrease in both p47-phox and p67-phox. The addition of purified or human recombinant p47-phox but not p67-phox corrected the diminished oxidase activity of cytosol from burn patients. Thus, decreased respiratory burst activity found in PMNs from individuals with thermal injury was associated with a specific, quantitative deficiency of p47-phox. (C) 1996 by The American Society of Hematology.
C1 UNIV COLORADO,HLTH SCI CTR,SCH MED,DEPT PEDIAT,DENVER,CO 80262.
UNIV COLORADO,SCH MED,DEPT SURG,DENVER,CO 80262.
BELLE BONFILS MEM BLOOD CTR,DENVER,CO.
NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892.
FU NHLBI NIH HHS [K07-HL02036]
NR 59
TC 35
Z9 36
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 DEC 1
PY 1996
VL 88
IS 11
BP 4321
EP 4329
PG 9
WC Hematology
SC Hematology
GA VV152
UT WOS:A1996VV15200029
PM 8943869
ER
PT J
AU Williams, S
Wakisaka, A
Zeng, QQ
Barnes, J
Martin, G
Wechter, WJ
Liang, CT
AF Williams, S
Wakisaka, A
Zeng, QQ
Barnes, J
Martin, G
Wechter, WJ
Liang, CT
TI Minocycline prevents the decrease in bone mineral density and trabecular
bone in ovariectomized aged rats
SO BONE
LA English
DT Article
DE bone formation; bone resorption; minocycline; estrogen; trabecular
connectivity; histomorphometry
ID I IGF-I; GROWTH-FACTOR; ESTROGEN-TREATMENT; MASS; CELLS; INTERLEUKIN-6;
OSTEOPOROSIS; OSTEOBLASTS; RESORPTION; EXPRESSION
AB In the current study, we examined the effects of minocycline, on the osteopenia of ovariectomized aged rats, Old female rats were randomly divided into five groups: sham, ovariectomized control and ovariectomized treated with minocycline, 17 beta-estradiol, or both agents, Bone samples were collected 8 wk after the treatment, Ovariectomy reduced bone mineral density of the whole femur and at the condylar, distal metaphyseal and head-neck-trochanter regions 10%-19% and the loss of bone density was prevented by treatment with minocycline or 17 beta-estradiol. Histomorphometric analysis of distal femur showed ovariectomy reduced the trabecular bone area, the trabecular bone number, trabecular bone thickness and increased the trabecular bone separation, The microanatomic structure of trabecular bone also showed that the number of nodes, node to node, cortical to node, node to free end was reduced by ovariectomy, Treatment with minocycline attenuated the effect of ovariectomy on trabecular bone in aged animals, In contrast, cortical bone was not affected by ovariectomy or minocycline treatment, The effect of minocycline on bone turnover was also examined, Minocycline increased osteoid surface, mineralizing surface, mineral apposition rate, bone formation rate and reduced eroded surface. We have therefore concluded that the modest increase in bone mineral density and the improvement in the trabecular bone status noted in minocycline treated ovariectomized aged rats is likely due to an increase in bone formation coupled with a decrease in bone resorption. (C) 1996 by Elsevier Science Inc.
C1 NIA,GERONTOL RES CTR,NATL INST HLTH,BALTIMORE,MD 21224.
LOMA LINDA UNIV,LOMA LINDA,CA 92350.
NR 35
TC 39
Z9 41
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 8756-3282
J9 BONE
JI Bone
PD DEC
PY 1996
VL 19
IS 6
BP 637
EP 644
DI 10.1016/S8756-3282(96)00302-X
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA VZ104
UT WOS:A1996VZ10400011
PM 8968031
ER
PT J
AU Chanock, SJ
Walsh, TJ
AF Chanock, SJ
Walsh, TJ
TI Evolving concepts of prevention and treatment of invasive fungal
infections in pediatric bone marrow transplant recipients
SO BONE MARROW TRANSPLANTATION
LA English
DT Article; Proceedings Paper
CT 2nd Meeting on Marrow Transplantation in Children - Current Results and
Controversies
CY JUN 01-03, 1995
CL HILTON HEAD ISL, SC
SP Amgen, Glaxo, Alpha Therapeut, Baxter, Caremark, Janssen, MedImmune, Rhone Poulenc Rorer, Bristol Myers Squibb, Burroughs Wellcome, Sandoz, SmithKline Beecham, Miles, Hoffman Laroche
DE supportive care; mycosis; antifungal therapy; immunocompromised host
ID LIPOSOMAL AMPHOTERICIN-B; IMMUNOCOMPROMISED PATIENTS; ANTIFUNGAL
PROPHYLAXIS; NEUTROPENIC PATIENTS; RISK-FACTORS; GRANULOCYTOPENIC
PATIENTS; DISSEMINATED CANDIDIASIS; PULMONARY ASPERGILLOSIS; FLUCONAZOLE
PROPHYLAXIS; NEOPLASTIC DISEASES
AB Fungal infections have emerged as a major complication of marrow transplantation in children, Most episodes occur within the first 100 days and are often difficult to diagnose, Until recently, a limited number of therapeutic options were available but with new antifungal agents, including azole compounds and less toxic preparations of amphotericin, there is promise for improvements in the prevention of fungal infections as well as the treatment of established infections. This review will summarize the current approach towards therapeutic options available for the supportive care of children undergoing marrow transplantation.
RP Chanock, SJ (reprint author), NCI,PEDIAT BRANCH,NIH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA.
NR 53
TC 9
Z9 10
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 DEC
PY 1996
VL 18
SU 3
BP S15
EP S20
PG 6
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA WA473
UT WOS:A1996WA47300005
PM 8971401
ER
PT J
AU Cupler, EJ
LeonMonzon, M
Miller, J
SeminoMora, C
Anderson, TL
Dalakas, MC
AF Cupler, EJ
LeonMonzon, M
Miller, J
SeminoMora, C
Anderson, TL
Dalakas, MC
TI Inclusion body myositis in HIV-1 and HTLV-1 infected patients
SO BRAIN
LA English
DT Article
DE inclusion body myositis; HIV-1; HTLV-1; superantigen
ID ACQUIRED IMMUNODEFICIENCY SYNDROME; MONOCLONAL-ANTIBODY ANALYSIS; HUMAN
FOAMY VIRUS; INFLAMMATORY MYOPATHIES; MONONUCLEAR-CELLS; TRANSGENIC
MICE; POLYMYOSITIS; EXPRESSION; RETROVIRUS; DISEASE
AB Sporadic inclusion body myositis (IBM) is the most common inflammatory myopathy affecting patients over the age of 50 years. Dysimmune and degenerative aetiologies have been postulated, but viral infections have not been associated with the disease. Two HIV-1 (human immunodeficiency virus type 1) infected men and one woman infected with HTLV-1 (human T cell leukaemia virus type 1) developed progressive proximal muscle weakness unrelated to antiretroviral therapy. Their muscle biopsies were studied by light and electron microscopy, by immunocytochemistry to determine the expression of major histocompatibility complex (MHC) molecules and identify the type of infiltrating cells and T cell receptor (TCR) subunits, and by reverse transcription-polymerase chain reaction (RT-PCR) and single or double immunocytochemistry to search for retrovirally infected endomysial cells. The clinical features were consistent with sporadic IBM. The muscle biopsies showed primary endomysial inflammation red-rimmed vacuoles, amyloid deposits, eosinophilic inclusions, and small round fibres in groups, all diagnostic of IBM. The muscle fibres expressed MHC class-I antigens and were invaded primarily by CD8+ T-lymphocytes preferentially bearing TCR V beta 5.1 and V beta 13 chains. The HIV-1 or HTLV-1 antigens were detected only on endomysial macrophages on or around muscle fibres, but not within the muscle fibres. We conclude that IBM occurs in HIV-1 and HTLV-1 infected individuals and has a clinical, histological and immunological pattern identical to sporadic IBM in the non-retrovirally infected patients. Retroviruses do not directly infect the muscle, but persistent retroviral infections may provide superantigenic stimulation and trigger an endomysial inflammatory response identical to that occurring in sporadic IBM.
C1 NINCDS,NEUROMUSCULAR DIS SECT,NIH,BETHESDA,MD 20892.
UNIV CALIF LOS ANGELES,HARBOR MED CTR,DEPT NEUROL,TORRANCE,CA 90509.
NR 27
TC 71
Z9 72
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0006-8950
J9 BRAIN
JI Brain
PD DEC
PY 1996
VL 119
BP 1887
EP 1893
DI 10.1093/brain/119.6.1887
PN 6
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA WE280
UT WOS:A1996WE28000006
PM 9009995
ER
PT J
AU Torrey, EF
Rawlings, RR
AF Torrey, EF
Rawlings, RR
TI Fluctuations in schizophrenic births by year
SO BRITISH JOURNAL OF PSYCHIATRY
LA English
DT Article
ID SEASON; RISK
AB Background. It has previously been reported that births of individuals who later develop schizophrenia vary by birth year.
Method. Birth data were analysed on 34 024 individuals diagnosed with DSM-III-R disorganised, catatonic, and undifferentiated schizophrenia using time series analysis.
Results. Minor yearly fluctuations were observed but did not achieve statistical significance. Thus earlier findings reported in the literature could not be replicated using a different statistical approach.
Conclusion. The findings do not support theories which assume major yearly fluctuations in the births of individuals with schizophrenia. Such theories include the perinatal effects of influenza, temperature variation, and the effects of severe weather.
C1 NIMH,CTR NEUROSCI,ST ELIZABETHS HOSP,WASHINGTON,DC 20032.
NIAAA,NIH,BETHESDA,MD 20892.
NR 12
TC 6
Z9 6
U1 0
U2 0
PU ROYAL COLLEGE OF PSYCHIATRISTS
PI LONDON
PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X
8PG
SN 0007-1250
J9 BRIT J PSYCHIAT
JI Br. J. Psychiatry
PD DEC
PY 1996
VL 169
IS 6
BP 772
EP 775
DI 10.1192/bjp.169.6.772
PG 4
WC Psychiatry
SC Psychiatry
GA VX570
UT WOS:A1996VX57000016
PM 8968637
ER
PT J
AU Alarcon, GS
Tilley, B
Cooper, S
Clegg, DO
Trentham, DE
Pillemer, SR
Neuner, R
Fowler, S
AF Alarcon, GS
Tilley, B
Cooper, S
Clegg, DO
Trentham, DE
Pillemer, SR
Neuner, R
Fowler, S
TI Another look at minocycline
SO BULLETIN ON THE RHEUMATIC DISEASES
LA English
DT Letter
ID PLACEBO-CONTROLLED TRIAL; RHEUMATOID-ARTHRITIS; DOUBLE-BLIND; THERAPY
C1 UNIV VERMONT,COLL MED,BURLINGTON,VT.
UNIV UTAH,MED CTR,SALT LAKE CITY,UT.
BETH ISRAEL HOSP,BOSTON,MA 02215.
NIH,BETHESDA,MD 20892.
US FDA,ROCKVILLE,MD 20857.
HENRY FORD HLTH CTR,MIRA,INVESTIGATORS GRP,DETROIT,MI.
RP Alarcon, GS (reprint author), UNIV ALABAMA,BIRMINGHAM,AL, USA.
NR 7
TC 0
Z9 0
U1 0
U2 0
PU ARTHRITIS FOUNDATION
PI ATLANTA
PA 1314 SPRING STREET NW, ATLANTA, GA 30309
SN 0007-5248
J9 B RHEUM DIS
JI Bull. Rheum. Dis.
PD DEC
PY 1996
VL 45
IS 8
BP 6
EP 7
PG 2
WC Rheumatology
SC Rheumatology
GA WC708
UT WOS:A1996WC70800002
PM 8997812
ER
PT J
AU Goans, RE
Weiss, GH
Vieira, NE
Sidbury, JB
Abrams, SA
Yergey, AL
AF Goans, RE
Weiss, GH
Vieira, NE
Sidbury, JB
Abrams, SA
Yergey, AL
TI Calcium kinetics in glycogen storage disease type 1a
SO CALCIFIED TISSUE INTERNATIONAL
LA English
DT Article
DE glycogen storage disease 1a; Von Gierke's disease; calcium metabolism;
calcium kinetics; calcium stable isotopes
ID PLASMA CALCIUM; BONE CALCIUM; CHILDREN; TRACER
AB Glycogen storage disease type 1a (Von Gierke's disease) is one of the more common glycogen storage diseases (GSD). GSD 1a patients can have severe idiopathic osteopenia, often beginning at a young age. Since calcium tracer studies offer a sensitive probe of the bone microenvironment and of calcium deposition, kinetics might be disturbed in patients with GSD 1a. Plasma dilution kinetics obtained using the stable isotope Ca-42 are shown in this paper to be quite different between GSD 1a patients and age-matched controls. Comparison of kinetic parameters in these two populations is made using a new binding site model for describing calcium dynamics at the plasma-bone interface. This model describes reversible binding of calcium ions to postulated short-term and lone-term sites by a retention probability density function psi (t). Using this analysis, adult GSD subjects exhibited a significant decrease (P = 0.023) in the apparent half-life of a calcium ion on the longer-term site compared with controls. The general theory of calcium tracer dilution kinetics is then discussed in terms of a new model of short-term calcium homeostasis recently proposed by Bronner and Stein [5].
C1 NICHHD,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892.
DCRT,LAB PHYS SCI,NIH,BETHESDA,MD 20892.
NICHHD,HUMAN GENET BRANCH,NIH,BETHESDA,MD 20892.
BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030.
BAYLOR UNIV,USDA ARS,CHILDRENS NUTR RES CTR,HOUSTON,TX 77030.
OI Abrams, Steven/0000-0003-4972-9233
NR 19
TC 7
Z9 7
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0171-967X
J9 CALCIFIED TISSUE INT
JI Calcif. Tissue Int.
PD DEC
PY 1996
VL 59
IS 6
BP 449
EP 453
DI 10.1007/BF00369209
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA VV310
UT WOS:A1996VV31000007
PM 8939770
ER
PT J
AU Schatzkin, A
Freedman, LS
Dorgan, J
McShane, LM
Schiffman, MH
Dawsey, SM
AF Schatzkin, A
Freedman, LS
Dorgan, J
McShane, LM
Schiffman, MH
Dawsey, SM
TI Surrogate end points in cancer research: A critique
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Editorial Material
ID HUMAN PAPILLOMAVIRUS INFECTION; CERVICAL INTRAEPITHELIAL NEOPLASIA; CELL
NUCLEAR ANTIGEN; POSTMENOPAUSAL WOMEN; GENETIC ALTERATIONS; CARCINOMA
SEQUENCE; COLORECTAL-CANCER; RELIABILITY; TRIALS; PLASMA
AB Studies using surrogate end points of malignant disease may be smaller, shorter, and less expensive than studies with incident cancer end points, Researchers have proposed a broad range of histological, cellular, and molecular markers as surrogate end points for cancer (SECs), We define a valid SEC as follows: the effect of an intervention on (or the association of a risk factor with) the SEC is concordant with its effect on (or association with) incident cancer, Adenomatous polyps and persistent human papillomavirus infections are examples of reasonably valid SECs (for colorectal and cervical cancer, respectively) because these markers are necessary precursors of most of these malignancies, Inferences from other potential SECs, however, are problematic if there exist major alternative causal pathways to malignancy bypassing the SEC, Furthermore, in such circumstances, an SEC that is valid for one intervention or exposure may not be valid for another, Even for those end points without such major alternative pathways, an intervention could differentially affect two intermediate markers on the same pathway, thus disturbing the concordance between its effect on a given SEC and its effect on cancer, Thus, an understanding of the causal structure underlying the relations of interventions/exposures, potential SECs, and cancer is critical in evaluating SECs, Three questions are pertinent to elucidating this structure: (a) What is the relation of the SEC to cancer? (b) What is the relation of the intervention/exposure to the SEC? and (c) To what extent does the SEC mediate the relation between the intervention/exposure and cancer? Ecological, metabolic, observational epidemiological, and intervention studies may provide data relevant to one or more of these questions, Data on SEC variability are critical in evaluating whether marker findings have been attenuated by random sources of intra-individual variation, We emphasize the importance of conducting studies, especially SEC-cancer and intervention/exposure-SEC-cancer mediation studies, to evaluate problematic SECs such as epithelial cell hyperproliferation, For some time to come, hard and policy-relevant evidence on cancer etiology and prevention will emerge only from studies with cancer end points or, at a somewhat lower level of certainty, SECs that are (for the most part) obligatory steps on the causal pathway to malignant disease.
RP Schatzkin, A (reprint author), NCI,DEPT HLTH & HUMAN SERV,NIH,9000 ROCKVILLE PIKE,EPN 211,BETHESDA,MD 20892, USA.
NR 42
TC 41
Z9 41
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 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 1996
VL 5
IS 12
BP 947
EP 953
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA VX384
UT WOS:A1996VX38400001
PM 8959315
ER
PT J
AU Longnecker, MP
Bernstein, L
PaganiniHill, A
Enger, SM
Ross, RK
AF Longnecker, MP
Bernstein, L
PaganiniHill, A
Enger, SM
Ross, RK
TI Risk factors for in situ breast cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID CARCINOMA IN-SITU; REPLACEMENT THERAPY; ESTROGEN; WOMEN; EPIDEMIOLOGY
AB Few data exist on risk factors for in situ breast carcinoma, We examined risk factors for lit situ breast carcinoma in data from two population-based case-control studies of breast cancer conducted among female residents of Los Angeles County, Cases with ill situ or invasive disease were identified through the cancer registry for Los Angeles County in the 1980s, We included all cases ages 40 years or younger diagnosed over a 5.5-year period and all cases ages 55-64 years diagnosed over a 3-year period, Control subjects were individually matched to cases by age (+/- 3 years), neighborhood of residence, and, for younger controls, parity (nulliparous versus parous), The analysis included 233 cases with in situ cancer, 2057 cases with invasive cancer, and 2203 controls, Odds ratios (ORs) and 95% confidence intervals (CIs) were adjusted for screening mammography and established risk factors, In general, risk factors for in situ breast cancer were similar to those for invasive disease in this population, In premenopausal women, however, the risk of in situ breast cancer decreased with increasing body mass index, whereas for invasive disease, body mass index was unrelated to risk, In addition, in postmenopausal women with known age at menopause, use of unopposed estrogen replacement therapy was associated with increased risk of in situ disease [OR for ever use of estrogen alone was 1.60 (95% CI, 1.00-2.58)], whereas for invasive disease the OR was 1.23 (95% CI, 1.00-1.50), A similar difference was seen for combined hormone replacement therapy, Unmeasured increased screening among estrogen or combined replacement hormone users compared with nonusers could account for some of the association of in situ breast cancer risk with hormone replacement use.
C1 UNIV SO CALIF,SCH MED,DEPT PREVENT MED,LOS ANGELES,CA 90033.
UNIV SO CALIF,KENNETH NORRIS JR COMPREHENS CANC CTR,LOS ANGELES,CA 90033.
RP Longnecker, MP (reprint author), NIEHS,EPIDEMIOL BRANCH,POB 12233,MC A3-05,RES TRIANGLE PK,NC 27709, USA.
OI Longnecker, Matthew/0000-0001-6073-5322
FU NCI NIH HHS [CA17054, CA44546, N01-CN25404]
NR 22
TC 48
Z9 49
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 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 1996
VL 5
IS 12
BP 961
EP 965
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA VX384
UT WOS:A1996VX38400003
PM 8959317
ER
PT J
AU Rothman, N
Hayes, RB
Zenser, TV
DeMarini, DM
Bi, WF
Hirvonen, A
Talaska, G
Bhatnagar, VK
Caporaso, NE
Brooks, LR
Lakshmi, VM
Feng, PW
Kashyap, SK
You, XJ
Eischen, BT
Kashyap, R
Shelton, ML
Hsu, FF
Jaeger, M
Parikh, DJ
Davis, BB
Yin, SN
Bell, DA
AF Rothman, N
Hayes, RB
Zenser, TV
DeMarini, DM
Bi, WF
Hirvonen, A
Talaska, G
Bhatnagar, VK
Caporaso, NE
Brooks, LR
Lakshmi, VM
Feng, PW
Kashyap, SK
You, XJ
Eischen, BT
Kashyap, R
Shelton, ML
Hsu, FF
Jaeger, M
Parikh, DJ
Davis, BB
Yin, SN
Bell, DA
TI The glutathione S-transferase M1 (GSTM1) null genotype and
benzidine-associated bladder cancer, urine mutagenicity, and exfoliated
urothelial cell DNA adducts
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID TRANS-STILBENE OXIDE; CARCINOGEN-METABOLISM; HOMOZYGOUS DELETION;
EXPOSED WORKERS; SUSCEPTIBILITY; GENE; SMOKERS; POLYMORPHISM; COMMON;
RISK
AB Multiple studies in the general population have suggested that subjects with the glutathione S-transferase M1 (GSTM1)-null genotype, who lack functional GSTM1, are at higher risk for bladder cancer, To evaluate the impact of the GSTM1-null genotype on bladder cancer caused by occupational exposure to benzidine and to determine its influence on benzidine metabolism, we carried out three complementary investigations: a case-control study of bladder cancer among workers previously exposed to benzidine in China, a cross-sectional study of urothelial cell DNA adducts and urinary mutagenicity in workers currently exposed to benzidine in India, and a laboratory study of the ability of human GSTM1 to conjugate benzidine and its known metabolites in vitro, There was no overall increase in bladder cancer risk for the GSTM1-null genotype among 38 bladder cancer cases and 43 controls (odds ratio, 1.0; 95% confidence interval, 0.4-2.7), although there was some indication that highly exposed workers with the GSTM1-null genotype were at greater risk of bladder cancer compared to similarly exposed workers without this allele. However, the GSTM1 genotype had no impact on urothelial cell DNA adduct and urinary mutagenicity levels in workers currently exposed to benzidine, Furthermore, human GSTM1 did not conjugate benzidine or its metabolites, These results led us to conclude that the GSTM1-null genotype does not have an impact on bladder cancer caused by benzidine, providing a contrast to its association with elevated bladder cancer risk in the general population.
C1 VET AFFAIRS MED CTR,ST LOUIS,MO 63125.
ST LOUIS UNIV,SCH MED,ST LOUIS,MO 63125.
US EPA,DIV ENVIRONM CARCINOGENESIS,RES TRIANGLE PK,NC 27711.
CHINESE ACAD PREVENT MED,BEIJING,PEOPLES R CHINA.
NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709.
UNIV CINCINNATI,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267.
NATL INST OCCUPAT HLTH,AHMEDABAD 380016,GUJARAT,INDIA.
TIANJIN BUR CHEM IND,INST LABOR HYG,TIANJIN,PEOPLES R CHINA.
SHANGHAI INST OCCUPAT MED,SHANGHAI,PEOPLES R CHINA.
RP Rothman, N (reprint author), NCI,NIH,DIV CANC EPIDEMIOL & GENET,EPN 418,BETHESDA,MD 20892, USA.
FU NCRR NIH HHS [RR-00954]; NIADDK NIH HHS [AM-20579]; NIEHS NIH HHS
[1-P30-ES06096-01]
NR 24
TC 27
Z9 30
U1 1
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 1996
VL 5
IS 12
BP 979
EP 983
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA VX384
UT WOS:A1996VX38400006
PM 8959320
ER
PT J
AU Harty, LC
Guinee, DG
Travis, WD
Bennett, WP
Jett, J
Colby, TV
Tazelaar, H
Trastek, V
Pairolero, P
Liotta, LA
Harris, CC
Caporaso, NE
AF Harty, LC
Guinee, DG
Travis, WD
Bennett, WP
Jett, J
Colby, TV
Tazelaar, H
Trastek, V
Pairolero, P
Liotta, LA
Harris, CC
Caporaso, NE
TI p53 mutations and occupational exposures in a surgical series of lung
cancers
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; NICKEL REFINERY WORKERS; TUMOR-SUPPRESSOR GENE;
CIGARETTE-SMOKING; OXIDATIVE DAMAGE; DNA; EXPRESSION; ANGIOSARCOMAS;
ASSOCIATION; CHROMIUM
AB p53 mutations are frequent in malignant lung tumors, Of 88 surgically treated lung cancers from cigarette smokers previously evaluated for p53 mutations, 45 tumors (51.1%) had mutations in exons 5-8 (D. G. Guinee, Jr, ef al., Carcinogenesis (Lend.), 16: 993-1002, 1995), We report here the examination of 13 occupational exposures and 13 high-risk occupations in relation to these p53 mutations, Two molecular abnormalities were associated with occupational exposures: (a) G:C-->T:A transversions on the coding (nontranscribed) strand (n = 13) were associated with chromate exposure and employment in the metal industry (P < 0.05) and marginally associated with nickel exposure (P = 0.056); and (b) G:C-->A:T transitions at non-CpG sites (n = 9) were associated with work in the petrochemical industry (P = 0.05), No association was found between p53 mutations and gender, cigarette pack-years, tumor histology, age at diagnosis, or family history of lung cancer, Because all three chromate-exposed subjects had large cell carcinomas exhibiting G: C-->T:A coding-strand transversions, follow-up of a cohort with this exposure should clarify the association with the p53 gene.
C1 NCI, GENET EPIDEMIOL BRANCH, NIH, BETHESDA, MD 20892 USA.
NCI, PATHOL LAB, NIH, BETHESDA, MD 20892 USA.
NCI, HUMAN CARCINOGENESIS LAB, NIH, BETHESDA, MD 20892 USA.
ARMED FORCES INST PATHOL, DEPT PULM & MEDIASTINAL PATHOL, WASHINGTON, DC 20306 USA.
MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA.
NR 34
TC 21
Z9 22
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 1996
VL 5
IS 12
BP 997
EP 1003
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA VX384
UT WOS:A1996VX38400009
PM 8959323
ER
PT J
AU Ohnuki, Y
Reddel, RR
Bates, SE
Lehman, TA
Lechner, JF
Harris, CC
AF Ohnuki, Y
Reddel, RR
Bates, SE
Lehman, TA
Lechner, JF
Harris, CC
TI Chromosomal changes and progressive tumorigenesis of human bronchial
epithelial cell lines
SO CANCER GENETICS AND CYTOGENETICS
LA English
DT Article
ID IMMORTAL HUMAN FIBROBLASTS; SHORT ARM; INDEFINITE DIVISION; TUMOR
PROGRESSION; HUMAN-LUNG; T-ANTIGEN; CARCINOMA; SENESCENCE; CANCER;
REGION
AB A simian virus 40 (SV40)-transformed human bronchial epithelial cell line, BEAS-2B, underwent progressive changes, including the development of tumorigenicity, during extended in vitro passaging. Karyotypic changes occurred in parallel with the phenotypic changes. For the first 12 passages following viral transformation, there were random karyotypic changes. Immortalization occurred between passages 12 and 21, corresponding with the accumulation of four characteristic abnormal chromosomes-m-1: add(15)(p11.1); m-2: der(8;9)(q10;q10); m-3: add(16)(p13); and m-4: mar4-and the loss of one homolog of chromosomes 8, 15, 16, 21, and 22. With further passaging (from 21 to 63), the acquisition of weak tumorigenicity was observed, accompanied by an increased frequency of cells containing all four common abnormal chromosomes, m-l through m-4, and missing one normal homolog of chromosomes 8, 15, 16, and 22. Four tumor cell lines (B39-TL, B39-TR, B61-T4 and B61-T7) were established from tumors induced by the injection of these weakly tumorigenic BEAS-2B 39th- and 61st- passage cells into athymic nude mice. One of the cell lines, B39-TL, is significantly more tumorigenic than the others. It is notable that B39-TL showed two specific abnormal chromosomes, del(3p);der(3;15) (q10;q10) and m-6; der(21)t(3;21)(p14.2;p12) inducing deletion of a short arm of chromosome 3. Fluorescence in situ hybridization analysis with a probe for protein tyrosine phosphatase-gamma demonstrated loss of heterozygosity in the 3p14 region. The development of step-wise karyotypic changes in this in vitro carcinogenesis model parallels changes documented in several common human cancers. (C) Elsevier Science Inc., 1996
C1 CHILDRENS MED RES INST,WESTMEAD,NSW,AUSTRALIA.
NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892.
RP Ohnuki, Y (reprint author), HUNTINGTON MED RES INST,99 N EL MOLINO AVE,PASADENA,CA 91101, USA.
RI Reddel, Roger/A-6635-2014
OI Reddel, Roger/0000-0002-6302-6107
NR 51
TC 16
Z9 16
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0165-4608
J9 CANCER GENET CYTOGEN
JI Cancer Genet. Cytogenet.
PD DEC
PY 1996
VL 92
IS 2
BP 99
EP 110
DI 10.1016/S0165-4608(96)00156-2
PG 12
WC Oncology; Genetics & Heredity
SC Oncology; Genetics & Heredity
GA VZ231
UT WOS:A1996VZ23100002
PM 8976365
ER
PT J
AU Ting, CC
Wang, J
Yang, YL
AF Ting, CC
Wang, J
Yang, YL
TI Interleukin-2 and interleukin-7 augment the cytolytic activity and
expand the antitumor killing spectrum of alpha CD3-induced activated
killer cells: Potential use in the immunotherapy of non-immunogenic
tumors
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE cytokines; alpha CD3-induced killer cells; immunotherapy
ID INFILTRATING LYMPHOCYTES; MONOCLONAL-ANTIBODY; MEDIATED-IMMUNITY;
T-LYMPHOCYTES; IN-VITRO; INVIVO; SUFFICIENT; GENERATION; MELANOMA;
EFFICACY
AB This study investigates the effect of different cytokines on the growth and antitumor activity of the a CD3-induced killer cells CD3-AK, and the potential of the use of CD3-AK cells in cancer immunotherapy. Eight cytokines were tested. Only three (interleukin-2, -4 and 7) were able to support the growth of CD3-AK cells, which selectively killed different tumor targets of diversified origin. Culturing in interleukin-4 (IL-4) or IL-7 alone could maintain the growth of CD3-AK cells for 6-8 days. Only IL-2 could maintain long-term growth, but further addition of IL-4 exerted an inhibitory effect, which terminated the cell growth in 2 weeks. In contrast, despite the fact that 11,-7 inhibited the proliferation of CD3-AK cells cultured in IL-2, as determined by [H-3]thymidine uptake, the recovery of viable cells was not reduced. In 10 days, CD3-AK cells cultured in IL-2 alone or IL-2 plus IL-7 increased 160- or 176-fold respectively. There is an inverse relationship between the in vitro growth ability and Fas expression on the CD3-AK cells. Further, IL-7 increased the cytolytic activity of the CD3-AK cells two- to threefold. CD3-AK cells could be maintained in IL-2 or IL-2 plus IL-7 for 60-240 days or more. The long-term-cultured CD3-AK cells not only possessed a high level of cytolytic activity, but also showed a wide spectrum of killing with different tumor targets; the normally ''resistant'' targets, such as EL-4 lymphoma, fibrosarcoma, or melanoma, became susceptible. When the in vivo antitumor activity of the CD3-AK cells against a non-immunogenic tumor, EL-4, was tested by tumor-neutralization experiments, we found that only the long-term-cultured cells gave significant protection, with those maintained in both IL-2 and IL-7 giving the highest degree of protection. Thus, these long-term-cultured CD3-AK cells may have the potential to be used for immunotherapy of a variety of tumors whatever their immunogenicity.
RP Ting, CC (reprint author), NCI,LAB IMMUNE CELL BIOL,DIV BASIC SCI,NIH,BETHESDA,MD 20892, USA.
NR 30
TC 8
Z9 9
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD DEC
PY 1996
VL 43
IS 5
BP 283
EP 292
PG 10
WC Oncology; Immunology
SC Oncology; Immunology
GA WF505
UT WOS:A1996WF50500005
PM 9024505
ER
PT J
AU Krizman, DB
Chuaqui, RF
Meltzer, PS
Trent, JM
Duray, PH
Linehan, WM
Liotta, LA
EmmertBuck, MR
AF Krizman, DB
Chuaqui, RF
Meltzer, PS
Trent, JM
Duray, PH
Linehan, WM
Liotta, LA
EmmertBuck, MR
TI Construction of a representative cDNA library from prostatic
intraepithelial neoplasia
SO CANCER RESEARCH
LA English
DT Article
ID CLONING; CANCER; CELLS
AB We report the construction of a plasmid-based cDNA library made from microdissected cells derived from prostatic intraepithelial neoplasia, Total RNA was extracted and converted to blunt-ended double-stranded cDNA by oligo(dT)-mediated reverse transcription followed by linker addition. A linker-specific primer with UDG-compatible ends was used to amplify the cDNA and the resulting PCR product was subcloned. A total of 154 clones were sequenced and results indicated that 81.5% of the clones derived from either known genes, anonymous expressed sequence tags, or novel transcripts with very little redundancy of screened clones. These results demonstrate the feasibility of constructing complex representative cDNA libraries from specific microdissected cell populations that represent microscopic precursor stages of cancer progression. This method should facilitate identification of transcripts specifically expressed in cells of a distinct histological origin and tumorigenic stage.
C1 NCI,PATHOL LAB,BETHESDA,MD 20892.
NCI,SURG BRANCH,BETHESDA,MD 20892.
RP Krizman, DB (reprint author), NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BLDG 49,ROOM 4A15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 18
TC 66
Z9 67
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 DEC 1
PY 1996
VL 56
IS 23
BP 5380
EP 5383
PG 4
WC Oncology
SC Oncology
GA VV562
UT WOS:A1996VV56200015
PM 8968089
ER
PT J
AU Petersen, LN
Mamenta, EL
Stevnsner, T
Chaney, SG
Bohr, VA
AF Petersen, LN
Mamenta, EL
Stevnsner, T
Chaney, SG
Bohr, VA
TI Increased gene specific repair of cisplatin induced interstrand
crosslinks in cisplatin resistant cell lines, and studies on carrier
ligand specificity
SO CARCINOGENESIS
LA English
DT Article
ID HUMAN OVARIAN-CANCER; MURINE LEUKEMIA-L1210 CELLS; DNA ADDUCT FORMATION;
CYTO-TOXICITY; L1210 CELLS; PLATINUM RESISTANCE; ACQUIRED-RESISTANCE;
CIS-DIAMMINEDICHLOROPLATINUM(II); LINKS; MECHANISM
AB Development of resistance to cisplatin in previously treatment-responsive malignancies is a major obstacle to successful treatment, Enhanced DNA repair as well as enhanced replicative bypass of DNA adducts have been suggested to play a role in the development of resistance to cisplatin, However, the relative contribution of these mechanisms is unknown, Second generation platinum compounds containing the 1,2-diaminocyclohexane (dach) carrier ligand have been of particular interest in the studies of resistance mechanisms since they have been effective in treatment of cells resistant to cisplatin, We have investigated the formation and repair of interstrand crosslinks (ICL) in the mouse leukemia cell line L1210/0 and its carrier ligand specific resistant derivatives L1210/DDP and L1210/DACH after treatment with ethylenediamine (en)-Pt and diaminocyclohexane (dach)-Pt compounds, ICL in the overall genome were examined using a modification of the alkaline elution assay, A Southern blot technique was employed for the study of ICL in specific regions of the genome. In the overall genome we found decreased formation of ICL with either -en or -dach carrier ligands in the two resistant cell lines without carrier ligand specificity, Some carrier ligand specificity of ICL formation was observed in the dihydrofolate reductase (DHFR) gene, but it did not correlate with the carrier ligand specificity of resistance. At the level of the overall genome there was no difference in repair of ICL between the sensitive and the two resistant cell lines, When measured in the DHFR gene, however, there was enhanced repair of ICL in the two resistant cell lines compared with the sensitive cell line, The enhanced repair at the level of the gene did not display any carrier ligand specificity.
C1 NIA,GENET MOL LAB,NIH,BALTIMORE,MD 21224.
UNIV N CAROLINA,SCH MED,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599.
FU NCI NIH HHS [CA 34082]
NR 46
TC 32
Z9 32
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 1996
VL 17
IS 12
BP 2597
EP 2602
DI 10.1093/carcin/17.12.2597
PG 6
WC Oncology
SC Oncology
GA WC820
UT WOS:A1996WC82000009
PM 9006094
ER
PT J
AU Selmin, O
Lucier, GW
Clark, GC
Tritscher, AM
VandenHeuvel, JP
Gastel, JA
Walker, NJ
Sutter, TR
Bell, DA
AF Selmin, O
Lucier, GW
Clark, GC
Tritscher, AM
VandenHeuvel, JP
Gastel, JA
Walker, NJ
Sutter, TR
Bell, DA
TI Isolation and characterization of a novel gene induced by
2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver
SO CARCINOGENESIS
LA English
DT Article
ID DOSE-RESPONSE RELATIONSHIPS; POLYMERASE CHAIN-REACTION; DIFFERENTIAL
DISPLAY; MESSENGER-RNAS; CDNA LIBRARY; RECEPTOR; DIOXIN; EXPRESSION;
CLONING; CANCER
AB The differential display technique was used to identify genes whose expression was regulated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), Expression of a novel sequence was up-regulated in a dose-dependent fashion in liver of Sprague-Dawley male rats exposed to both chronic and acute treatment with TCDD, as measured by densitometry of Northern blot analyses (P < 0.01). A rapid amplification of cDNA ends (RACE) procedure was used to isolate a 1.8 kb cDNA from a rat liver cDNA preparation, This cloned cDNA, called 25-Dx, was sequenced and found to encode a peptide of 223 amino acids, In control rats, the 25-Dx gene was expressed at high levels in lung and liver, A hydrophobic domain of 14 residues followed by a proline-rich domain, both located in the N-terminal region, showed 71% homology with the transmembrane domain of the precursor for the interleukin-6 receptor and a conserved consensus sequence found in the cytokine/growth factor/prolactin receptor superfamily respectively.
C1 NIEHS,LAB COMPUTAT BIOL & RISK ANAL,RES TRIANGLE PK,NC 27709.
JOHNS HOPKINS MED INST,DEPT ENVIRONM HLTH SCI,BALTIMORE,MD 21205.
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
NR 35
TC 100
Z9 103
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 1996
VL 17
IS 12
BP 2609
EP 2615
DI 10.1093/carcin/17.12.2609
PG 7
WC Oncology
SC Oncology
GA WC820
UT WOS:A1996WC82000011
PM 9006096
ER
PT J
AU Higinbotham, KG
Rice, JM
Reed, CD
Watatani, M
Enomoto, T
Anderson, LM
Perantoni, AO
AF Higinbotham, KG
Rice, JM
Reed, CD
Watatani, M
Enomoto, T
Anderson, LM
Perantoni, AO
TI Variant mutational activation of the K-ras oncogene in renal mesenchymal
tumors induced in newborn F344 rats by methyl(methoxymethyl)nitrosamine
SO CARCINOGENESIS
LA English
DT Article
ID POINT MUTATIONS; MICROSATELLITE INSTABILITY; LUNG CARCINOMAS;
DNA-DAMAGE; MOUSE; CANCER; GENE; DIMETHYLNITROSAMINE; PROTOONCOGENE;
TRANSVERSIONS
AB Renal mesenchymal tumors were induced at high incidence in F344 rats by a single intraperitoneal injection of methyl(methoxymethyl) nitrosamine (DMN-OMe) within 48 h after birth, DNAs from 18 of 35 mesenchymal tumors contained transforming ras sequences in NIH3T3 transfection assays: K-ras (17/18) or N-ras (1/18), Single-stranded conformational polymorphism analysis or dideoxy sequencing of polymerase chain reaction-amplified K-rns gene fragments revealed that these neoplasms contained a variety of activating mutations in the K-ras oncogene, Alterations in codon 12 predominated and included GGT --> GAT transitions, GGT --> GTT or TGT transversions, and previously reported insertion mutations, although some tumors expressed more than one mutation and the pattern of mutations even varied within tumors, Mutations were also found in exons 2 and 3, In addition, tumor transplantability into syngeneic hosts correlated positively and significantly with K-ms activation, Renal mesenchymal tumors with transforming mutations in exon 1 were often successfully passaged (10/12) while tumors which lacked mutations in exon 1 were infrequently transplantable (2/14), While the observed base substitutions in K-rns are consistent with adduct formation, the presence of insertion mutations and intratumor heterogeneity of alterations suggest that ras activation in DMN-OMe-induced tumors is not necessarily an early event in tumorigenesis.
C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702.
NR 35
TC 3
Z9 3
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 1996
VL 17
IS 12
BP 2625
EP 2630
DI 10.1093/carcin/17.12.2625
PG 6
WC Oncology
SC Oncology
GA WC820
UT WOS:A1996WC82000013
PM 9006098
ER
PT J
AU Munoz, EF
Diwan, BA
Calvert, RJ
Weghorst, CM
Anderson, J
Rice, JM
Buzard, GS
AF Munoz, EF
Diwan, BA
Calvert, RJ
Weghorst, CM
Anderson, J
Rice, JM
Buzard, GS
TI Transplacental mutagenicity of cisplatin: H-ras codon 12 and 13
mutations in skin tumors of SENCAR mice
SO CARCINOGENESIS
LA English
DT Article
ID POLYCYCLIC AROMATIC-HYDROCARBONS; MAJOR DNA ADDUCT; DRUG CISPLATIN; COLD
SSCP; GENE; CARCINOGENESIS; AMPLIFICATION; CHEMOTHERAPY; MUTAGENESIS;
PCR
AB Cisplatin is an anticancer agent sometimes used in pregnant women, It is also a potent initiator of skin tumors in mice when administered transplacentally, For characterization of the transplacental mutagenicity of cisplatin, tumors initiated in fetal skin by cisplatin or 7,12-dimethylbenz-[n]anthracene (DMBA) and promoted by postnatal 12-O-tetradecanoyl-phorbol-13-acetate (TPA) were analyzed for H-ms mutations by 'cold' single-strand conformation polymorphism analysis and direct sequencing, The expected high incidence of exon II codon 61 mutations (20/20) was found in transplacental DMBA-initiated tumors, with no exon I change, By contrast, 6/10 cisplatin tumors had seven mutations in codons 12 or 13 of exon I, all at GpG dinucleotides, Four of these were unique codon 13 GGC --> GTC changes, significantly different from the DMBA group and from historical TPA-only controls, The activation of codons 12 and 13 by cisplatin is in accord with the known in vitro preference of cisplatin for GpG sites for intrastrand cross-linking adduct formation, These results provide the first evidence that cisplatin can act transplacentally to cause specific mutations in fetal skin that are not seen in skin tumors caused by treatment of adult skin with this agent, This is evidence for unique molecular fetal carcinogenic pathways and underscores concern about human fetal risk due to maternal cisplatin treatment.
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,INTRAMURAL RES SUPPORT PROGRAM,FREDERICK,MD 21702.
US FDA,OFF SPECIAL NUTRIT,MOD LAB 1,CLIN RES & REVIEW STAFF,LAUREL,MD 20708.
NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702.
NR 32
TC 15
Z9 15
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD DEC
PY 1996
VL 17
IS 12
BP 2741
EP 2745
DI 10.1093/carcin/17.12.2741
PG 5
WC Oncology
SC Oncology
GA WC820
UT WOS:A1996WC82000029
PM 9006114
ER
PT J
AU Veech, RL
Fell, DA
AF Veech, RL
Fell, DA
TI Distribution control of metabolic flux
SO CELL BIOCHEMISTRY AND FUNCTION
LA English
DT Article
ID STEADY-STATE TREATMENT; TOP-DOWN APPROACH; CONTROL COEFFICIENTS;
ENZYMATIC CHAINS; RAT-LIVER; SYSTEMS; YEAST; RESPIRATION; EFFECTOR;
ENZYMES
C1 OXFORD BROOKES UNIV,SCH BIOL & MOL SCI,OXFORD OX3 0BP,ENGLAND.
NIAAA,METAB & MOL BIOL LAB,ROCKVILLE,MD 20852.
RI Fell, David/B-2109-2009
OI Fell, David/0000-0001-6669-2247
NR 27
TC 10
Z9 10
U1 0
U2 0
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0263-6484
J9 CELL BIOCHEM FUNCT
JI Cell Biochem. Funct.
PD DEC
PY 1996
VL 14
IS 4
BP 229
EP 236
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA VY020
UT WOS:A1996VY02000002
PM 8952041
ER
PT J
AU Knull, H
Minton, AP
AF Knull, H
Minton, AP
TI Structure within eukaryotic cytoplasm and its relationship to glycolytic
metabolism
SO CELL BIOCHEMISTRY AND FUNCTION
LA English
DT Review
ID ACTIN-CONTAINING-FILAMENTS; RED-CELL MEMBRANE; RABBIT MUSCLE
PHOSPHOFRUCTOKINASE; MICROTUBULE-ASSOCIATED PROTEINS; PERMEABILIZED
L-929 CELLS; VASCULAR SMOOTH-MUSCLE; CROSS-LINKING PROTEINS;
GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; F-ACTIN; SKELETAL-MUSCLE
C1 NIDDKD, BIOCHEM PHARMACOL LAB, SECT PHYS BIOCHEM, NIH, BETHESDA, MD 20892 USA.
RP Knull, H (reprint author), UNIV N DAKOTA, SCH MED, DEPT BIOCHEM, GRAND FORKS, ND 58202 USA.
NR 124
TC 24
Z9 24
U1 1
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0263-6484
J9 CELL BIOCHEM FUNCT
JI Cell Biochem. Funct.
PD DEC
PY 1996
VL 14
IS 4
BP 237
EP 248
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA VY020
UT WOS:A1996VY02000003
PM 8952042
ER
PT J
AU Sheikh, MS
Garcia, M
Zhan, QM
Liu, YS
Fornace, AJ
AF Sheikh, MS
Garcia, M
Zhan, QM
Liu, YS
Fornace, AJ
TI Cell cycle-independent regulation of p(21Waf1/Cip1) and retinoblastoma
protein during okadaic acid-induced apoptosis is coupled with induction
of Bax protein in human breast carcinoma cells
SO CELL GROWTH & DIFFERENTIATION
LA English
DT Article
ID DEPENDENT KINASES; GROWTH ARREST; P53; DEATH; CANCER; GENE; EXPRESSION;
INHIBITOR; BCL-2; LINES
AB Okadaic acid (OA) is a serine/threonine protein phosphatase inhibitor and has been shown to induce apoptosis in a number of different tumor cell lines, including human breast carcinoma (HBC) cells. The molecular basis of OA-induced apoptosis remains to be investigated, Here, we demonstrate that the OA concentration that inhibits only protein phosphatase 1 and 2A was sufficient to induce apoptosis in HBC cells. In MCF-7 cells, the OA-induced apoptosis was coupled with the overexpression of endogenous p53, p21(Waf1/Cip1), and Bax proteins, whereas the Rb protein levels were decreased. OA also induced apoptosis and concomitantly enhanced the p21(Waf1/Clp1) and Bax levels in human papilloma virus protein EG-transfected variants of MCF-7 cells, in which p53 function had been disrupted, OA, by contrast, had no effect on the levels or the subcellular localization of Gadd45 and Bcl2 proteins in either wild-type or EG-transfected MCF-7 cells, Bcl-x(L), Bcl-x(s), and Bak levels were also unchanged after OA treatment in both cell types. OA-induced apoptosis and its effect on the expression of the above molecular markers occurred in the absence of any detectable changes in the cell cycle phase distribution. On the basis of our findings, we conclude the following: (a) OA-induced apoptosis in HBC cells occurs independently of cell cycle arrest; (b) the wild-type p53 function is not an absolute prerequisite for OA-induced cell death; and (c) OA-induced apoptosis is associated with up-regulation of endogenous p21(Waf1/Clp1) and Bax protein levels.
C1 INSERM, U148, F-34090 MONTPELLIER, FRANCE.
NIA, SECT GENE EXPRESS & AGING, GERONTOL RES CTR, NIH, BALTIMORE, MD 21224 USA.
RP Sheikh, MS (reprint author), NCI, MOL PHARMACOL LAB, NIH, ROOM 5D02, BLDG 37, BETHESDA, MD 20892 USA.
RI Fornace, Albert/A-7407-2008; Liu, Yusen/E-3527-2011
OI Fornace, Albert/0000-0001-9695-085X;
NR 39
TC 48
Z9 48
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1044-9523
J9 CELL GROWTH DIFFER
JI Cell Growth Differ.
PD DEC
PY 1996
VL 7
IS 12
BP 1599
EP 1607
PG 9
WC Cell Biology
SC Cell Biology
GA VX052
UT WOS:A1996VX05200002
PM 8959327
ER
PT J
AU Gorospe, M
Shack, S
Guyton, KZ
Samid, D
Holbrook, NJ
AF Gorospe, M
Shack, S
Guyton, KZ
Samid, D
Holbrook, NJ
TI Up-regulation and functional role of p21(Waf1/Cip1) during growth arrest
of human breast carcinoma MCF-7 cells by phenylacetate
SO CELL GROWTH & DIFFERENTIATION
LA English
DT Article
ID TUMOR-SUPPRESSOR PROTEIN; CYCLE CONTROL; PHENOTYPIC REVERSION; P53;
DIFFERENTIATION; EXPRESSION; CANCER; INDUCTION; LEUKEMIA; GLIOMAS
AB Phenylacetate (PA) and related aromatic fatty acids constitute a novel class of relatively nontoxic antineoplastic agents. These compounds induce tumor cytostasis and growth inhibition and differentiation of cancer cells, but little is known regarding the molecular events mediating these biological effects. Using human breast carcinoma MCF-7 cells as a model, we show here that PA-induced growth arrest is associated with enhanced expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1) and dephosphorylation of the retinoblastoma protein (PRB). The induction of p21(WAF1/CIP1) mRNA by PA was independent of the cellular p53 status. To directly assess the contribution of p21(Waf1/Cip1) to PA-mediated cytostasis, we compared the effects of PA in parental MCF-7 cells and cells expressing reduced levels of p21(Waf1/Cip1) protein (clones AS.3 and AS.4), accomplished through constitutive expression of antisense p21(Waf1/Cip1) transcripts. In contrast to parental cells, AS.3 and AS.4 cells did not show reduced pRB phosphorylation following PA treatment, indicating that p21(Waf1/Cip1) induction by PA is required for dephosphorylation (inactivation) of pRB, a known mediator of cell cycle control. A prominent role for p21(Waf1/Clp1) in mediating PA-induced growth arrest was further supported by the demonstration that embryonal fibroblasts derived from a p21(WAF1/CIP1) knockout mouse (p21(-/-) mouse embryonal fibroblasts) did not growth arrest following PA treatment, whereas PA effectively induced p21(WAF1/CIP1) mRNA and growth inhibition of the wild-type mouse embryonal fibroblasts. Taken together, our findings strongly support a role for p21(Waf1/Cip1) the PA-mediated inhibition of cell growth.
C1 NIA,MOL & CELLULAR BIOL LAB,GERONTOL RES CTR,NIH,BALTIMORE,MD 21224.
UNIV VIRGINIA,CTR CANC,EXPT THERAPEUT PROGRAM,CHARLOTTESVILLE,VA 22908.
NR 43
TC 54
Z9 56
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 1044-9523
J9 CELL GROWTH DIFFER
JI Cell Growth Differ.
PD DEC
PY 1996
VL 7
IS 12
BP 1609
EP 1615
PG 7
WC Cell Biology
SC Cell Biology
GA VX052
UT WOS:A1996VX05200003
PM 8959328
ER
PT J
AU Kenney, NJ
Smith, GH
Rosenberg, K
Cutler, ML
Dickson, RB
AF Kenney, NJ
Smith, GH
Rosenberg, K
Cutler, ML
Dickson, RB
TI Induction of ductal morphogenesis and lobular hyperplasia by
amphiregulin in the mouse mammary gland
SO CELL GROWTH & DIFFERENTIATION
LA English
DT Article
ID EPIDERMAL GROWTH-FACTOR; BREAST-CANCER CELLS; EPITHELIAL-CELLS;
FACTOR-ALPHA; FACTOR RECEPTOR; TRANSGENIC MICE; TGF-ALPHA; EXPRESSION;
CRIPTO-1; DIFFERENTIATION
AB As the juvenile mouse mammary gland matures, it undergoes extensive epithelial proliferation, leading to a network of ductal branching that transverses the organ. Recent evidence suggests that the epidermal growth factor-related peptide amphiregulin (AR) may play multiple roles in the proliferation, differentiation, and neoplastic conversion of the mouse mammary gland. Using a dual approach of recombinant AR in slow-release pellets and retroviral expression of AR, we explored the roles of this growth factor in the mouse mammary gland in vivo. We first noted that recombinant AR can reestablish longitudinal ductal proliferation in growth quiescent mammary glands of ovariectomized mice. Furthermore, retrovirally transduced mammary transplants overexpressing AR developed into hyperplastic tertiary ducts and hyperplastic lobules with increased lateral branching, apparent 9 weeks after transplantation into cleared mammary fat pads. This is the first study to demonstrate that AR can reestablish the early developmental activity of ductal mammary epithelium and induce hyperplasia in vivo. These data, coupled with previous findings that demonstrated nearly universal overexpression of AR in human breast cancer and rodent mammary tumorigenesis, suggest that AR may be an important intermediary in glandular maturation and early malignant progression.
C1 GEORGETOWN UNIV,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007.
NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892.
NR 39
TC 42
Z9 43
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 1044-9523
J9 CELL GROWTH DIFFER
JI Cell Growth Differ.
PD DEC
PY 1996
VL 7
IS 12
BP 1769
EP 1781
PG 13
WC Cell Biology
SC Cell Biology
GA VX052
UT WOS:A1996VX05200021
PM 8959346
ER
PT J
AU Jeffers, M
Rao, MS
Rulong, S
Reddy, JK
Subbarao, V
Hudson, E
VandeWoude, GF
Resau, JH
AF Jeffers, M
Rao, MS
Rulong, S
Reddy, JK
Subbarao, V
Hudson, E
VandeWoude, GF
Resau, JH
TI Hepatocyte growth factor scatter factor-met signaling induces
proliferation, migration, and morphogenesis of pancreatic oval cells
SO CELL GROWTH & DIFFERENTIATION
LA English
DT Article
ID FACTOR SCATTER FACTOR; EPITHELIAL-CELLS; PROTOONCOGENE PRODUCT; LIVER
DEVELOPMENT; RECEPTOR; RAT; EXPRESSION; IDENTIFICATION; DIFFERENTIATION;
INDUCTION
AB Hepatocyte growth factor/scatter factor (HGF/SF) is a pleiotropic effector for cells expressing the Met tyrosine kinase receptor, In this investigation, we show that pancreatic oval cells express Met and exhibit a proliferative response to HGF/SF. Additionally, we found that oval cells treated transiently with this factor become ''scattered,'' whereas those exposed to HGF/SF for extended periods of time form branching tubular structures. These structures possess true lumens, which are lined by cells with ductal features, including apical microvilli, well-developed intercellular junctions, interdigitation of plasma membranes, and abundant cytoplasmic organelles. Interestingly, these ductal structures are formed by HGF/SF-treated cells cultured on plastic dishes in the absence of exogenous extracellular matrix components. Consistent with their ability to form ductal structures in vitro, we found that pancreatic oval cells form ductal adenocarcinomas in nude mice. This study supports the involvement of HGF/SF-Met signaling in the growth, migration, and morphogenesis of pancreatic oval cells and may have important implications for the expansion and morphogenic differentiation of these cells during developmental, regenerative, and neoplastic growth.
C1 NCI,ABL BASIC RES PROGRAM,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS INC,BASIC RES PROGRAM,FREDERICK,MD 21702.
NORTHWESTERN UNIV,SCH MED,DEPT PATHOL,CHICAGO,IL 60611.
FU NIDDK NIH HHS [DK37958]
NR 50
TC 37
Z9 38
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 1044-9523
J9 CELL GROWTH DIFFER
JI Cell Growth Differ.
PD DEC
PY 1996
VL 7
IS 12
BP 1805
EP 1813
PG 9
WC Cell Biology
SC Cell Biology
GA VX052
UT WOS:A1996VX05200024
PM 8959349
ER
PT J
AU Waller, CL
Oprea, TI
Chae, K
Park, HK
Korach, KS
Laws, SC
Wiese, TE
Kelce, WR
Gray, LE
AF Waller, CL
Oprea, TI
Chae, K
Park, HK
Korach, KS
Laws, SC
Wiese, TE
Kelce, WR
Gray, LE
TI Ligand-based identification of environmental estrogens
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID MOLECULAR-FIELD ANALYSIS; POLYCHLORINATED HYDROXYBIPHENYLS; RECEPTOR;
BINDING; COMFA; VALIDATION; REGRESSION; DIOXINS; MODELS; QSAR
AB Comparative molecular field analysis (CoMFA), a three-dimensional quantitative structure-activity relationship (3D-QSAR) paradigm, was used to examine the estrogen receptor (ER) binding affinities of a series of structurally diverse natural, synthetic, and environmental chemicals of interest. The CoMFA/3D-QSAR model is statistically robust and internally consistent, and successfully illustrates that the overall steric and electrostatic properties of structurally diverse ligands for the estrogen receptor are both necessary and sufficient to describe the binding affinity. The ability of the model to accurately predict the En binding affinity of an external test set of molecules suggests that structure-based 3D-QSAR models may be used to supplement the process of endocrine disrupter identification through prioritization of novel compounds for bioassay. The general application of this 3D-QSAR model within a toxicological framework is, at present, limited only by the quantity and quality of biological data for relevant biomarkers of toxicity and hormonal responsiveness.
C1 US EPA,REPROD TOXICOL DIV,NATL HLTH & ENVIRONM EFFECTS RES LAB,RES TRIANGLE PK,NC 27711.
LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87545.
NATL INST ENVIRONM HLTH SCI,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709.
UNIV N CAROLINA,CURRICULUM TOXICOL,CHAPEL HILL,NC 27599.
RP Waller, CL (reprint author), US EPA,DIV EXPT TOXICOL,NATL HLTH & ENVIRONM EFFECTS RES LAB,RES TRIANGLE PK,NC 27711, USA.
RI Oprea, Tudor/A-5746-2011;
OI Oprea, Tudor/0000-0002-6195-6976; Korach, Kenneth/0000-0002-7765-418X
NR 25
TC 183
Z9 186
U1 0
U2 13
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD DEC
PY 1996
VL 9
IS 8
BP 1240
EP 1248
DI 10.1021/tx960054f
PG 9
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA VV616
UT WOS:A1996VV61600004
PM 8951225
ER
PT J
AU Lee, VM
Keefer, LK
Archer, MC
AF Lee, VM
Keefer, LK
Archer, MC
TI An evaluation of the roles of metabolic denitrosation and
alpha-hydroxylation in the hepatotoxicity of N-nitrosodimethylamine
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID ISOLATED RAT HEPATOCYTES; CONTROLLED BIOLOGICAL RELEASE; NITRIC-OXIDE
GENERATION; DNA-DAMAGE; HUMAN-CELLS; LIVER; TOXICITY; AGENTS;
METHYLAMINE; MECHANISMS
AB N-Nitrosodimethylamine (NDMA) is a potent hepatotoxic agent in rats. NDMA causes cell death that does not correlate with known mechanisms of toxicity such as the production of oxidative stress or covalent binding to proteins. The following studies were designed to determine whether NDMA cytotoxicity is the result of metabolic denitrosation or alpha-hydroxylation of the nitrosamine. We determined the toxicity of various metabolites of NDMA in monolayer cultures of primary rat hepatocytes. NDMA was toxic at 0.1 mM in our cultures, but the metabolites formaldehyde, methanol, and methylamine were not toxic at this concentration. We used diazeniumdiolates that spontaneously release nitric oxide (NO) in aqueous media to deliver NO to hepatocytes in culture. The results show that, while NO released from diazeniumdiolates causes death in hepatocytes, the levels of NO produced during NDMA metabolism are insufficient to account for the toxicity of the nitrosamine. NDMA-dB, the fully deuteriated form of NDMA that undergoes approximately twice as much denitrosation in vivo as NDMA, was significantly less cytotoxic than NDMA. In contrast, N-nitroso-(acetoxymethyl)methylamine (AcO-NDMA), a stable precursor of the methanediazonium ion, was found to cause toxicity equivalent to NDMA on a molar basis. Altogether, our results with methylamine, formaldehyde, methanol, the diazeniumdiolates, and NDMA-d(6) indicate that NDMA toxicity is not the result of metabolic denitrosation, while the toxicity of AcO-NDMA provides strong evidence that the formation of the methanediazonium ion via alpha-hydroxylation leads to cell death.
C1 UNIV TORONTO,FAC MED,DEPT NUTR SCI,TORONTO,ON M5S 3E2,CANADA.
UNIV TORONTO,FAC MED,DEPT MED BIOPHYS,TORONTO,ON M5S 3E2,CANADA.
NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702.
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
NR 67
TC 20
Z9 22
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD DEC
PY 1996
VL 9
IS 8
BP 1319
EP 1324
DI 10.1021/tx960077u
PG 6
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA VV616
UT WOS:A1996VV61600014
PM 8951235
ER
PT J
AU Porter, DW
Nelson, VC
Fivash, MJ
Kasprzak, KS
AF Porter, DW
Nelson, VC
Fivash, MJ
Kasprzak, KS
TI Mechanistic studies of the inhibition of MutT dGTPase by the
carcinogenic metal Ni(II)
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI; DNA-SYNTHESIS; NUCLEOSIDE TRIPHOSPHATASE; MUTAGENIC
SUBSTRATE; MOLECULAR-CLONING; TERNARY COMPLEXES; HYDROXYLATION; MUTATOR;
2'-DEOXYGUANOSINE; REPLICATION
AB Promutagenic 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) levels are increased in DNA of animals exposed to carcinogenic metals, such as Ni(II). Besides being generated directly in genomic DNA, 8-oxo-dG may be incorporated there from 8-oxo-7,8-dihydro-2'-deoxyguanosine 5'-triphosphate (8-oxo-dGTP), a product of oxidative damage to the nucleotide pool. The Escherichia coli dGTPase MutT, and analogous dGTPases in rats and humans, have been suggested as a defense against such incorporation because they hydrolyze 8-oxo-dGTP to 8-oro-7,8-dihydro-2'-deoxyguanosine 5'-monophosphate (8-oxo-dGMP). MutT and its mammalian counterparts are Mg(II)-dependent enzymes. Ni(II), in turn, is known to interact antagonistically with Mg(II) in biological systems. Thus, we hypothesized that Ni(II) might inhibit the activity of MutT. As an initial examination of this hypothesis, we conducted enzyme kinetic studies of MutT to determine the effect of Ni(II) on MutT activity and the mechanisms involved. As found, NI(II) inhibited MutT in a concentration-dependent manner when either dGTP or 8-oxo-dGTP was the nucleotide substrate. Ni(II) was determined to be an uncompetitive inhibitor of MutT with respect to Mg(II) when dGTP was the substrate, with apparent K-i of 1.2 mM Ni(II), and a noncompetitive inhibitor with respect to Mg(II) when 8-oxo-dGTP was the substrate, with apparent K-i of 0.9 mM Ni(II). Hence, the two metal cations did not compete with each other for binding at the MutT active site. This makes it difficult to predict Ni(II) effects on 8-oxo-dGTPases of other species. However, based upon the amino acid sequences of human and rat MutT-like dGTPases, their capacity for Ni(II) binding should be greater than that of MutT. Whether this could lead to stronger inhibition of those enzymes by Ni(II), or not, remains to be investigated.
C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV INC,FREDERICK,MD 21702.
NR 36
TC 8
Z9 8
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD DEC
PY 1996
VL 9
IS 8
BP 1375
EP 1381
DI 10.1021/tx9600816
PG 7
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA VV616
UT WOS:A1996VV61600022
PM 8951243
ER
PT J
AU Lamb, ME
Hershkowitz, I
Sternberg, KJ
Boat, B
Everson, MD
AF Lamb, ME
Hershkowitz, I
Sternberg, KJ
Boat, B
Everson, MD
TI Investigative interviews of alleged sexual abuse victims with and
without anatomical dolls
SO CHILD ABUSE & NEGLECT
LA English
DT Article
DE anatomical dolls; interview processes; investigative interviews
ID CHILDRENS REPORTS; DETAILED DOLLS; CORRECT DOLLS; PROFESSIONALS; MEMORY
AB Verbal and nonverbal responses by alleged victims of child sexual abuse were coded for length, amount of information, and the manner in which they were elicited by the interviewer. In 16 of the interviews, anatomical dolls were employed for the purposes of demonstration, whereas they were not used in another eight cases matched with respect to other characteristics of the children and the alleged events. Children interviewed with dolls provided an equivalent number of details and spoke as many words in the substantive portion of the interview as did children interviewed without dolls, and interviewers in the two groups used similar probes to elicit information. However, the average responses by the children were significantly longer and more detailed when dolls were not used. Children gave longer and more detailed responses to open-ended invitations when dolls were not used. Caution is necessary when interpreting these findings. Copyright (C) 1996 Elsevier Science Ltd
C1 UNIV CINCINNATI, DEPT PSYCHIAT, CINCINNATI, OH USA.
UNIV N CAROLINA, DEPT PSYCHIAT, CHAPEL HILL, NC USA.
RP Lamb, ME (reprint author), NICHHD, SECT SOCIAL & EMOT DEV, 9190 ROCKVILLE PIKE, BETHESDA, MD 20814 USA.
NR 26
TC 35
Z9 35
U1 1
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2134
J9 CHILD ABUSE NEGLECT
JI Child Abuse Negl.
PD DEC
PY 1996
VL 20
IS 12
BP 1251
EP 1259
DI 10.1016/S0145-2134(96)00121-4
PG 9
WC Family Studies; Psychology, Social; Social Work
SC Family Studies; Psychology; Social Work
GA VV282
UT WOS:A1996VV28200013
PM 8985616
ER
PT J
AU Bornstein, MH
Haynes, OM
OReilly, AW
Painter, KM
AF Bornstein, MH
Haynes, OM
OReilly, AW
Painter, KM
TI Solitary and collaborative pretense play in early childhood: Sources of
individual variation in the development of representational competence
SO CHILD DEVELOPMENT
LA English
DT Article
ID SOCIOECONOMIC-STATUS; SYMBOLIC PLAY; INFANT TEMPERAMENT; BEHAVIOR;
MOTHER; ATTACHMENT; LANGUAGE; PARENTS; PERFORMANCE; ENVIRONMENT
AB This study evaluates sources of individual variation in child pretense play as an expression of emerging mental representation. Family sociodemographic characteristics, maternal personological characteristics, and maternal affective and cognitive play behaviors, as well as children's gender, language competence, and play, were examined simultaneously. Naturalistic child solitary play and child collaborative play with mother were videorecorded in 141 20-month-olds. Child solitary play, child-initiated and mother-initiated collaborative play with mother, and maternal demonstrations and solicitations of play were then coded into nonsymbolic and symbolic acts. Zero-order relations obtained between child play and, respectively, child gender and language, family SES, and maternal verbal intelligence, personality, physical affection, and play demonstrations and solicitations. Structural equation modeling supported the following unique predictive relations: Child language and mothers' symbolic play positively influenced child collaborative play, and child gender and mothers' verbal intelligence predicted child solitary play. Child gender and mothers' verbal intelligence and physical affection influenced mothers' play and so influenced child collaborative play indirectly. The cognitive advantages of child play and maternal influences on child play are placed in an adaptive parenting framework.
C1 W VIRGINIA UNIV,MORGANTOWN,WV 26506.
RP Bornstein, MH (reprint author), NICHHD,BLDG 31,ROOM B2B15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 96
TC 62
Z9 64
U1 1
U2 10
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0009-3920
J9 CHILD DEV
JI Child Dev.
PD DEC
PY 1996
VL 67
IS 6
BP 2910
EP 2929
DI 10.1111/j.1467-8624.1996.tb01895.x
PG 20
WC Psychology, Educational; Psychology, Developmental
SC Psychology
GA WN235
UT WOS:A1996WN23500018
PM 9071765
ER
EF