FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Leferson, JD
Kleiner, DE
StetlerStevenson, WG
AF Leferson, JD
Kleiner, DE
StetlerStevenson, WG
TI Macromolecular substrate inhibition of matrix metalloproteinases
demonstrated using a competing thiopeptolide assay.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,PATHOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 765
EP 765
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86100997
ER
PT J
AU Johnson, AC
Reed, AL
AF Johnson, AC
Reed, AL
TI Molecular cloning and characterization of a eukaryotic transcriptional
repressor
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,DIV BASIC SCI,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 824
EP 824
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101054
ER
PT J
AU Kopantzev, E
Roschke, V
Rudikoff, S
AF Kopantzev, E
Roschke, V
Rudikoff, S
TI Immunomodulatory effects of murine plasmacytoma cells transfected with a
retroviral vector encoding interleukin-2 cDNA
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 852
EP 852
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101082
ER
PT J
AU Roschke, V
Kopantzev, E
Hausner, P
Rudikoff, S
AF Roschke, V
Kopantzev, E
Hausner, P
Rudikoff, S
TI Dissemination pattern of murine plasmacytoma.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 854
EP 854
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101086
ER
PT J
AU Yu, W
Sipowicz, MA
Kasprzak, KS
Haines, D
Anderson, LM
AF Yu, W
Sipowicz, MA
Kasprzak, KS
Haines, D
Anderson, LM
TI Pathological effects of preconception exposure to urethane or chromium
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 858
EP 858
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101088
ER
PT J
AU Quan, X
Akiyama, SK
Godfrey, HP
AF Quan, X
Akiyama, SK
Godfrey, HP
TI Activation of endothelial cells by T cell fibronectin (FN).
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NEW YORK MED COLL,VALHALLA,NY 10595.
NIDR,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 874
EP 874
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101105
ER
PT J
AU Medin, JA
Tudor, M
Simovitch, R
Quirk, JM
Jacobson, S
Murray, GJ
Brady, RO
AF Medin, JA
Tudor, M
Simovitch, R
Quirk, JM
Jacobson, S
Murray, GJ
Brady, RO
TI Gene therapy for fabry disease: Expression, secretion and uptake of
alpha-galactosidase A (alpha-gal A) driven by a high titer recombinant
retroviral
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS,UNIT THERAPEUT GENE TRANSFER,DEV & METAB NEUROL BRANCH,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 885
EP 885
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101114
ER
PT J
AU Curiel, RE
Lahesmaa, R
Cippitelli, M
Subleski, J
Young, HA
Ghosh, P
AF Curiel, RE
Lahesmaa, R
Cippitelli, M
Subleski, J
Young, HA
Ghosh, P
TI Identification of an IL-4-responsive element in the promoter of human
IL-4 gene.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,DBS,FREDERICK,MD 21702.
SYNTEX RES,DEPT LEUKO BIOL,PALO ALTO,CA 94304.
SAIC FREDERICK,BCDP,FREDERICK,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 890
EP 890
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101119
ER
PT J
AU Choudhury, BK
Mannen, H
Sharief, FS
Hou, EW
Li, SSL
AF Choudhury, BK
Mannen, H
Sharief, FS
Hou, EW
Li, SSL
TI Cloning, structure and evolution of the enhancer of split groucho and
related genes from human, mouse, alligator, Xenopus and nematode
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS,GENET MOLEC LAB,NIH,RES TRIANGLE PK,NC 27709.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 896
EP 896
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101124
ER
PT J
AU Park, SI
Lee, BJ
Hatfield, DL
AF Park, SI
Lee, BJ
Hatfield, DL
TI Drosophila as a model to study the effects of selenium on aging, cancer
and heart disease.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,LEC,NIH,BETHESDA,MD 20892.
SEOUL NATL UNIV,INST MOLEC BIOL & GENET,LMG,SEOUL,SOUTH KOREA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 904
EP 904
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101134
ER
PT J
AU Burshtyn, DN
Scharenberg, AM
Wagtmann, N
Rajagopalan, S
Berrada, K
Yi, T
Kinet, JP
Long, EO
AF Burshtyn, DN
Scharenberg, AM
Wagtmann, N
Rajagopalan, S
Berrada, K
Yi, T
Kinet, JP
Long, EO
TI Signal transduction by killer cell inhibitory receptors involves
recruitment of tyrosine phosphatase SHP-1
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852.
CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 915
EP 915
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101145
ER
PT J
AU Marth, T
Seder, RA
Strober, W
Kelsall, BL
AF Marth, T
Seder, RA
Strober, W
Kelsall, BL
TI Regulation of transforming growth factor B production by interleukin-12.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,MUCOSAL IMMUN SECT,LCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 937
EP 937
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101167
ER
PT J
AU Asai, O
Funakoshi, S
Beckwith, M
Fanslow, W
Longo, DL
Murphy, WJ
AF Asai, O
Funakoshi, S
Beckwith, M
Fanslow, W
Longo, DL
Murphy, WJ
TI Inhibition of murine B-cell lymphoma growth by soluble recombinant
murine CD40 ligand
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD 21702.
NCI,DBS,LLB,FREDERICK,MD 21702.
IMMUNEX CORP,SEATTLE,WA.
NIA,BALTIMORE,MD 21224.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 944
EP 944
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101174
ER
PT J
AU Pospisil, R
Fitts, M
Mage, RG
AF Pospisil, R
Fitts, M
Mage, RG
TI CD5 on rabbit appendix B-lymphocytes is a potential selecting ligand for
B-cell surface immunoglobulin framework region sequences
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD.
RI Pospisil, Richard/B-7467-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 951
EP 951
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101180
ER
PT J
AU Zhang, J
Berenstein, EH
Evans, RL
Siraganian, RP
AF Zhang, J
Berenstein, EH
Evans, RL
Siraganian, RP
TI Transfection of Syk reconstitutes high affinity IgE mediated
degranulation in Syk negative variants of rat basophilic leukemia
RBL-2H3 cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 959
EP 959
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101189
ER
PT J
AU Song, JS
HaleemSmith, H
Szallasi, Z
Blumberg, PM
Rivera, J
AF Song, JS
HaleemSmith, H
Szallasi, Z
Blumberg, PM
Rivera, J
TI Association of PKC-delta with Src kinase family members in the RBL-2H3
mucosal mast cell line: Implications on the regulation of PKC-delta
activity.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAMS,BETHESDA,MD 20892.
NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 961
EP 961
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101190
ER
PT J
AU SchartonKersten, T
Butcher, B
Denkers, E
Gazzinelli, R
Grunvald, E
Sher, A
AF SchartonKersten, T
Butcher, B
Denkers, E
Gazzinelli, R
Grunvald, E
Sher, A
TI Endogenous IFN-gamma is not required for the induction of macrophage and
granulocyte IL-12 responses during acute infection with Toxoplasma
gondii.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 966
EP 966
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101198
ER
PT J
AU Chen, HT
Alexander, CB
Chen, FF
Mage, RG
AF Chen, HT
Alexander, CB
Chen, FF
Mage, RG
TI Rabbit DQ52 and D-H gene rearrangements in early B-cell development.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,IMMUNOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1004
EP 1004
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101232
ER
PT J
AU Zhu, XJ
SadeghNasseri, S
Bavari, S
Ulrich, RG
Mage, M
AF Zhu, XJ
SadeghNasseri, S
Bavari, S
Ulrich, RG
Mage, M
TI Recombinant single chain human HLA-DR1 molecules as biologically active
covalently linked heterotrimers of antigenic peptide, beta chain, and
alpha chain.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
AMER RED CROSS,ROCKVILLE,MD.
ARMY MED RES INST,FREDERICK,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1013
EP 1013
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101245
ER
PT J
AU Han, M
Robinson, M
Kindt, TJ
AF Han, M
Robinson, M
Kindt, TJ
TI Mapping of the rabbit MHC.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LIG,NIH,ROCKVILLE,MD 20852.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1019
EP 1019
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101251
ER
PT J
AU Currier, JR
Robinson, MA
AF Currier, JR
Robinson, MA
TI Distinctive patterns of TCR diversity generated in response to mitogen,
superantigen and nominal antigen.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,IMMUNOGENET LAB,ROCKVILLE,MD 20852.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1029
EP 1029
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101259
ER
PT J
AU Hieny, S
Grunvald, E
Morita, Y
Englund, PT
Gazzinelli, RT
Sher, A
AF Hieny, S
Grunvald, E
Morita, Y
Englund, PT
Gazzinelli, RT
Sher, A
TI Characterization of IL-12 and TNF-alpha inducing activities in
Toxoplasma gondii as protein-associated glycolipids.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 JOHNS HOPKINS SCH MED,BALTIMORE,MD 21205.
NIAID,LPD,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1045
EP 1045
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101275
ER
PT J
AU Zhou, P
Sieve, MC
Tewari, RP
Seder, RA
AF Zhou, P
Sieve, MC
Tewari, RP
Seder, RA
TI IL-12 and amphotericin B prolong survival in SCID mice infected with
Histoplasma capsulatum.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,BETHESDA,MD 20892.
SO ILLINOIS MED SCH,SPRINGFIELD,IL.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1050
EP 1050
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101278
ER
PT J
AU Camargo, M
Almeida, IC
Rizzo, LV
Travassos, LR
Gazzinelli, RT
AF Camargo, M
Almeida, IC
Rizzo, LV
Travassos, LR
Gazzinelli, RT
TI A Trypanosoma cruzi derived glycoconjugate is potent inducer of IL-12
synthesis by macrophages.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV FED MINAS GERAIS,DEPT BIOCHEM & IMMUNOL,BR-30161 BELO HORIZONT,MG,BRAZIL.
FIOCRUZ MS,CTR PESQUISAS RENE RACHOU,LAB CHAGAS DIS,BR-30161 BELO HORIZONT,MG,BRAZIL.
EPM,DISC CELLULAR BIOL,SAO PAULO,BRAZIL.
NEI,NIH,BETHESDA,MD 20982.
RI Rizzo, Luiz Vicente/B-4458-2009; Travassos, Luiz/J-3631-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1052
EP 1052
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101282
ER
PT J
AU McDyer, JF
Seder, RA
AF McDyer, JF
Seder, RA
TI Characterization of cytokine production from patients with multi-drug
resistant tuberculosis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1063
EP 1063
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101293
ER
PT J
AU Peruzzi, M
Wagtmann, N
Malnati, M
Parker, K
Long, EO
AF Peruzzi, M
Wagtmann, N
Malnati, M
Parker, K
Long, EO
TI A single killer cell inhibitory receptor (KIR) can discriminate among
peptides bound to HLA-B*2705.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,MOLEC STRUCT LAB,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852.
RI Long, Eric/G-5475-2011
OI Long, Eric/0000-0002-7793-3728
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1076
EP 1076
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101305
ER
PT J
AU Sconocchia, G
Titus, IA
Pericle, F
Segal, DM
AF Sconocchia, G
Titus, IA
Pericle, F
Segal, DM
TI A tyrosine phosphorylated protein may link CD44 to NK cytotoxicity
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1085
EP 1085
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101315
ER
PT J
AU Jakob, T
Udey, MC
AF Jakob, T
Udey, MC
TI E-cadherin-associated proteins and tyrosinephosphorylation status in
Langerhans cell-like dendritic cells (FSDC) propagated from fetal murine
skin
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,DERMATOL BRANCH,NIH,BETHESDA,MD.
RI Jakob, Thilo/J-1621-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1182
EP 1182
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101411
ER
PT J
AU Yamashita, Y
Hodes, RJ
AF Yamashita, Y
Hodes, RJ
TI Regulation of mouse CD44 epitopes associated with expression of variable
exon-containing isoforms.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NIA,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1183
EP 1183
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101414
ER
PT J
AU Caspi, RR
Jones, LS
Agarwal, R
Silver, PB
Chan, CC
Rizzo, LV
AF Caspi, RR
Jones, LS
Agarwal, R
Silver, PB
Chan, CC
Rizzo, LV
TI Interferon gamma (IFN-gamma)-deficient mice are susceptible to induction
of experimental autoimmune uveitis (EAU)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892.
HHMI,NIH,RES SCHOLARS PROG,BETHESDA,MD 20892.
RI Rizzo, Luiz Vicente/B-4458-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1188
EP 1188
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101417
ER
PT J
AU Silver, P
Hathcock, K
Chan, CC
Green, JM
Thompson, CB
Caspi, R
AF Silver, P
Hathcock, K
Chan, CC
Green, JM
Thompson, CB
Caspi, R
TI CD28 costimulation is required for induction of autoimmune, but not for
endotoxin-induced, uveitis.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NEI,NIH,BETHESDA,MD 20892.
NCI,NIH,BETHESDA,MD 20892.
UNIV CHICAGO,GWEN KNAPP CTR,CHICAGO,IL 60637.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1189
EP 1189
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101420
ER
PT J
AU Tuscano, J
Tedder, TF
Kehrl, JH
AF Tuscano, J
Tedder, TF
Kehrl, JH
TI Engagement of the adhesion receptor CD22 triggers a potent stimulatory
signal for B cells and blocking CD22/CD22L interactions impairs T-cell
proliferation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LIR,NIH,BETHESDA,MD 20892.
DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1213
EP 1213
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101441
ER
PT J
AU Chen, ZJ
Shimizu, F
Wheeler, J
Notkins, AL
AF Chen, ZJ
Shimizu, F
Wheeler, J
Notkins, AL
TI Properties of polyreactive antigen-binding B cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,DEPT ORAL MED,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1217
EP 1217
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101446
ER
PT J
AU Bouloc, A
Walker, P
Grivel, JC
Vogel, J
Katz, SL
AF Bouloc, A
Walker, P
Grivel, JC
Vogel, J
Katz, SL
TI A role for Langerhans cells in intracutaneous DNA immunization.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1232
EP 1232
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101459
ER
PT J
AU Swieter, M
Berenstein, EH
Siraganian, RP
AF Swieter, M
Berenstein, EH
Siraganian, RP
TI Protein tyrosine phosphatases in RBL-2H3 cells and their possible
involvement in IgE receptor (Fc epsilon RI) signaling.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20893.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1242
EP 1242
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101470
ER
PT J
AU Hamawy, MM
Sagawa, K
Zhang, J
Mergenhagen, SE
Siraganian, RP
AF Hamawy, MM
Sagawa, K
Zhang, J
Mergenhagen, SE
Siraganian, RP
TI A 72 kDa protein downstream of Syk that is tyrosine phosphorylated by
the aggregation of the high affinity IgE receptor (Fc epsilon RI).
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1243
EP 1243
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101473
ER
PT J
AU Berenstein, EH
Swieter, M
Siraganian, RP
AF Berenstein, EH
Swieter, M
Siraganian, RP
TI CD45 and signaling through the Fc epsilon RI in RBL-2H3 mast cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1245
EP 1245
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101474
ER
PT J
AU Kimura, T
Sakamoto, H
Apella, E
Siraganian, RP
AF Kimura, T
Sakamoto, H
Apella, E
Siraganian, RP
TI Conformational changes induced in protein tyrosine kinase Syk by
tyrosine phosphorylation or by binding of phosphorylated ITAM peptides.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,BETHESDA,MD 20892.
NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1252
EP 1252
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101481
ER
PT J
AU Amichay, D
Gazzinelli, R
Karupiah, G
Sher, A
Farber, I
AF Amichay, D
Gazzinelli, R
Karupiah, G
Sher, A
Farber, I
TI Chemokine expression patterns suggest unique biological roles in-vivo.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1290
EP 1290
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101520
ER
PT J
AU Kioka, N
Humphries, MJ
Akiyama, SK
AF Kioka, N
Humphries, MJ
Akiyama, SK
TI Effects of integrin activation on cell proliferation and the cell cycle.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,BETHESDA,MD 20892.
UNIV MANCHESTER,SCH BIOL SCI,MANCHESTER,LANCS,ENGLAND.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1326
EP 1326
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101555
ER
PT J
AU Yang, LH
Ahmed, SA
Miles, EW
AF Yang, LH
Ahmed, SA
Miles, EW
TI Roles of conserved and variable C-terminal residues in the beta subunit
of tryptophan synthase.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1374
EP 1374
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101605
ER
PT J
AU Gladyshev, VN
Jeang, KT
Stadtman, TC
AF Gladyshev, VN
Jeang, KT
Stadtman, TC
TI Selenium in normal and HIV-infected human T-cells: Selenocysteine in a
C-terminal tripeptide of T-cell thioredoxin reductase corresponds to TGA
in the gene.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892.
NIAID,NIH,MOLEC MICROBIOL LAB,BETHESDA,MD 20892.
RI Jeang, Kuan-Teh/A-2424-2008
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1405
EP 1405
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101632
ER
PT J
AU Kang, JH
Yim, HS
Kwak, HS
Chock, PB
Stadtman, ER
Yim, MB
AF Kang, JH
Yim, HS
Kwak, HS
Chock, PB
Stadtman, ER
Yim, MB
TI A gain-of-function of an amyotrophic lateral sclerosis-associated
Cu,Zn-superoxide dismutase mutant.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1422
EP 1422
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101652
ER
PT J
AU Qin, KF
Wang, YX
Huang, CY
AF Qin, KF
Wang, YX
Huang, CY
TI Characteristics of a novel Mg2+-dependent, Ca2+-inhibitable
serine/threonine phosphatase revealed by molecular cloning.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1457
EP 1457
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101686
ER
PT J
AU Huang, K
Sommers, CL
Grinberg, A
Kozak, CA
Love, PE
AF Huang, K
Sommers, CL
Grinberg, A
Kozak, CA
Love, PE
TI Cloning and characterization of PTPK1, a novel nonreceptor protein
tyrosine phosphatase highly expressed in bone marrow.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD,NIH,BETHESDA,MD 20892.
NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1463
EP 1463
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101692
ER
PT J
AU deMendez, I
Leto, T
AF deMendez, I
Leto, T
TI The molecular basis of p47(phox) SH3 domain binding specificities.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1515
EP 1515
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101744
ER
PT J
AU Leto, TL
AF Leto, TL
TI The p67-phox NADPH oxidase component is comprised of several
tetratricopeptide repeats (TPR) that are disrupted in a rare form of
chronic granulomatous disease
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1516
EP 1516
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101745
ER
PT J
AU Roche, PA
Chawla, A
Ravichandran, V
AF Roche, PA
Chawla, A
Ravichandran, V
TI Identification and characterization of SNAP-23, the non-neuronal homolog
of the membrane fusion protein receptor SNAP-25.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1530
EP 1530
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101758
ER
PT J
AU Kong, SK
Chock, PB
AF Kong, SK
Chock, PB
TI Ubiquitin carrier protein kinase activity of normal rat tissues.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1549
EP 1549
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101779
ER
PT J
AU MacGregor, D
Marrogi, AJ
Lockyer, JM
Gendelman, R
Lu, M
Ensoli, B
AF MacGregor, D
Marrogi, AJ
Lockyer, JM
Gendelman, R
Lu, M
Ensoli, B
TI Expression of Bcl-2 in AIDS-associated and classical Kaposi's Sarcoma.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 TULANE UNIV,MED CTR,NEW ORLEANS,LA 70112.
NCI,NIH,BETHESDA,MD 20892.
RI Ensoli, Barbara/J-9169-2016
OI Ensoli, Barbara/0000-0002-0545-8737
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1571
EP 1571
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101801
ER
PT J
AU Oliver, GW
EmmertBuck, M
StetlerStevenson, WG
Lim, MS
Kleiner, DE
AF Oliver, GW
EmmertBuck, M
StetlerStevenson, WG
Lim, MS
Kleiner, DE
TI Quantitative analysis of picogram amounts of metalloproteinase
inhibitors in human tumor tissues.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,PATHOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1579
EP 1579
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101808
ER
PT J
AU Utz, U
Banks, D
McFarland, HF
Jacobson, S
Biddison, WE
AF Utz, U
Banks, D
McFarland, HF
Jacobson, S
Biddison, WE
TI TCR usage in human demyelinating diseases: MBP-reactive TCR in MS versus
HTLV-I tax-reactive TCR in HAM/TSP.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
INST RECH CLIN MONTREAL,IMMUNOL LAB,MONTREAL,PQ H2W 1R7,CANADA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1589
EP 1589
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101819
ER
PT J
AU Omori, M
Evarts, RP
Hu, Z
Omori, N
Marsden, ER
Thorgeirsson, SS
AF Omori, M
Evarts, RP
Hu, Z
Omori, N
Marsden, ER
Thorgeirsson, SS
TI Activation of stem cell compartment in bile duct ligated young rats.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,LEC,DBS,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1629
EP 1629
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101857
ER
PT J
AU Omori, N
Evarts, RP
Omori, M
Hu, Z
Marsden, ER
Thorgeirsson, SS
AF Omori, N
Evarts, RP
Omori, M
Hu, Z
Marsden, ER
Thorgeirsson, SS
TI Expression of leukemia inhibitory factor and its receptor during liver
regeneration in the adult rat
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,LEC,DBS,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1637
EP 1637
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101864
ER
PT J
AU Schweighoffer, E
Fowlkes, BJ
AF Schweighoffer, E
Fowlkes, BJ
TI alpha beta/gamma delta lineage decisions in T cell development
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NATL INST HLTH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1739
EP 1739
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101968
ER
PT J
AU Magner, WJ
Chang, AC
Hong, MJP
Brooks, A
Owens, J
Coligan, JE
AF Magner, WJ
Chang, AC
Hong, MJP
Brooks, A
Owens, J
Coligan, JE
TI Aberrant differentiation of thymocytes in mice lacking laminin-2
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,MOLEC STRUCT LAB,ROCKVILLE,MD 20852.
NCRR,NIH,LAB SCI SECT,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1740
EP 1740
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101970
ER
PT J
AU Parker, K
Turner, R
Coligan, J
Biddison, W
AF Parker, K
Turner, R
Coligan, J
Biddison, W
TI HLA-A2/HTLV-1 tax peptide single-chain molecules are recognized by
tax-specific and HLA-A2 allo-specific T cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,ROCKVILLE,MD 20852.
NINCDS,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1750
EP 1750
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101981
ER
PT J
AU Fenske, TS
Farner, NL
deJong, JLO
OShea, JJ
Sondel, PM
AF Fenske, TS
Farner, NL
deJong, JLO
OShea, JJ
Sondel, PM
TI Interleukin-2 mediated activation of JAK3 in the absence of a detectable
64 kDa common gamma chain.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV WISCONSIN,MADISON,WI 53706.
NIAMSD,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1752
EP 1752
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101982
ER
PT J
AU Drew, PD
Franzoso, G
Biddison, WE
Siebenlist, U
Ozato, K
AF Drew, PD
Franzoso, G
Biddison, WE
Siebenlist, U
Ozato, K
TI Interferon regulatory factor and NF kappa B proteins physically interact
and coordinately regulate major histocompatibility class I gene
expression.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1755
EP 1755
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101984
ER
PT J
AU Tagaya, Y
Burton, JD
Miyamoto, Y
Waldmann, TA
AF Tagaya, Y
Burton, JD
Miyamoto, Y
Waldmann, TA
TI Interleukin-15/T utilizes a novel receptor signal transduction pathway
in mast cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,METAB BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1757
EP 1757
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101985
ER
PT J
AU Segal, BM
Shevach, EM
AF Segal, BM
Shevach, EM
TI The role of cytokines in resistance to an autoimmune disease.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,IMMUNOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1759
EP 1759
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101988
ER
PT J
AU Weiss, RA
Madaio, MP
Schwartz, RH
AF Weiss, RA
Madaio, MP
Schwartz, RH
TI Cadmium chloride induces B7.1 expression in murine renal tubular cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20894.
UNIV PENN,SCH MED,PHILADELPHIA,PA 19104.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1765
EP 1765
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101994
ER
PT J
AU Wu, AJ
Shimizu, F
Baum, BJ
Fox, PC
Notkins, AL
Chen, ZJ
AF Wu, AJ
Shimizu, F
Baum, BJ
Fox, PC
Notkins, AL
Chen, ZJ
TI Interferon-gamma induces the expression of B7 on a human salivary gland
cell line.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,CIPCB,BETHESDA,MD 20892.
NIDR,LOM,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1766
EP 1766
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86101997
ER
PT J
AU Schwartz, LB
Sakai, K
Worobec, A
Metcalfe, D
Ren, S
AF Schwartz, LB
Sakai, K
Worobec, A
Metcalfe, D
Ren, S
TI A novel heparin-dependent processing pathway for human tryptase may
account for different mechanisms of release of alpha and beta forms of
this enzyme
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 VIRGINIA COMMONWEALTH UNIV,RICHMOND,VA 23298.
NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1773
EP 1773
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102003
ER
PT J
AU Rumsaeng, V
Cruikshank, WW
Foster, B
Kornfeld, H
Center, DM
Metcalfe, DD
AF Rumsaeng, V
Cruikshank, WW
Foster, B
Kornfeld, H
Center, DM
Metcalfe, DD
TI Interleukin-16 production by human leukemic mast cells (HMC-1)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
BOSTON UNIV,BOSTON,MA 02118.
NR 0
TC 1
Z9 1
U1 0
U2 5
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1776
EP 1776
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102005
ER
PT J
AU Huang, H
HuLi, J
BenSasson, SZ
Seder, R
Li, WEP
AF Huang, H
HuLi, J
BenSasson, SZ
Seder, R
Li, WEP
TI A STAT-6-binding element in the IL-4 promoter
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1793
EP 1793
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102022
ER
PT J
AU Tarrant, T
Rizzo, LV
Silver, PB
Caspi, RR
AF Tarrant, T
Rizzo, LV
Silver, PB
Caspi, RR
TI TGF-beta suppresses antigen stimulation of a uveitogenic T cell line
through an effect on antigen-presenting cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,HHMI,RES SCHOLARS PROGRAM,LAB IMMUNOL,NEI,BETHESDA,MD 20892.
RI Rizzo, Luiz Vicente/B-4458-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1799
EP 1799
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102030
ER
PT J
AU Nishimura, MI
McKee, MD
Rosenberg, SA
AF Nishimura, MI
McKee, MD
Rosenberg, SA
TI Use of competitive PCR to quantitate TCR V beta gene usage in cultured T
cell lines and patient samples.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1822
EP 1822
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102051
ER
PT J
AU SuriPayer, E
Shevach, E
AF SuriPayer, E
Shevach, E
TI Identification of H/K ATP'ase-reactive T cells in autoimmune gastritis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1827
EP 1827
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102056
ER
PT J
AU Deulofeut, H
Robinson, MA
AF Deulofeut, H
Robinson, MA
TI Characterization of the TCRBV repertoire utilized in response to HBsAg.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1829
EP 1829
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102060
ER
PT J
AU Apasov, SG
Koshiba, M
Chused, TM
Sitkovsky, MV
AF Apasov, SG
Koshiba, M
Chused, TM
Sitkovsky, MV
TI Differential susceptibility of T cell subsets to effects of
extracellular adenosine and ATP: Possible role for purinergic receptors.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1843
EP 1843
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102073
ER
PT J
AU Ryan, JJ
McReynolds, LJ
Paul, WE
AF Ryan, JJ
McReynolds, LJ
Paul, WE
TI A movable IL-4 receptor sequence capable of enhancing CD23 expression.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1873
EP 1873
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102100
ER
PT J
AU Melillo, G
Taylor, LS
Brook, A
Cox, GW
Varesio, L
AF Melillo, G
Taylor, LS
Brook, A
Cox, GW
Varesio, L
TI Cooperative interaction between hypoxia and lipopolysaccharide (LPS) in
the activation of the inducible nitric oxide synthase (iNOS) promoter.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD.
NCI,FREDERICK CANC RES & DEV CTR,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD.
RI varesio, luigi/J-8261-2016
OI varesio, luigi/0000-0001-5659-2218
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1878
EP 1878
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102108
ER
PT J
AU Nelms, K
Paul, WE
AF Nelms, K
Paul, WE
TI The I4R motif of the IL-4 receptor: Critical residues and novel
interactions.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1879
EP 1879
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102106
ER
PT J
AU Kuhns, DB
Gallin, EK
Gallin, JI
AF Kuhns, DB
Gallin, EK
Gallin, JI
TI Thapsigargin induces Ca2+-dependent production and release of IL-8 in
human neutrophils (PMNs)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 SAIC FREDERICK,FREDERICK,MD 21702.
NIAID,NIH,HOST DEF LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1915
EP 1915
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102144
ER
PT J
AU Druey, KM
Blumer, KJ
Kang, VH
Kehrl, JH
AF Druey, KM
Blumer, KJ
Kang, VH
Kehrl, JH
TI A novel mammalian gene family that regulates G protein-mediated signal
transduction.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,BETHESDA,MD 20892.
WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1919
EP 1919
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102146
ER
PT J
AU Bosco, MC
Zea, A
Rowe, T
Ortaldo, J
Varesio, L
EspinozaDelgado, I
AF Bosco, MC
Zea, A
Rowe, T
Ortaldo, J
Varesio, L
EspinozaDelgado, I
TI Involvement of protein tyrosine kinases in IL-2-induced activation of
human monocytes.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 SAIC,BCDP,FREDERICK,MD 21702.
SAIC,CSP,FREDERICK,MD 21702.
FCRDC,NCI,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD 21702.
RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016
OI Bosco, Maria Carla/0000-0003-1857-7193; varesio,
luigi/0000-0001-5659-2218
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1960
EP 1960
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102187
ER
PT J
AU Ito, N
Li, Y
Dileepan, KN
Stechschulte, DJ
Rice, N
Suzuki, T
AF Ito, N
Li, Y
Dileepan, KN
Stechschulte, DJ
Rice, N
Suzuki, T
TI Phagocytosis of mast cell granules (MCG) leads to degradation of
NF-kappa B proteins in mouse macrophages.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV KANSAS,MED CTR,KANSAS CITY,KS 66160.
NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1968
EP 1968
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102197
ER
PT J
AU EspinozaDelgado, I
Rottschafer, S
Bosco, MC
Ortaldo, JR
AF EspinozaDelgado, I
Rottschafer, S
Bosco, MC
Ortaldo, JR
TI Interleukin-2 enhances B7-1 mRNA and protein expression.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 SAIC,BCDP,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD 21702.
RI Bosco, Maria Carla/J-7928-2016
OI Bosco, Maria Carla/0000-0003-1857-7193
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1973
EP 1973
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102202
ER
PT J
AU Jankovic, D
Kullberg, M
Yap, G
Epstein, M
Cheever, A
Sher, A
AF Jankovic, D
Kullberg, M
Yap, G
Epstein, M
Cheever, A
Sher, A
TI B cell-deficient mice exposed to Schistosoma mansoni develop exacerbated
egg pathology which fails to down-modulate during chronic infection.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOBIOL SECT,PARASIT DIS LAB,BETHESDA,MD 20892.
NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 1995
EP 1995
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102225
ER
PT J
AU PitchekianHalabi, H
Kim, S
MackenzieGraham, A
McFarland, HF
Raine, CS
Voskuhl, RR
AF PitchekianHalabi, H
Kim, S
MackenzieGraham, A
McFarland, HF
Raine, CS
Voskuhl, RR
TI Gender differences in autoimmune demyelination in the mouse;
Implications for multiple sclerosis.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90095.
NIH,BETHESDA,MD 20892.
YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2038
EP 2038
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102267
ER
PT J
AU Smith, ME
Eller, NL
AF Smith, ME
Eller, NL
TI Gender influences EAE both before and after sexual maturation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,PEDIAT MED BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2039
EP 2039
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102268
ER
PT J
AU Qui, JX
Murozono, M
Weng, N
Marcus, DM
Padian, EA
AF Qui, JX
Murozono, M
Weng, N
Marcus, DM
Padian, EA
TI Molecular models of antibodies against GM1 ganglioside and related
structures.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK,NIH,BETHESDA,MD 20892.
BAYLOR COLL MED,HOUSTON,TX 77030.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2071
EP 2071
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102301
ER
PT J
AU Bonney, EA
Matzinger, P
AF Bonney, EA
Matzinger, P
TI Beyond fetal cell migration into the maternal circulation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,SECT T CELL TOLERANCE,CELLULAR & MOLEC IMMUNOL LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2104
EP 2104
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102333
ER
PT J
AU Ubagai, T
Chamberlin, ME
Mudd, SH
Chou, JY
AF Ubagai, T
Chamberlin, ME
Mudd, SH
Chou, JY
TI Demyelination of the brain is associated with defects in the hepatic
form of methionine adenosyl transferase
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD,HERITABLE DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
NIMH,LAB GEN & COMPARAT BIOCHEM,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2147
EP 2147
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102375
ER
PT J
AU Napolitano, M
Hockman, S
Taira, M
Pepin, L
Degerman, E
Manganiello, V
AF Napolitano, M
Hockman, S
Taira, M
Pepin, L
Degerman, E
Manganiello, V
TI Molecular cloning and expression of mouse adipocyte cGMP-inhibited
cyclic nucleotides phosphodiesterase (cGI PDE)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2160
EP 2160
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102390
ER
PT J
AU Warner, DR
Fishman, PH
AF Warner, DR
Fishman, PH
TI A human G(s)alpha mutant that is is unable to couple to adenylate
cyclase and associate with membranes
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS,MBS,LMCN,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2161
EP 2161
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102388
ER
PT J
AU Basi, NS
Rebois, RV
AF Basi, NS
Rebois, RV
TI Fast rate zonal sedimentation of GTP gamma S-activated Gs.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS,MEMBRANE BIOCHEM SECT,LMCN,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2163
EP 2163
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102392
ER
PT J
AU Garcia, MC
Kim, HY
AF Garcia, MC
Kim, HY
TI Activation of serotonin receptors is coupled to the release of
polyunsaturated fatty acids from C6 glioma cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA,LMBB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2199
EP 2199
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102430
ER
PT J
AU Wolff, EC
Joe, YA
Park, MH
Folk, JE
AF Wolff, EC
Joe, YA
Park, MH
Folk, JE
TI Specific labeling of deoxyhypusine synthase by [H-3]spermidine
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,LCDO,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2207
EP 2207
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102434
ER
PT J
AU Liu, SY
Stadtman, TC
AF Liu, SY
Stadtman, TC
TI Two types of selenium-containing thioredoxin reductase from human lung
tumor and HeLa cell lines.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2208
EP 2208
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102437
ER
PT J
AU Joe, YA
Wolff, E
Park, MH
AF Joe, YA
Wolff, E
Park, MH
TI Site-directed mutagenesis studies of the recombinant human deoxyhypusine
synthase
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2209
EP 2209
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102438
ER
PT J
AU Ciotti, M
Owens, IS
AF Ciotti, M
Owens, IS
TI Comparison of bilirubin and 17 alpha-ethynylestradiol glucuronidation by
HUG-Br1 and some of its mutants.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD,DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2212
EP 2212
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102442
ER
PT J
AU Webster, JC
Oakley, RH
Sar, M
Cidlowski, JA
AF Webster, JC
Oakley, RH
Sar, M
Cidlowski, JA
TI Regulation of the alpha and beta isoforms of the human glucocorticoid
receptor by TNF-alpha
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS,MOL ENDOCRINOL GRP,LAB INTEGRAT BIOL,RES TRIANGLE PK,NC 27709.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2249
EP 2249
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102478
ER
PT J
AU Pak, JH
Mahoney, CW
Huang, FL
Huang, KP
AF Pak, JH
Mahoney, CW
Huang, FL
Huang, KP
TI Nitric oxide oxidation of neurogranin attenuates its phosphorylation by
protein kinase C and affinity for calmodulin.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2298
EP 2298
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102526
ER
PT J
AU Saito, H
Oka, T
AF Saito, H
Oka, T
TI Hormonally regulated double- and single-stranded DNA binding complexes
involved in mouse beta-casein gene transcription
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK,LMCB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2311
EP 2311
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102538
ER
PT J
AU Friguet, B
Conconi, M
Szweda, LI
Levine, RL
Stadtman, ER
AF Friguet, B
Conconi, M
Szweda, LI
Levine, RL
Stadtman, ER
TI Multicatalytic proteinase activity: Age-related decline and protection
from oxidative inactivation by Hsp 90.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 INST PASTEUR,UNITE BIOCHIM CELLULAIRE,F-75015 PARIS,FRANCE.
CASE WESTERN RESERVE UNIV,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106.
NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
RI Levine, Rodney/D-9885-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2320
EP 2320
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102551
ER
PT J
AU Corcoran, ML
StetlerStevenson, WG
AF Corcoran, ML
StetlerStevenson, WG
TI TIMP-2 suppresses cell growth by stimulating tyrosine phosphatase
activity
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,EXTRACELLULAR MATRIX PATHOL SECT,PATHOL LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2352
EP 2352
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102579
ER
PT J
AU Yamada, KM
Miyamoto, S
Aota, S
Katz, BZ
AF Yamada, KM
Miyamoto, S
Aota, S
Katz, BZ
TI Fibronectin and integrin signaling and cytoskeletal regulation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,DEV BIOL LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2433
EP 2433
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102661
ER
PT J
AU Wlodawer, A
Bujacz, G
Jaskolski, M
Alexandratos, J
Merkel, G
Katz, RA
Skalka, AM
AF Wlodawer, A
Bujacz, G
Jaskolski, M
Alexandratos, J
Merkel, G
Katz, RA
Skalka, AM
TI Retroviral integrase - Crystal structure of a new target for designing
drugs against AIDS.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702.
FOX CHASE CANC CTR,PHILADELPHIA,PA 19111.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2440
EP 2440
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102667
ER
PT J
AU Kiss, A
Thorgeirsson, SS
AF Kiss, A
Thorgeirsson, SS
TI Analysis of TGF-alpha/EGFR, HGF/c-met, TGF-beta-RII and p53 expression
in 85 human hepatocellular carcinomas (HCCs) from Chinese patients.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,DBS,LEC,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2475
EP 2475
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102704
ER
PT J
AU Yap, G
Cheever, A
Jankovic, D
Sher, A
AF Yap, G
Cheever, A
Jankovic, D
Sher, A
TI Immunomodulation of the granulomatous response to schistosome eggs
proceeds normally IFN-gamma and beta-2 microglobulin-deficient mice.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2500
EP 2500
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102730
ER
PT J
AU Murphy, WJ
Asai, O
Tian, Z
Hornung, R
Longo, DL
AF Murphy, WJ
Asai, O
Tian, Z
Hornung, R
Longo, DL
TI Activated natural killer (NK) cells mediate graft-versus-tumor (GVT)
effects but inhibit graft-versus-host disease (GVHD) after allogeneic
bone marrow transplantation (BMT).
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,LLB,DBS,FREDERICK,MD 21702.
NCI,BCDP,SAIC FREDERICK,FCRDC,FREDERICK,MD 21702.
NIA,BALTIMORE,MD 21224.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2509
EP 2509
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102737
ER
PT J
AU Karp, CL
Wysocka, M
Wahl, LM
Cuomo, PJ
Ahearn, JM
Trinchieri, G
Griffin, DE
AF Karp, CL
Wysocka, M
Wahl, LM
Cuomo, PJ
Ahearn, JM
Trinchieri, G
Griffin, DE
TI Inhibition of interleukin-12 production by measles virus
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21287.
SCH HYG & PUBL HLTH,BALTIMORE,MD 21287.
WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104.
NIDR,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2515
EP 2515
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102745
ER
PT J
AU Goletz, TJ
Zhan, S
Pendleton, CD
Helman, LJ
Berzofsky, JA
AF Goletz, TJ
Zhan, S
Pendleton, CD
Helman, LJ
Berzofsky, JA
TI Generation of cytotoxic T cells against tumor-specific translocations:
Potential anti-cancer vaccines for Ewing's sarcoma and alveolar
rhabdomyosarcoma.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2521
EP 2521
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102751
ER
PT J
AU Chen, W
Chesebro, B
Qin, H
Cheever, MA
AF Chen, W
Chesebro, B
Qin, H
Cheever, MA
TI Cytotoxic T lymphocytes elicited by priming with tumor-associated
peptide can eradicate established leukemia.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV WASHINGTON,DIV ONCOL,SEATTLE,WA 98195.
NIAID,ROCKY MT LABS,LPVD,HAMILTON,MT 59840.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2522
EP 2522
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102749
ER
PT J
AU Anderson, H
Roche, P
AF Anderson, H
Roche, P
TI Role of invariant chain phosphorylation in intracellular transport.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2530
EP 2530
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102756
ER
PT J
AU Reeves, ME
Rosenberg, SA
Hwu, P
AF Reeves, ME
Rosenberg, SA
Hwu, P
TI Transduction and differentiation of dendritic cells from human
hematopoietic progenitor cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,SURG BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2552
EP 2552
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102779
ER
PT J
AU Chen, H
Paul, WE
AF Chen, H
Paul, WE
TI Cultured splenic NK1.1+, CD4+ T cells produce IL4.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2560
EP 2560
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102790
ER
PT J
AU Smith, P
Apasov, S
Jelonik, M
Margulies, D
Sitkovsky, MV
AF Smith, P
Apasov, S
Jelonik, M
Margulies, D
Sitkovsky, MV
TI Constitutive intracellular Ser/Thr phosphorylation of the extracellular
domain of alpha beta TCR.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2569
EP 2569
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102795
ER
PT J
AU Huang, S
Smith, P
Apasov, S
Sitkovsky, M
AF Huang, S
Smith, P
Apasov, S
Sitkovsky, M
TI T-cell plasma membrane association of PP2A protein phosphatase.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2589
EP 2589
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102817
ER
PT J
AU Correa, MR
Ghosh, P
Longo, DL
Ochoa, AC
AF Correa, MR
Ghosh, P
Longo, DL
Ochoa, AC
TI Alterations in signal transduction and nuclear transcription factors in
chronically stimulated T cells through the TCR.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,IMMUNOTHERAPY LAB,FREDERICK,MD 21702.
ONCOTHERAPEUT INC,CRANBURY,NJ 08512.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2599
EP 2599
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102825
ER
PT J
AU Ishaq, M
Natarajan, V
AF Ishaq, M
Natarajan, V
TI Down regulation of an RXR alpha related gene expression during T cell
receptor (TCR) mediated activation of human T cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,FREDERICK,MD 21702.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2600
EP 2600
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102828
ER
PT J
AU Luo, G
Kazansky, A
Liu, X
Henninghausen, L
YuLee, L
AF Luo, G
Kazansky, A
Liu, X
Henninghausen, L
YuLee, L
TI Structure and function analysis of a prolactin-inducible Stat factor,
Stat 5b, in T cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 BAYLOR COLL MED,HOUSTON,TX 77030.
NIDDK,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2604
EP 2604
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102833
ER
PT J
AU Koshiba, M
Apasov, S
Sverdlov, V
Erb, L
Turner, J
Weisman, G
Sitkovsky, MV
AF Koshiba, M
Apasov, S
Sverdlov, V
Erb, L
Turner, J
Weisman, G
Sitkovsky, MV
TI Transient up-regulation of the expression of p2y(2) purinergic receptors
in thymocytes as an immediate early gene response.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,LI,BETHESDA,MD 20892.
UNIV MISSOURI,DEPT BIOCHEM,COLUMBIA,MO.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2606
EP 2606
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102834
ER
PT J
AU Kwon, TK
Nagel, J
Buchholz, M
Nordin, A
AF Kwon, TK
Nagel, J
Buchholz, M
Nordin, A
TI Characterization of the murine cyclin-dependent kinase inhibitor gene
p27(Kip).
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2608
EP 2608
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102838
ER
PT J
AU Matsubara, H
Shearer, GM
AF Matsubara, H
Shearer, GM
TI Suggestion or a unique CD28 costimulatory mechanism in human T cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,EIB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2619
EP 2619
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102847
ER
PT J
AU Palmer, L
Saha, B
Hodes, R
Abe, R
AF Palmer, L
Saha, B
Hodes, R
Abe, R
TI Immune-mediated responses against mouse mammary tumor virus (MMTV) in
CD28-deficient mice.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 USN,RES INST,NATL NAVAL MED CTR,BETHESDA,MD 20892.
NIA,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2639
EP 2639
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102866
ER
PT J
AU Cole, DJ
Wilson, M
Rivoltini, L
Custer, M
Nishimura, MI
AF Cole, DJ
Wilson, M
Rivoltini, L
Custer, M
Nishimura, MI
TI T-cell response in matched MART-1 peptide stimulated peripheral blood
lymphocytes and tumor infiltrating lymphocytes.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NATL TUMOR INST MILAN,I-20133 MILAN,ITALY.
MED UNIV S CAROLINA,DEPT SURG,CHARLESTON,SC 29425.
NCI,SURG BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2687
EP 2687
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102915
ER
PT J
AU Pericle, F
Sconocchia, G
Segal, DM
AF Pericle, F
Sconocchia, G
Segal, DM
TI Hyaluronan binding to CD44 on human neutrophils induces PMN tumoricidal
activity.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2696
EP 2696
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102929
ER
PT J
AU Loftus, D
Castelli, C
Marincola, F
Parmiani, G
Appella, E
Rivoltini, L
AF Loftus, D
Castelli, C
Marincola, F
Parmiani, G
Appella, E
Rivoltini, L
TI A possible role for epitope mimicry in shaping the CTL response to
melanoma antigen MART-1
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,NIH,BETHESDA,MD 20892.
IST NAZL TUMORI,I-20133 MILAN,ITALY.
RI castelli, chiara/K-6899-2012
OI castelli, chiara/0000-0001-6891-8350
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2705
EP 2705
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102933
ER
PT J
AU Rivoltini, L
Loftus, DJ
Barracchini, K
Arienti, F
Mazzocchi, A
Squarcina, P
Biddison, WE
Appella, E
Parmiani, G
Marincola, FM
AF Rivoltini, L
Loftus, DJ
Barracchini, K
Arienti, F
Mazzocchi, A
Squarcina, P
Biddison, WE
Appella, E
Parmiani, G
Marincola, FM
TI Binding, presentation and immunogenicity of peptides derived from
melanoma antigens MART-1 and GP100 by HLA-A2 subtypes
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NATL TUMOR INST MILAN,DIV EXPT ONCOL D,I-20133 MILAN,ITALY.
NCI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2706
EP 2706
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102931
ER
PT J
AU Irvine, KR
Chamberlain, RS
Bronte, V
Rosenberg, SA
Restifo, NP
AF Irvine, KR
Chamberlain, RS
Bronte, V
Rosenberg, SA
Restifo, NP
TI The route of administration of recombinant vaccinia virus (rVV) vaccines
effects the active treatment of cancer.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892.
RI Restifo, Nicholas/A-5713-2008
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2711
EP 2711
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102939
ER
PT J
AU Cain, SA
Padlan, EA
Helm, BA
AF Cain, SA
Padlan, EA
Helm, BA
TI Expression of human IgE-Fc and the extracellular domains of the
alpha-chain of the high affinity receptor for IgE in Pichia pastoris.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV SHEFFIELD,DEPT MOLEC BIOL & BIOTECHNOL,KREBS INST,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND.
NIDDK,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2746
EP 2746
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102973
ER
PT J
AU Helm, BA
Sayers, I
Machado, DC
Padlan, EA
AF Helm, BA
Sayers, I
Machado, DC
Padlan, EA
TI Potential applications of hIgE-Fc derived peptides as rational
antagonists of the allergic response.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV SHEFFIELD,KREBS INST,DEPT MOLEC BIOL & BIOTECHNOL,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND.
NIDDK,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2747
EP 2747
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102971
ER
PT J
AU Sayers, I
Machado, DC
Ahmad, K
Padlan, EA
Helm, BA
AF Sayers, I
Machado, DC
Ahmad, K
Padlan, EA
Helm, BA
TI Identification of the sites(s) on human IgE that are involved in the
interaction with its high (Fc epsilon RI) and low (Fc epsilon RII)
affinity receptors.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 UNIV SHEFFIELD,KREBS INST,DEPT MOL BIOL & BIOTECH,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND.
NIDDK,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2748
EP 2748
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86102981
ER
PT J
AU Su, HC
Kulkarni, AB
Karlsson, S
Biron, CA
AF Su, HC
Kulkarni, AB
Karlsson, S
Biron, CA
TI Aberrant NK cell responses in TGF-beta 1-deficient mice
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 BROWN UNIV,PROVIDENCE,RI 02912.
NINCDS,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2800
EP 2800
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103033
ER
PT J
AU Veech, RL
Kashiwaya, Y
Keon, CA
Radda, GK
Clarke, K
AF Veech, RL
Kashiwaya, Y
Keon, CA
Radda, GK
Clarke, K
TI A new P-31 NMR method to measure intracellular free [Mg2+]
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA,LMBB,ROCKVILLE,MD 20852.
UNIV OXFORD,DEPT BIOCHEM,OXFORD OX1 3QU,ENGLAND.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2858
EP 2858
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103082
ER
PT J
AU Zimmerman, SB
Murphy, LD
AF Zimmerman, SB
Murphy, LD
TI Stabilization of isolated nucleoids from Escherichia coli under crowded
conditions.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2861
EP 2861
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103091
ER
PT J
AU Rabinovitz, M
AF Rabinovitz, M
TI Consequences of amino acid deprivation: A unifying theory
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2898
EP 2898
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103125
ER
PT J
AU Venkatachalam, KV
Strott, CA
AF Venkatachalam, KV
Strott, CA
TI Isolation of a 55 kD protein from the guinea pig adrenal that catalyzes
production of the sulfotransferase sulfonate donor molecule
3'-phosphoadenosine 5'-phosphosulfate (PAPS): Evidence for intrinsic
sulfatase activity.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2951
EP 2951
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103178
ER
PT J
AU Kallarakal, AT
Jeng, J
Popov, KM
Song, BJ
AF Kallarakal, AT
Jeng, J
Popov, KM
Song, BJ
TI Naturally occurring mutant (H263L) of pyruvate dehydrogenase complex E1
alpha subunit: Implications in thiamine binding and phosphorylation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 INDIANA UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,INDIANAPOLIS,IN 46202.
NIAAA,NIH,NEUROGENET LAB,ROCKVILLE,MD 20852.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2952
EP 2952
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103176
ER
PT J
AU Srivastava, RK
ChoChung, YS
AF Srivastava, RK
ChoChung, YS
TI Protein kinase A RII beta regulatory subunit binds to cAMP-response
element in reverse transformation.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2967
EP 2967
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103192
ER
PT J
AU Nesterova, M
Noguchi, K
Srivastava, RK
ChoChung, YS
AF Nesterova, M
Noguchi, K
Srivastava, RK
ChoChung, YS
TI Protein kinase A type I - Directed antisense restrains tumor growth:
Sequence specific inhibition of gene expression.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2968
EP 2968
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103195
ER
PT J
AU Sweitzer, TD
Hanover, JA
AF Sweitzer, TD
Hanover, JA
TI A calmodulin-dependent pathway for nuclear protein import that does not
require GTP in vitro.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK,NIH,LAB CELL BIOL & BIOCHEM,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 2995
EP 2995
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103224
ER
PT J
AU Ponsalle, P
Buchholz, M
Nordin, A
AF Ponsalle, P
Buchholz, M
Nordin, A
TI Decreased G(1) cdk2 kinase activity in activated T cells from old mice.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 3002
EP 3002
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103231
ER
PT J
AU Patton, WA
Moss, J
Vaughan, M
Colombo, MI
Stahl, PD
AF Patton, WA
Moss, J
Vaughan, M
Colombo, MI
Stahl, PD
TI Evidence for cholera toxin and beta gamma subunit interaction domains in
ARF, a regulator of vesicular trafficking.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,NIH,PULM CRIT CARE MED BRANCH,BETHESDA,MD 20892.
WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 3008
EP 3008
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103233
ER
PT J
AU Cieplak, W
Mead, DJ
AF Cieplak, W
Mead, DJ
TI Inhibition of endosomal acidification or microtubule function
potentiates the cytotoxic activity of Escherichia coli heat-labile toxin
in CHO-K1 cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,NIH,ROCKY MT LABS,HAMILTON,MT 59840.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 3009
EP 3009
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103236
ER
PT J
AU Zhang, ZI
Panda, D
Mukherjee, AB
AF Zhang, ZI
Panda, D
Mukherjee, AB
TI Is human uteroglobin gene a tumor suppressor?
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD,HERITABLE DISORDERS BRANCH,SECT DEV GENET,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP 3028
EP 3028
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86103252
ER
PT J
AU Torchia, DA
AF Torchia, DA
TI Flexibility and function in HIV protease.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIDR,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP C10
EP C10
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86100060
ER
PT J
AU Umar, A
Koi, M
Risinger, JI
Barrett, JC
Kunkel, TA
AF Umar, A
Koi, M
Risinger, JI
Barrett, JC
Kunkel, TA
TI Correction of mismatch repair defective lines via chromosome transfer.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS,RES TRIANGLE PK,NC 27709.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP D14
EP D14
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86100014
ER
PT J
AU Cissel, DS
Fraundorfer, PF
Beaven, MA
AF Cissel, DS
Fraundorfer, PF
Beaven, MA
TI A requirement for phospholipase (PL) D for mediation of Ca2+/protein
kinase C (PKC)-dependent secretion in a mast cell line.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI,LMI,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP L46
EP L46
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86100137
ER
PT J
AU Burshtyn, DN
Scharenberg, AM
Wagtmann, N
Rajagopalan, S
Berrada, K
Yis, T
Kinet, JP
Long, EO
AF Burshtyn, DN
Scharenberg, AM
Wagtmann, N
Rajagopalan, S
Berrada, K
Yis, T
Kinet, JP
Long, EO
TI Signal transduction by killer cell inhibitory receptors involves
recruitment of the tyrosine phosphatase SHP-1.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852.
CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR 30
PY 1996
VL 10
IS 6
BP P29
EP P29
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA UK861
UT WOS:A1996UK86100192
ER
PT J
AU Chung, KW
Lee, YM
Park, TK
Kim, SJ
Lee, CC
AF Chung, KW
Lee, YM
Park, TK
Kim, SJ
Lee, CC
TI Cooperative transcriptional activation by two glutamine-rich regions of
twist product in Drosophila melanogaster
SO MOLECULES AND CELLS
LA English
DT Article
ID DNA-BINDING; DORSAL; PROTEIN; MESODERM; GENE; SEQUENCE; DOMAINS; EMBRYO;
MOTIF; DAUGHTERLESS
AB twist is one of the important genes that determine dorsal-ventral (D-V) axis during embryogenesis in Drosophila. The twist which is expressed in the ventral part of an embryo encodes a transcription factor which contains a basic helix-loop-helix (bHLH) domain. Twist (twist product) has two distinct glutamine-rich regions (QRs) on the upstream of the bHLH domain (major QR: QR-A, minor QR: QR-B). Domain analysis on the QRs using modified yeast two-hybrid assay has revealed that the QR-A has the function of a transcriptional activation domain. Although the QR-A alone could play the role of transcriptional activation domain, the QR-B may be required for stronger transcriptional activation.
C1 NHLBI, NIH, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA.
KONKUK UNIV, DEPT MOLEC BIOL, CHUNGJU 380701, SOUTH KOREA.
CHEJU NATL UNIV, DEPT BIOL, CHEJU 690756, SOUTH KOREA.
SEOUL NATL UNIV, DEPT BIOL, SEOUL 151742, SOUTH KOREA.
SEOUL NATL UNIV, RES CTR CELL DIFFERENTIAT, SEOUL 151742, SOUTH KOREA.
RP Chung, KW (reprint author), KONGJU NATL UNIV, DEPT BIOL, KONG JU 314701, SOUTH KOREA.
NR 29
TC 3
Z9 3
U1 0
U2 1
PU KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
PI SEOUL
PA 635-4, YUCKSAM-DONG, GANGNAM-GU, SEOUL 135-703, SOUTH KOREA
SN 1016-8478
J9 MOL CELLS
JI Mol. Cells
PD APR 30
PY 1996
VL 6
IS 2
BP 197
EP 202
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UG984
UT WOS:A1996UG98400012
ER
PT J
AU AlexanderMiller, MA
Leggatt, GR
Berzofsky, JA
AF AlexanderMiller, MA
Leggatt, GR
Berzofsky, JA
TI Selective expansion of high- or low-avidity cytotoxic T lymphocytes and
efficacy for adoptive immunotherapy
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE viral immunity; virus clearance; T-cell therapy; determinant density;
antigen dose
ID TUMOR-INFILTRATING LYMPHOCYTES; INFECTED TARGET-CELLS; ENVELOPE
GLYCOPROTEIN; VIRUS; INVIVO; PEPTIDE; INDUCTION; CLONES; PROTECTION;
ANTIGEN
AB The conventional approach to cytotoxic T-lymphocyte (CTL) induction uses maximal antigen concentration with the intent of eliciting more CTL. However, the efficacy of this approach has not been systematically explored with regard to the quality of the CTLs elicited or their in vivo functionality. Here, we show that a diametrically opposite approach elicits CTLs that are much more effective at clearing virus. CTLs specific for a defined peptide epitope were selectively expanded with various concentrations of peptide antigen. CTLs generated with exceedingly low-dose peptide lysed targets sensitized with >100-fold less peptide than CTLs generated with high-dose peptide. Differences in expression of T-cell antigen receptors or a number of other accessory molecules did not account for the functional differences. Further, high-avidity CTLs adoptively transferred into severe combined immunodeficient mire were 100- to 1000-fold more effective at viral clearance than the low-avidity CTLs, despite the fact that all CTL lines lysed virus-infected targets in vitro. Thus, the quality of CTLs is as important as the quantity of CTLs for adoptive immunotherapy, and the ability to kill virally infected targets in vitro is not predictive of in vivo efficacy, whereas the determinant density requirement described here is predictive. Application of these principles may be critical in developing effective adoptive cellular immunotherapy for viral infections and cancer.
C1 NCI, METAB BRANCH, NIH, BETHESDA, MD 20892 USA.
RI Leggatt, Graham/G-1924-2010;
OI Leggatt, Graham/0000-0002-4078-5653
NR 28
TC 416
Z9 418
U1 1
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 APR 30
PY 1996
VL 93
IS 9
BP 4102
EP 4107
DI 10.1073/pnas.93.9.4102
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700068
PM 8633023
ER
PT J
AU Sekido, Y
Bader, S
Latif, F
Chen, JY
Duh, FM
Wei, MH
Albanesi, JP
Lee, CC
Lerman, MI
Minna, JD
AF Sekido, Y
Bader, S
Latif, F
Chen, JY
Duh, FM
Wei, MH
Albanesi, JP
Lee, CC
Lerman, MI
Minna, JD
TI Human semaphorins A(V) and IV reside in the 3p21.3 small cell lung
cancer deletion region and demonstrate distinct expression patterns
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE growth cone guidance; collapsin; recessive oncogene; G protein
ID GROWTH; GENE; CHROMOSOME-3; 3P(14-23); SEQUENCE; PROTEIN; LINES
AB Semaphorins acid collapsins make up a family of conserved genes that encode nerve growth cone guidance signals. We have identified two additional members of the human semaphorin family [human semaphorin A(V) and human semaphorin IV] in chromosome region 3p21.3, where several small cell lung cancer (SCLC) cell lines exhibit homozygous deletions indicative of a tumor suppressor gene. Human semaphorin A(V) has 86% amino acid homology with murine semaphorin A, whereas semaphorin IV is most closely related to murine semaphorin E, with 50% homology. These semaphorin genes are approximate to 70 kb apart flanking two GTP-binding protein genes, GNAI-2 and GNAT-1. In contrast, other human semaphorin gene sequences (human semaphorin LII and homologues of murine semaphorins B and C) are not located on chromosome 3. Human semaphorin A(V) is translated in vitro into a 90-kDa protein, which accumulates at the endoplasmic reticulum. The human semaphorin A(V) (3.4-kb mRNA) and IV (3.9- and 2.9-kb mRNAs) genes are expressed abundantly but differentially in a variety of human neural and nonneural tissues. Human semaphorin A(V) was expressed in only 1 out of 23 SCLCs and 7 out of 16 non-SCLCs, whereas semaphorin IV was expressed in 19 out of 23 SCLCs and 13 out of 16 non-SCLCs. Mutational analysis in semaphorin A(V) revealed mutations (germ line in one case) in 3 of 40 lung cancers. Our data suggest the need to determine the function of human semaphorins A(V) and IV in nonneural tissues and their role in the pathogenesis of lung cancer.
C1 UNIV TEXAS,SW MED CTR,DEPT PHARMACOL,DALLAS,TX 75235.
UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED,DALLAS,TX 75235.
NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,IMMUNOBIOL LAB,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
BAYLOR COLL MED,DEPT MOL & HUMAN GENET,HOUSTON,TX 77030.
RP Sekido, Y (reprint author), UNIV TEXAS,SW MED CTR,HAMON CTR THERAPEUT ONCOL RES,DALLAS,TX 75235, USA.
RI Sekido, Yoshitaka/P-9756-2015
FU NCI NIH HHS [P20 CA58220]
NR 30
TC 205
Z9 213
U1 0
U2 9
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4120
EP 4125
DI 10.1073/pnas.93.9.4120
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700071
PM 8633026
ER
PT J
AU Lane, MA
Baer, DJ
Rumpler, WV
Weindruch, R
Ingram, DK
Tilmont, EM
Cutler, RG
Roth, GS
AF Lane, MA
Baer, DJ
Rumpler, WV
Weindruch, R
Ingram, DK
Tilmont, EM
Cutler, RG
Roth, GS
TI Calorie restriction lowers body temperature in rhesus monkeys,
consistent with a postulated anti-aging mechanism in rodents
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE aging; Macaca mulatta; locomotor activity; circadian rhythm; heart rate
ID DIETARY RESTRICTION; FOOD RESTRICTION; METABOLIC-RATE;
DEOXYRIBONUCLEIC-ACID; ENERGY-METABOLISM; FISCHER-344 RATS; MICE; ADULT;
VARIABLES; LONGEVITY
AB Many studies of caloric restriction (CR) in rodents and lower animals indicate that this nutritional manipulation retards aging processes, as evidenced by increased longevity, reduced pathology, and maintenance of physiological function in a more youthful state. The anti-aging effects of CR are believed to relate, at least in part, to changes in energy metabolism. We are attempting to determine whether similar effects occur in response to CR in nonhuman primates. Core (rectal) body temperature decreased progressively with age from 2 to 30 years in rhesus monkeys fed ad lib (controls) and is reduced by approximate to 0.5 degrees C in age-matched monkeys subjected to 6 years of a 30% reduction in caloric intake. A short-term (1 month) 30% restriction of 2.5-year-old monkeys lowered subcutaneous body temperature by 1.0 degrees C. Indirect calorimetry showed that 24-hr energy expenditure was reduced by approximately 24% during short-term CR. The temporal association between reduced body temperature and energy expenditure suggests that reductions in body temperature relate to the induction of an energy conservation mechanism during CR. These reductions in body temperature and energy expenditure are consistent with findings in rodent studies in which aging rate was retarded by CR, now strengthening the possibility that CR may exert beneficial effects in primates analogous to those observed in rodents.
C1 USDA ARS,BELTSVILLE HUMAN NUTR RES CTR,DIET & HUMAN PERFORMANCE LAB,BELTSVILLE,MD 20705.
UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706.
WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53706.
RP Lane, MA (reprint author), NIA,MOLEC PHYSIOL & GENET SECT,NATHAN W SHOCK LABS,GERONTOL RES CTR,NIH,BAYVIEW MED CTR,BALTIMORE,MD 21224, USA.
NR 43
TC 204
Z9 207
U1 0
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4159
EP 4164
DI 10.1073/pnas.93.9.4159
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700078
PM 8633033
ER
PT J
AU Cabiscol, E
Levine, RL
AF Cabiscol, E
Levine, RL
TI The phosphatase activity of carbonic anhydrase III is reversibly
regulated by glutathiolation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID S-THIOLATION; RAT-LIVER; TYROSINE KINASE; PROTEIN; REDUCTION; SITE;
DETHIOLATION; SPECIFICITY; DISULFIDES; BINDING
AB Carbonic anhydrase isozyme III (CAIII) is unique among the carbonic anhydrases because it demonstrates phosphatase activity. CAIII forms a disulfide link between glutathione and two of its five cysteine residues, a profess termed S-glutathiolation. Glutathiolation of CAIII occurs in Fire and is increased during aging and under acute oxidative stress. We show that glutathiolation serves to reversibly regulate the phosphatase activity of CAIII. Glutathiolation of Cys-186 is required for phosphatase activity, while glutathiolation of Cys-181 blocks activity. Phosphotyrosine is the preferred substrate, although phosphoserine and phosphothreonine can also be cleaved. Thus, glutathiolation is a reversible covalent modification that can regulate CAIII, a phosphatase that may function in the cellular response to oxidative stress.
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
RI Cabiscol, Elisa/A-4584-2009; Levine, Rodney/D-9885-2011
OI Cabiscol, Elisa/0000-0003-2795-7999;
NR 37
TC 106
Z9 115
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4170
EP 4174
DI 10.1073/pnas.93.9.4170
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700080
PM 8633035
ER
PT J
AU Podgornik, R
Strey, HH
Gawrisch, K
Rau, DC
Rupprecht, A
Parsegian, VA
AF Podgornik, R
Strey, HH
Gawrisch, K
Rau, DC
Rupprecht, A
Parsegian, VA
TI Bond orientational order, molecular motion, and free energy of
high-density DNA mesophases
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID DOUBLE HELICES; INTERMOLECULAR FORCES; HYDRATION FORCES; PHASES;
FLUCTUATIONS; DYNAMICS; INVITRO; INVIVO
AB By equilibrating condensed DNA arrays against reservoirs of known osmotic stress and examining them with several structural probes, it has been possible to achieve a detailed thermodynamic and structural characterization of the change between two distinct regions on the liquid-crystalline phase diagram: (i) a higher density hexagonally packed region with long-range bond orientational order in the plane perpendicular to the average molecular direction and (ii) a lower density cholesteric region with fluid-like positional order. X-ray scattering on highly ordered DNA arrays at high density and with the helical axis oriented parallel to the incoming beam showed a sixfold azimuthal modulation of the first-order diffraction peak that reflects the macroscopic bond-orientational order. Transition to the less-dense cholesteric phase through osmotically controlled swelling shows the loss of this bond orientational order, which had been expected from the change in optical birefringence patterns and which is consistent with a rapid onset of molecular positional disorder. This change in order was previously inferred from intermolecular force measurements and is now confirmed by P-31 NMR. Controlled reversible swelling and compaction under osmotic stress, spanning a range of densities between approximate to 120 mg/ml to approximate to 600 mg/ml, allow measurement of the free-energy changes throughout each phase and at the phase transition, essential information for theories of liquid-crystalline states.
C1 NIDDKD, STRUCT BIOL LAB, DIV COMP RES & TECHNOL, NIH, BETHESDA, MD 20892 USA.
NIDDKD, OFF DIRECTOR, DIV INTRAMURAL RES, NIH, BETHESDA, MD 20892 USA.
NIAAA, DIV INTRAMURAL CLIN & BIOL RES, NIH, BETHESDA, MD 20892 USA.
UNIV STOCKHOLM, ARRHENIUS LAB, STOCKHOLM, SWEDEN.
RI Strey, Helmut/B-5456-2009; Podgornik, Rudolf/C-6209-2008;
OI Podgornik, Rudolf/0000-0002-3855-4637; Rupprecht,
Allan/0000-0002-2772-1620
NR 29
TC 81
Z9 83
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4261
EP 4266
DI 10.1073/pnas.93.9.4261
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700097
PM 8633052
ER
PT J
AU Yap, N
Yu, CL
Cheng, SY
AF Yap, N
Yu, CL
Cheng, SY
TI Modulation of the transcriptional activity of thyroid hormone receptors
by the tumor suppressor p53
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene regulation; transcription factors; protein-protein interaction
ID RETINOID-X-RECEPTOR; WILD-TYPE P53; NUCLEAR RECEPTOR; BINDING ACTIVITY;
GENE-EXPRESSION; RXR-BETA; ACID; PROMOTER; PROTEIN; FORMS
AB Thyroid hormone nuclear receptors (TRs) are ligand-dependent transcriptional factors that regulate growth, differentiation, and development. The molecular mechanisms by which TRs mediate these effects are unclear. One prevailing hypothesis suggests that TRs may cooperate with other transcriptional factors to mediate their biological effects. In this study, we tested this hypothesis by examining whether the activity of TRs is modulated by the tumor suppressor p53. p53 is a nuclear protein that regulates gene expression via sequence-specific DNA binding and/or direct protein-protein interaction. We found that the human TR subtype beta 1 (h-TR beta 1) physically interacted with p53 via its DNA binding domain. As a result of this physical interaction, binding of h-TR beta 1 to its hormone response elements either as homodimer or as a heterodimer with the retinoic X receptor was inhibited by p53 in a concentration-dependent manner. In transfected cells, wild-type p53 repressed the hormone-dependent transcriptional activation of h-TR beta 1. In contrast, mutant p53 either had no effect or activated the transcriptional activity of h-TR beta 1 depending on the type of hormone response elements. These results indicate the gene regulating activity of TRs was modulated by p53, suggesting that the cross talk between these two transcriptional factors may play an important role in the biology of normal and cancer cells.
C1 NCI,GENE REGULAT SECT,MOLEC BIOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892.
NR 40
TC 73
Z9 73
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4273
EP 4277
DI 10.1073/pnas.93.9.4273
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700099
PM 8633054
ER
PT J
AU Butt, J
Kim, HY
Basilion, JP
Cohen, S
Iwai, K
Philpott, CC
Altschul, S
Klausner, RD
Rouault, TA
AF Butt, J
Kim, HY
Basilion, JP
Cohen, S
Iwai, K
Philpott, CC
Altschul, S
Klausner, RD
Rouault, TA
TI Differences in the RNA binding sites of iron regulatory proteins and
potential target diversity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID FERRITIN MESSENGER-RNA; RESPONSIVE ELEMENT; TRANSFERRIN RECEPTOR;
UNTRANSLATED REGION; HEART ACONITASE; IDENTIFICATION; DNA; POLYMERASE;
SYNTHASE; CLONING
AB Posttranscriptional regulation of genes of mammalian iron metabolism is mediated by the interaction of iron regulatory proteins (IRPs) with RNA stem-loop sequence elements known as iron-responsive elements (IREs). There are two identified IRPs, IRP1 and IRP2, each of which binds consensus IREs present in eukaryotic transcripts with equal affinity. Site-directed mutagenesis of IRP1 and IRP2 reveals that, although the binding affinities for consensus IREs are indistinguishable, the contributions of arginine residues in the active-site cleft to the binding affinity are different in the two RNA binding sites. Furthermore, although each IRP binds the consensus IRE with high affinity, each IRP also binds a unique alternative ligand, which was identified in an in vitro systematic evolution of ligands by exponential enrichment procedure. Differences in the two binding sites may be important in the function of the IRE-IRP regulatory system.
C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892.
NR 37
TC 105
Z9 106
U1 2
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4345
EP 4349
DI 10.1073/pnas.93.9.4345
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700113
PM 8633068
ER
PT J
AU Khleif, SN
DeGregori, J
Yee, CL
Otterson, GA
Kaye, FJ
Nevins, JR
Howley, PM
AF Khleif, SN
DeGregori, J
Yee, CL
Otterson, GA
Kaye, FJ
Nevins, JR
Howley, PM
TI Inhibition of cyclin D-CDK4/CDK6 activity is associated with an
E2F-mediated induction of cyclin kinase inhibitor activity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE human papillomaviruses; cervical cancer; E7 oncoprotein; retinoblastoma
protein
ID RETINOBLASTOMA GENE-PRODUCT; HUMAN PAPILLOMAVIRUS TYPE-16; CARCINOMA
CELL-LINES; CERVICAL-CARCINOMA; DEPENDENT REGULATION; PROTEIN;
PHOSPHORYLATION; EXPRESSION; TRANSCRIPTION; BINDING
AB Alterations of various components of the cell cycle regulatory machinery that controls the progression of cells from a quiescent to a growing state contribute to the development of many human cancers. Such alterations include the deregulated expression of G(1) cyclins, the loss of function of activities such as those of protein p16(INK4a) that control G(1) cyclin-dependent kinase activity, and the loss of function of the retinoblastoma protein (RB),which is normally regulated by the G(1) cyclin-dependent kinases. Various studies have revealed an inverse relationship in the expression of p16(INK4a) protein and the presence of functional RB in many cell lines. In this study we show that p16(INK4a) is expressed in cervical cancer cell lines in which the RB gene, Rb, is not functional, either as a consequence of Rb mutation or expression of the human papillomavirus E7 protein. We also demonstrate that p16(INK4a) levels are increased in primary cells in which RB has been inactivated by DNA tumor virus proteins. Given the role of RB in controlling E2F transcription factor activity, we investigated the role of E2F in controlling p16(INK4a) expression. We found that E2F1 overexpression leads to an inhibition of cyclin D1-dependent kinase activity and induces the expression of a p16-related transcript. We conclude that the accumulation of G(1) cyclin-dependent kinase activity during normal G(1) progression leads to E2F accumulation through the inactivation of RB, and that this then leads to the induction of cyclin kinase inhibitor activity and a shutdown of G(1) kinase activity.
C1 USN,NCI,MED ONCOL BRANCH,BETHESDA,MD 20889.
UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814.
DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT GENET,DURHAM,NC 27710.
NCI,DERMATOL BRANCH,BETHESDA,MD 20892.
HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115.
RI kaye, frederic/E-2437-2011
NR 59
TC 232
Z9 241
U1 0
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4350
EP 4354
DI 10.1073/pnas.93.9.4350
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700114
PM 8633069
ER
PT J
AU Tellier, R
Bukh, J
Emerson, SU
Purcell, RH
AF Tellier, R
Bukh, J
Emerson, SU
Purcell, RH
TI Amplification of the full-length hepatitis A virus genome by long
reverse transcription-PCR and transcription of infectious RNA directly
from the amplicon
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID COMPLETE NUCLEOTIDE-SEQUENCE; A VIRUS; POLIOVIRUS RNA; CELL-CULTURE;
POLYMERASE; CDNA; DNA; INHIBITION; TEMPLATES; INVITRO
AB The genetic study of RNA viruses is greatly facilitated by the availability of infectious cDNA clones. However, their construction has often been difficult. While exploring ways to simplify the construction of infectious clones, we have successfully modified and applied the newly described technique of ''long PCR'' to the synthesis of a full-length DNA amplicon from the RNA of a cytopathogenic mutant (HM 175/24a) of the hepatitis A virus (HAV). Primers were synthesized to match the two extremities of the HAV genome. The antisense primer, homologous to the 3' end, was used in both the reverse transcription (RT) and the PCR steps. With these primers we reproducibly obtained a full-length amplicon of approximate to 7.5 kb. Further, since we engineered a T7 promoter in the sense primer, RNA could be transcribed directly from the amplicon with T7 RNA polymerase. Following transfection of cultured fetal rhesus kidney cells with the transcription mixture containing both the HAV cDNA and the transcribed RNA, replicating HAV was detected by immunofluorescence microscopy and, following passage to other cell cultures, by focus formation. The recovered virus displayed the cytopathic effect and targe plaque phenotype typical of the original virus; this result highlights the fidelity of the modified long reverse transcription-PCR procedure and demonstrates the potential of this method for providing cDNAs of viral genomes and simplifying the construction of infectious clones.
C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,NIH,BETHESDA,MD 20892.
NR 30
TC 32
Z9 36
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 APR 30
PY 1996
VL 93
IS 9
BP 4370
EP 4373
DI 10.1073/pnas.93.9.4370
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700118
PM 8633073
ER
PT J
AU Graziosi, C
Gantt, KR
Vaccarezza, M
Demarest, JF
Daucher, M
Saag, MS
Shaw, GM
Quinn, TC
Cohen, OJ
Welbon, CC
Pantaleo, G
Fauci, AS
AF Graziosi, C
Gantt, KR
Vaccarezza, M
Demarest, JF
Daucher, M
Saag, MS
Shaw, GM
Quinn, TC
Cohen, OJ
Welbon, CC
Pantaleo, G
Fauci, AS
TI Kinetics of cytokine expression during primary human immunodeficiency
virus type 1 infection
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID PRIMARY HIV-1 INFECTION; STEP
AB In the present study, se have determined the kinetics of constitutive expression of a panel of cytokines [interleukin (IL) 2, IL-4, IL-6, IL-10, interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha)] in sequential peripheral blood mononuclear cell samples from nine individuals with primary human immunodeficiency virus infection. Expression of IL-2 and IL-4 was barely detected in peripheral blood mononuclear cells. However, substantial levels of IL-2 expression were found in mononuclear cells isolated from lymph node. Expression of IL-6 was detected in only three of nine patients, and IL-6 expression was observed when transition from the acute to the chronic phase had already occurred. Expression of IL-10 and TNF-alpha was consistently observed in all patients tested, and levels of both cytokines were either stable or progressively increased over time. Similar to IL-10 and TNF-alpha, IFN-gamma expression was detected in all patients; however, in five of nine patients, IFN-gamma expression peaked very early during primary infection. The early peak in IFN-gamma expression coincided with oligoclonal expansions of CD8(+) T cells in five of six patients, and CD8(+) T cells mostly accounted for the expression of this cytokine. These results indicate that high levels of expression of proinflammatory cytokines are associated with primary infection and that the cytokine response during this phase of infection is strongly influenced by oligoclonal expansions of CD8(+) T cells.
C1 UNIV ALABAMA,BIRMINGHAM,AL 35294.
RP Graziosi, C (reprint author), NIAID,IMMUNOREGULAT LAB,NIH,BLDG 10,BETHESDA,MD 20892, USA.
RI Quinn, Thomas/A-2494-2010; Pantaleo, Giuseppe/K-6163-2016;
OI VACCAREZZA, Mauro/0000-0003-3060-318X
NR 32
TC 107
Z9 107
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 30
PY 1996
VL 93
IS 9
BP 4386
EP 4391
DI 10.1073/pnas.93.9.4386
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700121
PM 8633076
ER
PT J
AU Arya, SK
Gallo, RC
AF Arya, SK
Gallo, RC
TI Human immunodeficiency virus (HIV) type 2-mediated inhibition of HIV
type 1: A new approach to gene therapy of HIV infection
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE AIDS; transcriptional downmodulation; mutational analysis; chimeric
genomes; retroviral vectors
ID TRANS-ACTIVATOR GENE; TRANSACTIVATOR TAT; HTLV-III; CD4; TRANSMISSION;
ORGANIZATION; RETROVIRUSES; REPLICATION; EXPRESSION; ISOLATE
AB Human immunodeficiency virus (HIV) type 2, the second AIDS-associated human retrovirus, differs from HIV-1 in its natural history, infectivity, and pathogenicity, as Kell as in details of its genomic structure and molecular behavior. We report here that HIV-2 inhibits the replication of HIV-I at the molecular level. This inhibition was selective, dose-dependent, and nonreciprocal. The closely related simian immunodeficiency provirus also inhibited HIV-1. The selectivity of inhibition was shown by the observation that HIV-2 did not significantly downmodulate the expression of the unrelated murine leukemia virus; neither did the murine leukemia virus markedly affect HIV-1 or HIV-2 expression. Moreover, while HIV-2 potently inhibited HIV-I, the reverse did not happen, thus identifying Set another and remarkable difference between HIV-I and HIV-2. Mutational analysis of the HIV-1, genome suggested that the inhibition follows a complex pathway, possibly involving multiple genes and redundant mechanisms. Introduction of inactivating mutations into the structural and regulatory/accessory genes did not render the HIV-2 provirus ineffective. Some of the HIV-2 gene defects, such as that of tat and rev genes, were phenotypically transcomplemented by HIV-1. The HIV-2 proviruses,vith deletions in the putative packaging signal and defective for virus replication were effective in inducing the suppressive phenotype. Though the exact mechanism remains to be defined, the inhibition appeared to be mainly due to an intracellular molecular event because it could not be explained solely on the basis of cell surface receptor mediated interference. The results support the notion that the inhibition likely occurred at the level of viral RNA, possibly involving competition between viral RNAs for some transcriptional factor essential for virus replication. Induction of a cytokine is another possibility. These findings might be relevant to the clinical-epidemiological data suggesting that infection with HIV-2 may offer some protection against HIV-1 infection.
RP Arya, SK (reprint author), NCI,TUMOR CELL BIOL LAB,NIH,BLDG 37,ROOM 6C24,37 CONVENT DR,BETHESDA,MD 20892, USA.
NR 32
TC 32
Z9 33
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 APR 30
PY 1996
VL 93
IS 9
BP 4486
EP 4491
DI 10.1073/pnas.93.9.4486
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UK557
UT WOS:A1996UK55700139
PM 8633095
ER
PT J
AU Guerrini, R
Capasso, A
Sorrentino, L
Anacardio, R
Bryant, SD
Lazarus, LH
Attila, M
Salvadori, S
AF Guerrini, R
Capasso, A
Sorrentino, L
Anacardio, R
Bryant, SD
Lazarus, LH
Attila, M
Salvadori, S
TI Opioid receptor selectivity alteration by single residue replacement:
Synthesis and activity profile of [Dmt]deltorphin B
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE antinociception; bioassay; deltorphin; opioid receptor; peptide
synthesis
ID MORPHINE ANTINOCICEPTION; HIGH-AFFINITY; MU-RECEPTOR; DEXAMETHASONE;
ANALGESIA; PEPTIDE; MICE; AGONIST; DESIGN
AB The single amino acid replacement of 2',6'-dimethyl-L-tyrosine in deltorphin B (H-Dmt-D-Ala-Phe-Glu-Val-Val-Gly-NH2) yielded high affinity for mu- and delta-binding sites. [Dmt(1)]Deltorphin B lacks activity at kappa-opioid binding sites. Bioactivity in vitro with guinea-pig ileum confirmed that [Dmt(1)]deltorphin B interacted with mu-opioid receptors by reducing electrically induced contractions in a naloxone-reversible manner and was 150-fold more potent than morphine and comparable to [D-Ala(2),NMePhe(4),Gly-ol(5)]enkephalin (DAGO). The inhibition of spontaneous contractions of rabbit jejunum provided evidence for delta-opioid receptor interaction. Analgesia (hot plate and tail flick tests) revealed that [Dmt(1)]deltorphin B was 180- to 200-fold more potent than morphine. Pretreatment with naloxone, naltrindole or H-Dmt-Tic-Ala-OH (a highly selective delta-opioid receptor antagonist) prevented [Dmt(1)]deltorphin B antinociception. Thus, [Dmt(1)]deltorphin B exhibited remarkably high dual affinity and bioactivity toward delta- and mu-opioid receptors.
C1 UNIV FERRARA,DIPARTIMENTO SCI FARMACEUT,I-44100 FERRARA,ITALY.
UNIV SALERNO,SCH PHARM,I-84084 SALERNO,ITALY.
UNIV NAPLES FEDERICO II,DEPT EXPTL PHARMACOL,I-80131 NAPLES,ITALY.
DOMPE SPA,I-67100 LAQUILA,ITALY.
NIEHS,RES TRIANGLE PK,NC 27709.
HELSINKI UNIV,DEPT PHARMACOL,DIV PHARMACOL & TOXICOL,SF-00014 HELSINKI,FINLAND.
OI Guerrini, Remo/0000-0002-7619-0918
NR 29
TC 43
Z9 44
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 APR 29
PY 1996
VL 302
IS 1-3
BP 37
EP 42
DI 10.1016/0014-2999(96)00067-2
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UQ817
UT WOS:A1996UQ81700006
PM 8790989
ER
PT J
AU VonLubitz, DKJE
Beenhakker, M
Lin, RCS
Carter, MF
Paul, IA
Bischofberger, N
Jacobson, KA
AF VonLubitz, DKJE
Beenhakker, M
Lin, RCS
Carter, MF
Paul, IA
Bischofberger, N
Jacobson, KA
TI Reduction of postischemic brain damage and memory deficits following
treatment with the selective adenosine A(1) receptor a agonist
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE cerebral ischemia; adenosine receptor; spatial memory; water maze;
(gerbil)
ID FOREBRAIN ISCHEMIA; CEREBRAL-ISCHEMIA; HIPPOCAMPUS; GERBILS; RATS
AB Agonists of adenosine A(1) receptors have been frequently proposed as candidate, for clinical development in treatment of cerebral ischemia and stroke, Numerous experimental studies have shown that pre- and postischemic administration of these drugs results in a very significant reduction of postischemic brain damage. However, only a few studies determined the impact of cerebral ischemia and drug treatment on postischemic recovery of spatial memory. Thr present paper demonstrates that preischemic i.p. administration of adenosine amine congener(ADAC) at 100 mu g/kg in gerbils results in a significant (P < 0.05) reduction of postischemic mortality and hippocampal, cortical and striatal morbidity. Postischemic Morris' water maze tests show that preischemic treatment with ADAC also leads to a very significant (P < 0.001) reduction of postischemic spatial memory loss, Our results indicate feasibility of further consideration of adenosine A(1) receptor agonists as a clinically applicable acute treatment of brain ischemia. Recent development of neuroprotective adenosine A(1) receptor agonists that are free of cardiovascular side effects supports such development.
C1 MED COLL PENN & HAHNEMANN UNIV, DEPT ANAT & NEUROBIOL, PHILADELPHIA, PA 19102 USA.
UNIV MISSISSIPPI, MED CTR, LAB NEUROBEHAV PHARMACOL & IMMUNOL, JACKSON, MS 39216 USA.
GILEAD SCI INC, FOSTER CITY, CA 94404 USA.
RP VonLubitz, DKJE (reprint author), NIDDK, MOLEC RECOGNIT SECT, 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 [Z99 DK999999, Z01 DK031117-20]
NR 34
TC 35
Z9 36
U1 0
U2 1
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 APR 29
PY 1996
VL 302
IS 1-3
BP 43
EP 48
DI 10.1016/0014-2999(96)00101-X
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UQ817
UT WOS:A1996UQ81700007
PM 8790990
ER
PT J
AU Wynn, TA
Sher, A
AF Wynn, TA
Sher, A
TI Hot Papers - Immunology Parasitology - Endogenous interleukin 12 (IL-12)
regulates granuloma formation induced by eggs of Schistosoma mansoni and
exogenous IL-12 both inhibits and prophylactically immunizes against egg
pathology by T.A. Wynn, I. Eltoum, I.P. Oswald, A.W. Cheever, A. Sher -
Comments
SO SCIENTIST
LA English
DT Editorial Material
AB Hot papers: Parasitologist Thomas A. Wynn and Alan Sher report on use of interleukin 12 to regulate granuloma formation induced by eggs of Schistosoma mansoni.
RP Wynn, TA (reprint author), NIAID,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
RI Wynn, Thomas/C-2797-2011
NR 3
TC 0
Z9 0
U1 0
U2 0
PU SCIENTIST INC
PI PHILADELPHIA
PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104
SN 0890-3670
J9 SCIENTIST
JI Scientist
PD APR 29
PY 1996
VL 10
IS 9
BP 14
EP 14
PG 1
WC Information Science & Library Science; Multidisciplinary Sciences
SC Information Science & Library Science; Science & Technology - Other
Topics
GA UH057
UT WOS:A1996UH05700013
ER
PT J
AU Bigbee, WL
Jensen, RH
Veidebaum, T
Tekkel, M
Rahu, M
Stengrevics, A
Kesminiene, A
Kurtinaitis, J
Auvinen, A
Hakulinen, T
Servomaa, E
Rytomaa, T
Obrams, GI
Boice, JD
AF Bigbee, WL
Jensen, RH
Veidebaum, T
Tekkel, M
Rahu, M
Stengrevics, A
Kesminiene, A
Kurtinaitis, J
Auvinen, A
Hakulinen, T
Servomaa, E
Rytomaa, T
Obrams, GI
Boice, JD
TI Glycophorin A biodosimetry in Chernobyl cleanup workers from the Baltic
countries
SO BRITISH MEDICAL JOURNAL
LA English
DT Article
C1 UNIV PITTSBURGH,INST CANC,MOL CARCINOGENESIS PROGRAM,PITTSBURGH,PA 15238.
UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143.
INST EXPT & CLIN MED,DEPT EPIDEMIOL & BIOSTAT,TALLINN,ESTONIA.
LATVIA CANC REGISTRY,RIGA,LATVIA.
LITHUANIAN CHERNOBYL MED CTR,VILNIUS,LITHUANIA.
LITHUANIAN CANC REGISTRY,MITHUANIAN ONCOL CTR,VILNIUS,LITHUANIA.
FINNISH CTR RADIAT & NUCL SAFETY,HELSINKI,FINLAND.
FINNISH CANC REGISTRY,SF-00170 HELSINKI,FINLAND.
NCI,EXTRAMURAL PROGRAMS BRANCH,BETHESDA,MD 20892.
NCI,RADIAT EPIDEMIOL BRANCH,BETHESDA,MD 20892.
RP Bigbee, WL (reprint author), UNIV PITTSBURGH,CTR ENVIRONM & OCCUPAT HLTH & TOXICOL,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15238, USA.
RI Rahu, Mati/A-9981-2008;
OI Auvinen, Anssi/0000-0003-1125-4818
FU NCI NIH HHS [N01-CP-50520]
NR 5
TC 23
Z9 23
U1 1
U2 4
PU BRITISH MED JOURNAL PUBL GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR
SN 0959-8138
J9 BRIT MED J
JI Br. Med. J.
PD APR 27
PY 1996
VL 312
IS 7038
BP 1078
EP 1079
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA UH816
UT WOS:A1996UH81600027
PM 8616416
ER
PT J
AU Dong, ZG
Xu, RH
Kim, JB
Zhan, SN
Ma, WY
Colburn, NH
Kung, HF
AF Dong, ZG
Xu, RH
Kim, JB
Zhan, SN
Ma, WY
Colburn, NH
Kung, HF
TI AP-1/jun is required for early Xenopus development and mediates mesoderm
induction by fibroblast growth factor but not by activin
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTION FACTOR; JUN; RECEPTOR; FOS; EXPRESSION; EMBRYOS; FGF;
ONCOGENE; ENHANCER; KINASE
AB In Xenopus, normal mesoderm formation depends on signaling through the fibroblast growth factor (FGF) tyrosine kinase receptor. An important signaling pathway from receptor tyrosine kinases involves Ras/Raf/MAP kinase, However, the downstream pathway that occurs in the nucleus to finally trigger gene expression for mesoderm formation remains unknown, We report here that a high level of activator protein-1 (AP-1)-dependent transcriptional activity is detected during the early development of Xenopus embryos. Injection of a dominant negative mutant jun (DNM-jun or TAM67) RNA into the two-cell stage embryos inhibited endogenous AP-1 activity and blocked normal embryonic development with severe posterior truncation in tadpoles. The inhibition of AP-1 activity and the phenotypic change induced by TAM67 was rescued by co-injection of wild-type c-jun RNA, but not by the control beta-galactosidase RNA. The FGF-stimulated mesoderm induction was markedly inhibited in animal cap explants from the embryos injected with TAM67. Activin induction of mesoderm, on the other hand, was normal in the embryos injected with TAM67 RNA. These findings suggest that AP-1 mediates FGF, but not activin, receptor signaling during mesoderm induction and the AP-1/Jun is a key signaling molecule in the development of posterior structure.
C1 SAIC,LAB BIOCHEM PHYSIOL,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD.
NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,NIH,CELL BIOL SECT,DIV BASIC SCI,FREDERICK,MD 21702.
RP Dong, ZG (reprint author), UNIV MINNESOTA,HORMEL INST,801 16TH AVE NE,AUSTIN,MN 55912, USA.
RI Xu, Ren-He/M-3125-2016
NR 38
TC 42
Z9 42
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 26
PY 1996
VL 271
IS 17
BP 9942
EP 9946
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG257
UT WOS:A1996UG25700015
PM 8626631
ER
PT J
AU Sackett, DL
KoskKosicka, D
AF Sackett, DL
KoskKosicka, D
TI The active species of plasma membrane Ca2+-ATPase are a dimer and a
monomer-calmodulin complex
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ERYTHROCYTE CA-2+-ATPASE; MOLECULAR-CLONING; OLIGOMERIZATION;
FLUORESCENCE; ASSOCIATION; ACTIVATION; ISOFORMS; BINDING; ATPASE; STATES
AB The purified plasma membrane Ca2+-ATPase is fully activated through the enzyme concentration-dependent self-association at physiologically relevant Ca2+ concentrations (Kosk-Kosicka, D., and Bzdega, T. (1988) J. Biol. Chem. 263, 18184-18189; Kosk-Kosicka, D., Bzdega, T., and Wawrzynow, A. (1989) J. Biol. Chem. 264, 19495-19499). We have previously shown that the Ca2+-ATPase activity of the oligomeric enzyme is independent of calmodulin, in contrast to another active enzyme species, a presumable monomer, that is activated by calmodulin binding, Presently, we have succeeded in determining the molecular mass of the two active enzyme species by equilibrium ultracentrifugation. For the calmodulin dependent species, the molecular mass is 170 +/- 30 kDa, which is consistent with predominantly monomeric Ca2+-ATPase with bound calmodulin, The molecular mass of calmodulin-independent oligomers is 260 +/- 34 kDa, indicating that they are dimers, Results of experiments performed under different calcium and potassium concentrations and in the presence of dextran that causes molecular crowding verify a strict Ca2+ requirement of the dimerization process, We conclude that the active species of the Ca2+-ATPase are a monomer-calmodulin complex and a dimer.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21287.
NIDDK,NIH,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892.
FU NIGMS NIH HHS [GM 447130]
NR 24
TC 21
Z9 22
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 26
PY 1996
VL 271
IS 17
BP 9987
EP 9991
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG257
UT WOS:A1996UG25700022
PM 8626638
ER
PT J
AU Frederikse, PH
Garland, D
Zigler, JS
Piatigorsky, J
AF Frederikse, PH
Garland, D
Zigler, JS
Piatigorsky, J
TI Oxidative stress increases production of beta-amyloid precursor protein
and beta-amyloid (A beta) in mammalian lenses, and A beta has toxic
effects on lens epithelial cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ALPHA-B-CRYSTALLIN; ALZHEIMERS-DISEASE; PHASE-SEPARATION; CATARACT
FORMATION; ACTIVATION; MOUSE; OPACIFICATION; FIBROBLASTS; DEPOSITION;
MECHANISM
AB Many amyloid diseases are characterized by protein aggregations linked to oxidative stress. Such diseases including those of the brain, muscle, and blood vessels exhibit plaques containing beta-amyloid (A beta). Here we demonstrate that Alzheimer's precursor protein (beta APP) and A beta are present at low levels in normal lenses and increase in intact cultured monkey lenses treated with H2O2 or UV radiation (known cataractogenic agents), and with phorbol 12-myristate 13-acetate. AP-1 factor binding, shown by others to up-regulate beta APP expression, increased in the monkey lenses treated with H2O2, UV radiation, or phorbol 12-myristate 13-acetate and paralleled the increase in beta APP expression. Rat lenses exposed to oxidative stress showed increased beta APP in the anterior epithelium and cortex. Incubation of cultured rabbit lens N/N1003A epithelial cells with A beta induced inclusions and vacuoles and was cytotoxic. A beta cross-reacting protein was readily detected in the cortex of a cataractous human lens. Our data show that beta APP and A beta increase in mammalian lenses as part of a response to H2O2 or UV radiation and suggest that they may contribute to the mechanism by which oxidative damage leads to lens opacification.
C1 NEI,LAB MECHANISMS OCULAR DIS,NIH,BETHESDA,MD 20892.
RP Frederikse, PH (reprint author), NEI,MOLEC & DEV BIOL LAB,NIH,6 CTR DR,MSC 2730,BETHESDA,MD 20892, USA.
NR 79
TC 138
Z9 143
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 26
PY 1996
VL 271
IS 17
BP 10169
EP 10174
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG257
UT WOS:A1996UG25700050
PM 8626578
ER
PT J
AU Hu, ZZ
Zhuang, L
Dufau, ML
AF Hu, ZZ
Zhuang, L
Dufau, ML
TI Multiple and tissue-specific promoter control of gonadal and non-gonadal
prolactin receptor gene expression
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RAT OVARY; CELLS
AB Prolactin receptors (PRLRs) are widely expressed, and multiple mRNA transcripts encoding PRLRs are present in prolactin target tissues. The molecular basis for the control of the PRLR gene expression is currently unknown. Analyses of the 5'-untranslated regions of PRLR mRNAs expressed in gonadal and non-gonadal tissues and their genomic organization revealed three alternative first exons designated as El(1), El(2), and El(3). Each of these exons is alternatively spliced to a common noncoding exon (exon 2, nucleotides -115 to -56) that precedes the third exon containing the translation initiation codon. Alternative utilization of exons El(1), El(2), and El(3), as well as alternative splicing of exon 2, generates multiple 5'-untranslated regions in PRLR transcripts. These alternative first exons (El(1), El(2), and El(3)) were found to be utilized in a tissue-specific manner in vivo. El(1) is predominantly expressed in the ovary, El(2) is specifically expressed in the liver, and El(3) is expressed as a predominant form in the Leydig cell and as a minor form in the ovary and liver. Genomic 5'-flanking regions containing the three putative PRLR gene promoters (PI, PII, and PIII) that initiate the transcription of El(1), El(2), and El(3), respectively, were identified. El(1) was found to initiate from a single site at -549, El(2) from multiple sites at -405, -461, and -506, and El(3) from two major sites at -340 and -351. These findings indicate that multiple promoters control transcription of the PRLR gene and provide a molecular basis for the differential regulation of PRLR expression in diverse tissues.
C1 NICHHD,SECT MOL ENDOCRINOL,ENDOCRINOL & REPROD RES BRANCH,NIH,BETHESDA,MD 20892.
NR 19
TC 54
Z9 54
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 26
PY 1996
VL 271
IS 17
BP 10242
EP 10246
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG257
UT WOS:A1996UG25700062
PM 8626590
ER
PT J
AU Choi, D
Stables, JP
Kohn, H
AF Choi, D
Stables, JP
Kohn, H
TI Synthesis and anticonvulsant activities of
N-benzyl-2-acetamidopropionamide derivatives
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID AMINO-ACIDS; SERIES
AB Studies have demonstrated that 2-substituted N-benzyl-2-acetamidoacetamides (2) are potent anticonvulsants. A recent investigation has led to the hypothesis that an important structural feature in 2 for maximal anticonvulsant activity is the placement of a small, substituted heteroatom moiety one atom from the C(2) sate. This paper validates this hypothesis. Twelve derivatives of N-benzyl-2-acetamidopropionamide have been prepared in which six different heteroatom substituents (chloro, bromo, iodo, oxygen, nitrogen, and sulfur) were incorporated at the C(3) site. Highly potent activities were observed for the two oxygen-substituted derivatives, N-benzyl-2-acetamido-3-methoxypropionamide (18) and N-benzyl-2-acetamido-3-ethoxypropionamide (19). The ED(50) values in mice following intraperitoneal (ip) dosing for the maximal electroschock-induced seizure test for 18 and 19 were 8.3 and 17.3 mg/kg, respectively. These values compared favorably to the ED(50) value found for phenytoin (ED(50) = 6.5 mg/kg). Comparable activities were observed for 18 and 19 upon oral (po) administration to rats (18, ED(50) = 3.9 mg/kg; 19, ED(50) = 19 mg/kg; phenytoin, ED(50) = 23 mg/kg). Evaluation of the individual stereoisomers for 18 demonstrated that the principal anticonvulsant activity resided in the (R)-stereoisomer. The ED(50) value for (R)-18 was 4.5 mg/kg, and the ED(50) for (S)-18 exceeded 100 mg/kg. This difference in activity for the two stereochemical isomers surpassed comparable values for other members within this class of compounds. The protective indices (PI = TD50/ED(50)) (where TD50 represents a neurotoxic dose impairing rotorod performance) for (R)-18 in mice (ip) and in rats (po) were 6.0 and >130, respectively.
C1 UNIV HOUSTON, DEPT CHEM, HOUSTON, TX 77204 USA.
NINCDS, EPILEPSY BRANCH, NIH, BETHESDA, MD 20892 USA.
NR 33
TC 96
Z9 102
U1 3
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD APR 26
PY 1996
VL 39
IS 9
BP 1907
EP 1916
DI 10.1021/jm9508705
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA UJ112
UT WOS:A1996UJ11200019
PM 8627614
ER
PT J
AU Liu, RY
Hu, RJ
Zhang, PW
Skolnick, P
Cook, JM
AF Liu, RY
Hu, RJ
Zhang, PW
Skolnick, P
Cook, JM
TI Synthesis and pharmacological properties of novel 8-substituted
imidazobenzodiazepines: High-affinity, selective probes for alpha
5-containing GABA(A) receptors
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID BENZODIAZEPINE RECEPTORS; A RECEPTORS; PHARMACOPHORE; SUBUNIT; BRAIN;
ANXIETY; CLONING; SITE
AB The synthesis and pharmacological properties of imidazobenzodiazepines with both high affinity and selectivity for alpha 5-containing GABAA receptors are described. Four of these compounds (5, 6, 8, and 9) inhibited [H-3]flunitrazepam binding to recombinant alpha 5 beta 2 gamma 2 GABA(A) receptors with IC50 values between similar to 0.4 and 5 nM. These compounds were greater than or equal to 24-75-fold more selective for recombinant receptors containing alpha 5 subunits compared to other, ''diazepam-sensitive'' GABA(A) receptors containing either alpha 1, alpha 2, or alpha 3 subunits. Imidazobenzodiazepine 9 (used as the prototypical alpha 5 selective ligand) inhibited [H-3]flunitrazepam binding to hippocampal membranes with high- and low-affinity components (IC50 0.6 +/- 0.2 and 85.6 +/- 13.1 nM, respectively), representing similar to 16% and similar to 84% of the receptor pool. Inhibition of [H-3]flunitrazepam binding to cerebellar membranes with imidazobenzodiazepine 9 was best fitted to a single population of sites with an IC50 of 79.8 +/- 18.3 nM. These imidazobenzodiazepines behaved as GABA negative ligands in recombinant GABA(A) receptors expressed in Xenopus oocytes and were convulsant in mice after parenteral administration. The relative potencies of flumazenil and zolpidem in blocking convulsions induced by 9 and DMCM, respectively, indicated that occupation of alpha 5-containing GABA(A) receptors substantially contributed to the convulsant properties of acetylene analog 9. These 8-substituted imidazobenzodiazepines (5, 6, 8, and 9) should prove useful in examining the physiological roles of GABA(A) receptors bearing an alpha 5 subunit and may also lead to the development of novel, subtype selective therapeutic agents.
C1 UNIV WISCONSIN, DEPT CHEM, MILWAUKEE, WI 53201 USA.
NIDDK, NEUROSCI LAB, NIH, BETHESDA, MD 20892 USA.
NR 37
TC 72
Z9 73
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD APR 26
PY 1996
VL 39
IS 9
BP 1928
EP 1934
DI 10.1021/jm950887n
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA UJ112
UT WOS:A1996UJ11200022
PM 8627617
ER
PT J
AU Kiser, R
Makovsky, S
Terpening, SJ
Laing, N
Clanton, DJ
AF Kiser, R
Makovsky, S
Terpening, SJ
Laing, N
Clanton, DJ
TI Assessment of a cytoprotection assay for the discovery and evaluation of
anti-human immunodeficiency virus compounds utilizing a
genetically-impaired virus
SO JOURNAL OF VIROLOGICAL METHODS
LA English
DT Article
DE human immunodeficiency virus; cytoprotection assay; antiviral activity
ID REVERSE-TRANSCRIPTASE; NATURAL-PRODUCTS; TYPE-1; HIV-1; RETROVIRUSES;
REPLICATION; INHIBITORS; MECHANISM; AIDS
AB A biologically contained cytoprotection assay was developed to screen inhibitors of the human immunodeficiency virus without the need for high level containment or practices. The virus used has multiple point mutations that have destroyed its ability to produce both Rev and Tat, proteins essential for virus replication in vitro. The original cell line employed (CEM-SSTART) contains a genetic construct that allows for the continuous expression of both Rev and Tat, and a subclone (1A2) was developed that provides for maximum acute cytopathic effect. The National Cancer Institute's AIDS drug screening assay was used to rest known drugs with both HIVIIIB virus in the T4 lymphocytic cell line CEM-SS and mutant virus in the 1A2 subclone. This cell-based assay uses the tetrazolium salt, XTT, as an indicator of cellular metabolism after the cells have been infected with virus. The results of extensive testing have shown that the assay using mutant virus is comparable to the current NCI AIDS drug screen. After 42 days in 1A2 or CEM-SS cell culture, the virus or the integrated genome did not revert to wild-type, and the virus produced in 1A2 cells was unable to replicate in PBMCs. Mutant viral stocks were devoid of wild-type virus as determined by a PCR assay that would have found 60-600 copies of mutant RNA. These materials, which are now available to the scientific community (NIH AIDS Research and Reference Reagent Program), should be useful tools to screen and test compounds for potential inhibition of HIV in laboratories not equipped to maintain and use wild-type infectious virus.
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS DRUG SCREENING & DEV LAB,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-56000]
NR 29
TC 26
Z9 26
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-0934
J9 J VIROL METHODS
JI J. Virol. Methods
PD APR 26
PY 1996
VL 58
IS 1-2
BP 99
EP 109
DI 10.1016/0166-0934(95)01998-7
PG 11
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Virology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Virology
GA UQ674
UT WOS:A1996UQ67400011
PM 8783155
ER
PT J
AU Mellon, I
Rajpal, DK
Koi, M
Boland, CR
Champe, GN
AF Mellon, I
Rajpal, DK
Koi, M
Boland, CR
Champe, GN
TI Transcription-coupled repair deficiency and mutations in human mismatch
repair genes
SO SCIENCE
LA English
DT Article
ID NONPOLYPOSIS COLORECTAL-CANCER; NUCLEOTIDE EXCISION REPAIR;
ESCHERICHIA-COLI; COCKAYNE-SYNDROME; DNA DAMAGE; PREFERENTIAL REPAIR;
SELECTIVE REPAIR; STRAND; YEAST; MECHANISM
AB Deficiencies in mismatch repair have been linked to a common cancer predisposition syndrome in humans, hereditary nonpolyposis colorectal cancer (HNPCC), and a subset of sporadic cancers. Here, several mismatch repair-deficient tumor cell lines and HNPCC-derived lymphoblastoid cell lines were found to be deficient in an additional DNA repair process termed transcription-coupled repair (TCR). The TCR defect was corrected in a mutant cell line whose mismatch repair deficiency had been corrected by chromosome transfer. Thus, the connection between excision repair and mismatch repair previously described in Escherichia coli extends to humans. These results imply that deficiencies in TCR and exposure to carcinogens present in the environment may contribute to the etiology of tumors associated with genetic defects in mismatch repair.
C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27706.
UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093.
RP Mellon, I (reprint author), UNIV KENTUCKY,MARKEY CANC CTR,TOXICOL PROGRAM,DEPT PATHOL,LEXINGTON,KY 40536, USA.
RI Koi, Minoru/C-3489-2012; Koi, Minoru/G-9197-2014
FU NIGMS NIH HHS [GM45535-03]
NR 46
TC 238
Z9 238
U1 0
U2 3
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD APR 26
PY 1996
VL 272
IS 5261
BP 557
EP 560
DI 10.1126/science.272.5261.557
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UG826
UT WOS:A1996UG82600047
PM 8614807
ER
PT J
AU Oh, CK
Metcalfe, DD
AF Oh, CK
Metcalfe, DD
TI Activated lymphocytes induce promoter activity of the TCA3 gene in mast
cells following cell-to-cell contact
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID DE-GRANULATION; HYPERSENSITIVITY; INVITRO
AB Aggregates of mast cells and lymphocytes have been found in inflamed tissues suggesting that lymphocytes may have the ability to activate mast cells through cell-to-cell contact. To examine this hypothesis, murine mast cells were transfected with a T cell activation gene-3 (TCA3)-chloramphenicol acetyl transferase (CAT) construct, and these cells co-cultured with murine EL-4 (T), CH12.LX (B), WEHI-3 (myelomonocytic) or 3T3(fibroblast) cell lines. Go-culture of activated EL-4 or CH12.LX cells, but not WEHI-3 or 3T3 cells, with transfected mast cells induced a 5 to 7 fold increase in CAT expression which was dependent on the lymphocyte to mast cell ratio. Supernatants from activated EL-4 or CH12.LX cells did not induce CAT expression in transfected mast cells. These data demonstrate that activated lymphocytes have the ability to induce the promoter of the TCA3 gene in mast cells through a mechanism requiring cell-to-cell contact, and suggest the possibility that activated lymphocytes may effect other biologic processes in mast cells as well through such heterotypic activation. (C) 1996 Academic Press, Inc.
RP Oh, CK (reprint author), NIAID,LAB ALLERG DIS,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 11
TC 11
Z9 11
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD APR 25
PY 1996
VL 221
IS 3
BP 510
EP 514
DI 10.1006/bbrc.1996.0627
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UH698
UT WOS:A1996UH69800004
PM 8629992
ER
PT J
AU McDermott, JB
Cvekl, A
Piatigorsky, J
AF McDermott, JB
Cvekl, A
Piatigorsky, J
TI Lens-specific expression of a chicken beta A3/Al-crystallin promoter
fragment in transgenic mice
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID A-CRYSTALLIN PROMOTER; CHLORAMPHENICOL ACETYLTRANSFERASE;
GENE-EXPRESSION; ELEMENTS; PROTEINS; SITES; CELLS
AB beta A3/A1-crystallin is one of the major refractive proteins of the chicken eye lens. Previously we showed that a fragment from -382 to +22 bp of the beta A3/A1-crystallin gene functions as a promoter in transfected lens cells. Here we show by use of the bacterial chloramphenicol acetyltransferase reporter gene that the -143/+22 fragment is sufficient for lens-specific promoter activity in transgenic mice. DNase I footprinting shows that lens nuclear proteins protect several regions within the minimal promoter fragment. (C) 1996 Academic Press, Inc.
C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892.
RI Cvekl, Ales/B-2427-2013
NR 28
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 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD APR 25
PY 1996
VL 221
IS 3
BP 559
EP 564
DI 10.1006/bbrc.1996.0635
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UH698
UT WOS:A1996UH69800012
PM 8630000
ER
PT J
AU Haxby, JV
AF Haxby, JV
TI Memory - Medial temporal lobe imaging
SO NATURE
LA English
DT Editorial Material
RP Haxby, JV (reprint author), NIMH,SECT FUNCT BRAIN IMAGING,BETHESDA,MD 20892, USA.
NR 10
TC 16
Z9 16
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 APR 25
PY 1996
VL 380
IS 6576
BP 669
EP 670
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UG827
UT WOS:A1996UG82700024
PM 8614458
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 Structure of the UmuD' protein and its regulation in response to DNA
damage
SO NATURE
LA English
DT Article
ID RECA-MEDIATED CLEAVAGE; MUTANT LEXA PROTEINS; ANOMALOUS DIFFRACTION;
DEPENDENT CLEAVAGE; ESCHERICHIA-COLI; SOS MUTAGENESIS; AUTODIGESTION;
POLYMERASE
AB FOR life to be sustained, mistakes in DNA repair must be tolerated when damage obscures the genetic information. In bacteria such as Escherichia coli, DNA damage elicits the well regulated 'SOS response' (reviewed in ref. 1). For the extreme case of damage that cannot be repaired by conventional enzymes, there are proteins that allow the replication of DNA through such lesions, but with a reduction in the fidelity of replication(2). Essential proteins in this mutagenic process are RecA, DNA polymerase III, UmuD, UmuD' and UmuC (umu: UV mutagenesis)(1-3). Regulation of this response involves a RecA-mediated self-cleavage of UmuD to produce UmuD'. To understand this system in more detail, we have determined the crystal structure of the E. coli UmuD' mutagenesis protein at 2.5 Angstrom resolution. Globular heads folded in an unusual beta-structure associate to form molecular dimers, and extended amino-terminal tails associate to produce crystallized filaments. The structure provides insight into the mechanism of the self-cleavage reaction that UmuD-like proteins undergo as part of the global SOS response(4-8).
C1 COLUMBIA UNIV,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032.
COLUMBIA UNIV,HOWARD HUGHES MED INST,NEW YORK,NY 10032.
NICHHD,SECT DNA REPLICAT REPAIR & MUTAGENESIS,NIH,BETHESDA,MD 20892.
RI Peat, Thomas/F-9817-2010
OI Peat, Thomas/0000-0002-6488-0831
NR 30
TC 134
Z9 136
U1 0
U2 3
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF
SN 0028-0836
J9 NATURE
JI Nature
PD APR 25
PY 1996
VL 380
IS 6576
BP 727
EP 730
DI 10.1038/380727a0
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UG827
UT WOS:A1996UG82700056
PM 8614470
ER
PT J
AU Hoofnagle, J
McKenzie, R
Straus, S
AF Hoofnagle, J
McKenzie, R
Straus, S
TI Severe toxicity of fialuridine (FIAU) - Reply
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
RP Hoofnagle, J (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 25
PY 1996
VL 334
IS 17
BP 1137
EP 1137
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA UG457
UT WOS:A1996UG45700021
ER
PT J
AU Fiore, MC
Wetter, DW
Bailey, WC
Bennett, G
Cohen, SJ
Dorfman, SF
Goldstein, MG
Gritz, ER
Hasselblad, V
Henningfield, JE
Heyman, RB
Holbrook, J
Husten, C
Jaen, CR
Kohler, C
Kottke, TE
Lando, HA
Manley, M
Mecklenburg, R
Melvin, C
Mullen, PD
Nett, LM
Piasecki, TM
Robinson, L
Rothstein, D
Schriger, DL
Stitzer, ML
Stachenko, S
Tommasello, A
Villejo, L
Wewers, ME
Baker, TB
AF Fiore, MC
Wetter, DW
Bailey, WC
Bennett, G
Cohen, SJ
Dorfman, SF
Goldstein, MG
Gritz, ER
Hasselblad, V
Henningfield, JE
Heyman, RB
Holbrook, J
Husten, C
Jaen, CR
Kohler, C
Kottke, TE
Lando, HA
Manley, M
Mecklenburg, R
Melvin, C
Mullen, PD
Nett, LM
Piasecki, TM
Robinson, L
Rothstein, D
Schriger, DL
Stitzer, ML
Stachenko, S
Tommasello, A
Villejo, L
Wewers, ME
Baker, TB
TI The Agency for Health Care Policy and Research Smoking Cessation
Clinical Practice Guideline
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID WEIGHT-GAIN; NICOTINE REPLACEMENT; CIGARETTE-SMOKING; UNITED-STATES;
QUIT SMOKING; BODY-WEIGHT; WOMEN; INTERVENTION; POPULATION; PHYSICIAN
AB Objective.-To summarize the Smoking Cessation Clinical Practice Guideline that provides recommendations for 3 groups of professionals: primary care clinicians, smoking cessation specialists, and health care administrators, insurers, and purchasers.
Participants.-An independent panel of scientists, clinicians, consumers, and methodologists selected by the US Agency for Health Care Policy and Research.
Evidence.-English-language, peer-reviewed literature published between 1975 and 1994 that addresses the assessment and treatment of tobacco dependence, nicotine addiction, and clinical practice.
Consensus Process.-Four panel meetings were held over 2 years to evaluate meta-analytic and other results, to synthesize the results, and to develop recommendations. The Guideline was repeatedly reviewed and revised.
Conclusions.-The panel recommendations address 3 audiences, Major recommendations for primary care clinicians are to use officewide systems to identify smokers, treat every smoker with a cessation or motivational intervention, offer nicotine replacement except in special circumstances, and schedule follow-up contact to occur after cessation, Major recommendations to smoking cessation specialists are to use multiple individual or group counseling sessions lasting at least 20 minutes each with sessions spanning multiple weeks, offer nicotine replacement, and provide problem-solving and social support counseling, Major recommendations for health care administrators, insurers, and purchasers are that tobacco-user identification systems be used in all clinics and that smoking cessation treatment be supported through staff education and training, dedicated staff, changes in hospital policies, and the provision of reimbursement for tobacco-dependence treatment.
C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX.
UNIV ALABAMA,BIRMINGHAM,AL.
NHLBI,NIH,BETHESDA,MD 20892.
WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC.
BROWN UNIV,SCH MED,MIRIAM HOSP,PROVIDENCE,RI 02912.
DUKE UNIV,DURHAM,NC.
NIDA,NIH,BALTIMORE,MD.
AMER ACAD PEDIAT,CINCINNATI,OH.
UNIV UTAH,SCH MED,SALT LAKE CITY,UT.
CTR DIS CONTROL & PREVENT,OFF SMOKING & HLTH,ATLANTA,GA 30341.
SUNY BUFFALO,CTR URBAN RES PRIMARY CARE,BUFFALO,NY.
MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905.
UNIV MINNESOTA,MINNEAPOLIS,MN 55455.
NCI,NIH,ROCKVILLE,MD.
NCI,POTOMAC,MD.
UNIV TEXAS,CTR HLTH PROMOT RES & DEV,HOUSTON,TX.
CTR HLTH SCI STUDIES,PSL HLTH ONE,DENVER,CO.
UNIV WISCONSIN,SCH MED,CTR TOBACCO RES & INTERVENT,MADISON,WI.
OFF DIS PREVENT & HLTH PROMOT,WASHINGTON,DC.
DEPT PUBL HLTH,WASHINGTON,DC.
UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA.
JOHNS HOPKINS UNIV HOSP,BAYVIEW MED CTR,BALTIMORE,MD.
HLTH CANADA,OTTAWA,ON,CANADA.
UNIV MARYLAND,SCH PHARM,BALTIMORE,MD 21201.
OHIO STATE UNIV,COLL NURSING,COLUMBUS,OH 43210.
RP Fiore, MC (reprint author), UNIV WISCONSIN,SCH MED,CTR TOBACCO RES & INTERVENT,1300 UNIV AVE,MADISON,WI 53706, USA.
NR 68
TC 222
Z9 222
U1 2
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 APR 24
PY 1996
VL 275
IS 16
BP 1270
EP 1280
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA UF478
UT WOS:A1996UF47800032
ER
PT J
AU Lee, H
Darden, TA
Pedersen, LG
AF Lee, H
Darden, TA
Pedersen, LG
TI An ab initio quantum mechanical model for the catalytic mechanism of
HIV-1 protease
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID IMMUNODEFICIENCY VIRUS-1 PROTEASE; ASPARTIC PROTEINASES; CHEMICAL
MECHANISM; ELUCIDATE DETAILS; ACTIVE-SITE; INHIBITOR; RESONANCE;
BARRIERS
AB The catalytic mechanism of the HIV-1 protease (HIV-PR) is studied through ab initio theoretical model calculations. This model consists of a formate/formic acid pair, a structurally important water molecule, and a formamide molecule. The proposed catalytic mechanism is composed of five steps, two of which are transition states separated by a third step (an intermediate state). The remaining two steps are related to product release. The overall forward hydrolysis reaction barrier is approximately 22 kcal/mol, with a reverse hydrolysis barrier of approximately 34 kcal/mol at the RHF/6-31G* level. The second transition state is related to a nucleophilic attack of the water molecule on the carbon atom of the substrate scissile bond, and is essential for the collapse of the substrate. That the transition state structures of HIV-PR have not been identified makes a theoretical study of this kind particularly valuable for understanding the HIV-PR mechanism.
C1 UNIV N CAROLINA,DEPT CHEM,CHAPEL HILL,NC 27599.
RP Lee, H (reprint author), NIEHS,LAB QUANTITAT & COMPUTAT BIOL,POB 12233,RES TRIANGLE PK,NC 27709, USA.
RI Pedersen, Lee/E-3405-2013
OI Pedersen, Lee/0000-0003-1262-9861
NR 33
TC 32
Z9 33
U1 0
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 APR 24
PY 1996
VL 118
IS 16
BP 3946
EP 3950
DI 10.1021/ja9513188
PG 5
WC Chemistry, Multidisciplinary
SC Chemistry
GA UG695
UT WOS:A1996UG69500019
ER
PT J
AU Siebler, T
Kiess, W
Linder, B
Kessler, U
Schwarz, HP
Nissley, SP
AF Siebler, T
Kiess, W
Linder, B
Kessler, U
Schwarz, HP
Nissley, SP
TI Pertussis toxin sensitive G-proteins are not involved in the mitogenic
signaling pathway of insulin-like growth factor-I in normal rat kidney
epithelial (NRKE) cells
SO REGULATORY PEPTIDES
LA English
DT Article
DE IGF-I; IGF-II; G-protein; signal transduction; pertussis toxin; NRKE
cell
ID MANNOSE 6-PHOSPHATE RECEPTOR; PHENOTYPIC TRANSFORMATION;
GENE-EXPRESSION; CALCIUM INFLUX; IGF BINDING; TRANSDUCTION
AB There is controversy as to whether or not a pertussis toxin sensitive G-protein is involved in the signaling pathway of insulin-like growth factor-I. We have used normal rat kidney epithelial (NRKE) cells to ask whether or not a pertussis toxin sensitive G-protein was involved in IGF-I stimulated DNA synthesis. NRKE cells express both IGF-I and IGF-II/M6P receptors and respond to IGF-I with increased thymidine incorporation into DNA. Under many circumstances incubation of cells/cell membranes with GTP analogues will inhibit binding of ligands that are linked to a G-protein-receptor pathway, However, when NRKE membrane preparations were incubated with I-125-IGF-I or I-125-IGF-II in the presence or absence of GTP gamma S, ATP and GTP, binding of the radioligands was not affected by the GTP-analogue. IGF-I and factors from serum of hypophysectomized rats (HRS) stimulated [H-3]thymidine incorporation into DNA of NRKE cells. Under serum-free conditions in the presence of EGF (2 ng/ml) and PDGF (1 ng/ml) pertussis toxin over a wide range of doses had no effect upon IGF-I stimulated [H-3]thymidine incorporation into DNA of NRKE cells, In addition, PT at a dose of 100 ng/ml had no effect on IGF-I (0.2-50 ng/ml) stimulated DNA synthesis of NRKE cells, However, PT at doses of 5, 50, 500, 5000 and 50 000 ng/ml was capable to ADP-ribosylate a 40 kDa protein in NRKE cell plasma membrane preparations corresponding to known PT-sensitive G-proteins. We conclude, that (1) PT-sensitive G-proteins and both IGF-I and IGF-II/M6P receptors are present in NRKE cell plasma membrane preparations, and most importantly, that (2) PT-sensitive G-proteins are not involved in the mitogenic signaling pathway of IGF-I in NRKE cells.
C1 UNIV MUNICH,CHILDRENS HOSP,D-80336 MUNICH,GERMANY.
NCI,NIH,METAB BRANCH,BETHESDA,MD 20892.
NR 26
TC 7
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-0115
J9 REGUL PEPTIDES
JI Regul. Pept.
PD APR 23
PY 1996
VL 62
IS 2-3
BP 65
EP 71
DI 10.1016/0167-0115(95)00159-X
PG 7
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA UR476
UT WOS:A1996UR47600001
PM 8795068
ER
PT J
AU Matsumoto, RR
Bowen, WD
Walker, JM
Patrick, SL
Zambon, AC
Vo, VN
Truong, DD
DeCosta, BR
Rice, KC
AF Matsumoto, RR
Bowen, WD
Walker, JM
Patrick, SL
Zambon, AC
Vo, VN
Truong, DD
DeCosta, BR
Rice, KC
TI Dissociation of the motor effects of (+)-pentazocine from binding to
sigma(1) sites
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE opiate; (+)-pentazocine; sigma site; red nucleus; substantia nigra
ID GUINEA-PIG BRAIN; RAT-BRAIN; AUTORADIOGRAPHIC LOCALIZATION; H-3
(+)-PENTAZOCINE; LOW-AFFINITY; RECEPTORS; FOREBRAIN; SUGGEST; POTENT;
LIGAND
AB Radioligand binding and behavioral studies were conducted to determine whether a relationship existed between the motor effects produced by (+)-pentazocine and its binding to sigma sites. Scatchard analyses revealed decreased [H-3](+)-pentazocine binding in middle aged rats (5-6 months old) compared to young adult rats (2-3 months old). However, there was no difference between the extent of circling behavior or dystonia produced by microinjection of (+)-pentazocine into the substantia nigra or red nucleus in the older animals compared to the young adult rats. There was also a significant decrease in [H-3](+)-pentazocine binding in rats chronically treated with haloperidol. Again, however, despite the reduction in [H-3](+)-pentazocine binding, there was no difference between the extent of dystonia produced by unilateral intrarubral microinjection of (+)-pentazocine into animals chronically treated with haloperidol vs. saline. The postural changes produced by (+)-pentazocine could not be attenuated with coadministration of the putative sigma receptor antagonist BD1047 (N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine), or the opiate receptor antagonist naloxone. However, the (+)-opiate, (+)-nordihydrocodeinone, partially attenuated the postural effects of(+)-pentazocine, despite its very low affinity for sigma(1), sigma(2) or opiate receptors. Taken together with previous studies, the results suggest that [H-3](+)-pentazocine is a potent and selective probe for sigma(1) binding sites, but the in vivo effects of (+)-pentazocine cannot be fully attributed to actions through these sites. Some of the in vivo effects of (+)-pentazocine appear to involve other binding sites that are not detected under the conditions normally used in in vitro assays.
C1 BROWN UNIV,DEPT PSYCHOL,PROVIDENCE,RI 02912.
BROWN UNIV,DEPT PSYCHOL,PROVIDENCE,RI 02912.
BROWN UNIV,DIV BIOL & MED,BIOCHEM SECT,PROVIDENCE,RI 02912.
NIDDK,MED CHEM LAB,NIH,BETHESDA,MD 20892.
RP Matsumoto, RR (reprint author), UNIV CALIF IRVINE,DEPT NEUROL,154 MED SURGE 1,IRVINE,CA 92717, USA.
FU NIDA NIH HHS [DA04988]; NIMH NIH HHS [MH50564]
NR 37
TC 13
Z9 13
U1 0
U2 1
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 APR 22
PY 1996
VL 301
IS 1-3
BP 31
EP 40
DI 10.1016/0014-2999(96)00008-8
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UP247
UT WOS:A1996UP24700005
PM 8773444
ER
PT J
AU Yoshiji, H
Gomez, DE
Thorgeirsson, UP
AF Yoshiji, H
Gomez, DE
Thorgeirsson, UP
TI Enhanced RNA expression of tissue inhibitor of metalloproteinases-1
(TIMP-1) in human breast cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID ERYTHROID-POTENTIATING ACTIVITY; LOCALIZATION; INVASION; PROTEINASES;
LYMPHOMAS; MEMBER; FAMILY; CELLS
AB Tissue inhibitor of metalloproteinases-1 (TIMP-1) is known to have at least 2 distinct types of activity, i.e., as a regulator of collagenolytic activity, and erythroid potentiating activity (ERA). In this study, we examined the expression of TIMP-1 in human mammary carcinomas, non-malignant breast tissues and benign breast tumors. A total of 53 samples were subjected to Northern-blot analysis, including 23 of primary breast cancer, 26 of non-malignant breast tissues, and 4 of benign tumors. Of the 53 samples, 10 were paired malignant and non-malignant breast-tissue samples from the same patient. TIMP-1 RNA expression was significantly higher in the malignant tumor tissues than in the non-malignant counterpart. Similar differences were observed in the level of TIMP-1 protein expression in the paired breast samples examined. Moreover, breast-cancer cell lines secreted larger amounts of TIMP-1 in vitro than non-neoplastic breast epithelial lines. The up-regulation of TIMP-1 expression in breast cancer may suggest that TIMP-1 has an additional role to that of metalloproteinase inhibitor. (C) 1996 Wiley-Liss, Inc.*
C1 NCI,DIV BASIC SCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,TUMOR BIOL & CARCINOGENESIS SECT,BETHESDA,MD 20892.
OI Gomez, Daniel E/0000-0002-8629-0787
NR 22
TC 60
Z9 60
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD APR 22
PY 1996
VL 69
IS 2
BP 131
EP 134
DI 10.1002/(SICI)1097-0215(19960422)69:2<131::AID-IJC11>3.0.CO;2-C
PG 4
WC Oncology
SC Oncology
GA UH135
UT WOS:A1996UH13500011
PM 8608981
ER
PT J
AU Pahor, M
Guralnik, JM
Furberg, CD
Carbonin, P
Havlik, RJ
AF Pahor, M
Guralnik, JM
Furberg, CD
Carbonin, P
Havlik, RJ
TI Risk of gastrointestinal haemorrhage with calcium antagonists in
hypertensive persons over 67 years old
SO LANCET
LA English
DT Article
ID PLATELET-AGGREGATION; CLINICAL-TRIAL; DIHYDROPYRIDINES; HEMORRHAGE
AB Background Calcium antagonists are used frequently in management of hypertension, In addition to their cardiovascular effects, these drugs inhibit platelet aggregation. Therefore we examined whether the use of calcium antagonists was associated with an increased risk of gastrointestinal haemorrhage (GIH).
Methods A prospective cohort study was conducted from 1985 through 1992 on 1636 hypertensive persons aged greater than or equal to 68 years living in three communities. The participants were taking beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, or calcium antagonists; those taking combinations of these drugs were excluded, The incidence of GIH was assessed by surveying hospital discharge deaths. Age, gender, disability, arterial pressure, other drugs, and comorbid conditions were examined as confounders.
Findings Compared with beta-blockers (4819 person-years, 65 events), after adjustment for confounders the relative risk for GIH associated with ACE inhibitors (772 person-years, 13 events) was 1 . 23 (95% CI 0 . 66-2 . 28) and with calcium antagonists (1510 person-years, 42 events) it was 1 . 86 (1 . 22-2 . 82). The risks for verapamil, diltiazem, and nifedipine did not differ significantly. The results were unchanged when the analyses were restricted to severe events (GIH in conjunction with blood transfusion or death).
Interpretation Calcium antagonists were associated with an increased risk of GIH in this population. Therefore caution is needed in prescription of these agents to old patients who have other risk factors for gastrointestinal bleeding.
C1 NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892.
WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27103.
RP Pahor, M (reprint author), UNIV CATTOLICA SACRO CUORE,IST MED INTERNA & GERIATRIA,LARGO F VITO 1,I-00168 ROME,ITALY.
NR 30
TC 203
Z9 205
U1 0
U2 1
PU LANCET LTD
PI LONDON
PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL
SN 0140-6736
J9 LANCET
JI Lancet
PD APR 20
PY 1996
VL 347
IS 9008
BP 1061
EP 1065
DI 10.1016/S0140-6736(96)90276-7
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA UG042
UT WOS:A1996UG04200009
PM 8602055
ER
PT J
AU Quintero, RA
Romero, R
Dzieczkowski, J
Mammen, E
Evans, MI
AF Quintero, RA
Romero, R
Dzieczkowski, J
Mammen, E
Evans, MI
TI Sealing of ruptured amniotic membranes with intra-amniotic
platelet-cryoprecipitate plug
SO LANCET
LA English
DT Letter
ID PREMATURE RUPTURE
C1 HUTZEL HOSP,DEPT PATHOL & MED,DETROIT,MI 48201.
HUTZEL HOSP,DEPT PHYSIOL,DETROIT,MI 48201.
NICHHD,PERINATOL BRANCH,BETHESDA,MD 20892.
RP Quintero, RA (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNECOL,FETAL ENDOSCOPY PROGRAM,DETROIT,MI 48201, USA.
NR 5
TC 42
Z9 44
U1 0
U2 2
PU LANCET LTD
PI LONDON
PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL
SN 0140-6736
J9 LANCET
JI Lancet
PD APR 20
PY 1996
VL 347
IS 9008
BP 1117
EP 1117
DI 10.1016/S0140-6736(96)90316-5
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA UG042
UT WOS:A1996UG04200056
PM 8602087
ER
PT J
AU Dunnick, JK
Elwell, MR
Haseman, JK
AF Dunnick, JK
Elwell, MR
Haseman, JK
TI Decreased incidence of spontaneous mammary gland neoplasms in female
F344 rats treated with amphetamine, methylphenidate, or codeine
SO CANCER LETTERS
LA English
DT Article
DE mammary gland neoplasm; amphetamine; methylphenidate; codeine; F344 rats
ID SPONTANEOUS TUMORS; EXPRESSION; RECEPTOR; MICE; GROWTH
AB Three drugs that affect the neuroendocrine system (amphetamine, methylphenidate, and codeine) caused decreases in body weights and in the incidence of spontaneously occurring mammary gland neoplasms in the female F344/N rat in 2-year carcinogenicity studies. Using a mathematical model that relates body weight changes to the incidence of mammary gland neoplasms, we find that the decrease in mammary gland tumors seen in female rats cannot be fully explained by body weight decreases relative to control animals. Further, the observed decreases in body weight in treated female rats were not a function of differences in feed consumption between treated and control groups. These pharmaceuticals are thought to affect the biologic system through interaction with membrane receptors. This interaction and/or subsequent cell signaling events may play a role in the observed decrease in spontaneously occurring mammary gland neoplasms in the female rat treated with amphetamine, methylphenidate, or codeine.
RP Dunnick, JK (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 28
TC 11
Z9 11
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 APR 19
PY 1996
VL 102
IS 1-2
BP 77
EP 83
DI 10.1016/0304-3835(96)04168-7
PG 7
WC Oncology
SC Oncology
GA UB974
UT WOS:A1996UB97400011
PM 8603383
ER
PT J
AU Craigie, R
AF Craigie, R
TI Quality control in Mu DNA transposition
SO CELL
LA English
DT Review
ID RECOMBINATION
RP Craigie, R (reprint author), NIDDK,NIH,BLDG 5,ROOM 301,BETHESDA,MD 20892, USA.
NR 9
TC 17
Z9 17
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138
SN 0092-8674
J9 CELL
JI Cell
PD APR 19
PY 1996
VL 85
IS 2
BP 137
EP 140
DI 10.1016/S0092-8674(00)81089-2
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UG255
UT WOS:A1996UG25500001
PM 8612265
ER
PT J
AU Savilahti, H
Mizuuchi, K
AF Savilahti, H
Mizuuchi, K
TI Mu transpositional recombination: Donor DNA cleavage and strand transfer
in trans by the Mu transposase
SO CELL
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; POLYNUCLEOTIDYL TRANSFER; INTEGRASE
PROTEIN; INVITRO PROCEEDS; BACTERIOPHAGE-MU; SITE; MECHANISM; DOMAINS;
IDENTIFICATION; COMPLEX
AB Central to the Mu transpositional recombination are the two chemical steps; donor DNA cleavage and strand transfer. These reactions occur within the Mu transpososome that contains two Mu DNA end segments bound to a tetramer of MuA, the transposase. To investigate which MuA-monomer catalyzes which chemical reaction, we made transpososomes containing wild-type and active site mutant MuA. By preloading the MuA variants onto Mu end DNA fragments of different length prior to transpososome assembly, we could track the catalysis by MuA bound to each Mu end segment. The donor DNA end that underwent the chemical reaction was identified. Both the donor DNA cleavage and strand transfer were catalyzed in trans by the MuA monomers bound to the partner Mu end. This arrangement explains why the transpososome assembly is a prerequisite for the chemical steps.
C1 NIDDKD, MOLEC BIOL LAB, NIH, BETHESDA, MD 20892 USA.
NR 59
TC 80
Z9 81
U1 1
U2 2
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 APR 19
PY 1996
VL 85
IS 2
BP 271
EP 280
DI 10.1016/S0092-8674(00)81103-4
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UG255
UT WOS:A1996UG25500015
PM 8612279
ER
PT J
AU BeitnerJohnson, D
Blakesley, VA
ShenOrr, Z
Jimenez, M
Stannard, B
Wang, LM
Pierce, J
LeRoith, D
AF BeitnerJohnson, D
Blakesley, VA
ShenOrr, Z
Jimenez, M
Stannard, B
Wang, LM
Pierce, J
LeRoith, D
TI The proto-oncogene product c-Crk associates with insulin receptor
substrate-1 and 4PS - Modulation by insulin growth factor-1 (IGF) and
enhanced IGF-1 signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PHOSPHATIDYLINOSITOL 3'-KINASE; HEMATOPOIETIC-CELLS; IRS-1; SH2;
PHOSPHORYLATION; PROTEINS; ELEMENTS; PATHWAYS; DOMAINS; BINDING
AB The Crk proto-oncogene product is an SH2 and SH3 domain-containing adaptor protein which we have previously shown to become rapidly tyrosine phosphorylated in response to stimulation with insulin-like growth factor I (IGF-I) in NIH-3T3 cells, In order to further characterize the role of Crk in the IGF-I signaling pathway, NIH-3T3 and 293 cells were stably transfected with an expression vector containing the Crk cDNA, The various resultant 3T3-Crk clones expressed Crk at approximately 2-15-fold higher levels than parental 3T3 cells, In 3T3-Crk cells, Crk immunoreactivity was detected in insulin receptor substrate-1 (IRS-1) immunoprecipitates, Stimulation with IGF-I resulted in a dissociation of Crk protein from IRS-1, In contrast, the association of the related adaptor protein Grb2 with IRS-1 was enhanced by IGF-I stimulation. Similar results were obtained in stably transfected 293-Crk cells, which express both IRS-I and the IRS-1-related signaling protein 4PS. In these cells, IRS-1 and 4PS both associated with Crk, and this association was also decreased by IGF-I treatment, whereas the association of Grb2 with IRS-1 and 4PS was enhanced by IGF-I. Overexpression of Crk also enhanced IGF-I-induced mitogenesis of NIH-3T3 cells, as measured by [H-3]thymidine incorporation. The levels of IGF-I-induced mitogenesis were proportional to the level of Crk expression, These results suggest that Crk is a positive effector of IGF-I signaling, and may mediate its effects via interaction with IRS-1 and/or 4PS.
C1 NIDDK,DIABET BRANCH,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
NCI,NIH,BETHESDA,MD 20892.
NR 31
TC 69
Z9 70
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 19
PY 1996
VL 271
IS 16
BP 9287
EP 9290
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400021
PM 8621590
ER
PT J
AU Oakley, RH
Sar, M
Cidlowski, JA
AF Oakley, RH
Sar, M
Cidlowski, JA
TI The human glucocorticoid receptor beta isoform - Expression, biochemical
properties, and putative function
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HORMONE-BINDING DOMAIN; HUMAN PROGESTERONE-RECEPTOR; 3' UNTRANSLATED
REGION; GENE-EXPRESSION; DNA-BINDING; MULTIPLE; TRANSCRIPTION;
LOCALIZATION; ACTIVATION; RESISTANCE
AB Alternative splicing of the human glucocorticoid receptor (hGR) primary transcript produces two receptor isoforms, hGR alpha and hGR beta, which differ at their carboxyl termini. The hGR alpha isoform conveys endocrine information to target tissues by altering patterns of gene expression in a hormone-dependent fashion, In contrast to hGR alpha, very little is known about the hGR beta splice variant. Using hGR alpha- and hGR beta-specific riboprobes on human multiple tissue Northern blots, we show that the hGR beta message has a widespread tissue distribution. We also prove by reverse transcriptase-polymerase chain reaction that the alternative splicing event underlying the formation of the hGR beta message occurs in these tissues. Because the hGR beta protein differs from hGR alpha at the extreme COOH terminus, we investigated several of the biochemical properties of hGR beta expressed in transfected cells. hGR beta does not bind the glucocorticoid agonist dexamethasone nor the glucocorticoid antagonist RU38486 in vivo. Moreover, in contrast to hGR beta, hGR beta is located primarily in the nucleus of transfected cells independent of hormone administration, Finally, in the absence of hGR alpha, hGR beta is transcriptionally inactive on a glucocorticoid-responsive enhancer. However, when both isoforms are expressed in the same cell, hGR beta inhibits the hormone-induced, hGR alpha-mediated stimulation of gene expression. Thus, hGR beta potentially functions as a dominant negative inhibitor of hGR alpha activity.
C1 NIEHS,LAB INTEGRAT BIOL,RES TRIANGLE PK,NC 27709.
UNIV N CAROLINA,DEPT PHYSIOL,CHAPEL HILL,NC 27599.
NR 53
TC 379
Z9 410
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 APR 19
PY 1996
VL 271
IS 16
BP 9550
EP 9559
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400059
PM 8621628
ER
PT J
AU vanLeeuwen, JEM
Kearse, KP
AF vanLeeuwen, JEM
Kearse, KP
TI Calnexin associates exclusively with individual CD3 delta and T cell
antigen receptor (TCR) alpha proteins containing incompletely trimmed
glycans that are not assembled into multisubunit TCR complexes
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODY; TRANSGENIC MICE;
DELTA-CHAIN; IDENTIFICATION; CHAPERONE; IP90
AB Most T lymphocytes express on their surfaces an oligomeric protein complex consisting of clonotypic alpha beta polypeptides associated with invariant CD3-gamma delta epsilon and zeta chains, designated the T cell antigen receptor (TCR) complex. Assembly and intracellular transport of nascent TCR proteins is believed to be assisted by their interaction with the molecular chaperone calnexin, which for certain molecules functions as a lectin for monoglucosylated glycans. However, as most of our knowledge about calnexin-TCR protein associations has been obtained under conditions of limited TCR assembly, the role of calnexin in the formation of nascent TCR complexes is unclear, Here, we studied the role of glucose (Glc) trimming and calnexin association in the oligomerization of TCR alpha and CD3 delta glycoproteins in murine splenic T lymphocytes, a model cell type for efficient assembly of complete TCR complexes. We show that removal of Glc residues from both CD3 delta proteins and TCR alpha proteins occurred prior to their association with any other TCR components and that calnexin specifically interacted with unassembled TCR alpha and CD3 delta proteins containing incompletely trimmed oligosaccharides, Interestingly, we found that removal of Glc residues from glycan chains was necessary for efficient association of calnexin with TCR alpha glycoproteins but not with CD3 delta glycoproteins. These studies define Glc trimming and calnexin association as initial molecular events in the translation of CD3 delta and TCR alpha proteins, occurring coincident with or immediately after their translocation into the endoplasmic reticulum and preceding the ordered pairing of TCR chains, In addition, these data document that calnexin assembly with CD36 and TCR alpha glycoproteins involves both glycan-dependent and glycan-independent mechanisms.
C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892.
RI van Leeuwen, Jeroen/G-3555-2010
NR 33
TC 41
Z9 41
U1 1
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 19
PY 1996
VL 271
IS 16
BP 9660
EP 9665
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400072
PM 8621641
ER
PT J
AU ODea, MH
Tamura, JK
Gellert, M
AF ODea, MH
Tamura, JK
Gellert, M
TI Mutations in the B subunit of Escherichia coli DNA gyrase that affect
ATP-dependent reactions
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID N-TERMINAL FRAGMENT; NUCLEOTIDE BINDING; TOPOISOMERASE-II;
NALIDIXIC-ACID; BASE-PAIRS; PROTEIN; MECHANISM; ENERGY; ENZYME; SITE
AB We have previously reported specific labeling of Escherichia coli DNA gyrase by the ATP affinity analog pyridoxal 5'-diphospho-5'adenosine (PLP-AMP), which resulted in inhibition of ATP-dependent reactions,The analog was found to be covalently bound at Lys(103) and Lys(110) on the gyrase B subunit (Tamura, J, K,, and Gellert, M, (1990) J, Biol, Chem, 265, 21342-21349), In this study, the importance of these two lysine residues is examined by site-directed mutagenesis.
Substitutions of Lys(103) result in the loss of ATP-dependent functions, These mutants are unable to supercoil DNA, to hydrolyze ATP, or to bind a nonhydrolysable ATP analog, 5'-adenylyl-beta, gamma-imidodiphosphate (ADPNP), The ATP-independent functions of gyrase, such as relaxation of negatively supercoiled DNA and oxolinic acid induced cleavage of double-stranded DNA, are unaffected by these mutations, suggesting that the mutant B subunits are assembling correctly with the A subunits, Gyrase with substitutions of Lys(110) retains all activities, However, the affinity of ATP is decreased, The DNA supercoiling activity of gyrase A(2)B(2) tetramers reconstituted with varying ratios of inactive mutant and wild-type gyrase B subunits is consistent with a mechanism of DNA supercoiling that requires the interdependent activity of both B subunits in ATP binding and hydrolysis.
C1 NIDDK,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892.
NR 35
TC 28
Z9 28
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 19
PY 1996
VL 271
IS 16
BP 9723
EP 9729
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400081
PM 8621650
ER
PT J
AU Semmes, OJ
Barrett, JF
Dang, CV
Jeang, KT
AF Semmes, OJ
Barrett, JF
Dang, CV
Jeang, KT
TI Human T-cell leukemia virus type I Tax masks c-myc function through a
cAMP-dependent pathway
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LONG TERMINAL REPEAT; PRIMARY HUMAN-LYMPHOCYTES; RECEPTOR
GENE-EXPRESSION; PROTEIN-KINASE-A; HTLV-I; CYCLIC-AMP; DNA-BINDING;
NEOPLASTIC TRANSFORMATION; TRANSCRIPTION FACTOR; ACTIVATES TRANSCRIPTION
AB Human T-cell leukemia virus type I Tax is a pleiotropic gene regulator that functions through CREB/ATF- and NF-kappa B-mediated pathways, In most contexts, Tax is a potent gene activator. Here, we describe an unexpected finding of Myc repression by Tax. In cells that overexpress human T-cell leukemia virus type I Tax, the detection of c-Myc protein in the nucleus by a monoclonal antibody was masked. Tax prevented immunological visualization of a Myc epitope contained within amino acids 45-104, resulting in interference with Myc function in transcription and in anchorage-independent cell growth, Tax did not affect steady-state protein levels since detection of c-Myc with other antibodies was unperturbed. Four observations suggest that this Tax-Myc interaction is mediated through CREB/ATF signal transduction. 1) Tax point mutants, selectively defective for activation of CREB/ATF but not NF-kappa B, failed to mask. c-Myc; 2) masking of Myc was abolished when Tax-expressing cells were treated with protein kinase inhibitor H-9; 3) Tax-specific shielding of Myc is absent in cells (B1R) that are genetically defective for cAMP signaling; and 4) forskolin treatment of cells mimicked Tax in masking the Myc epitope, Considered collectively, these findings suggest a regulation of Myc function at the level of localized protein conformation.
C1 NIAID,MOL VIROL SECT,MOLEC MICROBIOL LAB,NIH,BETHESDA,MD 20892.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV HEMATOL,BALTIMORE,MD 21205.
RI Jeang, Kuan-Teh/A-2424-2008
NR 95
TC 24
Z9 24
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 19
PY 1996
VL 271
IS 16
BP 9730
EP 9738
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400082
PM 8621651
ER
PT J
AU Honkakoski, P
Moore, R
Gynther, J
Negishi, M
AF Honkakoski, P
Moore, R
Gynther, J
Negishi, M
TI Characterization of phenobarbital-inducible mouse Cyp2b10 gene
transcription in primary hepatocytes
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ADULT-RAT HEPATOCYTES; TISSUE-SPECIFIC EXPRESSION; CYTOCHROME-P-450
GENE; GROWTH-HORMONE; MESSENGER-RNA; TESTOSTERONE 16-ALPHA-HYDROXYLASE;
CHROMOSOME LOCALIZATION; INVITRO TRANSCRIPTION; GLYCOPROTEIN GENE;
LIVER-MICROSOMES
AB The mouse phenobarbital (PB)-inducible Cyp2b10 gene promoter has been isolated and sequenced, and control of its expression has been characterized, The 1405-base pair (bp) Cyp2b10 promoter sequence is 83% identical to the corresponding region from the rat CYP2B2 gene. In addition to the lack of CA repeats, differences include insertion of 42 base pairs (-123/-82 bp) into the middle of a consensus sequence to the so called ''Barbie box.'' In this report, we have developed a primary mouse hepatocyte culture system in which endogenous 2B10 mRNA as well as Cyp2b10-driven CAT activity were induced by PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), but not by the 3-chloro derivative of TCPOBOP, Deletion analysis of the Cyp2b10 promoter identified a basal transcription element at -64/-34 bp and a negative element at -971/-775 bp. Sequences contained within the -1404/-971 bp region are responsible for the induced CAT activity. DNase I protection and gel shift assays detected five major protein binding sites within the -1404/-971 bp fragment, one of which shared high sequence identity with a portion of a regulatory element in CYP2B2 gene (Trottier, E,, Belzil, A., Stoltz, C,, and Anderson, A, (1995) Gene 158, 263-268). Our results indicate that sequences important for PB-induced transcription of Cyp2b10 gene are located in the distal promoter.
C1 NIEHS,PHARMACOGENET SECT,REPROD & DEV TOXICOL LAB,NIH,RES TRIANGLE PK,NC 27709.
UNIV KUOPIO,DEPT PHARMACEUT CHEM,SF-70211 KUOPIO,FINLAND.
OI Honkakoski, Paavo/0000-0002-4332-3577
NR 68
TC 103
Z9 104
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 19
PY 1996
VL 271
IS 16
BP 9746
EP 9753
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG044
UT WOS:A1996UG04400084
PM 8621653
ER
PT J
AU Boix, E
Wu, YN
Vasandani, VM
Saxena, SK
Ardelt, W
Ladner, J
Youle, RJ
AF Boix, E
Wu, YN
Vasandani, VM
Saxena, SK
Ardelt, W
Ladner, J
Youle, RJ
TI Role of the N terminus in RNase a homologues: Differences in catalytic
activity, ribonuclease inhibitor interaction and cytotoxicity
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE human pancreatic RNase; Rana pipiens RNase; pyroglutamic acid;
ribonuclease inhibitor; cytotoxicity
ID BOVINE PANCREATIC RIBONUCLEASE; HUMAN PLACENTAL RIBONUCLEASE;
AMINO-ACID-SEQUENCE; C-PEPTIDE HELIX; SEMINAL RIBONUCLEASE; LIVER
RIBONUCLEASE; RANA-CATESBEIANA; P-30 PROTEIN; ANGIOGENIN; SUPERFAMILY
AB A number of biochemical properties differ dramatically among homologues within the pancreatic ribonuclease superfamily Human pancreatic ribonuclease (hRNase) has high enzyme activity, extreme sensitivity to ribonuclease inhibitor (RI) and is non-toxic, whereas a homologous RNase from frog eggs, called onconase, has much lower enzyme activity, is not sensitive to RI and is cytotoxic to cancer cell lines and animals. To explore the structural basis of these differences among members in the RNase family we synthesized genes for onconase, hRNase, a mutant onconase (K9Q) and onconase-hRNase N-terminal hybrids and expressed the proteins in Escherichia coli with final yields of 10 to 50 mg per liter of culture after purification. A recombinant version of onconase with an N-terminal methionine instead of the native pyroglutamyl residue had decreased cytotoxicity and enzyme activity. Cleavage of the recombinant onconase Met-1 residue, and cyclization of the Gln1 residue to reform the pyroglutamyl N terminus, reconstituted cytotoxicity and enzyme activity Thus a unique role of the pyroglutamyl residue in the active site of amphibian RNases is indicated. Replacement of one to nine residues of onconase with the homologous residues of hRNase increased the enzymatic activity against most of the substrates tested with a simultaneous shift in the enzyme specificity from high preference for poly(U) to slight preference for poly(C). Cytotoxicity of the chimera decreased, dissociating cytotoxicity from enzymatic activity: The molecular basis for the low binding affinity of onconase for RI has been examined experimentally with the recombinant RNases and by fitting onconase and RNase A structures to the coordinates from the recently published RNase A-RI complex. (C) 1996 Academic Press Limited
C1 NINCDS,BIOCHEM SECT,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892.
ALFACELL CORP,BLOOMFIELD,NJ 07003.
UNIV MARYLAND,MARYLAND BIOTECHNOL INST,CTR ADV RES BIOTECHNOL,ROCKVILLE,MD 20850.
NATL INST STAND & TECHNOL,ROCKVILLE,MD 20850.
RI Boix, Ester/B-9038-2012;
OI Boix, Ester/0000-0003-1790-2142; Saxena, Shailendra
K/0000-0003-2856-4185
NR 77
TC 164
Z9 168
U1 2
U2 6
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 APR 19
PY 1996
VL 257
IS 5
BP 992
EP 1007
DI 10.1006/jmbi.1996.0218
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UG014
UT WOS:A1996UG01400010
PM 8632481
ER
PT J
AU Vondrasek, J
Wlodawer, A
AF Vondrasek, J
Wlodawer, A
TI New database
SO SCIENCE
LA English
DT Letter
RP Vondrasek, J (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702, USA.
RI Vondrasek, JIri/A-4244-2008
NR 3
TC 6
Z9 6
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 APR 19
PY 1996
VL 272
IS 5260
BP 337
EP 338
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UG252
UT WOS:A1996UG25200009
PM 8602518
ER
PT J
AU Wolffe, AP
AF Wolffe, AP
TI Histone deacetylase: A regulator of transcription
SO SCIENCE
LA English
DT Editorial Material
ID DNA; ACETYLATION; INVITRO; YEAST
RP Wolffe, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,NIH,BETHESDA,MD 20892, USA.
NR 16
TC 227
Z9 233
U1 1
U2 12
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD APR 19
PY 1996
VL 272
IS 5260
BP 371
EP 372
DI 10.1126/science.272.5260.371
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UG252
UT WOS:A1996UG25200036
PM 8602525
ER
PT J
AU Shimoda, K
vanDeursen, J
Sangster, MY
Sarawar, SR
Carson, RT
Tripp, RA
Chu, C
Quelle, FW
Nosaka, T
Vignali, DAA
Doherty, PC
Grosveld, G
Paul, WE
Ihle, JN
AF Shimoda, K
vanDeursen, J
Sangster, MY
Sarawar, SR
Carson, RT
Tripp, RA
Chu, C
Quelle, FW
Nosaka, T
Vignali, DAA
Doherty, PC
Grosveld, G
Paul, WE
Ihle, JN
TI Lack of IL-4-induced Th2 response and IgE class switching in mice with
disrupted Stat6 gene
SO NATURE
LA English
DT Article
ID IL-4; GENERATION; INVIVO; CELLS
AB Signal transducers and activators of transcription (Stats) are activated by tyrosine phosphorylation in response to cytokines, and are thought to mediate many of their functional responses(1-4) Stat6 is activated in response to interleukin (IL)-4 (refs 5,6) and may contribute to various functions including mitogenesis, T-helper cell differentiation and immunoglobulin isotype switching(7). To evaluate the role of Stat6, we generated Stat6-null mice (Stat6(-/-)) by gene disruption in embryonic stem cells. The mice were viable, indicating the lack of a non-redundant function in normal development. Although naive lymphoid cell development was normal, Stat6(-/-) mice were deficient in IL-4-mediated functions including Th2 helper T-cell differentiation, expression of cell surface markers, and immunoglobulin class switching to IgE. In contrast, IL-4-mediated proliferation was only partly affected.
C1 ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, MEMPHIS, TN 38105 USA.
ST JUDE CHILDRENS RES HOSP, DEPT GENET, MEMPHIS, TN 38105 USA.
ST JUDE CHILDRENS RES HOSP, DEPT IMMUNOL, MEMPHIS, TN 38105 USA.
NIAID, IMMUNOL LAB, NIH, BETHESDA, MD 20892 USA.
RI Doherty, Peter Charles/C-4185-2013;
OI Doherty, Peter Charles/0000-0002-5028-3489; Tripp,
Ralph/0000-0002-2924-9956
NR 29
TC 975
Z9 989
U1 3
U2 22
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD APR 18
PY 1996
VL 380
IS 6575
BP 630
EP 633
DI 10.1038/380630a0
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF741
UT WOS:A1996UF74100047
PM 8602264
ER
PT J
AU Choi, OH
Kim, JH
Kinet, JP
AF Choi, OH
Kim, JH
Kinet, JP
TI Calcium mobilization via sphingosine kinase in signalling by the Fc
epsilon RI antigen receptor
SO NATURE
LA English
DT Article
ID CELL; TRANSDUCTION; PLATELETS
AB Calcium mobilization through antigen receptors, including high-affinity IgE receptors (Fc epsilon RI), is thought to be mediated by inositol-1,4,5-trisphosphate production (InsP(3))(1-4). Here we show that antigen clustering of Fc epsilon RI on the rat mast-cell line (RBC 2H3) activates a sphingosine kinase (SK) and produces sphingosine-l-phosphate (S1P), an alternative second messenger for intracellular calcium mobilization, The sphingosine analogue, D-L-threo-dihydrosphingosine (DHS), inhibits the SK enzyme competitively with a dissociation constant, K-i, of 5 to 18 mu M. This inhibition substantially suppresses the Fc epsilon RI-mediated calcium signal, but leaves intact the syk tyrosine kinase activation and the small InsP(3) production. The entire InsP(3)-dependent pathway activated by a transfected G-protein coupled receptor, used here as a positive control, also remained intact. Thus Fc epsilon RI principally utilizes a SK pathway to mobilize calcium.
C1 BETH ISRAEL HOSP,LAB ALLERGY & IMMUNOL,BOSTON,MA 02215.
HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02215.
RP Choi, OH (reprint author), NIAID,LAB ALLERG DIS,NIH,ROCKVILLE,MD 20852, USA.
NR 17
TC 350
Z9 357
U1 0
U2 8
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF
SN 0028-0836
J9 NATURE
JI Nature
PD APR 18
PY 1996
VL 380
IS 6575
BP 634
EP 636
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF741
UT WOS:A1996UF74100048
PM 8602265
ER
PT J
AU Collier, AC
Coombs, RW
Schoenfeld, DA
Bassett, RL
Timpone, J
Baruch, A
Jones, M
Facey, K
Whitacre, C
McAuliffe, VJ
Friedman, HM
Merigan, TC
Reichman, RC
Hooper, C
Corey, L
AF Collier, AC
Coombs, RW
Schoenfeld, DA
Bassett, RL
Timpone, J
Baruch, A
Jones, M
Facey, K
Whitacre, C
McAuliffe, VJ
Friedman, HM
Merigan, TC
Reichman, RC
Hooper, C
Corey, L
TI Treatment of human immunodeficiency virus infection with saquinavir,
zidovudine, and zalcitabine
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; REVERSE-TRANSCRIPTASE;
AZIDOTHYMIDINE AZT; PROTEASE INHIBITOR; NATURAL-HISTORY; HIV PROTEINASE;
DOUBLE-BLIND; RO 31-8959; RESISTANCE
AB Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment with several agents may increase the effectiveness of antiviral therapy. We studied the safety and efficacy of saquinavir, an HIV-protease inhibitor, given with one or two nucleoside antiretroviral agents, as compared with the safety and efficacy of a combination of two nucleosides alone.
Methods. In this double-blind trial, patients with HIV infection were randomly assigned to receive either saquinavir (1800 mg per day) plus both zidovudine (600 mg per day) and zalcitabine (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine. The 302 patients enrolled had CD4+ counts of 50 to 300 cells per cubic millimeter and had previously received zidovudine for a median of 27 months. The study lasted 24 weeks, with an optional double-blind extension period of an additional 12 to 32 weeks.
Results. Ninety-six percent of the patients completed the 24-week study. In all three treatment groups, CD4+ cell counts rose at first and then fell gradually. The normalized area under the curve for the CD4+ cell count was greater with the three-drug combination than with either saquinavir and zidovudine (P=0.017) or zalcitabine and zidovudine (P<0.001). There were significantly greater reductions in plasma HIV with the three-drug combination than with the other regimens when peripheral-blood mononuclear cells were cultured for HIV and HIV RNA was assessed, and there were greater decreases in serum neopterin and beta(2)-microglobulin levels. There were no major differences in toxic effects among the three treatments.
Conclusions. Treatment with saquinavir, zalcitabine, and zidovudine was well tolerated. This drug combination reduced HIV-1 replication, increased CD4+ cell counts, and decreased levels of activation markers in serum more than did treatment with zidovudine and either saquinavir or zalcitabine. Studies are warranted to evaluate whether the three-drug combination will reduce morbidity and mortality.
C1 UNIV WASHINGTON,SCH MED,SEATTLE,WA.
HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115.
NIAID,BETHESDA,MD 20892.
HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110.
ROCHE PROD,WELWYN GARDEN CIT,HERTS,ENGLAND.
OHIO STATE UNIV,COLUMBUS,OH 43210.
NYU,NEW YORK,NY.
UNIV PENN,PHILADELPHIA,PA 19104.
STANFORD UNIV,PALO ALTO,CA 94304.
UNIV ROCHESTER,ROCHESTER,NY.
FU NCRR NIH HHS [RR00044]; NIAID NIH HHS [AI-27658, AI-27664]
NR 42
TC 561
Z9 567
U1 5
U2 17
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 18
PY 1996
VL 334
IS 16
BP 1011
EP 1017
DI 10.1056/NEJM199604183341602
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA UE733
UT WOS:A1996UE73300002
PM 8598838
ER
PT J
AU Lindpaintner, K
Lee, MA
Larson, MG
Rao, VS
Pfeffer, MA
Ordovas, JM
Schaefer, EJ
Wilson, AF
Wilson, PWF
Vasan, RS
Myers, RH
Levy, D
AF Lindpaintner, K
Lee, MA
Larson, MG
Rao, VS
Pfeffer, MA
Ordovas, JM
Schaefer, EJ
Wilson, AF
Wilson, PWF
Vasan, RS
Myers, RH
Levy, D
TI Absence of association or genetic linkage between the
angiotensin-converting-enzyme gene and left ventricular mass
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HEART-FAILURE; HYPERTROPHY; TWINS; CELLS; CAPTOPRIL; RATS; POLYMORPHISM;
HYPERTENSION; DYSFUNCTION; EXPRESSION
AB Background. Homozygous carriers of the D allele of the angiotensin-converting-enzyme (ACE) gene have been reported to be at increased risk for various cardiovascular disorders, including left ventricular hypertrophy. We investigated the potential role of the ACE gene in influencing left ventricular mass.
Methods. Quantitative echocardiographic data and DNA samples were available for 2439 subjects from the Framingham Heart Study. ACE genotypes were determined by an assay based on the polymerase chain reaction. (The D allele of the ACE gene contains a deletion, whereas the I [insertion] allele does not.) Left ventricular mass and the prevalence of left ventricular hypertrophy, adjusted for clinical covariates, were analyzed according to genotype, Genetic linkage between the ACE locus and left ventricular mass was evaluated by quantitative analysis of pairs of siblings.
Results. The ACE genotype was associated neither with left ventricular mass nor with the prevalence of left ventricular hypertrophy. Mean (+/-SE) left ventricular mass (adjusted for sex) among subjects carrying the DD, DI, and II genotypes was 165+/-1.6, 165+/-1.3, and 166+/-2.0 g, respectively (P=0.90). The prevalence of left ventricular hypertrophy among the three genotype groups was 15.6 percent, 13.6 percent, and 15.6 percent, respectively (P=0.36), and the adjusted relative risk of left ventricular hypertrophy associated with the DD genotype was 1.10 (95 percent confidence interval, 0.86 to 1.19). Linkage analysis in 759 pairs of siblings using both the ACE D/I marker and a microsatellite polymorphism at the neighboring locus for the human growth hormone gene failed to support any role of ACE in influencing left ventricular mass.
Conclusions. The ACE genotype showed no association with echocardiographically determined left ventricular mass, nor did it confer an increased risk of left ventricular hypertrophy. We found no appreciable role of the ACE gene in influencing left ventricular mass.
C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT CARDIOL,BOSTON,MA 02115.
HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV CARDIOL,BOSTON,MA.
HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,DIV CLIN EPIDEMIOL,BOSTON,MA.
BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118.
BOSTON UNIV,SCH MED,DIV EPIDEMIOL,BOSTON,MA.
BOSTON UNIV,SCH MED,DEPT MED,DIV PREVENT MED,BOSTON,MA 02118.
TUFTS UNIV,SCH MED,HUMAN NUTR RES CTR AGING,USDA,LIPID METAB LAB,BOSTON,MA.
FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA.
LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112.
NHLBI,BETHESDA,MD 20892.
RP Lindpaintner, K (reprint author), HARVARD UNIV,DIV CARDIOVASC DIS,DEPT MED,BRIGHAM & WOMENS HOSP,SCH MED,75 FRANCIS ST,BOSTON,MA 02115, USA.
RI Wilson, Alexander/C-2320-2009;
OI Ramachandran, Vasan/0000-0001-7357-5970; Ordovas,
Jose/0000-0002-7581-5680
FU NCRR NIH HHS [RR03655]; NHLBI NIH HHS [K04-HL03138-01]; PHS HHS
[N01-38038]
NR 52
TC 219
Z9 225
U1 0
U2 0
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 18
PY 1996
VL 334
IS 16
BP 1023
EP 1028
DI 10.1056/NEJM199604183341604
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA UE733
UT WOS:A1996UE73300004
PM 8598840
ER
PT J
AU Okimoto, T
Kohno, K
Kuwano, M
Gopas, J
Kung, HF
Ono, M
AF Okimoto, T
Kohno, K
Kuwano, M
Gopas, J
Kung, HF
Ono, M
TI Regulation of epidermal growth factor receptor by activated H-ras and
V-myc oncogenes in mouse Balb/3T3 cells: Possible roles of AP-1
SO ONCOGENE
LA English
DT Article
DE H-ras; EGF receptor; AP-1; dominant negative c-jun
ID DENSITY-LIPOPROTEIN RECEPTOR; TRANSCRIPTION FACTOR AP-1;
TUMOR-NECROSIS-FACTOR; MIDDLE T-ANTIGEN; C-FOS GENE; PROTO-ONCOGENE;
MALIGNANT TRANSFORMATION; CHEMICAL CARCINOGENS; MOLECULAR-CLONING;
TYROSINE KINASE
AB We previously reported that introduction of H-ras oncogene decreases the epidermal growth factor (EGF) binding activity to cell surface EGF receptor in mouse Balb/3T3, In this study, we have further isolated four H-ras transfectants, four v-myc transfectants and three both H-ras and v-myc (H-ras/v-myc) transfectants of mouse Balb/3T3 cells. In comparison with introduction of v-myc alone or both H-ras and v-myc oncogenes, introduction of H-ras alone resulted in a loss of [I-125]EGF binding activity to the cell surface EGF receptor, RT-PCR analysis also showed much lower levels of EGF receptor gene expression in H-ras transfectants compared to that of parental untransformed cells (Balb-Neo1), v-myc and H-ras/v-myc transfectants, Our results demonstrated the activated binding of a transcription factor, Stat1 p84/p91, which directly interacts with EGF receptor, to c-sis-inducible element (SIE) in both v-myc and H-ras/v-myc transfectants, but not in H-ras transfectants, Among transcription factors which we have analysed, activator protein 1 (AP-1) but not SP-1 was modulated by H-ras. Gel shift assays demonstrated the mobility pattern of TPA-responsive element (TRE) binding complex with AP-1 derived from H-ras transfectants migrated faster than those from Balb-Neo1, v-myc and H-ras/v-myc. Expression of c-Jun and Fra-1 was increased more than threefold in H-ras transfectants compared with Balb-Neo1, v-myc and H-ras/v-myc transfectants, but that of c-Fos, Jun B and SP-1 was unchanged, Both transient and permanent expression of H-ras enhanced AP-1 activity in mouse cells, but further co-introduction of dominant negative c-jun mutant encoding a transcriptionally inactive product inhibited the H-ras dependent AP-1 induction, Transfection of the dominant negative c-jun mutant also restored down-regulation of EGF binding by activated H-ras oncogene, Down-regulation of EGF receptor by activated H-ras and the possible involvement of a transcription factor, AP-1, will be discussed.
C1 KYUSHU UNIV,SCH MED,DEPT BIOCHEM,FUKUOKA 81282,JAPAN.
SOROKA MED CTR,LAB ONCOL,IL-84101 BEER SHEVA,ISRAEL.
BEN GURION UNIV NEGEV,FAC HLTH SCI,DEPT MICROBIOL & IMMUNOL,IL-84105 BEER SHEVA,ISRAEL.
NCI,FREDERICK CANC RES & DEV CTR,LAB BIOCHEM PHYSIOL,FREDERICK,MD 21702.
NR 59
TC 22
Z9 22
U1 0
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD APR 18
PY 1996
VL 12
IS 8
BP 1625
EP 1633
PG 9
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA UG458
UT WOS:A1996UG45800004
PM 8622882
ER
PT J
AU Lee, JE
Beck, TW
Wojnowski, L
Rapp, UR
AF Lee, JE
Beck, TW
Wojnowski, L
Rapp, UR
TI Regulation of A-raf expression
SO ONCOGENE
LA English
DT Article
DE A-raf; steroid hormones; glucocorticoid receptor; transcription
ID MAMMARY-TUMOR VIRUS; DNA-BINDING DOMAIN; ESTROGEN-RESPONSIVE ELEMENT;
STEROID-HORMONE RECEPTORS; GLUCOCORTICOID RECEPTOR; GENE-EXPRESSION;
TRANSCRIPTION FACTORS; MMTV PROMOTER; GROWTH-FACTOR; AMINO-ACIDS
AB The Raf family proto-oncogenes encode cytoplasmic protein serine/threonine kinases which play a critical role in cell growth and development, A-raf shares several functional properties with Raf-1 including transforming activity, stimulation of the Raf/MAPK pathway and the ability of dominant negative versions to functionally block Ras signalling, A-raf transcripts are predominantly expressed in the mouse urogenital tissues, Interestingly, the human A-raf promoter region contains three potential glucocorticoid response elements GRE-1, GRE-2 and GRE-3, at positions -17, -34 and -168 respectively from the transcriptional start site, DNA sequence analysis of the mouse A-raf promoter region demonstrated that GRE-1 and -2 were conserved evolutionarily, To determine whether the human A-raf GREs represent functional motifs, an expression vector for the glucocorticoid receptor was cotransfected with A-raf promoter/reporter constructs into HeLa cells, A fivefold dexamethasone-dependent induction of A-raf promoter activity was observed using constructs containing all three GRE motifs whereas point mutations in the GREs either diminished or abolished dexamethasone induction, Electrophoretic mobility shift assays (EMSAs) using purified glucocorticoid receptor DNA binding domain (DBD) demonstrated that both GRE-2 and -3 motifs interact with DBD and oligonucleotide competition experiments established that these have different affinities for DBD, Using nuclear extracts from human and rodent cell lines in EMSAs, a specific protein-DNA complex was observed with GRE-1 which displayed binding properties unlike that of glucocorticoid receptor, These results demonstrate that the A-raf promoter is regulated in part by members of the glucocorticoid family of steroid hormone receptors and suggest a model for the regulation of A-raf expression in urogenital tissues.
C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,DYN CORP,PROGRAM RESOURCES,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,VIRAL PATHOL SECT,FREDERICK,MD 21702.
NR 41
TC 14
Z9 16
U1 0
U2 3
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD APR 18
PY 1996
VL 12
IS 8
BP 1669
EP 1677
PG 9
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA UG458
UT WOS:A1996UG45800009
PM 8622887
ER
PT J
AU Cobb, JP
Danner, RL
AF Cobb, JP
Danner, RL
TI Nitric oxide and septic shock
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID VASCULAR SMOOTH-MUSCLE; METHYL-L-ARGININE; INDUCED HYPOTENSION;
HEMODYNAMIC-CHANGES; INHIBITION; SYNTHASE; SEPSIS; ENDOTOXIN;
EXPRESSION; REVERSAL
C1 NIH,DEPT CRIT CARE MED,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD 20892.
NR 59
TC 125
Z9 132
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 APR 17
PY 1996
VL 275
IS 15
BP 1192
EP 1196
DI 10.1001/jama.275.15.1192
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA UE625
UT WOS:A1996UE62500032
PM 8609688
ER
PT J
AU Lancaster, JM
Cochran, CJ
Brownlee, HA
Evans, AC
Berchuck, A
Futreal, PA
Wiseman, RW
AF Lancaster, JM
Cochran, CJ
Brownlee, HA
Evans, AC
Berchuck, A
Futreal, PA
Wiseman, RW
TI Detection of BRCA1 mutations in women with early-onset ovarian cancer by
use of the protein truncation test
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,DURHAM,NC 27710.
DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710.
DUKE UNIV,MED CTR,DEPT GENET,DURHAM,NC 27710.
RP Lancaster, JM (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,MAIL DROP C4-06,111 ALEXANDER DR,RES TRIANGLE PK,NC 27709, USA.
NR 21
TC 11
Z9 11
U1 0
U2 2
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD APR 17
PY 1996
VL 88
IS 8
BP 552
EP 554
DI 10.1093/jnci/88.8.552
PG 3
WC Oncology
SC Oncology
GA UE732
UT WOS:A1996UE73200017
PM 8606385
ER
PT J
AU Barnes, KM
Dickstein, B
Cutler, GB
Fojo, T
Bates, SE
AF Barnes, KM
Dickstein, B
Cutler, GB
Fojo, T
Bates, SE
TI Steroid transport, accumulation, and antagonism of P-glycoprotein in
multidrug-resistant cells
SO BIOCHEMISTRY
LA English
DT Article
ID REDUCED DRUG ACCUMULATION; BREAST CANCER-CELLS; HUMAN-KB CELLS;
SECRETORY EPITHELIUM; EXPRESSION; GENE; PROGESTERONE; PHOSPHORYLATION;
LINES; CYTOTOXICITY
AB According to multiple reports, progesterone is not transported by P-glycoprotein (Pgp), which mediates multidrug resistance through active drug efflux. However, progesterone has been shown to block Pgp-mediated efflux of other drugs. To extend these observations, and to examine the effect of modulating Pgp phosphorylation, the accumulation of progesterone and 14 other steroids in untreated and calphostin C-treated multidrug-resistant human colon carcinoma SW620 Ad300 cells was compared to the accumulation in parental SW620 cells. The accumulation of progesterone in untreated multidrug resistant cells expressing Pgp was not reduced compared to parental cells. However, the accumulation of more hydrophilic steroids was reduced by as much as 50%. Progesterone and progesterone-like compounds, however, were potent inhibitors of Pgp-mediated vinblastine efflux; increased antagonism correlated with increased steroid hydrophobicity. Treatment with calphostin C, a PKC inhibitor which decreases Pgp phosphorylation, increased progesterone efflux, modulated Pgp antagonism by steroids, and inhibited photoaffinity labeling of Pgp by progesterone. These results extend previous observations that Pgp can mediate the transport of, and be antagonized by, a variety of steroids and that these properties vary with both a steroid's hydrophobicity and the phosphorylated state of Pgp.
C1 NICHHD,DEV ENDOCRINOL BRANCH,NIH,BETHESDA,MD 20892.
NCI,MED BRANCH,DCS,BETHESDA,MD 20892.
NR 50
TC 140
Z9 144
U1 3
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 16
PY 1996
VL 35
IS 15
BP 4820
EP 4827
DI 10.1021/bi952380k
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UF521
UT WOS:A1996UF52100020
PM 8664272
ER
PT J
AU Reeves, R
Wolffe, AP
AF Reeves, R
Wolffe, AP
TI Substrate structure influences binding of the non-histone protein
HMG-I(Y) to free and nucleosomal DNA
SO BIOCHEMISTRY
LA English
DT Article
ID TRANSCRIPTION FACTOR ACCESS; BOVINE INTERLEUKIN-2 CDNA;
SEQUENCE-SPECIFIC BINDING; CHROMATIN CORE PARTICLES; TUMOR VIRUS
PROMOTER; HMG-I; B-DNA; POSITIONED NUCLEOSOMES; HELICAL PERIODICITY;
BASE-PAIRS
AB High mobility group protein HMG-I(Y) selectively binds to stretches of A . T-rich B-form DNA in vitro by recognition of substrate structure rather nucleotide sequence. Recognition of altered DNA structures has also been proposed to explain the preferential binding of this non-histone protein to four-way junction DNA as well as to restricted regions of DNA on random-sequence nucleosome core particles. Here we describe experiments that examine the influence of intrinsic DNA structure, and of structure imposed by folding of DNA around histone cores, on the binding of HMG-I(Y). As substrates for binding, we chose defined-sequence DNA molecules containing A . T-rich segments demonstrated previously to have very different structures in solution. These segments are either intrinsically bent (phased A . T tracts), flexible (oligo[d(A-T)]), or straight and rigid [oligo(dA). oligo(dT)]. DNase-I and hydroxyl radical footprinting techniques were employed to analyze protein binding to these DNAs either free in solution or when they were reconstituted into monomer or dinucleosomes in vitro. Results indicate that the DNA structure exerts a significant influence on HMG-I(Y) binding both when substrates are free in solution and when they are wrapped into nucleosomal structures. For example, when DNA is free in solution, HMG-I(Y) prefers to bind to the narrow minor groove of A . T sequences but sometimes also binds to certain GpC residues having narrowed major grooves that are embedded in such sequences. On the other hand, depending on the structure and/or orientation assumed by particular A . T-rich segments on the surface of reconstituted histone octamers, HMG-I(Y) binding site selection on individual nucleosomes differs considerably. Two observations are of particular importance: (i) HMG-I(Y) can preferentially bind to certain types of A . T-DNA located on the surface of nucleosomes; and (ii) HMG-I(Y) binding can induce localized alterations in the helical periodicity and/or rotational setting of DNA on the surface of some nucleosomes. These abilities of HMG-I(Y) suggests that in vivo the protein may play an important role in recognizing and altering the structure of localized regions of chromatin.
C1 WASHINGTON STATE UNIV,DEPT GENET & CELL BIOL,PULLMAN,WA 99164.
NICHHD,MOLEC EMBRYOL LAB,NIH,BETHESDA,MD 20892.
RP Reeves, R (reprint author), WASHINGTON STATE UNIV,DEPT BIOCHEM BIOPHYS,PULLMAN,WA 99164, USA.
NR 95
TC 62
Z9 62
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 16
PY 1996
VL 35
IS 15
BP 5063
EP 5074
DI 10.1021/bi952424p
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UF521
UT WOS:A1996UF52100047
PM 8664299
ER
PT J
AU Zolkiewski, M
Redowicz, MJ
Korn, ED
Ginsburg, A
AF Zolkiewski, M
Redowicz, MJ
Korn, ED
Ginsburg, A
TI Thermal unfolding of Acanthamoeba myosin 11 and skeletal muscle myosin
SO BIOPHYSICAL CHEMISTRY
LA English
DT Article
DE protein unfolding; myosin; muscle, skeletal; unfolding, thermal;
Acanthamoeba
ID DIFFERENTIAL SCANNING CALORIMETRY; 3 PHOSPHORYLATION SITES;
ACTIN-ACTIVATED ATPASE; AMINO-ACID-SEQUENCE; HEAVY-CHAIN;
LIGHT-MEROMYOSIN; SUBFRAGMENT-1; STABILITY; PROTEINS; DOMAINS
AB Studies on the thermal unfolding of monomeric Acanthamoeba myosin II and other myosins, in particular skeletal muscle myosin, using differential scanning calorimetry (DSC) are reviewed. The unfolding transitions for intact myosin or its head fragment are irreversible, whereas those of the rod part and its fragments are completely reversible, Acanthamoeba myosin II unfolds with a high degree of cooperativity from ca, 40-45 degrees C at pH 7.5 in 0.6 M KCl, producing a single, sharp endotherm in DSC. In contrast, thermal transitions of rabbit skeletal muscle myosin occur over a broader temperature range (ca, 40-60 degrees C) under the same conditions, The DSC studies on the unfolding of the myosin rod and its fragments allow identification of cooperative domains, each of which unfolds according to a two-state mechanism, Also, DSC data show the effect of the nucleotide-induced conformational changes in the myosin head on the protein stability.
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892.
RI Korn, Edward/F-9929-2012; Redowicz, Maria Jolanta/R-4083-2016
NR 45
TC 8
Z9 8
U1 1
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-4622
J9 BIOPHYS CHEM
JI Biophys. Chem.
PD APR 16
PY 1996
VL 59
IS 3
BP 365
EP 371
DI 10.1016/0301-4622(95)00129-8
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical
SC Biochemistry & Molecular Biology; Biophysics; Chemistry
GA UK319
UT WOS:A1996UK31900015
PM 8672724
ER
PT J
AU Merril, CR
Biswas, B
Carlton, R
Jensen, NC
Creed, GJ
Zullo, S
Adhya, S
AF Merril, CR
Biswas, B
Carlton, R
Jensen, NC
Creed, GJ
Zullo, S
Adhya, S
TI Long-circulating bacteriophage as antibacterial agents
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE phage; bacteria; reticuloendothelial system; toxins; antibiotic
resistance
ID PROTEIN
AB The increased prevalence of multidrug-resistant bacterial pathogens motivated us to attempt to enhance the therapeutic efficacy of bacteriophages. The therapeutic application of phages as antibacterial agents was impeded by several factors: (i) the failure to recognize the relatively narrow host range of phages; (ii) the presence of toxins in crude phage lysates; and (iii) a lack of appreciation for the capacity of mammalian host defense systems, particularly the organs of the reticuloendothelial system, to remove phage particles from the circulatory system, In our studies involving bacteremic mice, the problem of the narrow host range of phage was dealt with by using selected bacterial strains and virulent phage specific for them, Toxin levels were diminished by purifying phage preparations, To reduce phage elimination by the host defense system, we developed a serial-passage technique in mice to select for phage mutants able to remain in the circulatory system for longer periods of time, By this approach we isolated long-circulating mutants of Escherichia coli phage lambda and of Salmonella typhimurium phage P22. We demonstrated that the long-circulating lambda mutants also have greater capability as antibacterial agents than the corresponding parental strain in animals infected with lethal doses of bacteria, Comparison of the parental and mutant lambda capsid proteins revealed that the relevant mutation altered the major phage head protein E. The use of toxin free, bacteria-specific phage strains, combined with the serial-passage technique, may provide insights for developing phage into therapeutically effective antibacterial agents.
C1 EXPONENTIAL BIOTHERAPIES INC, NEW YORK, NY 10001 USA.
NCI, MOLEC BIOL LAB, NIH, BETHESDA, MD 20892 USA.
RP Merril, CR (reprint author), NIMH, NEUROSCI CTR ST ELIZABETHS, LAB BIOCHEM GENET, WASHINGTON, DC 20032 USA.
NR 21
TC 228
Z9 249
U1 5
U2 47
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 16
PY 1996
VL 93
IS 8
BP 3188
EP 3192
DI 10.1073/pnas.93.8.3188
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000007
PM 8622911
ER
PT J
AU Moskovitz, J
Jenkins, NA
Gilbert, DJ
Copeland, NG
Jursky, F
Weissbach, H
Brot, N
AF Moskovitz, J
Jenkins, NA
Gilbert, DJ
Copeland, NG
Jursky, F
Weissbach, H
Brot, N
TI Chromosomal localization of the mammalian peptide-methionine sulfoxide
reductase gene and its differential expression in various tissues
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID RETINAL-PIGMENT EPITHELIUM; ENZYMATIC REDUCTION; PROTEINS; RESIDUES;
CLONING; DAMAGE; MOUSE
AB Peptide methionine sulfoxide reductase (MsrA; EC 1.8.4.6) is a ubiquitous protein that can reduce methionine sulfoxide residues in proteins as well as in a large number of methyl sulfoxide compounds, The expression of MsrA in various rat tissues was determined by using immunocytochemical staining. Although the protein was found in all tissues examined, it,vas specifically localized to renal medulla and retinal pigmented epithelial cells, and it was prominent in neurons and throughout the nervous system. In addition, blood and alveolar macrophages showed high expression of the enzyme, The msrA gene was mapped to the central region of mouse chromosome 14, in a region of homology with human chromosomes 13 and 8p21.
C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA.
RP Moskovitz, J (reprint author), ROCHE INST MOLEC BIOL, ROCHE RES CTR, NUTLEY, NJ 07110 USA.
NR 27
TC 115
Z9 118
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 16
PY 1996
VL 93
IS 8
BP 3205
EP 3208
DI 10.1073/pnas.93.8.3205
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000010
PM 8622914
ER
PT J
AU Dix, DJ
Allen, JW
Collins, BW
Mori, C
Nakamura, N
PoormanAllen, P
Goulding, EH
Eddy, EM
AF Dix, DJ
Allen, JW
Collins, BW
Mori, C
Nakamura, N
PoormanAllen, P
Goulding, EH
Eddy, EM
TI Targeted gene disruption of Hsp70-2 results in failed meiosis, germ cell
apoptosis, and male infertility
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gametogenesis; heat shock protein; programmed cell death;
spermatogenesis; stress protein
ID MOUSE SPERMATOGENIC CELLS; HEAT-SHOCK PROTEINS; NUCLEOTIDE-SEQUENCE;
EXPRESSION; CLONING; FAMILY; IDENTIFICATION; MEMBER; P70
AB In addition to the five 70-kDa heat shock proteins (HSP70) common to germ cells and somatic tissues of mammals, spermatogenic cells synthesize HSP70-2 during meiosis, To determine if this unique stress protein has a critical role in meiosis, we used gene-targeting techniques to disrupt Hsp70-2 in mice. Male mice homozygous for the mutant allele (Hsp70-2(-/-)) did not synthesize HSP70-2, lacked postmeiotic spermatids and mature sperm, and were infertile, However, neither meiosis nor fertility was affected in female Hsp70-2(-/-) mice, We previously found that HSP70-2 is associated with synaptonemal complexes in the nucleus of meiotic spermatocytes from mice and hamsters. While synaptonemal complexes assembled in Hsp70-2(-/-) spermatocytes, structural abnormalities became apparent in these cells by late prophase, and development rarely progressed to the meiotic divisions, Furthermore, analysis of nuclei and genomic DNA indicated that the failure of meiosis in Hsp70-2(-/-) mice was coincident with a dramatic increase in spermatocyte apoptosis. These results suggest that HSP70-2 participates in synaptonemal complex function during meiosis in male germ cells and is linked to mechanisms that inhibit apoptosis.
C1 US EPA,DIV ENVIRONM CARCINOGENESIS,NATL HLTH & ENVIRONM EFFECTS RES LAB,RES TRIANGLE PK,NC 27711.
NIEHS,GAMETE BIOL SECT,REPROD & DEV TOXICOL LAB,NIH,RES TRIANGLE PK,NC 27709.
KYOTO UNIV,FAC MED,DEPT ANAT,KYOTO 60601,JAPAN.
GLAXO INC,DIV MED SAFETY EVALUAT,RES TRIANGLE PK,NC 27709.
RP Dix, DJ (reprint author), US EPA,REPROD TOXICOL DIV,GAMETE & EARLY EMBRYO BIOL BRANCH,MAIL DROP 72,RES TRIANGLE PK,NC 27711, USA.
NR 35
TC 384
Z9 403
U1 1
U2 12
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 16
PY 1996
VL 93
IS 8
BP 3264
EP 3268
DI 10.1073/pnas.93.8.3264
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000021
PM 8622925
ER
PT J
AU Kong, SK
Yim, MB
Stadtman, ER
Chock, PB
AF Kong, SK
Yim, MB
Stadtman, ER
Chock, PB
TI Peroxynitrite disables the tyrosine phosphorylation regulatory
mechanism: Lymphocyte-specific tyrosine kinase fails to phosphorylate
nitrated cdc2(6-20)NH2 peptide
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE tyrosine nitration; tyrosine kinase; signal transduction; cell cycle
ID NITRIC-OXIDE; SUPEROXIDE-DISMUTASE; SUBSTRATE; ACID; NO
AB To determine if nitration of tyrosine residues by peroxynitrite (PN), which can be generated endogenously, can disrupt the phosphorylation of tyrosine residues in proteins involved in cell signaling networks, we studied the effect of PN-promoted nitration of tyrosine residues in a penta-decameric peptide, cdc2(6-20)NH2, on the ability of the peptide to be phosphorylated, cdc2(6-20)NH2 corresponds to the tyrosine phosphorylation site of p34(cdc2) kinase, which is phosphorylated by lck kinase (lymphocyte-specific tyrosine kinase, p56(lck)). PN nitrates both Tyr-15 and Tyr-19 of the peptide in phosphate buffer (pH 7.5) at 37 degrees C. Nitration of Tyr-15, which is the phosphorylated amino acid residue, inhibits completely the phosphorylation of the peptide. The nitration reaction is enhanced by either Fe(III)EDTA or Cu(II)-Zn(II)-superoxide dismutase (Cu,Zn-SOD). The kinetic data are consistent with the view that reactions of Fe(III)EDTA or Cu,Zn-SOD with the cis form of PN yield complexes in which PN decomposes more slowly to form NO2+, the nitrating agent, Thus, the nitration efficiency of PN is enhanced, These results are discussed from the point of view that PN-promoted nitration will result in permanent impairment of cyclic cascades that control signal transduction processes and regulate cell cycles.
C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 27
TC 269
Z9 273
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 APR 16
PY 1996
VL 93
IS 8
BP 3377
EP 3382
DI 10.1073/pnas.93.8.3377
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000043
PM 8622943
ER
PT J
AU Maraia, RJ
AF Maraia, RJ
TI Transcription termination factor La is also an initiation factor for RNA
polymerase III
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE autoimmune antigen; ribonucleoprotein; transcription complexes
ID GENE-TRANSCRIPTION; PROTEIN; COMPLEXES; INVITRO; BINDING; INTERMEDIATE;
ANTIBODIES; FRACTION; ANTIGEN
AB La RNA-binding protein is a transcription termination factor that facilitates recycling of template and RNA polymerase (pot) III. Transcription complexes preassembled on immobilized templates were depleted of pol III after a single round of RNA synthesis in the presence of heparin and sarkosyl. The isolated complexes could then be complemented with highly purified pol III and/or recombinant La to test if La is required for transcription reinitiation. VA1, 7SL, and B1 transcription complexes cannot be transcribed by supplemental pol III in single or multiple-round transcription assays unless La is also provided, La mediates concentration-dependent activation of pol III initiation and thereby controls the use of preassembled stable transcription complexes. The initiation factor activity of La augments its termination factor activity to produce a novel mechanism of activated reinitiation. A model in which La serves pol III upon transcription initiation and again at termination is discussed.
RP Maraia, RJ (reprint author), NICHHD,LAB MOLEC GROWTH REGULAT,NIH,BLDG 6,ROOM 416,BETHESDA,MD 20892, USA.
NR 30
TC 90
Z9 90
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 APR 16
PY 1996
VL 93
IS 8
BP 3383
EP 3387
DI 10.1073/pnas.93.8.3383
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000044
PM 8622944
ER
PT J
AU Weihe, E
TaoCheng, JH
Schafer, MKH
Erickson, JD
Eiden, LE
AF Weihe, E
TaoCheng, JH
Schafer, MKH
Erickson, JD
Eiden, LE
TI Visualization of the vesicular acetylcholine transporter in cholinergic
nerve terminals and its targeting to a specific population of small
synaptic vesicles
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE vesicular monoamine transporter; immunohistochemistry; small synaptic
vesicles; large dense-core vesicles; regulated secretion
ID ADRENAL PHEOCHROMOCYTOMA CELLS; GROWTH-FACTOR; MONOAMINE TRANSPORTER;
CLONAL LINE; IDENTIFICATION; MICROVESICLES; CLONING; RESPOND
AB Immunohistochemical visualization of the rat vesicular acetylcholine transporter (VAChT) in cholinergic neurons and nerve terminals has been compared to that for choline acetyltransferase (ChAT), heretofore the most specific marker for cholinergic neurons, VAChT-positive cell bodies were visualized in cerebral cortex, basal forebrain, medial habenula, striatum, brain stem, and spinal cord by using a polyclonal anti-VAChT antiserum, VAChT-immunoreactive fibers and terminals were also visualized in these regions and in hippocampus, at neuromuscular junctions within skeletal muscle, and in sympathetic and parasympathetic autonomic ganglia and target tissues, Cholinergic nerve terminals contain more VAChT than ChAT immunoreactivity after routine fixation, consistent with a concentration of VAChT within terminal neuronal arborizations in which secretory vesicles are clustered. These include VAChT-positive terminals of the median eminence of the hypothalamus, not observed with ChAT antiserum after routine fixation, Subcellular localization of VAChT in specific organelles in neuronal cells was examined by immunoelectron microscopy in a rat neuronal cell line (PC12-c4) expressing VAChT as well as the endocrine and neuronal forms of the vesicular monoamine transporters (VMAT1 and VMAT2). VAChT is targeted to small synaptic vesicles, while VMAT1 is found mainly but not exclusively on large dense-core vesicles. VMAT2 is found on large dense-core vesicles but not on the small synaptic vesicles that contain VAChT in PC12-c4 cells, despite the presence of VMAT2 immunoreactivity in central and peripheral nerve terminals known to contain monoamines in small synaptic vesicles, Thus, VAChT and VMATZ may be specific markers for ''cholinergic'' and ''adrenergic'' small synaptic vesicles, with the latter not expressed in nonstimulated neuronally differentiated PC12-c4 cells.
C1 NIMH,NIH,CELL BIOL LAB,MOLEC NEUROSCI SECT,BETHESDA,MD 20892.
UNIV MARBURG,DEPT ANAT & CELL BIOL,W-3550 MARBURG,GERMANY.
NINCDS,NIH,NEUROBIOL LAB,BETHESDA,MD 20892.
OI Eiden, Lee/0000-0001-7524-944X
NR 32
TC 237
Z9 241
U1 4
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 16
PY 1996
VL 93
IS 8
BP 3547
EP 3552
DI 10.1073/pnas.93.8.3547
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000074
PM 8622973
ER
PT J
AU Levine, M
ConryCantilena, C
Wang, YH
Welch, RW
Washko, PW
Dhariwal, KR
Park, JB
Lazarev, A
Graumlich, JF
King, J
Cantilena, LR
AF Levine, M
ConryCantilena, C
Wang, YH
Welch, RW
Washko, PW
Dhariwal, KR
Park, JB
Lazarev, A
Graumlich, JF
King, J
Cantilena, LR
TI Vitamin C pharmacokinetics in healthy volunteers: Evidence for a
recommended dietary allowance
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE ascorbic acid; bioavailability
ID COULOMETRIC ELECTROCHEMICAL DETECTION; PERFORMANCE
LIQUID-CHROMATOGRAPHY; ASCORBIC-ACID; DEHYDROASCORBIC ACID; CHROMAFFIN
GRANULES; INSITU KINETICS; HEART-DISEASE; PLASMA; DEPLETION; TRANSPORT
AB Determinants of the recommended dietary allowance (RDA) for vitamin C include the relationship between vitamin C dose and steady state plasma concentration, bioavailability, urinary excretion, cell concentration, and potential adverse effects. Because current data are inadequate, an in-hospital depletion-repletion study was conducted. Seven healthy volunteers were hospitalized for 4-6 months and consumed a diet containing <5 mg of vitamin C daily. Steady-state plasma and tissue concentrations were determined at seven daily doses of vitamin C from 30 to 2500 mg. Vitamin C steady-state plasma concentrations as a function of dose displayed sigmoid kinetics. The steep portion of the curve occurred between the 30- and 100-mg daily dose, the current RDA of 60 mg daily was on the lower third of the curve, the first dose beyond the sigmoid portion of the curve was 200 mg daily, and complete plasma saturation occurred at 1000 mg daily. Neutrophils, monocytes, and lymphocytes saturated at 100 mg daily and contained concentrations at least 14-fold higher than plasma. Bioavailability was complete for 200 mg of vitamin C as a single dose. No vitamin C was excreted in urine of six of seven volunteers until the 100-mg dose. At single doses of 500 mg and higher, bioavailability declined and the absorbed amount was excreted. Oxalate and urate excretion were elevated at 1000 mg of vitamin C daily compared to lower doses. Based on these data and Institute of Medicine criteria, the current RDA of 60 ng daily should be increased to 200 mg daily, which can be obtained from fruits and vegetables. Safe doses of vitamin C are less than 1000 mg daily, and vitamin C daily doses above 400 mg have no evident value.
C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892.
UNIFORMED SERV UNIV HLTH SCI,DIV CLIN PHARMACOL,BETHESDA,MD 20814.
NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT NUTR,BETHESDA,MD 20892.
RP Levine, M (reprint author), NIDDKD,MOL & CLIN NUTR SECT,NIH,BLDG 10,ROOM 4D52,MSC 1372,BETHESDA,MD 20892, USA.
NR 56
TC 629
Z9 645
U1 2
U2 36
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 16
PY 1996
VL 93
IS 8
BP 3704
EP 3709
DI 10.1073/pnas.93.8.3704
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UF740
UT WOS:A1996UF74000103
PM 8623000
ER
PT J
AU Licinio, J
Magistretti, P
Bolis, CL
AF Licinio, J
Magistretti, P
Bolis, CL
TI The World Health Organization sponsored study group on anorexia nervosa
(AN): Basic mechanisms, clinical approaches and treatment - Introduction
SO PSYCHIATRY RESEARCH
LA English
DT Editorial Material
C1 UNIV LAUSANNE,INST PHYSIOL,CH-1005 LAUSANNE,SWITZERLAND.
WHO,CH-1211 GENEVA,SWITZERLAND.
UNIV MILAN,MILAN,ITALY.
RP Licinio, J (reprint author), NIMH,NIH,CLIN NEUROENDOCRINOL BRANCH,UNIT CLIN RES,BLDG 10,RM 3S231,10 CTR DR MSC 1284,BETHESDA,MD 20892, USA.
RI Licinio, Julio/L-4244-2013
OI Licinio, Julio/0000-0001-6905-5884
NR 10
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD APR 16
PY 1996
VL 62
IS 1
BP 1
EP 2
DI 10.1016/0165-1781(96)01007-4
PG 2
WC Psychiatry
SC Psychiatry
GA UL142
UT WOS:A1996UL14200001
ER
PT J
AU Licinio, J
Wong, ML
Gold, PW
AF Licinio, J
Wong, ML
Gold, PW
TI The hypothalamic-pituitary-adrenal axis in anorexia nervosa
SO PSYCHIATRY RESEARCH
LA English
DT Article; Proceedings Paper
CT WHO Study Group on Anorexia Nervosa (AN) Meeting - Basic Mechanisms,
Clinical Approaches and Treatment
CY SEP 27-29, 1993
CL GENEVA, SWITZERLAND
SP WHO, Study Grp Anorexia Nervosa
DE cortisol; adrenocorticotropic hormone; corticotropin-releasing hormone;
circadian rhythms; depression
ID CORTICOTROPIN-RELEASING-FACTOR; PRIMARY CORTISOL RESISTANCE;
GLUCOCORTICOID RECEPTORS; ARGININE VASOPRESSIN; WEIGHT-LOSS; HORMONE;
DEPRESSION; SECRETION; SYSTEM; PLASMA
AB Studies examining the function of the hypothalamic-pituitary-adrenal (HPA) axis in anorexia nervosa are reviewed. A principal finding is that of hypercortisolism, associated with increased central corticotropin-releasing hormone levels and normal circulating levels of adrenocorticotropic hormone. Similarities between neuroendocrine findings in anorexia nervosa and in affective disorder are reviewed. The contribution of circadian rhythm disturbances and malnutrition to observed HPA axis abnormalities in anorexia nervosa is also considered. Directions for future research are discussed.
RP Licinio, J (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,INTRAMURAL RES PROGRAM,BLDG 10,RM 3S231,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013
OI Licinio, Julio/0000-0001-6905-5884
NR 46
TC 93
Z9 93
U1 2
U2 4
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD APR 16
PY 1996
VL 62
IS 1
BP 75
EP 83
DI 10.1016/0165-1781(96)02991-5
PG 9
WC Psychiatry
SC Psychiatry
GA UL142
UT WOS:A1996UL14200010
PM 8739117
ER
PT J
AU Chyou, PH
White, LR
Yano, K
Sharp, DS
Burchfiel, CM
Chen, R
Rodriguez, BL
Curb, JD
AF Chyou, PH
White, LR
Yano, K
Sharp, DS
Burchfiel, CM
Chen, R
Rodriguez, BL
Curb, JD
TI Pulmonary function measures as predictors and correlates of cognitive
functioning in later life
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE aging; cognition; forced expiratory volume
ID SLEEP-APNEA; DISEASE; PERFORMANCE; RISK; MEN; POPULATION; HAWAII
AB The relation between pulmonary function and cognitive functioning was investigated in a cohort of 3,036 Japanese-American men living in Hawaii. Pulmonary function, as indicated by forced expiratory volume in 1 second (FEV(1)), was measured at the baseline examination from 1965 to 1968. Cognitive function was assessed by the Cognitive Abilities Screening Instrument (CASI) test at least 23 years later (1991-1993). Baseline FEV(1) was significantly correlated with follow-up CASI score (r = 0.22, p = 0.0001). Although the strength of the association was reduced by controlling for the effects of other factors, stepwise multiple linear regression showed that FEV(1) during middle age was a significant predictor of CASI in later life, after taking into account the effects of age, education, stroke, sedentary job activity, nonmanual occupation, height, generation, and Japanese speaking ability. The mean CASI value was significantly greater for men whose FEV(1) exceeded 2.8 liter compared with those whose FEV(1) levels were in the lowest (<2.5 liters) quartile. Furthermore, the test on the effect of interaction between FEV(1) and age was statistically significant (p = 0.0024), with subjects less than 55 years of age at the baseline examination showing a stronger direct association of FEV(1) with CASI than the men aged 55 or older. These findings suggest that pulmonary function impairment may be associated with cognitive function impairment in later life.
C1 MARSHFIELD MED RES FDN,MARSHFIELD CLIN,DEPT EPIDEMIOL & BIOSTAT,MARSHFIELD,WI 54449.
NIA,HONOLULU,HI.
HONOLULU ASIA AGING STUDY,HONOLULU,HI.
KUAKINI MED CTR,HONOLULU HEART PROGRAM,HONOLULU,HI 96817.
NHLBI,HONOLULU EPIDEMIOL RES UNIT,EPIDEMIOL & BIOMETRY PROGRAM,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892.
FU NHLBI NIH HHS [N01-HC-05102]
NR 32
TC 53
Z9 53
U1 0
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 APR 15
PY 1996
VL 143
IS 8
BP 750
EP 756
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UE759
UT WOS:A1996UE75900002
PM 8610684
ER
PT J
AU Beckett, LA
Brock, DB
Lemke, JH
deLeon, CFM
Guralnik, JM
Fillenbaum, GG
Branch, LG
Wetle, TT
Evans, DA
AF Beckett, LA
Brock, DB
Lemke, JH
deLeon, CFM
Guralnik, JM
Fillenbaum, GG
Branch, LG
Wetle, TT
Evans, DA
TI Analysis of change in self-reported physical function among older
persons in four population studies
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE activities of daily living; aging; longitudinal studies; population
surveillance
ID ELDERLY FINNISH MEN; PREVALENCE RATES; ALAMEDA COUNTY; FOLLOW-UP;
DISABILITY; PREDICTORS; MORTALITY; MODELS; LIFE
AB Change in self-reported physical function was examined using baseline and 5 years of follow-up data between 1982 and 1991 from the four Established Populations for Epidemiologic Studies of the Elderly studies. In East Boston, Massachusetts (n = 3,809), Iowa and Washington Counties, Iowa (n = 3,673), New Haven, Connecticut (n = 2,812), and North Carolina (n = 4,163), noninstitutionalized persons aged 65 years and older were asked a series of questions to assess their physical function: a modified Katz Activities of Daily Living (ADL) scale, three items from the Rosow-Breslau Functional Health Scale, and questions on physical performance, adapted from Nagi, as well as information on demographic, social, and health characteristics. Longitudinal statistical analyses (random effects and Markov transition models) were used to evaluate improvement, stability, and deterioration in functional ability at both an individual and a population level over multiple years of data. The average decline in physical function associated with age was found to be greater than previous cross-sectional studies have suggested, and the rate of decline increased with increasing age. Considerable individual variation was evident. Although many people experienced declines, a smaller but substantial portion experienced recovery. Women reported a greater rate of decline in physical function and were less likely to recover from disability.
C1 RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612.
NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892.
UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242.
YALE UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510.
DUKE UNIV,MED CTR,CTR STUDY AGING & HUMAN DEV,DURHAM,NC 27710.
ABT ASSOCIATES INC,CAMBRIDGE,MA 02138.
BOSTON UNIV,SCH MED,BOSTON,MA 02118.
UNIV CONNECTICUT,SCH MED,INST LIVING,BRACELAND CTR MENTAL HLTH & AGING,HARTFORD,CT 06112.
UNIV CONNECTICUT,SCH MED,DEPT COMMUNITY MED & HLTH CARE,HARTFORD,CT 06112.
RP Beckett, LA (reprint author), RUSH UNIV,RUSH INST AGING,1645 W JACKSON BLVD,CHICAGO,IL 60612, USA.
FU NIA NIH HHS [N01AG02105, N01AG02106, N01AG02107]
NR 41
TC 202
Z9 204
U1 2
U2 5
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 APR 15
PY 1996
VL 143
IS 8
BP 766
EP 778
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UE759
UT WOS:A1996UE75900004
PM 8610686
ER
PT J
AU Fest, T
Pron, B
Lefranc, MP
Pierre, C
Angonin, R
deWazieres, B
Soua, Z
Dupond, JL
AF Fest, T
Pron, B
Lefranc, MP
Pierre, C
Angonin, R
deWazieres, B
Soua, Z
Dupond, JL
TI Detection of a clonal BCL2 gene rearrangement in tissues from a patient
with Whipple disease
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID FOLLICULAR LYMPHOMAS; IMMUNE-RESPONSE; MUCOSA; PYLORI
C1 HOP NECKER ENFANTS MALAD,MICROBIOL SERV,F-75743 PARIS 15,FRANCE.
INST GENET MOLEC,UMR CNRS 9942,IMMUNOGENET MOLEC LAB,F-34033 MONTPELLIER 1,FRANCE.
HOP UNIV JEAN MINJOZ,SERV ANATOMOPATHOL,F-25030 BESANCON,FRANCE.
HOP UNIV JEAN MINJOZ,SERV MED INTERNE,F-25030 BESANCON,FRANCE.
RP Fest, T (reprint author), NEI,PATHOL LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2N109,BETHESDA,MD 20892, USA.
NR 11
TC 10
Z9 10
U1 0
U2 0
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572
SN 0003-4819
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD APR 15
PY 1996
VL 124
IS 8
BP 738
EP 740
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA UD936
UT WOS:A1996UD93600006
PM 8633834
ER
PT J
AU Candotti, F
Johnston, JA
Puck, JM
Sugamura, K
OShea, JJ
Blaese, M
AF Candotti, F
Johnston, JA
Puck, JM
Sugamura, K
OShea, JJ
Blaese, M
TI Retroviral-mediated gene correction for X-linked severe combined
immunodeficiency
SO BLOOD
LA English
DT Article
ID RECEPTOR GAMMA-CHAIN; BONE-MARROW TRANSPLANTATION; HUMAN
ADENOSINE-DEAMINASE; FUNCTIONAL COMPONENT; CELLS; EXPRESSION; VIRUS
AB X-linked severe combined immunodeficiency (XSCID) is a lethal disease caused by a defect in the gene encoding the common gamma chain (gamma(c)) of the receptor for interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15. Allogeneic bone marrow transplantation, the current therapy of choice for this defect, is often complicated by graft-versus-host disease and/or incomplete reconstitution of B-lymphocyte functions. Correction of the gene defect at the level of the autologous lymphohematopoietic progenitors could therefore represent an improvement in the medical management of these patients. To study the feasibility of a gene therapy approach for XSCID, a retroviral vector expressing gamma(c) was used to transduce Epstein-Barr virus-transformed B-cell lines derived from patients with XSCID. After transduction, XSCID cells newly expressed gamma(c) on the cell surface at levels comparable to those observed on B-cell lines obtained from normal donors. Moreover, the reconstituted gamma(c) restored function to the IL-2 and IL-4 receptors as shown by signal transduction mediated by phosphorylation of the JAK1 and JAK3 members of the Janus family of tyrosine kinases and by restoration of cellular proliferation in response to IL-2.
This is a US government work. There are no restrictions on its use.
C1 NIAMS,LEUKOCYTE CELL BIOL SECT,NIH,BETHESDA,MD.
NIH,IMMUNOL GENET SECT,NCHGR,BETHESDA,MD 20892.
TOHOKU UNIV,SCH MED,DEPT MICROBIOL,SENDAI,MIYAGI 980,JAPAN.
RP Candotti, F (reprint author), NIH,CLIN GENE THERAPY BRANCH,NCHGR,BLDG 10-ROOM 10C103,10 CTR DR,BETHESDA,MD 20892, USA.
NR 47
TC 60
Z9 61
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 15
PY 1996
VL 87
IS 8
BP 3097
EP 3102
PG 6
WC Hematology
SC Hematology
GA UF381
UT WOS:A1996UF38100004
PM 8605322
ER
PT J
AU Hernandez, L
Fest, T
Cazorla, M
TeruyaFeldstein, J
Bosch, F
Peinado, MA
Piris, MA
Montserrat, E
Cardesa, A
Jaffe, ES
Campo, E
Raffeld, M
AF Hernandez, L
Fest, T
Cazorla, M
TeruyaFeldstein, J
Bosch, F
Peinado, MA
Piris, MA
Montserrat, E
Cardesa, A
Jaffe, ES
Campo, E
Raffeld, M
TI p53 gene mutations and protein overexpression are associated with
aggressive variants of mantle cell lymphomas
SO BLOOD
LA English
DT Article
ID LYMPHOCYTIC LYMPHOMA; CENTROCYTIC LYMPHOMA; INTERMEDIATE
DIFFERENTIATION; GEL-ELECTROPHORESIS; CYCLIN D1; EXPRESSION;
PROGRESSION; ONCOGENE; CANCER; REARRANGEMENT
AB Mantle cell lymphoma (MCL) is molecularly characterized by bcl-1 rearrangement and cyclin D1/PRAD-1 gene overexpression. Some aggressive variants have been recognized with a blastic or large cell morphology, higher proliferative activity, and shorter survival. p53 gene mutations in lymphoid neoplasms have been detected mainly in high grade lymphomas and have been associated with tumor progression in follicular and small lymphocytic lymphomas. To determine the role of p53 alterations in MCL, we examined 35 typical and 8 aggressive variants (5 blastic and 3 large cell) of MCLs by a combination of immunohistochemistry. single-strand conformational polymorphism analysis of genomic DNA and/or cDNA obtained by reverse transcriptase-polymerase chain reaction, denaturing gradient gel electrophoresis, and sequencing. Of the 8 aggressive MCLs, 3 (38%) contained missense point mutations in exon 8 codon 278 (Pro --> Leu), exon 8 codon 273 (Arg --> His), and exon 5 codon 151 (Pro --> Ser), respectively. A diffuse p53 protein overexpression was observed in more than 50% of the tumor cells in these 3 cases. A fourth blastic MCL also showed strong p53 immunoreactivity. However, no mutations were detected in exons 5-9 in this case. p53 expression was also detected in 10% of the cells in an additional large cell type of MCL and in less than 1% of the cells in 6 typical cases. No mutations were detected in any of these cases or in the remaining cases with no expression of the protein. Four nucleotide changes were observed by single-strand conformational polymorphism analysis in 4 typical MCLs with no overexpression of the protein. Direct sequencing showed that these nucleotide changes were located at exon 6 (1 case), intron 7 (2 cases), and intron 8 (1 case). The changes in exon 6 and intron 7 were known polymorphisms. The nucleotide change in intron 8 was outside splicing sites of the neighboring exons. The overall survival of the 3 patients with p53 mutations (median, 18.3 months) was significantly shorter than that of pateints with the nonmutated MCLs (median, 49 months; P < .01). These findings indicate that p53 gene mutations are an infrequent phenomenon in MCLs and are associated with a subset of aggressive variants.
This is a US government work. There are no restrictions on its use.
C1 UNIV BARCELONA,ANAT PATHOL LAB,HOSP CLIN PROV,E-08036 BARCELONA,SPAIN.
UNIV BARCELONA,HOSP CLIN PROV,POSTGRAD SCH HEMATOL FARRERAS VALENTI,BARCELONA,SPAIN.
INST RECERCA ONCOL,BARCELONA,SPAIN.
HOSP VIRGEN DE LA SALUD,DEPT PATHOL ANAT,TOLEDO,SPAIN.
UNIV LLEIDA,SCH MED,DEPT BASIC MED SCI,LLEIDA,SPAIN.
NCI,HEMATOPATHOL SECT,PATHOL LAB,NIH,BETHESDA,MD 20892.
RI Peinado, Miguel A./A-5591-2008;
OI Peinado, Miguel A./0000-0002-4090-793X; Bosch,
Francesc/0000-0001-9241-2886; Piris, Miguel A/0000-0001-5839-3634;
Campo, elias/0000-0001-9850-9793
NR 47
TC 206
Z9 207
U1 1
U2 3
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 15
PY 1996
VL 87
IS 8
BP 3351
EP 3359
PG 9
WC Hematology
SC Hematology
GA UF381
UT WOS:A1996UF38100034
PM 8605352
ER
PT J
AU Gamel, JW
Meyer, JS
Feuer, E
Miller, BA
AF Gamel, JW
Meyer, JS
Feuer, E
Miller, BA
TI The impact of stage and histology on the long-term clinical course of
163,808 patients with breast carcinoma
SO CANCER
LA English
DT Article
DE breast cancer; histologic type; cured fraction; survival time; stage
ID CELL-KINETICS; CANCER
AB BACKGROUND, Stage and histologic type have a significant impact on the long term clinical course of breast carcinoma. Clinical course is governed by two components: likelihood of cure and median tumor-related survival time among uncured patients. Estimates of these components can be derived only by using survival models that incorporate cured fraction as a specific parameter.
METHODS. The prognostic value of stage and histologic type was determined for 163,808 patients with breast carcinoma using the log normal and log legit cure-based survival models. Follow-up ranged from 1 month to 19 years and was obtained from the SEER Program.
RESULTS, In approximate terms, ductal carcinoma was diagnosed in 70% of the patients, with estimated cured fractions of 2/3 and 1/3 for local, and regional disease, respectively. Estimates of median survival times for uncured patients were 10 and 5 years. Findings were similar for patients with tumors of miscellaneous histologic types. For patients with medullary carcinoma, cured fractions were relatively high at 82% and 64%, but median survival times were relatively short at 4 and 3 years. Corresponding values for patients with invasive comedo carcinoma were 82% and 50%, with median survival rimes of 6 and 4 years. For patients with mucinous, lobular, and ductolobular carcinomas, parametric analysis gave inconsistent estimates of cured fraction, but findings suggested unusually long tumor-related survival times.
CONCLUSIONS, Cure-based parametric survival models offer valuable insight into the impact of stage and histology on the clinical course of breast cancer. (C) 1996 American Cancer Society.
C1 UNIV LOUISVILLE,SCH MED,VET ADM MED CTR,LOUISVILLE,KY 40292.
UNIV LOUISVILLE,SCH MED,DEPT OPHTHALMOL,LOUISVILLE,KY 40292.
ST LUKES HOSP,ST LOUIS,MO.
NCI,NIH,SURVEILLANCE PROGRAM,BETHESDA,MD 20892.
NR 17
TC 41
Z9 41
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0008-543X
J9 CANCER
JI Cancer
PD APR 15
PY 1996
VL 77
IS 8
BP 1459
EP 1464
DI 10.1002/(SICI)1097-0142(19960415)77:8<1459::AID-CNCR6>3.0.CO;2-7
PG 6
WC Oncology
SC Oncology
GA UD430
UT WOS:A1996UD43000006
PM 8608529
ER
PT J
AU Kato, S
Onda, M
Matsukura, N
Tokunaga, A
Matsuda, N
Yamashita, K
Shields, PG
AF Kato, S
Onda, M
Matsukura, N
Tokunaga, A
Matsuda, N
Yamashita, K
Shields, PG
TI Genetic polymorphisms of the cancer related gene and Helicobacter pylori
infection in Japanese gastric cancer patients an age and gender matched
case-control study
SO CANCER
LA English
DT Article; Proceedings Paper
CT 7th Annual Meeting of the
Japanese-Research-Society-for-Gastroenterological-Carcinogenesis
CY SEP 08-09, 1995
CL OITA, JAPAN
SP Japanese Res Soc Gastroenterol Carcinogenesis
DE genetic polymorphism; cytochrome p450; Helicobacter pylori; gastric
cancer susceptibility; glutathione-S-transferase; L-myc protooncogene
ID FRAGMENT-LENGTH-POLYMORPHISM; SERUM PEPSINOGEN-I; L-MYC GENE;
LUNG-CANCER; STOMACH-CANCER; CYTOCHROME-P450IIE1; METASTASIS; RISK;
CARCINOGENESIS; SUSCEPTIBILITY
AB BACKGROUND. Gastric cancer is a multistage process, each caused by numerous factors. The objective of this study was to elucidate the risk factors for gastric cancer by using molecular epidemiologic techniques and serum markers.
METHODS. Serum pepsinogen I levels, pepsinogen I/pepsinogen II (I/II) ratios, serum IgG antibody against Helicobacter pylori (H. pylori), and genetic polymorphisms of cytochrome p450 2E1 (CYP2E1), glutathione-S-transferase M1 (GSTM1), and L-myc protooncogenes were analyzed in 82 persons with gastric cancer and in 151 age- and sex-matched controls, who were selected from 208 gastric cancer patients and 375 noncancer patients, respectively. Statistical analysis was performed to elucidate which risk factors for gastric cancer were contributing the most to gastric carcinogenicity.
RESULTS. Serum pepsinogen I level (odds ratio [OR] = 1.81; 95% confidence interval [CI], 1.04-3.16) and pepsinogen I/II ratios (OR = 3.09; 95% CI, 1.74-5.49) were significantly associated with gastric cancer risk in a case-control study. Seropositivity of serum IgG antibody against H. pylori (OR = 1.25; 95% CI, 0.84-1.85) and specific genotypes of a L-myc genetic polymorphism (OR = 1.33; 95% CI, 0.59-2.99) were more commonly observed in gastric cancer cases, but this was not statistically significant. Specific genotypes of the CYP2E1 RsaI polymorphism and GSTM1 gene deletion were not associated with gastric cancer.
CONCLUSIONS. Atrophic mucosal change, indicated by serum pepsinogen levels, is possible a risk factor for gastric cancer. X. pylori infection and genetic polymorphisms of CYP2E1, L-myc, and GSTM1 genetic polymorphisms were not risk factors in this study. (C) 1996 American Cancer Society.
C1 NCI,HUMAN CARCINOGENESIS LAB,DIV CANC ETIOL,NIH,BETHESDA,MD 20892.
RP Kato, S (reprint author), NIPPON MED COLL,DEPT SURG 1,BUNKYO KU,1-1-5 SENDAGI,TOKYO 113,JAPAN.
RI Shields, Peter/I-1644-2012
NR 39
TC 67
Z9 68
U1 0
U2 5
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0008-543X
J9 CANCER
JI Cancer
PD APR 15
PY 1996
VL 77
IS 8
SU S
BP 1654
EP 1661
DI 10.1002/(SICI)1097-0142(19960415)77:8+<1654::AID-CNCR11>3.0.CO;2-X
PG 8
WC Oncology
SC Oncology
GA UE554
UT WOS:A1996UE55400011
PM 8608558
ER
PT J
AU McCormick, DL
Rao, KVN
Johnson, WD
BowmanGram, TA
Steele, VE
Lubet, RA
Kelloff, GJ
AF McCormick, DL
Rao, KVN
Johnson, WD
BowmanGram, TA
Steele, VE
Lubet, RA
Kelloff, GJ
TI Exceptional chemopreventive activity of low-dose dehydroepiandrosterone
in the rat mammary gland
SO CANCER RESEARCH
LA English
DT Article
ID LONG-TERM TREATMENT; INHIBITION; MICE; 7,12-DIMETHYLBENZANTHRACENE;
CARCINOGENESIS; 3-BETA-METHYLANDROST-5-EN-17-ONE; SUSCEPTIBILITY;
TUMORIGENESIS; METABOLISM; DHEA
AB To determine if the chemopreventive activity of dehydroepiandrosterone (DHEA) in the rat mammary gland can be dissociated from its toxicity, two studies were conducted in which low doses of DHEA were administered alone and in combination with other agents to rats treated with N-methyl-N-nitrosourea, Beginning 1 week prior to administration of 35 mg N-methyl-N-nitrosourea per kg body weight, groups of 20 female Sprague-Dawley rats were fed AIN-76A diet supplemented with DHEA alone (800 or 400 mg/kg diet), DHEA + tamoxifen (80 or 40 mu g/kg diet), DHEA + carbenoxolone (3500 or 1750 mg/kg diet), or DHEA + tamoxifen + carbenoxolone. When administered alone at either 800 or 100 mg/kg diet, DHEA reduced mammary cancer incidence from >70% in dietary controls to 0%; mammary cancer incidence in all DHEA combination regimens was also less than or equal to 5%. The dose levels of DHEA used induced no toxicity or alteration in body weight gain, These results indicate that dietary supplementation with low doses of DHEA has chemopreventive efficacy greater than or equal to that of endocrine ablation, This protection may be mediated by the induction of differentiation in the mammary parenchyma.
C1 NCI,CHEMOPREVENT INVEST STUDIES BRANCH,BETHESDA,MD 20852.
RP McCormick, DL (reprint author), IIT,DEPT LIFE SCI,10 W 35TH ST,CHICAGO,IL 60616, USA.
FU NCI NIH HHS [CA-30646, N01-CN-85097-11]
NR 24
TC 47
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 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 1996
VL 56
IS 8
BP 1724
EP 1726
PG 3
WC Oncology
SC Oncology
GA UE735
UT WOS:A1996UE73500005
PM 8620482
ER
PT J
AU Steller, MA
Delgado, CH
Bartels, CJ
Woodworth, CD
Zou, ZQ
AF Steller, MA
Delgado, CH
Bartels, CJ
Woodworth, CD
Zou, ZQ
TI Overexpression of the insulin-like growth factor-1 receptor and
autocrine stimulation in human cervical cancer cells
SO CANCER RESEARCH
LA English
DT Article
ID FACTOR-I RECEPTOR; PAPILLOMAVIRUS TYPE-16; DNA
AB We characterized mechanisms of growth control involving insulin-like growth factor-1 (IGF-I), IGF-2, and IGF-I receptor (IGF-IR) by investigating their expression in human cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical epithelial cells maintained in short-term culture, By reverse transcription followed by PCR, IGF-1 mRNA was not detected in any of the cell lines, whereas IGF-2-mRNA transcripts were detected in all of them, Using the RNase protection assay, low levels of IGF-2 mRNA were also detected in all of the cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical cultures tested, but no IGF-1 transcripts were detected, Scatchard analysis revealed 3- and 5-fold increases in IGF-1R expression by the primary cervical cancer cell cultures and cervical cancer cell lines, respectively, compared with the normal ectocervical cells, In proliferation assays, epidermal growth factor (EGF) consistently enhanced cervical cancer cell growth, but an antisense oligonucleotide to IGF-2 uniformly inhibited the EGF-induced mitogenic effect, These studies suggest that autocrine production of IGF-2 and overexpression of the IGF-1R are important components controlling the proliferation of cervical carcinoma cells, and that autocrine IGF-2 production in cervical cancer cells may participate in the mitogenic signaling of EGF.
C1 NCI,BIOL LAB,BETHESDA,MD 20892.
RP Steller, MA (reprint author), NCI,GYNECOL ONCOL SECT,SURG BRANCH,BLDG 10,ROOM 2B-42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 30
TC 63
Z9 66
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 1996
VL 56
IS 8
BP 1761
EP 1765
PG 5
WC Oncology
SC Oncology
GA UE735
UT WOS:A1996UE73500013
PM 8620490
ER
PT J
AU Gallahan, D
Jhappan, C
Robinson, G
Hennighausen, L
Sharp, R
Kordon, E
Callahan, R
Merlino, G
Smith, GH
AF Gallahan, D
Jhappan, C
Robinson, G
Hennighausen, L
Sharp, R
Kordon, E
Callahan, R
Merlino, G
Smith, GH
TI Expression of a truncated Int3 gene in developing secretory mammary
epithelium specifically retards lobular differentiation resulting in
tumorigenesis
SO CANCER RESEARCH
LA English
DT Article
ID TRANSGENIC MICE; TGF-ALPHA; GLAND; OVEREXPRESSION; CELLS
AB Insertional mutation of the Int3 gene, a member of the Notch gene family, is frequently associated with primary mouse mammary tumors induced by the mouse mammary tumor virus (MMTV). A major consequence of these mutations Is the production of a shortened 2,4-kb tumor-specific Int3 RNA transcript that encodes the entire intracellular domain of the Int3 protein, Previous studies have demonstrated that mammary gland development and function was severely impaired in transgenic mice expressing the truncated Int3 gene product from the MMTV viral promoter, Both mammary ductal growth and secretory lobule development were curtailed in these mice, These results were attributed to a gain of function modification of the Int3 gene, which led to a restriction of cell fate selection in the affected mammary epithelial cells, To confirm and extend these findings, truncated Int3 was expressed from the whey acidic protein (WAP) promoter, the activity of which, unlike that of the MMTV long terminal repeat, is restricted to the secretory mammary epithelial population, In transgenic mice carrying the WAP/Int3 construct, mammary ductal growth was unaffected in virgin females, but growth and differentiation of secretory lobules during gestation was profoundly inhibited, Coincidental with the block in lobular secretory differentiation, mammary dysplasia and tumorigenesis occurred in all breeding females by 25 weeks of age, In nonbreeding WAP/Int3 females, mammary tumor incidence also reached 100%, but only after 70 weeks. The WAP/Int3 mammary tumors were highly malignant, and most tumor-bearing females, irrespective of breeding history, developed metastatic lung lesions, These results suggest that WAP promoter-targeted Int3 function is associated with mammary secretory cell differentiation and maintenance in this transgenic model, Consistent with the conclusion that WAP-driven truncated Int3 expression influenced only lobular differentiation and not ductal growth and extension during mammary gland development, transplants of I VAP/Int3 gland into nontransgenic mammary fat pads produced complete mammary ductal outgrowths in virgin FVB/N mice but failed to develop secretory lobules when the females were impregnated.
C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892.
NIDDK,BIOCHEM & METAB LAB,NIH,BETHESDA,MD 20892.
RI Robinson, Gertraud/I-2136-2012
NR 26
TC 134
Z9 138
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 1996
VL 56
IS 8
BP 1775
EP 1785
PG 11
WC Oncology
SC Oncology
GA UE735
UT WOS:A1996UE73500016
PM 8620493
ER
PT J
AU Blagosklonny, MV
Schulte, T
Nguyen, P
Trepel, J
Neckers, LM
AF Blagosklonny, MV
Schulte, T
Nguyen, P
Trepel, J
Neckers, LM
TI Taxol-induced apoptosis and phosphorylation of Bcl-2 protein involves
c-Raf-1 and represents a novel c-Raf-1 signal transduction pathway
SO CANCER RESEARCH
LA English
DT Article
ID KINASE; RAF-1
AB c-Raf-l (Raf-l) is a central component of signal transduction pathways stimulated by various growth factors, protein kinase C, and other protein kinases. Raf-l activation is thought to be initiated at the plasma membrane after its recruitment by Ras, Raf-l activation is associated primarily with proliferation and cell survival, but it has also been implicated in apoptosis, Raf-l has also been shown to form complexes with both R-Ras and Bcl-2, raising the possibility that this component of cellular Raf-l plays a role in apoptosis, Recently, taxol was reported to induce Bcl-2 phosphorylation and inactivation, We have previously demonstrated Raf-l activation following taxol in MCF7 cells, We now present evidence that taxol fails to stimulate either apoptosis or phosphorylation of Bcl-2 in the absence of Raf-l, Moreover, Raf-l activation by taxol coincided with Bcl-2 phosphorylation, showing similar dose and time dependence, Thus, our data support a role for a distinct subcellular component of Raf-l, which is taxol but not phorbol myristate acetate sensitive, in mediating an apoptotic pathway involving Bcl-2.
C1 NCI,CLIN PHARMACOL BRANCH,NIH,BETHESDA,MD 20892.
NR 27
TC 355
Z9 368
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 1996
VL 56
IS 8
BP 1851
EP 1854
PG 4
WC Oncology
SC Oncology
GA UE735
UT WOS:A1996UE73500026
PM 8620503
ER
PT J
AU vanderPluijm, G
Vloedgraven, HJM
Ivanov, B
Robey, FA
Grzesik, WJ
Robey, PG
Papapoulos, SE
Lowik, CWGM
AF vanderPluijm, G
Vloedgraven, HJM
Ivanov, B
Robey, FA
Grzesik, WJ
Robey, PG
Papapoulos, SE
Lowik, CWGM
TI Bone sialoprotein peptides are potent inhibitors of breast cancer cell
adhesion to bone
SO CANCER RESEARCH
LA English
DT Article
ID CYCLIC RGD PEPTIDE; MESSENGER-RNA; DEVELOPMENTAL EXPRESSION; VITRONECTIN
RECEPTOR; TUMOR-METASTASIS; RAT OSTEOCLASTS; MATRIX; OSTEOPONTIN;
INTEGRINS; RESORPTION
AB Bone and bone marrow are important sites of metastasis formation in breast cancer. Extracellular matrix proteins with attachment properties are generally believed to play a key role in tumorigenesis and metastasis formation, We have investigated whether mammary carcinoma cells (MDA-MB-231) can recognize constructs of the fairly bone-specific human bone sialoprotein, which encompass the RGD sequence (EPRGDNYR), Exogenously added bone sialoprotein peptides with this amino acid sequence in their backbone structure, but not the more common fibronectin-derived GRGDS peptide, strongly inhibited breast cancer cell adhesion to extracellular bone matrix at micromolar concentrations, Most cyclic derivatives with the EPRGDNYR sequence were more effective inhibitors of tumor cell adhesion to bone than their linear equivalents, Furthermore, changes in the RGD-tripeptide of the backbone structure of the constructs, removal of the NYR flanking sequence, or a different tertiary cyclic structure significantly decreased their inhibitory potencies, In addition, the RGE-analogue EPRGENYR was capable of inhibiting breast cancer cell adhesion to bone, albeit to a lesser extent.
We conclude, therefore, that the inhibitory potency of the bone sialoprotein-derived peptides on breast cancer cell adhesion to bone is not solely due to a properly positioned RGD-motif alone but is also determined by its flanking regions, together with the tertiary structure of the EPRGDNYR peptide, Synthetic cyclic constructs with the EPRGDNYR sequence may, therefore, be potentially useful as antiadhesive agents for cancer cells to bone in vivo.
C1 NIDR, CELLULAR DEV & ONCOL LAB, PEPTIDE & IMMUNOCHEM UNIT, NIH, BETHESDA, MD 20892 USA.
RP vanderPluijm, G (reprint author), LEIDEN UNIV HOSP, DEPT ENDOCRINOL & METAB DIS C489, POB 9600, 2300 RC LEIDEN, NETHERLANDS.
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
NR 59
TC 56
Z9 57
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 APR 15
PY 1996
VL 56
IS 8
BP 1948
EP 1955
PG 8
WC Oncology
SC Oncology
GA UE735
UT WOS:A1996UE73500041
PM 8620518
ER
PT J
AU Lauer, MS
Okin, PM
Larson, MG
Evans, JC
Levy, D
AF Lauer, MS
Okin, PM
Larson, MG
Evans, JC
Levy, D
TI Impaired heart rate response to graded exercise - Prognostic
implications of chronotropic incompetence in the Framingham Heart Study
SO CIRCULATION
LA English
DT Article
DE mortality; heart rate; exercise testing; coronary heart disease
ID PHYSICAL-ACTIVITY; DISEASE; RISK; MEN
AB Background Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample.
Methods and Results In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise (''chronotropic response index''). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P<.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors.
Conclusions An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.
C1 NEW YORK HOSP,CORNELL MED CTR,DEPT CARDIOL,NEW YORK,NY.
BOSTON UNIV,SCH MED,DEPT EPIDEMIOL & PREVENT MED,BOSTON,MA.
NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA.
RP Lauer, MS (reprint author), CLEVELAND CLIN FDN,DEPT CARDIOL,DESK F-15,9500 EUCLID AVE,CLEVELAND,OH 44195, USA.
RI Lauer, Michael/L-9656-2013
OI Lauer, Michael/0000-0002-9217-8177
NR 26
TC 306
Z9 322
U1 1
U2 14
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 15
PY 1996
VL 93
IS 8
BP 1520
EP 1526
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA UE620
UT WOS:A1996UE62000009
PM 8608620
ER
PT J
AU Antinore, MJ
Birrer, MJ
Patel, D
Nader, L
McCance, DJ
AF Antinore, MJ
Birrer, MJ
Patel, D
Nader, L
McCance, DJ
TI The human papillomavirus type 16 E7 gene product interacts with and
trans-activates the AP1 family of transcription factors
SO EMBO JOURNAL
LA English
DT Article
DE AP1; E7; human papillomavirus; Jun
ID DNA-BINDING ACTIVITY; ADENOVIRUS E1A PROTEINS; CASEIN KINASE-II;
EPITHELIAL-CELL DIFFERENTIATION; OPEN READING FRAME; RAT EMBRYO CELLS;
C-JUN; HUMAN KERATINOCYTES; CERVICAL-CARCINOMA; NUCLEAR-PROTEIN
AB The E7 gene product of human papillomavirus type 16 (HPV16) binds to the retinoblastoma gene product (pRb) and dissociates pRb-E2F complexes. However, the observation that the ability of E7 to bind pRb is not required for the HPV16-induced immortalization of primary keratinocytes prompted a search for other cellular factors bound by E7. Using a glutathione-S-transferase (GST) fusion protein system, we show that E7 complexes with AP1 transcription factors including c-Jun, JunB, JunD and c-Fos. The ability of E7 to complex with c-Jun in vivo is demonstrated by co-immunoprecipitation and the yeast two-hybrid system. An analysis of E7 point mutants in the GST system indicates that the E7 zinc-finger motif, but not the pRb binding domain, is involved in these interactions. Using c-Jun deletion mutants, E7 binding maps between amino acids 224 and 286 of c-Jun. E7 trans-activates c-Jun-induced transcription from a Jun responsive promoter, and this activity correlates with the ability of E7 mutants to bind Jun proteins. Finally, a transcriptionally inactive c-Jun deletion, which can bind E7, interferes with the E7-induced transformation of rat embryo fibroblasts in cooperation with an activated ras, indicating that the Jun-E7 interaction is physiologically relevant and that Jun factors may be targeted in the E7 transformation pathway.
C1 UNIV ROCHESTER,DEPT MICROBIOL & IMMUNOL,ROCHESTER,NY 14642.
NCI,BIOMARKERS & PREVENT RES BRANCH,DIV CANC PREVENT & CONTROL,ROCKVILLE,MD 20850.
FU NIAID NIH HHS [AI 30798-05, T32 AI07362-01]
NR 72
TC 156
Z9 158
U1 0
U2 1
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0261-4189
J9 EMBO J
JI Embo J.
PD APR 15
PY 1996
VL 15
IS 8
BP 1950
EP 1960
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UG748
UT WOS:A1996UG74800023
PM 8617242
ER
PT J
AU Tuomisto, J
Sewall, CH
Unkila, M
Pohjanvirta, R
Clark, GC
Viluksela, M
Rozman, K
Lucier, GW
AF Tuomisto, J
Sewall, CH
Unkila, M
Pohjanvirta, R
Clark, GC
Viluksela, M
Rozman, K
Lucier, GW
TI Differences in binding of epidermal growth factor to liver membranes of
TCDD-resistant and TCDD-sensitive rats after a single dose of TCDD
SO ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
LA English
DT Article
DE dioxin; TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin); EGF (epidermal
growth factor); EGF receptor; phosphoenolpyruvate carboxykinase (PEPCK);
TCDD-resistant rat; TCDD-sensitive rat; strain difference; liver, rat
ID HEPATIC PLASMA-MEMBRANE; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD;
FACTOR RECEPTOR; PHOSPHOENOLPYRUVATE CARBOXYKINASE; EGF RECEPTOR;
EXPRESSION; INVIVO; STRAIN; TOXICITY; INCREASE
AB Epidermal growth factor (EGF) receptor has been implied as having a role in certain actions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). After a single dose of TCDD, the receptor has been shown to be downregulated in several tissues including the liver. Two rat substrains, the Han/Wistar (Kuopio; H/W) rat and the Long-Evans (Turku AB; L-E) rat exhibit over a 1000-fold difference in their sensitivity to the lethal effect of TCDD, This large sensitivity difference was utilized in the current study to investigate whether or not a correlation exists between TCDD lethality and biochemical endpoints related to the hepatic EGF receptor. In the TCDD-sensitive L-E strain both the B-max of the EGF receptor and the receptor protein as measured by Western blots, decreased dose and time dependently. Ten days after a lethal dose of TCDD (50 mu g/kg), the downregulation was 80%. In the resistant H/W strain, two non-lethal doses were used (50 and 500 mu g/kg), since the lethal dose is not known, These doses caused a downregulation already at 4 days after dosing, but no further decrease by day 10. The activity of phosphoenolpyruvate carboxykinase (PEPCK, the main gluconeogenetic enzyme in the liver and a proposed target of TCDD) decreased in H/W rats at least to the same extent as in L-E rats at both 4 and 10 days, It is concluded that EGF receptor downregulation is different in the two rat strains studied, despite the fact that a classical Ah receptor-regulated response (CYP1Al induction) is similar. The results demonstrate that downregulation of the EGF receptor by TCDD is strain-dependent as well as dose- and time-dependent.
C1 NATL INST ENVIRONM HLTH,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709.
UNIV KANSAS,MED CTR,DEPT PHARMACOL TOXICOL & THERAPEUT,KANSAS CITY,KS 66160.
RP Tuomisto, J (reprint author), NATL PUBL HLTH INST,DEPT TOXICOL,DIV ENVIRONM HLTH,POB 95,FIN-70701 KUOPIO,FINLAND.
NR 33
TC 3
Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1382-6689
J9 ENVIRON TOXICOL PHAR
JI Environ. Toxicol. Pharmacol.
PD APR 15
PY 1996
VL 1
IS 2
BP 109
EP 116
DI 10.1016/1382-6689(95)00016-X
PG 8
WC Environmental Sciences; Pharmacology & Pharmacy; Toxicology
SC Environmental Sciences & Ecology; Pharmacology & Pharmacy; Toxicology
GA UT284
UT WOS:A1996UT28400004
PM 21781670
ER
PT J
AU Mermelstein, F
Yeung, K
Cao, J
Inostroza, JA
ErdjumentBromage, H
Eagelson, K
Landsman, D
Levitt, P
Tempst, P
Reinberg, D
AF Mermelstein, F
Yeung, K
Cao, J
Inostroza, JA
ErdjumentBromage, H
Eagelson, K
Landsman, D
Levitt, P
Tempst, P
Reinberg, D
TI Requirement of a corepressor for Dr1-mediated repression of
transcription
SO GENES & DEVELOPMENT
LA English
DT Article
DE Dr1-mediated repression; corepression of transcription; HeLa cells;
heterodimer formation
ID RNA POLYMERASE-II; TATA-BINDING-PROTEIN; SACCHAROMYCES-CEREVISIAE;
PREINITIATION COMPLEX; PROMOTER INTERACTIONS; GENE-TRANSCRIPTION; LESS
PROMOTER; TFIID COMPLEX; PURIFICATION; ACTIVATION
AB A Dr1-associated polypeptide (DRAP1) was isolated from HeLa cells and found to function as a corepressor of transcription. Corepressor function requires an interaction between DRAP1 and Dr1. Heterodimer formation was dependent on a histone fold moth present at the amino terminus of both polypeptides. Association of DRAP1 with Dr1 results in higher stability of the Dr1-TBP-TATA moth complex and precluded the entry of TPIIA and/or TFIIB to preinitiation complexes. DRAP1 was found to be expressed in all tissues analyzed with higher levels in tissues with a low mitotic index. Analysis of DRAP1 in the developing brain of rat demonstrated undetectable levels of DRAP1 in actively dividing cells but high levels of DRAP1 expression in differentiated non dividing cells. Dr1 was immunodetected in all cells analyzed. A model for DRAP1-dependent, Dr1-mediated repression of transcription is proposed.
C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT BIOCHEM,HOWARD HUGHES MED INST,PISCATAWAY,NJ 08854.
MEM SLOAN KETTERING CANC CTR,PROGRAM MOLEC BIOL,NEW YORK,NY 10021.
UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROBIOL,PISCATAWAY,NJ 08854.
NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,NIH,BETHESDA,MD 20894.
RI Landsman, David/C-5923-2009;
OI Landsman, David/0000-0002-9819-6675
NR 82
TC 105
Z9 108
U1 0
U2 1
PU COLD SPRING HARBOR LAB PRESS
PI PLAINVIEW
PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD APR 15
PY 1996
VL 10
IS 8
BP 1033
EP 1048
DI 10.1101/gad.10.8.1033
PG 16
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA UJ343
UT WOS:A1996UJ34300011
PM 8608938
ER
PT J
AU Wang, JY
Walker, H
Lin, Q
Jenkins, N
Copeland, NG
Watanabe, T
Burrows, PD
Cooper, MD
AF Wang, JY
Walker, H
Lin, Q
Jenkins, N
Copeland, NG
Watanabe, T
Burrows, PD
Cooper, MD
TI The mouse BP-1 gene: Structure, chromosomal localization, and regulation
of expression by type I interferons and interleukin-7
SO GENOMICS
LA English
DT Article
ID TRANSFORMATION-ASSOCIATED ANTIGEN; PRE-B-CELLS; MURINE INTERLEUKIN-7;
MOLECULAR-CLONING; AMINOPEPTIDASE-A; BONE-MARROW; DIFFERENTIATION;
ORGANIZATION; RECEPTOR; DISTINCT
AB The BP-1/6C3 antigen is a homodimeric, phosphorylated type II membrane integral glycoprotein expressed on immature B-lineage cells, bone marrow stromal cells, thymic cortical epithelial cells, endothelial cells, enterocytes, and renal proximal tubular cells. Biochemical and molecular analysis identified BP-1 as glutamyl aminopeptidase, an ectoenzyme that catalyzes the hydrolysis of acidic amino acid residues from the amino termini of regulatory peptides. We have isolated genomic clones that encode the BP-1 gene (gene symbol Enpep). The gene spans more than 110 kb and contains 20 exons. Except for the first and the last exons, it is composed of small exons ranging from 56 to 171 bp that are separated by introns ranging from less than 100 bp to approximately 10 kb. The zinc binding motif HEXXH and the glutamic acid residue 19 amino acids downstream, which also binds zinc, are encoded in exons 5 and 6. Primer extension analysis revealed a common major transcriptional start site in a pre-B cell line, in a bone marrow stromal cell line, and in kidney cells. The promoter region contains a TATA-like element and potential DNA-binding motifs for lymphocyte-specific transcription factors including Ikaros, BSAP, PU.1, and octamer binding proteins, as well as DNA binding motifs for several ubiquitous transcription factors. An interferon responsive element also located in the promoter region appeared to be functional, since type I interferons (IFN-alpha/IFN-beta) upregulated BP-1 expression in pre-B cell lines. A 2.1-kb promoter fragment, when fused to a luciferase reporter gene, was able to drive luciferase expression in pre-B cells, which normally express BP-1, and ill Ag8 cells, in which BP-1 expression is extinguished. The BP-1/Enpep gene was localized to a distal region of mouse chromosome 3 in a region homologous to human chromosome 4q25. Interestingly, while interleukin-7 (IL-7) induced both cell growth and increased BP-1 expression, IFN-alpha/IFN-beta upregulated BP-1 expression but inhibited IL-7-induced proliferation. This finding indicates that the upregulated BP-1 expression can be disassociated from the cell growth signal. (C) 1996 Academic Press, Inc.
C1 UNIV ALABAMA,WALLACE TUMOR INST 386,HOWARD HUGHES MED INST,BIRMINGHAM,AL 35294.
UNIV ALABAMA,DIV DEV & CLIN IMMUNOL,BIRMINGHAM,AL 35294.
UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294.
UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL 35294.
UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294.
NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702.
KYUSHU UNIV,MED INST BIOREGULAT,FUKUOKA 81282,JAPAN.
FU NCI NIH HHS [N01-CO-46000]; NIAID NIH HHS [AI 34568, AI 39816]
NR 48
TC 32
Z9 32
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD APR 15
PY 1996
VL 33
IS 2
BP 167
EP 176
DI 10.1006/geno.1996.0180
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA UH006
UT WOS:A1996UH00600003
PM 8660964
ER
PT J
AU Long, GL
Winfield, S
Adolph, KW
Ginns, EI
Bornstein, P
AF Long, GL
Winfield, S
Adolph, KW
Ginns, EI
Bornstein, P
TI Structure and organization of the human metaxin gene (MTX) and
pseudogene
SO GENOMICS
LA English
DT Article
ID GLUCOCEREBROSIDASE GENE; GAUCHER DISEASE; TARGETED DISRUPTION; LEADER
SEQUENCE; EVOLUTION; MODEL; EXPRESSION; MURINE; MUCIN
AB Metaxin encodes a mitochondrial protein and is an essential nuclear gene in mice. The cDNA sequence and genomic organization of the human metaxin gene (MIX) have now been determined, MIX is 6 kb and consists of eight protein-encoding exons, The gene is contiguous to thrombospondin 3 (THBS3) and to the pseudogene for glucocerebrosidase (psGBA), but is transcribed in a direction opposite to the latter two genes. Thus, MIX and THBS3 share a common promoter region and are transcribed divergently, whereas MIX and psGBA are transcribed convergently and have closely apposed polyadenylation sites, Human metaxin contains 317 amino acids and is 91.5% identical to mouse metaxin. Metaxin is rich in leucine (14.2%) and in basic (12.9%) and acidic (12.0%) amino acids, The predicted protein lacks an amino-terminal signal sequence and N-glycosylation sites, but contains a putative transmembrane domain near its carboxy terminus, A DNA duplication has led to a direct repeat and the evolution of a pseudogene for GBA. A pseudogene for metaxin (psMTX) is also located within the 16 kb of DNA separating GBA from psGBA. The psMTX sequence is nearly identical to the 3' part of exon 2 through exon 8 of MTX, and both the intronic and the 3'-flanking sequences are highly conserved, Thus, there is a 278 amino acid open reading frame that is 97.8% identical to metaxin. However, psMTX lacks the first intron and promoter present in MIX and at least in liver, the pseudogene is not expressed. (C) 1996 Academic Press, Inc.
C1 UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195.
NIMH,CLIN NEUROSCI BRANCH,IRP,BETHESDA,MD 20892.
FU NCI NIH HHS [CO6-HL39745]; NIDCR NIH HHS [DE 08229]
NR 24
TC 32
Z9 33
U1 0
U2 2
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD APR 15
PY 1996
VL 33
IS 2
BP 177
EP 184
DI 10.1006/geno.1996.0181
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA UH006
UT WOS:A1996UH00600004
PM 8660965
ER
PT J
AU Savitsky, K
Ziv, Y
BarShira, A
Gilad, S
Tagle, DA
Smith, S
Uziel, T
Sfez, S
Nahmias, J
Sartiel, A
Eddy, RL
Shows, TB
Collins, FS
Shiloh, Y
Rotman, G
AF Savitsky, K
Ziv, Y
BarShira, A
Gilad, S
Tagle, DA
Smith, S
Uziel, T
Sfez, S
Nahmias, J
Sartiel, A
Eddy, RL
Shows, TB
Collins, FS
Shiloh, Y
Rotman, G
TI A human gene (DDX10) encoding a putative DEAD-box RNA helicase at
11q22-q23
SO GENOMICS
LA English
DT Article
ID TRANSLATION INITIATION FACTOR-4A; A-D BOX; ESCHERICHIA-COLI;
RIBOSOMAL-RNA; PROTEIN; DROSOPHILA; SEQUENCE; SIMILARITY; DISEASE;
HYBRIDS
AB A human gene encoding a putative RNA helicase, designated DDX10, was identified 400 kb telomeric to the ataxia-telangiectasia gene at chromosome 11q22-q23. The predicted amino acid sequence shows very high similarity to a subgroup of DEAD-box RNA helicases involved in ribosome biogenesis. This novel gene encodes a 3.2-kb transcript in a variety of human tissues. A processed pseudogene of DDX10 was detected at chromosome 9q21-q22. We observed a rare trinucleotide repeat length polymorphism within the coding sequence of DDX10. (C) 1996 Academic Press, Inc.
C1 TEL AVIV UNIV, SACKLER SCH MED, DEPT HUMAN GENET, IL-69978 RAMAT AVIV, ISRAEL.
NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA.
UCL, GALTON LAB, MRC, HUMAN BIOCHEM GENET UNIT, LONDON NW1 2HE, ENGLAND.
NEW YORK STATE DEPT HLTH, ROSWELL PK CANC INST, DEPT HUMAN GENET, BUFFALO, NY 14263 USA.
FU NINDS NIH HHS [NS31763]
NR 39
TC 40
Z9 42
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
J9 GENOMICS
JI Genomics
PD APR 15
PY 1996
VL 33
IS 2
BP 199
EP 206
DI 10.1006/geno.1996.0184
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA UH006
UT WOS:A1996UH00600007
PM 8660968
ER
PT J
AU Lopez, JV
Cevario, S
OBrien, SJ
AF Lopez, JV
Cevario, S
OBrien, SJ
TI Complete nucleotide sequences of the domestic cat (Felis catus)
mitochondrial genome and a transposed mtDNA tandem repeat (Numt) in the
nuclear genome
SO GENOMICS
LA English
DT Article
ID D-LOOP REGION; MOLECULAR PHYLOGENY; DNA DAMAGE; FIN WHALE; EVOLUTION;
GENES; MUTATION; ORGANIZATION; HETEROPLASMY; SUBSTITUTION
AB The complete 17,009-bp mitochondrial genome of the domestic cat, Felis catus, has been sequenced and conforms largely to the typical organization of previously characterized mammalian mtDNAs. Codon usage and base composition also followed canonical vertebrate patterns, except for an unusual ATC (non-AUG) codon initiating the NADH dehydrogenase subunit 2 (ND2) gene. Two distinct repetitive motifs at opposite ends of the control region contribute to the relatively large size (1559 bp) of this carnivore mtDNA. Alignment of the feline mtDNA genome to a homologous 7946-bp nuclear mtDNA tandem repeat DNA sequence in the cat, Numt, indicates simple repeat motifs associated with insertion/deletion mutations. Overall DNA sequence divergence between Numt and cytoplasmic mtDNA sequence was only 5.1%. Substitutions predominate at the third codon position of homologous feline protein genes. Phylogenetic analysis of mitochondrial gene sequences confirms the recent transfer of the cytoplasmic mtDNA sequences to the domestic cat nucleus and recapitulates evolutionary relationships between mammal species. (C) 1996 Academic Press, Inc.
C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC FREDERICK,FREDERICK,MD 21702.
NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702.
GEORGE MASON UNIV,DEPT BIOL,FAIRFAX,VA 22030.
RI Lopez, Jose/F-8809-2011
OI Lopez, Jose/0000-0002-1637-4125
NR 86
TC 180
Z9 204
U1 1
U2 15
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD APR 15
PY 1996
VL 33
IS 2
BP 229
EP 246
DI 10.1006/geno.1996.0188
PG 18
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA UH006
UT WOS:A1996UH00600011
PM 8660972
ER
PT J
AU Cerretti, DP
Lyman, SD
Kozlosky, CJ
Copeland, NG
Gilbert, DJ
Jenkins, NA
Valentine, V
Kirstein, MN
Shapiro, DN
Morris, SW
AF Cerretti, DP
Lyman, SD
Kozlosky, CJ
Copeland, NG
Gilbert, DJ
Jenkins, NA
Valentine, V
Kirstein, MN
Shapiro, DN
Morris, SW
TI The genes encoding the Eph-related receptor tyrosine kinase ligands
LERK-1 (EPLG1, Epl1), LERK-3 (EPLG3, Epl3), and LERK-4 (EPLG4, EPl4) are
clustered on human chromosome 1 and mouse chromosome 3
SO GENOMICS
LA English
DT Article
ID FAMILY; IDENTIFICATION; EXPRESSION; HINDBRAIN; CLONING; CHICKEN; TUMOR;
ELK
AB Hek and elk are members of the eph-related family of receptor tyrosine kinases. Recently, we isolated five cDNAs encoding membrane-bound ligands to hek and elk. Because of the promiscuous nature of their binding, we have termed these proteins ligands of the ephrelated kinases or LERKs. The LERKs can be divided into two subgroups by virtue of their sequence identity, binding properties, and mode of cell membrane attachment. For example, LERK-2 (EPLG2, Ep12) and LERK-5 (EPLG5, Epl5) are type 1 transmembrane proteins, while LERK-1 (EPLG1, Epl1), LERK-3 (EPLG3, Epl3), and LERK-4 (EPLG4, Epl4) are anchored to the membrane by glycosyl-phosphatidylinositol (GPI) linkage. Using Southern hybridization analysis of human x rodent somatic cell hybrid DNAs, we have assigned the genes that encode the GPI-anchored LERKs (EPLG1, EPLG3, and EPLG4) to human chromosome 1. Fluorescence in situ hybridization to metaphase chromosome preparations using genomic clones from each locus refined this localization to chromosome 1, bands q21-q22. In addition, Southern blot analysis of DNA from interspecific backcross mice indicated that the mouse homologues Epl1, Epl3, and Epl4 map to a homologous region on mouse chromosome 3. (C) 1996 Academic Press, Inc.
C1 NCI, FREDERICK CANC RES & DEV CTR, MAMMALIAN GENET LAB, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA.
ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38101 USA.
ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA.
RP Cerretti, DP (reprint author), IMMUNEX RES & DEV CORP, 51 UNIV ST, SEATTLE, WA 98101 USA.
FU NCI NIH HHS [CA23099, CA01702, CA21765]
NR 36
TC 14
Z9 14
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
J9 GENOMICS
JI Genomics
PD APR 15
PY 1996
VL 33
IS 2
BP 277
EP 282
DI 10.1006/geno.1996.0192
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA UH006
UT WOS:A1996UH00600015
PM 8660976
ER
PT J
AU Carrington, M
Martin, M
Newell, W
Beck, S
Klitz, W
AF Carrington, M
Martin, M
Newell, W
Beck, S
Klitz, W
TI Association of alleles at loci located throughout the HLA complex
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD.
IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND.
UNIV CALIF BERKELEY,BERKELEY,CA.
RI Newell, William/C-7995-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP O06
EP O06
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500007
ER
PT J
AU Cullen, M
Noble, J
Erlich, H
Thorpe, K
Beck, S
Trowsdale, J
Carrington, M
AF Cullen, M
Noble, J
Erlich, H
Thorpe, K
Beck, S
Trowsdale, J
Carrington, M
TI Mapping recombination sites in the HLA class II region.
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702.
IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND.
ROCHE MOL SYST,ALAMEDA,CA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP O02
EP O02
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500005
ER
PT J
AU Mann, DL
Nelson, G
Carrington, M
Geodert, J
Kaslow, R
AF Mann, DL
Nelson, G
Carrington, M
Geodert, J
Kaslow, R
TI Combinations of mhc genes influence HIV-1 disease course
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NCI,SIAC INC,BETHESDA,MD 20892.
NIAID,ROCKVILLE,MD.
NIAID,FREDERICK,MD.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP O647
EP O647
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500648
ER
PT J
AU Wade, JA
Ng, CM
Harding, A
Malasky, M
Carrington, M
AF Wade, JA
Ng, CM
Harding, A
Malasky, M
Carrington, M
TI Stratified testing for HLA matching: Selection of identical SIB pairs
using microsatellite loci across HLA
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 UNIV TORONTO,TTH REG HISTOCOMPATIBIL LAB,TORONTO,ON,CANADA.
NCI,FRDC,SAIC,FREDERICK,MD.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP O439
EP O439
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500438
ER
PT J
AU Assefi, N
Kim, E
Hodgson, W
Ribaudo, R
AF Assefi, N
Kim, E
Hodgson, W
Ribaudo, R
TI Engineering higher affinity variants of beta 2-microglobulin
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NATL CANC INST,NIH,BETHESDA,MD.
HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,COCONUT GROVE,FL 33133.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P502
EP P502
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500502
ER
PT J
AU Begovich, AB
Chang, JD
Steiner, LL
Aldrich, CA
Zimmerman, PA
AF Begovich, AB
Chang, JD
Steiner, LL
Aldrich, CA
Zimmerman, PA
TI A comparison of HLA class II allele frequencies within Africa:
Implications for vaccine development
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 ROCHE MOLEC SYST,ALAMEDA,CA.
NIAID,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P574
EP P574
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500577
ER
PT J
AU Hackett, JA
Simonis, TB
Mixon, A
Wunderlich, J
Ferrone, S
Marincola, FM
AF Hackett, JA
Simonis, TB
Mixon, A
Wunderlich, J
Ferrone, S
Marincola, FM
TI Variability in HLA-A2 antigen expression by melanoma cell lines.
Functional implications
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NEW YORK MED COLL,VALHALLA,NY 10595.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P110
EP P110
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500110
ER
PT J
AU Hollenbach, JA
Barcellos, LF
Thomson, G
Winkler, C
Winter, M
Klitz, W
AF Hollenbach, JA
Barcellos, LF
Thomson, G
Winkler, C
Winter, M
Klitz, W
TI HLA differentiation among Mesoamerican natives
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NCI,FREDERICK,MD 21701.
UNIV CALIF BERKELEY,BERKELEY,CA 94720.
INST NATL ANTROPOL & HIST,OAXACA,MEXICO.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P329
EP P329
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500330
ER
PT J
AU Manns, A
Mann, D
Wilks, R
Carrington, M
Cranston, B
Hanchard, B
Blattner, W
AF Manns, A
Mann, D
Wilks, R
Carrington, M
Cranston, B
Hanchard, B
Blattner, W
TI HLA associated with HTLV-I seroconversion after transfusion
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
UNIV W INDIES,KINGSTON 7,JAMAICA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P660
EP P660
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500663
ER
PT J
AU Martayan, A
Fiscella, M
Setini, A
Ciccarelli, G
Gambari, R
Beretta, A
Siccardi, A
Appella, E
Giacomini, P
AF Martayan, A
Fiscella, M
Setini, A
Ciccarelli, G
Gambari, R
Beretta, A
Siccardi, A
Appella, E
Giacomini, P
TI Conformation and surface expression of free HLA-CW1 heavy chains in
beta(2)m defective cells
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 IST REGINA ELENA,I-00161 ROME,ITALY.
UNIV FERRARA,I-44100 FERRARA,ITALY.
DIBIT,HSR,MILAN,ITALY.
NCI,NIH,BETHESDA,MD 20892.
RI Gambari, Roberto/F-9555-2015
OI Gambari, Roberto/0000-0001-9205-6033
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P503
EP P503
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500505
ER
PT J
AU Thomsen, M
Cullen, M
Carrington, M
Foissac, A
Abbal, M
dePreval, C
CrouauRoy, B
CambonThomsen, A
AF Thomsen, M
Cullen, M
Carrington, M
Foissac, A
Abbal, M
dePreval, C
CrouauRoy, B
CambonThomsen, A
TI Localisation of the recombination points in a family with two DR/DP
recombinations
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 CHU PURPAN,INSERM U395,TOULOUSE,FRANCE.
CHU PURPAN,CNRS UPR 8291,TOULOUSE,FRANCE.
CHU RANGUEIL,IMMUNOL LAB,F-31054 TOULOUSE,FRANCE.
NCI,FREDERICK,MD 21701.
RI Thomsen, Mogens/B-7651-2011
OI Thomsen, Mogens/0000-0002-4546-0129
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P359
EP P359
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500361
ER
PT J
AU Wang, ZG
Marincola, FM
Ferrone, S
AF Wang, ZG
Marincola, FM
Ferrone, S
TI Molecular analysis of the selective loss of HLA-A2 antigen expression by
melanoma cells 624MEL28
SO HUMAN IMMUNOLOGY
LA English
DT Meeting Abstract
C1 NEW YORK MED COLL,VALHALLA,NY 10595.
NATL CANC INST,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0198-8859
J9 HUM IMMUNOL
JI Hum. Immunol.
PD APR 15
PY 1996
VL 47
IS 1-2
BP P108
EP P108
PG 1
WC Immunology
SC Immunology
GA UM455
UT WOS:A1996UM45500109
ER
PT J
AU Brousseau, ME
SantamarinaFojo, S
Zech, LA
Berard, AM
Vaisman, BL
Meyn, SM
Powell, D
Brewer, HB
Hoeg, JM
AF Brousseau, ME
SantamarinaFojo, S
Zech, LA
Berard, AM
Vaisman, BL
Meyn, SM
Powell, D
Brewer, HB
Hoeg, JM
TI Hyperalphalipoproteinemia in human lecithin cholesterol acyltransferase
transgenic rabbits - In vivo apolipoprotein A-I catabolism is delayed in
a gene dose-dependent manner
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE high density lipoproteins; lipoproteins; apolipoprotein A-I; metabolism;
cholesterol
ID HIGH-DENSITY-LIPOPROTEIN; ESTER TRANSFER PROTEIN; HEPATIC LIPASE;
PARTICLE-SIZE; PLASMA; METABOLISM; DEFICIENCY; RECEPTOR; KINETICS; LCAT
AB Lecithin cholesterol acyltransferase (LCAT) is an enzyme involved in the intravascular metabolism of high density lipoproteins (HDLs). Overexpression of human LCAT (hLCAT) in transgenic rabbits leads to gene dose-dependent increases of total and HDL cholesterol concentrations. To elucidate the mechanisms responsible for this effect, I-131-HDL apoA-I kinetics were assessed in age- and sex-matched groups of rabbits (n = 3 each) with high, low, or no hLCAT expression. Mean total and HDL cholesterol concentrations (mg/dl), respectively, were 162 +/- 18 and 121 +/- 12 for high expressors (HE), 55 +/- 6 and 55 +/- 10 for low expressors (LE), and 29 +/- 2 and 28 +/- 4 for controls. Fast protein liquid chromatography analysis of plasma revealed that the HDL of both HE and LE were cholesteryl ester and phospholipid enriched, as compared with controls, with the greatest differences noted between HE and controls. These compositional changes resulted in an incremental shift in apparent HDL particle size which correlated directly with the level of hLCAT expression, such that HE had the largest HDL particles and controls the smallest. In vivo kinetic experiments demonstrated that the fractional catabolic rate (FCR, d(-1)) of apoA-I was slowest in HE (0.328 +/-0.03) followed by LE (0.408 +/- 0.01) and, lastly, by controls (0.528 +/- 0.04). ApoA-I FCR was inversely associated with HDL cholesterol level (r = -0.851, P < 0.01) and hLCAT activity (r = -0.816, P < 0.01). These data indicate that fractional catabolic rate is the predominant mechanism by which hLCAT overexpression differentially modulates HDL concentrations in this animal model. We hypothesize that LCAT-induced changes in HDL composition and size ultimately reduce apoA-I catabolism by altering apoA-I conformation and/or HDL particle regeneration.
C1 NHLBI,LAB ANIM MED & SURG,NIH,BETHESDA,MD 20892.
RP Brousseau, ME (reprint author), NHLBI,MOLEC DIS BRANCH,NIH,BLDG 10-ROOM 7N116,10 CTR DR MSC 1666,BETHESDA,MD 20892, USA.
NR 56
TC 37
Z9 37
U1 0
U2 0
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 222 E 70TH STREET, NEW YORK, NY 10021
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD APR 15
PY 1996
VL 97
IS 8
BP 1844
EP 1851
DI 10.1172/JCI118614
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA UG083
UT WOS:A1996UG08300008
PM 8621767
ER
PT J
AU Taub, DD
Anver, M
Oppenheim, JJ
Longo, DL
Murphy, WJ
AF Taub, DD
Anver, M
Oppenheim, JJ
Longo, DL
Murphy, WJ
TI T lymphocyte recruitment by interleukin-8 (IL-8) - IL-8-induced
degranulation of neutrophils releases potent chemoattractants for human
T lymphocytes both in vitro and in vivo
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE chemotaxis; T lymphocytes; neutrophils; granules
ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; PHORBOL MYRISTATE ACETATE; LYSOSOMAL
ENZYME RELEASE; DELAYED-TYPE HYPERSENSITIVITY; HOST DEFENSE CYTOKINES;
INVIVO IMMUNE-RESPONSE; TUMOR-NECROSIS-FACTOR; RED-BLOOD-CELLS;
MESSENGER-RNA; RABBIT SKIN
AB IL-8 has been shown to be a human neutrophil and T cell chemoattractant in vitro. In an effort to assess the in vivo effects of IL-8 on human leukocyte migration, we examined the ability of rhIL-8 to induce human T cell infiltration using a human/mouse model in which SCID mice were administered human peripheral blood lymphocytes intraperitoneally, followed by subcutaneous injections of rhIL-8. rhIL-8 induced predominantly murine neutrophil accumulation by 4 h after administration while recombinant human macrophage inflammatory protein-1 beta (rhMIP-1 beta)induced both murine monocytes and human T cell infiltration during the same time period as determined by immunohistology, Interestingly, 72 h after chemokine administration, a marked human T cell infiltrate was observed in the IL-8 injection site suggesting that rhIL-8 may be acting indirectly possibly through a murine neutrophil-derived T cell chemoattractant, This hypothesis was confirmed using granulecyte-depleted SCID mice. Moreover, human neutrophils stimulated in vitro with IL-8 were found to release granule-derived factor(s) that induce in vitro T cell and monocyte chemotaxis and chemokinesis. This T cell and monocyte chemotactic activity was detected in extracts of both azurophilic and specific granules. Together, these results demonstrate that neutrophils store and release, upon stimulation with IL-8 or other neutrophil activators, chemoattractants that mediate T cell and monocyte accumulation at sites of inflammation.
C1 NCI, FREDERICK CANC RES & DEV CTR, BIOL CARCINOGENESIS & DEV PROGRAM, FREDERICK, MD 21702 USA.
NCI, FREDERICK CANC RES & DEV CTR, PATHOL HISTOTECHNOL LAB, FREDERICK, MD 21702 USA.
NCI, FREDERICK CANC RES & DEV CTR, MOLEC IMMUNOREGULAT LAB, FREDERICK, MD 21702 USA.
NIA, OFF SCI DIRECTOR, BALTIMORE, MD 21224 USA.
RP Taub, DD (reprint author), NCI, FREDERICK CANC RES & DEV CTR,SAIC FREDERICK, CLIN SERV PROGRAM,BLDG 560, RM 11-23, FREDERICK, MD 21702 USA.
NR 59
TC 177
Z9 179
U1 0
U2 3
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD APR 15
PY 1996
VL 97
IS 8
BP 1931
EP 1941
DI 10.1172/JCI118625
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA UG083
UT WOS:A1996UG08300019
PM 8621778
ER
PT J
AU Marples, D
Frokiaer, J
Dorup, J
Knepper, MA
Nielsen, S
AF Marples, D
Frokiaer, J
Dorup, J
Knepper, MA
Nielsen, S
TI Hypokalemia-induced downregulation of aquaporin-2 water channel
expression in rat kidney medulla and cortex
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE aquaporins; water channels; vasopressin; nephrogenic diabetes insipidus;
polyuria
ID INVIVO
AB Prolonged hypokalemia causes vasopressin-resistant polyuria. We have recently shown that another cause of severe polyuria, chronic lithium therapy, is associated with decreased aquaporin-2 (AQP2) water channel expression (Marples, D., S. Christensen, E.I, Christensen, P.D, OttoSen, and S. Nielsen, 1995. J. Clin. Invest., 95: 1838-1845), Consequently, we studied the effect in rats of 11 days' potassium deprivation on urine production and AQP2 expression and distribution, Membrane fractions were prepared from one kidney, while the contralateral kidney was perfusion-fixed for immunocytochemistry. Immunoblotting and densitometry revealed a decrease in AQP2 levels to 27 +/- 3.4% of control levels (n = 11, P < 0.001) in inner medulla, and 34 +/- 15% of controls (n = 5, P < 0.05) in cortex. Urine production increased in parallel, from 11 +/- 1.4 to 30 +/- 4.4 ml/day (n = 11, P < 0.01), After return to a potassium-containing diet both urine output and AQP2 levels normalized within 7 d. Immunocytochemistry confirmed decreased AQP2 labeling in principal cells of both inner medullary and cortical collecting ducts, AQP2 labeling was predominantly associated with the apical plasma membrane and intracellular vesicles. Lithium treatment for 24 d caused a more extensive reduction of AQP2 levels, to 4 +/- 1% of control levels in the inner medulla and 4 +/- 2% in cortex, in association with severe polyuria, The similar degree of downregulation in medulla and cortex suggests that interstitial tonicity is not the major factor in the regulation of AQP2 expression, Consistent with this furosemide treatment did not alter AQP2 levels. In summary, hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level of polyuria induced, supporting the view that there is a causative link.
C1 AARHUS UNIV,INST ANAT,DEPT CELL BIOL,DK-8000 AARHUS,DENMARK.
AARHUS UNIV HOSP,DEPT CLIN PHYSIOL,DK-8000 AARHUS,DENMARK.
AARHUS UNIV,INST EXPTL CLIN RES,DK-8000 AARHUS,DENMARK.
NHLBI,NIH,BETHESDA,MD 20892.
NR 30
TC 190
Z9 191
U1 0
U2 1
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 222 E 70TH STREET, NEW YORK, NY 10021
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD APR 15
PY 1996
VL 97
IS 8
BP 1960
EP 1968
DI 10.1172/JCI118628
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA UG083
UT WOS:A1996UG08300022
PM 8621781
ER
PT J
AU Tsui, CC
Copeland, NG
Gilbert, DJ
Jenkins, NA
Barnes, C
Worley, PF
AF Tsui, CC
Copeland, NG
Gilbert, DJ
Jenkins, NA
Barnes, C
Worley, PF
TI Narp, a novel member of the pentraxin family, promotes neurite outgrowth
and is dynamically regulated by neuronal activity
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE growth factors; immediate-early genes; lectins; long-term potentiation;
neurite outgrowth; pentraxins
ID LONG-TERM POTENTIATION; AMYLOID-P-COMPONENT; C-REACTIVE PROTEIN;
IMMEDIATE-EARLY GENES; FACTOR MESSENGER-RNAS; CONCANAVALIN-A; RAT-BRAIN;
NICOTINIC TRANSMISSION; SELECTIVE EXPRESSION; HIPPOCAMPAL-NEURONS
AB Stimulus-linked RNA and protein synthesis is required for establishment of long-term neuroplasticity. To identify molecular mechanisms underlying long-term neuroplasticity, we have used differential cDNA techniques to clone a novel immediate-early gene (IEG) that is rapidly induced in neurons of the hippocampus and cortex by physiological synaptic activity. Analysis of the deduced amino acid sequence indicates homology to members of the pentraxin family of secreted lectins that include C-reactive protein and serum amyloid P component. Regions of homology include an 8 amino acid ''pentraxin signature'' sequence and a characteristic pentraxin calcium-binding domain. We have termed this gene and the encoded protein Narp (from neuronal activity-regulated pentraxin). Biochemical analyses confirm the presence of a functional signal sequence, and Narp is secreted by transfected COS-1 cells in culture. Additionally, Narp binds to agar matrix in a calcium-dependent manner consistent with the lectin properties of the pentraxin family. When cocultured with Narp-secreting COS-1 cells, neurons of cortical explants exhibit enhanced growth of neuronal dendritic processes. Neurite outgrowth-promoting activity is also observed using partially purified Narp and can be specifically immunodepleted, demonstrating that Narp is the active principle. Narp is fully active at a concentration of similar to 40 ng/ml, indicating a potency similar to known peptide growth factors. Because Narp is rapidly regulated by neuronal activity, its lectin and growth-promoting activities are likely to play role in the modification of cellular properties that underlie long-term plasticity.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205.
UNIV ARIZONA,DEPT PSYCHOL NEUROL,TUCSON,AZ 85724.
UNIV ARIZONA,DIV NEURONAL SYST MEMORY & AGING,TUCSON,AZ 85724.
NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-74101]; NIA NIH HHS [AG09219]; NIMH NIH HHS
[MH53608]
NR 90
TC 186
Z9 192
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 15
PY 1996
VL 16
IS 8
BP 2463
EP 2478
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA UD671
UT WOS:A1996UD67100005
PM 8786423
ER
PT J
AU Gallo, V
Zhou, JM
McBain, CJ
Wright, P
Knutson, PL
Armstrong, RC
AF Gallo, V
Zhou, JM
McBain, CJ
Wright, P
Knutson, PL
Armstrong, RC
TI Oligodendrocyte progenitor cell proliferation and lineage progression
are regulated by glutamate receptor-mediated K+ channel block
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE AMPA receptors; O-2A cells; glia; cell migration; tetraethylammonium;
delayed rectifier K+ channels
ID CENTRAL NERVOUS-SYSTEM; RAT CEREBELLAR CULTURES; EXCITATORY AMINO-ACIDS;
TYPE-2 ASTROCYTES; MACROGLIAL CELLS; DEVELOPMENTAL CLOCK; POTASSIUM
CHANNELS; GLIAL PROGENITORS; NMDA RECEPTORS; GROWTH-FACTOR
AB We have analyzed the role of glutamate and its receptors (GluRs) in regulating the development of oligodendrocytes. Activation of AMPA-preferring GluRs with selective agonists inhibited proliferation of purified cortical oligodendrocyte progenitor (O-2A) cells cultured with different mitogens, as measured by [H-3]thymidine incorporation or bromodeoxyuridine staining. In contrast, activation of GABA or muscarinic receptors did not affect O-2A proliferation. Cell viability and apoptosis assays demonstrated that the inhibition of O-2A proliferation was not attributable to a cytotoxic action of GluR agonists, and was reversible. Activation of GluRs prevented lineage progression from the O-2A (GD3(+)/nestin(+)) stage to the pro-oligodendroblast (O4(+)) stage, but did not affect O-2A migration. Additional experiments examined the membrane ionic channels mediating these GlUR activation effects. We found that proliferating O-2A cells expressed functional delayed rectifier K+ channels, which were absent in pro-oligodendroblasts. GluR agonists and the K+ channel blocker tetraethylammonium (TEA) strongly inhibited delayed rectifier K+ currents in O-2A cells. TEA reproduced the effects of GluR activation on O-2A proliferation and lineage progression in the same concentration range that blocked delayed rectifier K+ currents. These results indicate that glutamate regulates oligodendrogenesis specifically at the O-2A stage by modulating K+ channel activity.
C1 UNIFORMED SERV UNIV HLTH SCI,DEPT ANAT & CELL BIOL,BETHESDA,MD 20814.
RP Gallo, V (reprint author), NICHHD,NATL INST HLTH,LAB CELLULAR & MOL NEUROPHYSIOL,BLDG 49,ROOM 5A78,BETHESDA,MD 20892, USA.
RI Messier, Claude/A-2322-2008
OI Messier, Claude/0000-0002-4791-1763
FU NCI NIH HHS [R070CB]
NR 70
TC 266
Z9 267
U1 2
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 15
PY 1996
VL 16
IS 8
BP 2659
EP 2670
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA UD671
UT WOS:A1996UD67100024
PM 8786442
ER
PT J
AU Sadato, N
Campbell, G
Ibanez, V
Deiber, MP
Hallett, M
AF Sadato, N
Campbell, G
Ibanez, V
Deiber, MP
Hallett, M
TI Complexity affects regional cerebral blood flow change during sequential
finger movements
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE regional cerebral blood flow; sequential finger movements; positron
emission tomography; sensorimotor cortex; premotor cortex; supplementary
motor area
ID POSITRON EMISSION TOMOGRAPHY; SUPPLEMENTARY MOTOR AREA;
NEURONAL-ACTIVITY; PREMOTOR CORTEX; CORTICOSPINAL PROJECTIONS;
WORKING-MEMORY; CORTICAL AREAS; FRONTAL-LOBE; PET IMAGES; MONKEY
AB Brain regions activated with complex sequential finger movements were localized by measuring regional cerebral blood flow (rCBF) with positron emission tomography. Whereas the total number and frequency of finger movements were kept constant, the complexity of auditory cued sequential finger movements of the right hand varied, with sequence length as the independent variable. In four conditions of differing complexity, the bilateral primary sensorimotor area, left ventral premotor cortex, posterior supplementary motor area, right superior part of the cerebellum, and left putamen were consistently and equally activated. This finding suggests an executive role in running sequences, regardless of their length. The right dorsal premotor cortex (Brodmann area 6) and the right precuneus (Brodmann area 7) showed a linear increase of rcBF as sequence complexity increased. This finding is consistent with the hypothesis that these areas function in the storage of motor sequences in spatial working memory and the production of ongoing sequential movement with reference to that of buffered memory. A similar increase in the cerebellar vermis and the left thalamus likewise suggests a role of these subcortical structures in complexity of sequential finger movements. Conversely, the left inferior parietal lobule showed a decrease of rCBF as complexity increased. Because short-term phonological storage is localized to this area, we suggest that the visuospatial working memory system may suppress other systems not in use. Our findings suggest that complex sequential finger movements recruit a discrete set of brain areas, in addition to areas underlying the execution of simple movement sequences.
C1 NINDS,NIH,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,BETHESDA,MD 20892.
NINDS,NIH,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892.
RI Deiber, Marie-Pierre/M-5949-2014
NR 67
TC 76
Z9 78
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 15
PY 1996
VL 16
IS 8
BP 2693
EP 2700
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA UD671
UT WOS:A1996UD67100027
ER
PT J
AU Su, XZ
Wu, YM
Sifri, CD
Wellems, TE
AF Su, XZ
Wu, YM
Sifri, CD
Wellems, TE
TI Reduced extension temperatures required for PCR amplification of
extremely A+T-rich DNA
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID PLASMODIUM-FALCIPARUM; SEQUENCE; GENERATION; GENOME
C1 NIAID,NIH,PARASIT DIS LAB,BETHESDA,MD 20892.
OI Su, Xinzhuan/0000-0003-3246-3248
NR 17
TC 74
Z9 76
U1 1
U2 10
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR 15
PY 1996
VL 24
IS 8
BP 1574
EP 1575
DI 10.1093/nar/24.8.1574
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UH370
UT WOS:A1996UH37000026
PM 8628694
ER
PT J
AU Hjalmars, U
Kulldorff, M
Gustafsson, G
Nagarwalla, N
AF Hjalmars, U
Kulldorff, M
Gustafsson, G
Nagarwalla, N
TI Childhood leukaemia in Sweden: Using GIS and a spatial scan-statistic
for cluster detection
SO STATISTICS IN MEDICINE
LA English
DT Article; Proceedings Paper
CT Conference on Statistics and Computing in Disease Clustering
CY JUL 21-22, 1994
CL UNIV BRITISH COLUMBIA, VANCOUVER, CANADA
SP BioMedware, Elect Power Res Inst, Natl Canc Inst
HO UNIV BRITISH COLUMBIA
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; BRITAIN; POWER
AB The study of disease clustering is becoming increasingly common in the field of medical epidemiology. There is great public concern and numerous reports on perceived clusters of various diseases, with cancers, and especially leukaemia, being the most commonly studied. We present a population based study on acute childhood leukaemia in Sweden 1973-1993, illustrating the possibility of a system for full-scale spatial epidemiological study design. The aim of the study is to test a large set of childhood leukaemia cases for the presence of geographical clusters. Necessary prerequisites, in the form of extensive population and disease data, a tool for geographical spatial analysis and a proper statistical method were fulfilled. No significant clusters were found.
C1 NCI,BIOMETRY BRANCH,DCPC,BETHESDA,MD 20892.
UNIV UPPSALA,DEPT STAT,S-75120 UPPSALA,SWEDEN.
KAROLINSKA INST,REG ONCOL CTR,S-10401 STOCKHOLM,SWEDEN.
HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,BOSTON,MA 02115.
HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115.
RP Hjalmars, U (reprint author), OSTERSUND CENT HOSP,DEPT PAEDIAT,S-83183 OSTERSUND,SWEDEN.
RI Kulldorff, Martin/H-4282-2011;
OI Kulldorff, Martin/0000-0002-5284-2993
NR 26
TC 86
Z9 89
U1 2
U2 9
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD APR 15
PY 1996
VL 15
IS 7-9
BP 707
EP 715
DI 10.1002/(SICI)1097-0258(19960415)15:7/9<707::AID-SIM242>3.3.CO;2-W
PG 9
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA UG357
UT WOS:A1996UG35700004
PM 9132898
ER
PT J
AU Melnick, RL
Elwell, MR
Roycroft, JH
Chou, BJ
Ragan, HA
Miller, RA
AF Melnick, RL
Elwell, MR
Roycroft, JH
Chou, BJ
Ragan, HA
Miller, RA
TI Toxicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344 rats
and B6C3F(1) mice
SO TOXICOLOGY
LA English
DT Article
DE chloroprene; butadiene; inhalation toxicology; hepatocellular necrosis;
anemia; olfactory epithelial degeneration
ID INHALATION EXPOSURE; 1,3-BUTADIENE; CARCINOGENICITY; TOXICOLOGY;
ISOPRENE; TISSUE; RODENT
AB Chloroprene (2-chloro-1,3-butadiene) is a high production chemical used almost exclusively in the production of polychloroprene (neoprene) elastomer. Because of its structural similarity to isoprene (2-methyl-1,3-butadiene) and to 1,3-butadiene, a potent trans-species carcinogen, inhalation studies were performed on chloroprene to characterize its toxicological potential and to provide a basis for selecting exposure concentrations for chronic toxicity and carcinogenicity studies. Thirteen-week inhalation toxicology studies were conducted in male and female F344 rats and B6C3F(1) mice at exposure concentrations of 0, 5, 12, 32 or 80 ppm (6 h/day; 5 days/week). A 200 ppm exposure group was also included for rats only, because a previous study showed that this concentration of chloroprene is lethal to mice. In mice, exposure to 80 ppm chloroprene caused a marginal decrease in body weight gain in males and epithelial hyperplasia of the forestomach in males and females. This lesion has been observed in mice exposed to isoprene or 1,3-butadiene. In rats, exposure to 80 ppm chloroprene or higher concentrations caused degeneration and metaplasia of the olfactory epithelium and exposure to 200 ppm caused anemia, hepatocellular necrosis and reduced sperm motility. These lesions have not been observed in rats exposed to isoprene or 1,3-butadiene. The profile of toxic effects of chloroprene is considerably different from that of isoprene or 1,3-butadiene; this may be due to differences in exposure concentrations that were used in toxicology studies of these compounds and/or to the influence of the chlorine substitution on the toxicokinetics of these compounds, on their biotransformation, or on the reactivity of metabolic intermediates with tissue macromolecules.
C1 NIEHS, RES TRIANGLE PK, NC 27709 USA.
PACIFIC NW LAB, RICHLAND, WA 99352 USA.
NR 36
TC 14
Z9 14
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD APR 15
PY 1996
VL 108
IS 1-2
BP 79
EP 91
DI 10.1016/0300-483X(95)03286-O
PG 13
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA UC593
UT WOS:A1996UC59300011
PM 8644121
ER
PT J
AU Vowells, SJ
Fleisher, TA
Malech, HL
AF Vowells, SJ
Fleisher, TA
Malech, HL
TI Testing for chronic granulomatous disease
SO LANCET
LA English
DT Letter
RP Vowells, SJ (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 3
TC 18
Z9 19
U1 0
U2 2
PU LANCET LTD
PI LONDON
PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL
SN 0140-6736
J9 LANCET
JI Lancet
PD APR 13
PY 1996
VL 347
IS 9007
BP 1048
EP 1049
DI 10.1016/S0140-6736(96)90189-0
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA UF380
UT WOS:A1996UF38000060
PM 8606593
ER
PT J
AU Lee, MD
Bhakta, KY
Raina, S
Yonescu, R
Griffin, CA
Copeland, NG
Gilbert, DJ
Jenkins, NA
Preston, GM
Agre, P
AF Lee, MD
Bhakta, KY
Raina, S
Yonescu, R
Griffin, CA
Copeland, NG
Gilbert, DJ
Jenkins, NA
Preston, GM
Agre, P
TI The human aquaporin-5 gene - Molecular characterization and chromosomal
localization
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RNA POLYMERASE-II; WATER CHANNEL; DNA-SEQUENCES; LINKAGE MAP;
RAT-KIDNEY; TRANSCRIPTION; INITIATOR; ORGANIZATION; ELEMENTS; CLONING
AB The cDNA for the fifth mammalian aquaporin (AQP5) was isolated from rat, and expression was demonstrated in rat salivary and lacrimal glands, cornea, and lung (Raina, S., Preston, G. M., Guggino, W. B., and Agre, P. (1995) J. Biol. Chem. 270, 1908-1912). Here we report the isolation and characterization of the human AQP5 cDNA and gene. The AQP5 cDNA from a human submaxillary gland library contains a 795-base pair open reading frame encoding a 265-amino acid protein. The deduced amino acid sequences of human and rat AQP5 are 91% identical with 6 substitutions in the 22-amino acid COOH-terminal domain. Expression of human AQP5 in Xenopus oocytes conferred mercurial-sensitive osmotic water permeability (Pf) equivalent to other aquaporins. The human AQP5 structural gene resides within a 7.4-kilobase SalI-EcoRI fragment with four exons corresponding to amino acids 1-121, 122-176, 177-204, and 205-265 separated by introns of 1.2, 0.5, and 0.9 kilobases. A transcription initiation site was identified 518 base pairs upstream of the initiating methionine. Genomic Southern analysis indicated that AQP5 is a single copy gene which localized to human chromosome 12q13; this coincides with the chromosomal locations of the homologous human genes MIP and AQP2, thus confirming 12q13 as the site of an aquaporin gene cluster. The mouse gene localized to distal chromosome 15. This information may permit molecular characterization of AQP5 expression during normal development and in clinical disorders.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV PULM & CRIT CARE MED,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205.
NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,NIH,FREDERICK,MD 21702.
FU NEI NIH HHS [EY11239]; NHLBI NIH HHS [HL33991, HL48268]
NR 43
TC 60
Z9 63
U1 1
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8599
EP 8604
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000020
PM 8621489
ER
PT J
AU Ahmed, SA
McPhie, P
Miles, EW
AF Ahmed, SA
McPhie, P
Miles, EW
TI A thermally induced reversible conformational transition of the
tryptophan synthase beta(2) subunit probed by the spectroscopic
properties of pyridoxal phosphate and by enzymatic activity
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; L-SERINE; 5'-PHOSPHATE; ALPHA;
SYNTHETASE; MECHANISM; SPECTRA; INDOLE; BASES
AB A reversible thermally induced conformational transition of the beta(2) subunit of tryptophan synthase from Salmonella typhimurium has been detected by use of the pyridoxal 5'-phosphate coenzyme as a spectroscopic probe. Increasing the temperature converts the major form of pyridoxal 5'-phosphate bound to the beta(2) subunit from a ketoenamine species with lambda(max) at 410 nm to a enolimine species with lambda(max) at 336 nm (T-m = similar to 43 degrees C) and results in loss of the circular dichroism signal at 410 nm and of fluorescence emission at 510 nm, The results indicate that increasing the temperature favors a conformer of the enzyme that binds pyridoxal 5'-phosphate in a more nonpolar environment and leads to loss of asymmetric pyridoxal 5'-phosphate binding. The internal aldimine between pyridoxal 5'-phosphate and the E-amino group of lysine 87 is not disrupted by increased temperature because sodium borohydride treatment of the enzyme at either 15 or 60 degrees C results in covalent attachment of [4'-H-3]pyridoxal 5'-phosphate. The thermal transition of the beta(2) subunit below 60 degrees C produces reversible thermal inactivation (T-i = similar to 52 degrees C) and occurs at a much lower temperature than the major reversible unfolding at similar to 80 degrees C (Remeta, D. P., Miles, E. W., and Ginsburg, A. (1995) Pure Appl. Chem. 67, 1859-1866). Our new results indicate that the 410 nm absorbing species of pyridoxal 5'-phosphate is the catalytically active form of the cofactor in the beta(2) subunit and that the low temperature reversible conformational transition disturbs the active site and causes loss of catalytic activity.
C1 NIDDKD, BIOCHEM PHARMACOL LAB, NIH, BETHESDA, MD 20892 USA.
NR 32
TC 9
Z9 9
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8612
EP 8617
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000022
PM 8621491
ER
PT J
AU Cenciarelli, C
Wilhelm, KG
Guo, A
Weissman, AM
AF Cenciarelli, C
Wilhelm, KG
Guo, A
Weissman, AM
TI T cell antigen receptor ubiquitination is a consequence of
receptor-mediated tyrosine kinase activation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FACTOR BETA-RECEPTOR; SIGNAL TRANSDUCTION; ZETA-CHAIN; LYMPHOCYTES-T;
PHOSPHORYLATION; COMPLEX; PATHWAY; CD45; INHIBITOR; INVITRO
AB Engagement of the T cell antigen receptor results in both its phosphorylation and its ubiquitination. T cell antigen receptor ubiquitination was evaluated in Jurkat, a well characterized human T leukemia cell line. Treatment of cells with the tyrosine kinase inhibitor herbimycin A resulted in an inhibition of receptor ubiquitination, Consistent with this, pervanadate, which increases cellular tyrosine phosphorylation, enhanced receptor ubiquitination, A requirement for receptor-mediated tyrosine kinase activity for ubiquitination was confirmed in cells lacking the tyrosine kinase p56(lck) and also in cells that are defective in expression of CD45, a tyrosine phosphatase that regulates the activity of p56(lck). The need for tyrosine kinase activation for ubiquitination was not bypassed by directly activating protein kinase C and stimulating endocytosis of receptors. These observations establish ubiquitination of the T cell antigen receptor as a tyrosine kinase-dependent manifestation of transmembrane signaling and suggest a role for tyrosine phosphorylation in the ligand-dependent ubiquitination of mammalian transmembrane receptors.
C1 NCI,NIH,DIV BASIC SCI,LAB IMMUNE CELL BIOL,BETHESDA,MD 20892.
NR 54
TC 71
Z9 71
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8709
EP 8713
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000034
PM 8621503
ER
PT J
AU Liu, J
Wess, J
AF Liu, J
Wess, J
TI Different single receptor domains determine the distinct G protein
coupling profiles of members of the vasopressin receptor family
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID 3',5'-CYCLIC ADENOSINE-MONOPHOSPHATE; BETA-ADRENERGIC RECEPTORS;
MOLECULAR-CLONING; MUSCARINIC RECEPTOR; BINDING PROTEINS; EXPRESSION;
SIGNAL; GENES; RAT; IDENTIFICATION
AB The vasopressin receptor family is unique among all classes of peptide receptors in that its individual members couple to different subsets of G proteins. The V-1n vasopressin receptor, for example, is preferentially linked to G proteins of the G(q/11) class (biochemical response: stimulation of phosphatidylinositol hydrolysis), whereas the V-2 vasopressin receptor is selectively coupled to G(s) (biochemical response: stimulation of adenylyl cyclase). To elucidate the structural basis underlying this functional heterogeneity, we have systematically exchanged different intracellular domains between the V-1a and V-2 receptors. Transient expression of the resulting hybrid receptors in COS-7 cells showed that all mutant receptors containing V-1a receptor sequence in the second intracellular loop were able to activate the phosphatidylinositol pathway with high efficiency. On the other hand, only those hybrid receptors containing V-2 receptor sequence in the third intracellular loop were capable of efficiently stimulating cAMP production. These findings suggest that the differential G protein coupling profiles of individual members of a structurally closely related receptor subfamily can be determined by different single intracellular receptor domains.
C1 NIDDK, NIH, BIOORGAN CHEM LAB, BETHESDA, MD 20892 USA.
NR 53
TC 111
Z9 111
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8772
EP 8778
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000044
PM 8621513
ER
PT J
AU Toyoshige, M
Basi, NS
Rebois, RV
AF Toyoshige, M
Basi, NS
Rebois, RV
TI Chloride effects on G(s) subunit dissociation - Fluoroaluminate binding
to G(s) does not cause subunit dissociation in the absence of chloride
ion
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ADENYLATE-CYCLASE; REGULATORY COMPONENT; G-PROTEINS;
CONFORMATIONAL-CHANGES; GUANINE-NUCLEOTIDES; ALPHA-SUBUNIT; RECEPTOR;
PURIFICATION
AB The stimulatory guanine nucleotide binding protein (G(s)) is heterotrimeric (alpha beta gamma), and mediates activation of adenylyl cyclase by a ligand-receptor complex. The cu subunit of G(s) (G(s) alpha) has a guanine nucleotide binding site, and activation occurs when tightly bound GDP is displaced by GTP. Together, GDP and fluoroaluminate (AlF4-) form a transition state analog of GTP that activates G(s). The work of other investigators suggests that AlF4- causes subunit dissociation when it activates G(s). We have observed that in solution AlF4- did not cause G(s) subunits to dissociate unless NaCl was also present. The effect of NaCl was concentration dependent (10-200 mM). Omitting F-, Al3+, or Mg2+ prevented the NaCl-induced dissociation of G(s) subunits. Na2SO4 could not substitute for NaCl in causing subunit dissociation, but KCl could, suggesting that the anion was responsible for the effect. G(s) subunit reassociation occurred when the concentration of Cl- was reduced even though the concentrations of AlF4- and Mg2+ were maintained. The absence of Cl- did not prevent AlF4- binding to G(s) alpha. We have concluded that AlF4- a ligand which is capable of activating G proteins, can bind to G(s) in solution without causing subunit dissociation.
C1 NINCDS,NIH,MEMBRANE BIOCHEM SECT,LAB MOL & CELLULAR NEUROBIOL,BETHESDA,MD 20892.
NR 29
TC 14
Z9 14
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8791
EP 8795
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000047
PM 8621516
ER
PT J
AU Najjar, SM
Boisclair, YR
Nabih, ZT
Phillippe, N
Imai, Y
Suzuki, Y
Suh, DS
Ooi, GT
AF Najjar, SM
Boisclair, YR
Nabih, ZT
Phillippe, N
Imai, Y
Suzuki, Y
Suh, DS
Ooi, GT
TI Cloning and characterization of a functional promoter of the rat pp120
gene, encoding a substrate of the insulin receptor tyrosine kinase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MEMBRANE ECTO-ATPASE; LIVER-SPECIFIC GENES; RNA POLYMERASE-II;
ENDOGENOUS SUBSTRATE; TRANSCRIPTION FACTOR; GROWTH-FACTOR;
CARCINOEMBRYONIC ANTIGEN; ADHESION MOLECULE; PROTEIN-KINASE; LESS
PROMOTER
AB Cloning of the 5'-flanking region of the rat pp120 gene has indicated that it is a housekeeping gene: it lacks a functional TATA bog and contains several Spl binding sites and multiple transcription initiation sites at nucleotides -101, -71, -41, and -27 spread over a GC-rich area, A fragment between nucleotides -21 and -1609 exhibited promoter activity when ligated in a sense orientation into a promoterless luciferase reporter plasmid and transiently transfected into rat H4-II-E hepatoma cells, 5' progressive deletion and block substitution analyses revealed that the three proximal Spl boxes (boxes 3, 5, and 6) are required for basal transcription of the pp120 gene. Promoter activity was stimulated 2-3-fold in response to insulin, dexamethasone, insulin plus dexamethasone, and cAMP. Although unaltered by phorbol esters alone, promoter activity was stimulated 4-5-fold in response to phorbol esters plus cAMP. Several motifs resembling response elements for insulin (in the rat phosphoenolpyruvate carboxykinase gene), glucocorticoids, cAMP, and phorbol esters as well as a number of putative binding sites for activating proteins-1 (Jun/Fos) and -2, and liver-specific factors were detected, The role of these sites in tissue-specific expression of pp120 remains to be investigated.
C1 NIDDK,NIH,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892.
CORNELL UNIV,DEPT ANIM SCI,ITHACA,NY 14853.
RP Najjar, SM (reprint author), MED COLL OHIO,DEPT PHARMACOL & THERAPEUT,HLTH SCI BLDG,RM 270,TOLEDO,OH 43614, USA.
NR 55
TC 22
Z9 22
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8809
EP 8817
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000050
PM 8621519
ER
PT J
AU Saito, H
Oka, T
AF Saito, H
Oka, T
TI Hormonally regulated double- and single-stranded DNA-binding complexes
involved in mouse beta-casein gene transcription
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MAMMARY EPITHELIAL-CELLS; MULTIGENE FAMILY; NUCLEAR FACTOR;
FINE-STRUCTURE; PROTEINS; GROWTH; PROMOTER; IDENTIFICATION; EXPRESSION;
INDUCTION
AB Transcription of the 252-base pair-long mouse beta-casein gene promoter is induced by the synergistic action of insulin, prolactin, and glucocorticoid in a primary mammary epithelial cell culture, The promoter contains a region termed block C having a highly conserved sequence and position among many casein genes, Mutation of block C reduced the response of the promoter to lactogenic hormones 84%. Nuclear extracts from lactating mouse mammary glands contained both a double-stranded and a single-stranded DNA binding protein complex (DS1 and SS), which specifically bind to the sequences AAATTAGCATGT and CCACAA of block C, respectively, The DS1 and the SS protein complexes were approximately 400 and 280 kDa, respectively, Each complex contained a DNA-binding component(s) having a molecular mass of approximately 120 kDa for DS1 and 80 and 65 kDa for SS, Deoxycholate, which interferes with the protein-protein interactions, inhibited the binding activities of DS1 and SS, The maximal increase in the binding activity of DS1 and SS in the mammary gland occurred during pregnancy and during lactation, respectively. In organ culture, the DSI activity is increased by epidermal growth factor or prolactin in combination with insulin, whereas the SS activity is enhanced by insulin, prolactin, and glucocorticoid, These results suggest that multiprotein complexes binding to the double- and single-stranded DNA of block C mediate hormonal induction of beta-casein gene transcription.
C1 NIDDK,LMCB,BETHESDA,MD 20892.
NR 38
TC 25
Z9 26
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 12
PY 1996
VL 271
IS 15
BP 8911
EP 8918
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE730
UT WOS:A1996UE73000065
PM 8621534
ER
PT J
AU Driscoll, JS
Siddiqui, MA
Ford, H
Kelley, JA
Roth, JS
Mitsuya, H
Tanaka, M
Marquez, VE
AF Driscoll, JS
Siddiqui, MA
Ford, H
Kelley, JA
Roth, JS
Mitsuya, H
Tanaka, M
Marquez, VE
TI Lipophilic, acid-stable, adenosine deaminase-activated anti-HIV prodrugs
for central nervous system delivery .3. 6-Amino prodrugs of
2'-beta-fluoro-2',3'-dideoxyinosine
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID NUCLEOSIDES; INFECTION; 2',3'-DIDEOXYADENOSINE; THERAPY; ANALOGS; AGENTS
AB A series of 6-substituted amino analogs of 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl) purines (F-ddN) has been synthesized and characterized with the objective of finding compounds which might be superior to existing chugs for the treatment of HIV in the central nervous system. These compounds are intended to be more lipophilic than the currently approved anti-HIV drugs for better blood-brain barrier penetration. Subsequent adenosine deaminase (ADA)-catalyzed hydrolysis of these prodrugs in the brain is expected to produce the anti-HIV agent, 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl)hypoxanthine (F-ddI). The new compounds, synthesized from the corresponding 6-chloro analog, include F-ddN which contain methylamino, ethylamino, dimethylamino, hydroxylamino, methoxyamino, benzyloxyamino, hydrazino, and nitro substituents in the 6-position. The 6-nitro analog was isolated as an unexpected product during the preparation of the 6-chloro derivative. Among the analogs with anti-HIV activity, the ethylamino and dimethylamino compounds are ca. 100 times more Lipophilic than ddI or F-ddI. As expected, 2'-fluoro substitution protects the compounds from acid-catalyzed glycosylic cleavage. Only the hydroxylamino and nitro analogs underwent any nonenzymatic hydrolysis at pH 1.0 or 7.4. This reaction, however, results in hydrolysis of the group in the 6-position rather than glycosylic bond cleavage. ADA catalyzes the hydrolysis of the 6-substituents at rates which vary from slightly slower (NO2, 1.7x) to much slower (NHEt, 5000 x) than F-ddA. The 6-dimethylamino analog is the only compound which possesses anti-HIV activity (ED(50) is mu M) without ADA hydrolysis. With the exception of the two inactive alkoxyamino compounds, the other prodrugs exhibited cellular protection in the HIV-1/PHA-PBM system with IC50 potencies of 7-40 mu M.
C1 NCI, NIH, DIV CLIN SCI, EXPTL RETROVIROL SECT, BETHESDA, MD 20892 USA.
RP Driscoll, JS (reprint author), NCI, NIH, DIV BASIC SCI, MED CHEM LAB, BETHESDA, MD 20892 USA.
NR 41
TC 20
Z9 21
U1 1
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD APR 12
PY 1996
VL 39
IS 8
BP 1619
EP 1625
DI 10.1021/jm9509197
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA UE818
UT WOS:A1996UE81800007
PM 8648601
ER
PT J
AU Gussio, R
Pattabiraman, N
Zaharevitz, DW
Kellogg, GE
Topol, IA
Rice, WG
Schaeffer, CA
Erickson, JW
Burt, SK
AF Gussio, R
Pattabiraman, N
Zaharevitz, DW
Kellogg, GE
Topol, IA
Rice, WG
Schaeffer, CA
Erickson, JW
Burt, SK
TI All-atom models for the non-nucleoside binding site of HIV-1 reverse
transcriptase complexed with inhibitors: A 3D QSAR approach
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; NONNUCLEOSIDE INHIBITORS; ANTIVIRAL
ACTIVITY; REPLICATION; DERIVATIVES; NEVIRAPINE; ZIDOVUDINE; INVITRO;
POTENT; SERIES
AB Several molecular modeling techniques were used to generate an all-atom molecular model of a receptor binding site starting only from Ca atom coordinates. The model consists of 48 noncontiguous residues of the non-nucleoside binding site of HIV-1 reverse transcriptase and was generated using a congeneric series of nevirapine analogs as structural probes. On the basis of the receptor-ligand atom contacts, the program HINT was used to develop a 3D quantitative structure activity relationship that predicted the rank order of binding affinities for the series of inhibitors. Electronic profiles of the ligands in their docked conformations were characterized using electrostatic potential maps and frontier orbital calculations. These results led to the development of a 3D stereoelectronic pharmacophore which was used to construct 3D queries for database searches. A search of the National Cancer Institute's open database identified a lead compound that exhibited moderate antiviral activity.
C1 SAIC FREDERICK,NCI,FREDERICK CANC RES & DEV CTR,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702.
SAIC FREDERICK,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702.
VIRGINIA COMMONWEALTH UNIV,SCH PHARM,DEPT MED CHEM,RICHMOND,VA 23298.
RI Kellogg, Glen/A-8008-2011
NR 37
TC 50
Z9 51
U1 1
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 APR 12
PY 1996
VL 39
IS 8
BP 1645
EP 1650
DI 10.1021/jm9508088
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA UE818
UT WOS:A1996UE81800010
PM 8648604
ER
PT J
AU Drgonova, J
Drgon, T
Tanaka, K
Kollar, R
Chen, GC
Ford, RA
Chan, CSM
Takai, Y
Cabib, E
AF Drgonova, J
Drgon, T
Tanaka, K
Kollar, R
Chen, GC
Ford, RA
Chan, CSM
Takai, Y
Cabib, E
TI Rho1p, a yeast protein at the interface between cell polarization and
morphogenesis
SO SCIENCE
LA English
DT Article
ID RAS SUPERFAMILY GENES; SACCHAROMYCES-CEREVISIAE; BETA-(1->3)GLUCAN
SYNTHETASE; WALL; BIOSYNTHESIS; GROWTH; DEFECT; GTP
AB The enzyme that catalyzes the synthesis of the major structural component of the yeast cell wall, beta(1-->3)-D-glucan synthase (also known as 1,3-beta-glucan synthase), requires a guanosine triphosphate (GTP) binding protein for activity. The GTP binding protein was identified as Rho1p. The rho1 mutants were defective in GTP stimulation of glucan synthase, and the defect was corrected by addition of purified or recombinant Rho1p. A protein missing in purified preparations from a rho1 strain was identified as Rho1p. Rho1p also regulates protein kinase C, which controls a mitogen-activated protein kinase cascade. Experiments with a dominant positive PKC1 gene showed that the two effects of Rho1p are independent of each other. The colocalization of Rho1p with actin patches at the site of bud emergence and the role of Rho1p in cell wall synthesis emphasize the importance of Rho1p in polarized growth and morphogenesis.
C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892.
OSAKA UNIV,SCH MED,DEPT MOLEC BIOL & BIOCHEM,SUITA,OSAKA 565,JAPAN.
UNIV TEXAS,DEPT MICROBIOL,AUSTIN,TX 78712.
RI Drgonova, Jana/B-2903-2008;
OI Drgonova, Jana/0000-0002-4623-8466
NR 24
TC 275
Z9 279
U1 0
U2 5
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD APR 12
PY 1996
VL 272
IS 5259
BP 277
EP 279
DI 10.1126/science.272.5259.277
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UE729
UT WOS:A1996UE72900044
PM 8602514
ER
PT J
AU Sadato, N
PascualLeone, A
Grafman, J
Ibanez, V
Deiber, MP
Dold, G
Hallett, M
AF Sadato, N
PascualLeone, A
Grafman, J
Ibanez, V
Deiber, MP
Dold, G
Hallett, M
TI Activation of the primary visual cortex by Braille reading in blind
subjects
SO NATURE
LA English
DT Article
ID MONKEY; MACAQUE
AB PRIMARY visual cortex receives visual input from the eyes through the lateral geniculate nuclei, but is not known to receive input from other sensory modalities'. Its level of activity, both at rest and during auditory or tactile tasks, is higher in blind subjects than in normal controls(2), suggesting that it can subserve nonvisual functions; however, a direct effect of non-visual tasks on activation has not been demonstrated(2-4). To determine whether the visual cortex receives input from the somatosensory system(5-8), we used positron emission tomography (PET) to measure activation during tactile discrimination tasks in normal subjects and in Braille readers blinded in early life. Blind subjects showed activation of primary and secondary visual cortical areas during tactile tasks, whereas normal controls showed deactivation, A simple tactile stimulus that did not require discrimination produced no activation of visual areas in either group. Thus, in blind subjects, cortical areas normally reserved for vision may be activated by other sensory modalities.
C1 NINCDS,HUMAN MOTOR CONTROL SECT,NIH,BETHESDA,MD 20892.
NINCDS,COGNIT NEUROSCI SECT,MED NEUROL BRANCH,NIH,BETHESDA,MD 20892.
FUKUI MED SCH,BIOMED IMAGING RES CTR,MATUOKA,FUKUI 91011,JAPAN.
RI Deiber, Marie-Pierre/M-5949-2014;
OI Grafman, Jordan H./0000-0001-8645-4457
NR 24
TC 624
Z9 632
U1 5
U2 54
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF
SN 0028-0836
J9 NATURE
JI Nature
PD APR 11
PY 1996
VL 380
IS 6574
BP 526
EP 528
DI 10.1038/380526a0
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UE663
UT WOS:A1996UE66300049
PM 8606771
ER
PT J
AU Kirschstein, RL
AF Kirschstein, RL
TI Women physicians - Good news and bad news
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
RP Kirschstein, RL (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 8
TC 4
Z9 4
U1 0
U2 0
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 11
PY 1996
VL 334
IS 15
BP 982
EP 983
DI 10.1056/NEJM199604113341510
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA UD596
UT WOS:A1996UD59600010
ER
PT J
AU Mireskandari, A
Reid, RL
Kashanchi, F
Dittmer, J
Li, WB
Brady, JN
AF Mireskandari, A
Reid, RL
Kashanchi, F
Dittmer, J
Li, WB
Brady, JN
TI Isolation of a cDNA clone, TRX, encoding a human T-cell lymphotrophic
virus type-I Tax(1) binding protein
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
LA English
DT Article
DE HTLV-1 Tax(1); Tax(1) binding protein
ID TRANSCRIPTIONAL ACTIVATOR TAX; HTLV-I; REGULATORY ELEMENTS;
TRANSACTIVATION; MYELOPATHY; SEQUENCES; PROMOTER; ENHANCER; REPEATS;
BLOOD
AB Tax, is essential for human T-cell lymphotropic virus type I (HTLV-I) virus replication and transformation. We have identified and characterized a Tax(1) binding protein, TRX, by cDNA screening of a Jurkat T-cell cDNA library. TRX mRNA is ubiquitously expressed in human tissues tested and cell lines analyzed.
C1 NCI,MOLEC VIROL LAB,NIH,BETHESDA,MD 20892.
US FDA,ONCOL BRANCH,DIB CLIN TRIAL DESIGN & ANAL,CTR BIOL & RES,ROCKVILLE,MD 20852.
LIFE TECHNOL,GAITHERSBURG,MD.
RI Dittmer, Juergen/G-1160-2011
NR 19
TC 8
Z9 9
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-4781
J9 BBA-GENE STRUCT EXPR
JI Biochim. Biophys. Acta-Gene Struct. Expression
PD APR 10
PY 1996
VL 1306
IS 1
BP 9
EP 13
DI 10.1016/0167-4781(96)00012-7
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UF670
UT WOS:A1996UF67000003
PM 8611628
ER
PT J
AU Fisher, GH
Lenardo, MJ
ZunigaPflucker, JC
AF Fisher, GH
Lenardo, MJ
ZunigaPflucker, JC
TI Synergy between T cell receptor and Fas (CD95/APO-1) signaling in mouse
thymocyte death
SO CELLULAR IMMUNOLOGY
LA English
DT Article
ID CLONAL DELETION; MONOCLONAL-ANTIBODIES; IMMATURE THYMOCYTES; NEGATIVE
SELECTION; CD4+8+ THYMOCYTES; AUTOIMMUNE MICE; LYMPHOCYTES-T;
EXPRESSION; ANTIGEN; APOPTOSIS
AB Administration of anti-TCR/CD3 epsilon antibody in vivo or in thymic organ culture results in the apoptotic death of CD4(+)/CD8(+) thymocytes. In contrast, purified thymocytes in suspension culture are resistant to TCR/CD3 epsilon-induced apoptotic death. We show that induction of thymocyte death, in suspension culture, can be induced by the combination of TCR/CD3 epsilon and Fas (CD95/Apo-1) signaling. No significant thymocyte death was observed after in vitro Fas cross-linking unless TCR/CD3 epsilon was simultaneously co-cross-linked or metabolic inhibitors such as actinomycin D were added. Furthermore, TCR/CD3 epsilon and Fas synergy did not operate through upregulation of Fas but by facilitation of the Fas-mediated death signal. Both TCR(mid/lo)/HSA(hi)/CD4(+)/CD8(+) (double positive) and TCR(hi)/HSA(lo)/CD4(+)/CD8(-) or CD4(-)/CD8(+) (single positive) thymocytes were susceptible to death induced by co-cross-linking of TCR/CD3 epsilon and Fas. Our results reveal a signaling synergy between the Fas and TCR/CD3 epsilon complex that has important implications for our understanding of in vivo vs in vitro models of thymocyte deletion. (C) 1996 Academic Press, Inc.
C1 UNIV TORONTO,DEPT IMMUNOL,TORONTO,ON M5S 1A8,CANADA.
RP Fisher, GH (reprint author), NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892, USA.
RI Zuniga-Pflucker, Juan/H-1295-2012;
OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178
NR 47
TC 17
Z9 17
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 APR 10
PY 1996
VL 169
IS 1
BP 99
EP 106
DI 10.1006/cimm.1996.0096
PG 8
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA UF065
UT WOS:A1996UF06500014
PM 8612301
ER
PT J
AU Ujike, H
Akiyama, K
Kuroda, S
AF Ujike, H
Akiyama, K
Kuroda, S
TI [H-3]YM-09151-2 (nemonapride), a potent radioligand for both sigma(1)
and sigma(2) receptor subtypes
SO NEUROREPORT
LA English
DT Article
DE sigma receptors; nemonapride; [H-3]YM-09151-2; (+)-[H-3]SKF-10047;
[H-3]DTG, (+)-[H-3]3-PPP; (+)-[H-3]pentazocine; binding study;
autoradiography; rat
ID GUINEA-PIG BRAIN; BINDING-SITES; H-3 YM-09151-2; RAT; ANTAGONISTS;
AFFINITY; LIGANDS; CELLS
AB USING K+ phosphate buffer with 25 nM spiperone, [H-3]YM-09151-2 binding showed a high affinity for sigma receptors but no affinity for D-2 dopamine or 5-HT1A receptors in rat brain. The order of pK(i) values of various sigma compounds at [H-3]YM-09151-2 binding sites and stereoisomer selectivity were consistent with previous studies using other sigma ligands such as (+)-[H-3]SKF-10047, [H-3]DTG and (+)-[H-3]3-PPP. Although Scatchard analysis fitted a one-site model, competition between [H-3]YM-09151-2 and (+)-pentazocine revealed two sites, sigma(1) and sigma(2) receptors, at which the K-i values of YM-09151-2 were 8.4nM and 9.6nM, respectively. Autoradiography using [H-3]YM-09151-2 also showed a characteristic distribution of sigma receptors in rat brain. [H-3]YM-09151-2 is, therefore, a potent and useful radioligand for sigma(1)/sigma(2) receptor subtypes.
C1 NIDA,MOL NEUROBIOL BRANCH,BALTIMORE,MD 21224.
RP Ujike, H (reprint author), OKAYAMA UNIV,SCH MED,DEPT NEUROPSYCHIAT,2-5-1 SHIKATA CHO,OKAYAMA 700,JAPAN.
NR 19
TC 18
Z9 19
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 APR 10
PY 1996
VL 7
IS 5
BP 1057
EP 1061
DI 10.1097/00001756-199604100-00021
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA VF117
UT WOS:A1996VF11700021
PM 8804051
ER
PT J
AU Winokur, G
Coryell, W
Endicott, J
Keller, M
Akiskal, H
Solomon, D
AF Winokur, G
Coryell, W
Endicott, J
Keller, M
Akiskal, H
Solomon, D
TI Familial alcoholism in manic-depressive (bipolar) disease
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE familial alcoholism; bipolar; mania; hyperactivity
ID HYPERACTIVE CHILD SYNDROME; DISORDER; CRITERIA
AB A previous analysis found a relatively high rate of alcoholism in a cohort of bipolar I subjects, and a trend for increased rates of alcoholism in relatives of subjects with both bipolar I disorder and alcoholism, compared to relatives of subjects with bipolar I disorder and no alcoholism. The sample of subjects with bipolar I disorder has been enlarged through continued follow-up, permitting new analyses to address the association and heritability of bipolar I disorder with alcoholism. Probands with bipolar I disorder were followed for 10 years as part of the NIMH Collaborative Depression Study. The rate of alcoholism in relatives of probands with both bipolar I disorder and alcoholism was compared to the rate of alcoholism in relatives of probands with bipolar disorder and no alcoholism. The prevalence of alcoholism in relatives of subjects with bipolar I disorder was compared to the rate of alcoholism in relatives of control subjects, Relatives of probands with bipolar I disorder showed a higher rate of alcoholism than relatives of controls. Relatives of probands with bipolar I disorder and alcoholism showed a higher rate of alcoholism than relatives of probands with bipolar I disorder without alcoholism. These data suggest that familial alcoholism may contribute to a vulnerability to bipolar I disorder, and that there is a shared heritability for the two disorders. (C) 1996 Wiley-Liss, Inc.
C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS CLIN STUDIE,WASHINGTON,DC.
FU NIMH NIH HHS [R01 MH025478]
NR 18
TC 39
Z9 39
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 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD APR 9
PY 1996
VL 67
IS 2
BP 197
EP 201
DI 10.1002/(SICI)1096-8628(19960409)67:2<197::AID-AJMG10>3.0.CO;2-E
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA UH661
UT WOS:A1996UH66100012
PM 8723047
ER
PT J
AU Gershon, ES
Badner, JA
DeteraWadleigh, SD
Ferraro, TN
Berrettini, WH
AF Gershon, ES
Badner, JA
DeteraWadleigh, SD
Ferraro, TN
Berrettini, WH
TI Maternal inheritance and chromosome 18 allele sharing in unilineal
bipolar illness pedigrees
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE genetic linkage; affected-sib-pairs; manic-depressive illness
AB We have replicated the observation of McMahon et al, [1995] that there is excess maternal transmission of illness in a series of previously described unilineal Bipolar manic-depressive illness extended pedigrees [Berrettini et al., 1991], (''Transmission'' is defined for any ill person in a pedigree when father or mother has a personal or immediate family history of major affective disorder.) We divided our pedigrees into exclusively maternal transmission (Mat) and mixed maternal-paternal transmission (in different pedigree branches) (Pat). Using affected sib-pair-analysis, linkage to a series of markers on chromosome 18p-cen was observed in the Pat but not the Mat pedigrees, with significantly greater identity by descent (IBD) at these markers in the Pat pedigrees. As compared with the pedigree series as a whole, the proportion of alleles IBD in the linkage region is much increased in the Pat pedigrees. As shown by Kruglyak and Lander [1995], as the sharing proportion of alleles in affected relative pairs increases, the number of such pairs needed to resolve the linkage region to a 1 cM interval becomes smaller. Genetic subdivision of an illness by clinical or pedigree configuration criteria may thus play an important role in discovery of disease susceptibility mutations (C) 1996 Wiley-Liss, Inc.
C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107.
RP Gershon, ES (reprint author), NIMH,BETHESDA,MD 20892, USA.
FU PHS HHS [49181]
NR 10
TC 105
Z9 106
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 APR 9
PY 1996
VL 67
IS 2
BP 202
EP 207
DI 10.1002/(SICI)1096-8628(19960409)67:2<202::AID-AJMG11>3.0.CO;2-N
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA UH661
UT WOS:A1996UH66100013
PM 8723048
ER
PT J
AU Rothschild, LG
Badner, J
Cravchik, A
Gershon, ES
Gejman, PV
AF Rothschild, LG
Badner, J
Cravchik, A
Gershon, ES
Gejman, PV
TI No association detected between a D-3 receptor gene-expressed variant
and schizophrenia
SO AMERICAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE schizophrenia; dopamine D-3 receptor gene; DRD3; polymorphism;
transmission for linkage disequilibrium test; TDT
ID DOPAMINE D3 RECEPTOR; SCHIZOAFFECTIVE DISORDER; HOMOZYGOSITY; LINKAGE;
FAMILY
AB A missense polymorphism (glycine to serine) in the first exon of the dopamine D-3 (DRDS) gene was examined in a sib-pairs schizophrenia collection by the transmission test for linkage disequilibrium (TDT). No association due to linkage disequilibrium was detected using TDT. Additionally, no evidence for excess homozygosity was found. (C) 1996 Wiley-Liss, Inc.
C1 NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892.
NR 26
TC 21
Z9 21
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-7299
J9 AM J MED GENET
JI Am. J. Med. Genet.
PD APR 9
PY 1996
VL 67
IS 2
BP 232
EP 234
DI 10.1002/(SICI)1096-8628(19960409)67:2<232::AID-AJMG18>3.0.CO;2-K
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA UH661
UT WOS:A1996UH66100020
PM 8723055
ER
PT J
AU Warner, DR
Hoffman, JL
AF Warner, DR
Hoffman, JL
TI Suicide inactivation of thioether S-methyltransferase by ethyl vinyl
sulfide
SO BIOCHEMISTRY
LA English
DT Article
ID SULFONIUM; PROTEIN; ENZYME; SULFUR
AB Thioether S-methyltransferase is an important enzyme in the metabolism of sulfur and selenium-containing compounds in animals. Ethyl vinyl sulfide was previously shown to be a substrate for this enzyme yielding methyl ethyl vinyl sulfonium ion (MEVS(+)) upon reaction with S-adenosylmethionine. Since vinyl sulfonium ions are reactive toward nucleophiles, the inactivation of thioether S-methyltransferase as a result of its methylation of ethyl vinyl sulfide was investigated, Ethyl vinyl sulfide was found to inactivate thioether S-methyltransferase in a time-dependent, pseudo-first-order process with k(inact) and K-I values of 0.05 min(-1) and 0.275 mM, respectively, Calculation of the partition ratio revealed one inactivation event for every 100 turnovers, Dimethyl sulfide, an alternate substrate for thioether S-methyltransferase which yields the nonreactive product trimethyl sulfonium ion, protected the enzyme from inactivation by ethyl vinyl sulfide. The inactivation is a result of covalent reaction of methyl ethyl vinyl sulfonium ion with the enzyme as shown by comigration of radioactivity with the enzyme during denaturing gel filtration of reaction mixtures containing thioether S-methyltransferase, ethyl vinyl sulfide, and S-adenosyl[methyl-H-3]methionine, Using this method the stoichiometry of inactivation was determined to be 1 mel of [H-3]-methyl group/mol of thioether S-methyltransferase inactivated, Both the alternate substrate, dimethyl sulfide, and the competitive product inhibitor, S-adenosylhomocysteine, inhibited such covalent labeling of the enzyme by ethyl vinyl sulfide and S-adenosyl[methyl-H-3]methionine, Chemically synthesized MEVS(+) inactivated thioether S-methyltransferase, and [methyl-C-14]MEVS(+) covalently labeled the enzyme with C-14. These results reveal a previously unrecognized mechanism for biochemical activation of vinyl thioethers by methylation to form reactive vinyl sulfonium ions.
C1 UNIV LOUISVILLE,DEPT BIOCHEM,SCH MED,LOUISVILLE,KY 40292.
NINCDS,MEMBRANE BIOCHEM SECT,NIH,BETHESDA,MD 20892.
FU NIEHS NIH HHS [ES-4887]
NR 17
TC 5
Z9 5
U1 2
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 9
PY 1996
VL 35
IS 14
BP 4480
EP 4484
DI 10.1021/bi9600815
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE612
UT WOS:A1996UE61200025
PM 8605197
ER
PT J
AU Barnett, SM
Dracheva, S
Hendler, RW
Levin, IW
AF Barnett, SM
Dracheva, S
Hendler, RW
Levin, IW
TI Lipid-induced conformational changes of an integral membrane protein: An
infrared spectroscopic study of the effects of triton X-100 treatment on
the purple membrane of Halobacterium halobium ET1001
SO BIOCHEMISTRY
LA English
DT Article
ID X-RAY-DIFFRACTION; BACTERIORHODOPSIN PHOTOCYCLE; PROTON TRANSLOCATION;
SECONDARY STRUCTURE; REVISED STRUCTURE; RAMAN; MODEL; INTERMEDIATE;
SPECTRA; RECONSTITUTION
AB Exposure of purple membrane from Halobacterium halobium to sublytic concentrations of Triton X-100 results in significant changes in the bacteriorhodopsin (BR) photocycle (Mukhopadhyay et al., 1994). Infrared spectra of purple membrane samples exposed briefly to Triton indicate that this change in protein function accompanies the preferential release of purple membrane glycolipids and squalenes, an association of Triton with purple membrane, and a perturbation of specific lipid headgroup interactions within the membrane. Specifically, the bilayer alterations induced by Triton entail a disruption of lipid headgroup hydrogen bonding in addition to protein conformational changes involving a loss in beta-turn and alpha(II)-helical structures in BR. We propose that the purple membrane glycolipids and squalenes are critical for the normal functioning of the BR photocycle and that perturbations of these lipids cause the profound photocycle changes induced by exposure to Triton. Lipid reconstitution studies demonstrated that although several of the infrared spectral parameters characteristic of the structural changes induced by Triton were reversed, the photocycle characteristics of BR in native purple membrane were not regained. The observed changes in the vibrational spectra induced by lipid-mediated bilayer perturbations suggest a useful approach for clarifying structure-function relationships of intrinsic membrane proteins exhibiting transmembrane helices.
C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892.
NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892.
NR 80
TC 33
Z9 33
U1 1
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 9
PY 1996
VL 35
IS 14
BP 4558
EP 4567
DI 10.1021/bi952258l
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UE612
UT WOS:A1996UE61200034
PM 8605206
ER
PT J
AU Bowen, T
Planalp, RP
Brechbiel, MW
AF Bowen, T
Planalp, RP
Brechbiel, MW
TI An improved synthesis of cis,cis-1,3,5-triaminocyclohexane. Synthesis of
novel hexadentate ligand derivatives for the preparation of gallium
radiopharmaceuticals
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
ID METAL-IONS; COMPLEXES; DESIGN; PET
AB An improved synthesis of cis,cis-1,3,5-triaminocyclohexane in 82% yield involves reaction of the commercially available cis,cis-1,3,5-cyclohexanetricarboxylic acid with DPPA to afford the tri(benzylcarbamate) as the Curtius rearrangement product Deprotection yields the triamine which serves as a platform from which a variety of chelating structures may be assembled. Novel tris(2-methylenepyridyl)triamine and tris(2-methylenethienyl)triamine ligands are prepared to investigate their suitability for use as gallium radiopharmaceuticals.
C1 UNIV NEW HAMPSHIRE,DEPT CHEM,DURHAM,NH 03824.
RP Bowen, T (reprint author), NIH,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892, USA.
NR 25
TC 61
Z9 61
U1 2
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD APR 9
PY 1996
VL 6
IS 7
BP 807
EP 810
DI 10.1016/0960-894X(96)00110-2
PG 4
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA UG180
UT WOS:A1996UG18000015
ER
PT J
AU Ichikawa, H
Deguchi, T
Fujiyoshi, Y
Nakago, T
Jacobowitz, DM
Sugimoto, T
AF Ichikawa, H
Deguchi, T
Fujiyoshi, Y
Nakago, T
Jacobowitz, DM
Sugimoto, T
TI Calbindin-D28k-immunoreactivity in the trigeminal ganglion neurons and
molar tooth pulp of the rat
SO BRAIN RESEARCH
LA English
DT Article
DE calbindin-D28k; calretinin; carbonic anhydrase; trigeminal ganglion;
tooth pulp; immunohistochemistry; rat
ID GENE-RELATED-PEPTIDE; CARBONIC-ANHYDRASE ACTIVITY; DORSAL-ROOT GANGLIA;
PRIMARY SENSORY NEURONS; CENTRAL NERVOUS-SYSTEM; SUBSTANCE-P;
HORSERADISH-PEROXIDASE; CYTOCHEMICAL-LOCALIZATION; TRANSGANGLIONIC
TRANSPORT; CENTRAL PROJECTIONS
AB The cell body size and coexpression of carbonic anhydrase (CA), calretinin (CR) and calcitonin gene-related peptide (CGRP) of primary neurons with calbindin-D28k (CB) was examined in the trigeminal ganglion (TG) of the rat. CB-immunoreactive (-ir) cells were mostly large and preferentially distributed in the maxillary and mandibular divisions of the TG. 48% of CB-ir TG cells exhibited enzyme CA activity. 10% of CB-ir TG cells contained CR-ir. Most TC cells coexpressing CB- and CR-irs were localized to the maxillary and mandibular divisions and exhibited CA activity. 6.5% of CB-ir TG cells coexisted with CGRP-ir. 46% of TG cells coexpressing CB and CGRP exhibited CA activity, The innervation of the molar tooth pulp by CB-ir TG primary neurons was also examined. CB-ir thick and smooth nerve fibers projected from the root pulp to the pulp horn and the roof of the pulp chamber, where they became thinner and rarely entered the subodontoblastic layer. However, they could not be traced to the odontoblastic layer, predentin or dentine. The distribution pattern of CB-ir pulpal fibers was different from that of CR-ir ones. The trigeminal neuronal cells retrogradely labeled with fast blue (FB) from the maxillary molar tooth pulp contained CB- and CR-irs. 23% and 1% of the labeled cells were immunoreactive for CB and CR, respectively. The coexpression of CB- and CR-immunoreactivities (-irs) in FB-labeled cells was negligible. An immunoelectron microscopic method revealed that 21% of pulpal nerve fibers were immunoreactive for CB, and that all CB-ir nerve fibers in the root pulp were myelinated. The present study indicated that the tooth pulp primary neurons contained CB-ir but did not coexpress CB- and CR-irs and that these neurons projected their myelinated axons to the pulp.
C1 OKAYAMA UNIV,SCH DENT,DEPT ORTHODONT,OKAYAMA 700,JAPAN.
NIMH,CLIN SCI LAB,BETHESDA,MD 20892.
RP Ichikawa, H (reprint author), OKAYAMA UNIV,SCH DENT,DEPT ORAL ANAT 2,2-5-1 SHIKATA CHO,OKAYAMA 700,JAPAN.
NR 40
TC 30
Z9 30
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 APR 9
PY 1996
VL 715
IS 1-2
BP 71
EP 78
DI 10.1016/0006-8993(95)01550-7
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA UK609
UT WOS:A1996UK60900009
PM 8739624
ER
PT J
AU Jain, R
Cohen, LA
AF Jain, R
Cohen, LA
TI Regiospecific alkylation of histidine and histamine at N-1 (tau)
SO TETRAHEDRON
LA English
DT Article
ID 3-SUBSTITUTED L-HISTIDINES; SIDE-CHAINS; METHYLHISTIDINE
AB Series of 1-alkyl histidines and histamines have been synthesized by the alkylation of the corresponding 5,6,7,8-tertrahydro-5-oxoimidazo[1,5-c]pyrimidines with alkyl halides in aprotic solvents. The method of conversion of the intermediate quaternary salt to the aminoacid or amine depends oil the nature of the alkyl group.
C1 NIDDK,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892.
NR 21
TC 43
Z9 43
U1 0
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0040-4020
J9 TETRAHEDRON
JI Tetrahedron
PD APR 8
PY 1996
VL 52
IS 15
BP 5363
EP 5370
DI 10.1016/0040-4020(96)00187-1
PG 8
WC Chemistry, Organic
SC Chemistry
GA UD909
UT WOS:A1996UD90900006
ER
PT J
AU Hasbahceci, M
Kiyan, M
Eyol, E
Ewalt, LC
Lodmell, DL
AF Hasbahceci, M
Kiyan, M
Eyol, E
Ewalt, LC
Lodmell, DL
TI Human diploid-cell rabies vaccine: Efficacy of four doses
SO LANCET
LA English
DT Letter
C1 NIAID,ROCKY MT LABS,LAB PERSISTENT DIS,HAMILTON,MT.
RP Hasbahceci, M (reprint author), HACETTEPE UNIV HOSP,DEPT SURG,CENT CAMPUS SIHHIYE,ANKARA,TURKEY.
RI Kiyan, Mehmet/D-2527-2015
OI Kiyan, Mehmet/0000-0002-6748-2070
NR 3
TC 4
Z9 5
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 APR 6
PY 1996
VL 347
IS 9006
BP 976
EP 977
DI 10.1016/S0140-6736(96)91467-1
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA UD591
UT WOS:A1996UD59100067
PM 8598794
ER
PT J
AU Angeles, TS
Steffler, C
Bartlett, BA
Hudkins, RL
Stephens, RM
Kaplan, DR
Dionne, CA
AF Angeles, TS
Steffler, C
Bartlett, BA
Hudkins, RL
Stephens, RM
Kaplan, DR
Dionne, CA
TI Enzyme-linked immunosorbent assay for trkA tyrosine kinase activity
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
ID NERVE GROWTH-FACTOR; PHOSPHOLIPASE-C-GAMMA; FACTOR RECEPTOR; EGF
RECEPTOR; NEUROTROPHIN RECEPTORS; SELECTIVE INHIBITOR; INSULIN-RECEPTOR;
CELLULAR ACTIONS; BINDING-SITE; PROTEIN
AB A 96-well microtiter enzyme-linked immunosorbent assay was developed to assay the activity of the cytoplasmic domain of trkA tyrosine kinase. The assay involves immobilization of phospholipase C-gamma/glutathione S-transferase fusion protein on a microtiter plate, addition of the kinase reaction mixture, and detection by an antibody to phosphotyrosine followed by an alkaline phosphatase-conjugated second antibody. The substrate used in this system, phospholipase C-gamma, is one of several biologically important substrates for the phosphorylation reaction of receptor-linked tyrosine kinases. The assay was then used to characterize kinase inhibitory activities of various small molecules including analogs of K-252a. (C) 1996 Academic Press, Inc.
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,EUKARYOT SIGNAL TRANSDUCT SECT,FREDERICK,MD 21702.
CEPHALON INC,DEPT CHEM,W CHESTER,PA 19380.
RP Angeles, TS (reprint author), CEPHALON INC,DEPT CELL BIOL,145 BRANDYWINE PKWY,W CHESTER,PA 19380, USA.
NR 31
TC 40
Z9 40
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD APR 5
PY 1996
VL 236
IS 1
BP 49
EP 55
DI 10.1006/abio.1996.0130
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA UE209
UT WOS:A1996UE20900008
PM 8619495
ER
PT J
AU Pergami, P
Jaffe, H
Safar, J
AF Pergami, P
Jaffe, H
Safar, J
TI Semipreparative chromatographic method to purify the normal cellular
isoform of the prion protein in nondenatured form
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
ID SODIUM DODECYL-SULFATE; MEMBRANE-PROTEINS; LIQUID-CHROMATOGRAPHY;
PRECURSOR PROTEIN; MOLTEN GLOBULE; SCRAPIE AGENT; PURIFICATION; BRAIN;
SIZE; PRP
AB A fundamental step in the pathogenesis of spongiform encephalopathies (prion diseases) is the conversion of the cellular isoform of prion protein (PrPC) into the infectious form (scrapie isoform, PrPSc), apparently by a conformational mechanism, Comparison of the native secondary and tertiary structures of both proteins is essential to elucidate the molecular basis of this transformation, To obtain sufficient quantities of native-like PrPC, we have developed a semipreparative method to purify PrPC from hamster brains, PrPC was solubilized from purified synaptosomal and microsomal membranes by the nonionic detergent n-octyl-beta-glucopyranoside; the soluble fraction was loaded at pH 7.5 onto a semipreparative cation-exchange TSK-SP-BPW (HPLC) column, The fr actions eluted by linear NaCl gradient and enriched for PrPC were sequentially purified using an immobilized ion-affinity HPLC column charged by Co2+, followed by wheat germ agglutinin (WGA)-affinity HPLC or size-exclusion HPLC (SE-HPLC) using a TSK G3000SW column, More than 95% purity was achieved after SE-HPLC as estimated by quantitative densitometry of the silver-stained SDS-PAGE gel; the recovery of total brain PrPC was greater than or equal to 8%. The purified PrPC was a monomer with an intact N-terminus, and with a Stoke's radius of 26 Angstrom, corresponding to that expected from the molecular weight for a native protein, The presence of the native-like conformation was further verified by peptide mapping after limited trypsin proteolysis, and by the apparent unfolding in guanidine hydrochloride, as detected by SE-HPLC. (C) 1906 Academic Press, Inc.
C1 NINCDS,NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892.
NINCDS,NIH,DIV INTRAMURAL RES,PROT PEPTIDE SEQUENCING FACIL,BETHESDA,MD 20892.
RI Safar, Jiri/G-6512-2013
NR 40
TC 67
Z9 70
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD APR 5
PY 1996
VL 236
IS 1
BP 63
EP 73
DI 10.1006/abio.1996.0132
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA UE209
UT WOS:A1996UE20900010
PM 8619497
ER
PT J
AU Steinert, PM
Chung, SI
Kim, SY
AF Steinert, PM
Chung, SI
Kim, SY
TI Inactive zymogen and highly active proteolytically processed
membrane-bound forms of the transglutaminase 1 enzyme in human epidermal
keratinocytes
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID ANCHORAGE REGION; ENVELOPE; EXPRESSION; DIFFERENTIATION; INVOLUCRIN;
PROTEIN; CELLS; GENE
AB The transglutaminase 1 enzyme is important for the formation of a cornified cell envelope in terminally differentiating keratinocytes. We show here that it is present in low levels in proliferating foreskin or cultured epidermal cells as an inactive zymogen full length form of 106 kDa, of which >95% is attached to membranes. In terminally differentiating keratinocytes, there is a greater than or equal to 100-fold induction of mRNA and protein. In addition to some cytosolic protein, most of the newly expressed protein is attached to membranes, of which about half exists in the zymogen form. Other protein consists of a 67/33/10 kDa complex formed by proteolytic processing at specific sites, and is anchored by way of the 10 kDa fragment. This processed form is very highly active and thus accounts for almost all transglutaminase 1 activity in keratinocytes. (C) 1996 Academic Press, Inc.
C1 GREEN CROSS CO,KIHEUNG EUP,SOUTH KOREA.
PACIFIC CORP,KYOUNGGI DO 449900,SOUTH KOREA.
RP Steinert, PM (reprint author), NIAMSD,SKIN BIOL LAB,NIH,BLDG 6,ROOM 425,BETHESDA,MD 20892, USA.
NR 25
TC 57
Z9 57
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD APR 5
PY 1996
VL 221
IS 1
BP 101
EP 106
DI 10.1006/bbrc.1996.0552
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UF049
UT WOS:A1996UF04900019
PM 8660317
ER
PT J
AU vanGent, DC
Ramsden, DA
Gellert, M
AF vanGent, DC
Ramsden, DA
Gellert, M
TI The RAG1 and RAG2 proteins establish the 12/23 rule in V(D)J
recombination
SO CELL
LA English
DT Article
ID MOUSE THYMOCYTES; SIGNALS; DNA
AB V(D)J recombination requires a pair of signal sequences with spacer lengths of 12 and 23 base pairs. Cleavage by the RAG1 and RAG2 proteins was previously shown to demand only a single signal sequence. Here, we establish conditions where 12- and 23-spacer signal sequences are both necessary for cleavage. Coupled cutting at both sites requires only the RAG1 and RAG2 proteins, but depends on the metal ion. In Mn2+, a single signal sequence supports efficient double strand cleavage, but cutting in Mg2+ requires two signal sequences and is best with the canonical 12/23 pair. Thus, the RAG proteins determine both aspects of the specificity of V(D)J recombination, the recognition of a single signal sequence and the correct 12/23 coupling in a pair of signals.
RP vanGent, DC (reprint author), NIDDKD,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892, USA.
NR 18
TC 223
Z9 224
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA
SN 0092-8674
J9 CELL
JI Cell
PD APR 5
PY 1996
VL 85
IS 1
BP 107
EP 113
DI 10.1016/S0092-8674(00)81086-7
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UE559
UT WOS:A1996UE55900013
PM 8620529
ER
PT J
AU Phelps, DE
Dressler, GR
AF Phelps, DE
Dressler, GR
TI Identification of novel Pax-2 binding sites by chromatin precipitation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TRANSCRIPTION FACTOR BSAP; B-CELL DIFFERENTIATION; HOMEOTIC
GENE-CONTROL; PAIRED BOX GENE; EARLY NEUROGENESIS; SWITCH REGIONS;
IN-VIVO; EXPRESSION; PROTEIN; DROSOPHILA
AB The Pax genes encode a family of developmental transcription factors that bind to specific DNA sequences via the paired domain and are necessary for the morphogenesis of a variety of tissues, The murine Pax-2 gene, through alternative splicing, encodes two nuclear proteins, Pax-2A and Pax-2B, which are transiently expressed during the differentiation of specific neural cell types and early kidney formation. In order to identify potential in vivo Pax-2 target sequences, chromatin from embryonic neural tube was immunoprecipitated with Pax-2 specific antibodies and cloned. Two unique immunoprecipitated clones containing three specific Pax-2 binding sites were identified by functional binding assays using Pax-2 proteins produced in both Escherichia coli and eukaryotic cells. In vitro DNA binding assays, using Pax-5 and Pax-8 DNA recognition sequences as well as the three immunopurified Pax-2 binding sites, demonstrated that both forms of the Pax-2 protein bind DNA with a similar specificity and that this binding is mediated by the paired domain. The binding sites identified in this report share significant homology among themselves and with previously defined consensus sequences for Pax-5 and Pax-2. The genomic clones can now be used as sequence tags to identify potential target loci.
C1 NICMD, NIH, BETHESDA, MD 20892 USA.
NR 58
TC 52
Z9 52
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 5
PY 1996
VL 271
IS 14
BP 7978
EP 7985
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UD600
UT WOS:A1996UD60000018
PM 8626478
ER
PT J
AU Roesler, WJ
Crosson, SM
Vinson, C
McFie, PJ
AF Roesler, WJ
Crosson, SM
Vinson, C
McFie, PJ
TI The alpha-isoform of the CCAAT/enhancer-binding protein is required for
mediating cAMP responsiveness of the phosphoenolpyruvate carboxykinase
promoter in hepatoma cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID 3 C/EBP ISOFORMS; GTP GENE; TRANSCRIPTIONAL REGULATION; RESPONSE
ELEMENT; KINASE-C; EXPRESSION; ACTIVATION; ENHANCER; FAMILY;
IDENTIFICATION
AB The gene coding for phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) is expressed in all gluconeogenic tissues, but stimulation of its rate of transcription by cAMP is robust only in liver, Evidence has accumulated which suggests that a liver-enriched transcription factor, likely a member of the CCAAT/enhancer binding protein (C/EBP) family, is required along with other ubiquitously expressed transcription factors to mediate this liver-specific response to cAMP. In this study, we examined the ability of C/EBP to participate in the cAMP-mediated activation of phosphoenolpyruvate carboxykinase (PEPCK) gene transcription in hepatoma cells, Expression of a dominant repressor of C/EBP in hepatoma cells significantly inhibited the protein kinase A-stimulated transcription of the PEPCK promoter, suggesting that a C/EBP family member was required for maximal transcriptional activation by protein kinase A. To provide additional support for this hypothesis, we prepared GAL4 fusion proteins containing C/EBP domains. Both C/EBP alpha and C/EBP beta GAL4 fusion proteins were capable of stimulating transcription from promoters containing binding sites for the DNA-binding domain of GAL4, However, only the GAL4-C/EBP alpha fusion protein demonstrated the ability to synergize with the other transcription factors bound to the PEPCK promoter which are required to mediate cAMP responsiveness, The DNA-binding domain of C/EBP alpha was not required for this activity in hepatoma cells, although in non-hepatoma cells the basic region leucine zipper domain appeared to inhibit the ability of C/EBP alpha to participate in mediating cAMP responsiveness, These results suggest that the liver-specific nature of the cAMP responsiveness of the PEPCK promoter involves the recruitment of C/EBP alpha to the cAMP response unit.
C1 NCI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
RP Roesler, WJ (reprint author), UNIV SASKATCHEWAN,DEPT BIOCHEM,SASKATOON,SK S7N 5E5,CANADA.
NR 43
TC 50
Z9 50
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 5
PY 1996
VL 271
IS 14
BP 8068
EP 8074
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UD600
UT WOS:A1996UD60000031
PM 8626491
ER
PT J
AU Gladyshev, VN
Boyington, JC
Khangulov, SV
Grahame, DA
Stadtman, TC
Sun, PD
AF Gladyshev, VN
Boyington, JC
Khangulov, SV
Grahame, DA
Stadtman, TC
Sun, PD
TI Characterization of crystalline formate dehydrogenase H from Escherichia
coli - Stabilization, EPR spectroscopy, and preliminary crystallographic
analysis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MOLYBDENUM COFACTORS; HYDROGEN-LYASE; SELENOCYSTEINE; SEQUENCE;
BIOCHEMISTRY; SELENIUM; ENZYMES
AB The selenocysteine-containing formate dehydrogenase H (FDH) is an 80-kDa component of the Escherichia coli formate-hydrogen lyase complex. The molybdenum-coordinated selenocysteine is essential for catalytic activity of the native enzyme, FDH in dilute solutions (30 mu g/ml) was rapidly inactivated at basic pH or in the presence of formate under anaerobic conditions, but at higher enzyme concentrations (greater than or equal to 3 mg/ml) the enzyme was relatively stable, The formate-reduced enzyme was extremely sensitive to air inactivation under all conditions examined. Active formate-reduced FDH was crystallized under anaerobic conditions in the presence of ammonium sulfate and PEG 400. The crystals diffract to 2.6 Angstrom resolution and belong to a space group of P4(1)2(1)2 or P4(3)2(1)2 with unit cell dimensions a = b = 146.1 Angstrom and c = 82.7 Angstrom. There is one monomer of FDH per crystallographic asymmetric unit. Similar diffraction quality crystals of oxidized FDH could be obtained by oxidation of crystals of formate-reduced enzyme with benzyl viologen. By EPR spectroscopy, a signal of a single reduced FeS cluster was found in a crystal of reduced FDH, but not in a crystal of oxidized enzyme, whereas Mo(V) signal was not detected in either form of crystalline FDH. This suggests that Mo(IV)- and the reduced FeS cluster-containing form of the enzyme was crystallized and this could be converted into Mo(VI)- and oxidized FeS cluster form upon oxidation. A procedure that combines anaerobic and cryocrystallography has been developed that is generally applicable to crystallographic studies of oxygen-sensitive enzymes. These data provide the first example of crystallization of a substrate-reduced form of a Se- and Mo-containing enzyme.
C1 NHLBI,NIH,LB,BETHESDA,MD 20892.
NIAID,MOLEC STRUCT LAB,NIH,ROCKVILLE,MD 20852.
UNIFORMED SERV UNIV HLTH SCI,DEPT BIOCHEM,BETHESDA,MD 20814.
NR 26
TC 34
Z9 35
U1 1
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 APR 5
PY 1996
VL 271
IS 14
BP 8095
EP 8100
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UD600
UT WOS:A1996UD60000035
PM 8626495
ER
PT J
AU Nashed, EM
Glaudemans, CPJ
AF Nashed, EM
Glaudemans, CPJ
TI Observations on the binding of four anti-carbohydrate monoclonal
antibodies to their homologous ligands
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MYELOMA PROTEINS; CHEMICAL SYNTHESIS; O-ANTIGEN; OLIGOSACCHARIDES;
GLYCOSIDES; SUBSITES; DEXTRAN; THERMODYNAMICS; SPECIFICITY; SALMONELLA
AB The binding of four monoclonal immunoglobulins, two with specificity for beta(1-->6)-linked D-galactopyranans (IgA X24 and IgA J539) and two with specificity for the chain terminus of alpha(1-->6)-linked D-glucopyranans (IgA W3129 and IgA 16.4.12E), was measured with a number of their homologous oligosaccharide ligands at different temperatures. The results show a linear relationship between lnk(alpha) and 1/T, where K-alpha is the affinity constant and T is the absolute temperature. The unitary free energy of binding, Delta G(u), is virtually independent of T, and the Delta S-u is small when compared with Delta G(u). The enthalpy changes derived from van't Hoff plots are large and negative, indicating an exothermic binding effect, whereas the entropy changes are small and negative, indicating minor overall hydrophobic contributions. Measurements of the free energies of binding, in low and high salt buffers, of methyl beta-D-galactopyranoside and the methyl glycoside of beta(1-->6)-D-galactopyranotetraose with anti-galactan IgA X24 indicate that the monosaccharide has no hydrophobic interaction with the highest affinity subsite of IgA, whereas the tetraoside might have a modest hydrophobic interaction with the three other hapten-binding subsites of IgA. The standard entropy change of binding of the two groups (galactosyl and glucosyl) of oligosaccharides to the two respective sets (anti-galactan and anti-dextran) of antibodies shows a distinct, differing correlation with the hapten chain length within each set. This correlation agrees with the type of association previously established between the antibodies and either the interior determinants of the antigen (in the case of the anti-galactans) or the chain terminus (in the case of the anti-dextrans).
RP Nashed, EM (reprint author), NIDDK,NIH,BETHESDA,MD 20892, USA.
NR 33
TC 7
Z9 7
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 5
PY 1996
VL 271
IS 14
BP 8209
EP 8214
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UD600
UT WOS:A1996UD60000053
PM 8626513
ER
PT J
AU Funada, M
Schutz, CG
Shippenberg, TS
AF Funada, M
Schutz, CG
Shippenberg, TS
TI Role of delta-opioid receptors in mediating the aversive stimulus
effects of morphine withdrawal in the rat
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE naltrindole; naltriben; delta-opioid receptor; opioid withdrawal
ID STRESS-INDUCED ANTINOCICEPTION; ANTAGONIST NALTRINDOLE; YOUNG-RATS;
DEPENDENCE; NALOXONE; MAINTENANCE; PEPTIDES; BINDING; POTENT; DRUGS
AB An unbiased place preference conditioning procedure was used to examine the role of delta-opioid receptors in mediating the aversive effects of opioid withdrawal. Rats were implanted s.c. with two pellets each containing placebo or 75 mg morphine. Single-trial conditioning sessions with saline and the opioid receptor antagonists naloxone (0.001-1.0 mg/kg, s.c.), naltrindole (0.01-3.0 mg/kg, s.c.) or naltriben (0.01-3.0 mg/kg, s.c.) commenced 4 days later. During these conditioning sessions, physical signs of withdrawal were also quantified. Tests of conditioning were conducted on day 5. Naloxone in doses of 0.01-1.0 mg/kg produced significant conditioned place aversions in morphine-implanted animals. A dose of 0.01 mg/kg produced few physical withdrawal signs whereas higher doses resulted in marked wet dog shakes, body weight loss, ptosis and diarrhea. No such effects were observed in control (placebo-implanted) animals. Administration of the selective delta-opioid receptor antagonists naltrindole and naltriben produced dose-related place aversions in morphine-implanted animals. The magnitude of these effects did not differ from that observed with naloxone. The minimum effective doses of naltrindole and naltriben were 0.1 mg/kg. Doses of 0.1-1.0 mg/kg produced few, if any, somatic signs of withdrawal whereas higher doses of these antagonists only produced diarrhea and wet-dog shakes. Other withdrawal signs were absent. In contrast to the opioid receptor antagonists tested, the dopamine D-1 receptor antagonist SCH23390 failed to produced conditioned place aversions or physical signs of withdrawal in morphine-pelleted animals. These data demonstrate that the selective blockade of either delta- or mu-opioid receptors is sufficient to induce conditioned aversive effects in morphine-dependent animals. They also indicate that physical symptoms associated with precipitated morphine withdrawal differ depending upon the opioid receptor antagonist employed.
C1 NIDA,DIV INTRAMURAL RES,PRECLIN PHARMACOL BRANCH,BALTIMORE,MD 21224.
RP Funada, M (reprint author), NIDA,DIV INTRAMURAL RES,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA.
NR 34
TC 20
Z9 20
U1 0
U2 1
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 APR 4
PY 1996
VL 300
IS 1-2
BP 17
EP 24
DI 10.1016/0014-2999(95)00860-8
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UG949
UT WOS:A1996UG94900003
PM 8741160
ER
PT J
AU Silberman, JD
Sogin, ML
Leipe, DD
Clark, CG
AF Silberman, JD
Sogin, ML
Leipe, DD
Clark, CG
TI Human parasite finds taxonomic home
SO NATURE
LA English
DT Letter
ID BLASTOCYSTIS-HOMINIS
C1 NIH, NCBI GENBANK, NATL LIB MED, BETHESDA, MD 20984 USA.
UNIV LONDON LONDON SCH HYG & TROP MED, DEPT MED PARASITOL, LONDON WC1E 7HT, ENGLAND.
RP Silberman, JD (reprint author), MARINE BIOL LAB, CTR MOLEC EVOLUT, WOODS HOLE, MA 02543 USA.
RI Clark, C Graham/H-3683-2011
OI Clark, C Graham/0000-0002-0521-0977
NR 13
TC 130
Z9 136
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD APR 4
PY 1996
VL 380
IS 6573
BP 398
EP 398
DI 10.1038/380398a0
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD590
UT WOS:A1996UD59000045
PM 8602239
ER
PT J
AU Chackalaparampil, I
Peri, A
Nemir, M
Mckee, MD
Lin, PH
Mukherjee, BB
Mukherjee, AB
AF Chackalaparampil, I
Peri, A
Nemir, M
Mckee, MD
Lin, PH
Mukherjee, BB
Mukherjee, AB
TI Cells in vivo and in vitro from osteopetrotic mice homozygous for c-src
disruption show suppression of synthesis of osteopontin, a
multifunctional extracellular matrix protein
SO ONCOGENE
LA English
DT Article
DE osteopontin; src-deficient; epidermal growth factor (EGF); homozygous;
osteopetrosis
ID TYROSINE KINASE; GROWTH-FACTOR; PHOSPHOPROTEIN; BONE; OSTEOCLASTS;
EXPRESSION; ACTIVATION; INDUCTION; PATHWAYS
AB Mice carrying homozygous disruption of the c-src protooncogene (Src-/-) develop osteopetrosis due to an impaired ability of osteoclasts to adhere to the bone surface and/or to form bone-resorbing ruffled border. It has also been reported that osteopontin (OPN), a secreted phosphoprotein, mediates osteoclast adherence to the bone matrix. We report here that cells from Src-/- mice, both in vitro and in vivo, express OPN mRNA and protein at a significantly reduced level as compared to cells from Src+/- and +/+ animals, suggesting a potential role for the proto-oncogene c-src in the regulation of OPN gene expression. Our data also show that OPN gene expression can be induced by treatment of Src -/- cells with epidermal growth factor (EGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA). Results obtained from studies using inhibitors of receptor tyrosine kinases (RTKs) and protein kinase C (PKC) suggest that PKC and RTK are positioned in a pathway with PKC as the downstream effector for the EGF-induced OPN gene expression in Src-/- cells, and that pp60(c-src) and EGF may regulate OPN gene expression through a common signalling pathway. Furthermore, contrary to published reports, our study shows that EGF-mediated cell signalling does not require functional interaction between the EGF-receptor and pp60(c-src).
C1 MCGILL UNIV,DEPT BIOL,MONTREAL,PQ H3A 1B1,CANADA.
NICHHD,SECT DEV GENET,HERITABLE DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
UNIV MONTREAL,FAC DENT,DEPT STOMATOL,MONTREAL,PQ H3C 3J7,CANADA.
RUTGERS STATE UNIV,WAKSMAN INST,DEPT MICROBIOL,PISCATAWAY,NJ 08855.
RI Lin, Pei-Hui/I-3011-2015
OI Lin, Pei-Hui/0000-0002-3894-5099
NR 38
TC 39
Z9 40
U1 0
U2 0
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD APR 4
PY 1996
VL 12
IS 7
BP 1457
EP 1467
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA UF076
UT WOS:A1996UF07600010
PM 8622862
ER
PT J
AU Murphy, EL
Bryzman, S
Williams, AE
CoChien, H
Schreiber, GB
Ownby, HE
Gilcher, RO
Kleinman, SH
Matijas, L
Thomson, RA
Nemo, GJ
AF Murphy, EL
Bryzman, S
Williams, AE
CoChien, H
Schreiber, GB
Ownby, HE
Gilcher, RO
Kleinman, SH
Matijas, L
Thomson, RA
Nemo, GJ
TI Demographic determinants of hepatitis C virus seroprevalence among blood
donors
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID RISK-FACTORS; UNITED-STATES; INFECTION; ANTIBODIES; ASSOCIATION;
SEROEPIDEMIOLOGY; EPIDEMIOLOGY; PREVALENCE; VIREMIA; DISEASE
AB Objective.-To measure demographic determinants of hepatitis C virus (HCV) seroprevalence among blood donors in the United States.
Design.-Cross-sectional epidemiological study.
Setting.-Five blood centers in different regions of the United States.
Subjects.-A total of 862 398 consecutive volunteer blood donors with one or more nonautologous donations from March 1992 through December 1993.
Methods.-Demographic data collection, serological screening with second-generation anti-HCV enzyme immunoassay, and confirmation with anti-HCV recombinant immunoblot.
Results.-There were 3126 donors with at least one blood donation confirmed HCV-seropositive, for a crude prevalence of 3.6 per 1000. Age-specific HCV seroprevalence rose from 0.5 per 1000 in donors younger than 20 years to a maximum of 6.9 per 1000 in donors aged 30 to 39 years and declined in older age groups. There was interaction between age and educational attainment, with 30- to 49-year-olds with less than a high school diploma at highest risk of HCV infection (odds ratio [OR], 33.0; 95% confidence interval [CI], 23.0 to 47.2 compared with those younger than 30 years with a bachelor's degree or higher degree), Other independent risk factors for HCV seropositivity included male sex (OR, 1.9, 95% CI, 1.8 to 2.1), black race (OR, 1.7, 95% CI, 1.6 to 1.9), Hispanic ethnicity (OR, 1.3, 95% CI, 1.1 to 1.5), previous blood transfusion (OR, 2.8; 95% CI, 2.5 to 3.1), and first/only time donor status (OR, 4.2; 95% CI, 3.9 to 4.5, compared with repeat donors), Seropositivity for human T-lymphotropic virus types I and II, human immunodeficiency virus, or hepatitis B core antigen was highly associated with HCV seropositivity (OR, 10.4; 95% CI, 9.6 to 11.4 for one vs no marker).
Conclusions.-Despite a low overall HCV prevalence in blood donors in the United States, there is marked variation in HCV seroprevalence by demographic subgroup, even after controlling for prior blood transfusion, a recognized risk factor for HCV. Further study of the prevalence of other parenteral risk factors such as past injection drug use among blood donors is needed.
C1 HIGHLAND GEN HOSP,OAKLAND,CA.
AMER RED CROSS,JEROME H HOLLAND LAB,ROCKVILLE,MD.
WESTAT CORP,ROCKVILLE,MD.
AMER RED CROSS,BLOOD SERV,DETROIT,MI.
OKLAHOMA BLOOD INST,OKLAHOMA CITY,OK.
UNIV CALIF LOS ANGELES,BLOOD & PLATELET CTR,LOS ANGELES,CA 90024.
NHLBI,BETHESDA,MD 20892.
RP Murphy, EL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT LAB MED,BOX 0884,SAN FRANCISCO,CA 94143, USA.
FU NHLBI NIH HHS [N01-HB-97079, N01-HB-97078, N01-HB-97077]
NR 33
TC 95
Z9 97
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 APR 3
PY 1996
VL 275
IS 13
BP 995
EP 1000
DI 10.1001/jama.275.13.995
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA UC123
UT WOS:A1996UC12300026
PM 8596257
ER
PT J
AU Smith, MA
McCaffrey, RP
Karp, JE
AF Smith, MA
McCaffrey, RP
Karp, JE
TI The secondary leukemias: Challenges and research directions
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Review
ID ACUTE MYELOID-LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA;
DNA-TOPOISOMERASE-II; CELL NUCLEAR ANTIGEN; DEBRISOQUINE METABOLIC
PHENOTYPE; ACUTE LYMPHOBLASTIC-LEUKEMIA; BREAKAGE-REUNION REACTION;
WILD-TYPE P53; LUNG-CANCER; HODGKINS-DISEASE
AB Acute myelogenous leukemia (AML) arising following exposure to genotoxic agents has been recognized as a distinctive entity for more than 40 years. Secondary, or therapy-related, AML accounts for 10%-20% of all AML cases. This review addresses four overarching areas of investigation focused on secondary AMLs: 1) dissection of the molecular structure of the induced genetic lesions and identification of the functional consequences of these changes, thereby providing clues to the pathogenesis of secondary AML and potentially serving as a basis for innovative therapeutic interventions; 2) identification and characterization of mechanisms of DNA damage and the orderly repair of such damage; 3) identification and application of accurate biomarkers of leukemogenesis for the purpose of risk prediction and quantification, potentially allowing recognition of patients especially susceptible to the leukemogenic effects of chemotherapy (for genetic or acquired reasons) and allowing their treatment for cancer to be modified on the basis of this susceptibility; and 4) design and implementation of longitudinal clinical and genetic monitoring of high-risk populations (i.e., individuals undergoing cytotoxic therapies for primary cancers). This review of the literature relating to these areas builds upon these themes and attempts to synthesize these seemingly disparate areas of research so that they can be more effectively utilized together to address the problem of secondary AML. Ultimately, the evaluation of these areas will improve our understanding of de novo leukemia and will serve as a springboard for the development of new concepts of therapy and prevention.
C1 NCI, NIH, CLIN TRIALS EVALUAT PROGRAM, DIV CANC TREATMENT DIAGNOSIS & CTR, BETHESDA, MD 20892 USA.
NCI, NIH, CHEMOPREVENT BRANCH, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA.
BOSTON UNIV, EVANS DEPT CLIN RES, SECT MED ONCOL, BOSTON, MA 02215 USA.
NR 201
TC 141
Z9 145
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD APR 3
PY 1996
VL 88
IS 7
BP 407
EP 418
DI 10.1093/jnci/88.7.407
PG 12
WC Oncology
SC Oncology
GA UD518
UT WOS:A1996UD51800010
PM 8618232
ER
PT J
AU Popescu, NC
Zimonjic, DB
LeventonKriss, S
Bryant, JL
LunardiIskandar, Y
Gallo, RC
AF Popescu, NC
Zimonjic, DB
LeventonKriss, S
Bryant, JL
LunardiIskandar, Y
Gallo, RC
TI Deletion and translocation involving chromosome 3(p14) in two
tumorigenic Kaposi's sarcoma cell lines
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID ACQUIRED IMMUNODEFICIENCY SYNDROME; SHORT ARM; CANCER; CARCINOMA;
HETEROZYGOSITY; ABERRATIONS; GENE
AB Background: Two neoplastic Kaposi's sarcoma (KS) cell lines, KS Y-1 (derived from a patient with KS associated with acquired immunodeficiency syndrome) and KS SLK (derived from an immunosuppressed patient with a renal transplant and KS or iatrogenic KS), have been shown to have abnormal chromosome constitution and to require no exogenous growth factors. They produce malignant tumors in immunodeficient mice. In contrast, all other cell cultures prepared in the past from KS specimens have been shown to have normal diploid characteristics, are hyperplastic, and depend on cytokines for growth, but they do not produce malignant tumors in immunodeficient mice. Purpose: We investigated whether the chromosomal changes that occurred in these KS cell lines were random or nonrandom and if such changes contribute to the pathogenesis of KS. Methods: We used the conventional G-banding technique and fluorescence in situ hybridization to identify structural and numerical chromosomal changes in the KS cell lines. Results: We demonstrated that both cell lines are aneuploid and have some additional features in common, i.e., loss of copies of chromosomes 14 and 21 and nonrandom translocations and deletions in the short arm of chromosome 3 at region 3p14. These KS cell lines also exhibit loss of heterozygosity of loci at region 3p14-ter. Conclusion: This is the first time nonrandom chromosomal alterations have been described in KS neoplastic cells. On the basis of information available on other cancers, the chromosome 3 alterations observed here can be expected to contribute to the neoplastic process in KS. Implications: Future research should focus on the identification of cytogenetic markers, thus facilitating generation of specific molecular probes for detecting neoplastic cells early in the disease process.
C1 TEL AVIV UNIV,SCH MED,CHAIM SHEBA MED CTR,CENT VIRUS LAB,TEL HASHOMER,ISRAEL.
NIDR,ANIM CARE UNIT,BETHESDA,MD 20892.
NCI,BIOL LAB,DIV BASIC SCI,BETHESDA,MD.
NCI,TUMOR CELL BIOL LAB,DIV BASIC SCI,BETHESDA,MD 20892.
NR 36
TC 23
Z9 24
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 APR 3
PY 1996
VL 88
IS 7
BP 450
EP 455
DI 10.1093/jnci/88.7.450
PG 6
WC Oncology
SC Oncology
GA UD518
UT WOS:A1996UD51800015
PM 8618237
ER
PT J
AU Clerici, M
Clerici, E
Shearer, GM
AF Clerici, M
Clerici, E
Shearer, GM
TI The tumor enhancement phenomenon: Reinterpretation from a Th1/Th2
perspective
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
ID INTERLEUKIN-12
C1 UNIV MILAN,CATTEDRA IMMUNOL,MILAN,ITALY.
NCI,EXPTL IMMUNOL BRANCH,DIV BASIC SCI,BETHESDA,MD 20892.
NR 20
TC 29
Z9 30
U1 1
U2 2
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD APR 3
PY 1996
VL 88
IS 7
BP 461
EP 462
DI 10.1093/jnci/88.7.461
PG 2
WC Oncology
SC Oncology
GA UD518
UT WOS:A1996UD51800017
PM 8618239
ER
PT J
AU Rhee, S
Parris, KD
Ahmed, SA
Miles, EW
Davies, DR
AF Rhee, S
Parris, KD
Ahmed, SA
Miles, EW
Davies, DR
TI Exchange of K+ or Cs+ for Na+ induces local and long-range changes in
the three-dimensional structure of the tryptophan synthase
alpha(2)beta(2) complex
SO BIOCHEMISTRY
LA English
DT Article
ID D-SERINE DEHYDRATASE; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BIENZYME
COMPLEX; ALPHA-SUBUNIT; HINGE REGION; BETA-SUBUNIT; MECHANISM;
SYNTHETASE; SUBSTRATE
AB Monovalent cations activate the pyridoxal phosphate-dependent reactions of tryptophan synthase and affect intersubunit communication in the alpha(2) beta(2) complex. We report refined crystal structures of the tryptophan synthase alpha(2) beta(2) complex from Salmonella typhimurium in the presence of K+ at 2.0 Angstrom and of Cs+ at 2.3 Angstrom. Comparison of these structures with the recently refined structure in the presence of Na+ shows that each monovalent cation binds at approximately the same position about 8 Angstrom from the phosphate of pyridoxal phosphate. Na+ and K+ are coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, and beta Gly-232 and to two or one water molecule, respectively. Cs+ is coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, beta Gly-232, beta Val-231, beta Gly-268, and beta Leu-304. A second binding site for Cs+ is located in the pip interface on the 2-fold axis with four carbonyl oxygens in the coordination sphere. In addition to local changes in structure close to the cation binding site, a number of long-range changes are observed. The K+ and Cs+ structures differ from the Na+ structure with respect to the positions of beta Asp-305, beta Lys-167, and alpha Asp-56. One unexpected result of this investigation is the movement of the side chains of beta Phe-280 and beta Tyr-279 from a position partially blocking the tunnel in the Na+ structure to a position lining the surface of the tunnel in the K+ and Cs+ structures. The results provide a structural basis for understanding the effects of cations on activity and intersubunit communication.
C1 NIDDK, NIH, MOLEC BIOL LAB, BETHESDA, MD 20892 USA.
NIDDK, NIH, BIOCHEM PHARMACOL LAB, BETHESDA, MD 20892 USA.
NR 70
TC 118
Z9 119
U1 2
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 2
PY 1996
VL 35
IS 13
BP 4211
EP 4221
DI 10.1021/bi952506d
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UC977
UT WOS:A1996UC97700042
PM 8672457
ER
PT J
AU Scherf, U
Pastan, I
Willingham, MC
Brinkmann, U
AF Scherf, U
Pastan, I
Willingham, MC
Brinkmann, U
TI The human CAS protein which is homologous to the CSE1 yeast chromosome
segregation gene product is associated with microtubules and mitotic
spindle
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Pseudomonas exotoxin; tumor necrosis factor; microtubule-associated
protein; apoptosis; cyclin B
AB Human CAS cDNA contains a 971-aa open reading frame that is homologous to the essential yeast gene CSE1. CSE1 is involved in chromosome segregation and is necessary for B-type cyclin degradation in mitosis, Using antibodies to GAS, it was shown that CAS levels are high in proliferating and low in nonproliferating cells, Here we describe the distribution of GAS in cells and tissues analyzed with antibodies against GAS. CAS is an approximate to 100-kDa protein present in the cytoplasm of proliferating cells at levels between 2 x 10(5) and 1 x 10(6) molecules per cell. The intracellular distribution of CAS resembles that of tubulin, In interphase cells, anti-GAS antibody shows microtubule-like patterns and in mitotic cells it labels the mitotic spindle. CAS Is removed from microtubules by mild detergent treatment (cytoskeleton preparations) and in vincristine- or taxol-treated cells, CAS is diffusely distributed in the cytoplasm with only traces present in tubulin paracrystals or bundles, Thus, CAS appears to be associated with but not to be an integral part of microtubules. Immunohistochemical staining of frozen tissues shows elevated amounts of GAS in proliferating cells such as testicular spermatogonia and cells in the basal layer cells of the colon, CAS was also concentrated in the respiratory epithelium of the trachea and in axons and Purkinje cells in the cerebellum, These cells contain many microtubules. The cellular location of CAS is consistent with an important role in cell division as well as in ciliary movement and vesicular transport.
C1 NCI,MOLEC BIOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892.
MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425.
NR 20
TC 51
Z9 52
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2670
EP 2674
DI 10.1073/pnas.93.7.2670
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500009
PM 8610099
ER
PT J
AU Neel, JV
Major, EO
Awa, AA
Glover, T
Burgess, A
Traub, R
Curfman, B
Satoh, C
AF Neel, JV
Major, EO
Awa, AA
Glover, T
Burgess, A
Traub, R
Curfman, B
Satoh, C
TI Hypothesis: ''Rogue cell''-type chromosomal damage in lymphocytes is
associated with infection with the JC human polyoma virus and has
implications for oncopenesis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE viral chromosome damage; JC viral oncogenesis
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HUMAN-DIPLOID FIBROBLASTS;
LARGE T-ANTIGEN; CHERNOBYL ACCIDENT; SIMIAN VIRUS-40; SV40-T ANTIGEN;
ABERRATIONS; TRANSFORMATION; PATHOGENESIS; FALLOUT
AB The hemagglutination inhibition antibody titers against the JC and BK polyoma viruses (JCV and BKV, respectively) are significantly elevated in individuals exhibiting ''rogue'' cells among their cultured lymphocytes. However, the elevation is so much greater with respect to JCV that the BKV elevation could readily be explained by cross reactivity to the capsid protein of these two closely related viruses, The JCV exhibits high sequence homology with the simian papovavirus, simian virus 40 (SV40), and Inoculation of human fetal brain cells with JCV produces polyploidy and chromosomal damage very similar to that produced by SV40. We suggest, by analogy with the effects of SV40, that these changes are due to the action of the viral large tumor antigen, a pluripotent DNA binding protein that acts in both transcription and replication, The Implications of these findings for oncogenesis are briefly discussed.
C1 NINCDS,MOLEC MED & VIROL SECT,LAB MOLEC MED & NEUROSCI,NIH,BETHESDA,MD 20892.
RADIAT EFFECTS RES FDN,MINAMI KU,HIROSHIMA 732,JAPAN.
RP Neel, JV (reprint author), UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109, USA.
NR 45
TC 99
Z9 103
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 APR 2
PY 1996
VL 93
IS 7
BP 2690
EP 2695
DI 10.1073/pnas.93.7.2690
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500013
PM 8610102
ER
PT J
AU Yoritaka, A
Hattori, N
Uchida, K
Tanaka, M
Stadtman, ER
Mizuno, Y
AF Yoritaka, A
Hattori, N
Uchida, K
Tanaka, M
Stadtman, ER
Mizuno, Y
TI Immunohistochemical detection of 4-hydroxynonenal protein adducts in
Parkinson disease
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID SUBSTANTIA-NIGRA; CELL-DEATH; COMPLEX-I; LIPID-PEROXIDATION; IRON;
GLUTATHIONE; DEFICIENCY; NEURONS; BRAINS
AB There is growing evidence that oxidative stress and mitochondrial respiratory failure with attendant decrease in energy output are implicated in nigral neuronal death in Parkinson disease (PD), It is not known, however, which cellular elements (neurons or glial cells) are major targets of oxygen-mediated damage, 4-Hydroxy-2-nonenal (HNE) was shown earlier to react with proteins to form stable adducts that can be used as markers of oxidative stress-induced cellular damage, We report here results of immunochemical studies using polyclonal antibodies directed against HNE-protein conjugates to label the site of oxidative damage in control subjects (ages 18-99 years) and seven patients that died of PD (ages 57-78 years), All the nigral melanized neurons in one of the midbrain sections were counted and classified into three groups according to the intensity of immunostaining for HNE-modified proteins-i.e., no staining, weak staining, and intensely positive staining, On average, 58% of nigral neurons were positively stained for HNE-modified proteins in PD; in contrast only 9% of nigral neurons were positive in the control subjects; the difference was statistically significant (Mann-Whitney U test; P < 0.01), In contrast to the substantia nigra, the oculomotor neurons in the same midbrain sections showed no or only weak staining for HNE-modified proteins in both PD and control subjects; young control subjects did not show any immunostaining; however, aged control subjects showed weak staining in the oculomotor nucleus, suggesting age-related accumulation of HNE-modified proteins in the neuron, Our results indicate the presence of oxidative stress within nigral neurons in PD, and this oxidative stress may contribute to nigral cell death.
C1 JUNTENDO UNIV,SCH MED,DEPT NEUROL,BUNKYO KU,TOKYO 113,JAPAN.
NAGOYA UNIV,FAC MED,DEPT BIOMED CHEM,SHOWA KU,NAGOYA,AICHI 46401,JAPAN.
NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
NR 28
TC 672
Z9 688
U1 3
U2 23
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2696
EP 2701
DI 10.1073/pnas.93.7.2696
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500014
PM 8610103
ER
PT J
AU deAzevedo, WF
MuellerDieckmann, HJ
SchulzeGahmen, U
Worland, PJ
Sausville, E
Kim, SH
AF deAzevedo, WF
MuellerDieckmann, HJ
SchulzeGahmen, U
Worland, PJ
Sausville, E
Kim, SH
TI Structural basis for specificity and potency of a flavonoid inhibitor of
human CDK2, a cell cycle kinase
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE cyclin-dependent kinase; protein kinase inhibitors; cancer; drug design;
flavopiridol
ID CATALYTIC SUBUNIT; PROTEIN-KINASE; DEPENDENT KINASE-2;
CRYSTAL-STRUCTURE; CRYSTALLIZATION; P21
AB The central role of cyclin-dependent kinases (CDKs) in cell cycle regulation makes them a promising target for studying inhibitory molecules that can modify the degree of cell proliferation, The discovery of specific inhibitors of CDKs such as polyhydroxylated flavones has opened the way to investigation and design of antimitotic compounds, A novel flavone, (-)-cis-5,7-dihydroxyphenyl-8-[4-(3-hydroxy-1-methyl)piperidinyl]-4H-1-benzopyran-4-one hydrochloride hemihydrate (L868276), is a potent inhibitor of CDKs. A chlorinated form, flavopiridol, is currently in phase I clinical trials as a drug against breast tumors, We determined the crystal structure of a complex between CDK2 and L868276 at 2.33-Angstrom resolution and refined to an R(factor) of 20.3%. The aromatic portion of the inhibitor binds to the adenine-binding pocket of CDK2, and the position of the phenyl group of the inhibitor enables the inhibitor to make contacts with the enzyme not observed in the ATP complex structure, The analysis of the position of this phenyl ring not only explains the great differences of kinase inhibition among the flavonoid inhibitors but also explains the specificity of L868276 to inhibit CDK2 and CDC2.
C1 UNIV CALIF BERKELEY,DEPT CHEM,BERKELEY,CA 94720.
UNIV CALIF BERKELEY,LAWRENCE BERKELEY LAB,BERKELEY,CA 94720.
NCI,DIV CANC TREATMENT,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
NR 36
TC 328
Z9 333
U1 1
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2735
EP 2740
DI 10.1073/pnas.93.7.2735
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500021
PM 8610110
ER
PT J
AU Botos, I
Scapozza, L
Zhang, DC
Liotta, LA
Meyer, EF
AF Botos, I
Scapozza, L
Zhang, DC
Liotta, LA
Meyer, EF
TI Batimastat, a potent matrix metalloproteinase inhibitor, exhibits an
unexpected mode of binding
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE metastasis; drug design; crystallography; molecular modelling
ID CARCINOMA; MACROMOLECULES; ASSOCIATION; EXPRESSION; GELATINASE;
MOLECULES; INVASION; PROGRAM; VENOM
AB Matrix metalloproteinase enzymes have been implicated in degenerative processes like tumor cell invasion, metastasis, and arthritis, Specific metalloproteinase inhibitors have been used to block tumor cell proliferation. We have examined the interaction of batimastat (BB-94) with a metalloproteinase [atrolysin C (Ht-d), EC 3.4.24.42] active site at 2.0-Angstrom resolution (R = 16.8%). The title structure exhibits an unexpected binding geometry, with the thiophene ring deeply inserted into the primary specificity site, This unprecedented binding geometry dramatizes the significance of the cavernous primary specificity site, pointing the way for the design of a new generation of potential antitumor drugs.
C1 TEXAS A&M UNIV,DEPT BIOCHEM & BIOPHYS,BIO LAB,COLLEGE STN,TX 77843.
NCI,PATHOL LAB,BETHESDA,MD 20892.
NR 36
TC 109
Z9 110
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 APR 2
PY 1996
VL 93
IS 7
BP 2749
EP 2754
DI 10.1073/pnas.93.7.2749
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500024
PM 8610113
ER
PT J
AU Pedone, PV
Ghirlando, R
Clore, GM
Gronenborn, AM
Felsenfeld, G
Omichinski, JG
AF Pedone, PV
Ghirlando, R
Clore, GM
Gronenborn, AM
Felsenfeld, G
Omichinski, JG
TI The single Cys(2)-His(2) zinc finger domain of the GAGA protein flanked
by basic residues is sufficient for high-affinity specific DNA binding
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene expression; DNA-protein interaction
ID NITROGEN REGULATORY GENE; TRANSCRIPTION FACTOR; CRYSTAL-STRUCTURE;
SACCHAROMYCES-CEREVISIAE; DISTINCT ROLES; SEQUENCE; COMPLEX;
RECOGNITION; ACTIVATION; EXPRESSION
AB Specific DNA binding to the core consensus site GAGAGAG has been shown with an 82-residue peptide (residues 310-391) taken from the Drosophila transcription factor GAGA. Using a series of deletion mutants, it was demonstrated that the minimal domain required for specific binding (residues 310-372) includes a single zinc finger of the Cys(2)-His(2) family and a stretch of basic amino acids located on the N-terminal end of the zinc finger, In gel retardation assays, the specific binding seen with either the peptide or the whole protein Is zinc dependent and corresponds to a dissociation constant of approximate to 5 x 10(-9) M for the purified peptide. It has previously been thought that a single zinc finger of the Cys(2)-His(2) family is incapable of specific, high-affinity binding to DNA. The combination of an N-terminal basic region with a single Cys(2)-His(2) zinc finger in the GAGA protein can thus be viewed as a novel DNA binding domain. This raises the possibility that other proteins carrying only one Cys(2)-His(2) finger are also capable of high-affinity specific binding to DNA.
C1 NIH,MOLEC BIOL LAB,BETHESDA,MD 20892.
NIH,PHYS CHEM LAB,BETHESDA,MD 20892.
RI Clore, G. Marius/A-3511-2008; Ghirlando, Rodolfo/A-8880-2009
OI Clore, G. Marius/0000-0003-3809-1027;
NR 33
TC 106
Z9 107
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 APR 2
PY 1996
VL 93
IS 7
BP 2822
EP 2826
DI 10.1073/pnas.93.7.2822
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500038
PM 8610125
ER
PT J
AU Fijalkowska, IJ
Schaaper, RM
AF Fijalkowska, IJ
Schaaper, RM
TI Mutants in the Exo I motif of Escherichia coli dnaQ: Defective
proofreading and inviability due to error catastrophe
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE fidelity of DNA replication; dnaQ and dnaE genes; mutD5 mutator; dnaE
antimutators; saturation of mismatch repair
ID POLYMERASE-III HOLOENZYME; MISMATCH REPAIR; MUTATOR MUTD5;
SALMONELLA-TYPHIMURIUM; REPLICATION ERRORS; 3'-5' EXONUCLEASE; CODING
PROPERTIES; LAC REPRESSOR; ACTIVE-SITE; AMINO-ACID
AB The Escherichia coli dnaQ gene encodes the proofreading 3' exonuclease (epsilon subunit) of DNA polymerase III holoenzyme and is a critical determinant of chromosomal replication fidelity, We constructed by site-specific mutagenesis a mutant, dnaQ926, by changing two conserved amino acid residues (Asp-12-->Ala and Glu-14-->Ala) in the Exo I motif, which, by analogy to other proofreading exonucleases, is essential for the catalytic activity, When residing on a plasmid, dnaQ926 confers a strong, dominant mutator phenotype, suggesting that the protein, although deficient in exonuclease activity, still binds to the polymerase subunit (cu subunit or dnaE gene product), When dnaQ926 was transferred to the chromosome, replacing the wild-type gene, the cells became inviable, However, viable dnaQ926 strains could be obtained if they contained one of the dnaE alleles previously characterized in our laboratory as antimutator alleles or if it carried a multicopy plasmid containing the E. coli mutL(+) gene, These results suggest that loss of proofreading exonuclease activity in dnaQ926 is lethal due to excessive error rates (error catastrophe), Error catastrophe results from both the loss of proofreading and the subsequent saturation of DNA mismatch repair, The probability of lethality by excessive mutation is supported by calculations estimating the number of inactivating mutations in essential genes per chromosome replication.
C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709.
RI Fijalkowska, Iwona/I-7796-2016
NR 45
TC 105
Z9 107
U1 2
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2856
EP 2861
DI 10.1073/pnas.93.7.2856
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500044
PM 8610131
ER
PT J
AU Bamford, RN
Battiata, AP
Burton, JD
Sharma, H
Waldmann, TA
AF Bamford, RN
Battiata, AP
Burton, JD
Sharma, H
Waldmann, TA
TI Interleukin (IL) 15/IL-T production by the adult T-cell leukemia cell
line HuT-102 is associated with a human T-cell lymphotrophic virus type
I R region/IL-15 fusion message that lacks many upstream AUGs that
normally attenuate IL-15 mRNA translation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID MESSENGER-RNA; UNTRANSLATED REGION; HTLV-I; INTEGRATION; ACTIVATION;
SEQUENCES; PROVIRUS
AB We reported previously that the human T-cell lymphotrophic virus type I (HTLV-I)-associated adult T-cell leukemia line HuT-102 produces a cytokine designated interleukin (IL) T that requires interleukin (IL) 2 receptor beta-subunit expression for its action, Using anti-cytokine antibodies, we demonstrated that IL-T is identical to the simultaneously described IL-15, When compared to activated monocytes, IL-15 mRNA expression was 6- to 10-fold greater in HuT-102 cells, The predominant IL-15 message from HuT-102 is a chimeric mRNA joining a segment of the R region of the long terminal repeat of HTLV-I and the 5'-untranslated region (UTR) of IL-15, Normally, by alternative splicing, this 118-nucleotide R element represents the most 5' region of several HTLV-I transcripts including tax, rex, and env, The introduction of the R element eliminated over 200 nucleotides of the IL-15 5'-UTR, including 8 of 10 upstream AUGs that are present in normal IL-15 messages, On analysis of the 5'-UTR of normal IL-15, we demonstrated that the presence of these 10 upstream AUGs interferes with IL-15 mRNA translation, Thus, IL-15 synthesis by the adult T-cell leukemia line HuT-102 involves an increase in IL-15 mRNA transcription and translation secondary to the production of an HTLV-I R element fusion message that lacks many upstream AUGs.
C1 GENZYME CORP,CAMBRIDGE,MA 02139.
RP Bamford, RN (reprint author), NCI,NIH,METAB BRANCH,BETHESDA,MD 20892, USA.
NR 26
TC 173
Z9 175
U1 1
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2897
EP 2902
DI 10.1073/pnas.93.7.2897
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500052
PM 8610139
ER
PT J
AU Kundu, GC
Mantile, G
Miele, L
CordellaMiele, E
Mukherjee, AB
AF Kundu, GC
Mantile, G
Miele, L
CordellaMiele, E
Mukherjee, AB
TI Recombinant human uteroglobin suppresses cellular invasiveness via a
novel class of high-affinity cell surface binding site
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Clara cell 10-kDa protein; invasion; extracellular matrix; metastasis
ID KDA PROTEIN; PHOSPHOLIPASE-A2 ACTIVITY; RABBIT UTEROGLOBIN; 10-KDA
PROTEIN; EXPRESSION; GENE; PEPTIDES; REGION; CC10; RAT
AB The mechanism(s) that regulates invasion of trophoblasts through the uterine epithelium during embryo implantation and nidation in hemochorial placental mammals is poorly understood. While limited trophoblast invasion is essential for the establishment of normal pregnancy, dysregulation of this process may contribute to the pathogenesis of choriocarcinoma, a highly invasive and lethal form of cancer arising from the trophoblasts. We have previously demonstrated that rabbit uteroglobin (UG), a cytokine-like, antiinflammatory protein, produced by the endometrial epithelium during pregnancy, has a potent antichemotactic effect on neutrophils and monocytes in vitro. Here, we report that recombinant human UG (hUG) dramatically suppresses invasion of human trophoblasts and NIH 3T3 cells through an artificial basement membrane (Matrigel) in vitro but has no effect on that of human choriocarcinoma cells. We identified a previously unreported high-affinity, high molecular weight (approximate to 190 kDa), nonglycosylated hUG-binding protein, readily detectable on human trophoblasts and NIH 3T3 cells but totally lacking on choriocarcinoma cells. Taken together, these results raise the possibility that (i) hUG plays a critical role in regulating cellular invasiveness, at least in part, via its previously unrecognized cell surface binding site, and (ii) some of the numerous biological activities of proteins of the UG family, reported so far, may be mediated via this binding site.
C1 NICHHD,NIH,SECT DEV GENET,HUMAN GENET BRANCH,BETHESDA,MD 20892.
NR 35
TC 59
Z9 61
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 APR 2
PY 1996
VL 93
IS 7
BP 2915
EP 2919
DI 10.1073/pnas.93.7.2915
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500055
PM 8610142
ER
PT J
AU Wimley, WC
Gawrisch, K
Creamer, TP
White, SH
AF Wimley, WC
Gawrisch, K
Creamer, TP
White, SH
TI Direct measurement of salt-bridge solvation energies using a peptide
model system: Implications for protein stability
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE protein folding; electrostatics; hydrophobicity; octanol partitioning;
C-13 NMR)
ID T4 LYSOZYME; HYDROPHOBIC CORE; PACKING; ACIDS
AB The solvation energies of salt bridges formed between the terminal carboxyl of the host pentapeptide AcWL-X-LL and the side chains of Arg or Lys in the guest (X) position have been measured. The energies were derived from octanol-to-buffer transfer free energies determined between pH 1 and pH 9, C-13 NMR measurements show that the salt bridges form in the octanol phase, but not in the buffer phase, when the side chains and the terminal carboxyl group are charged. The free energy of salt-bridge formation in octanol is approximately -4 kcal/mol (1 cal = 4.184 J), which is equal to or slightly larger than the sum of the solvation energies of noninteracting pairs of charged side chains, This is about one-half the free energy that would result from replacing a charge pair in octanol with a pair of hydrophobic residues of moderate size. Therefore, salt bridging in octanol can change the favorable aqueous solvation energy of a pair of oppositely charged residues to neutral or slightly unfavorable but cannot provide the same free energy decrease as hydrophobic residues. This is consistent with recent computational and experimental studies of protein stability.
C1 UNIV CALIF IRVINE,DEPT PHYSIOL & BIOPHYS,IRVINE,CA 92717.
NIAAA,NIH,NMR STUDIES SECT,MEMBRANE BIOPHYS & BIOCHEM LAB,BETHESDA,MD 20892.
JOHNS HOPKINS UNIV,SCH MED,DEPT BIOPHYS & BIOPHYS CHEM,BALTIMORE,MD 21205.
RI Creamer, Trevor/A-5252-2008; White, Stephen/B-1053-2009
OI White, Stephen/0000-0001-8540-7907
FU NIGMS NIH HHS [GM29458, GM46823]
NR 33
TC 101
Z9 102
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 2
PY 1996
VL 93
IS 7
BP 2985
EP 2990
DI 10.1073/pnas.93.7.2985
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA UD375
UT WOS:A1996UD37500068
PM 8610155
ER
PT J
AU Shulman, LE
AF Shulman, LE
TI Clinical research 1996: Stirrings from the academic health centers
SO ACADEMIC MEDICINE
LA English
DT Editorial Material
RP Shulman, LE (reprint author), NIAMSD,NIH,BETHESDA,MD 20892, USA.
NR 0
TC 20
Z9 20
U1 0
U2 0
PU HANLEY & BELFUS INC
PI PHILADELPHIA
PA 210 S 13TH ST, PHILADELPHIA, PA 19107
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD APR
PY 1996
VL 71
IS 4
BP 362
EP &
DI 10.1097/00001888-199604000-00013
PG 3
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA UF246
UT WOS:A1996UF24600016
PM 8645401
ER
PT J
AU Stein, DH
Salive, ME
AF Stein, DH
Salive, ME
TI Adequacy of training in preventive medicine and public health: A
national survey of residency graduates
SO ACADEMIC MEDICINE
LA English
DT Article
AB Purpose. To evaluate training in general preventive medicine and public health, determining which experiences and institutional sponsors best prepare residents for practice and where improvements are most needed.
Method. A 1991 survey of the 1,070 graduates of preventive medicine residencies from 1979 through 1989 asked the graduates to measure the adequacy of their training in preventive medicine topic areas by using a Likert-type scale of 1 (poor) to dr (excellent), Adequacy was analyzed for variation against practice emphasis during training, training program sponsor, and other variables. The statistical methods included Student's t-test, analysis of variance, and linear regression.
Results. A total of 797 graduates (74.5%) responded. The overall mean ratings of adequacy of training were 3.1 (SD, 0.9) for epidemiology, 2.5 (SD, 1.0) for clinical preventive medicine, 2.4 (SD, 0.9) for environmental health, 2.3 (SD, 0.9) for health administration, 2.3 (SD, 0.9) for health education and behavioral sciences, and 2.2 (SD, 0.9) for occupational medicine. Training was rated highest for topics emphasized during practice experiences. Adequacy varied by type of institution sponsoring the residency. Women rated their training as being less adequate than did men in all areas except clinical preventive medicine. The graduates tended ultimately to practice in topic areas emphasized during training.
Conclusion. The graduates' ratings suggest that improvements are most needed in health administration, environment health, health education, and occupational medicine. Potential improvement strategies include highly focused practice experiences and increased emphasis on training in actual practice settings and community sites.
C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,BALTIMORE,MD.
NIA,NIH,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892.
NR 17
TC 7
Z9 7
U1 0
U2 0
PU HANLEY & BELFUS INC
PI PHILADELPHIA
PA 210 S 13TH ST, PHILADELPHIA, PA 19107
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD APR
PY 1996
VL 71
IS 4
BP 375
EP 380
DI 10.1097/00001888-199604000-00016
PG 6
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA UF246
UT WOS:A1996UF24600020
PM 8645404
ER
PT J
AU Shtern, F
AF Shtern, F
TI Technology assessment: A perspective from the National Cancer Institute
SO ACADEMIC RADIOLOGY
LA English
DT Article; Proceedings Paper
CT International Symposium on Costs and Benefits of Radiology
CY 1995
CL OXFORD, ENGLAND
ID DIAGNOSTIC-ONCOLOGY-GROUP; CLINICAL-EXPERIENCE; BREAST; CT
RP Shtern, F (reprint author), NCI,DIAGNOST IMAGING RES BRANCH,RADIAT RES PROGRAM,DEPT HLTH & HUMAN SERV,DIV CANC TREATMENT,ROCKVILLE,MD 20852, USA.
NR 23
TC 2
Z9 2
U1 0
U2 0
PU ASSOC UNIV RADIOLOGISTS
PI RESTON
PA 1891 PRESTON WHITE DR, RESTON, VA 22091
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD APR
PY 1996
VL 3
SU 1
BP S84
EP S87
DI 10.1016/S1076-6332(96)80494-6
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA UE519
UT WOS:A1996UE51900033
PM 8796524
ER
PT J
AU Verny, M
Jellinger, KA
Hauw, JJ
Bancher, C
Litvan, I
Agid, Y
AF Verny, M
Jellinger, KA
Hauw, JJ
Bancher, C
Litvan, I
Agid, Y
TI Progressive supranuclear palsy: A clinicopathological study of 21 cases
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
DE progressive supranuclear palsy; symptoms; diagnostic criteria
ID DISEASE
AB The symptoms and signs used to diagnose progressive supranuclear palsy (PSP) should be easily identifiable by neuropathologists and neurologists as well as by movement disorder experts. The presence, at the time of death, of symptoms and signs that are used in published clinical criteria for the diagnosis of this disorder was searched for in 21 pathologically confirmed typical PSP cases. The following items, present in at least 80% of pathologically confirmed cases, can be considered as the most accurate clinical data for the diagnosis of PSP: nonfamilial parkinsonism, not improved by L-dopa therapy, with vertical voluntary gaze palsy; postural instability and falls; pseudobulbar palsy and dementia with frontal lobelike syndrome; and a progressive course of less than 10 years. The definite diagnosis of PSP must be clinicopathological, and these minimal clinical data may be used for this purpose.
C1 HOP LA PITIE SALPETRIERE,DIV MAZARIN,DEPT NEUROL,PARIS,FRANCE.
KRANKENHAUS STADT WIEN LAINZ,LUDWIG BOLTZMANN INST CLIN NEUROBIOL,A-1130 VIENNA,AUSTRIA.
NINCDS,NIH,NEUROEPIDEMIOL BRANCH,BETHESDA,MD 20892.
HOP LA PITIE SALPETRIERE,INSERM U289,F-75651 PARIS,FRANCE.
HOP LA PITIE SALPETRIERE,FEDERAT NEUROL,F-75651 PARIS,FRANCE.
RP Verny, M (reprint author), HOP LA PITIE SALPETRIERE,INSERM U360,LAB NEUROPATHOL R ESCOUROLLE,ASSOC CLAUDE BERNARD,F-75651 PARIS 13,FRANCE.
OI Litvan, Irene/0000-0002-3485-3445
NR 29
TC 60
Z9 61
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 APR
PY 1996
VL 91
IS 4
BP 427
EP 431
PG 5
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA UB191
UT WOS:A1996UB19100015
PM 8928621
ER
PT J
AU Johanson, CE
Duffey, FF
Anthony, JC
AF Johanson, CE
Duffey, FF
Anthony, JC
TI Associations between drug use and behavioral repertoire in urban youths
SO ADDICTION
LA English
DT Article
ID SUBSTANCE USE; COCAINE; SCHOOL; DRINKING; STUDENTS; SMOKING; MONKEYS;
ABUSE
AB Converging with psyche-social research findings, animal and human laboratory studies indicate that behavioral alternatives are important determinants of drug-taking. To investigate associations between how early adolescents spend their time, i.e. their behavioral repertoire and drug use (use of marijuana, crack/cocaine or inhalants), we analyzed data from an epidemiological sample of 1516 urban middle-school students who had completed private interviews in spring 1993. The interview included a 36-item questionnaire to assess how frequently the youth engaged in different activities; history of drug-taking was assessed separately. Multiple logistic regression was wed to estimate associations between drug we and each of seven behavioral domains as well as sex, age and racial-ethnic status. Youths spending a great deal of time working for pay and assuming other adult-like roles were more likely to have initiated drug use (estimated odds ratio, OR = 3.49; p = 0.002). Those who spent much time in religious activities were less likely (OR = 0.2, p < 0.001). An exploratory search for interactions disclosed other associations that merit attention in future research. These results corroborate evidence on the potential etiological significance of behavioral repertoire in relation to risk of drug use.
C1 NIDA,ETIOL BRANCH,INTRAMURAL RES PROGRAM,BALTIMORE,MD.
NR 40
TC 18
Z9 18
U1 8
U2 15
PU CARFAX PUBL CO
PI ABINGDON
PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE
SN 0965-2140
J9 ADDICTION
JI Addiction
PD APR
PY 1996
VL 91
IS 4
BP 523
EP 534
DI 10.1111/j.1360-0443.1996.tb02310.x
PG 12
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA UE993
UT WOS:A1996UE99300012
PM 8857378
ER
PT J
AU Corti, MC
Guralnik, JM
Bilato, C
AF Corti, MC
Guralnik, JM
Bilato, C
TI Coronary heart disease risk factors in older persons
SO AGING CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Review
DE aged; atherosclerosis; cardiovascular disease; coronary heart disease;
risk factors
ID POSTMENOPAUSAL ESTROGEN USE; HIGH BLOOD CHOLESTEROL; BODY-MASS INDEX;
SERUM URIC-ACID; FACTOR INTERVENTION TRIAL; 10-YEAR FOLLOW-UP;
CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; PHYSICAL-ACTIVITY;
SYSTOLIC HYPERTENSION
AB In most Western nations, coronary heart disease (CHD) is the leading cause of death and one of the most important causes of physical disability in persons over 65 years of age. The importance of traditional CHD risk factors has been well documented in middle-aged populations, whereas their role in older populations is still under debate. This paper reviews the epidemiologic evidence from observational studies and randomized clinical trials that established risk factors for CHD predict level of risk of CHD, and identify high risk individuals among older men and women. Hypertension and cigarette smoking have been clearly associated with an increased risk of CHD events, and their modification has been proven to be highly effective in the primary and secondary prevention of CHD in older persons. For other highly prevalent risk factors, such as lipid abnormalities, obesity and physical inactivity, evidence of an independent association with CHD risk has been demonstrated by the majority of observational studies. However, definitive proof from controlled clinical trials of the beneficial effects of their modification is still lacking in the older population. The role of estrogen replacement therapy in the primary and secondary prevention of CHD in older women is still an open question. In evaluating the impact of these risk factors in older persons, elements such as comorbidity, frailty, and age-related changes in risk profile should also be taken into consideration; Given the complexity of the relationship between risk factors and multiple disease statuses, other important outcomes, such as osteoporosis, cancer, falls and physical disability, should be considered when evaluating the risks and benefits of risk factor modifications in older persons.
RP NIA, EPIDEMIOL DEMOG BIOMETRY PROGRAM, NIH, 7201 WISCONSIN AVE, RM 3C309, BETHESDA, MD 20892 USA.
NR 154
TC 17
Z9 17
U1 4
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1594-0667
EI 1720-8319
J9 AGING CLIN EXP RES
JI Aging Clin. Exp. Res.
PD APR
PY 1996
VL 8
IS 2
BP 75
EP 89
PG 15
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA UJ079
UT WOS:A1996UJ07900002
PM 8737605
ER
PT J
AU Faris, M
Ensoli, B
Stahl, N
Yancopoulos, G
Nguyen, A
Wang, S
Nel, AE
AF Faris, M
Ensoli, B
Stahl, N
Yancopoulos, G
Nguyen, A
Wang, S
Nel, AE
TI Differential activation of the extracellular signal-regulated kinase,
Jun Kinase and Janus Kinase-Stat pathways by oncostatin M and basic
fibroblast growth factor in AIDS-derived Kaposi's sarcoma cells
SO AIDS
LA English
DT Article
DE JAK-Stat; ERK; Kaposi's sarcoma
ID RECEPTOR TYROSINE KINASES; PROTEIN-KINASE; FOS; PHOSPHORYLATION;
IDENTIFICATION; PATHOGENESIS; TRANSDUCTION; CYTOKINES; PROMOTER; COMPLEX
AB Objectives: To determine the integration of signalling pathways associated with two recognized Kaposi's sarcoma (KS) growth factors, oncostatin M (OSM) and basic fibroblast growth factor (bFGF), in the induction of KS cell proliferation.
Design and methods: We used protein kinase assays, protein-DNA interactions and AP-1 luciferase assays to study the extracellular signal-regulated kinase (ERK), janus kinase (JAK)-Stat and Jun kinase (JNK) pathways in AIDS-derived KS cells during stimulation with OSM and bFGF.
Results: Treatment with OSM-induced activation of receptor-associated JAK and phosphorylation of Stat1 and Stat3. Stat1/Stat3 heterodimers interacted with known gamma-interferon-activated sites like elements such as the sis-inducible element (SIE) in the c-fos promoter. In contrast, ligation of the bFGF receptor induced Stat3 phosphorylation and its association with the bFGF receptor, but failed to induce IAK activity or protein complexes which interact with GAS-like oligonucleotides. OSM also induced the activation of ERK2 by activating the serine/threonine kinases Raf-1 and [mitogen-activated protein kinase (MAPK) ERK kinase (MEK1)]-1, while bFGF failed to activate any of the above components. Both OSM and bFGF activated the JNK pathway, along with the activation of MEKkinase (MEKK)-1.JNK control the transcriptional activation of c-Jun. Because the above pathways exert an effect on the expression or activation of activation protein (AP)-1 components, we confirm that OSM and bFGF induce TPA response element (TRE)-luciferase activity synergistically.
Conclusion We demonstrate that OSM and bFGF activate distinct as well as shared signalling cascades in KS cells, which integrate to provide a synergistic AP-1 response by which OSM and bFGF may sustain KS cell growth.
C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,CIA,LOS ANGELES,CA 90024.
NCI,NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892.
REGENERON PHARMACEUT INC,TARRYTOWN,NY 10591.
RI Nel, Andre/J-2808-2012; Ensoli, Barbara/J-9169-2016
OI Ensoli, Barbara/0000-0002-0545-8737
FU CSR NIH HHS [02104-15-RG]; NCI NIH HHS [CA6532901, CA09120-20]
NR 58
TC 34
Z9 34
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 APR
PY 1996
VL 10
IS 4
BP 369
EP 378
DI 10.1097/00002030-199604000-00004
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA UE997
UT WOS:A1996UE99700004
PM 8728040
ER
PT J
AU Hitchcock, PJ
AF Hitchcock, PJ
TI Adolescents and sexually transmitted diseases
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID HIV INFECTION; RISK; TRANSMISSION; HERPES
AB This paper presents a brief overview of sexually transmitted diseases (STDs), including acquired immunodeficiency syndrome (AIDS), in adolescent populations. Using the framework of a mathematical model (which considers how, why, and whether an infection spreads within a population), the epidemic of STDs among adolescent populations is considered. The unique aspects of adolescent behavior, adolescent biology, and the social context of adolescents' lives are highlighted.
RP Hitchcock, PJ (reprint author), NIAID,SEXUALLY TRANSMITTED DIS BRANCH,9000 ROCKVILLE PIKE,SOLAR BLDG 3A24,BETHESDA,MD 20892, USA.
NR 26
TC 3
Z9 3
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1087-2914
J9 AIDS PATIENT CARE ST
JI Aids Patient Care STDS
PD APR
PY 1996
VL 10
IS 2
BP 79
EP 85
DI 10.1089/apc.1996.10.79
PG 7
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA UN022
UT WOS:A1996UN02200004
PM 11361711
ER
PT J
AU Grant, BF
AF Grant, BF
TI Toward an alcohol treatment model: A comparison of treated and untreated
respondents with DSM-IV alcohol use disorders in the general population
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE alcohol treatment; help-seeking for alcohol problems; alcohol treatment
utilization; access to alcohol treatment
ID PROBLEM DRINKERS; DRINKING; HELP
AB The purpose of this study was to compare characteristics of person with alcohol use disorders who sought alcohol treatment with those who did not using data from a nationally representative sample of the United States. Applying an organizing framework from the larger literature on service utilization, a logistic regression analysis was conducted to examine the interaction among factors influencing treatment, The results identified unemployment status and lower educational level as barriers to alcohol treatment, but the impact of these factors differed depending on whether the respondent had previous experience with alcohol treatment. The major findings of this study are discussed in terms of consumer satisfaction, minimizing barriers to alcohol treatment services, and the need to examine individual determinants of alcohol treatment within the larger context of organizational and sociopolitical factors.
RP Grant, BF (reprint author), NIAAA,DEPT BIOMETRY & EPIDEMIOL,BIOMETRY BRANCH,SUITE 514,6000 EXECUT BLVD,MSC 7003,BETHESDA,MD 20892, USA.
NR 25
TC 80
Z9 80
U1 0
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD APR
PY 1996
VL 20
IS 2
BP 372
EP 378
DI 10.1111/j.1530-0277.1996.tb01655.x
PG 7
WC Substance Abuse
SC Substance Abuse
GA UE737
UT WOS:A1996UE73700027
PM 8730232
ER
PT J
AU Kalkwarf, HJ
Specker, BL
Heubi, JE
Vieira, NE
Yergey, AL
AF Kalkwarf, HJ
Specker, BL
Heubi, JE
Vieira, NE
Yergey, AL
TI Intestinal calcium absorption of women during lactation and after
weaning
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE intestinal calcium absorption; lactation; weaning; stable isotopes
ID METABOLISM; PREGNANCY
AB We investigated whether intestinal calcium absorption and serum 1,25-dihydroxycholecalciferol (calcitriol) concentrations are higher in women during lactation and after weaning to compensate for calcium lost in breast milk. Measurements were obtained at 4.6 mo postpartum in 24 lactating women and 24 nonlactating women, at 9.6 mo postpartum in 24 lactating women (2.6 mo after complete weaning) and 24 nonlactating women. One-half of the women in each group were randomly assigned to receive 1 g supplemental Ca/d as calcium carbonate. Fractional calcium absorption was measured by using stable isotopic tracers Ca-42 and Ca-44. Fractional absorption was 0.32 +/- 0.02 (+/- SEM) in both lactating and nonlactating women, but was higher in lactating women after weaning (0.37 +/- 0.02) compared with nonlactating postpartum control subjects (0.31 +/- 0.02). These effects were independent of calcium intake. Changes in serum calcitriol paralleled changes in fractional absorption. There were no differences in calcitriol concentrations between lactating and nonlactating women, but calcitriol was greater in women after weaning compared with postpartum control subjects. Lactating women who had resumed menses had higher fractional absorption and serum calcitriol than did lactating women who had not. Serum calcium and phosphorus concentrations were greater in lactating compared with nonlactating women; there were no differences between groups after weaning. We conclude that lactation stimulates increases in fractional calcium absorption and serum calcitriol, but the responses are only apparent after weaning or the resumption of menses.
C1 NICHHD,NIH,BETHESDA,MD 20892.
RP Kalkwarf, HJ (reprint author), CHILDRENS HOSP,MED CTR,DIV NEONATOL,ML-0541,3333 BURNET AVE,CINCINNATI,OH 45229, USA.
FU NCRR NIH HHS [MO1 RR 08084]; NIAMS NIH HHS [R01 AR41366]
NR 16
TC 59
Z9 61
U1 0
U2 4
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 APR
PY 1996
VL 63
IS 4
BP 526
EP 531
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA UC185
UT WOS:A1996UC18500008
PM 8599316
ER
PT J
AU Mark, SD
Wang, W
Fraumeni, JF
Li, JY
Taylor, PR
Wang, GQ
Guo, W
Dawsey, SM
Li, B
Blot, WJ
AF Mark, SD
Wang, W
Fraumeni, JF
Li, JY
Taylor, PR
Wang, GQ
Guo, W
Dawsey, SM
Li, B
Blot, WJ
TI Lowered risks of hypertension and cerebrovascular disease after vitamin
mineral supplementation - The Linxian nutrition intervention trial
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE antioxidants; cerebrovascular disorders; hypertension; minerals;
nutrition; randomized controlled trials; stroke; vitamins
ID BLOOD-PRESSURE; CANCER INCIDENCE; VEGETABLES PROTECT; SERUM SELENIUM;
UNITED-STATES; HEART-DISEASE; DIETARY FATS; FOLLOW-UP; STROKE; MORTALITY
AB A total of 3,318 men and women from a region in rural China were randomized to receive daily either a multiple vitamin/mineral supplement or a placebo. Deaths that occurred in the participants were ascertained and classified according to cause over the 6-year period from 1985 to 1991, At the end of supplementation, blood pressure readings were taken, and the prevalence of hypertension was determined, There was a slight reduction in overall mortality in the supplement group (relative risk (RR) = 0.93, 95% confidence interval (CI) 0.75-1.16), with the decreased relative risk most pronounced for cerebrovascular disease deaths (RR = 0.63, 95% CI 0.37-1.07). This benefit was greater for men (RR = 0.42, 95% CI 0.19-0.93) than for women (RR = 0.93, 95% CI 0.44-1.98). Among the survivors, the presence of elevations in both systolic and diastolic blood pressures was less common in those who received the supplement (RR for men = 0.43, 95% CI 0.28-0.65; RR for women = 0.92, 95% CI 0.68-1.24). This study indicates that supplementation with a multivitamin/mineral combination may have reduced mortality from cerebrovascular disease and the prevalence of hypertension in this rural population with a micronutrient-poor diet.
C1 CHINESE ACAD MED SCI, INST CANC, BEIJING 100021, PEOPLES R CHINA.
INT EPIDEMIOL INST, ROCKVILLE, MD USA.
RP Mark, SD (reprint author), NCI, BETHESDA, MD 20892 USA.
NR 47
TC 79
Z9 91
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD APR 1
PY 1996
VL 143
IS 7
BP 658
EP 664
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UD948
UT WOS:A1996UD94800002
PM 8651227
ER
PT J
AU Cushman, M
Yanez, D
Psaty, BM
Fried, LP
Heiss, G
Lee, M
Polak, JF
Savage, PJ
Tracy, RP
AF Cushman, M
Yanez, D
Psaty, BM
Fried, LP
Heiss, G
Lee, M
Polak, JF
Savage, PJ
Tracy, RP
TI Association of fibrinogen and coagulation factors VII and VIII with
cardiovascular risk factors in the elderly - The cardiovascular health
study
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE aged; blood coagulation factors; cardiovascular disease; risk factors
ID POSTMENOPAUSAL ESTROGEN THERAPY; ISCHEMIC-HEART-DISEASE;
VON-WILLEBRAND-FACTOR; PLASMA-FIBRINOGEN; INDUSTRIAL-POPULATION;
HEMOSTATIC FUNCTION; BASELINE DATA; ATHEROSCLEROSIS; CHOLESTEROL;
MENOPAUSE
AB The cross-sectional correlates of three hemostatic factors-fibrinogen, factor VII, and factor VIII-were examined in the Cardiovascular Health Study, a population-based cohort study of 5,201 subjects over age 65 years. Subjects were recruited in 1989-1990 in Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. In multivariate linear regression models, cardiac risk factors significantly associated with fibrinogen were current smoking, race, lipids, and white blood count. In women, alcohol use, obesity, physical activity, and insulin level were also significant, while in men hypertension was correlated. The significant correlates of factor VII were lipids and white blood count in men and estrogen use, alcohol use, race, lipids, insulin level, white blood count, and obesity in women. The independent correlates of factor VIII were insulin, glucose, and race in both sexes; low density lipoprotein cholesterol, white blood count, and diuretic use in men; and alcohol use in women. In multivariate models, factors known to be modifiable risk factors for cardiovascular disease accounted for more of the population variance of these hemostatic factors in women than in men, especially for factor VII. The hemostatic factors may mediate some effects of risk factors on disease, and this should be considered in longitudinal studies.
C1 UNIV VERMONT,DEPT PATHOL & MED,BURLINGTON,VT.
UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195.
UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195.
UNIV WASHINGTON,DEPT HLTH SERV,SEATTLE,WA 98195.
UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195.
JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD.
JOHNS HOPKINS UNIV,DEPT EPIDEMIOL,BALTIMORE,MD.
UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC.
UNIV CALIF DAVIS,DEPT MED,DAVIS,CA 95616.
BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115.
NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892.
UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405.
UNIV VERMONT,DEPT BIOCHEM,BURLINGTON,VT 05405.
FU NHLBI NIH HHS [N01-HC-85081, N01-HC-85079, N01-HC-85080]
NR 56
TC 97
Z9 99
U1 0
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 APR 1
PY 1996
VL 143
IS 7
BP 665
EP 676
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UD948
UT WOS:A1996UD94800003
PM 8651228
ER
PT J
AU Hayes, RB
Brown, LM
Schoenberg, JB
Greenberg, RS
Silverman, DT
Schwartz, AG
Swanson, GM
Benichou, J
Liff, JM
Hoover, RN
Pottern, LM
AF Hayes, RB
Brown, LM
Schoenberg, JB
Greenberg, RS
Silverman, DT
Schwartz, AG
Swanson, GM
Benichou, J
Liff, JM
Hoover, RN
Pottern, LM
TI Alcohol use and prostate cancer risk in US blacks and whites
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE alcohol; case-control studies; prostatic neoplasms
ID CHRONIC ETHANOL; GROWTH-HORMONE; CONSUMPTION; LIVER; RAT; PERSPECTIVE;
SECRETION; INGESTION; TOBACCO; COHORT
AB Prostate cancer is the most common malignancy in US men (more than 165,000 cases per annum) and occurs substantially more frequently in blacks than in whites. The causes of this disease are, however, poorly understood. Alcohol consumption, which has been clearly related to malignancies of the upper aerodigestive tract, may also increase risk of cancer at other sites, including the prostate. The authors investigated alcohol use as a risk factor for prostate cancer among US blacks and whites. A population-based, case-control study was carried out among 981 men (479 blacks and 502 whites) with pathologically confirmed prostate cancer diagnosed between August 1, 1986, and April 30, 1989, and 1,315 controls (594 blacks and 721 whites) who resided in Atlanta, Georgia; Detroit, Michigan; and 10 counties in New Jersey, geographic areas covered by three population-based cancer registries. In-person interviews elicited information on alcohol use and other factors possibly related to prostate cancer. Compared with never-users, risk for prostate cancer increased with amount of alcohol drunk (chi(trend)(2), p < 0.001), with significantly elevated risks seen for those who had 22-56 drinks per week (odds ratio = 1.4; 95% confidence interval 1.0-1.8) and 57 or more drinks per week (odds ratio = 1.9; 95% confidence interval 1.3-2.7). The finding was consistent among blacks (chi(trend)(2), p < 0.01) and whites (chi(trend)(2), p < 0.05), and among young and old subjects; it was not restricted to a specific type of alcoholic beverage. In this first large study among US blacks and whites, increased risk for prostate cancer was associated with increased alcohol use. The risk was similar for whites and blacks and could not be attributed to tobacco use or to a number of other potential confounders.
C1 NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892.
NEW JERSEY STATE DEPT HLTH,SPECIAL EPIDEMIOL PROGRAM,TRENTON,NJ 08625.
EMORY UNIV,SCH PUBL HLTH,DIV EPIDEMIOL,ATLANTA,GA.
UNIV PITTSBURGH,SCH MED & FAMILY MED,DEPT CLIN EPIDEMIOL,PITTSBURGH,PA.
MICHIGAN STATE UNIV,COLL HUMAN MED,E LANSING,MI 48824.
FU NCI NIH HHS [N01-CP-51089, N01-CN-05225, N01-CP-5109]
NR 41
TC 55
Z9 56
U1 0
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 APR 1
PY 1996
VL 143
IS 7
BP 692
EP 697
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UD948
UT WOS:A1996UD94800006
PM 8651231
ER
PT J
AU Swanson, CA
Coates, RJ
Schoenberg, JB
Malone, KE
Gammon, MD
Stanford, JL
Shorr, IJ
Potischman, NA
Brinton, LA
AF Swanson, CA
Coates, RJ
Schoenberg, JB
Malone, KE
Gammon, MD
Stanford, JL
Shorr, IJ
Potischman, NA
Brinton, LA
TI Body size and breast cancer risk among women under age 45 years
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE anthropometry; body height; body weight; breast neoplasms
ID FAT DISTRIBUTION; PREMENOPAUSAL WOMEN; MENSTRUAL EVENTS; RELATIVE
WEIGHT; HEIGHT; OBESITY; MASS
AB In a multicenter population-based case-control study that included 1,588 cases and 1,394 controls less than age 45 years, the authors examined the relation of adult body size and breast cancer risk among young women. Breast cancer patients and healthy controls were identified in Atlanta, Georgia; Seattle/Puget Sound, Washington; and central New Jersey. Cases were newly diagnosed with in situ or invasive breast cancer during the period of May 1, 1990, through December 31, 1992. Anthropometric variables thought to reflect early environmental factors (e.g., height, sitting height, frame size), obesity, and body fat distribution were measured directly. Height, but not sitting height or frame size, was a breast cancer risk factor. Risk of the disease was increased 46 percent among women in the fourth quartile of height (>167 cm) compared with women in the first quartile (<159 cm). Body weight, but not body fat distribution, was related to breast cancer risk. Risk of the disease was 35 percent lower among women in the highest quartile of Quetelet index (>28.8 kg/m(2)) compared with women in the lowest quartile (<22.0 kg/m(2)). Risk of the disease was increased about 2.1-fold (95 percent confidence interval 1.2-3.8) among women who were thin and tall compared with women who were heavy and short. Thus, breast cancer risk was increased substantially among younger women with a linear body type.
C1 EMORY UNIV, ROLLINS SCH PUBL HLTH, DEPT EPIDEMIOL, ATLANTA, GA 30322 USA.
NEW JERSEY STATE DEPT HLTH, SPECIAL EPIDEMIOL PROGRAM, TRENTON, NJ 08625 USA.
FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA.
COLUMBIA UNIV, SCH PUBL HLTH, DIV EPIDEMIOL, NEW YORK, NY USA.
RP Swanson, CA (reprint author), NCI, NUTR EPIDEMIOL SECT,ENVIRONM EPIDEMIOL BRANCH, DIV CANC EPIDEMIOL & GENET,NIH, EPN ROOM 443, BETHESDA, MD 20892 USA.
RI Brinton, Louise/G-7486-2015
OI Brinton, Louise/0000-0003-3853-8562
NR 39
TC 88
Z9 89
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD APR 1
PY 1996
VL 143
IS 7
BP 698
EP 706
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UD948
UT WOS:A1996UD94800007
PM 8651232
ER
PT J
AU Cohen, MR
Anderson, RW
Attilio, RM
Green, L
Muller, RJ
Pruemer, JM
AF Cohen, MR
Anderson, RW
Attilio, RM
Green, L
Muller, RJ
Pruemer, JM
TI Preventing medication errors in cancer chemotherapy
SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY
LA English
DT Article
ID INTRATHECAL VINCRISTINE; OVERDOSE; MYELOENCEPHALOPATHY; CISPLATIN
AB Recommendations for preventing medication errors in cancer chemotherapy are made.
Before a health care provider is granted privileges to prescribe, dispense, or administer antineoplastic agents, he or she should undergo a tailored educational program and possibly testing or certification. Appropriate reference materials should be developed. Each institution should develop a dose-verification process with as many independent checks as possible. A detailed checklist covering prescribing, transcribing, dispensing, and administration should be used. Oral orders are not acceptable. All doses should be calculated independently by the physician, the pharmacist, and the nurse. Dosage limits should be established and a review process set up for doses that exceed the limits. These limits should be entered into pharmacy computer systems, listed on preprinted order forms, stated on the product packaging, placed in strategic locations in the institution, and communicated to employees. The prescribing vocabulary must be standardized. Acronyms, abbreviations, and brand names must be avoided and steps taken to avoid other sources of confusion in the written orders, such as trailing zeros. Preprinted anti neoplastic drug order forms containing checklists can help avoid errors. Manufacturers should be encouraged to avoid or eliminate ambiguities in drug names and dosing information. Patients must be educated about all aspects of their cancer chemotherapy, as patients represent a last line of defense against errors. An interdisciplinary team at each practice site should review every medication error reported. Pharmacists should be involved at all sites where antineoplastic agents are dispensed.
Although it may not be possible to eliminate all medication errors in cancer chemotherapy, the risk can be minimized through specific steps. Because of their training and experience, pharmacists should take the lead in this effort.
C1 UNIV TEXAS,MD ANDERSON CANC CTR,DIV PHARM,HOUSTON,TX.
LEHIGH VALLEY HOSP,JOHN & DOROTHY MORGAN CANC CTR,DEPT PHARM,ALLENTOWN,PA.
NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892.
MEM SLOAN KETTERING CANC CTR,DIV PHARM SERV,NEW YORK,NY.
UNIV CINCINNATI,DEPT PHARM,CINCINNATI,OH.
RP Cohen, MR (reprint author), INST SAFE MEDICAT PRACTICES,320 W ST RD,WARMINSTER,PA 18974, USA.
NR 66
TC 44
Z9 46
U1 0
U2 2
PU AMER SOC HEALTH-SYSTEM PHARMACISTS
PI BETHESDA
PA 7272 WISCONSIN AVE, BETHESDA, MD 20814
SN 1079-2082
J9 AM J HEALTH-SYST PH
JI Am. J. Health-Syst. Pharm.
PD APR 1
PY 1996
VL 53
IS 7
BP 737
EP 746
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UD644
UT WOS:A1996UD64400006
PM 8697025
ER
PT J
AU Rick, ME
Krizek, DM
AF Rick, ME
Krizek, DM
TI Identification of a His54Gln substitution in von Willebrand factor from
a patient with defective binding of factor VIII
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
DE von Willebrand factor; Normandy variant; genetic defect; factor VIII
binding defect
ID VONWILLEBRAND-FACTOR GENE; ACTIVATED PROTEIN-C; AMINO-ACID-RESIDUES;
FACTOR VWF; NORMANDY VARIANT; POINT MUTATIONS; DISEASE; PLASMA; DOMAIN;
INACTIVATION
AB A patient with type 2N (''Normandy'' variant) von Willebrand's disease is described. Her von Willebrand factor level was borderline low, while her factor VIII was markedly decreased to 7%. Her plasma von Willebrand factor demonstrated a decreased ability to complex with factor VIII in vitro, binding less than 10% when compared to normal plasma von Willebrand factor. The factor VIII released into the circulation after the patient received DDAVP had a shortened survival in vivo. Nucleotide sequence analysis revealed a T-to-A transition at nucleotide 2451 on both alleles. This transition results in a substitution of Gln for His at amino acid 54 in the mature subunit of von Willebrand factor. (C) lees Wiley Liss, Inc.*
RP Rick, ME (reprint author), NIH,HEMATOL SECT,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,ROOM 2C 390,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 39
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 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD APR
PY 1996
VL 51
IS 4
BP 302
EP 306
PG 5
WC Hematology
SC Hematology
GA UC620
UT WOS:A1996UC62000009
PM 8602631
ER
PT J
AU Davis, S
Schroeder, M
Goldin, LR
Weeks, DE
AF Davis, S
Schroeder, M
Goldin, LR
Weeks, DE
TI Nonparametric simulation-based statistics for detecting linkage in
general pedigrees
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID MEMBER METHOD; TRAITS; PAIRS
AB We present here four nonparametric statistics for linkage analysis that test whether pairs of affected relatives share marker alleles more often than expected. These statistics are based on simulating the null distribution of a given statistic conditional on the unaffecteds' marker genotypes. Each statistic uses a different measure of marker sharing: the SimAPM statistic uses the simulation-based affected-pedigree-member measure based on identity-by-state (IBS) sharing. The SimKIN (kinship) measure is 1.0 for identity-by-descent (IBD) sharing, 0.0 for no IBD sharing, and the kinship coefficient when the IBD status is ambiguous. The simulation-based IBD (SimIBD) statistic uses a recursive algorithm to determine the probability of two affecteds sharing a specific allele IBD. The SimISO statistic is identical to SimIBD, except that it also measures marker similarity between unaffected pairs. We evaluated our statistics on data simulated under different two-locus disease models, comparing our results to those obtained with several other nonparametric statistics. Use of IBD information produces dramatic increases in power over the SimAPM method, which uses only IBS information. The power of our best statistic in most cases meets or exceeds the power of the other nonparametric statistics. Furthermore, our statistics perform comparisons between all affected relative pairs within general pedigrees and are not restricted to sib pairs or nuclear families.
C1 UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA 15261.
UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA.
NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892.
UNIV OXFORD,WELLCOME TRUST CTR HUMAN GENET,OXFORD,ENGLAND.
RI Weeks, Daniel/B-2995-2012;
OI Davis, Sean/0000-0002-8991-6458; Weeks, Daniel/0000-0001-9410-7228
FU NCRR NIH HHS [1 P41 RR03655]; NHGRI NIH HHS [HG00719]; Wellcome Trust
NR 32
TC 94
Z9 95
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 APR
PY 1996
VL 58
IS 4
BP 867
EP 880
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA UA380
UT WOS:A1996UA38000025
PM 8644751
ER
PT J
AU Cannon, RO
AF Cannon, RO
TI The heart in hypertension - Thinking small
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Editorial Material
ID LEFT-VENTRICULAR HYPERTROPHY; DIPYRIDAMOLE-ECHOCARDIOGRAPHY TEST; NORMAL
CORONARY-ARTERIES; ANGINA-PECTORIS; CHEST PAIN; SYNDROME-X; DISEASE;
CIRCULATION; RESERVE
RP Cannon, RO (reprint author), NHLBI,CARDIOL BRANCH,NIH,BLDG 10,ROOM 7B15,10 CTR DR MSC-1650,BETHESDA,MD 20892, USA.
NR 19
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD APR
PY 1996
VL 9
IS 4
BP 406
EP 408
PN 1
PG 3
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA UF251
UT WOS:A1996UF25100017
PM 8722445
ER
PT J
AU Alciati, MH
AF Alciati, MH
TI Intervention research: A model from the national cancer institute's
smoking and tobacco control program
SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
LA English
DT Article
DE cancer control; intervention research tobacco control; disease
prevention
AB Recognizing that the scientific method is as critical to cancer control as it is to basic laboratory research, the National Cancer Institute (NCI) established a well-defined, systematic strategy for attaining its cancer control goals and objectives. This strategy, operationalized in the early 1980s as a five-phase process, emphasized cancer control as a research science rather than a demonstration science. The five phases of NCI's cancer control research strategy progress from hypothesis development, to methods development to controlled intervention trials, to defined population studies, and finally to demonstration and implementation programs. This research base provides the foundation for nationwide prevention and health services programs. The application of this five-phase approach to NCI's efforts to reduce morbidity and mortality attributable to tobacco use is described and some of the challenges that faced the Institute in this process ale identified. These experiences provide an important framework for other disciplines faced with the challenge of translating science into practice. (C) 1996 Wiley-Liss, Inc.*
C1 NCI,PUBL HLTH AGCY SECT,ROCKVILLE,MD.
OI Alciati, Marianne/0000-0001-6294-1090
NR 23
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 0271-3586
J9 AM J IND MED
JI Am. J. Ind. Med.
PD APR
PY 1996
VL 29
IS 4
BP 324
EP 328
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA UD075
UT WOS:A1996UD07500009
PM 8728133
ER
PT J
AU Striker, GE
AF Striker, GE
TI NIDDK goes on-line
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT News Item
RP Striker, GE (reprint author), NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD 20892, USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD APR
PY 1996
VL 27
IS 4
BP 603
EP 603
DI 10.1016/S0272-6386(96)90175-4
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA UC864
UT WOS:A1996UC86400021
ER
PT J
AU Regan, JA
Klebanoff, MA
Nugent, RP
Eschenbach, DA
Blackwelder, WC
Lou, Y
Gibbs, RS
Rettig, PJ
Martin, DH
Edelman, R
AF Regan, JA
Klebanoff, MA
Nugent, RP
Eschenbach, DA
Blackwelder, WC
Lou, Y
Gibbs, RS
Rettig, PJ
Martin, DH
Edelman, R
TI Colonization with group B streptococci in pregnancy and adverse outcome
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE Group B streptococci; Streptococcus agalactiae; low birth weight;
preterm birth
ID SELECTIVE INTRAPARTUM CHEMOPROPHYLAXIS; EARLY-ONSET DISEASE;
CHLAMYDIA-TRACHOMATIS; PREMATURE RUPTURE; PRETERM LABOR; VAGINAL FLORA;
MEMBRANES; INFECTION; PREVENTION; DELIVERY
AB OBJECTIVE: Our purpose was to study the association of cervicovaginal colonization with group B streptococci with pregnancy and neonatal outcome.
STUDY DESIGN: A prospective study was conducted at seven medical centers between 1984 and 1989. Genital tract cultures were obtained at 23 to 26 weeks' gestation and at delivery. Prematurity and neonatal sepsis rates were compared between group B streptococci positive and negative women.
RESULTS: Group B streptococci was recovered from 2877 (21%) of 13,646 women at enrollment. Heavy colonization was associated with a significant risk of delivering a preterm infant who had a low birth weight (odds ratio = 1.5, 95% confidence interval 1.1 to 1.9). Heavily colonized women given antibiotics effective against group B streptococci had little increased risk of a preterm, low-birth-weight birth. Women with light colonization were at the same risk of adverse outcome as the uncolonized women. Neonatal group B streptococci sepsis occurred in 2.6 of 1000 live births in women with and 1.6 of 1000 live births in women without group B streptococci at 23 to 26 weeks' gestation (p = 0.11). However, sepsis occurred in 16 of 1000 live births to women with and 0.4 of 1000 live births to women without group B streptococci at delivery (p < 0.001).
CONCLUSIONS: Heavy group B streptococci colonization at 23 to 26 weeks' gestation was associated with an increased risk of delivering a preterm, low-birth-weight infant. Cervicovaginal colonization with group B streptococci at 23 to 26 weeks' gestation was not a reliable predictor of neonatal group B streptococci sepsis. Colonization at delivery was associated with sepsis.
C1 NICHHD,NIH,DESPR,BETHESDA,MD 20892.
COLUMBIA UNIV,DEPT PEDIAT,NEW YORK,NY 10027.
UNIV WASHINGTON,DEPT OBSTET & GYNECOL,SEATTLE,WA 98195.
NIAID,NIH,BETHESDA,MD 20892.
RES TRIANGLE INST,RES TRIANGLE PK,NC 27709.
UNIV TEXAS,DEPT OBSTET & GYNECOL,SAN ANTONIO,TX.
UNIV OKLAHOMA,DEPT PEDIAT,NORMAN,OK 73019.
LOUISIANA STATE UNIV,DEPT MED,NEW ORLEANS,LA.
TULANE UNIV,NEW ORLEANS,LA 70118.
HARLEM HOSP MED CTR,NEW YORK,NY.
FU NICHD NIH HHS [HD-3-2833, HD-3-2832, HD-3-2834]
NR 25
TC 127
Z9 143
U1 0
U2 8
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 APR
PY 1996
VL 174
IS 4
BP 1354
EP 1360
DI 10.1016/S0002-9378(96)70684-1
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA UH184
UT WOS:A1996UH18400052
PM 8623869
ER
PT J
AU deSmet, MD
StarkVancs, V
Kohler, DR
Smith, J
Wittes, R
Nussenblatt, RB
AF deSmet, MD
StarkVancs, V
Kohler, DR
Smith, J
Wittes, R
Nussenblatt, RB
TI Intraocular levels of methotrexate after intravenous administration
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID LYMPHOMA; THERAPY
AB PURPOSE: To determine if adequate intraocular levels of methotrexate are achieved after intravenous administration.
METHODS: After intravenous administration, methotrexate levels were determined in the serum, the anterior chamber, and the cerebrospinal fluids of a patient with recurrent ocular lymphoma. A fluorescence polarization immunoassay was used to make the determinations.
RESULTS: At seven hours into a 24-hour intravenous infusion, methotrexate was at cytotoxic level in all samples. At 74 hours, cytotoxic levels were present only in the aqueous humor.
CONCLUSION: Sustained cytotoxic ocular methotrexate levels are achievable after systemic administration.
C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892.
NCI,DIV CANC TREATMENT,NIH,BETHESDA,MD.
NIH,DEPT PHARM,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD.
RP deSmet, MD (reprint author), NEI,CLIN IMMUNOL SECT,NIH,BLDG 10,RM 10N112,10 CTR DR,MSC 1858,BETHESDA,MD 20892, USA.
OI de Smet, Marc/0000-0002-9217-5603
NR 5
TC 29
Z9 31
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 APR
PY 1996
VL 121
IS 4
BP 442
EP 444
PG 3
WC Ophthalmology
SC Ophthalmology
GA UD610
UT WOS:A1996UD61000014
PM 8604740
ER
PT J
AU Baumrind, S
Korn, EL
Boyd, RL
Maxwell, R
AF Baumrind, S
Korn, EL
Boyd, RL
Maxwell, R
TI The decision to extract .2. Analysis of clinicians' stated reasons for
extraction
SO AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS
LA English
DT Article
AB In a recently reported study, the pretreatment records of each subject in a randomized clinical trial of 148 patients with Class I and Class II malocclusions presenting for orthodontic treatment were evaluated independently by five experienced clinicians (drawn from a panel of 14). The clinicians displayed a higher incidence of agreement with each other than had been expected with respect to the decision as to whether extraction was indicated in each specific case. To improve our understanding of how clinicians made their decisions on whether to extract or not, the records of a subset of 72 subjects randomly selected from the full sample of 148, have now been examined in greater detail. In 21 of these cases, all five clinicians decided to treat without extraction. Among the remaining 51 cases, there were 202 decisions to extract (31 unanimous decision cases and 20 split decision cases). The clinicians cited a total of 469 reasons to support these decisions. Crowding was cited as the first reason in 49% of decisions to extract, followed by incisor protrusion (14%), need for profile correction (8%), Class II severity (5%), and achievement of a stable result (5%). When all the reasons for extraction in each clinician's decision were considered as a group, crowding was cited in 73% of decisions, incisor protrusion in 35%, need for profile correction in 27%, Class II severity in 15% and posttreatment stability in 9%. Tooth size anomalies, midline deviations, reduced growth potential, severity of overjet, maintenance of existing profile, desire to close the bite, periodontal problems, and anticipation of poor cooperation accounted collectively for 12% of the first reasons and were mentioned in 54% of the decisions, implying that these considerations play a consequential, if secondary, role in the decision-making process. All other reasons taken together were mentioned in fewer than 20% of cases. In this sample at least, clinicians focused heavily on appearance-related factors that are qualitatively determinable by physical examination of the surface structures of the face and teeth. They appear to have made primary use of indicators available on study casts and facial photographs and relatively little use of information that is available only on cephalograms or that involves the application of specialized orthodontic theories.
C1 UNIV CALIF SAN FRANCISCO,DEPT GROWTH & DEV,DIV ORTHODONT,SAN FRANCISCO,CA 94143.
UNIV MED & DENT NEW JERSEY,NEWARK,NJ 07103.
NCI,CLIN TRIALS SECT,BIOMETR RES BRANCH,BETHESDA,MD 20892.
FU NIDCR NIH HHS [DE08713]
NR 9
TC 20
Z9 25
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0889-5406
J9 AM J ORTHOD DENTOFAC
JI Am. J. Orthod. Dentofac. Orthop.
PD APR
PY 1996
VL 109
IS 4
BP 393
EP 402
DI 10.1016/S0889-5406(96)70121-X
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA UF041
UT WOS:A1996UF04100010
PM 8638581
ER
PT J
AU Smith, ML
Fornace, AJ
AF Smith, ML
Fornace, AJ
TI The two faces of tumor suppressor p53
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID CELL
RP Smith, ML (reprint author), NCI,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT,NIH,BLDG 37,ROOM 5C09,BETHESDA,MD 20892, USA.
RI Fornace, Albert/A-7407-2008
OI Fornace, Albert/0000-0001-9695-085X
NR 39
TC 52
Z9 54
U1 0
U2 0
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 1996
VL 148
IS 4
BP 1019
EP 1022
PG 4
WC Pathology
SC Pathology
GA UD966
UT WOS:A1996UD96600001
PM 8644842
ER
PT J
AU Morris, CB
Gendelman, R
Marrogi, AJ
Lu, M
Lockyer, JM
AlperinLea, W
Ensoli, B
AF Morris, CB
Gendelman, R
Marrogi, AJ
Lu, M
Lockyer, JM
AlperinLea, W
Ensoli, B
TI Immunohistochemical detection of bcl-2 in AIDS-associated and classical
Kaposi's sarcoma
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; PROGRAMMED CELL-DEATH; YOUNG HOMOSEXUAL
MEN; TAT PROTEIN; TUMOR-SUPPRESSOR; WILD-TYPE; P53; GROWTH; EXPRESSION;
APOPTOSIS
AB Kaposi's Sarcoma (KS) is an angioproliferative disease that is characterized by, proliferation of spindle-shaped cells predominantly of vascular endothelial cell origin, neoangiogenesis, inflammatory cell infiltration, and edema. Although the lesions of classical KS and AIDS-associated KS (AIDS-KS) share common histological features, AIDS-KS occurs at a markedly higher frequency with a more aggressive clinical course Immunohistochemical analyses of 26 evolutionarily staged AIDS-KS lesions derived from HIV-infected patients demonstrate significant cytoplasmic levels of Bcl-2, a protooncogene known to prolong cellular viability and to antagonize apoptosis. Bcl-2 expression increases as the pathological stage of KS advances. Immunohistochemical analyses of classical KS lesions demonstrate prevalent expression of Bcl-2 as well, indicating that upregulation of Bcl-2 may be important in the pathogenesis of both classical and AIDS-associated KS. Coexpression of Bcl-2 and factor VIII-related antigen in spindle-shaped cells present within RS lesions suggests that Bcl-2 is upregulated within the vascular endothelial spindle-shaped cells of KS. The consequences of upregulated Bcl-2 expression within RS lesions may be prolonged spindle cell viability which, when coupled with dysregulated cellular proliferation due in part to synergistic activities of inflammatory and angiogenic cytokines and NN-I Tat protein, may result in the maintenance, growth, and progression of KS.
C1 TULANE UNIV,MED CTR,DEPT PATHOL & LAB MED,TULANE CANC CTR,MOL & CELLULAR BIOL PROGRAM,NEW ORLEANS,LA.
NCI,TUMOR CELL BIOL LAB,NIH,BETHESDA,MD 20892.
TULANE UNIV,MED CTR,DEPT MED,SECT CARDIOL,MOL & CELLULAR BIOL PROGRAM,NEW ORLEANS,LA 70112.
RI Ensoli, Barbara/J-9169-2016
OI Ensoli, Barbara/0000-0002-0545-8737
FU NIAID NIH HHS [AI 32880]
NR 39
TC 34
Z9 35
U1 0
U2 0
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 1996
VL 148
IS 4
BP 1055
EP 1063
PG 9
WC Pathology
SC Pathology
GA UD966
UT WOS:A1996UD96600006
PM 8644847
ER
PT J
AU Tseng, CC
Boylan, MO
Jarboe, LA
Usdin, TB
Wolfe, MM
AF Tseng, CC
Boylan, MO
Jarboe, LA
Usdin, TB
Wolfe, MM
TI Chronic desensitization of the glucose-dependent insulinotropic
polypeptide receptor in diabetic rats
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE downregulation; non-insulin-dependent diabetes mellitus
ID GASTRIC-INHIBITORY POLYPEPTIDE; PANCREATIC ALPHA-CELL; PEPTIDE-1 7-36
AMIDE; HOMOLOGOUS DESENSITIZATION; ADENYLATE-CYCLASE; GIP; RELEASE;
BLOOD
AB Rats were rendered diabetic by streptozotocin, after which serum glucose-dependent insulinotropic polypeptide (GIP) levels, duodenal mucosal GIP content, and GIP mRNA levels were nine times, 50%, and 80%, respectively, greater than in control rats. To determine whether an increase in GIP gene expression might induce chronic desensitization of its receptor, normal rats were subjected to continuous intravenous GIP infusion. Serum GIP levels increased gradually in GIP-infused rats, and by 4 h a threefold increase was detected. In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. The response to glucagon-like peptide-1 (GLP-1) was preserved, indicating that desensitization was ligand specific. To determine the mechanisms governing desensitization of this receptor, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. GIP stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in LGIPR2 cells, which was first detected after 1 h of stimulation, reached maximum level at 4 h, and returned to basal concentrations by 16 h. Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. In contrast, a response to prostaglandin E(1) or forskolin in GIP-desensitized LGIPR2 cells was unchanged, suggesting that desensitization was a receptor-specific process. The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line.
C1 HARVARD UNIV, SCH MED, DIV GASTROENTEROL, HARVARD DIGEST DIS CTR, BOSTON, MA 02115 USA.
NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA.
RP Tseng, CC (reprint author), BRIGHAM & WOMENS HOSP, DIV GASTROENTEROL, 75 FRANCIS ST, BOSTON, MA 02115 USA.
FU NIDDK NIH HHS [DK-02277, DK-48042, P30-DK-34854]
NR 30
TC 45
Z9 47
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 APR
PY 1996
VL 270
IS 4
BP E661
EP E666
PG 6
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA UE561
UT WOS:A1996UE56100018
PM 8928774
ER
PT J
AU Ecelbarger, CA
Chou, CL
Lolait, SJ
Knepper, MA
DiGiovanni, SR
AF Ecelbarger, CA
Chou, CL
Lolait, SJ
Knepper, MA
DiGiovanni, SR
TI Evidence for dual signaling pathways for V-2 vasopressin receptor in rat
inner medullary collecting duct
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY
LA English
DT Article
DE water permeability; V-1a receptor; adenosine 3',5'-cyclic monophosphate;
intracellular calcium; secondary messengers; signaling; vasopressin
analogues; oxytocin
ID POLYMERASE CHAIN-REACTION; WATER PERMEABILITY; ADENYLYL CYCLASE;
PHOSPHOLIPASE-C; CA2+ MOBILIZATION; NEPHRON SEGMENTS; V2 RECEPTOR;
CELLS; OXYTOCIN; TUBULES
AB Previous studies have demonstrated that both the V-2-receptor agonist, 1-desamino-8-D-arginine vasopressin (dDAVP), and the V-1a-receptor agonist, [Phe(2),Orm(8)]vasotocin (PO-VT), increase intracellular calcium concentration( [Ca2+](i)) in the rat inner medullary collecting duct (IMCD). The present studies were done to clarify the receptor subtype(s) responsible for calcium mobilization. Measurements of [Ca2+](i) using fura 2 in microdissected IMCD segments, confirmed that arginine vasopressin (AVP), dDAVP, and PO-VT stimua late an increase in [Ca2+](i) and that the response to all three agents could be blocked by the specific V-2-receptor antagonist, [d(CH2)(5)(1),D-Ile(2),Ile(4),Arg(8)]vasopressin (II-VP). These results would suggest that all three agents acted through the V-2 receptor. Furthermore, we showed that PO-VT increased cAMP production in IMCD suspensions and water permeability in isolated perfused tubules. These responses were also blocked by II-VP, indicating that PO-VT is also a V-2 agonist in the IMCD. Finally, we utilized the quantitative reverse transcription-polymerase chain reaction technique of Wiesner (Nucleic Acids Res. 20: 5863-5864, 1992) to evaluate V-1a and V-2 mRNA levels in rat collecting duct. In terminal IMCD, we estimated >30 copies/cell for V-2 receptor mRNA but less than 1 copy/cell of V-1a receptor mRNA, thus there is little or no V-1a mRNA expression in the terminal IMCD. These results suggest that calcium mobilization in response to vasopressin analogues is associated with the V-2 receptor and that the V-2 receptor is linked to both adenylyl cyclase and calcium mobilization in the rat IMCD.
C1 NHLBI, KIDNEY & ELECTROLYTE METAB LAB, NIH, BETHESDA, MD 20892 USA.
NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA.
FU NIDDK NIH HHS [DK-00832]
NR 40
TC 81
Z9 82
U1 0
U2 2
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 APR
PY 1996
VL 270
IS 4
BP F623
EP F633
PG 11
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA UE696
UT WOS:A1996UE69600007
PM 8967340
ER
PT J
AU Frokiaer, J
Marples, D
Knepper, MA
Nielsen, S
AF Frokiaer, J
Marples, D
Knepper, MA
Nielsen, S
TI Bilateral ureteral obstruction downregulates expression of
vasopressin-sensitive AQP-2 water channel in rat kidney
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY
LA English
DT Article
DE polyuria; nephrongenic diabetes insipidus; postobstructive diuresis
ID POSTOBSTRUCTIVE DIURESIS; TRANSPORT DEFECTS; DEEP NEPHRON; YOUNG RAT;
SEGMENTS; PROTEIN; CELLS
AB Polyuria after release of bilateral ureteral obstruction (BUO) is frequently seen in patients with urological disorders. In this study, we examined the effect of BUO and release of BUO on the expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in rat kidney. Ureters were obstructed for 24 h in all experiments, and BUO was either not released or released for 24 or 48 h or 7 days. Each group of experimental rats were matched with sham-operated controls. One kidney was used for membrane fractionation and immunoblotting, whereas the contralateral was fixed for immunocytochemistry. Immunoblotting demonstrated a significant reduction in AQP-2 expression in inner medulla during 24 h of BUO to 26 +/- 8% (P < 0.001). Release of BUO was associated with immediate onset of a predominant osmotic-dependent polyuria. Forty-eight hours after release of BUO, the reduction in AQP-2 expression persisted (19 +/- 8%, P < 0.001), concurrent with a marked nonosmotic postobstructive polyuria, as determined by a significant reduction in free-water clearance (-50 +/- 7 vs. -85 +/- 10 mu l . min(-1). kg(-1), P < 0.05). Immunofluorescence and immunoelectron microscopy confirmed the reduced levels of AQP-2 in collecting duct principal cells. Seven days after release, the renal excretion of water and electrolytes had almost normalized. However, the downregulation of AQP-2 was only partly reversed (49 +/- 14%, P < 0.001), and, consistent with this, the urinary concentrating capacity was significantly reduced 7 days after release of BUO compared with sham-operated rats in response to an 18-h period of thirst. This strongly suggests that the persistent downregulation of AQP-2 is the cause of the slow recovery in concentrating capacity. In conclusion, BUO and release of BUO were associated with a marked reduction in expression of AQP-2, coincident with the development and maintenance of postobstructive polyuria. Thus reduced AQP-2 levels may represent an important factor in the slow recovery from postobstructive diuresis.
C1 AARHUS UNIV, INST ANAT, DEPT CELL BIOL, DK-8000 AARHUS C, DENMARK.
AARHUS UNIV HOSP, DEPT CLIN PHYSIOL, DK-8000 AARHUS, DENMARK.
AARHUS UNIV, INST EXPTL CLIN RES, DK-8000 AARHUS C, DENMARK.
NHLBI, KIDNEY & ELECTROLYTE METAB LAB, BETHESDA, MD 20892 USA.
NR 37
TC 134
Z9 138
U1 0
U2 2
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 APR
PY 1996
VL 270
IS 4
BP F657
EP F668
PG 12
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA UE696
UT WOS:A1996UE69600011
PM 8967344
ER
PT J
AU Liu, LT
Khastgir, A
McCauley, JM
Dunn, ST
Morrissey, JH
Christakos, S
Hughes, MR
Bourdeau, JE
AF Liu, LT
Khastgir, A
McCauley, JM
Dunn, ST
Morrissey, JH
Christakos, S
Hughes, MR
Bourdeau, JE
TI RT-PCR microlocalization of mRNAS for calbindin D-28k and vitamin D
receptor in the murine nephron
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY
LA English
DT Article
DE reverse transcription; polymerase chain reaction; messenger ribonucleic
acid
ID CALCIUM-BINDING PROTEINS; MOUSE KIDNEY; GENE-EXPRESSION; RAT-KIDNEY;
LOCALIZATION; VERTEBRATES
AB The spatial relationship between vitamin D receptor (VDR) and calbindin D-28k [calcium binding protein D-28k (CaBP-D-28k)] gene expression within the murine kidney was studied by localizing their mRNAs in discrete nephron structures using reverse transcription-polymerase chain reaction (RT-PCR). Primers for beta-actin mRNA were used as a control for the presence of tissue during RT-PCR for CaBP-D-28k mRNA. mRNA for CaBP-D-28k was found only in distal convoluted tubules (DCTs), connecting tubules (CNTs), and cortical collecting ducts (CCDs). In contrast, VDR mRNA was detected in glomeruli, S2 proximal convoluted tubules, cortical thick ascending limbs of Henle's loop, DCTs, CNTs, and initial CCDs. The presence of both VDR and CaBP-D-28k mRNA in DCTs, CNTs, and CCDs is consistent with the hypothesis that calcitriol acts via the VDR to stimulate CaBP-D-28k synthesis. Conversely, the presence of VDR mRNA in other parts of the nephron suggests that calcitriol has genomically mediated actions within the kidney in addition to stimulation of CaBP-D-28k synthesis.
C1 UNIV OKLAHOMA, HLTH SCI CTR, DEPT MED, NEPHROL SECT, OKLAHOMA CITY, OK USA.
UNIV OKLAHOMA, HLTH SCI CTR, DEPT PATHOL, OKLAHOMA CITY, OK USA.
UNIV OKLAHOMA, HLTH SCI CTR, DEPT PHYSIOL & BIOPHYS, OKLAHOMA CITY, OK USA.
DEPT VET AFFAIRS MED CTR, MED SERV, OKLAHOMA CITY, OK USA.
OKLAHOMA MED RES FDN, CARDIOVASC BIOL PROGRAM, OKLAHOMA CITY, OK 73104 USA.
NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA.
UNIV MED & DENT NEW JERSEY, NEW JERSEY MED SCH, DEPT BIOCHEM & MOLEC BIOL, NEWARK, NJ 07103 USA.
FU NIDDK NIH HHS [DK-41427, DK-35985, DK-38961]
NR 22
TC 16
Z9 18
U1 0
U2 1
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 APR
PY 1996
VL 270
IS 4
BP F677
EP F681
PG 5
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA UE696
UT WOS:A1996UE69600013
PM 8967346
ER
PT J
AU Coryell, W
Leon, A
Winokur, G
Endicott, J
Keller, M
Akiskal, H
Solomon, D
AF Coryell, W
Leon, A
Winokur, G
Endicott, J
Keller, M
Akiskal, H
Solomon, D
TI Importance of psychotic features to long-term course in major depressive
disorder
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID DEXAMETHASONE SUPPRESSION TEST; FOLLOW-UP; DELUSIONAL DEPRESSION;
UNIPOLAR DEPRESSION; SEPARATE ENTITY; SUICIDE; SUBTYPES
AB Objective: Most efforts to describe the prognostic significance of psychotic features in depression have been limited to single assessments 1 year or less after the initial evaluation. However, the various biological and treatment response differences between patients with psychotic and nonpsychotic depression suggest that prognostic differences may be very long-term. Method: The 787 patients described here entered the study as they sought treatment at one of five academic medical centers; they had either RDC major depressive disorder or schizoaffective depression (other than the mainly schizophrenic subtype) and completed at least 6 months of follow-up. Of these, 144 (18.3%) had psychotic depression as defined here. Patients provided follow-up interviews at 6-month intervals for 5 years and annually thereafter; 98 of those with psychotic depression and 434 of those with nonpsychotic depression were followed for 10 years. Results: Those who began follow-up with psychotic depression had fewer weeks with minimal symptoms in each of the 10 years of follow-up and reported more psychosocial impairment at both 5 and 10 years. Both the index episode and the first recurrence of psychotic depression lasted longer than nonpsychotic episodes, but nonpsychotic episodes among previously psychotic individuals were relatively brief. Intervals between episodes were significantly shorter for patients who had ever been psychotic. Conclusions: Together with evidence that psychotic features are highly recurrent, these data show 1) that psychotic features denote a lifetime illness of greater severity and 2) that within individuals, psychotic features may emerge in only the more severe episodes.
C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESSION CLIN STU,BETHESDA,MD 20892.
RP Coryell, W (reprint author), UNIV IOWA,DEPT PSYCHIAT,200 HAWKINS DR,IOWA CITY,IA 52242, USA.
FU NIMH NIH HHS [R01 MH025478]
NR 38
TC 115
Z9 117
U1 2
U2 4
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD APR
PY 1996
VL 153
IS 4
BP 483
EP 489
PG 7
WC Psychiatry
SC Psychiatry
GA UC478
UT WOS:A1996UC47800006
PM 8599395
ER
PT J
AU Frazier, JA
Giedd, JN
Kaysen, D
Albus, K
Hamburger, S
AlaghbandRad, J
Lenane, MC
McKenna, K
Breier, A
Rapoport, JL
AF Frazier, JA
Giedd, JN
Kaysen, D
Albus, K
Hamburger, S
AlaghbandRad, J
Lenane, MC
McKenna, K
Breier, A
Rapoport, JL
TI Childhood-onset schizophrenia: Brain MRI rescan after 2 years of
clozapine maintenance treatment
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID CORTEX
AB Objective: The effect of clozapine on striatal morphology was examined in adolescents with childhood-onset schizophrenia. Method: Eight adolescent patients with onset of psychosis before age 12 and eight matched comparison subjects had initial and 2-year follow-up brain magnetic resonance imaging scans. Basal ganglia and lateral ventricle volumes were measured. The patients were on a clozapine regimen during the 2-year interim. Results: Caudate volume was larger in the patients at the initial scanning, decreased in the patients between scans, and did not differ significantly between the patients and the comparison subjects at the second scanning. Conclusions: Caudate enlargement in patients with childhood-onset schizophrenia who are taking typical neuroleptics appears to be secondary to medication exposure. Rescanning to examine basal ganglia morphology is indicated for these patients when they are taking an atypical neuroleptic.
C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892.
NIMH,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892.
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 15
TC 103
Z9 105
U1 0
U2 2
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD APR
PY 1996
VL 153
IS 4
BP 564
EP 566
PG 3
WC Psychiatry
SC Psychiatry
GA UC478
UT WOS:A1996UC47800021
PM 8599409
ER
PT J
AU Avila, NA
Worobec, AS
Ling, A
Hijazi, Y
Metcalfe, DD
AF Avila, NA
Worobec, AS
Ling, A
Hijazi, Y
Metcalfe, DD
TI Pulmonary and ovarian manifestations of systemic mastocytosis
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
ID MAST-CELL DISEASE
C1 NIAID,ALLERG DIS SECT,NIH,BETHESDA,MD 20892.
NIH,DEPT PATHOL,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892.
RP Avila, NA (reprint author), NIH,DEPT DIAGNOST RADIOL,HENRY M JACKSON FDN,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,RM 1C660,BETHESDA,MD 20892, USA.
NR 8
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 APR
PY 1996
VL 166
IS 4
BP 969
EP 970
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA UB521
UT WOS:A1996UB52100040
PM 8610583
ER
PT J
AU Zhong, M
McCarthy, J
Bierwert, L
LizotteWaniewski, M
Chanteau, S
Nutman, TB
Ottesen, EA
Williams, SA
AF Zhong, M
McCarthy, J
Bierwert, L
LizotteWaniewski, M
Chanteau, S
Nutman, TB
Ottesen, EA
Williams, SA
TI A polymerase chain reaction assay for detection of the parasite
Wuchereria bancrofti in human blood samples
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID SPECIES-SPECIFIC DETECTION; REPEATED DNA-SEQUENCES; OLIGONUCLEOTIDE
PROBES; BRUGIA-PAHANGI; FILARIASIS; MALAYI
AB To identify Wuchereria bancrofti DNA sequences that could be used as the basis for a simple and rapid parasite detection assay, a genomic library of W. bancrofti was constructed and screened for highly repeated DNA. The repeat found with the highest copy number was 195 basepairs (bps) long, 77% AT, and 300 copies per haploid genome. This sequence was designated the Ssp I repeat because it has a unique recognition site for that restriction endonuclease in all or most of the repeat copies. The Ssp I repeat DNA family is dispersed, genus-specific, and exists in all of the different geographic isolates of W. bancrofti tested. Based on DNA sequence analysis of this repeat, we have developed an assay to detect very small quantities of W. bancrofti DNA using the polymerase chain reaction (PCR). With this PCR assay, the Ssp I repeat was detected in as little as 1 pg of W. bancrofti genomic DNA (about 1% of the DNA in one microfilaria) added to 100 mu l of human blood. The PCR assay also amplified Ssp I repeat DNA from geographic isolates of W. bancrofti from around the world but not from other species of filariae or from human or mosquito DNA. Microfilaria-positive human blood samples collected in Mauke, Cook Islands were shown to be Ssp I PCK-positive, while microfilaria-negative samples were PCR-negative. The specificity and sensitivity of the Ssp I PCR assay indicates that this approach has significant potential for improved screening of large human populations for active W. bancrofti infection.
C1 INST TERRITORIAL RECH MED LOUIS MALARDE,PAPEETE,TAHITI,FR POLYNESIA.
NIAID,NATL INST HLTH,PARASIT DIS LAB,BETHESDA,MD 20892.
RP Zhong, M (reprint author), SMITH COLL,CLARK SCI CTR,DEPT BIOL SCI,NORTHAMPTON,MA 01063, USA.
RI McCarthy, James/C-1681-2009; yu, yan/C-2322-2012
FU PHS HHS [636005]
NR 12
TC 81
Z9 82
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD APR
PY 1996
VL 54
IS 4
BP 357
EP 363
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA UJ490
UT WOS:A1996UJ49000009
PM 8615447
ER
PT J
AU Vernick, KD
Keister, DB
Toure, A
Toure, YT
AF Vernick, KD
Keister, DB
Toure, A
Toure, YT
TI Quantification of Plasmodium falciparum sporozoites by ribosomal RNA
detection
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID CIRCUMSPOROZOITE PROTEIN; MALARIA SPOROZOITES; ANTIBODIES; TARGET; GENES
AB We used sequences specific to the small subunit ribosomal RNA (SSU rRNA) of the sporogonic stages of Plasmodium falciparum to design a reverse transcriptase-polymerase chain reaction (RT-PCR) assay that can detect 0.1 sporozoites in total RNA purified from potentially infected mosquitoes. We made a synthetic RNA that is amplified in the RT-PCR by the same primers as the parasite SSU rRNA and that serves as an internal control and competitive quantitation standard. We calibrated the assay for quantitation of sporozoites by making a standard curve with RNA from purified and counted sporozoites. The assay accurately measured sporozoite number with a linear range of at least three orders of magnitude in a single reaction. Some applications and limitations of the assay are discussed.
C1 ECOLE NATL MED & PHARM,DEPT EPIDEMIOL AFFECTAT PARASITAIRES,BAMAKO,MALI.
RP Vernick, KD (reprint author), NIAID,NATL INST HLTH,PARASIT DIS LAB,BETHESDA,MD 20892, USA.
NR 15
TC 14
Z9 16
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD APR
PY 1996
VL 54
IS 4
BP 430
EP 438
PG 9
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA UJ490
UT WOS:A1996UJ49000022
PM 8615460
ER
PT J
AU Ma, Y
Ito, Y
AF Ma, Y
Ito, Y
TI Affinity countercurrent chromatography using a ligand in the stationary
phase
SO ANALYTICAL CHEMISTRY
LA English
DT Article
AB In countercurrent chromatography (CCC), an addition of a ligand to the liquid stationary phase remarkably improved both retention time and peak resolution of the analytes: various amino acid derivatives were separated by N-dodecanoyl-L-proline-3,5-dimethylanilide, while polar catecholamines and dipeptides were separated by bis(2-ethylhexyl)phosphoric acid. By selecting an appropriate ligand and dissolving it in the liquid stationary phase, the present CCC technique can perform a variety of separations comparable to chiral chromatography, ion chromatography, and affinity chromatography. Leakage of the ligand from the column can be entirely eliminated by introducing a small volume of a ligand-free stationary phase at the end of the column as an absorbent. The method further facilitates application of pH-zone-refining CCC and can uncrease the sample loading capacity over 10 times for a given column.
C1 NHLBI,NATL INST HLTH,BIOPHYS CHEM LAB,BETHESDA,MD 20892.
NR 13
TC 22
Z9 24
U1 4
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD APR 1
PY 1996
VL 68
IS 7
BP 1207
EP 1211
DI 10.1021/ac9509263
PG 5
WC Chemistry, Analytical
SC Chemistry
GA UC182
UT WOS:A1996UC18200028
PM 8651493
ER
PT J
AU Kirch, W
Horneber, M
Tamm, ER
AF Kirch, W
Horneber, M
Tamm, ER
TI Characterization of Meibomian gland innervation in the cynomolgus monkey
(Macaca fascicularis)
SO ANATOMY AND EMBRYOLOGY
LA English
DT Article
DE neuropeptide; nitric oxide; eyelid; double-labeling method;
immunocytochemistry
ID GENE-RELATED PEPTIDE; VASOACTIVE INTESTINAL POLYPEPTIDE; NITRIC-OXIDE
SYNTHASE; CRANIAL PARASYMPATHETIC NEURONS; IMMUNOREACTIVE NERVE-FIBERS;
SUBSTANCE-P; NEUROPEPTIDE-Y; GUINEA-PIG; TRIGEMINAL GANGLION; NADPH
DIAPHORASE
AB To characterize the innervation of the cynomolgus monkey (Macaca fascicularis) Meibomian (tarsal) glands, upper lids of six cynomolgus monkeys were investigated with electronmicroscopical and double-labeling immunocytochemical methods. Antibodies against calcitonin gene-related peptide (CGRP), dopamine-beta-hydroxylase (DBH), neuropeptide Y (NPY), nitric oxide synthase (NOS), protein gene product 9.5 (PGP 9.5), substance P (SP), tyrosine hydroxylase (TH), and vasoactive intestinal peptide (VIP) were used. In addition, sections were processed for NADPH-diaphorase (NADPH-d) histochemistry. Staining for PGP 9.5 and electron microscopy showed that Meibomian gland acini were surrounded by a network of unmyelinated nerves and terminal varicose axons. The terminals contained small agranular (30-60 nm) and large granular vesicles (65-110 nm), and were observed in close contact with the basal lamina of the acini, but never internally to the basal lamina. Meibomian axons showed like-immunoreactivity (LI) for the neuropeptides SP, CGRP, NPY, and VIP. In addition, the axons stained for TH, DBH, NOS, and NADPH-d. VIP-LI, NOS- and NADPH-d-positive axons appeared to be more numerous, TH- and DBH-positive axons more rare than others. Most SP-LI axons were double-labelled for CGRP-LI, some for VIP-LI or NPY-LI. In addition, some VIP-LI axons were double-labeled for NPY-LI. NPY/VIP-LI and NPY/SP-LI axons were only observed close to the Meibomian acini. Conversely, NPY-LI colocalized with TH-IR or DBH-IR predominated in perivascular nerves of Meibomian gland vasculature. The close association of varicose axons with the acini of Meibomian glands indicates that nervous signals modulate meibomian secretion. Meibomian gland nerve fibers in the cynomolgus monkey appear to utilize various neuropeptides, catecholamines and nitric oxide as transmitter substances, and seem to derive from the pterygopalatine, superior cervical and trigeminal ganglion respectively.
C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892.
UNIV ERLANGEN NURNBERG,DEPT ANAT 2,UNIVERSITATSSTR 19,D-91054 ERLANGEN,GERMANY.
NR 74
TC 20
Z9 20
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0340-2061
J9 ANAT EMBRYOL
JI Anat. Embryol.
PD APR
PY 1996
VL 193
IS 4
BP 365
EP 375
PG 11
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA UC857
UT WOS:A1996UC85700006
PM 8694272
ER
PT J
AU Martin, JL
Laster, MJ
Kandel, L
Kerschmann, RL
Reed, GF
Eger, EI
AF Martin, JL
Laster, MJ
Kandel, L
Kerschmann, RL
Reed, GF
Eger, EI
TI Metabolism of compound A by renal cysteine-S-conjugate beta-lyase is not
the mechanism of compound A-induced renal injury in the rat
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
ID GLUTATHIONE DEPLETION; DEGRADATION PRODUCTS; SEVOFLURANE;
NEPHROTOXICITY; KIDNEY
AB Compound A [CF2=C(CF3)OCH2F], a vinyl ether produced by CO2 absorbents acting on sevoflurane, can produce corticomedullary junction necrosis (injury to the outer stripe of the outer medullary layer, i.e., corticomedullary junction) in rats. Several halogenated alkenes produce a histologically similar corticomedullary necrosis by converting glutathione conjugates of these alkenes to halothionoacetyl halides. To test whether this mechanism explained the nephrotoxicity of Compound A, we blocked three metabolic steps which would lead to formation of a halothionoacetyl halide: 1) we depleted glutathione by administering dl-buthionine-S,R-sulfoximine (BSO); 2) we blocked cysteine S-conjugate formation by administering acivicin (AT-125); and 3) we inhibited subsequent metabolism by renal cysteine conjugate beta-lyase to the nephrotoxic acetic acid (AOAA). These treatments were given alone or in combination to separate groups of 10 or 20 Wistar rats before their exposure to Compound A. We hypothesized that blocking these metabolic steps should decrease the injury produced by breathing 150 ppm of Compound A for 3 h. However, we found either no change or an increase in renal injury, suggesting that this pathway mediates detoxification rather than toxicity. Our findings suggest that the cysteine-S-conjugate-mediated pathway is not the mechanism of Compound A nephrotoxicity and, therefore, observed interspecies differences in the activity of this activating pathway may not be relevant in the prediction of the nephrotoxic potential of Compound A in clinical practice.
C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205.
NIAID,NIH,DIV MICROBIOL & INFECT DIS,BIOMETRY BRANCH,BETHESDA,MD 20892.
UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143.
UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143.
UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143.
NR 25
TC 35
Z9 35
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0003-2999
J9 ANESTH ANALG
JI Anesth. Analg.
PD APR
PY 1996
VL 82
IS 4
BP 770
EP 774
DI 10.1097/00000539-199604000-00017
PG 5
WC Anesthesiology
SC Anesthesiology
GA UC482
UT WOS:A1996UC48200017
PM 8615496
ER
PT J
AU Cohen, SG
Settipane, GA
AF Cohen, SG
Settipane, GA
TI Hymenoptera honored again
SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY
LA English
DT Letter
C1 BROWN UNIV,PROVIDENCE,RI 02912.
RP Cohen, SG (reprint author), NIAID,NIH,BETHESDA,MD 20892, USA.
NR 6
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY
PI ARLINGTON HTS
PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005
SN 1081-1206
J9 ANN ALLERG ASTHMA IM
JI Ann. Allergy Asthma Immunol.
PD APR
PY 1996
VL 76
IS 4
BP 379
EP 380
PG 2
WC Allergy; Immunology
SC Allergy; Immunology
GA UF806
UT WOS:A1996UF80600016
ER
PT J
AU Cohen, SG
Bianchini, PJ
AF Cohen, SG
Bianchini, PJ
TI Hymenoptera honored again
SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY
LA English
DT Letter
C1 BROWN UNIV,PROVIDENCE,RI 02912.
RP Cohen, SG (reprint author), NIAID,NIH,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY
PI ARLINGTON HTS
PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005
SN 1081-1206
J9 ANN ALLERG ASTHMA IM
JI Ann. Allergy Asthma Immunol.
PD APR
PY 1996
VL 76
IS 4
BP 379
EP 379
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA UF806
UT WOS:A1996UF80600015
ER
PT J
AU Licht, T
Pastan, I
Gottesman, MM
Herrmann, F
AF Licht, T
Pastan, I
Gottesman, MM
Herrmann, F
TI The multidrug-resistance gene in gene therapy of cancer and
hematopoietic disorders
SO ANNALS OF HEMATOLOGY
LA English
DT Review
DE chemotherapy; myelosuppression; hematopoietic stem cells;
P-glycoprotein; dihydrofolate reductase
ID BONE-MARROW CELLS; DIHYDROFOLATE-REDUCTASE GENE; ADENOSINE-DEAMINASE
GENE; MDR1 MESSENGER-RNA; P-GLYCOPROTEIN; TRANSGENIC MICE; STEM-CELLS;
MONOCLONAL-ANTIBODIES; DRUG-RESISTANCE; RETROVIRAL TRANSFER
AB Chemoresistance genes have been identified as an impediment to anticancer drug treatment. In particular, P-glycoprotein, the product of the multidrug-resistance (MDR1) gene, plays a major role in clinical treatment failure. Conversely, expression of an MDR1 cDNA in bone marrow of transgenic animals renders hematopoietic cells chemoresistant. Efficient transfer of drug-resistance genes to normal hematopoietic progenitor cells has been achieved with the use of retroviral vectors. In this article we review approaches which use the multidrug-resistance gene to protect bone marrow from myelosuppression following chemotherapy and as a selectable markerin vivo to increase the expression of nonselectable genes which correct hereditary diseases of the hematopoietic system.
C1 NCI,MOLEC BIOL LAB,DIV CANC BIOL DIAG & CTR,NIH,BETHESDA,MD 20892.
RP Licht, T (reprint author), UNIV ULM,DEPT INTERNAL MED 3,ROBERT KOCH STR 8,D-89081 ULM,GERMANY.
NR 119
TC 20
Z9 22
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0939-5555
J9 ANN HEMATOL
JI Ann. Hematol.
PD APR
PY 1996
VL 72
IS 4
BP 184
EP 193
DI 10.1007/s002770050159
PG 10
WC Hematology
SC Hematology
GA UG571
UT WOS:A1996UG57100005
PM 8624371
ER
PT J
AU Lenders, JWM
Keiser, HR
Eisenhofer, G
AF Lenders, JWM
Keiser, HR
Eisenhofer, G
TI Plasma metanephrines in the diagnosis of pheochromocytoma - In response
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Letter
RP Lenders, JWM (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA.
NR 1
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 APR 1
PY 1996
VL 124
IS 7
BP 695
EP 695
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA UB513
UT WOS:A1996UB51300020
ER
PT J
AU Dalakas, MC
Quarles, RH
AF Dalakas, MC
Quarles, RH
TI Autoimmune ataxic neuropathies (sensory ganglionopathies): Are
glycolipids the responsible autoantigens?
SO ANNALS OF NEUROLOGY
LA English
DT Editorial Material
ID MONOCLONAL IGM; PATIENT; POLYNEUROPATHY; GANGLIOSIDES; BINDS
C1 NINCDS,MOLEC & CELLULAR NEUROBIOL LAB,NIH,BETHESDA,MD 20892.
RP Dalakas, MC (reprint author), NINCDS,NEUROMUSCULAR DIS SECT,NIH,BETHESDA,MD 20892, USA.
NR 17
TC 46
Z9 47
U1 0
U2 0
PU LITTLE BROWN CO
PI BOSTON
PA 34 BEACON STREET, BOSTON, MA 02108-1493
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD APR
PY 1996
VL 39
IS 4
BP 419
EP 422
DI 10.1002/ana.410390402
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA UF808
UT WOS:A1996UF80800001
PM 8619518
ER
PT J
AU Goldfarb, LG
Vasconcelos, O
Platonov, FA
Lunkes, A
Kipnis, V
Kononova, S
Chabrashvili, T
Vladimirtsev, VA
Alexeev, VP
Gajdusek, DC
AF Goldfarb, LG
Vasconcelos, O
Platonov, FA
Lunkes, A
Kipnis, V
Kononova, S
Chabrashvili, T
Vladimirtsev, VA
Alexeev, VP
Gajdusek, DC
TI Unstable triplet repeat and phenotypic variability of spinocerebellar
ataxia type 1
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID HEREDITARY ATAXIA; CAG REPEAT; HLA; SIBERIA; LINKAGE
AB A Siberian kindred with spinocerebellar ataxia genetically linked to the SCA1 locus on chromosome 6p has been screened for the CAG triplet expansion within the coding region of the SCA1 gene. The kindred includes 1,484 individuals, 225 affected and 656 at risk, making this collection the largest spinocerebellar ataxia type 1 (SCA1) pedigree known. Each of the studied 78 SCA1 patients carried an expanded allele containing a stretch of 39 to 72 uninterrupted CAG repeats. Normal alleles had 25 to 37 trinucleotide repeats. Expanded alleles containing 40 to 55 repeats were found in 26 at-risk relatives. The number of CAG repeats in the mutated allele was inversely correlated with age at disease onset. Cerebellar deficiency was present in each patient and its severity was moderately affected by the number of CAG repeats. In contrast, the associated signs, dysphagia, diffuse skeletal muscle atrophy with fasciculations, and tongue atrophy were absent or mild in patients with low CAG repeat numbers, but severely complicated the course of illness in patients with a larger number of repeat units. One female mutation carrier was asymptomatic at age 66, more than 2 standard deviations beyond the average age of risk, suggesting incomplete penetrance. In 2 symptomatic individuals who had an expanded number of CAG repeats on both chromosomes, age at onset, rate of progression, and clinical manifestation corresponded to the size of the larger allele.
C1 NINDS,CLIN NEUROGENET UNIT,MED NEUROL BRANCH,BETHESDA,MD 20892.
NINDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892.
NCI,BIOMETRY BRANCH,NIH,BETHESDA,MD 20892.
RES CTR NEURODEGENERAT DISORDERS,YAKUTSK,SAKHA REPUBL,RUSSIA.
UNIV DUSSELDORF,DEPT NEUROL,W-4000 DUSSELDORF,GERMANY.
NR 25
TC 52
Z9 58
U1 2
U2 4
PU LITTLE BROWN CO
PI BOSTON
PA 34 BEACON STREET, BOSTON, MA 02108-1493
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD APR
PY 1996
VL 39
IS 4
BP 500
EP 506
DI 10.1002/ana.410390412
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA UF808
UT WOS:A1996UF80800011
PM 8619528
ER
PT J
AU DeJonge, BLM
Handwerger, S
Gage, D
AF DeJonge, BLM
Handwerger, S
Gage, D
TI Altered peptidoglycan composition in vancomycin-resistant Enterococcus
faecalis
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID STAPHYLOCOCCUS-AUREUS STRAIN; ALANYL-D-ALANINE; FAECIUM BM4147;
ESCHERICHIA-COLI; GLYCOPEPTIDE RESISTANCE; PENICILLIN; PRECURSORS;
BIOSYNTHESIS; CARBOXYPEPTIDASE; PROTEINS
AB The muropeptide compositions of isogenic vancomycin-resistant and -susceptible Enterococcus faecalis strains were analyzed by reverse-phase high-performance liquid chromatography combined with amino acid analysis and fast atom bombardment mass spectrometry, Peptidoglycan of the susceptible strain contained pentapeptides as stem peptides, whereas peptidoglycan of the isogenic resistant strain was composed of muropeptides with tetrapeptide stem peptides. Despite the synthesis of lactate-terminating peptidoglycan precursors, no lactate-containing muropeptides were detected In peptidoglycan of the resistant strain. These findings indicate that either lactate-terminating precursors are not incorporated into peptidoglycan of the resistant strain or that the lactate residues are removed from peptidoglycan during synthesis.
C1 MICHIGAN STATE UNIV,DEPT BIOCHEM,NIH,MASS SPECTROMETRY FACIL,E LANSING,MI 48824.
RP DeJonge, BLM (reprint author), ROCKEFELLER UNIV,MICROBIOL LAB,BOX 152,1230 YORK AVE,NEW YORK,NY 10021, USA.
FU NCRR NIH HHS [RR00480]; NIAID NIH HHS [R01 AI31612]
NR 41
TC 18
Z9 18
U1 2
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD APR
PY 1996
VL 40
IS 4
BP 863
EP 869
PG 7
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA UD248
UT WOS:A1996UD24800007
PM 8849241
ER
PT J
AU Gandjbakhche, AH
Bonner, RF
Nossal, R
Weiss, GH
AF Gandjbakhche, AH
Bonner, RF
Nossal, R
Weiss, GH
TI Absorptivity contrast in transillumination imaging of tissue
abnormalities
SO APPLIED OPTICS
LA English
DT Article
DE random walks; optical imaging; detectability; optical contrast
ID SCATTERING MEDIA; TIME
AB We calculate the time-resolved flux of photons transmitted across an optically turbid slab containing a partially absorbing inclusion. An analytical expression is obtained for the flux at a detector positioned opposite a point source (at a distance equal to the thickness of the slab) when the center of the inclusion lies on the line connecting those points. The calculation employs a discrete-time lattice random-walk model of photon transport. The resulting expression is used to assess the affects of time resolution on the detectability of the inclusion.
C1 NIH,PHYS SCI LAB,DIV COMP RES & TECHNOL,BETHESDA,MD 20892.
RP Gandjbakhche, AH (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892, USA.
RI Bonner, Robert/C-6783-2015
NR 30
TC 29
Z9 30
U1 0
U2 0
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036
SN 0003-6935
J9 APPL OPTICS
JI Appl. Optics
PD APR 1
PY 1996
VL 35
IS 10
BP 1767
EP 1774
DI 10.1364/AO.35.001767
PG 8
WC Optics
SC Optics
GA UC179
UT WOS:A1996UC17900025
PM 21085300
ER
PT J
AU Cohn, JA
Tsai, L
Friguet, B
Szweda, LI
AF Cohn, JA
Tsai, L
Friguet, B
Szweda, LI
TI Chemical characterization of a protein-4-hydroxy-2-nonenal cross-link:
Immunochemical detection in mitochondria exposed to oxidative stress
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE free radicals; lipid peroxidation; 4-hydroxy-2-nonenal; protein
cross-linking; Mitochondria
ID LOW-DENSITY-LIPOPROTEIN; LIPID-PEROXIDATION; ISCHEMIA REPERFUSION;
APOLIPOPROTEIN-B; PROTEIN ADDUCTS; FREE-RADICALS; OXIDIZED LDL;
MACROPHAGES; OXYGEN; PRODUCTS
AB We have previously shown that incubation of the model protein glucose-6-phosphate dehydrogenase (Glu-6-PDH) from the bacterium Leuconostoc mesenteroides with 4-hydroxy-2-nonenal (HNE), a major product of lipid peroxidation, results in the formation of cross-linked protein, HNE-modified protein is resistant to proteolytic degradation and acts as an inhibitor of the multicatalytic proteinase, It was therefore important to establish the chemistry of the cross-linking reaction. The formation of cross-linked Glu-6-PDH is associated with the nearly exclusive loss of lysine residues, For this reason the reaction of N-acetyllysine with HNE has been investigated. The E-amino group of lysine reacts with the double bond (C3) and the carbonyl (C1) functions of HNE via Michael addition and Schiff base formation resulting in the production of a 2:1 amino acid-HNE cross-link. Chromatographic detection of this adduct in the acid hydrolysate of HNE-treated Glu-6-PDH reveals that this chemistry is responsible for the formation of cross-linked protein. Antibody to the reduced form of the 2:1 lysine-HNE adduct was prepared, The antibody was used to demonstrate that exposure of isolated liver mitochondria to oxidative stress led to the formation of intra- and intermolecular protein-HNE cross-links. The results of the present study indicate that modifications to protein by lipid peroxidation products may be physiologically relevant and could contribute to the disease- and age-related buildup of damaged protein. (C) 1996 Academic Press, Inc.
C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106.
NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892.
INST PASTEUR,UNITE BIOCHIM CELLULAIRE,F-75724 PARIS 15,FRANCE.
NR 43
TC 111
Z9 115
U1 0
U2 5
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD APR 1
PY 1996
VL 328
IS 1
BP 158
EP 164
DI 10.1006/abbi.1996.0156
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UD396
UT WOS:A1996UD39600022
PM 8638925
ER
PT J
AU Shou, MG
Krausz, KW
Gonzalez, FJ
Gelboin, HV
AF Shou, MG
Krausz, KW
Gonzalez, FJ
Gelboin, HV
TI Metabolic activation of the potent carcinogen dibenzo[a,h]anthracene by
cDNA-expressed human cytochromes P450
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE dibenzo[a,h]anthracene; cytochrome P450; cDNA expression; human liver
microsomes; metabolism; high-performance liquid chromatography
ID VACCINIA VIRUS; HUMAN-TISSUES; DIHYDRODIOLS; DIBENZO(A,H)ANTHRACENE;
DIBENZANTHRACENE; INDUCTION; ENZYMES
AB The metabolic activation of the potent carcinogen dibenzo[a,h] anthracene (DB[a,h]A) was investigated with recombinant human cytochrome P450 enzymes 1A2, 2B6, 2C8, 2C9, 2E1, 3A3, 3A4, and 3A5 expressed in hepatoma G2 cells and with 14 different human liver microsomes. Three dihydrodiols, three phenols, and one diphenol were formed and separated by high-performance liquid chromatography and identified by UV absorption and mass spectra. Of all P450s tested, 1A2 and 2C9 were the most active and 2B6 was moderately active in the rate of total DB[a,h]A metabolism (2.5- to 12-fold greater activity than that for other P450s). The trans-3,4-dihydrodiol, generally recognized as a precursor of the ultimate carcinogenic 3,4-diol-1,2-epoxides, was produced most actively by 2C9, then 1A2 and 2B6. The values of enzymatic kinetics (K-m and V-max) indicated that 2C9 had the highest catalytic efficiency (V-max/K-m = 9.7) in the formation of 3,4-dihydrodiol, in contrast to 1A2 (5.9) and 2B6 (4.4). 1A2 had the highest activity toward production of the 1,2-dihydrodiol, which is considered to be a weakly carcinogenic metabolite. Although specific activities of human liver microsomes in overall metabolism of DB[a,h]A markedly differed between individuals, metabolic patterns were observed similar to that generated from 1A2. Since human 1A1, a predominant enzyme for metabolism of polycyclic aromatic hydrocarbons, is not significantly expressed in the liver, hepatic microsomal 2C9, 1A2, and 2B6 all probably contribute to the metabolic activation of DB[a,h]A. (C) 1996 Academic Press, Inc.
RP Shou, MG (reprint author), NCI,MOLEC CARCINOGENESIS LAB,NIH,BLDG 37,BETHESDA,MD 20892, USA.
NR 26
TC 35
Z9 37
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 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD APR 1
PY 1996
VL 328
IS 1
BP 201
EP 207
DI 10.1006/abbi.1996.0161
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UD396
UT WOS:A1996UD39600027
PM 8638931
ER
PT J
AU Hommer, D
Momenan, R
Rawlings, R
Ragan, P
Williams, W
Rio, D
Eckardt, M
AF Hommer, D
Momenan, R
Rawlings, R
Ragan, P
Williams, W
Rio, D
Eckardt, M
TI Decreased corpus callosum size among alcoholic women
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID LIVER-DISEASE; WHITE MATTER; SEX; MRI; CONSUMPTION; INSTRUMENT;
METABOLISM; HISTORY; ATROPHY; DAMAGE
AB Background: Although females appear to be more sensitive to the hepatic consequences of alcoholism, it is not clear if women are more sensitive to the effects of excessive alcohol consumption on the brain than men.
Subjects and Methods: We compared the cross-sectional area of the corpus callosum in a group of 14 hospitalized alcoholic women and 13 hospitalized alcoholic men with a group of nine nonalcoholic women and 10 nonalcoholic men. All subjects were between the ages of 30 and 50 years. The cross-sectional areas of the corpus callosum and the inner table of the skull were measured on midsagittal T-1-weighted magnetic resonance images.
Results: Females had smaller intracranial areas than males, but there was no difference in intracranial area between the alcoholics and nonalcoholics. The corpus callosum area was significantly smaller among the alcoholic women compared with either. the control women or the alcoholic men. Alcoholic men did not differ from control men in the corpus callosum area. These results did not change when the corpus callosum area was adjusted for intracranial area by analysis of covariance. When the corpus callosum was divided into four segments of equal length, the reduction in area was not localized to any particular region.
Conclusion: These results suggest an increased sensitivity to alcohol-induced brain damage among alcoholic women compared with alcoholic men.
C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,NIH,BETHESDA,MD 20892.
NR 27
TC 105
Z9 107
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD APR
PY 1996
VL 53
IS 4
BP 359
EP 363
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA UD631
UT WOS:A1996UD63100013
PM 8929159
ER
PT J
AU Sternberg, P
Brown, JM
Curtis, L
Fremstad, A
Gibbs, D
Gilman, J
Swords, R
Waldron, RG
Bressler, NM
Belt, J
Bressler, SB
Muth, T
Elman, MJ
George, T
Haller, JA
Herring, M
Orr, PR
Schachat, AP
Sotirakos, P
Starr, J
Singerman, LJ
Brown, P
Coreno, K
DeLisio, M
Novak, M
Pinter, AS
Rice, TA
SmithBrewer, S
Fish, GE
Aguado, H
Anderson, T
Crockett, E
Jost, BF
Nork, CP
Orth, DH
Baczewski, D
Bryant, D
Doherty, D
Fitzgerald, J
Flood, TP
Graff, S
Kwiatkowski, K
Packo, KH
Garcia, CA
Bloome, MA
Foreman, J
Horton, J
Matheny, J
Ruiz, RS
Folk, JC
Fountain, C
Griffin, M
Heffron, E
Kimura, AE
Northway, R
Vogel, C
Ward, B
Chandra, SR
Harrison, R
Knutson, G
Lewis, B
Lyngaas, H
Myers, RL
Quackenboss, D
Saine, PJ
Somers, G
Stevens, TS
Weber, GB
Gass, JDM
Cubillas, T
Chuang, E
Duria, L
HessJacobsen, D
Lewis, ML
Pall, M
Rams, I
Soler, A
Burton, TC
Laabs, J
Mieler, WF
Phillips, J
Wipplinger, W
Zarling, D
Gitter, K
Schomacker, K
Wilkinson, CP
Wheeler, A
Klein, ML
Evans, M
Nolte, SK
Vahrenwald, D
Wallace, P
Watzke, RC
Wilson, DJ
Margherio, RR
Bridges, C
Cox, S
Cumming, K
Huston, G
Johnson, JL
Murphy, PL
Regan, VS
Stenic, C
Streasik, P
Burgess, DB
Blank, J
Breeding, L
Dahl, J
Hoffmeyer, G
Kacizak, R
Meredith, TA
Olk, RJ
Ort, E
Wilder, A
Fine, SL
Fatula, E
Hawkins, BS
Maguire, MG
Cramer, LD
Goldsborough, IL
Keller, JA
Marsh, MJ
McCaffrey, L
MillerHart, A
Newhouse, MM
White, VL
Alexander, J
EureCooper, R
Hiner, CJ
Javornik, NB
Phillips, DA
Tian, Y
Walker, VG
Ward, RG
Whitehead, GR
McLaughlin, JA
Donald, J
Gass, M
Meinert, CL
McCormick, P
Hillis, AI
Jampol, LM
McLean, EB
Rosner, B
Safriet, B
AF Sternberg, P
Brown, JM
Curtis, L
Fremstad, A
Gibbs, D
Gilman, J
Swords, R
Waldron, RG
Bressler, NM
Belt, J
Bressler, SB
Muth, T
Elman, MJ
George, T
Haller, JA
Herring, M
Orr, PR
Schachat, AP
Sotirakos, P
Starr, J
Singerman, LJ
Brown, P
Coreno, K
DeLisio, M
Novak, M
Pinter, AS
Rice, TA
SmithBrewer, S
Fish, GE
Aguado, H
Anderson, T
Crockett, E
Jost, BF
Nork, CP
Orth, DH
Baczewski, D
Bryant, D
Doherty, D
Fitzgerald, J
Flood, TP
Graff, S
Kwiatkowski, K
Packo, KH
Garcia, CA
Bloome, MA
Foreman, J
Horton, J
Matheny, J
Ruiz, RS
Folk, JC
Fountain, C
Griffin, M
Heffron, E
Kimura, AE
Northway, R
Vogel, C
Ward, B
Chandra, SR
Harrison, R
Knutson, G
Lewis, B
Lyngaas, H
Myers, RL
Quackenboss, D
Saine, PJ
Somers, G
Stevens, TS
Weber, GB
Gass, JDM
Cubillas, T
Chuang, E
Duria, L
HessJacobsen, D
Lewis, ML
Pall, M
Rams, I
Soler, A
Burton, TC
Laabs, J
Mieler, WF
Phillips, J
Wipplinger, W
Zarling, D
Gitter, K
Schomacker, K
Wilkinson, CP
Wheeler, A
Klein, ML
Evans, M
Nolte, SK
Vahrenwald, D
Wallace, P
Watzke, RC
Wilson, DJ
Margherio, RR
Bridges, C
Cox, S
Cumming, K
Huston, G
Johnson, JL
Murphy, PL
Regan, VS
Stenic, C
Streasik, P
Burgess, DB
Blank, J
Breeding, L
Dahl, J
Hoffmeyer, G
Kacizak, R
Meredith, TA
Olk, RJ
Ort, E
Wilder, A
Fine, SL
Fatula, E
Hawkins, BS
Maguire, MG
Cramer, LD
Goldsborough, IL
Keller, JA
Marsh, MJ
McCaffrey, L
MillerHart, A
Newhouse, MM
White, VL
Alexander, J
EureCooper, R
Hiner, CJ
Javornik, NB
Phillips, DA
Tian, Y
Walker, VG
Ward, RG
Whitehead, GR
McLaughlin, JA
Donald, J
Gass, M
Meinert, CL
McCormick, P
Hillis, AI
Jampol, LM
McLean, EB
Rosner, B
Safriet, B
TI Occult choroidal neovascularization - Influence on visual outcome in
patients with age-related molecular degeneration
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID MACULAR DEGENERATION
AB Objective: To determine whether the presence of occult choroidal neovascularization (CNV) influenced the anatomic and visual acuity outcomes in a randomized clinical trial of krypton red laser photocoagulation to treat juxtafoveal neovascular lesions in age-related macular degeneration.
Design, getting, and Patients: The fluorescein angiograms obtained at the baseline examination at tertiary retinal referral centers between April 1, 1981, and December 31, 1987, as part of the Macular Photocoagulation Study (MPS) Age-Related Macular Degeneration Study-Krypton Laser were evaluated retrospectively at the MPS Fundus Photograph Reading Center by two senior readers independently (with open adjudication of any differences) from 1992 to 1994. Criteria for classifying classic and occult CNV by the MPS Group were established by 1989, 2 years after the last patient had been assigned randomly to treatment or observation in the krypton laser study.
Main Outcome Measures: Treatment coverage of classic and occult CNV, persistent CNV, recurrent CNV, and visual acuity from scheduled follow-up examinations for up to 5 years were analyzed for the absence or presence of occult CNV at baseline.
Results: The number of eyes with classic CNV but no occult CNV, classic and occult CNV, and occult CNV but no classic CNV were almost identical for the eyes assigned randomly to treatment or observation. Classic CNV almost always was covered completely with intense laser treatment; nevertheless, recurrent CNV developed in more than half of these eyes within 1 year after initial laser treatment. In contrast, in more than half of the eyes with occult CNV, more than 50% of the occult CNV was not covered with heavy laser treatment. Laser treatment was clearly beneficial for eyes with classic CNV but no occult CNV and almost equivalent to no treatment for eyes with classic and occult CNV. The few eyes with occult CNV but no classic CNV precluded conclusions about the value of treatment in this subgroup.
Conclusions: These results strengthen previous reports that laser treatment is beneficial for eyes with juxtafoveal choroidal neovascular lesions when classic CNV is present, even though CNV often recurs. Treatment of classic CNV alone in eyes with classic and occult CNV was not beneficial in this study. Distinguishing classic CNV from occult CNV can aid in the selection of patients who will benefit most from laser treatment.
C1 JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205.
EMORY EYE CTR,ATLANTA,GA.
RETINA ASSOCIATES,CLEVELAND,OH.
TEXAS RETINA ASSOCIATES,DALLAS,TX.
INGALLS MEM HOSP,HARVEY,IL.
INGALLS MEM HOSP,CHICAGO,IL.
HERMANN EYE CTR,HOUSTON,TX.
UNIV IOWA,IOWA CITY,IA.
UNIV WISCONSIN,MADISON,WI.
UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL.
MED COLL WISCONSIN,MILWAUKEE,WI 53226.
TOURO INFIRM,NEW ORLEANS,LA.
UNIV OKLAHOMA,MCGEE EYE INST,OKLAHOMA CITY,OK.
OREGON HLTH SCI UNIV,PORTLAND,OR.
WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072.
RETINA CONSULTANTS LTD,ST LOUIS,MO.
UNIV PENN,SCHEIE EYE INST,PHILADELPHIA,PA 19104.
NEI,NIH,BETHESDA,MD 20892.
NR 25
TC 104
Z9 104
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD APR
PY 1996
VL 114
IS 4
BP 400
EP 412
PG 13
WC Ophthalmology
SC Ophthalmology
GA UD951
UT WOS:A1996UD95100005
ER
PT J
AU Elsas, FJ
Braune, K
Jones, J
Kimble, JA
Kline, L
Lampton, G
Witherspoon, D
Roth, AM
Erickson, R
Gilbert, WS
Chrousos, GA
Friendly, DS
Jaafar, M
Keys, MP
Kolsky, MP
Mercer, PA
ONeill, JF
Parelhoff, ES
Perraut, E
Pilkerton, AR
Plotsky, D
Flynn, JT
Bancalari, E
Clarkson, J
Vandenbroucke, R
Warman, R
Miller, MT
Cronin, C
Daily, M
Gieser, R
Mittelman, D
Squires, P
Vygantas, C
Kaufman, LM
Santiago, N
Shapiro, M
Ellis, FD
Helveston, EM
Plager, D
Schreiner, R
Sprunger, DT
Barr, CC
Douglas, CH
Fishman, PH
Whittington, GK
Gordon, RA
Bushaw, C
Haik, BG
Repka, MX
Loupe, DN
Haller, JA
Baker, JD
Trese, MT
Manatrey, P
Summers, CG
Balles, MW
Egbert, JE
Knobloch, DK
Knobloch, WH
Lavoie, JD
Maxwell, M
Ramsay, RC
Phelps, DL
Reynolds, JD
Torrisi, P
Asselin, D
Esposito, P
Gardner, K
Guillet, E
Hampton, R
Merriam, W
Metz, HS
Olsen, R
Platt, C
Simon, R
Spalding, SC
Tingley, D
Vanderlinde, RE
Wood, NE
Buckley, EG
Anderson, MM
Machemer, R
Valentine, G
Burke, MJ
Johnson, JC
Lipman, M
Szmyd, SM
Rogers, GL
Bremer, DL
Fellows, RR
Letson, AD
McGregor, MLK
Palmer, EA
Chao, J
LaFrance, SB
Robertson, J
Brown, GC
Hertle, RW
Kubacki, JJ
Menacker, SJ
Miller, DL
Schaffer, DB
Tasman, W
Biglan, AW
Cheng, KP
Schramm, M
Saunders, RA
Bluestein, E
King, LP
McPherson, J
Wilson, ME
Feman, SS
Law, AB
Spencer, R
Arnwine, J
Berry, PM
Leffler, JN
Stager, DR
vanHeuven, WAJ
Montez, MG
Hoffman, RO
Bracken, S
Teske, M
Mowery, RL
Krom, CP
Phillips, CL
Hardy, RJ
Davis, BR
Tung, B
Foos, RY
Dobson, V
Quinn, GE
Bartholomew, P
Evans, J
Hammel, N
Trueb, L
Verness, J
Scher, S
Connett, J
Davis, M
Hillis, A
Robb, R
Safriet, B
Saigal, S
Silverman, W
Roth, A
Palmer, EA
AF Elsas, FJ
Braune, K
Jones, J
Kimble, JA
Kline, L
Lampton, G
Witherspoon, D
Roth, AM
Erickson, R
Gilbert, WS
Chrousos, GA
Friendly, DS
Jaafar, M
Keys, MP
Kolsky, MP
Mercer, PA
ONeill, JF
Parelhoff, ES
Perraut, E
Pilkerton, AR
Plotsky, D
Flynn, JT
Bancalari, E
Clarkson, J
Vandenbroucke, R
Warman, R
Miller, MT
Cronin, C
Daily, M
Gieser, R
Mittelman, D
Squires, P
Vygantas, C
Kaufman, LM
Santiago, N
Shapiro, M
Ellis, FD
Helveston, EM
Plager, D
Schreiner, R
Sprunger, DT
Barr, CC
Douglas, CH
Fishman, PH
Whittington, GK
Gordon, RA
Bushaw, C
Haik, BG
Repka, MX
Loupe, DN
Haller, JA
Baker, JD
Trese, MT
Manatrey, P
Summers, CG
Balles, MW
Egbert, JE
Knobloch, DK
Knobloch, WH
Lavoie, JD
Maxwell, M
Ramsay, RC
Phelps, DL
Reynolds, JD
Torrisi, P
Asselin, D
Esposito, P
Gardner, K
Guillet, E
Hampton, R
Merriam, W
Metz, HS
Olsen, R
Platt, C
Simon, R
Spalding, SC
Tingley, D
Vanderlinde, RE
Wood, NE
Buckley, EG
Anderson, MM
Machemer, R
Valentine, G
Burke, MJ
Johnson, JC
Lipman, M
Szmyd, SM
Rogers, GL
Bremer, DL
Fellows, RR
Letson, AD
McGregor, MLK
Palmer, EA
Chao, J
LaFrance, SB
Robertson, J
Brown, GC
Hertle, RW
Kubacki, JJ
Menacker, SJ
Miller, DL
Schaffer, DB
Tasman, W
Biglan, AW
Cheng, KP
Schramm, M
Saunders, RA
Bluestein, E
King, LP
McPherson, J
Wilson, ME
Feman, SS
Law, AB
Spencer, R
Arnwine, J
Berry, PM
Leffler, JN
Stager, DR
vanHeuven, WAJ
Montez, MG
Hoffman, RO
Bracken, S
Teske, M
Mowery, RL
Krom, CP
Phillips, CL
Hardy, RJ
Davis, BR
Tung, B
Foos, RY
Dobson, V
Quinn, GE
Bartholomew, P
Evans, J
Hammel, N
Trueb, L
Verness, J
Scher, S
Connett, J
Davis, M
Hillis, A
Robb, R
Safriet, B
Saigal, S
Silverman, W
Roth, A
Palmer, EA
TI Multicenter trial of cryotherapy for retinopathy of prematurity -
Snellen visual acuity and structural outcome at 5 1/2 years after
randomization
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
AB Objective: To evaluate outcome at 5 1/2 years after randomization in eyes that underwent cryotherapy and in control eyes of patients in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity.
Design: During infancy, patients with bilateral threshold retinopathy of prematurity (ROP) were assigned to receive cryotherapy for one eye and no cryotherapy for the other eye. Those with threshold ROP in only one eye (asymmetric) were randomly assigned to cryotherapy or no cryotherapy for that eye. Then, 5 1/2 years later, testers who were masked to the treatment status of each eye measured the patients' monocular visual acuity by using the log of the minimum angle of resolution visual acuity chart that was used in the Early Treatment Diabetic Retinopathy Study. This was the most refined visual acuity testing yet performed on this cohort. Structural outcome was evaluated by participating ophthalmologists' assessment of ROP residua in the posterior pole of the fundus.
Patients: Patients were 291 children who had been preterm infants with birth weights of less than 1251 g in whom threshold ROP had developed. Two hundred forty patients had bilateral threshold ROP, and 51 had threshold ROP in only one eye.
Results: For the 234 children examined, both visual acuity and fundus structure showed a reduction in unfavorable outcomes in treated vs control eyes: 47.1% vs 61.7%, respectively (P<.005), for visual acuity and 26.9% vs 45.4%, respectively (P<.001), for fundus status. Detailed analysis uf visual acuity outcomes for all eyes revealed that while fewer treated eyes (31.5%) than control eyes (48%) were blind (P<.001), there was a slight trend toward fewer eyes with a visual acuity of 20/40 or better in the treated (13%) vs control (17%) groups (P=.19).
Conclusions: The results support the long-term efficacy and safety of cryotherapy in the treatment of severe ROP. However, the data show preliminary evidence of a possible adverse effect of this treatment on visual acuity.
C1 OREGON HLTH SCI UNIV,CASEY EYE INST,CRYO ROP HEADQUARTERS,PORTLAND,OR 97201.
CHILDRENS HOSP,BIRMINGHAM,AL.
UNIV CALIF DAVIS,MED CTR,SUTTER MEM HOSP,SACRAMENTO,CA 95817.
GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037.
CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010.
GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007.
WASHINGTON HOSP CTR,WASHINGTON,DC 20010.
JACKSON MEM HOSP,MIAMI,FL 33136.
UNIV ILLINOIS,EYE & EAR INFIRM,CHICAGO,IL 60612.
LOYOLA UNIV,MAYWOOD,IL 60153.
LUTHERAN GEN HOSP,PARK RIDGE,IL 60068.
RILEY HOSP,WISHARD MEM HOSP,INDIANAPOLIS,IN.
UNIV HOSP,INDIANAPOLIS,IN.
UNIV LOUISVILLE HOSP,LOUISVILLE,KY.
NORTON KOSAIR CHILDRENS HOSP,LOUISVILLE,KY.
TULANE UNIV,MED CTR,NEW ORLEANS,LA.
JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21287.
WILLIAM BEAUMONT HOSP,DETROIT,MI.
CHILDRENS HOSP MICHIGAN,DETROIT,MI.
UNIV MINNESOTA HOSP,MINNEAPOLIS CHILDRENS MED CTR,MINNEAPOLIS,MN.
UPSTATE NEW YORK CTR,ROCHESTER,NY.
UPSTATE NEW YORK CTR,SYRACUSE,NY.
UPSTATE NEW YORK CTR,BUFFALO,NY.
STRONG MEM HOSP,BUFFALO,NY.
CHILDRENS HOSP BUFFALO,BUFFALO,NY.
RETINA RES INST CENT NEW YORK,SYRACUSE,NY.
DUKE EYE CTR,DURHAM,NC.
UNIV HOSP,CHILDRENS HOSP MED CTR,CINCINNATI,OH.
CHILDRENS HOSP,COLUMBUS,OH 43205.
UNIV HOSP,COLUMBUS,OH.
CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104.
UNIV PITTSBURGH,PITTSBURGH,PA.
INST EYE & EAR,PITTSBURGH,PA.
MED UNIV HOSP,CHARLESTON,SC.
VANDERBILT UNIV SCH MED,NASHVILLE,TN.
METHODIST MED CTR,DALLAS,TX.
PARKLAND MEM HOSP & AFFILIATED INST,DALLAS,TX.
ST PAULS HOSP,DALLAS,TX.
MED CITY DALLAS HOSP,DALLAS,TX.
PRESBYTERIAN MED CTR,DALLAS,TX.
UNIV TEXAS,HLTH SCI CTR,MED CTR,SAN ANTONIO,TX.
UNIV UTAH HOSP,SALT LAKE CITY,UT.
NEI,BETHESDA,MD 20892.
UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,COORDINATING CTR CLIN TRIALS,HOUSTON,TX.
UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024.
NR 20
TC 131
Z9 137
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD APR
PY 1996
VL 114
IS 4
BP 417
EP 424
PG 8
WC Ophthalmology
SC Ophthalmology
GA UD951
UT WOS:A1996UD95100007
ER
PT J
AU Pattatucci, AML
AF Pattatucci, AML
TI Heterosexuality: A feminism & psychology reader - Wilkinson,S,
Kitzinger,C
SO ARCHIVES OF SEXUAL BEHAVIOR
LA English
DT Book Review
RP Pattatucci, AML (reprint author), NCI,LB,NIH,BLDG 37,ROOM 4A13,BETHESDA,MD 20892, USA.
NR 4
TC 0
Z9 0
U1 1
U2 1
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0004-0002
J9 ARCH SEX BEHAV
JI Arch. Sex. Behav.
PD APR
PY 1996
VL 25
IS 2
BP 221
EP 225
PG 5
WC Psychology, Clinical; Social Sciences, Interdisciplinary
SC Psychology; Social Sciences - Other Topics
GA UJ516
UT WOS:A1996UJ51600007
ER
PT J
AU Tayebi, N
Herman, J
Ginns, EI
Sidransky, E
AF Tayebi, N
Herman, J
Ginns, EI
Sidransky, E
TI Genotype D399N/R463C in a patient with type 3 Gaucher disease previously
assigned genotype N370S/R463C
SO BIOCHEMICAL AND MOLECULAR MEDICINE
LA English
DT Article
ID GLUCOCEREBROSIDASE GENE
AB A patient with type 3 Gaucher disease is described with a novel genotype, D399N/R463C, established by DNA sequencing. This patient was previously reported as having genotype N370S/R463C. This communication now establishes that no patients reported with mutation N370S have the neuronopathic forms of Gaucher disease and has important implications for genetic counseling. (C) 1996 Academic Press, Inc.
RP Tayebi, N (reprint author), NIMH,CLIN NEUROSCI BRANCH,NIH,BETHESDA,MD 20892, USA.
NR 20
TC 12
Z9 12
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 1077-3150
J9 BIOCHEM MOL MED
JI Biochem. Mol. Med.
PD APR
PY 1996
VL 57
IS 2
BP 149
EP 151
DI 10.1006/bmme.1996.0021
PG 3
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA UJ835
UT WOS:A1996UJ83500010
PM 8733893
ER
PT J
AU OmatsuKanbe, M
Zarnowski, MJ
Cushman, SW
AF OmatsuKanbe, M
Zarnowski, MJ
Cushman, SW
TI Hormonal regulation of glucose transport in a brown adipose cell
preparation isolated from rats that shows a large response to insulin
SO BIOCHEMICAL JOURNAL
LA English
DT Article
ID UNCOUPLING PROTEIN; SKELETAL-MUSCLE; TRANSGENIC MICE; PLASMA-MEMBRANE;
ADIPOCYTES; TISSUE; EXPRESSION; GLUT4; STIMULATION; NOREPINEPHRINE
AB Isolated brown adipose cells from rats are prepared whose viability is indicated by the expected stimulation of oxygen consumption by noradrenaline and counter-regulation of this oxygen consumption response by insulin. Insulin stimulates 3-O-methyl-D-glucose transport by approx. 15-fold in the absence of adenosine, and adenosine augments this response at least 2-fold. The insulin-stimulated translocation of the glucose transporter GLUT4 from an intracellular compartment to the plasma membrane is readily detected by subcellular fractionation and Western blotting, and the appearance of GLUT4 on the cell surface in response to insulin is demonstrated by bis-mannose photolabelling. Isoprenaline also stimulates glucose transport activity but only by approx, 3-fold; this effect is not altered by adenosine. Isoprenaline increases insulin-stimulated glucose transport activity in the absence of adenosine but decreases it in the presence of adenosine. These results demonstrate that although the regulation of glucose transport by insulin in brown adipose cells is qualitatively similar to that in white adipose cells, counter-regulation by adenosine and isoprenaline is at least quantitatively and may be qualitatively different. Isolated brown adipose cells from rats thus represent an excellent model for further examination of the mechanism by which multiple hormone signalling pathways interact to control glucose transport and GLUT4 subcellular trafficking.
C1 NIDDK,NATL INST HLTH,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892.
NR 31
TC 21
Z9 22
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 APR 1
PY 1996
VL 315
BP 25
EP 31
PN 1
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UF053
UT WOS:A1996UF05300005
PM 8670115
ER
PT J
AU Zang, LY
Shi, XL
Misra, HP
AF Zang, LY
Shi, XL
Misra, HP
TI EPR-spin trapping kinetic studies of superoxide radicals produced by
photosensitized hypocrellin A, a photodynamic therapeutic agent
SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL
LA English
DT Article
DE kinetics; superoxide radicals; hypocrellin A; EPR; spin trapping
ID GENERATION; PHOTOLYSIS
AB Kinetics of superoxide radicals generation by a photodynamic therapeutic agent, Hypocrellin A has been studied by EPR-spin trapping technique. The rate constant (k(g)) for superoxide radicals generation by Hypocrellin A was found to be 5.0 x 10(-3) s(-1). The first-order rate constant (k(1)) and the half-life time (t(0.5)) for DMPO-O-2(-) decay were 2.86 x 10(-3) s(-1) and 242.3 s, respectively. It appears that oxyradicals, generated during the photodynamic process, may be associated with the treatment of various skin diseases by photodynamic therapy of Hypocrellin A.
C1 VIRGINIA TECH,VIRGINIA MARYLAND REG COLL VET MED,DEPT BIOMED SCI,BLACKSBURG,VA 24061.
NCI,LAB EXPT PATHOL,BETHESDA,MD 20892.
RI Shi, Xianglin/B-8588-2012
NR 11
TC 2
Z9 2
U1 0
U2 0
PU ACADEMIC PRESS AUST
PI MARRICKVILLE
PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA
SN 1039-9712
J9 BIOCHEM MOL BIOL INT
JI Biochem. Mol. Biol. Int.
PD APR
PY 1996
VL 38
IS 4
BP 685
EP 691
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA VG882
UT WOS:A1996VG88200006
PM 8728097
ER
PT J
AU Kaye, W
Halmi, K
Berrettini, W
Goldman, D
Fichter, M
Strober, M
Treasurer, J
Kaplan, A
Woodside, B
Plotnikov, K
Pollice, C
Lilenfeld, L
AF Kaye, W
Halmi, K
Berrettini, W
Goldman, D
Fichter, M
Strober, M
Treasurer, J
Kaplan, A
Woodside, B
Plotnikov, K
Pollice, C
Lilenfeld, L
TI Clinical studies supporting genetic research in anorexia nervosa
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 UNIV PITTSBURGH,PITTSBURGH,PA 15213.
CORNELL UNIV,COLL MED,NEW YORK,NY 10605.
THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107.
NIAAA,NIH,BETHESDA,MD 20852.
UNIV MUNICH,MUNICH,GERMANY.
UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024.
INST PSYCHIAT,LONDON,ENGLAND.
UNIV TORONTO,TORONTO,ON,CANADA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 17
EP 17
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300013
ER
PT J
AU Hitri, A
Wyatt, RJ
AF Hitri, A
Wyatt, RJ
TI Dopamine transporter in schizophrenia: A progressive loss with age in
the cingulate cortex
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 VET ADM MED CTR,RES & DEV,WASHINGTON,DC 20422.
NIMH,CTR NEUROSCI,NPB,WASHINGTON,DC 20422.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 22
EP 22
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300018
ER
PT J
AU Rapoport, JL
AF Rapoport, JL
TI Childhood onset schizophrenia: New research
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 27
EP 27
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300023
ER
PT J
AU Putnam, F
AF Putnam, F
TI Post-traumatic stress disorder: A developmental perspective
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 28
EP 28
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300024
ER
PT J
AU London, ED
Grant, S
Newlin, D
Villemagne, V
Phillips, RL
Liu, X
Kimes, AS
Contoreggi, C
Margolin, A
AF London, ED
Grant, S
Newlin, D
Villemagne, V
Phillips, RL
Liu, X
Kimes, AS
Contoreggi, C
Margolin, A
TI Cocaine-related cues elicit craving and activate cortical circuits
relevant to episodic memory
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIDA,INTRAMURAL RES PROGRAM,NEUROSCI BRANCH,BALTIMORE,MD 21224.
YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06519.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 35
EP 35
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300031
ER
PT J
AU Rosenthal, NE
AF Rosenthal, NE
TI The use of light therapy in psychiatry
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,SECT ENVIRONM PSYCHIAT,CPB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 45
EP 45
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300041
ER
PT J
AU Breier, A
Su, TP
Weisenfeld, N
Elman, I
Adler, C
Malhotra, AK
Pickar, D
AF Breier, A
Su, TP
Weisenfeld, N
Elman, I
Adler, C
Malhotra, AK
Pickar, D
TI Assessment of striatal dopamine function in schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 48
EP 48
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300044
ER
PT J
AU Su, TP
Breier, A
Coppola, R
Hadd, K
Elman, I
Adler, C
Malhotra, AK
Watsky, E
Gorey, J
Weinberger, D
Pickar, D
AF Su, TP
Breier, A
Coppola, R
Hadd, K
Elman, I
Adler, C
Malhotra, AK
Watsky, E
Gorey, J
Weinberger, D
Pickar, D
TI D2 receptor occupancy in risperidone and clozapine-treated
schizophrenics
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD.
NIMH,CLIN BRAIN DISORDERS BRANCH,ST ELIZABETHS HOSP,NIH,NEUROSCI CTR,WASHINGTON,DC.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 51
EP 51
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300047
ER
PT J
AU Knable, MB
Heinz, A
Coppola, R
Gorey, J
Weinberger, DR
AF Knable, MB
Heinz, A
Coppola, R
Gorey, J
Weinberger, DR
TI IBZM SPECT measurement of D2 receptor occupancy by haloperidol and
risperidone
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 56
EP 56
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300052
ER
PT J
AU Bahro, M
Schreurs, BG
McIntosh, AR
Sunderland, T
Molchan, SE
AF Bahro, M
Schreurs, BG
McIntosh, AR
Sunderland, T
Molchan, SE
TI Scopolamine effects on rCBF during human eyeblink conditioning
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,SECT GERIATR PSYCHIAT,NIH,BETHESDA,MD 20892.
NINCDS,LAB ADAPT SYST,NIH,BETHESDA,MD 20892.
UNIV TORONTO,TORONTO,ON M6A 2E1,CANADA.
RI McIntosh, Anthony/G-4955-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 60
EP 60
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300056
ER
PT J
AU Jacobsen, LK
Giedd, JN
Rajapakse, JC
Hamburger, SD
Vaituzis, AC
Frazier, JA
Lenane, MC
Rapoport, JL
AF Jacobsen, LK
Giedd, JN
Rajapakse, JC
Hamburger, SD
Vaituzis, AC
Frazier, JA
Lenane, MC
Rapoport, JL
TI The corpus callosum in childhood onset schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 HARVARD UNIV,SCH MED,BOSTON,MA.
NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892.
RI Giedd, Jay/A-3080-2008; Rajapakse, Jagath/B-8485-2008; Giedd,
Jay/B-7302-2012; Giedd, Jay/J-9644-2015
OI Rajapakse, Jagath/0000-0001-7944-1658; Giedd, Jay/0000-0003-0827-3460;
Giedd, Jay/0000-0003-2002-8978
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 66
EP 66
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300062
ER
PT J
AU Kumra, S
Jacobsen, LK
Frazier, JA
McKenna, K
Gordon, CT
Smith, AK
Rapoport, JL
AF Kumra, S
Jacobsen, LK
Frazier, JA
McKenna, K
Gordon, CT
Smith, AK
Rapoport, JL
TI Clozapine treatment of childhood-onset schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,NIH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 106
EP 106
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300102
ER
PT J
AU Shoaf, SE
Schmall, B
AF Shoaf, SE
Schmall, B
TI Lumped constant for pharmacokinetic estimation of brain serotonin
synthesis rates
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,BETHESDA,MD 20892.
NIH,CTR CLIN,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 115
EP 115
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300111
ER
PT J
AU George, DT
Ragan, PW
Rawlings, R
Umhau, J
Phillips, M
Shoaf, S
Linnoila, M
AF George, DT
Ragan, PW
Rawlings, R
Umhau, J
Phillips, M
Shoaf, S
Linnoila, M
TI Cerebrospinal fluid 5-HIAA is low in perpetrators of domestic violence
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,NIH,DICBR,CLIN STUDIES LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 123
EP 123
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300119
ER
PT J
AU Williams, W
Andreason, P
Ruttimann, U
Kerich, M
Rio, D
Rawlings, R
Brown, G
Hommer, D
Linnoila, M
AF Williams, W
Andreason, P
Ruttimann, U
Kerich, M
Rio, D
Rawlings, R
Brown, G
Hommer, D
Linnoila, M
TI Brain glucose metabolic rates in alcoholic patients
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,NIH,DICBR,CLIN STUDIES LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 125
EP 125
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300121
ER
PT J
AU Hibbeln, JR
Umhau, JC
Salem, N
Rawlings, R
George, DT
Linnoila, M
AF Hibbeln, JR
Umhau, JC
Salem, N
Rawlings, R
George, DT
Linnoila, M
TI Plasma fatty acids predict CSF 5-HIAA and HVA in normals, early and late
onset alcoholics
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,MEMBRANE BIOPHYS LAB,BETHESDA,MD 20892.
NIAAA,BIOCHEM LAB,BETHESDA,MD 20892.
NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892.
NIAAA,DIV INTRAMURAL CLIN & BIOL RES,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 126
EP 126
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300122
ER
PT J
AU Feltner, DE
Hermesz, E
Grinberg, A
Mahon, KA
AF Feltner, DE
Hermesz, E
Grinberg, A
Mahon, KA
TI Targeted disruption of the mouse Rpx gene
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NICHHD,NIH,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 145
EP 145
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300141
ER
PT J
AU Heinz, A
Knable, MB
Pietzcker, A
Schmidt, LG
Weinberger, DR
AF Heinz, A
Knable, MB
Pietzcker, A
Schmidt, LG
Weinberger, DR
TI Positive symptoms in dopaminergic psychosis - Implications for the
dopamine hypothesis of schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,NIH,CLIN BRAIN DISORDERS BRANCH,BETHESDA,MD 20892.
FREE UNIV BERLIN,DEPT PSYCHIAT,W-1000 BERLIN,GERMANY.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 151
EP 151
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300147
ER
PT J
AU Waltrip, RW
Torrey, EF
King, LR
Weinberger, DR
Rickler, KC
Rubin, SA
Carbone, KM
AF Waltrip, RW
Torrey, EF
King, LR
Weinberger, DR
Rickler, KC
Rubin, SA
Carbone, KM
TI Schizophrenia, borna disease, and neurological signs in a monozygotic
twin study cohort
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228.
JOHNS HOPKINS UNIV,DEPT MED,VIRAL IMMUNOPATHOGENESIS LAB,BALTIMORE,MD 21218.
NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 152
EP 152
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300148
ER
PT J
AU Daniel, DG
Egan, M
Hyde, T
AF Daniel, DG
Egan, M
Hyde, T
TI Probable neuroleptic induced tardive dyskinesia in association with
combined fluoxetine and risperidone treatment
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 WASHINGTON CLIN RES CTR,FALLS CHURCH,VA 22044.
NIMH,DIRP,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 182
EP 182
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300178
ER
PT J
AU Skolnick, P
AF Skolnick, P
TI Adaptation of NMDA receptors following antidepressant treatments
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIDDK,NIH,NEUROSCI LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 203
EP 203
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300195
ER
PT J
AU Goldman, D
Nielsen, D
Okada, M
Adamson, M
Lappalainen, J
Malhotra, N
Pesonen, U
Koulu, M
Eggert, M
Virkkunen, M
Ozaki, N
Linnoila, M
AF Goldman, D
Nielsen, D
Okada, M
Adamson, M
Lappalainen, J
Malhotra, N
Pesonen, U
Koulu, M
Eggert, M
Virkkunen, M
Ozaki, N
Linnoila, M
TI Molecular genetics of impaired impulse control and early onset
alcoholism
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852.
RI Nielsen, David/B-4655-2009
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 212
EP 212
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300204
ER
PT J
AU Higley, JD
Mehlman, P
Suomi, SJ
Linnoila, M
AF Higley, JD
Mehlman, P
Suomi, SJ
Linnoila, M
TI A nonhuman primate model of type II excessive alcohol consumption
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,CLIN STUDIES LAB,PRIMATE UNIT,NIH,ANIM CTR,POOLESVILLE,MD 20837.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 213
EP 213
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300205
ER
PT J
AU Altemus, M
Paletzki, R
Gerfen, CR
Murphy, DL
AF Altemus, M
Paletzki, R
Gerfen, CR
Murphy, DL
TI Differential activation of ZIF268 in the amygdala in response to MCPP
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892.
NIMH,NEUROPHYSIOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 285
EP 285
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300277
ER
PT J
AU Malhotra, AK
Pinals, DA
Weisenfeld, N
Pickar, D
Breier, A
AF Malhotra, AK
Pinals, DA
Weisenfeld, N
Pickar, D
Breier, A
TI NMDA receptor function and schizophrenia: Studies with ketamine
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 296
EP 296
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300288
ER
PT J
AU Butler, PD
Printz, DJ
DeSanti, L
Issa, F
Gorman, JM
Carraway, RE
AF Butler, PD
Printz, DJ
DeSanti, L
Issa, F
Gorman, JM
Carraway, RE
TI Neurotensin and metabolites in CSF of patients with schizophrenia and
controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 DVAMC,PSYCHIAT SERV,NEW YORK,NY 10010.
NEW YORK STATE PSYCHIAT INST & HOSP,DEPT CLIN PSYCHOBIOL,NEW YORK,NY 10032.
NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032.
UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01604.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 300
EP 300
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300292
ER
PT J
AU Mosnaim, AD
Freitag, F
Karoum, F
Wolf, ME
Diamond, S
Salas, MA
AF Mosnaim, AD
Freitag, F
Karoum, F
Wolf, ME
Diamond, S
Salas, MA
TI Migraine and the contents of tyramine and phenylethylamine in food
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 UNIV HLTH SCI CHICAGO MED SCH,N CHICAGO,IL 60064.
N CHICAGO UAMO,DIAMOND HEADACHE CLIN,N CHICAGO,IL.
ST ELIZABETH HOSP,NIMH,NPB,WASHINGTON,DC.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 325
EP 325
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300317
ER
PT J
AU Frye, MA
Mathe, AA
Gary, KA
George, MS
CoraLocatelli, G
Huggins, T
Pazzaglia, PJ
Callahan, AM
Davis, C
Marangell, L
Rubinow, D
Winokur, A
Post, RM
AF Frye, MA
Mathe, AA
Gary, KA
George, MS
CoraLocatelli, G
Huggins, T
Pazzaglia, PJ
Callahan, AM
Davis, C
Marangell, L
Rubinow, D
Winokur, A
Post, RM
TI CSF neuropeptide dysregulation in patients with affective disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892.
KAROLINSKA INST,STOCKHOLM,SWEDEN.
UNIV PENN,SCH MED,PHILADELPHIA,PA 19104.
MED UNIV S CAROLINA,CHARLESTON,SC 29425.
UNIV MISSISSIPPI,SCH MED,JACKSON,MS.
MT SINAI MED CTR,NEW YORK,NY 10029.
VET ADM MED CTR,BRONX,NY 10468.
BAYLOR COLL MED,HOUSTON,TX 77030.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 327
EP 327
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300319
ER
PT J
AU Bigelow, LB
Torrey, EF
Kleinman, JE
AF Bigelow, LB
Torrey, EF
Kleinman, JE
TI Problems in post-mortem diagnosis can be solved
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032.
NIMH,CTR NEUROSCI,STANLEY RES FDN,WASHINGTON,DC 20032.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 328
EP 328
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300320
ER
PT J
AU Elman, I
Wiesenfeld, N
Su, TP
Malhotra, AK
Pickar, D
Breier, A
AF Elman, I
Wiesenfeld, N
Su, TP
Malhotra, AK
Pickar, D
Breier, A
TI The effects of metabolic and cognitive stress on cerebral blood flow
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,NIH,EXPTL THERAPEUT BRANCH,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 354
EP 354
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300346
ER
PT J
AU Wyatt, RJ
AF Wyatt, RJ
TI Early intervention in schizophrenia improves the long-term course of the
illness
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,NIH,DIV INTRAMURAL RES,NEUROPSYCHIAT BRANCH,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 384
EP 384
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300372
ER
PT J
AU Rubinow, DR
Schmidt, PJ
AF Rubinow, DR
Schmidt, PJ
TI Reproductive hormones and mood in women
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 386
EP 386
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300374
ER
PT J
AU Baumann, MH
Rothman, RB
AF Baumann, MH
Rothman, RB
TI Withdrawal from chronic cocaine in rats: A model of depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIDA,CLIN PSYCHOPHARMACOL SECT,NIH,IRP,BALTIMORE,MD 21224.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 399
EP 399
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300386
ER
PT J
AU Ragan, PW
George, DT
Shoaf, S
Eckardt, M
Linnoila, M
AF Ragan, PW
George, DT
Shoaf, S
Eckardt, M
Linnoila, M
TI CSF monoamine metabolites in alcoholics with and without nicotine
addiction
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIAAA,CLIN STUDIES LAB,DICBR,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 437
EP 437
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300422
ER
PT J
AU Bachus, SE
Hyde, TM
Herman, MM
Kleinman, JE
AF Bachus, SE
Hyde, TM
Herman, MM
Kleinman, JE
TI Elevated cholecystokinin mRNA in dorsolateral prefrontal cortex in
suicides
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NEUROSCI CTR ST ELIZABETHS,WASHINGTON,DC 20032.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 447
EP 447
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300432
ER
PT J
AU Bertolino, A
Callicott, JH
Elman, I
Duyn, JH
Tedeschi, G
Frank, JA
Pickar, D
Weinberger, DR
AF Bertolino, A
Callicott, JH
Elman, I
Duyn, JH
Tedeschi, G
Frank, JA
Pickar, D
Weinberger, DR
TI Proton magnetic resonance spectroscopic imaging in drug free patients
with schizophrenia: Regional neuronal damage
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
RI Duyn, Jozef/F-2483-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 460
EP 460
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300445
ER
PT J
AU Bertolino, A
Callicott, JH
Nawroz, S
Knable, MB
Mattay, VS
Duyn, JH
Tedeschi, G
Frank, JA
Weinberger, DR
AF Bertolino, A
Callicott, JH
Nawroz, S
Knable, MB
Mattay, VS
Duyn, JH
Tedeschi, G
Frank, JA
Weinberger, DR
TI Reproducibility of proton magnetic resonance spectroscopic imaging in
patients with schizophrenia and normal controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
RI Duyn, Jozef/F-2483-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 461
EP 461
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300446
ER
PT J
AU Bertolino, A
Saunders, RC
Frank, JA
Weinberger, DR
AF Bertolino, A
Saunders, RC
Frank, JA
Weinberger, DR
TI Proton magnetic resonance spectroscopic imaging in a monkey model of
schizophrenia: Preliminary results
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 463
EP 463
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300448
ER
PT J
AU Callicott, JH
Tallent, K
Bertolino, A
Ramsey, N
Santha, A
Knable, M
Coppola, R
Goldberg, T
Mattay, V
vanGelderen, P
Frank, JA
Moonen, CTW
Weinberger, DR
AF Callicott, JH
Tallent, K
Bertolino, A
Ramsey, N
Santha, A
Knable, M
Coppola, R
Goldberg, T
Mattay, V
vanGelderen, P
Frank, JA
Moonen, CTW
Weinberger, DR
TI 3-D fMRI of working memory in schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,CLIN BRAIN DISORDERS BRANCH,IRP,WASHINGTON,DC 20032.
NIH,INVIVO NMR CTR,BETHESDA,MD 20892.
NIH,LAB DIAGNOST RADIOL RES,BETHESDA,MD 20892.
RI Moonen, Chrit/K-4434-2016
OI Moonen, Chrit/0000-0001-5593-3121
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 466
EP 466
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300451
ER
PT J
AU Elman, I
Bir, C
Pickar, D
Breier, A
AF Elman, I
Bir, C
Pickar, D
Breier, A
TI Neuroendocrinological impacts of glucoprivic stress
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 494
EP 494
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300479
ER
PT J
AU Roca, CA
Rosenstein, DL
Schmidt, PJ
Danaceau, MA
Greenberg, B
Murphy, DL
Rubinow, DR
AF Roca, CA
Rosenstein, DL
Schmidt, PJ
Danaceau, MA
Greenberg, B
Murphy, DL
Rubinow, DR
TI Mechanism of efficacy of fluoxetine in premenstrual syndrome
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 497
EP 497
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300482
ER
PT J
AU Bloch, M
Schmidt, PJ
Su, TP
Tobin, MB
Rubinow, DR
AF Bloch, M
Schmidt, PJ
Su, TP
Tobin, MB
Rubinow, DR
TI ACTH & beta-endorphin over the menstrual cycle in women with PMS &
controls
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIMH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 506
EP 506
PG 2
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300491
ER
PT J
AU Pietrini, P
Dani, A
Furey, ML
Freo, U
Horwitz, B
Mentis, M
Alexander, GE
Grady, C
Schapiro, MB
Rapoport, SI
AF Pietrini, P
Dani, A
Furey, ML
Freo, U
Horwitz, B
Mentis, M
Alexander, GE
Grady, C
Schapiro, MB
Rapoport, SI
TI Brain stimulation reverses cerebral metabolic reductions in Alzheimer
disease
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 544
EP 544
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300529
ER
PT J
AU Mentis, MJ
Horwitz, B
Grady, C
Alexander, GE
Furey, ML
Schapiro, MB
Rapoport, SI
AF Mentis, MJ
Horwitz, B
Grady, C
Alexander, GE
Furey, ML
Schapiro, MB
Rapoport, SI
TI Visual processing is abnormal in striate and association areas in
Alzheimer's disease
SO BIOLOGICAL PSYCHIATRY
LA English
DT Meeting Abstract
C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 1
PY 1996
VL 39
IS 7
BP 549
EP 549
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA UE893
UT WOS:A1996UE89300534
ER
PT J
AU Shingarova, LN
Sagaidak, LN
Turetskaya, RL
Nedospasov, SA
Esipov, DS
Korobko, VG
AF Shingarova, LN
Sagaidak, LN
Turetskaya, RL
Nedospasov, SA
Esipov, DS
Korobko, VG
TI Mutants of human tumor necrosis factor: Preparation and properties
SO BIOORGANICHESKAYA KHIMIYA
LA Russian
DT Article
DE human tumor necrosis factor (TNF-alpha); mutants; polymerase chain
reaction; expression in E-coli
ID FACTOR-ALPHA; TNF RECEPTORS; MOLECULAR-CLONING; HUMAN LYMPHOTOXIN;
EXPRESSION; BETA; ACTIVATION; PROTEINS; INVITRO; FAMILY
AB Using polymerase chain reaction, a number of mutant genes encoding human tumor necrosis factor (TNF-alpha) with amino acid substitutions and a deletion were obtained. The mutant proteins (muteins) contained point mutations R32H, A33S, F144L, I118M, and I118A; double mutation R32H-F144L; and deletion of four amino acid residues 67-70. The mutant genes were expressed in E. coli under the control of constitutive promoters. A simple purification method for the muteins was developed and their physicochemical properties were studied. All the muteins obtained, except F144L and I118A, were shown by CD and cross-linking to form a spatial structure similar to that of the native TNF-alpha. The collection of muteins was characterized by their biological activity. Mutants R32H and A33S exerted a decreased cytotoxicity against murine fibroblast cell line L929, whereas point mutant F144L and double mutant R32H-F144L were essentially inactive.
C1 RUSSIAN ACAD SCI,SHEMYAKIN OVCHINNIKOV INST BIOORGAN CHEM,MOSCOW 117871,RUSSIA.
NCI,FREDERICK,MD 21701.
VA ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA.
RI Nedospasov, Sergei/J-5936-2013; Esipov, Dmitriy/J-9434-2012; Nedospasov,
Sergei/L-1990-2015; Nedospasov, Sergei/Q-7319-2016
OI Esipov, Dmitriy/0000-0003-3973-0898;
NR 36
TC 15
Z9 20
U1 0
U2 1
PU MEZHDUNARODNAYA KNIGA
PI MOSCOW
PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA
SN 0132-3423
J9 BIOORG KHIM+
JI Bioorg. Khim.
PD APR
PY 1996
VL 22
IS 4
BP 243
EP 251
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA UV957
UT WOS:A1996UV95700001
PM 8768260
ER
PT J
AU Wilbur, WJ
Major, F
Spouge, J
Bryant, S
AF Wilbur, WJ
Major, F
Spouge, J
Bryant, S
TI The statistics of unique native states for random peptides
SO BIOPOLYMERS
LA English
DT Article
ID PROTEIN; CONFORMATIONS; SEQUENCES
AB Given a probability distribution from which the energy spectrum of a random peptide is to be sampled, we derive a general expression for the probability that such a peptide will fold to a unique native state and for the probability distribution of the native energy. This latter results allows us to localize the energy of folding based on the model parameters and is one advantage of our formulation. Evidence from both the lattice theory of proteins and protein threading experiments suggest that the energy spectrum for the compact states of a peptide chain is Gaussian in form. For this reason we have derived from the more general framework the specific formulas that apply in the Gaussian case, where one requires only the number of states and the variance of the Gaussian distribution in order to apply the theory. This simplicity allows us to perform calculations that we compare with calculations previously made by others based on statistical thermodynamics. We find qualitative agreement, but a significant correction to prior estimates of folding probability derived from the Gaussian assumption is necessary. (C) 1996 John Wiley & Sons, Inc.
RP Wilbur, WJ (reprint author), NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BLDG 38A,RM 8S806,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA.
NR 21
TC 4
Z9 4
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI NEW YORK
PA 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0006-3525
J9 BIOPOLYMERS
JI Biopolymers
PD APR
PY 1996
VL 38
IS 4
BP 447
EP 459
DI 10.1002/(SICI)1097-0282(199604)38:4<447::AID-BIP2>3.3.CO;2-Y
PG 13
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA UA092
UT WOS:A1996UA09200003
PM 8867208
ER
PT J
AU BakerCairns, B
Meyers, K
Hamilton, R
Smith, C
Tornatore, C
AF BakerCairns, B
Meyers, K
Hamilton, R
Smith, C
Tornatore, C
TI Immunohistochemical staining of fixed tissue using antigen retrieval and
a thermal cycler
SO BIOTECHNIQUES
LA English
DT Article
ID PARAFFIN SECTIONS; CELLS
AB The use of monoclonal antibodies to identify antigens in perfused fixed tissue is currently very challenging, Recently, many antigen retrieval methods have been described that require heating the tissue on slides using a microwave oven.
Here, we describe a protocol for antigen retrieval that uses a commercially available solution called Citra and a DNA thermal cycler to heat the tissue sections. This method (i) allows for precise control of the temperature and time (unlike the microwave oven), (ii) uses very small quantities of the antigen retrieval solution, (iii) stains either free-floating sections or sections mounted on slides and (iv) achieves uniform staining throughout the tissue.
In the paraformaldehyde-perfused fired rat cerebellum, the monoclonal antibody glial fibrillary acidic protein conveys the clarity of the Bergmann and stellate glia in the strata. Scanning confocal images through the center of the tissue demonstrates the depth of antibody penetration achieved using this method. Finally, using a monoclonal antibody against the simian virus 40 (SV40) T antigen allowed positive, unequivocal identification of a grafted cell fine, immortalized using SV40 T protein, thus demonstrating the true value of this method in an experimental paradigm.
C1 NINCDS,NIH,LAB MOL MED & NEUROSCI,MOL THERAPEUT SECT,BETHESDA,MD 20892.
NR 13
TC 3
Z9 3
U1 0
U2 0
PU EATON PUBLISHING CO
PI NATICK
PA 154 E. CENTRAL ST, NATICK, MA 01760
SN 0736-6205
J9 BIOTECHNIQUES
JI Biotechniques
PD APR
PY 1996
VL 20
IS 4
BP 641
EP &
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA UD717
UT WOS:A1996UD71700020
PM 8800684
ER
PT J
AU Schwarzenberger, P
Spence, S
Lohrey, N
Kmiecik, T
Longo, DL
Murphy, WJ
Ruscetti, FW
Keller, JR
AF Schwarzenberger, P
Spence, S
Lohrey, N
Kmiecik, T
Longo, DL
Murphy, WJ
Ruscetti, FW
Keller, JR
TI Gene transfer of multidrug resistance into a factor-dependent human
hematopoietic progenitor cell line: In vivo model for genetically
transferred chemoprotection
SO BLOOD
LA English
DT Article
ID BONE-MARROW CELLS; HUMAN MDR1; TRANSGENIC MICE; DRUG-RESISTANCE;
EXPRESSION; AGENTS; CDNA
AB To develop a rapid preclinical in vivo model to study gene transfer into human hematopoietic progenitor cells, MO-7e cells (CD-34(+), c-kit(+)) were infected with multidrug resistance (MDR1)-containing retroviruses and then transplanted into nonobese diabetic severe combined immunodeficient mice (NOD SCID), MO-7e cells infected with a retrovirus encoding the human MDR1 cDNA showed integration, transcription, and expression of the transfered MDR1 gene. This resulted in a 20-fold increase in the resistance of MO-7e cells to paclitaxel in vitro. The expression of the MDR1 gene product was stable over a 6-month period in vitro without selection in colchicine, MO-7e and MDR1-infected MO-7e cells were transplanted into NOD SCID mice to determine whether MDR1 could confer drug resistance in vivo. A sensitive polymerase chain reaction method specific for human sequences was developed to quantitate the level of human cell engraftment in NOD SCID bone marrow (BM) cells. The percentage of human DNA in BM cells from MO-7e-transplanted mice was 10.9% and decreased to 0.7% in mice treated with paclitaxel, The percentage of human DNA in infected-MO-7e transplanted mice was 7.6% and that level was unchanged in mice treated with paclitaxel. These results show that expression of the MDR1 gene in human hematopoietic progenitor cells can confer functional drug resistance in an in vivo model. (C) 1996 by The American Society of Hematology.
C1 NCI,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
NCI,LAB LEUKOCYTE BIOL,BIOL RESPONSE MODIFIERS PROGRAM,DIV CANC TREATMENT,FREDERICK,MD 21701.
FU NCI NIH HHS [N01-CO-56000]
NR 22
TC 17
Z9 18
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 1
PY 1996
VL 87
IS 7
BP 2723
EP 2731
PG 9
WC Hematology
SC Hematology
GA UC776
UT WOS:A1996UC77600013
PM 8639888
ER
PT J
AU Kwak, LW
Pennington, R
Longo, DL
AF Kwak, LW
Pennington, R
Longo, DL
TI Active immunization of murine allogeneic bone marrow transplant donors
with B-cell tumor-derived idiotype: A strategy for enhancing the
specific antitumor effect of marrow grafts
SO BLOOD
LA English
DT Article
ID MAJOR HISTOCOMPATIBILITY COMPLEX; CHRONIC MYELOGENOUS LEUKEMIA;
MULTIPLE-MYELOMA; HOST-DISEASE; T-CELLS; LYMPHOMA; IMMUNOTHERAPY;
INDUCTION; IMMUNITY; ANTIGEN
AB Persistence of the underlying malignancy remains the major obstacle limiting the success of high-dose chemoradiotherapy with allogeneic bone marrow transplantation (BMT) for lymphomas and multiple myeloma, We used the C3H 38C13 murine B-cell lymphoma, which expresses and secretes clonally derived Ig, the idiotype of which can serve as a tumor-specific antigen, to test the principle of transfer of tumor idiotype-specific immunity with BM. BALB/c marrow donors were twice immunized with 38C13-derived Ig, or with an isotype-matched control Ig, conjugated to keyhole limpet hemocyanin. Lethally irradiated C3H recipients reconstituted with marrow from idiotype immune, but not nonspecifically immune, donors demonstrated protection against subsequent lethal tumor challenge. The immunoprotective effect of immune allogeneic marrow was abrogated by T-cell depletion of the marrow graft before infusion, Low levels of serum anti-idiotypic antibody remained unaltered in recipients of T-cell-depleted immune marrow, consistent with a primary role for T-cell immunity in the cellular mechanism of this phenomenon. A modest therapeutic effect of immune allogeneic marrow was observed against 10 day, 1 cm established subcutaneous tumors, but only in combination with a booster immunization of the recipient post-BMT. These results provide the rationale for a novel strategy for enhancing the specific antitumor effect of allogeneic marrow grafts.
C1 SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
RP Kwak, LW (reprint author), NCI,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK CANC RES & DEV CTR,DIV CLIN SCI,BLDG 567,ROOM 205,FREDERICK,MD 21702, USA.
NR 36
TC 33
Z9 34
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 1
PY 1996
VL 87
IS 7
BP 3053
EP 3060
PG 8
WC Hematology
SC Hematology
GA UC776
UT WOS:A1996UC77600054
PM 8639929
ER
PT J
AU Pines, M
Fukayama, S
Costas, K
Meurer, E
Goldsmith, PK
Xu, X
Muallem, S
Behar, V
Chorev, M
Rosenblatt, M
Tashjian, AH
Suva, LJ
AF Pines, M
Fukayama, S
Costas, K
Meurer, E
Goldsmith, PK
Xu, X
Muallem, S
Behar, V
Chorev, M
Rosenblatt, M
Tashjian, AH
Suva, LJ
TI Inositol 1-,4-,5-trisphosphate-dependent Ca2+ signaling by the
recombinant human PTH/PTHrP receptor stably expressed in a human kidney
cell line
SO BONE
LA English
DT Article
DE PTH/PTHrP receptor; hormone; intracellular calcium; signal transduction
ID OSTEO-SARCOMA CELLS; THYROTROPIN-RELEASING-HORMONE; ALKALINE-PHOSPHATASE
ACTIVITY; CYTOSOLIC FREE CALCIUM; PROTEIN KINASE-C; PARATHYROID-HORMONE;
OSTEOSARCOMA CELLS; BINDING PROTEINS; UMR-106-01 CELLS; PERTUSSIS TOXIN
AB We previously reported the preparation and partial characterization of a series of human embryonic kidney cell lines (HEK-293) stably expressing various numbers of the recombinant human (h) parathyroid hormone (PTH)/PTH-related protein (PTHrP) receptor (Rc), Using this expression system we examined ligand (PTH or PTHrP) binding characteristics and cyclic AMP responsiveness, We have now extended these studies to investigate the calcium signal transduction pathways activated by the hPTH/PTHrP Rc. In parental HEK-293 cells, which lack endogenous PTH/PTHrP Rc, incubation with hPTH(1-34) had no effect on cytosolic free Ca2+ concentration [Ca2+](i). In HEK-293 clone C-21, stably expressing similar to 400,000 Rc/cell, PTH stimulated an increase in [Ca2+](i) by Ca2+ release from intracellular stores; PTH released Ca2+ exclusively from the IP3 sensitive Ca2+ pool, Unlike previous studies, the ability of PTH to elicit both cAMP responses and [Ca2+](i) transients occurred over a wide range of Rc numbers (between 400,000 and 3000 Rc/cell); both responses were always observed at PTH concentrations in the same dose range although the magnitude of the responses decrease with Rc number, Pretreatment of C-21 cells with pertussis toxin for 24 h, which significantly enhanced PTH-stimulated cAMP accumulation, did not modulate PTH-stimulated [Ca2+](i) transients, At each PTH concentration tested which resulted in increased cAMP levels, there was also an increase in [Ca2+](i) transients. Treatment of C-21 cells with a battery of midregion and C-terminal PTH or PTHrP peptides showed no effect on either [Ca2+](i) transients or cAMP accumulation, indicating a lack of functional interactions between these peptides and the form of the hPTH/PTHrP Rc stably expressed in these cells, Immunological analysis of G-protein expression demonstrated the presence of G(s), G(i), and G(q) in all parental and transfected cell lines examined, Taken together, these data demonstrate that the hPTH/PTHrP Rc, stably expressed in HEK-293 cells, elicits responses in both the cAMP and IP3-dependent [Ca2+](i) pathways and is responsive only to N-terminal PTH/PTHrP peptides.
C1 BETH ISRAEL HOSP,HARVARD THORNDIKE LAB,DIV BONE & MINERAL METAB,DEPT MED,BOSTON,MA 02215.
BETH ISRAEL HOSP,CHARLES A DANA LABS,DEPT MED,BOSTON,MA 02215.
HARVARD UNIV,SCH PUBL HLTH,DEPT MOLEC & CELLULAR TOXICOL,BOSTON,MA.
HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115.
NIDDKD,METAB DIS BRANCH,BETHESDA,MD 20892.
UNIV TEXAS,SW MED CTR,DEPT PHYSIOL,DALLAS,TX 75235.
FU NIDDK NIH HHS [DK47940, DK46655]
NR 61
TC 51
Z9 51
U1 0
U2 0
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 APR
PY 1996
VL 18
IS 4
BP 381
EP 389
DI 10.1016/8756-3282(96)00008-7
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UG174
UT WOS:A1996UG17400015
PM 8726398
ER
PT J
AU Schmidt, EM
Bak, MJ
Hambrecht, FT
Kufta, CV
ORourke, DK
Vallabhanath, P
AF Schmidt, EM
Bak, MJ
Hambrecht, FT
Kufta, CV
ORourke, DK
Vallabhanath, P
TI Feasibility of a visual prosthesis for the blind based on intracortical
microstimulation of the visual cortex
SO BRAIN
LA English
DT Article
DE human; electrical stimulation; visual cortex
ID HUMAN OCCIPITAL CORTEX; ELECTRICAL-STIMULATION; VISION
AB The feasibility of producing a visual prosthesis for the blind using intracortical microstimulation (ICMS) of the visual cortex was studied in a 42-year-old woman who had been totally blind for 22 years secondary to glaucoma. Thirty-eight microelectrodes were implanted in the right visual cortex, near the occipital pole, for a period of 4 months. Percepts reported as small spots of light, called phosphenes, were produced with 34 of the 38 implanted microelectrodes. Threshold currents for phosphene generation with trains of biphasic pulses were as low as 1.9 mu A, and most of the microelectrodes had thresholds below 25 mu A. Phosphene brightness could be modified with stimulus amplitude, frequency and pulse duration. Repeated stimulation over a period of minutes produced a gradual decrease in phosphene brightness. Phosphenes did not flicker. The apparent size of phosphenes ranged from a 'pin-point' to a 'nickel' (20 mm diameter coin) held at arm's length. Phosphene size usually decreased as stimulation current was increased but increased slightly as the train length (TL) was increased. At levels of stimulation near threshold, the phosphenes were often reported to have colours. As the stimulation level was increased, the phosphenes generally became white, greyish or yellowish. Individual phosphenes appeared at different distances from the subject. When two phosphenes were simultaneously generated, the apparent distances of the individual phosphenes sometimes changed to make them appear to be at about the same distance. When three or more phosphenes were simultaneously generated, they became coplanar Except for rave occasions, phosphenes extinguished rapidly at the termination of the stimulation train. When stimulation TLs were increased beyond 1 s, phosphenes usually disappeared before the end of the train. The duration of phosphene perception could be increased by interrupting a long stimulation train with brief pauses in stimulation. Intracortical microelectrodes spaced 500 mu m apart generated separate phosphenes, but microelectrodes spaced 250 mu m typically did not. This two-point resolution was about Jive times closer than has typically been achieved with surface stimulation. With some individual microelectrodes, a second closely spaced phosphene was sometimes produced by increasing the stimulation current Phosphenes moved with eye movements. When up to six phosphenes were simultaneously elicited, they all moved with the same relative orientation during eye movements. All phosphenes were located in the left hemi-field with the majority above the horizontal meridian There was a clustering of most of the phosphenes within a relatively small area of visual space. The potentially greater microelectrode density and lower power requirements of ICMS compared with surface stimulation appears encouraging for a visual prosthesis. However, further studies with blind subjects are required to optimize stimulation parameters and test complex image recognition before the feasibility of a visual prosthesis based on ICMS can be established.
C1 NINCDS,NEURAL PROSTHESIS PROGRAM,NIH,BETHESDA,MD 20892.
NINCDS,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892.
HOWARD HUGHES MED INST,BETHESDA,MD 20817.
RP Schmidt, EM (reprint author), NINCDS,NEURAL CONTROL LAB,NIH,BLDG 49,ROOM 3A50,BETHESDA,MD 20892, USA.
NR 21
TC 335
Z9 350
U1 0
U2 23
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0006-8950
J9 BRAIN
JI Brain
PD APR
PY 1996
VL 119
BP 507
EP 522
DI 10.1093/brain/119.2.507
PN 2
PG 16
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA UN423
UT WOS:A1996UN42300015
PM 8800945
ER
PT J
AU Berardelli, A
Hallett, M
Rothwell, JC
Agostino, R
Manfredi, M
Thompson, PD
Marsden, CD
AF Berardelli, A
Hallett, M
Rothwell, JC
Agostino, R
Manfredi, M
Thompson, PD
Marsden, CD
TI Single-joint rapid arm movements in normal subjects and in patients with
motor disorders
SO BRAIN
LA English
DT Review
DE rapid movements; arm; normal subjects; motor disorders
ID ELBOW FLEXION MOVEMENTS; STEREOTYPED VOLUNTARY MOVEMENTS; ANTAGONIST
MUSCLE-ACTIVITY; AGONIST EMG BURST; PARKINSONS-DISEASE; ORGANIZING
PRINCIPLES; POSTURAL ADJUSTMENTS; ABDUCTION MOVEMENTS;
HUNTINGTONS-DISEASE; BALLISTIC MOVEMENT
AB In normal subjects the execution of single rapid one-joint movements is characterized by an electromyographic (EMG) pattern composed of three discrete bursts of activity: two bursts (first and second agonist bursts, or AG1 and AG2) are present in the agonist muscle separated by an almost complete period of electrical silence. During this pause, another burst (antagonist burst or ANT) occurs in the antagonist muscle. If a rapid movement is executed during tonic activation of the agonist muscle, tonic activity is inhibited just prior to AG1 onset (agonist inhibition). Similarly, if the movement is performed during tonic activation of the antagonist muscle, such activity is also inhibited prior to AG1 onset (antagonist inhibition). Antagonist inhibition also starts prior to AG1 onset and lasts until ANT onset. A general descriptor of the kinematic features related to the EMG pattern described above is a symmetrical and unimodal velocity profile that is bell-shaped and shows an acceleration time roughly equal to the deceleration time. This holds true for movements performed under low accuracy constraints; as accuracy demands become stricter and stricter the peak velocity decreases but as long as the movement is made with one continuous trajectory the velocity profile remains roughly symmetrical. In general terms, the function of AG1 is to provide the impulsive force to start the movement; the function of ANT is to halt the movement at the desired end-point; and the function of AG2 is to dampen out the oscillations which might occur at the end of the movement. The timing and size of the bursts vary according to the speed and amplitude of the movement. The origin of the EMG pattern is a central programme, but afferent inputs can modulate the voluntary activity. In this paper we also review the EMG and kinematic abnormalities that are present during the execution of single-joint, rapid arm movements in patients with Parkinson's disease, Huntington's disease, Sydenham's chorea, dystonia, athetosis, cerebellar deficits, upper motor neuron syndrome, essential tremor and large-fibre sensory neuropathy. The data from these studies lead us to the following conclusions: (i) the basal ganglia have a role in scaling the size of AG1, reinforcing the voluntary command and inhibiting inappropriate EMG activity; (ii) the cerebellum has a role in timing the voluntary bursts and probably in implementing muscle force phasically; (iii) the corticospinal tract has a role in determining spatial and temporal recruitment of motor units; (iv) proprioceptive feedback is not necessary reproduce the triphasic pattern but it contributes to the accuracy of both the trajectory and the end-point of rapid movements.
C1 NATL INST HLTH, BETHESDA, MD USA.
UCL NATL HOSP NEUROL & NEUROSURG, DEPT NEUROL, LONDON WC1N 3BG, ENGLAND.
UNIV ADELAIDE, DEPT MED, ADELAIDE, SA 5001, AUSTRALIA.
RP Berardelli, A (reprint author), UNIV ROMA LA SAPIENZA, DIPARTIMENTO SCI NEUROL, VIALE UNIV 30, I-00185 ROME, ITALY.
OI Rothwell, John/0000-0003-1367-6467
NR 76
TC 152
Z9 152
U1 2
U2 13
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD APR
PY 1996
VL 119
BP 661
EP 674
DI 10.1093/brain/119.2.661
PN 2
PG 14
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA UN423
UT WOS:A1996UN42300025
PM 8800955
ER
PT J
AU Brown, P
Tateishi, J
Budka, H
AF Brown, P
Tateishi, J
Budka, H
TI Inactivation of the causal agents of Creutzfeldt-Jakob disease and other
human prion diseases - Reply
SO BRAIN PATHOLOGY
LA English
DT Letter
C1 KYUSHU UNIV,INST NEUROL,FUKUOKA 812,JAPAN.
UNIV VIENNA,INST NEUROL,VIENNA,AUSTRIA.
RP Brown, P (reprint author), NINCDS,CNS STUDIES LAB,NIH,BLDG 36,RM 4D04,BETHESDA,MD 20892, USA.
NR 2
TC 1
Z9 1
U1 0
U2 0
PU INT SOC NEUROPATHOLOGY
PI ZURICH
PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND
SN 1015-6305
J9 BRAIN PATHOL
JI Brain Pathol.
PD APR
PY 1996
VL 6
IS 2
BP 198
EP 198
DI 10.1111/j.1750-3639.1996.tb00801.x
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA UF671
UT WOS:A1996UF67100015
ER
PT J
AU Hirata, H
Ladenheim, B
Carlson, E
Epstein, C
Cadet, JL
AF Hirata, H
Ladenheim, B
Carlson, E
Epstein, C
Cadet, JL
TI Autoradiographic evidence for methamphetamine-induced striatal
dopaminergic loss in mouse brain: Attenuation in CuZn-superoxide
dismutase transgenic mice
SO BRAIN RESEARCH
LA English
DT Article
DE methamphetamine; transgenic mouse; superoxide dismutase; superoxide
radical; dopamine uptake site; striatum; gender
ID PARKINSONS-DISEASE; CAUDATE-NUCLEUS; NITRIC-OXIDE; RAT-BRAIN;
AMPHETAMINE; NEUROTOXICITY; 6-HYDROXYDOPAMINE; GLUTAMATE; TOXICITY;
RELEASE
AB Methamphetamine (METH) has long-lasting neurotoxic effects on the nigrostriatal dopamine (DA) system of rodents. METH-induced neurotoxicity is thought to involve release of DA in presynaptic DA terminals, which is associated with increased formation of oxygen-based free radicals. We have recently shown that METH-induced striatal DA depletion is attenuated in transgenic (Tg) mice that express the human CuZn-superoxide dismutase (SOD) enzyme. That study did not specifically address the issue of loss of DA terminals. In the present study, we have used receptor autoradiographic studies of [I-125]RTI-121-labeled DA uptake sites to evaluate the effects of several doses of METH on striatal DA terminals of Non-Tg as well as of heterozygous and homozygous SOD-Tg mice. In Non-Tg mice, METH caused decreases in striatal DA uptake sites in a dose-dependent fashion. The loss of DA terminals was more prominent in the lateral region than in the medial subdivisions of the striatum. In SOD-Tg mice, the loss of DA terminals caused by METH was attenuated in a gene dosage-dependent fashion, with the homozygous mice showing the greatest protection. Female mice were somewhat more resistant than male mice against these deleterious effects of METH. These results provide further evidence for a role of superoxide radicals in the long-term effects of METH. They also suggest the notion of a gender-specific handling of oxidative stress.
C1 NIDA,MOLEC NEUROPSYCHIAT SECT,NIH,DIV INTRAMURAL RES,BALTIMORE,MD 21224.
UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143.
FU NIA NIH HHS [AG-08938]
NR 43
TC 91
Z9 92
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD APR 1
PY 1996
VL 714
IS 1-2
BP 95
EP 103
DI 10.1016/0006-8993(95)01502-7
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA UF668
UT WOS:A1996UF66800011
PM 8861613
ER
PT J
AU Melbye, M
Cote, TR
West, D
Kessler, L
Biggar, RJ
Lemp, G
Singleton, J
Young, J
Kerndt, P
Deapen, D
Ginzberg, M
AntonCulver, H
Lieb, S
Hopkins, R
Williams, B
Liff, J
Morgan, D
Parkin, W
AF Melbye, M
Cote, TR
West, D
Kessler, L
Biggar, RJ
Lemp, G
Singleton, J
Young, J
Kerndt, P
Deapen, D
Ginzberg, M
AntonCulver, H
Lieb, S
Hopkins, R
Williams, B
Liff, J
Morgan, D
Parkin, W
TI Nasopharyngeal carcinoma: An EBV-associated tumour not significantly
influenced by HIV-induced immunosuppression
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE human immunodeficiency virus; immunosuppression; nasopharyngeal
carcinoma; Epstein-Barr virus; registry linkage
ID RENAL-TRANSPLANT RECIPIENTS; HODGKINS-DISEASE; KAPOSIS-SARCOMA; CANCER;
RISK
AB We used a link between cancer (859 398 reports) and AIDS (50 050 reports) registries in the United States to study whether nasopharyngeal carcinoma (NPC) was increased in the population with AIDS. There was no indication of a significantly increased risk up to or after the AIDS diagnosis, which argues against progressively failing immunity being important in the development of this malignancy.
C1 NCI,DIV CANC ETIOL,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD 20852.
SAN FRANCISCO CANC REGISTRY,SAN FRANCISCO,CA.
NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,ROCKVILLE,MD 20852.
RP Melbye, M (reprint author), STATENS SERUM INST,DANISH EPIDEMIOL SCI CTR,COPENHAGEN,DENMARK.
NR 17
TC 9
Z9 9
U1 0
U2 0
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR
PY 1996
VL 73
IS 8
BP 995
EP 997
DI 10.1038/bjc.1996.194
PG 3
WC Oncology
SC Oncology
GA UE606
UT WOS:A1996UE60600019
PM 8611438
ER
PT J
AU Mellemkjaer, L
Gridley, G
Moller, H
Hsing, AW
Linet, MS
Brinton, LA
Olsen, JH
AF Mellemkjaer, L
Gridley, G
Moller, H
Hsing, AW
Linet, MS
Brinton, LA
Olsen, JH
TI Pernicious anaemia and cancer risk in Denmark
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE pernicious anaemia; cancer risk; cohort study
ID ANEMIA
AB A cohort of 5072 patients with pernicious anaemia was identified in the Danish Hospital Discharge Register from 1977 to 1989 and, through linkage to the Danish Cancer Registry, the occurrence of cancer in the cohort was determined up to 1991. Observed numbers of cancer cases during 1-15 years of follow-up were compared with expected numbers based on national incidence rates. Besides the well-established increased risk for stomach cancer, the analysis also revealed a 2-fold increase in the relative risk for cancer of the buccal cavity and pharynx among pernicious anaemia patients in accordance with previous studies; previously reported elevated risks for other digestive tract cancers were not confirmed. There was a non-significantly increased risk for lymphatic and haematological malignancy but the risk tended to disappear after 5 years of follow-up, indicating a possible selection bias. Decreased risks for cervical cancer and non-melanoma skin cancer were also seen.
C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892.
CTR RES HLTH & SOCIAL STAT,DK-2100 COPENHAGEN O,DENMARK.
RP Mellemkjaer, L (reprint author), DANISH CANC SOC,DIV CANC EPIDEMIOL,STRANDBLVD 49,DK-2100 COPENHAGEN O,DENMARK.
RI Brinton, Louise/G-7486-2015;
OI Brinton, Louise/0000-0003-3853-8562; Moller, Henrik/0000-0001-8200-5929
FU NCI NIH HHS [N01-CP-85639-04]
NR 11
TC 20
Z9 20
U1 1
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR
PY 1996
VL 73
IS 8
BP 998
EP 1000
DI 10.1038/bjc.1996.195
PG 3
WC Oncology
SC Oncology
GA UE606
UT WOS:A1996UE60600020
PM 8611439
ER
PT J
AU Coceani, F
Kelsey, L
Seidlitz, E
Korzekwa, Z
AF Coceani, F
Kelsey, L
Seidlitz, E
Korzekwa, Z
TI Inhibition of the contraction of the ductus arteriosus to oxygen by
1-aminobenzotriazole, a mechanism-based inactivator of cytochrome P450
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE foetus ductus arteriosus closure; oxygen; cytochrome P450; endothelin-1;
1-aminobenzotriazole
ID PROSTAGLANDIN-E2; EXPRESSION; TENSION; METABOLISM; CLOSURE; CELLS
AB 1 We have proposed that contractile tension of the ductus arteriosus is sustained by a cytochrome P450-linked mechanism acting as a limiting step in the synthesis of endothelin-1 (ET-1). In the present study, we have used the isolated ductus from near-term foetal lambs and guinea-pigs to investigate the effect on both muscle tone and ET-1 formation of 1-aminobenzotriazole (ABT), a suicide substrate for mono-oxygenase reactions.
2 ABT relaxed the lamb ductus at rest (2.5% O-2) and during the oxygen contraction (ii to 95% O-2) The effect was seen at 40 mu M, and at 0.8 mM active tone was almost completely abolished. ABT (1 mM) also reversed the oxygen contraction in the guinea-pig ductus.
3 In the lamb ductus, the ABT response was not affected by removal of the endothelium or by treatment with 2.8 mu M indomethacin (al 2.5% O-2) and the ensuing contraction.
4 At both low and high concentration, ABT relaxed marginally, or not at all, the potassium-contracted (55 mM) ductus from either species.
5 ET-1 release from either the intact or endothelium-denuded lamb ductus tended to decrease in the presence of ABT (1 mM), whilst during the same treatment cyclic GMP content of the tissue remained unchanged.
6 We conclude that ABT relaxation is due to suppression of a contractile mechanism and not to activation of prostaglandin- and NO-mediated relaxing mechanisms. This contractile mechanism has a cytochrome P450-based mono-oxygenase reaction as a key component.
C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892.
RP Coceani, F (reprint author), HOSP SICK CHILDREN,RES INST,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA.
RI Seidlitz, Eric/K-6765-2013
OI Seidlitz, Eric/0000-0001-9760-1133
NR 40
TC 22
Z9 26
U1 0
U2 2
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD APR
PY 1996
VL 117
IS 7
BP 1586
EP 1592
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UF138
UT WOS:A1996UF13800033
PM 8730758
ER
PT J
AU Jordan, NJ
Watson, ML
Williams, RJ
Roach, AG
Yoshimura, T
Westwick, J
AF Jordan, NJ
Watson, ML
Williams, RJ
Roach, AG
Yoshimura, T
Westwick, J
TI Chemokine production by human vascular smooth muscle cells: Modulation
by IL-13
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Meeting Abstract
C1 UNIV BATH,DEPT PHARMACOL,BATH BA2 7AY,AVON,ENGLAND.
RHONE POULENC RORER,DAGENHAM RES CTR,DAGENHAM RM10 7XS,ESSEX,ENGLAND.
NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
RI Jordan, Nicola/B-3341-2013
NR 3
TC 0
Z9 0
U1 0
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD APR
PY 1996
VL 117
SU S
BP P113
EP P113
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UD162
UT WOS:A1996UD16200113
ER
PT J
AU Wise, SP
diPellegrino, G
Boussaoud, D
AF Wise, SP
diPellegrino, G
Boussaoud, D
TI The premotor cortex and nonstandard sensorimotor mapping
SO CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT Symposium on Visuomotor Control - Planning and Execution
CY MAY 11-12, 1995
CL MONTREAL, CANADA
SP Univ Montreal, Ctr Rech Sci Neurol
DE premotor cortex; frontal cortex; sensorimotor mapping; behavioral
neurophysiology
ID MOTOR CORTICAL ACTIVITY; VISUALLY GUIDED ARM; STIMULUS-RESPONSE
COMPATIBILITY; MONKEY SUPERIOR COLLICULUS; MOVEMENT-RELATED ACTIVITY;
PRIMATE FRONTAL-CORTEX; NEURONAL-ACTIVITY; REACHING MOVEMENTS; HAND
MOVEMENTS; RHESUS-MONKEYS
AB We often gaze at and attend to an object while preparing to reach toward and grasp it, and continue doing so when the plan is executed. Elaborate machinery, much of it in the brainstem and spinal cord, provides control systems for the spatially congruent guidance of the eyes, limbs, and body toward targets in visual space. We will use the term standard mapping for the sensorimotor transformations that underlie such behavior. Despite the commonsense character of standard mapping, the targets of gaze, attention, and reaching can be dissociated from each other. We can attend to stimuli in locations that differ from the target of action. We can gaze in one direction while reaching in another. And we can guide spatial action with nonspatial stimuli, such as when, in conditional motor tasks, the color of an object instructs a movement elsewhere in space. All of these situations, and many others, call for a process that we term nonstandard mapping, wherein the central nervous system must reject the commonplace correspondences among visuospatial stimuli, gaze, attention, and reaching movements. We focus in this article on the possibility that premotor cortex underlies nonstandard mapping and, therefore, the behavioral flexibility that such a process allows.
RP Wise, SP (reprint author), NIMH, NEUROPHYSIOL LAB, POB 608, POOLESVILLE, MD 20837 USA.
RI Boussaoud, Driss/B-6932-2008;
OI di Pellegrino, Giuseppe/0000-0001-7080-4758
NR 92
TC 173
Z9 174
U1 1
U2 6
PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
PI OTTAWA
PA 1200 MONTREAL ROAD, BUILDING M-55, OTTAWA, ON K1A 0R6, CANADA
SN 0008-4212
J9 CAN J PHYSIOL PHARM
JI Can. J. Physiol. Pharmacol.
PD APR
PY 1996
VL 74
IS 4
BP 469
EP 482
DI 10.1139/cjpp-74-4-469
PG 14
WC Pharmacology & Pharmacy; Physiology
SC Pharmacology & Pharmacy; Physiology
GA UY560
UT WOS:A1996UY56000013
PM 8828893
ER
PT J
AU Cavazza, A
Travis, LB
Travis, WD
Wolfe, JT
Foo, ML
Gillespie, DJ
Weidner, N
Colby, TV
AF Cavazza, A
Travis, LB
Travis, WD
Wolfe, JT
Foo, ML
Gillespie, DJ
Weidner, N
Colby, TV
TI Post-irradiation malignant mesothelioma
SO CANCER
LA English
DT Article
DE mesothelioma; radiotherapy; Hodgkin's disease; breast carcinoma
ID PERITONEAL MESOTHELIOMA; PLEURAL MESOTHELIOMA; HODGKINS-DISEASE;
UNITED-STATES; WILMS TUMOR; CANCER; RADIATION; RADIOTHERAPY; EXPERIENCE;
THOROTRAST
AB BACKGROUND. Approximately 30 patients with malignant mesothelioma following radiotherapy have been described. Population-based studies of this occurrence have not been reported.
METHODS. Patients with malignant mesothelioma of the pleura were collected. All of the patients had a prior cancer and had received radiotherapy to the region in which the malignant mesothelioma developed. Data from the National Cancer Institute's Surveillance, Epidemiology and End Results Program and the Connecticut Tumor Registry were evaluated for cases of malignant mesothelioma of the pleura occurring in patients with a previous cancer. The literature on post-irradiation malignant mesotheliomas was reviewed.
RESULTS. Eight patients (4 men, 4 women) with malignant mesothelioma occurring in sites of radiotherapy for a prior tumor were identified. The mean age at diagnosis of mesothelioma was 45 years (range: 22-78 years), and the average interval between radiotherapy and the mesothelioma was 21 years (range: 11-29 years). Three of the patients had also received chemotherapy. Histologically, the mesotheliomas were epithelial in five cases, biphasic in one, and sarcomatous in one. One hundred forty-two patients were identified in the epidemiologic survey. The majority were men (89%), with a median age for all patients of 68.5 years (range: 35-86 years) and a median latency between first cancer and mesothelioma of 4.3 pears (range: 2 months-29.9 years).
CONCLUSIONS. Mesotheliomas rarely develop as second malignant neoplasms. Within a large, population-based survey of patients with cancer, temporal patterns and demographic features of most second primary mesotheliomas were similar to asbestos-related tumors, although the late effects of cancer treatment might have contributed to the occurrence of cancer in some patients. (C) 1996 American Cancer Society.
C1 NCI,RADIAT EPIDEMIOL BRANCH,NIH,BETHESDA,MD.
ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306.
MAYO CLIN SCOTTSDALE,DEPT LAB MED & PATHOL,SCOTTSDALE,AZ.
MAYO CLIN JACKSONVILLE,DEPT PATHOL,JACKSONVILLE,FL 32224.
MAYO CLIN JACKSONVILLE,DEPT RADIAT ONCOL,JACKSONVILLE,FL 32224.
MAYO CLIN,DEPT THORAC DIS,ROCHESTER,MN.
UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA 94143.
NR 33
TC 55
Z9 57
U1 0
U2 2
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0008-543X
J9 CANCER
JI Cancer
PD APR 1
PY 1996
VL 77
IS 7
BP 1379
EP 1385
DI 10.1002/(SICI)1097-0142(19960401)77:7<1379::AID-CNCR24>3.3.CO;2-5
PG 7
WC Oncology
SC Oncology
GA UA645
UT WOS:A1996UA64500024
PM 8608519
ER
PT J
AU Goto, M
Miller, RW
Ishikawa, Y
Sugano, H
AF Goto, M
Miller, RW
Ishikawa, Y
Sugano, H
TI Excess of rare cancers in Werner syndrome (adult progeria)
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID MELANOMA; TISSUE; CARCINOMA; CELLS; GENE
AB The association between genetic disorders and diverse cancers has provided clues for laboratory research into carcinogenesis, Such an opportunity now arises from studies of cancer in Werner syndrome (WRN). Soft-tissue sarcoma (STS) and benign meningioma have been associated with WRN, an autosomal recessive disorder characterized by premature aging, more commonly reported in Japan than elsewhere, in part because of inbreeding, In the literature we found 124 case-reports of neoplasia and WRN from Japan and 34 from outside Japan, 1939-August 1995, They reveal a greater diversity of neoplasia in WRN than was previously known, In Japanese, there were 127 cancers, 14 benign meningioma, and 5 myeloid disorders, as compared with 30, 7 and 2 respectively in non-Japanese, The ratio of epithelial to non-epithelial cancers was about 1:1 for Japanese and for non-Japanese instead of the usual 10:1, Both series had excesses of STS, osteosarcoma, myeloid disorders, and benign meningioma. In addition, the Japanese had an excess of thyroid cancer (20 versus 2 cases in non-Japanese) and melanoma (21 versus 3 cases), including 5 intranasal and 13 of the feet, STS, osteosarcoma, melanoma, and thyroid carcinoma accounted for 57% of all cancer in WRN as compared with 2% expected based on the Osaka population at 25-64 years of age, Multiple tumors were reported in 19 Japanese and 5 non-Japanese. In Japan, nine first-degree relatives had WRN and cancer, six of whom were concordant as to site and/or cell type, The WRN gene has been mapped to chromosome 8p, The high frequency of thyroid cancer and melanoma in Japanese, not found in Caucasians, may be related to a report of linkage disequilibrium with the WRN gene in Japanese but not in Caucasians and to haplotype differences within and between the two races, suggesting multiple independent mutations.
C1 NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892.
INST CANC RES,TOSHIMA KU,TOKYO 170,JAPAN.
TOKYO METROPOLITAN OTSUKA HOSP,DEPT RHEUMAT DIS,TOSHIMA KU,TOKYO 170,JAPAN.
NR 164
TC 280
Z9 287
U1 2
U2 5
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 APR
PY 1996
VL 5
IS 4
BP 239
EP 246
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA UE615
UT WOS:A1996UE61500001
PM 8722214
ER
PT J
AU Weed, DL
Gorelic, LS
AF Weed, DL
Gorelic, LS
TI The practice of causal inference in cancer epidemiology
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID ALCOHOLIC-BEVERAGE CONSUMPTION; UNITED-STATES MEN; BREAST-CANCER;
PROSTATE-CANCER; CIGARETTE-SMOKING; RISK-FACTORS; RETROSPECTIVE COHORT;
VASECTOMY; DIET; HEALTH
AB Causal inference is an important link between the practice of cancer epidemiology and effective cancer prevention, Although many papers and epidemiology textbooks have vigorously debated theoretical issues in causal inference, almost no attention has been paid to the issue of how causal inference is practiced, In this paper, we review two series of review papers published between 1985 and 1994 to find answers to the following questions: which studies and prior review papers were cited, which causal criteria were used, and what causal conclusions and public health recommendations ensued, Fourteen published reviews on alcohol and breast cancer and 6 published reviews on vasectomy and prostate cancer were examined, For both series of reviews, nearly all available published studies were cited except for ecological studies and prior reviews, Sources of causal criteria were often not provided, When they appeared, all citations were either the 1964 Surgeon General's report or works of Austin Bradford Hill, Reviews often excluded and sometimes altered criteria without giving reasons for these changes, The criteria of consistency and strength of association were almost always used accompanied by dose-response and biological plausibility in a majority of reviews, The criterion of temporality, considered by many methodologists to be a necessary causal condition, was infrequently used, Confounding and bias were often added considerations. Public health recommendations were not discussed in nearly one-half of the reviews.
C1 NCI,COMPREHENS MINOR BIOMED PROGRAM,BETHESDA,MD 20892.
RP Weed, DL (reprint author), NCI,PREVENT ONCOL BRANCH,EPS T-41,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 175
TC 59
Z9 61
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 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD APR
PY 1996
VL 5
IS 4
BP 303
EP 311
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA UE615
UT WOS:A1996UE61500010
PM 8722223
ER
PT J
AU DeLaPena, L
WooleryAntill, M
Tomaszewski, JG
Gantz, S
DiLorenzo, K
Kryk, JA
AF DeLaPena, L
WooleryAntill, M
Tomaszewski, JG
Gantz, S
DiLorenzo, K
Kryk, JA
TI Programmed instruction: Biotherapy module .5. Hematopoietic growth
factors
SO CANCER NURSING
LA English
DT Article
RP DeLaPena, L (reprint author), NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892, USA.
NR 12
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0162-220X
J9 CANCER NURS
JI Cancer Nurs.
PD APR
PY 1996
VL 19
IS 2
BP 135
EP 150
DI 10.1097/00002820-199604000-00008
PG 16
WC Oncology; Nursing
SC Oncology; Nursing
GA UE722
UT WOS:A1996UE72200008
PM 8635167
ER
PT J
AU Wei, MH
Latif, F
Bader, S
Kashuba, V
Chen, JY
Duh, FM
Sekido, Y
Lee, CC
Geil, L
Kuzmin, I
Zabarovsky, E
Klein, G
Zbar, B
Minna, JD
Lerman, MI
AF Wei, MH
Latif, F
Bader, S
Kashuba, V
Chen, JY
Duh, FM
Sekido, Y
Lee, CC
Geil, L
Kuzmin, I
Zabarovsky, E
Klein, G
Zbar, B
Minna, JD
Lerman, MI
TI Construction of a 600-kilobase cosmid clone contig and generation of a
transcriptional map surrounding the lung cancer tumor suppressor gene
(TSG) locus on human chromosome 3p21.3: Progress toward the isolation of
a lung cancer TSG
SO CANCER RESEARCH
LA English
DT Article
ID 3P(14-23); DELETION; REGION; DNA
AB The critical region on human chromosome 3p21.3 harboring a putative lung cancer tumor suppressor gene (TSG) was previously defined by allelotyping and recently refined by overlapping homozygous deletions. We report the construction of a 700-kb (cosmid and one P1 phage) clone contig covering the deletion overlap and its flanks. The minimal set of 23 cosmids comprises 600 kb and is extended by one P1 phage to 700 kb to cover the distal breakpoint of the overlap. The clone contig was extensively characterized by restriction and expression mapping to produce high resolution physical and transcription maps of the cloned region, Potential transcribed fragments were detected by hybridization with PCR-amplified cDNA libraries, direct cDNA selection, ''zoo'' blotting, cDNA screening, and identification of 24 CpG islands. Thus far, 15 new genes represented hy partial or full-length cDNAs were isolated, characterized, and precisely positioned on the contig. Two previously cloned genes, namely GNAI-2 and GNAT-1, mere also positioned, In addition, the telomeric breakpoint of the NCI H740 deletion and the centromeric breakpoint of the overlapping GLC20 deletion were discovered and mapped to define precisely the candidate TSG region. This large cosmid clone contig and high resolution maps will prove crucial in the identification of the lung cancer TSG(s).
C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702.
SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD.
UNIV TEXAS,SW MED CTR,SIMMONS CANC CTR,DALLAS,TX 75235.
KAROLINSKA INST,DEPT TUMOR BIOL,S-17177 STOCKHOLM,SWEDEN.
BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030.
RI Zabarovsky, Eugene/A-6645-2010; Sekido, Yoshitaka/P-9756-2015
FU NCI NIH HHS [P20 CA58220]
NR 23
TC 144
Z9 151
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 1996
VL 56
IS 7
BP 1487
EP 1492
PG 6
WC Oncology
SC Oncology
GA UC167
UT WOS:A1996UC16700006
PM 8603390
ER
PT J
AU Kondratyev, AD
Chung, KN
Jung, MO
AF Kondratyev, AD
Chung, KN
Jung, MO
TI Identification and characterization of a radiation-inducible
glycosylated human early-response gene
SO CANCER RESEARCH
LA English
DT Article
ID PROTEIN-KINASE-C; FACTOR-KAPPA-B; IONIZING-RADIATION; LEUKEMIA-CELLS;
PLASMACYTOID DIFFERENTIATION; HYDROGEN-PEROXIDE; MESSENGER-RNA;
EXPRESSION; ACTIVATION; SEQUENCE
AB A radiation-inducible immediate-early gene, IEX-1, was identified and characterized in human squamous carcinoma cells. Sequence analysis revealed 156-amino acid nucleotides, encoding a protein of M(r) 20,000. The protein is glycosylated (M(r) similar to 27,000) in the presence of microsomal membranes, Northern analysis reveals a 1.2-kb transcript. Treatment with cycloheximide was associated with superinduction of this transcript, suggesting that it is an immediate-early gene. The abundance of IEX-1 mRNA increased rapidly after exposure of the cells to ionizing radiation (2-10 Gy), reaching a maximum by 15 min and returning subsequently to basal levels by 4 h. Expression of IEX-1 was also induced significantly by the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate (TPA), the protein phosphatase inhibitor okadaic acid, and tumor necrosis factor-alpha, whereas treatment of cells with UV light and H2O2 had little effect on IEX-1 expression. Cells depleted of PKC by prolonged incubation with TPA showed no attenuated IEX-1 response to tumor necrosis factor-alpha. This is the first report of IEX-1, a radiation-inducible glycosylated human protein, whose expression can be mediated through multisignal transduction pathways.
C1 GEORGETOWN UNIV,MED CTR,DEPT RADIAT MED,DIV RADIAT RES,WASHINGTON,DC 20007.
NIH,NCI,MED BRANCH,BETHESDA,MD 20892.
NR 32
TC 81
Z9 84
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 1996
VL 56
IS 7
BP 1498
EP 1502
PG 5
WC Oncology
SC Oncology
GA UC167
UT WOS:A1996UC16700008
PM 8603392
ER
PT J
AU Travis, LB
Curtis, RE
Boice, JD
Platz, CE
Hankey, BF
Fraumeni, JF
AF Travis, LB
Curtis, RE
Boice, JD
Platz, CE
Hankey, BF
Fraumeni, JF
TI Second malignant neoplasms among long-term survivors of ovarian cancer
SO CANCER RESEARCH
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; BREAST-CANCER; MUCINOUS TUMORS;
COLON-CANCER; RISK; CARCINOMA; APPENDIX; CYCLOPHOSPHAMIDE;
TRANSLOCATION; CHEMOTHERAPY
AB Second malignant neoplasms were evaluated among 32,251 women with ovarian cancer, including 4,402 10-year survivors, within the nine population-based registries of the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute (1973-1992) and the Connecticut Tumor Registry (1935-1972). Overall, 1,296 second cancers occurred against 1,014 expected [observed/expected (O/E), 1.28; 95% confidence interval (CI), 1.21-1.35]. Sites contributing 25 or more excess cancers included leukemia (O/E, 4.17; O, 111; 95% CI, 3.43-5.03) and malignancies of colon (O/E, 1.33; O, 188; 95% CI, 1.15-1.51), rectum (O/E, 1.43; O, 76; 95% CI, 1.13-1.79), breast (O/E, 1.18; O, 404; 95%, CI 1.07-1.30), and bladder (O/E, 2.07; O, 65; 95% CI, 1.59-2.63). Ocular melanoma (O/E, 4.45; O, 8; 95% CI, 1.92-8.77) was also significantly increased. Second cancer risk was high during all follow-up intervals, and cumulative risk at 20 years was 18.2%, compared with a population expected risk of 11.5%, Statistically significant relationships existed between serous adenocarcinoma of the ovary and breast cancer (O/E, 1.29; 95% CI, 1.06-1.56) and mucinous ovarian adenocarcinoma and rectal cancer (O/E, 1.95; 95% CI, 1.09-3.22), Secondary leukemia appeared linked with antecedent chemotherapy, whereas radiotherapy was associated with cancers of connective tissue, bladder, and possibly pancreas, Genetic and reproductive factors predisposing to ovarian cancer may have contributed to the elevated risk of breast and colorectal neoplasms and possibly ocular melanoma, Thus, excess malignancies following ovarian cancer represent complications of curative therapies and/or underlying susceptibility states that have etiological and clinical ramifications.
C1 NCI,NIH,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,CANC STAT BRANCH,BETHESDA,MD 20892.
UNIV IOWA,DEPT PATHOL,IOWA CITY,IA 52242.
RP Travis, LB (reprint author), NCI,NIH,DIV CANC EPIDEMIOL & GENET,EPN 408,BETHESDA,MD 20892, USA.
NR 60
TC 81
Z9 81
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 1996
VL 56
IS 7
BP 1564
EP 1570
PG 7
WC Oncology
SC Oncology
GA UC167
UT WOS:A1996UC16700019
PM 8603403
ER
PT J
AU Buckwalter, CA
Lin, AH
Tanizawa, A
Pommier, YG
Cheng, YC
Kaufmann, SH
AF Buckwalter, CA
Lin, AH
Tanizawa, A
Pommier, YG
Cheng, YC
Kaufmann, SH
TI RNA synthesis inhibitors alter the subnuclear distribution of DNA
topoisomerase I
SO CANCER RESEARCH
LA English
DT Article
ID HELA-CELLS; PROTEIN B23; CAMPTOTHECIN ANALOGS; CATALYTIC ACTIVITY;
ANTITUMOR AGENTS; NUCLEAR MATRIX; TRANSCRIPTION; LOCALIZATION;
TRANSLOCATION; NUCLEOLUS
AB The acute effect of RNA and DNA synthesis inhibitors on DNA topoisomerase (topo)I localization within cells was examined. Indirect immunofluorescence revealed that topo I was distributed throughout the nuclei but was concentrated in nucleoli of untreated K562 leukemia cells and A549 non-small cell lung cancer cells, Treatment with the DNA polymerase inhibitor aphidicolin did not alter this distribution. In contrast, 30-60 min after addition of the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) at concentrations that inhibited [H-3]uridine incorporation into RNA by greater than or equal to 50%, topo I was visible throughout the nuclei without nucleolar accentuation, Western blotting and activity assays confirmed that the amount of topo I polypeptide and topo I activity were unaltered by the brief DRB treatment, Within 30 min of DRB removal, topo I relocalized to the nucleoli in the absence or presence of the protein synthesis inhibitor cycloheximide. Collectively, these results suggest a reversible translocation of topo I out of the nucleoli when RNA synthesis is inhibited, Treatment with the topo I poisons topotecan or camptothecin, agents that also inhibit RNA synthesis, likewise caused redistribution of topo I to nonnucleolar regions of the nucleus in a variety of cell types, In DC3F hamster lung fibroblasts, 2.5 mu M topotecan or 1.25 mu M camptothecin was sufficient to cause this topo I redistribution, In DC3F/C-10 cells that contain a mutant camptothecin-resistant topo I, topo I relocalization required 50-fold higher concentrations of topotecan or camptothecin but not DRB, These observations not only suggest that accumulation of topo I in the nucleolus is related to ongoing RNA synthesis but also raise the possibility of screening for some types of camptothecin resistance at the single-cell level using a rapid immunofluorescence-based assay.
C1 MAYO CLIN,DIV ONCOL RES,ROCHESTER,MN 55905.
MAYO CLIN & MAYO FDN,MAYO MED SCH,DEPT PHARMACOL,ROCHESTER,MN 55905.
JOHNS HOPKINS UNIV,BALTIMORE,MD 21203.
NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892.
YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06510.
FU NCI NIH HHS [CA44358]
NR 57
TC 63
Z9 64
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 1996
VL 56
IS 7
BP 1674
EP 1681
PG 8
WC Oncology
SC Oncology
GA UC167
UT WOS:A1996UC16700035
PM 8603419
ER
PT J
AU Lowry, DT
Li, LW
Hennings, H
AF Lowry, DT
Li, LW
Hennings, H
TI Thapsigargin, a weak skin tumor promoter, alters the growth and
differentiation of mouse keratinocytes in culture
SO CARCINOGENESIS
LA English
DT Article
ID ORNITHINE DECARBOXYLASE ACTIVITY; EPIDERMAL-CELLS; TERMINAL
DIFFERENTIATION; MURINE KERATINOCYTES; GENE-EXPRESSION; CALCIUM-ENTRY;
INVITRO; 12-0-TETRADECANOYLPHORBOL-13-ACETATE; CARCINOGENESIS;
ACTIVATION
AB Thapsigargin (Tg), applied twice weekly to the backs of CD-1 mice initiated with 7,12-dimethylbenz[a]anthracene, promoted papillomas on the skin of similar to 50% of the mice, Tg alone induced papillomas in 10% of the mice, Although Tg and 12-O-tetradecanoylphorbol-13-acetate (TPA) are synergistic in a keratinocyte co-culture assay for promotion, skin tumor promotion by TPA was inhibited by co-treatment with Tg, Treatment of cultured keratinocytes with non-toxic doses of Tg increased the level of intracellular free Ca2+ and delayed Ca2+-induced stratification, Tg blocked expression of the spinous layer differentiation marker keratin 1 (K1), while inducing cornification, a marker of differentiation in the granular layer/stratum corneum, In medium with 1.4 mM Ca2+, Tg prolonged keratinocyte proliferation and selected foci of monolayer cells. A Tg-independent cell line, TK-1, was developed from a single dish in which foci continued to expand after Tg removal, Grafting TK-1 cells on to the backs of nude mice as part of a reconstituted skin resulted in the development of dysplastic papillomas with a high rate of progression to squamous cell carcinomas.
C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892.
NR 36
TC 10
Z9 11
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD APR
PY 1996
VL 17
IS 4
BP 699
EP 706
DI 10.1093/carcin/17.4.699
PG 8
WC Oncology
SC Oncology
GA UG814
UT WOS:A1996UG81400013
PM 8625480
ER
PT J
AU Blomeke, B
Greenblatt, MJ
Doan, VD
Bowman, ED
Murphy, SE
Chen, CC
Kato, S
Shields, PG
AF Blomeke, B
Greenblatt, MJ
Doan, VD
Bowman, ED
Murphy, SE
Chen, CC
Kato, S
Shields, PG
TI Distribution of 7-alkyl-2'-deoxyguanosine adduct levels in human lung
SO CARCINOGENESIS
LA English
DT Article
ID TOBACCO-SPECIFIC NITROSAMINES; NON-ENZYMATIC METHYLATION;
HYDROCARBON-DNA ADDUCTS; P-32 POSTLABELING ASSAY; HUMAN CANCER;
CARCINOGEN METABOLISM; F344 RATS; II CELLS; SMOKING; EXPOSURE
AB Human lung tissue is frequently studied as a target organ for DNA damage from carcinogen-DNA adducts, In order to assess the distribution of carcinogen-DNA adducts in human lung, we measured 7-methyl-2'-deoxyguanosine-3'-monophosphate (7-methyl-dGp), 7-ethyl-2'-deoxyguanosine-3'-monophosphate (7-ethyl-dGp) and 4-hydroxy-(3-pyridyl)-1-butanone (HPB)-releasing DNA adducts in different lobes, The first two result from exposure to N-nitrosamines, including tobacco-specific nitrosamines, and the latter only from tobacco-specific nitrosamines. Using a chemically-specific P-32-postlabeling assay for 7-alkyl-2'-deoxyguanosines, adducts were measured in eight separate lung segments of ten autopsy donors, 7-Methyl-dGp levels were detected in all eighty samples (range from 0.3 to 11.5 adducts/10(7) dGp; mean 2.5 +/- 2.3 adducts/10(7) dGp), 7-Ethyl-dGp were detected in all but five of the samples (range from <0.1 to 7.1 adducts/10(7) dGp; mean 1.6 +/- 1.7 adducts/10(7) dGp). 7-Methyl-dGp levels were approximately 1.5-fold higher than 7-ethyl-dGp levels, and they were positively correlated with each other in most individuals. There was no consistent pattern of adduct distribution in the different lobar segments, Most individuals, especially those with the lowest levels, had similar levels among the lobes, while those with the highest levels had a widely variable pattern ranging as much as ten-fold, Moreover, 7-methyl-dGp and 7-ethyl-dGp levels in all people showed a highly significant inter-individual variation (P = 0.0001), The levels of 7-alkyl-2'-deoxyguanosine among individuals could not be explained by differences in tobacco exposure (measured by serum cotinine), onset of death, gender, age, race, blood ethanol, or ventilation and perfusion variability, In an effort to corroborate 7-alkyl-2'-deoxyguanosine adducts variability among lobes or individuals, we sought to determine a correlation with HPB-releasing DNA adducts as an independent marker of tobacco exposure. However, this tobacco-specific carcinogen-DNA adduct could not be detected in four individuals tested (detection limit: 0.3 adducts per 10(7) dGp), Based upon the lack of 7-alkyl-2'-deoxyguanosine discernible adduct patterns, no conclusions could be drawn regarding a potential relationship to lobar cancer incidence. The results indicate that in studies of carcinogen-DNA adducts, such as 7-alkyl-dGp in human lungs, for most individuals a random lung sample would be representative of other parts of the lungs, Some individuals however might be misclassified due to highly variable 7-alkyl-dGp levels.
C1 NCI,HUMAN CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892.
RI Shields, Peter/I-1644-2012
NR 61
TC 33
Z9 34
U1 0
U2 2
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD APR
PY 1996
VL 17
IS 4
BP 741
EP 748
DI 10.1093/carcin/17.4.741
PG 8
WC Oncology
SC Oncology
GA UG814
UT WOS:A1996UG81400018
PM 8625485
ER
PT J
AU Bishop, RE
Pauly, GT
Moschel, RC
AF Bishop, RE
Pauly, GT
Moschel, RC
TI O-6-ethylguanine and O-6-benzylguanine incorporated site-specifically in
codon 12 of the rat H-ras gene induce semi-targeted as well as targeted
mutations in Rat4 cells
SO CARCINOGENESIS
LA English
DT Article
ID O6-ETHYLGUANINE CARCINOGENIC LESIONS; MOLECULAR MECHANICS CALCULATIONS;
APURINIC APYRIMIDINIC SITE; MAMMALIAN-CELLS; ABASIC SITE;
O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; DODECANUCLEOTIDE DUPLEXES;
DEOXYADENOSINE STACKS; MUTAGENIC PROPERTIES; ADJACENT POSITIONS
AB To examine the miscoding properties of modified guanine residues bearing increasingly bulky O-6-substituents, Rat4 cells, grown in the presence of O-6-benzylguanine to deplete the DNA. repair protein O-6-alkylguanine-DNA alkyltransferase, were transfected with plasmids carrying H-ras genes in which O-6-methyl, O-6-ethyl- and O-6-benzylguanine were substituted for the first, second or both the first and second guanine residues of codon 12 (GGA). DNA from isolated transformed colonies was amplified by PCR and directly sequenced by high-temperature manual and automated methods, The results show that O-6-ethylguanine and O-6-benzylguanine induced semi-targeted as well as targeted mutations, in contrast to O-6-methylguanine, which induced only targeted mutations, When incorporated in place of the first guanine of H-ras codon 12, the targeted mutations induced by all these modified guanines were exclusively G-->A transitions. When incorporated at the second position of codon 12, O-6-benzylguanine induced G-->A, G-->T and G-->C mutations, O-6-Ethylguanine at the second position induced chiefly G-->A transitions, and O-6-methylguanine induced G-->A transitions exclusively, Semi-targeted mutations were strictly G-->A at the base 3' to a position 1 adduct or 5' to a position 2 adduct, The mechanism for induction of targeted mutations probably involves decreasing preference for thymidine incorporation opposite an O-6-modified guanine as the size of the O-6-substituent increases, while the mechanism for non-targeted mutations may be related to abasic site formation or to translesion synthesis which might be made error-prone by obstructive DNA lesions in this context.
C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702.
NR 53
TC 15
Z9 15
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD APR
PY 1996
VL 17
IS 4
BP 849
EP 856
DI 10.1093/carcin/17.4.849
PG 8
WC Oncology
SC Oncology
GA UG814
UT WOS:A1996UG81400033
PM 8625500
ER
PT J
AU Deakin, M
Elder, J
Hendrickse, C
Peckham, D
Baldwin, D
Pantin, C
Wild, N
Leopard, P
Bell, DA
Jones, P
Duncan, H
Brannigan, K
Alldersea, J
Fryer, AA
Strange, RC
AF Deakin, M
Elder, J
Hendrickse, C
Peckham, D
Baldwin, D
Pantin, C
Wild, N
Leopard, P
Bell, DA
Jones, P
Duncan, H
Brannigan, K
Alldersea, J
Fryer, AA
Strange, RC
TI Glutathione S-transferase GSTT1 genotypes and susceptibility to cancer:
Studies of interactions with GSTM1 in lung, oral, gastric and colorectal
cancers
SO CARCINOGENESIS
LA English
DT Article
ID CLASS-MU; CARCINOMA; PHENOTYPE; JAPANESE; MARKER
AB Allelism in glutathione S-transferase GSTM1 and GSTT1 has been suggested as a risk factor in various cancers, Accordingly, we describe a group of case-control studies carried out to identify associations between GSTT1 genotypes and susceptibility to lung, oral, gastric and colorectal cancers, The frequencies of the putatively high risk GSTT1 null genotype were not increased in the lung, oral or gastric cancer cases compared with controls but the frequency of this genotype was significantly increased (P = 0.0011, odds ratio = 1.88) in the colorectal cancer cases, No significant interactions between the GSTT1 and GSTM1 null genotypes were identified in the cancer groups studied, Indeed, no significant associations between GSTM1 genotypes and susceptibility were identified though further evidence was obtained that the protective effect of GSTM1*A and GSTM1*B is not equal, The data complement studies showing that GSTT1 null is associated with an increased susceptibility to total ulcerative colitis and suggests that this enzyme is important in the detoxification of unidentified xenobiotics in the large intestine.
C1 KEELE UNIV,N STAFFORDSHIRE HOSP,POSTGRAD MED SCH,DEPT SURG,KEELE,STAFFS,ENGLAND.
N STAFFORDSHIRE HOSP,DEPT RESP MED,STOKE ON TRENT,STAFFS,ENGLAND.
N STAFFORDSHIRE HOSP,DEPT ORAL & MAXILLOFACIAL SURG,STOKE ON TRENT,STAFFS,ENGLAND.
NIEHS,RES TRIANGLE PK,NC 27709.
KEELE UNIV,DEPT MATH,KEELE,STAFFS,ENGLAND.
NR 28
TC 274
Z9 287
U1 0
U2 3
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD APR
PY 1996
VL 17
IS 4
BP 881
EP 884
DI 10.1093/carcin/17.4.881
PG 4
WC Oncology
SC Oncology
GA UG814
UT WOS:A1996UG81400038
PM 8625505
ER
PT J
AU Packard, B
AF Packard, B
TI Prescription for the 21st century
SO CARDIOVASCULAR RISK FACTORS
LA English
DT Editorial Material
RP Packard, B (reprint author), NHLBI,INFORMAT CTR,SCI PROGRAM OPERAT,NIH,POB 30105,BETHESDA,MD 20824, USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1130-7501
J9 CARDIOVASC RISK FACT
JI Cardiovasc. Risk Factors
PD APR
PY 1996
VL 6
IS 2
BP 63
EP 65
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA UP304
UT WOS:A1996UP30400001
ER
PT J
AU Higgins, M
AF Higgins, M
TI Cardiovascular diseases in women: A public health problem
SO CARDIOVASCULAR RISK FACTORS
LA English
DT Article
DE heart; risk factors; women
ID CORONARY
AB Cardiovascular diseases (CVDs) are the leading causes of death and major causes of illness and disability in women. Forty-six percent of all deaths in U.S. women are attributed to CVD; 22% to coronary heart disease (CHD) and 8% to stroke. Although death and incidence rates are 2 to 3 times higher in men than in women during middle age, and CHD tends to occur similar to 10 years later in women, a higher proportion of women die soon after a heart attack, and more women who survive a heart attack have a recurrent event. Diagnostic procedures and surgical treatment may be delayed and are performed less frequently in women. Risk factors for CVD are highly prevalent among women. Recent national surveys estimate that: 23% have high levels of serum cholesterol, 25% have hypertension, 37% are overweight, and 25% smoke cigarettes. Obesity and diabetes mellitus are more prevalent in than in men. Premature menopause, oophorectomy, and oral contraceptive use are risk factors unique to women. There is substantial evidence that reducing cholesterol, blood pressure, and cigarette smoking and controlling weight are effective strategies for reducing CVD risk in women. Failure to prevent, diagnose, and treat CVD and to reduce prevalence of risk factors in women to the maximum extent possible should be considered a public health problem.
RP Higgins, M (reprint author), NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,2 ROCKLEDGE CTR,ROOM 8104,6701 ROCKLEDGE DR,BETHESDA,MD 20892, USA.
NR 23
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1130-7501
J9 CARDIOVASC RISK FACT
JI Cardiovasc. Risk Factors
PD APR
PY 1996
VL 6
IS 2
BP 66
EP 73
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA UP304
UT WOS:A1996UP30400002
ER
PT J
AU Bian, XP
Bird, GSJ
Putney, JW
AF Bian, XP
Bird, GSJ
Putney, JW
TI cGMP is not required for capacitative Ca2+ entry in Jurkat T-lymphocytes
SO CELL CALCIUM
LA English
DT Article
ID PANCREATIC ACINAR CELL; CALCIUM ENTRY; STORES; DEPLETION; MESSENGER
AB In this study, we have addressed the potential role of cGMP in regulating calcium entry in Jurkat T-lymphocytes. These cells display capacitative Ca2+-entry in response to the intracellular Ca2+-ATPase inhibitor, thapsigargin (TG). In the presence of extracellular Ca2+, TG stimulates a sustained elevation of intracellular cGMP levels. In the absence of extracellular Ca2+, TG induces no apparent increase in the levels of cGMP. However, experiments using Mn2+, as a. surrogate for Ca2+, demonstrated that TG increased the rate of divalent cation entry in the absence of extracellular Ca2+. Treatment of Jurkat cells with the guanylyl cyclase inhibitor, LY83583 (20 mu M), completely blocked cGMP formation in response to TG. However, LY83583 treated cells still exhibited a sustained, albeit partially reduced, Ca2+ response induced by TG. These data demonstrate that, in Jurkat cells, the sustained formation of cGMP is dependent on elevated intracellular Ca2+, and that elevated levels of cGMP are not necessary for the activation of capacitative Ca2+ entry.
C1 NIEHS,NIH,CELLULAR & MOLEC PHARMACOL LAB,CALCIUM REGULAT SECT,RES TRIANGLE PK,NC 27709.
NR 21
TC 13
Z9 14
U1 0
U2 0
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF
SN 0143-4160
J9 CELL CALCIUM
JI Cell Calcium
PD APR
PY 1996
VL 19
IS 4
BP 351
EP 354
DI 10.1016/S0143-4160(96)90075-5
PG 4
WC Cell Biology
SC Cell Biology
GA UM872
UT WOS:A1996UM87200008
PM 8983855
ER
PT J
AU Baez, A
Torres, K
Tan, EM
Pommier, Y
Casiano, CA
AF Baez, A
Torres, K
Tan, EM
Pommier, Y
Casiano, CA
TI Expression of proliferation-associated nuclear autoantigens,
p330(d)/CENP-F and PCNA, in differentiation and in drug-induced growth
inhibition using two-parameter flow cytometry
SO CELL PROLIFERATION
LA English
DT Article
ID MONOCLONAL-ANTIBODY KI-67; DNA POLYMERASE-DELTA; CELL-CYCLE ANALYSIS;
S-PHASE; HL-60 CELLS; CLINICAL-APPLICATIONS; AUXILIARY PROTEIN; LENS
REGENERATION; TOPOISOMERASE-I; RETINOIC ACID
AB p330(d)/CENP-F is a recently described nuclear autoantigen that was detected in PHA-stimulated but not in resting peripheral lymphocytes. This protein accumulates in the nucleus during S-phase and reaches maximum levels during the G(2) and M phases of the cell cycles. We compared the expression of p330(d)/CENP-F and proliferating cell nuclear antigen (PCNA) during the induction of terminal myeloid differentiation of HL-60 tumour cells. HL-60 cells were induced to differentiate with retinoic acid (RA), dimethyl sulfoxide (DMSO), and 3-nitrobenzothiazolo [3,2-]quinolinium (NBQ), and collected at different intervals. Control and treated cells were analyzed by two-parameter flow cytometry using propidium iodide and antibodies to p330(d)/CENP-F and PCNA. The percentage of p330(d)/CENP-F and PCNA positive cells was found to be proportional to the percentage of proliferating cells. After two cell cycles (65 h), the percentage of p330(d)/CENP-F and PCNA positive cells was reduced proportionately to the number of cells that had differentiated. Reduction in the expression of both antigens was completed after 120 h when 80% to 85% of the cells were arrested in G(1) and displayed the mature phenotype. The expression of p330(d)/CENP-F and PCNA was also assessed in the growth inhibition of HT-29 cells induced by various concentrations of camptothecin (CPT), etoposide (VP-16), and aphidicolin (APH). There was a dose-dependent displacement of cells to late S-phase by CPT while VP-16 induced cells to accumulate in G(2) + M, and as expected these effects caused a strong increase in the cellular levels of both antigens. The arrest of cells in G(1) by APH led to a significant decrease in their expression. The dramatic reduction in p330(d)/CENP-F levels during differentiation, and the correlation of its expression with the cell cycle effects of the cytotoxic drugs are consistent with the behaviour expected for a proliferation marker.
C1 WM KECK AUTOIMMUNE DIS CTR, DEPT MOLEC & EXPTL MED SRB6, SCRIPPS RES INST, LA JOLLA, CA USA.
NCI, MOLEC PHARMACOL LAB, DPT, DCT, NIH, BETHESDA, MD 20892 USA.
RP Baez, A (reprint author), UNIV PUERTO RICO, SCH MED, DEPT PHARMACOL, BOX 365067, SAN JUAN, PR 00936 USA.
FU NCI NIH HHS [CA569056]; NIAMS NIH HHS [AR320063]; NIGMS NIH HHS
[GM08224]
NR 39
TC 9
Z9 10
U1 0
U2 1
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0960-7722
J9 CELL PROLIFERAT
JI Cell Prolif.
PD APR
PY 1996
VL 29
IS 4
BP 183
EP 196
DI 10.1111/j.1365-2184.1996.tb00105.x
PG 14
WC Cell Biology
SC Cell Biology
GA UZ205
UT WOS:A1996UZ20500002
PM 8695747
ER
PT J
AU Lopez, FJ
Merchenthaler, I
Liposits, Z
NegroVilar, A
AF Lopez, FJ
Merchenthaler, I
Liposits, Z
NegroVilar, A
TI Steroid imprinting and modulation of sexual dimorphism in the
luteinizing hormone-releasing hormone neuronal system
SO CELLULAR AND MOLECULAR NEUROBIOLOGY
LA English
DT Article
DE luteinizing hormone-releasing hormone; sexual dimorphism; galanin;
estrogen
ID IMMORTALIZED HYPOTHALAMIC NEURONS; ESTROGEN-RECEPTOR; GALANIN;
EXPRESSION; RAT; GONADOTROPIN; SEQUENCE; BRAIN
AB 1. Sex differences in the control of gonadotropin secretion and reproductive functions are a distinct characteristic in all mammalian species, including humans. Ovulation and cyclicity are among the most distinct neuroendocrine markers of female brain differentiation, along with sex behavioral traits that are also evident in different species.
2. The luteinizing hormone-releasing hormone (LHRH) neuronal system is the prime regulator of neuroendocrine events leading to ovulation and hormonal changes during the menstrual cycle and, as such, is the potential site where many of these sex differences may be expressed or, at the very least, integrated. However, until recently, no significant differences were seen in LHRH neurons between male and female brains, including cell number, pattern of distribution, and expression of message or peptide (LHRH) levels.
3. Recently, we reported that galanin (GAL), a brain-gut peptide, is coexpressed in LHRH neurons and that this coexpression is sexually dimorphic. When GAL is used as a marker for this neuronal system, it is clear that estradiol as well as progesterone profoundly affects the message and expression of the peptide and that this regulation, at least in rodents, is neonatally predetermined by gonadal steroid imprinting.
4. Changes in GAL expression and message can also be seen at puberty, during pregnancy and lactation, and in aging, all situations that affect the function of the LHRH neuronal system. Using an immortalized LHRH neuronal cell line (GT1) we have recently observed that these neurons express estrogen receptor (ER) and GAL and that estradiol can increase the expression of GAL, indicating functional activation of the endogenous ER.
C1 WYETH AYERST RES,WOMENS HLTH RES INST,RADNOR,PA 19087.
NIEHS,NIH,RADNOR,PA.
NR 25
TC 15
Z9 15
U1 0
U2 2
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0272-4340
J9 CELL MOL NEUROBIOL
JI Cell. Mol. Neurobiol.
PD APR
PY 1996
VL 16
IS 2
BP 129
EP 141
DI 10.1007/BF02088172
PG 13
WC Cell Biology; Neurosciences
SC Cell Biology; Neurosciences & Neurology
GA UN346
UT WOS:A1996UN34600004
PM 8743965
ER
PT J
AU Agarwal, R
Canella, KA
Yagi, H
Jerina, DM
Dipple, A
AF Agarwal, R
Canella, KA
Yagi, H
Jerina, DM
Dipple, A
TI Benzo[c]phenanthrene-DNA adducts in mouse epidermis in relation to the
tumorigenicities of four configurationally isomeric 3,4-dihydrodiol
1,2-epoxides
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID REGION DIOL-EPOXIDES; EMBRYO CELL-CULTURES; DIHYDRODIOL-EPOXIDE;
MAMMALIAN-CELLS; DNA ADDUCTS; BENZO(C)PHENANTHRENE;
3,4-DIOL-1,2-EPOXIDES; SKIN; 7,12-DIMETHYLBENZ(A)ANTHRACENE; BINDING
AB P-32-Postlabeling assays were used to monitor the binding to epidermal DNA that resulted from the application of each of the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide to mouse skin in vivo. For three of these configurational isomers, there was a reasonable correlation between the relative level of binding to epidermal DNA and the known tumorigenic effects of these compounds. However, for the 4(S),3(R)-dihydrodiol a(S),1(R)-epoxide, the tumorigenic response was considerably greater in relation to the level of DNA modification than was the case for the other isomers. This greater tumorigenic response was consistent with previous observations indicating that this isomer was more mutagenic, at equivalent levels of DNA modification, than the other two tumorigenic dihydrodiol epoxides. Additionally, the 4(S),3(R)-dihydrodiol 2(S),1(R);epoxide reacts with DNA to generate predominantly (similar to 80%) adducts on the amino group of adenine residues. These findings might imply a greater intrinsic biological effect of such adenine adducts with respect to the other major adduct formed on the amino group of guanine residues.
C1 NIDDKD,NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892.
RP Agarwal, R (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702, USA.
NR 27
TC 28
Z9 28
U1 0
U2 0
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 APR-MAY
PY 1996
VL 9
IS 3
BP 586
EP 592
DI 10.1021/tx950148+
PG 7
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA UF846
UT WOS:A1996UF84600005
PM 8728502
ER
PT J
AU Putnam, FW
AF Putnam, FW
TI A brief history of multiple personality disorder
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
ID SATANIC RITUAL ABUSE; CLINICAL PHENOMENOLOGY; DISSOCIATIVE DISORDERS;
POSTTRAUMATIC-STRESS; CHILDHOOD; SCHIZOPHRENIA; CHILDREN
AB This brief review of multiple personality disorder (MPD) focuses on a number of historical threads of inquiry spanning the past century. Nineteenth-century investigations of dissociation paved the way for multilevel models of the mind and the development of dynamic psychiatry. Modern controversies, such as the role of trauma in dissociation, cultural influences on the expression of dissociation, the portrayal of MPD in the popular media, and the validity of MPD, grow out of nineteenth-century debates. The recognition of child and adolescent dissociative disorders and the adoption of a developmental focus of investigation offers an opportunity to resolve many of these contentious issues.
RP Putnam, FW (reprint author), NIMH,UNIT DEV TRAUMATOL,BIOL PSYCHOL BRANCH,DIV INTRAMURAL RES,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 61
TC 2
Z9 2
U1 2
U2 4
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD APR
PY 1996
VL 5
IS 2
BP 263
EP &
PG 10
WC Psychiatry
SC Psychiatry
GA UZ891
UT WOS:A1996UZ89100003
ER
PT J
AU Putnam, FW
AF Putnam, FW
TI Child development and dissociation
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
ID MULTIPLE PERSONALITY-DISORDER; POSTTRAUMATIC-STRESS-DISORDER; SEXUAL
ABUSE; CLINICAL PHENOMENOLOGY; FAMILY ENVIRONMENT; EXPERIENCES SCALE;
SYMPTOMS; VALIDITY; INTERVIEW; VETERANS
AB Increased recognition of dissociative symptoms and phenomena in children and adolescents has confronted clinicians with the challenge of differentiating normal from abnormal or pathologic dissociation. Reliable and valid measures of dissociation are increasingly being used both clinically and for research. These data strongly link pathologic dissociation with traumatic antecedents. They also point to family environmental experiences and attachment as important contributors to an individual's dissociativity. High levels of dissociation are linked with behavioral problems and psychopathology in maltreated children and adults.
RP Putnam, FW (reprint author), NIMH, UNIT DEV TRAUMATOL,BIOL PSYCHIAT BRANCH, DIV INTRAMURAL RES,BLDG 15K, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA.
NR 89
TC 20
Z9 20
U1 2
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
EI 1558-0490
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD APR
PY 1996
VL 5
IS 2
BP 285
EP +
PG 0
WC Psychiatry
SC Psychiatry
GA UZ891
UT WOS:A1996UZ89100005
ER
PT J
AU Putnam, FW
Hornstein, N
Peterson, G
AF Putnam, FW
Hornstein, N
Peterson, G
TI Clinical phenomenology of child and adolescent dissociative disorders -
Gender and age effects
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
ID MULTIPLE PERSONALITY-DISORDER
AB Clinicians have noted age and gender differences in the presentations of children and adolescents with dissociative disorders. This study uses a composite sample of 177 cases to explore developmental and gender differences in youth with pathologic dissociation. Females proved to be more symptomatic than males in five areas: anxiety and phobic symptoms, post-traumatic stress disorder symptoms, sleep problems, sexual acting out, and somatization. In general, there were more dissociative and comorbid symptoms with increasing age, although most age differences did not achieve statistical significance. Internalized auditory hallucinations, conversion symptoms, amnesias,suicidal ideation, and self-mutilation increased significantly with age. Preschool cases were essentially equally divided between males and females. By late adolescence, 83% of cases were female. Cases diagnosed with dissociative identity disorder/multiple personality disorder were significantly more symptomatic than those diagnosed with dissociative disorder not otherwise specified.
C1 UNIV ILLINOIS,DIV CHILD PSYCHIAT,CHICAGO,IL.
SO CALIF PSYCHOANAL INST,LOS ANGELES,CA.
UNIV N CAROLINA,DEPT PSYCHIAT,CHAPEL HILL,NC.
RP Putnam, FW (reprint author), NIMH,UNIT DEV TRAUMATOL,BIOL PSYCHIAT BRANCH,DIV INTRAMURAL RES,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 15
TC 15
Z9 15
U1 3
U2 12
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD APR
PY 1996
VL 5
IS 2
BP 351
EP &
PG 12
WC Psychiatry
SC Psychiatry
GA UZ891
UT WOS:A1996UZ89100008
ER
PT J
AU Lewis, DO
Putnam, FW
AF Lewis, DO
Putnam, FW
TI Dissociative identity disorder/multiple personality disorder - Preface
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 NIMH,UNIT DEV TRAUMATOL,BETHESDA,MD 20892.
RP Lewis, DO (reprint author), NYU,SCH MED,DEPT PSYCHIAT,NEW BELLEVUE 21S25,550 1ST AVE,NEW YORK,NY 10016, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD APR
PY 1996
VL 5
IS 2
BP R13
EP R14
PG 2
WC Psychiatry
SC Psychiatry
GA UZ891
UT WOS:A1996UZ89100002
ER
PT J
AU Dunn, PF
Newman, KD
Jones, M
Yamada, I
Shayani, V
Virmani, R
Dichek, DA
AF Dunn, PF
Newman, KD
Jones, M
Yamada, I
Shayani, V
Virmani, R
Dichek, DA
TI Seeding of vascular grafts with genetically modified endothelial cells -
Secretion of recombinant TPA results in decreased seeded cell retention
in vitro and in vivo
SO CIRCULATION
LA English
DT Article
DE carotid arteries; cells; plasminogen activators; viruses
ID MEDIATED GENE-TRANSFER; TISSUE PLASMINOGEN-ACTIVATOR; HUMAN UMBILICAL
VEIN; PROSTHESES; POLYTETRAFLUOROETHYLENE; EXPRESSION; UROKINASE;
MEMBRANE; INVITRO; BYPASS
AB Background Seeding of Small-diameter vascular grafts with endothelial cells (ECs) genetically engineered to secrete fibrinolytic or antithrombotic proteins offers the potential to improve graft patency rates.
Methods and Results Sheep venous ECs were transduced with a retroviral vector encoding human tissue plasminogen activator (TPA). The ECs were seeded onto 4-mm-ID synthetic (Dacron) grafts. Retention of the seeded ECs was measured 2 hours after placement of the seeded grafts both in vitro in a nonpulsatile flow system and in vivo (in sheep) as femoral and carotid interposition grafts. On exposure to flow in vitro, ECs transduced with TPA were retained at a significantly lower rate (median, 67%) than either untransduced ECs (81%)or ECs transduced with a control retroviral vector producing beta-galactosidase (beta-Gal) (80%) (P<.05 for TPA versus either control). On implantation in vivo, ECs transduced with TPA were retained at a very low rate (median, 0%), significantly less than the retention of ECs transduced with the beta-Gal vector (32%; P<.00001). Decreased in vivo retention of ECs transduced with TPA correlated modestly with increased in vitro cellular passage level (r(2)=.48; P<.0001) but not with in vivo blood flow rate (P=.45). Addition of the protease inhibitor aprotinin to the cell culture and graft perfusion media resulted in a significant (P<.05) increase in in vitro retention of ECs transduced with TPA.
Conclusions Increased TPA expression significantly decreases seeded EC adherence in vitro and in vivo. Gene therapy strategies for decreasing graft thrombosis may require expression of antithrombotic molecules that lack proteolytic activity.
C1 UNIV CALIF SAN FRANCISCO,GLADSTONE INST CARDIOVASC DIS,SAN FRANCISCO,CA 94141.
NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892.
NHLBI,LAB ANIM MED & SURG,BETHESDA,MD 20892.
CHILDRENS NATL MED CTR,DEPT SURG,WASHINGTON,DC 20010.
ARMED FORCES INST PATHOL,WASHINGTON,DC 20306.
NR 52
TC 68
Z9 74
U1 0
U2 0
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 1
PY 1996
VL 93
IS 7
BP 1439
EP 1446
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA UC189
UT WOS:A1996UC18900018
PM 8641034
ER
PT J
AU Zheng, JS
Boluyt, MO
Long, XL
ONeill, L
Lakatta, EG
Crow, MT
AF Zheng, JS
Boluyt, MO
Long, XL
ONeill, L
Lakatta, EG
Crow, MT
TI Extracellular ATP inhibits adrenergic agonist-induced hypertrophy of
neonatal cardiac myocytes
SO CIRCULATION RESEARCH
LA English
DT Article
DE ATP; purinergic receptors; cardiac hypertrophy; norepinephrine; cardiac
myocytes
ID SARCOPLASMIC-RETICULUM CA-2+-ATPASE; RAT MYOCARDIAL-CELLS;
PROTEIN-KINASE-C; GENE-EXPRESSION; VENTRICULAR MYOCYTES;
SIGNAL-TRANSDUCTION; MESSENGER-RNA; JUN PROTEINS; GROWTH; HEART
AB We have previously shown that extracellular ATP, like norepinephrine (NE) and many other hypertrophy-inducing agents, increases expression of the immediate-early genes c-Sos and junB in cultured neonatal cardiac myocytes but that the intracellular signaling pathways activated by ATP and responsible for these changes differ from those stimulated by NE. Furthermore, whereas NE increases incorporation of [C-14]phenylalanine (C-14-Phe) and cell size in neonatal cardiomyocytes, ATP does not. Since ATP is coreleased with NE from sympathetic nerve endings in the heart, we investigated whether ATP could modulate cardiac hypertrophy induced by adrenergic agonists, such as NE. We report in the present study that extracellular ATP inhibited the increase in incorporation of C-14-Phe into cellular protein and the increase in cell size in neonatal rat cardiac myocytes that was induced by NE, phenylephrine (PE), basic fibroblast growth factor, or endothelin-1. This inhibition was dose dependent, occurred predominantly through P-2 purinergic receptors, and was observed even when cells were treated with ATP for as little as 1 hour before the addition of the hypertrophy-inducing agent. ATP also selectively affected changes in gene expression associated with hypertrophy. It prevented PE-stimulated increases in atrial natriuretic factor and myosin light chain-2 mRNA levels, while appearing to augment basal and PE-stimulated skeletal cr-actin mRNA levels. ATP alone increased sarcoplasmic reticulum Ca2+-ATPase mRNA levels but had no effect when added with PE. ATP did not significantly affect the level of the constitutively expressed mRNA for GAPDH. Neither the PE-stimulated increase in immediate-early gene expression nor the initial induction of mitogen-activated protein kinase activity by PE was inhibited by ATP. These results demonstrate that extracellular ATP can inhibit hypertrophic growth of neonatal cardiac myocytes and differentially alter the changes in gene expression that accompany hypertrophy.
C1 NIA,NIH,CTR GERONTOL RES,CARDIOVASC SCI LAB,BALTIMORE,MD 21224.
NR 49
TC 47
Z9 47
U1 0
U2 2
PU AMER HEART ASSOC
PI DALLAS
PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD APR
PY 1996
VL 78
IS 4
BP 525
EP 535
PG 11
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA UC176
UT WOS:A1996UC17600003
PM 8635209
ER
PT J
AU Whelton, PK
Williamson, JD
Louis, GT
Davis, BR
Cutler, JA
AF Whelton, PK
Williamson, JD
Louis, GT
Davis, BR
Cutler, JA
TI Experimental approaches to determining the choice of first-step therapy
for patients with hypertension
SO CLINICAL AND EXPERIMENTAL HYPERTENSION
LA English
DT Article; Proceedings Paper
CT 3rd WHO/ISH Meeting on Prevention of Hypertension and Cardiovascular
Disease
CY JUN 15-17, 1995
CL PORTO CERVO, ITALY
SP WHO, Int Soc Hypertens
DE hypertension; high blood pressure; clinical trials; prevention;
epidemiology; cardiovascular disease; pharmacology
ID MYOCARDIAL-INFARCTION; DRUG-THERAPY; ANGINA; MILD
AB Detection, treatment and control of hypertension is one of the best proven approaches to prevention of cardiovascular disease. Antihypertensive treatment trials have convincingly demonstrated that diuretics and beta-blockers reduce the risk of stroke and coronary heart disease. Corresponding information is not yet available for newer classes of antihypertensive drug therapy such as calcium channel blockers, angiotensin converting enzyme inhibitors and alpha, receptor blockers. Several experimental studies are now addressing this question. The largest such trial (n=40,000) is the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). This manuscript describes two studies (TOMHS and the VA study on antihypertensive agents) that compared several classes of antihypertensive drugs with regard to blood pressure outcomes and ALLHAT, which is comparing the effect of four first-step approaches to antihypertensive therapy on combined incidence of fatal coronary heart disease and non-fatal myocardial infarction.
C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD.
UNIV TEXAS,SCH PUBL HLTH,CTR HLTH SCI,HOUSTON,TX.
NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892.
RP Whelton, PK (reprint author), JOHNS HOPKINS MED INST,WELCH CTR PREVENT EPIDEMIOL & CLIN RES,2024 E MONUMENT ST,SUITE 2-600,BALTIMORE,MD 21205, USA.
NR 17
TC 17
Z9 17
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016
SN 1064-1963
J9 CLIN EXP HYPERTENS
JI Clin. Exp. Hypertens.
PD APR-MAY
PY 1996
VL 18
IS 3-4
BP 569
EP 579
DI 10.3109/10641969609088986
PG 11
WC Pharmacology & Pharmacy; Peripheral Vascular Disease
SC Pharmacology & Pharmacy; Cardiovascular System & Cardiology
GA UF358
UT WOS:A1996UF35800026
PM 8743044
ER
PT J
AU Goldwasser, F
Valenti, M
Torres, R
Kohn, KW
Pommier, Y
AF Goldwasser, F
Valenti, M
Torres, R
Kohn, KW
Pommier, Y
TI Potentiation of cisplatin cytotoxicity by 9-aminocamptothecin
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID DNA TOPOISOMERASE-I; OVARIAN-CARCINOMA CELLS; CROSS-LINKING;
CYTO-TOXICITY; CIS-DIAMMINEDICHLOROPLATINUM(II); REPAIR; CAMPTOTHECIN;
RESISTANCE; LINE; MECHANISM
AB Camptothecin (CPT) derivatives are presently in ongoing Phase I/II clinical trials. The interactions between 9-aminocamptothecin (9AC) and cisplatin (CDDP) have been studied in the IGROV-1 human ovarian cancer cell line used in the National Cancer Institute Drug Discovery Anticancer Screen, One-h simultaneous treatment with 9AC and CDDP produced synergistic cytotoxicity. Under these conditions, 9AC delayed the reversal of CDDP-induced DNA interstrand cross-links (ISCs) without modifying the maximum ISC frequency at 6 h after drug treatment, CDDP did not affect the amount and the kinetics of reversion of 9AC-induced DNA single-strand breaks, Simultaneous treatment with CDDP and 9AC prolonged the DNA synthesis inhibition produced by each drug alone, Consistently, flow cytometry analyses showed enhanced S-phase arrest in cells treated with the CDDP-9AC combination, The DNA polymerase inhibitor aphidicolin also increased the residual CDDP-induced ISCs. These results suggest that prolonged inhibition of DNA synthesis by CPTs potentiate the cytotoxicity of CDDP by inhibiting the reversal of CDDP-induced DNA damage, Therefore, the combination of CPTs and CDDP appears to be worthwhile in cancer chemotherapy.
C1 NCI,MOLEC PHARMACOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892.
NR 51
TC 34
Z9 34
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
PHILADELPHIA, PA 19106
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR
PY 1996
VL 2
IS 4
BP 687
EP 693
PG 7
WC Oncology
SC Oncology
GA UD929
UT WOS:A1996UD92900010
PM 9816219
ER
PT J
AU Contois, JH
McNamara, JR
LammiKeefe, CJ
Wilson, PWF
Massov, T
Schaefer, EJ
AF Contois, JH
McNamara, JR
LammiKeefe, CJ
Wilson, PWF
Massov, T
Schaefer, EJ
TI Reference intervals for plasma apolipoprotein A-I determined with a
standardized commercial immunoturbidimetric assay: Results from the
framingham offspring study
SO CLINICAL CHEMISTRY
LA English
DT Article
DE lipids; lipoproteins; epidemiology; coronary heart disease;
standardization
ID HIGH-DENSITY-LIPOPROTEIN; CORONARY HEART-DISEASE; ARTERY DISEASE;
INTERNATIONAL-FEDERATION; MYOCARDIAL-INFARCTION; HDL-CHOLESTEROL;
CIGARETTE-SMOKING; SERUM-LIPIDS; MEN; WOMEN
AB We have evaluated a commercially available, standardized immunoturbidimetric assay of apolipoprotein (ape) A-I, the major protein constituent of high-density lipoproteins (HDL). We determined the reference ranges of plasma apo A-I concentration for white men and women and related these values to the risk of coronary heart disease (CHD). The mean between-run CV for this assay was 2.9%. As determined with individuals participating in cycle 4 of the Framingham Offspring Study, the mean (+/- SD) apo A-I concentration was 13 % lower in 1879 men (1.34 +/- 0.23 g/L) than in 1939 women (1.54 +/- 0.28 g/L) (P <0.001). An apo A-I concentration of 1.20 g/L roughly corresponded to the 25th percentile value in men and the 5th percentile in women, and subjects with a concentration below this value were significantly more likely to have CHD than subjects with a higher concentration (P <0.001).
C1 TUFTS UNIV,USDA,JEAN MAYER HUMAN NUTR RES CTR AGING,LIPID METAB LAB,BOSTON,MA 02111.
UNIV CONNECTICUT,DEPT NUTR SCI,STORRS,CT 06269.
NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA 01701.
FU NHLBI NIH HHS [HV-83-03]
NR 43
TC 103
Z9 110
U1 1
U2 1
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD APR
PY 1996
VL 42
IS 4
BP 507
EP 514
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA UD765
UT WOS:A1996UD76500006
PM 8605666
ER
PT J
AU Contois, JH
McNamara, JR
LammiKeefe, CJ
Wilson, PWF
Massov, T
Schaefer, EJ
AF Contois, JH
McNamara, JR
LammiKeefe, CJ
Wilson, PWF
Massov, T
Schaefer, EJ
TI Reference intervals for plasma apolipoprotein B determined with a
standardized commercial immunoturbidimetric assay: Results from the
Framingham Offspring Study
SO CLINICAL CHEMISTRY
LA English
DT Article
DE lipids; lipoproteins; coronary heart disease; epidemiology;
standardization
ID CORONARY HEART-DISEASE; DENSITY-LIPOPROTEIN CHOLESTEROL; MIDDLE-AGED
MEN; A-I; ARTERY DISEASE; INTERNATIONAL-FEDERATION;
MYOCARDIAL-INFARCTION; SUBCLASS PATTERNS; SERUM-LIPIDS; RISK
AB We evaluated a commercially available, standardized immunoturbidimetric assay for apolipoprotein (ape) B, the protein constituent of low-density lipoprotein (LDL), to establish reference ranges for men and women, and to determine the concentrations associated with increased risk of coronary heart disease (CHD). The between-run CV for assay of a normal-concentration control for this assay was 6.60%. The mean (+/- SD) apo B concentration was 1.03 +/- 0.24 g/L in 1880 men, significantly higher than the mean for 1944 women (0.96 +/- 0.26 g/L) participating in cycle 4 of the Framingham Offspring Study (P <0.001). An apo B value of 1.20 g/L corresponded roughly to the 75th percentile in men, similar to an LDL cholesterol concentration of 1.60 g/L, and subjects with concentrations greater than this were significantly more likely to have CHD than subjects with apo B concentrations less than 1.00 g/L, the approximate 50th percentile (P <0.05 in men and P <0.001 in women).
C1 TUFTS UNIV, USDA, JEAN MAYER HUMAN NUTR RES CTR AGING, LIPID METAB LAB, BOSTON, MA 02111 USA.
UNIV CONNECTICUT, DEPT NUTR SCI, STORRS, CT 06269 USA.
NHLBI, FRAMINGHAM HEART STUDY, FRAMINGHAM, MA 01701 USA.
FU NHLBI NIH HHS [HV-83-03]
NR 55
TC 137
Z9 144
U1 1
U2 2
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD APR
PY 1996
VL 42
IS 4
BP 515
EP 523
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA UD765
UT WOS:A1996UD76500007
PM 8605667
ER
PT J
AU Magiakou, MA
Mastorakos, G
Rabin, D
Margioris, AN
Dubbert, B
Calogero, AE
Tsigos, C
Munson, PJ
Chrousos, GP
AF Magiakou, MA
Mastorakos, G
Rabin, D
Margioris, AN
Dubbert, B
Calogero, AE
Tsigos, C
Munson, PJ
Chrousos, GP
TI The maternal hypothalamic-pituitary-adrenal axis in the third trimester
of human pregnancy
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID CORTICOTROPIN-RELEASING HORMONE; INSULIN-INDUCED HYPOGLYCEMIA;
PLASMA-CORTISOL; ARGININE VASOPRESSIN; MEDIAN-EMINENCE; BINDING-PROTEIN;
BETA-ENDORPHIN; HUMAN-PLACENTA; SECRETION; ADRENOCORTICOTROPIN
AB OBJECTIVE The third trimester of pregnancy is characterized by a mildly hyperactive hypothalamic-pituitary-adrenal (HPA) axis, possibly driven by elevated circulating levels of corticotrophin releasing hormone (CRH) of placental origin. In-vitro studies have demonstrated that glucocorticoids and oestrogen stimulate while progesterone inhibits the expression of CRH mRNA and/or protein, suggesting that several potential interactions between the placenta and the HPA axis may exist.
DESIGN AND PATIENTS To investigate the detailed pattern of circulating immunoreactive (ir) CRH, ACTH, cortisol, oestradiol and progesterone during the third trimester of pregnancy, plasma samples were drawn serially every 30 minutes from 22 healthy pregnant women (age 32.0 +/- 1.1 years, mean +/- SE) between the 34th and 36th week of gestation. Ten women had plasma samples drawn between 0800 h and 2000 h (daytime group), and 12 between 2000 h and 0300 h (night-time group). The hormone concentrations obtained were analysed for pulsatility by the Detect program, for detection of circadian rhythmicity by comparison between the first and second 6-hour periods within each group by Student's t-test, and for time-dependent correlations by cross-correlation analysis.
RESULTS All five hormones were secreted in a pulsatile fashion. There was no apparent circadian rhythm of CRH or oestradiol secretion, whereas there was a clear circadian rhythm in plasma ACTH, cortisol and progesterone secretion, with the latter in reverse phase (P<0.05). No significant correlations were observed between CRH and ACTH, whereas, as expected, ACTH and cortisol concentrations were strongly correlated with each other over time (r = 0.32 and 0.70 at lag time 30 minutes for the daytime and night-time groups, respectively), with ACTH leading cortisol. A weak positive correlation was observed between CRH and cortisol concentrations for the night-time group at lag time 0 minute, suggesting that the latter may have a positive effect on the former in vivo.
CONCLUSIONS These data suggest that placental CRH, although pulsatile, drives quantitatively the maternal HPA axis in the third trimester of pregnancy in a non-circadian, non-pulsatile fashion. The maternal HPA axis is probably driven in a circadian and pulsatile fashion by another major ACTH secretagogue, most likely AVP of parvocellular paraventricular nucleus origin.
C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892.
NIH,ANALYT BIOSTAT SECT,STRUCT BIOL LAB,DCRT,BETHESDA,MD 20892.
NR 54
TC 87
Z9 87
U1 1
U2 5
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0300-0664
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD APR
PY 1996
VL 44
IS 4
BP 419
EP 428
DI 10.1046/j.1365-2265.1996.683505.x
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UH463
UT WOS:A1996UH46300008
PM 8706308
ER
PT J
AU TreiberHeld, S
Stewart, DM
Kurman, CC
Nelson, DL
AF TreiberHeld, S
Stewart, DM
Kurman, CC
Nelson, DL
TI IL-15 induces the release of soluble IL-2R alpha from human peripheral
blood mononuclear cells
SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY
LA English
DT Article
ID RECEPTOR-BETA-CHAIN; HUMAN INTERLEUKIN-2 RECEPTOR; GAMMA-CHAIN;
MULTIPLE-SCLEROSIS; CLONING; EXPRESSION; INVITRO; CDNAS; P64
AB The recently identified and cloned cytokine IL-15 shares many of the T-cell and B-cell stimulatory activities of IL-2 and utilizes the beta and gamma chains of the IL-2R for binding and signaling. The present report shows that, like IL-2, IL-15 in a concentration and time-dependent manner causes the release of sIL-2R alpha from PHA-activated human peripheral blood mononuclear cells. This effect of IL-15 is largely direct and independent of IL-2. Blocking of the IL-2R beta chain with the antibody Mik-beta 1 prevented the release of sIL-2R alpha by IL-15 but not by IL-2. IL-7, another cytokine utilizing the gamma chain of the IL-2R, drove the release of sIL-2R alpha as well. Several clinical conditions are associated with abnormal serum sIL-2R alpha levels and are also monitored by the measurement of sIL-2R alpha. The reason for siL-2R alpha release is not fully understood. In this study, IL-15, like IL-2 was shown to be a potent inducer of sIL-2R alpha release in vitro. (C) 1996 Academic Press, Inc.
RP TreiberHeld, S (reprint author), NCI,IMMUNOL SECT,METAB BRANCH,NIH,BETHESDA,MD 20982, USA.
NR 36
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 0090-1229
J9 CLIN IMMUNOL IMMUNOP
JI Clin. Immunol. Immunopathol.
PD APR
PY 1996
VL 79
IS 1
BP 71
EP 78
DI 10.1006/clin.1996.0052
PG 8
WC Immunology; Pathology
SC Immunology; Pathology
GA UJ249
UT WOS:A1996UJ24900009
PM 8612353
ER
PT J
AU Yahnke, CJ
Johnson, WE
Geffen, E
Smith, D
Hertel, F
Roy, MS
Bonacic, CF
Fuller, TK
vanValkenburgh, B
Wayne, RK
AF Yahnke, CJ
Johnson, WE
Geffen, E
Smith, D
Hertel, F
Roy, MS
Bonacic, CF
Fuller, TK
vanValkenburgh, B
Wayne, RK
TI Darwin's fox: A distinct endangered species in a vanishing habitat
SO CONSERVATION BIOLOGY
LA English
DT Article
ID HUMAN MITOCHONDRIAL-DNA; POPULATION; CHILE; CONSERVATION; DIVERSITY;
SEQUENCES; EVOLUTION; GENETICS; TAXONOMY; FULVIPES
AB The temperate rain forest of Chiloe Island, Chile, is inhabited by an endemic fox (Dusicyon fulvipes) first described by Charles Darwin and now designated Darwin's fox. Despite morphological differences, Darwin's fox has been considered only an insular subspecies of the mainland chilla fox (D. griseus). This follows the assumption that the island population, with an estimated population of less than 500, has been separated from the mainland chilla fox for only about 15,000 years and may have received occasional immigrants from the mainland. Consequently, this island population has not been protected as endangered or bred in captivity. Recently, a population of Darwin's fox was discovered on the Chilena mainland 600 km north of Chiloe Island. This population exists in sympatry with chilla and possibly culpeo (D. culpaeus) foxes, which suggests that Darwin's fox may be reproductivity isolated. To clarify the phylogenetic position of Darwin's fox, we analyzed 344 bp of mitochondrial DNA control-region sequence of the three species of Chilean foxes. Darwin's foxes from the island and mainland populations compose a monophyletic group distinct from the two other Chilean fox species. This indicates that Darwin's fox was probably an early inhabitant of central Chile, and that its present distribution on the mainland may be a relict of a once much wider distribution. Our results highlight the ability of molecular genetic techniques to uncover historical relationships masked by recent events, such as local extinctions. The ''rediscovery'' of Darwin's fox as a distinct species implies that greater significance should be given to the protection of this species and its unique habitat and to documenting the extent of its mainland distribution.
C1 UNIV CALIF LOS ANGELES,DEPT BIOL,LOS ANGELES,CA 90024.
NO ILLINOIS UNIV,DEPT BIOL SCI,DE KALB,IL 60115.
NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702.
UNIV COPENHAGEN,DEPT POPULAT BIOL,DK-2100 COPENHAGEN,DENMARK.
PONTIFICIA UNIV CATOLICA CHILE,DEPT INGN FORESTAI,SANTIAGO,CHILE.
UNIV MASSACHUSETTS,DEPT FORESTRY & WILDLIFE MANAGEMENT,AMHERST,MA 01003.
RI Johnson, Warren/D-4149-2016
OI Johnson, Warren/0000-0002-5954-186X
NR 71
TC 17
Z9 19
U1 3
U2 14
PU BLACKWELL SCIENCE INC
PI CAMBRIDGE
PA 238 MAIN ST, CAMBRIDGE, MA 02142
SN 0888-8892
J9 CONSERV BIOL
JI Conserv. Biol.
PD APR
PY 1996
VL 10
IS 2
BP 366
EP 375
DI 10.1046/j.1523-1739.1996.10020366.x
PG 10
WC Biodiversity Conservation; Ecology; Environmental Sciences
SC Biodiversity & Conservation; Environmental Sciences & Ecology
GA UK801
UT WOS:A1996UK80100017
ER
PT J
AU Koonin, EV
Mushegian, AR
Rudd, KE
AF Koonin, EV
Mushegian, AR
Rudd, KE
TI Sequencing and analysis of bacterial genomes
SO CURRENT BIOLOGY
LA English
DT Review
ID ESCHERICHIA-COLI GENOME; POLYNUCLEOTIDE PHOSPHORYLASE; RIBOSOMAL
PROTEIN-S1; NUCLEOTIDE-SEQUENCE; GENE; DATABASE; REGIONS; SEARCH
AB The complete sequences of two small bacterial genomes have recently become available, and those of several more species should follow within the next two years. Sequence comparisons show that the most bacterial proteins are highly conserved in evolution, allowing predictions to be made about the functions of most products of an uncharacterized genome. Bacterial genomes differ vastly in their gene repertoires. Although genes for components of the translation and transcription machinery, and for molecular chaperones, are typically maintained, many regulatory and metabolic systems are absent in bacteria with small genomes. Mycoplasma genitalium, with the smallest known genome of any cellular life form, lacks virtually all known regulatory genes, and its gene expression may be regulated differently than in other bacteria, Genome organization is evolutionarily labile: extensive gene shuffling leaves only very few conserved gene arrays in distantly related bacteria.
RP NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, NIH, BETHESDA, MD 20894 USA.
OI Mushegian, Arcady/0000-0002-6809-9225
NR 81
TC 71
Z9 72
U1 0
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD APR 1
PY 1996
VL 6
IS 4
BP 404
EP 416
DI 10.1016/S0960-9822(02)00508-0
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UH684
UT WOS:A1996UH68400022
PM 8723345
ER
PT J
AU Lou, MF
Xu, GT
Zigler, S
York, B
AF Lou, MF
Xu, GT
Zigler, S
York, B
TI Inhibition of naphthalene cataract in rats by aldose reductase
inhibitors
SO CURRENT EYE RESEARCH
LA English
DT Article
DE naphthalene; cataract; aldose reductase inhibitor; rat
ID DIABETIC RATS; LENS; MECHANISM
AB Naphthalene-induced cataract in rat lenses can be completely prevented by AL01576, an aldose reductase inhibitor (ARI). In an attempt to understand the mechanism of this inhibition, several ARIs were examined to compare their efficacies in preventing naphthalene cataract, using both in vitro and in vivo models. Two classes of ARIs were tested: One group including AL01576, AL04114 (a AL01576 analog) and Sorbinil contained the spirohydantoin group, while Tolrestat contained a carboxylic acid group. Furthermore, to clarify if aldose reductase played a role in naphthalene-induced cataractogenesis in addition to its role in sugar cataract formation, a new dual cataract model was established for ARI evaluations. This was achieved by feeding rats simultaneously with high galactose and naphthalene or incubating rat lenses in culture media containing high galactose and naphthalene dihydrodiol. Under these conditions, both cortical cataract and perinuclear cataract developed in the same lens. It was found that at the same dosage of 10 mg/kg/day, both AL01576 and AL04114 completely prevented all morphological and biochemical changes in the lenses of naphthalene-fed rats. Sorbinil was less efficacious, while Tolrestat was inactive. AL01576 showed a dose-response effect in preventing naphthalene cataract and at 10 mg/kg/day, it was also effective as an intervention agent after cataractogenesis had begun. With the dual cataract model, Tolrestat prevented the high galactose-induced cortical cataract but showed no protection against the naphthalene-induced peri nuclear cataract. AL01576, on the other hand, prevented both cataract formations. Results for dulcitol and glutathione levels were in good agreement with the morphological findings. AL04114, an ARI as potent as AL01576 but without its property for cytochrome P-450 inhibition, displayed similar efficacy in preventing naphthalene cataract. Based on these results, it was concluded that the prevention of the naphthalene cataract probably results from inhibition of the conversion of naphthalene dihydrodiol to 1,2-dihydroxynaphthalene and that the effect of the ARIs cannot be explained by their inhibition of the dihydrodiol dehydrogenase activity of aldose reductase.
C1 UNIV NEBRASKA,MED CTR,DEPT OPHTHALMOL,OMAHA,NE 68198.
N TEXAS STATE UNIV,MED CTR,DEPT ANAT & CELL BIOL,FT WORTH,TX 76107.
ALCOA LABS,FT WORTH,TX 76134.
NEI,BETHESDA,MD 20892.
RP Lou, MF (reprint author), UNIV NEBRASKA,DEPT VET & BIOMED SCI,CTR BIOTECHNOL,LINCOLN,NE 68583, USA.
FU NEI NIH HHS [EY 10595]
NR 26
TC 11
Z9 11
U1 0
U2 1
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0271-3683
J9 CURR EYE RES
JI Curr. Eye Res.
PD APR
PY 1996
VL 15
IS 4
BP 423
EP 432
DI 10.3109/02713689608995833
PG 10
WC Ophthalmology
SC Ophthalmology
GA UG505
UT WOS:A1996UG50500009
PM 8670742
ER
PT J
AU ZunigaPflucker, JC
Lenardo, MJ
AF ZunigaPflucker, JC
Lenardo, MJ
TI Regulation of thymocyte development from immature progenitors
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID T-CELL DEVELOPMENT; HEMATOPOIETIC STEM-CELLS; FETAL THYMUS DEVELOPMENT;
C-KIT; PRECURSOR CELLS; ANTIGEN RECEPTORS; LYMPHOCYTES-T; MICE;
DIFFERENTIATION; MOUSE
AB T lymphocytes differentiate from hematopoietic stem cells that settle in the microenvironment of the thymus. The earliest stages of mouse alpha/beta T-cell differentiation occurring before surface expression of the TCR include three important events: proliferation, commitment to the T lineage, and rearrangement and expression of the TCR loci. Recent evidence suggests that the survival as well as differentiation of early thymocytes depends critically on molecular signals such as those generated by the recently described pre-TCR complex.
C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892.
RP ZunigaPflucker, JC (reprint author), UNIV TORONTO,DEPT IMMUNOL,TORONTO,ON M5S 1A8,CANADA.
RI Zuniga-Pflucker, Juan/H-1295-2012;
OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178
NR 96
TC 136
Z9 138
U1 0
U2 5
PU CURRENT BIOLOGY LTD
PI LONDON
PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB
SN 0952-7915
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD APR
PY 1996
VL 8
IS 2
BP 215
EP 224
DI 10.1016/S0952-7915(96)80060-4
PG 10
WC Immunology
SC Immunology
GA UM874
UT WOS:A1996UM87400009
PM 8725945
ER
PT J
AU Margulies, DH
Plaksin, D
Khilko, SN
Jelonek, MT
AF Margulies, DH
Plaksin, D
Khilko, SN
Jelonek, MT
TI Studying interactions involving the T-cell antigen receptor by surface
plasmon resonance
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID BIOSPECIFIC INTERACTION ANALYSIS; CLASS-I MOLECULE; ENDOGENOUS PEPTIDES;
MHC MOLECULE; BINDING; COMPLEX; PROTEIN; AFFINITY; IMMOBILIZATION;
RECOGNITION
AB T-lymphocyte activation is initiated by the interaction of the alpha beta TCR with a complex consisting of a class I or class II MHC-encoded molecule and an antigenic peptide, displayed on the surface of an antigen-presenting cell. Real-time binding measurements using surface plasmon resonance have revealed kinetic and equilibrium parameters for the interactions between purified MHC molecules and peptides, between TCR and MHC-peptide complexes, and between TCR and superantigens. The MHC-peptide interaction is characterized by its high affinity and long half-life, the TCR-MHC/peptide interaction by its low affinity and short half-life, and the TCR-superantigen interaction by its low-to-moderate affinity, which is dependent on the particular superantigen involved. The consistent finding is that both MHC-peptide complexes and superantigens interact with TCR with a low affinity attributable to rapid dissociation. That an MHC-peptide complex that encounters a single TCR only briefly can still deliver the necessary activation signals offers a mechanistic conundrum for which several solutions have been proposed.
RP Margulies, DH (reprint author), NIAID,MOLEC BIOL SECT,IMMUNOL LAB,NIH,BLDG 10,ROOM 11N311,BETHESDA,MD 20892, USA.
RI Margulies, David/H-7089-2013;
OI Margulies, David/0000-0001-8530-7375
NR 56
TC 26
Z9 28
U1 0
U2 2
PU CURRENT BIOLOGY LTD
PI LONDON
PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB
SN 0952-7915
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD APR
PY 1996
VL 8
IS 2
BP 262
EP 270
DI 10.1016/S0952-7915(96)80066-5
PG 9
WC Immunology
SC Immunology
GA UM874
UT WOS:A1996UM87400015
PM 8725950
ER
PT J
AU Suzuki, WA
AF Suzuki, WA
TI The anatomy, physiology and functions of the perirhinal cortex
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID INFERIOR TEMPORAL CORTEX; SHORT-TERM-MEMORY; HIPPOCAMPAL-FORMATION;
CORTICAL AFFERENTS; VISUAL RECOGNITION; ENTORHINAL CORTEX; LESIONS;
IMPAIRMENT; ANTERIOR; STIMULUS
AB The perirhinal cortex is a polymodal association area that contributes importantly to normal recognition memory. A convergence of recent findings from lesion and electrophysiological studies has provided new evidence that this area participates in an even broader range of memory functions than previously thought, including associative memory and emotional memory, as well as consolidation functions. These results are consistent with neuroanatomical research showing that this area has strong and reciprocal connections with widespread cortical sensory areas and with other memory-related structures, including the hippocampal formation and amygdala.
RP Suzuki, WA (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,49 CONVENT DR,BETHESDA,MD 20892, USA.
NR 60
TC 150
Z9 151
U1 7
U2 13
PU CURRENT BIOLOGY LTD
PI LONDON
PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD APR
PY 1996
VL 6
IS 2
BP 179
EP 186
DI 10.1016/S0959-4388(96)80071-7
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA UN151
UT WOS:A1996UN15100005
PM 8725959
ER
PT J
AU Theodore, WH
AF Theodore, WH
TI Positron emission tomography and single photon emission computed
tomography
SO CURRENT OPINION IN NEUROLOGY
LA English
DT Article
AB Neuroimaging techniques have had a dramatic impact on the evaluation and treatment of patients with epilepsy. In order to take full advantage of their potential, it is important to place them in clinical and electrophysiological context and to understand their technical limitations. Positron emission tomography with F-18-2-deoxyglucose and single photon emission computed tomography can provide valuable data for presurgical localization of epileptogenic zones. Interictal cerebral blood flow studies, however, using either positron emission tomography or simple photon emission computed tomography are unreliable. Positron emission tomography cerebral blood flow activation studies, on the other hand, are becoming very useful for presurgical cognitive mapping and may be able to replace the intracarotid amytal test for language and memory lateralization. There are a number of receptor ligands available for both positron emission tomography and simple photon emission computed tomography studies, including benzodiazepine, opiate, and cholinergic tracers. Increased mu opiate, decreased benzodiazepine, and increased monoamine oxidase B receptor binding have been reported.
RP Theodore, WH (reprint author), NIH,CLIN EPILEPSY SECT,BLDG 10,5C-205,BETHESDA,MD 20892, USA.
NR 37
TC 6
Z9 6
U1 1
U2 1
PU CURRENT SCIENCE
PI PHILADELPHIA
PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA
19106
SN 1350-7540
J9 CURR OPIN NEUROL
JI Curr. Opin. Neurol.
PD APR
PY 1996
VL 9
IS 2
BP 89
EP 92
DI 10.1097/00019052-199604000-00005
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA UN971
UT WOS:A1996UN97100005
PM 8782973
ER
PT J
AU Jernigan, RL
Bahar, I
AF Jernigan, RL
Bahar, I
TI Structure-derived potentials and protein simulations
SO CURRENT OPINION IN STRUCTURAL BIOLOGY
LA English
DT Article
ID GLOBULAR-PROTEINS; MEAN FORCE; MODELS; CONFORMATIONS; PREDICTION;
SEQUENCES; CRITERIA; FOLDS
AB There has recently been an explosion in the number of structure-derived potential functions that are based on the increasing number of high-resolution protein crystal structures. These functions differ principally in their reference states; the usual two classes correspond either to initial solvent exposure or to residue exposure of residues. Reference states are critically important for applications of these potentials functions. Inspection of the potential functions and their derivation can tell us not only about protein interaction strengths themselves, but can also provide suggestions for the design of better folding simulations. An appropriate goal in this field is achieving self-consistency between the details in the derivation of potentials and the applied simulations.
C1 BOGAZICI UNIV, ISTANBUL, TURKEY.
TUBITAK, POLYMER RES CTR, ISTANBUL, TURKEY.
RP Jernigan, RL (reprint author), NIH, MATH BIOL LAB, MSC 5677, ROOM B-116, BLDG 12A, BETHESDA, MD 20892 USA.
RI Jernigan, Robert/A-5421-2012
NR 92
TC 220
Z9 225
U1 2
U2 15
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-440X
J9 CURR OPIN STRUC BIOL
JI Curr. Opin. Struct. Biol.
PD APR
PY 1996
VL 6
IS 2
BP 195
EP 209
DI 10.1016/S0959-440X(96)80075-3
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UF605
UT WOS:A1996UF60500010
PM 8728652
ER
PT J
AU Lai, JC
Wawrousek, EF
Sipe, JD
Whitcup, SM
Gery, I
AF Lai, JC
Wawrousek, EF
Sipe, JD
Whitcup, SM
Gery, I
TI Reduced susceptibility to IL-1 and endotoxin in transgenic mice
expressing IL-1 in their lens
SO CYTOKINE
LA English
DT Article
DE endotoxin effects; IL-1 transgene; responses to IL-1; transgenic mice
ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1; LETHALITY; RATS
AB To learn about the effects of chronic exposure to IL-1 we generated a transgenic (Tg) mouse line that expresses human IL-1 beta under the control of the lens alpha A crystallin promoter. Expression of human IL-1 beta was restricted to the eye; neither the protein nor its mRNA were detected in various other organs of the Tg mice, The Tg mice develop severe ocular inflammation shortly after birth, which affects the lens and other eye tissues and apparently allows the release of IL-1 into the circulation. Here we report that the Tg mice exhibit decreased responsiveness to IL-1 and lipopolysaccharide (LPS), as compared to their wildtype littermate controls: (1) when injected with IL-1 the Tg mice produced lower levels of serum amyloid A than their controls; (2) thymocytes of the Tg mice responded less vigorously in culture to stimulation with IL-1; and (3) Tg mice showed lower morbidity and mortality than their controls when injected with toxic amounts of LPS, These data suggest that chronic exposure to IL-1 in the Tg mice induces partial resistance to this cytokine, analogous to the reduced responsiveness to IL-1 in animals pretreated with this proinflammatory cytokine. (C) 1996 Academic Press Limited
C1 NEI, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA.
NEI, NIH, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA.
NEI, NIH, CLIN BRANCH, BETHESDA, MD 20892 USA.
BOSTON UNIV, SCH MED, DEPT BIOCHEM, BOSTON, MA 02118 USA.
NIH, HOWARD HUGHES MED INST, RES SCHOLARS PROGRAM, BETHESDA, MD 20814 USA.
RI Wawrousek, Eric/A-4547-2008
NR 30
TC 7
Z9 7
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD APR
PY 1996
VL 8
IS 4
BP 288
EP 293
DI 10.1006/cyto.1996.0038
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA UF850
UT WOS:A1996UF85000003
PM 9162217
ER
PT J
AU BarrettConnor, E
Schrott, HG
Greendale, G
KritzSilverstein, D
Espeland, MA
Stern, MP
Bush, T
Perlman, JA
AF BarrettConnor, E
Schrott, HG
Greendale, G
KritzSilverstein, D
Espeland, MA
Stern, MP
Bush, T
Perlman, JA
TI Factors associated with glucose and insulin levels in wealthy
postmenopausal women
SO DIABETES CARE
LA English
DT Article
ID CARDIOVASCULAR RISK-FACTORS; DEPENDENT DIABETES-MELLITUS;
CARBOHYDRATE-METABOLISM; ALCOHOL-CONSUMPTION; PHYSICAL-ACTIVITY;
HEART-DISEASE; TOLERANCE; RESISTANCE; POPULATION; NIDDM
AB OBJECTIVE - Little is known about the covariates of hyperglycemia and hyperinsulinemia. We examined candidate factors in postmenopausal women.
RESEARCH DESIGN AND METHODS - We determined the cross-sectional associations of sociodemographic, body size, lifestyle, reproductive, and menopausal factors with pre-trial fasting and postchallenge glucose and insulin levels in 869 postmenopausal women aged 45-65 years. Women were participants in the Postmenopausal Estrogen/Progestin Interventions study who were not taking estrogen or insulin.
RESULTS - Plasma glucose levels increased significantly with age; serum insulin levels did not. BMI and waist-to-hip ratio (WHR) each showed graded positive and independent associations with glucose and insulin levels. Alcohol intake, cigarette smoking, physical activity, parity, education, and income were also associated with insulin or glucose in age-adjusted models. In multivariable models, BMI and WHR explained 18% of the variability in fasting glucose, 16% in postchallenge glucose, 28% in fasting insulin, and 17% in postchallenge insulin. Age and all other factors combined accounted for <6% of the variance in glucose or insulin. In multiply adjusted models, African-American and Hispanic women had higher fasting and 2-h insulin levels than non-Hispanic white women.
CONCLUSIONS - Most of the variance in glycemia and insulin is unexplained. Measures of obesity and fat distribution account for nearly all the explained variance.
C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA.
UNIV IOWA,IOWA CITY,IA.
WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC.
UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX.
JOHNS HOPKINS UNIV,BALTIMORE,MD.
NCI,BETHESDA,MD 20892.
RP BarrettConnor, E (reprint author), UNIV CALIF SAN DIEGO,DEPT FAMILY & PREVENT MED,9500 GILMAN DR,LA JOLLA,CA 92093, USA.
FU NHLBI NIH HHS [HL40154, U01-HL40185, HL40195]
NR 45
TC 28
Z9 28
U1 1
U2 1
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1660 DUKE ST, ALEXANDRIA, VA 22314
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD APR
PY 1996
VL 19
IS 4
BP 333
EP 340
DI 10.2337/diacare.19.4.333
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB885
UT WOS:A1996UB88500006
PM 8729156
ER
PT J
AU Nelson, RG
Pettitt, DJ
deCourten, MP
Hanson, RL
Knowler, WC
Bennett, PH
AF Nelson, RG
Pettitt, DJ
deCourten, MP
Hanson, RL
Knowler, WC
Bennett, PH
TI Parental hypertension and proteinuria in Pima Indians with NIDDM
SO DIABETOLOGIA
LA English
DT Article
DE diabetic nephropathy; hypertension; familial predisposition;
non-insulin-dependent diabetes mellitus; Pima Indians
ID SODIUM-LITHIUM COUNTERTRANSPORT; DEPENDENT DIABETES-MELLITUS; INCREASED
BLOOD-PRESSURE; RED-CELLS; FAMILIAL AGGREGATION; RENAL-DISEASE; URINE
SAMPLES; NEPHROPATHY; PREDISPOSITION; CHILDREN
AB To determine if parental hypertension is associated with proteinuria in offspring with non-insulin-dependent diabetes mellitus (NIDDM), 438 diabetic Pima Indians (172 men, 266 women) aged 20 years or more and both of their parents were examined. Hypertension was defined as a systolic blood pressure 140 mm Hg or more, diastolic blood pressure 90 mm Hg or more, or treatment with antihypertensive medicine. Sixty-three percent of the fathers and 80 % of the mothers had diabetes at the time their blood pressure was measured. Families in which either parent had proteinuria, defined as a urine protein-to-creatinine ratio greater than or equal to 0.5 g/g were excluded; 73 (16.7 %) of the offspring had proteinuria. The prevalence rates of proteinuria in the offspring were similar if neither parent or only one parent had hypertension (8.9 and 9.4%, respectively), but was significantly higher if both parents had hypertension (18.8 %), after adjustment for age, sex, duration of diabetes, and 2-h post-load plasma glucose concentration in the offspring and diabetes in the parents by logistic regression. The odds for proteinuria being present in the offspring if both parents had hypertension was 2.2 times (95 % confidence interval, 1.2 to 4.2) that if only one parent had hypertension. When mean arterial pressure and blood pressure treatment in the offspring were added to the model the relationship remained (odds ratio = 2.2; 95 % confidence interval, 1.1 to 4.3). Hypertension in both parents is associated with the development of proteinuria in offspring with NIDDM. This relationship was present even when controlled for the effects of blood pressure and its treatment in the offspring.
RP Nelson, RG (reprint author), NIDDK,PHOENIX EPIDEMIOL & CLIN RES BRANCH,NIH,1550 E INDIAN SCH RD,PHOENIX,AZ 85014, USA.
RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015; de Courten,
Maximilian/B-3300-2012
OI Hanson, Robert/0000-0002-4252-7068; de Courten,
Maximilian/0000-0001-9997-9359
NR 32
TC 25
Z9 26
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD APR
PY 1996
VL 39
IS 4
BP 433
EP 438
DI 10.1007/BF00400674
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB882
UT WOS:A1996UB88200007
PM 8777992
ER
PT J
AU Ghanayem, BI
Burka, LT
AF Ghanayem, BI
Burka, LT
TI Excretion and identification of methacrylonitrile metabolites in the
bile of male F344 rats
SO DRUG METABOLISM AND DISPOSITION
LA English
DT Article
ID 2-CYANOETHYLENE OXIDE; ACRYLONITRILE; INVITRO; CYANIDE; GLUTATHIONE;
MICE
AB Methacrylonitrile (MAN) is structurally similar to the known carcinogen acrylonitrile (AN), has similar industrial uses, and is occasionally used as its replacement, In contrast to AN, minimal information is available on the toxicity, carcinogenicity, or metabolism of MAN, Earlier work in this laboratory demonstrated that, in rats, MAN is primarily eliminated in the expired air as unchanged MAN, acetone, and CO2. Two mercapturic acids were identified in the urine of rats and mice treated with MAN, In the present work, the common bile duct of anesthetized rats was cannulated, The animals received a single gavage dose of 58 mg/kg 2-[C-14]MAN, Bile was collected before and after MAN administration, Bile flow and MAN-derived radioactivity were determined at each time point. MAN had a minimal effect on bile flow and 4 to 6% of the administered MAN dose was excreted in the bile within 6 hr after dosing, HPLC analysis of bile showed two major metabolites, which were identified as 1-(S-glutathionyl)-2-propanene and 1-(S-glutathionyl)-2-cyanopropane by using NMR spectra and chemical synthesis, The ratio of the two metabolites in MAN-treated rats was approximately 2:1. Pretreatment of rats with sodium phenobarbital caused minimal quantitative or qualitative changes in the biliary excretion of MAN metabolites. In contrast, pretreatment of rats with beta-diethylaminoethyl diphenylpropylacetate before MAN administration resulted in a significant decrease in the ratio of 1-(S-glutathionyl)-2-propanone to 1-(S-glutathionyl)-2-cyanopropane (1:2). These data, especially the identification of 1-(S-glutathionyl)-2-propanone, indirectly demonstrated that MAN is metabolized via an epoxide intermediate (1-cyano-1-methyloxirane), Modulation of MAN metabolism by the P450 modulators suggested that this metabolic pathway is catalyzed via the cytochrome P450 enzymes, This work also confirms that MAN undergoes direct reaction with reduced glutathione via a Michael addition, Because earlier work demonstrated that AN undergoes similar metabolism, MAN might have a qualitative toxicity profile similar to that of acryonitrile.
RP Ghanayem, BI (reprint author), NIEHS,NIH,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 14
TC 11
Z9 11
U1 0
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0090-9556
J9 DRUG METAB DISPOS
JI Drug Metab. Dispos.
PD APR
PY 1996
VL 24
IS 4
BP 390
EP 394
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UE830
UT WOS:A1996UE83000003
PM 8801052
ER
PT J
AU Bunnell, BA
Morgan, RA
AF Bunnell, BA
Morgan, RA
TI Gene therapy for HIV infection
SO DRUGS OF TODAY
LA English
DT Review
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOTOXIC LYMPHOCYTES-T; HUMAN
ADENOSINE-DEAMINASE; LONG-TERM EXPRESSION; WILD-TYPE VIRUS; ANTISENSE
RNA; RETROVIRAL VECTORS; INTRACELLULAR IMMUNIZATION; SEROPOSITIVE
INDIVIDUALS; TRANSDOMINANT MUTANTS
AB The ultimate goal of gene theray for HIV-I is to inhibit viral replication and the resultant AIDS pathogenesis. Gene therapy for HIV-1 requires the introduction of genes that effectively inhibit viral replication by blocking expression of viral genes or altering the normal function of HIV-1 associated proteins. This review details the various anti-HIV-1 gene therapy strategies that have been developed to effectively inhibit HIV-1 replication. The review covers three broad categories: i) gene tehrapy using nucleic acid moieties such as gene vaccines, antisense DNA/RNA, RNA decoys, and ribozymes; ii) protein approaches such as trans-dominant negative proteins and single chain antibodies; and iii) immunotherapy using HIV-1 specific cytotoxic T cells. The discussion focuses on the effectiveness of the various techniques in preclinical experiments and in animal models. Also, the status of all of the current RAC/FDA approved clinical protocols for anti-HIV-1 gene therapy strategies is reviewed.
RP Bunnell, BA (reprint author), NIH, CLIN GENE THERAPY BRANCH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA.
NR 109
TC 3
Z9 4
U1 0
U2 1
PU PROUS SCIENCE, SA-THOMSON REUTERS
PI BARCELONA
PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN
SN 1699-3993
J9 DRUG TODAY
JI Drugs Today
PD APR-MAY
PY 1996
VL 32
IS 3
BP 209
EP 224
PG 16
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA UT113
UT WOS:A1996UT11300002
ER
PT J
AU Chen, N
Chrambach, A
AF Chen, N
Chrambach, A
TI Enhanced field strength and resolution in gel electrophoresis upon
substitution of buffer by histidine at its isoelectric point
SO ELECTROPHORESIS
LA English
DT Article
DE electrophoresis; isoelectric histidine; field strength; dispersion
coefficient; resolution
AB Gel electrophoresis in isoelectric buffers, recently introduced by R. Westermeier and H. Schickle (Electrophoresis '95, Paris, Abstract No. 3, 1995), was applied to the automated HPGE-1000 apparatus in the expectation to be able to increase the field strength under the limiting conditions of heat dissipation capacity and voltage of that apparatus. A previous attempt to achieve that aim by reduction of gel thickness had not yielded more than a twofold increment in resolving power. Replacing 0.2 X Tris-boric acid-EDTA (TEE) buffer, conventionally applied in the apparatus at 15 V/cm, by 0.05 M histidine, pH 7.6 (close to the pI of 7.47), allows one to increase the field strength to 60 V/cm, thus providing a nearly fivefold increment in resolution under otherwise identical conditions (fluorescein carboxylate-labeled conalbumin-sodium dodecyl sulfate (SDS) and soybean trypsin inhibitor-SDS samples, 10 degrees C, 4% MetaPhor agarose). An additional decrease in band dispersion can be obtained by decreasing the starting zone width through buffer dilution in the sample phase.
C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892.
NR 10
TC 13
Z9 13
U1 1
U2 4
PU VCH PUBLISHERS INC
PI DEERFIELD BEACH
PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788
SN 0173-0835
J9 ELECTROPHORESIS
JI Electrophoresis
PD APR
PY 1996
VL 17
IS 4
BP 699
EP 703
DI 10.1002/elps.1150170413
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA UP016
UT WOS:A1996UP01600012
PM 8738330
ER
PT J
AU Chang, HT
Zakharov, SF
Chrambach, A
AF Chang, HT
Zakharov, SF
Chrambach, A
TI Separation and isolation of subcellular-sized particles by
electrophoresis in polymer solution using the commercial scanning
apparatus
SO ELECTROPHORESIS
LA English
DT Article
DE subcellular-sized particles; isolation; scanning apparatus
AB Electrophoresis of fluorescently labeled rat liver microsomes and polystyrene carboxylates of 10 and 30 nm radius was conducted in buffered 10-15% polyvinylpyrrolidone (M(r) = 10(6)) solutions, using a horizontal gel electrophoresis apparatus with intermittent scanning of fluorescence (HPGE-1000, LabIntelligence). Banding, constant migration rates and Ferguson plots were obtained in these polymer solutions. The major microsome band detected by the automated scan was located visually on the gel by means of its fluorescein label and was isolated by volumetric withdrawal; recovery was monitored by scanning and ascertained to be near quantitative after three consecutive steps, in each of which 30 mu L were withdrawn. This preparative method promises to be generally applicable to particles that are too large to enter into gels.
C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892.
RI Chang, Huan-Tsung/C-1183-2011
NR 11
TC 9
Z9 9
U1 0
U2 2
PU VCH PUBLISHERS INC
PI DEERFIELD BEACH
PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788
SN 0173-0835
J9 ELECTROPHORESIS
JI Electrophoresis
PD APR
PY 1996
VL 17
IS 4
BP 776
EP 780
DI 10.1002/elps.1150170426
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA UP016
UT WOS:A1996UP01600025
PM 8738343
ER
PT J
AU Weissenhorn, W
Wharton, SA
Calder, LJ
Earl, PL
Moss, B
Aliprandis, E
Skehel, JJ
Wiley, DC
AF Weissenhorn, W
Wharton, SA
Calder, LJ
Earl, PL
Moss, B
Aliprandis, E
Skehel, JJ
Wiley, DC
TI The ectodomain of HIV-1 env subunit gp41 forms a soluble, alpha-helical,
rod-like oligomer in the absence of gp120 and the N-terminal fusion
peptide
SO EMBO JOURNAL
LA English
DT Article
DE conformational change; envelope glycoprotein gp41; HIV-1; membrane
fusion
ID IMMUNODEFICIENCY-VIRUS TYPE-1; MURINE LEUKEMIA-VIRUS; ENVELOPE
GLYCOPROTEIN; TRANSMEMBRANE PROTEIN; CD4 BINDING; STRUCTURAL PROTEINS;
MEMBRANE-FUSION; HTLV-III; HEMAGGLUTININ; RECEPTOR
AB The human immunodeficiency virus-1 (HIV-1) envelope glycoprotein is composed of a soluble glycopolypeptide gp120 and a transmembrane glycopolypeptide gp41, These subunits form non-covalently linked oligomers on the surface of infected cells, virions and cells transfected with the complete env gene. Two length variants of the extracellular domain of gp41 (aa 21-166 and aa 39-166), that both lack the N-terminal fusion peptide and the C-terminal membrane anchor and cytoplasmic domain, have been expressed in insect cells to yield soluble oligomeric gp41 proteins. Oligomerization was confirmed by chemical cross-linking and gel filtration. Electron microscopy and circular dichroism measurements indicate a rod-like molecule with a high alpha-helical content and a high melting temperature (78 degrees C). The binding of monoclonal antibody Fab fragments dramatically increased the solubility of both gp41 constructs, We propose that gp41 folds into its membrane fusion-active conformation, when expressed alone.
C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,MOLEC MED LAB,BOSTON,MA 02215.
NIAID,NIH,BETHESDA,MD 20892.
HARVARD UNIV,HOWARD HUGHES MED INST,DEPT MOLEC & CELLULAR BIOL,CAMBRIDGE,MA 02138.
NATL INST MED RES,LONDON NW7 1AA,ENGLAND.
FU NIGMS NIH HHS [GM39589]
NR 37
TC 125
Z9 126
U1 0
U2 4
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0261-4189
J9 EMBO J
JI Embo J.
PD APR 1
PY 1996
VL 15
IS 7
BP 1507
EP 1514
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA UF658
UT WOS:A1996UF65800004
PM 8612573
ER
PT J
AU McSweegan, E
AF McSweegan, E
TI The infectious diseases impact statement: A mechanism for addressing
emerging diseases
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID EPIDEMIOLOGY; HEALTH
AB The use of an Infectious Diseases Impact Statement (IDIS) is proposed for predictive assessments of local changes in infectious diseases arising from human-engineered activities. IDIS is intended to be analogous to an Environmental Impact Statement. The drafting of an IDIS for specific activities, particularly in developing nations, would provide a formal mechanism for examining potential changes in local health conditions, including infected and susceptible populations, diseases likely to fluctuate in response to development, existing control measures, and vectors likely to be affected by human activities. The resulting survey data could provide a rational basis and direction for development, surveillance, and prevention measures. An IDIS process that balances environmental alterations, local human health, and economic growth could substantially alter the nature of international development efforts and infectious disease outbreaks.
RP McSweegan, E (reprint author), NIAID,NIH,SOLAR BLDG,RM 3A34,BETHESDA,MD 20892, USA.
NR 20
TC 6
Z9 6
U1 1
U2 2
PU CENTER DISEASE CONTROL
PI ATLANTA
PA ATLANTA, GA 30333
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD APR-JUN
PY 1996
VL 2
IS 2
BP 103
EP 108
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA UM787
UT WOS:A1996UM78700004
PM 8903209
ER
PT J
AU Pu, LP
Ma, W
Barker, JL
Loh, YP
AF Pu, LP
Ma, W
Barker, JL
Loh, YP
TI Differential coexpression of genes encoding prothyrotropin-releasing
hormone (Pro-TRH) and prohormone convertases (PC1 and PC2) in rat brain
neurons: Implications for differential processing of Pro-TRH
SO ENDOCRINOLOGY
LA English
DT Article
ID MESSENGER RIBONUCLEIC-ACID; CENTRAL-NERVOUS-SYSTEM; PROPROTEIN
CONVERTASE; INSITU HYBRIDIZATION; IDENTIFICATION; EXPRESSION; PEPTIDES;
KEX2; LOCALIZATION; ENDOPROTEASE
AB Pro-TRH is cleaved at paired basic residues to yield five copies of TRH and cryptic peptides. Recent studies have shown that the prohormone convertases, PC1 and PC2, can process pro-TRH correctly. To determine whether these two enzymes could play a role in pro-TRH processing in vivo, the regional and cellular colocalization of pro-TRH messenger RNA (mRNA) with the mRNAs encoding the prohormone convertases PC1 and PC2 was examined in rat brain, using in situ hybridization histochemistry. Differential regional distribution of pro-TRH mRNA with PC1 and/or PC2 mRNA was found in several brain regions. For example, in the olfactory regions, there was coexpression of pro-TRH mRNA in the glomerular layer with PC2 mRNA, but not PC1 mRNA, whereas in the tenia tecta, coexpression of pro-TRH and PC1 mRNAs was evident, but PC2 mRNA was absent. Pro-TRH mRNA in the paraventricular nucleus was coexpressed with both PC1 and PC2 mRNAs, whereas the basal lateral hypothalamus showed coexistence of pro-TRH mRNA with PC2 mRNA, but not PC1 mRNA. Interestingly, pro-TRH was expressed in the thalamic reticular nucleus, but neither PC1 nor PC2 was detectable in this region. Cellular colocalization studies using double in situ hybridization histochemistry showed the presence of PC2 mRNA in the pro-TRH neurons of the olfactory glomerular layer and basal lateral hypothalamus, and PC1 mRNA in the pro-TRH neurons in the paraventricular nucleus. These results suggest that PC1 and PC2 are enzyme candidates for the processing of pro-TRH in vivo. Moreover, the differential distribution of PC1 and PC2 mRNAs with pro-TRH mRNA may be responsible for the differential processing of this prohormone in the central nervous system. The absence of PC1 and PC2 mRNAs in certain TRH neurons raises the possibility that prohormone convertases other than PC1 and PC2 may be involved in the processing of brain pro-TRH.
C1 NICHHD, CELLULAR NEUROBIOL SECT, DEV NEUROBIOL LAB, NIH, BETHESDA, MD 20892 USA.
NINCDS, NEUROPHYSIOL LAB, NIH, BETHESDA, MD 20892 USA.
NR 39
TC 35
Z9 35
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD APR
PY 1996
VL 137
IS 4
BP 1233
EP 1241
DI 10.1210/en.137.4.1233
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB891
UT WOS:A1996UB89100013
PM 8625894
ER
PT J
AU Moy, E
Kimzey, LM
Nelson, LM
Blithe, DL
AF Moy, E
Kimzey, LM
Nelson, LM
Blithe, DL
TI Glycoprotein hormone alpha-subunit functions synergistically with
progesterone to stimulate differentiation of cultured human endometrial
stromal cells to decidualized cells: A novel role for free alpha-subunit
in reproduction
SO ENDOCRINOLOGY
LA English
DT Article
ID HUMAN CHORIONIC-GONADOTROPIN; FACTOR-BINDING PROTEIN-1; INVITRO
DECIDUALIZATION; PREMATURE LUTEINIZATION; LEUPROLIDE ACETATE; HUMAN
PROLACTIN; PREGNANCY; GROWTH; SECRETION; SERUM
AB Glycoprotein hormone-free alpha subunit is secreted by the pituitary throughout the menstrual cycle and by the placenta during pregnancy. We showed previously that free a subunit stimulated PRL secretion from term pregnancy decidual cells, suggesting a function for free alpha in pregnancy. However, no role has been ascribed to free alpha in the normal menstrual cycle. Using an in vitro model, we examined the role of alpha subunit in regulating human endometrial stromal cell differentiation (decidualization). PRL and insulin-like growth factor binding protein-1 (IGFBP-1), specific decidual secretory products, were used as markers of decidualization. We found that alpha subunit acted synergistically with progesterone (P) to induce more rapid decidualization with higher output (2- to 6-fold) of PRL and IGFBP-1, compared with P alone (P < 0.01). The effect of a was dose dependent, with stimulatory activity starting at 0.05 ng/ml and reaching maximal levels at 1-2 ng/ml. These levels correspond to serum concentrations of free alpha found during the luteal phase of the menstrual cycle when endometrial decidualization occurs in vivo. These findings demonstrate new biological activity for a subunit in the regulation of human endometrial decidualization and indicate that free alpha plays a role in human reproduction. Furthermore, demonstration of potential bioactivities of free a subunit has important implications for understanding normal endocrine function and various pathological conditions.
C1 NIH, CTR CLIN, DEPT NURSING, BETHESDA, MD 20892 USA.
NICHHD, DEV ENDOCRINOL BRANCH, SECT GYNECOL RES, BETHESDA, MD 20892 USA.
NICHHD, DEV ENDOCRINOL BRANCH, UNIT GLYCOBIOL, BETHESDA, MD 20892 USA.
NR 48
TC 36
Z9 36
U1 2
U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD APR
PY 1996
VL 137
IS 4
BP 1332
EP 1339
DI 10.1210/en.137.4.1332
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB891
UT WOS:A1996UB89100027
PM 8625908
ER
PT J
AU Gomez, G
Padilla, L
Udupi, V
Tarasova, N
Sundler, F
Townsend, CM
Thompson, JC
Greeley, GH
AF Gomez, G
Padilla, L
Udupi, V
Tarasova, N
Sundler, F
Townsend, CM
Thompson, JC
Greeley, GH
TI Regulation of peptide YY homeostasis by gastric acid and gastrin
SO ENDOCRINOLOGY
LA English
DT Article
ID RELEASE; SECRETION; GUT; DOG; PANCREAS; RAT
AB Peptide YY (PYY) is a gut hormone localized primarily in the distal bowel. Because circulating PW inhibits gastric acid secretion, we investigated the effects of gastric acid secretion and gastrin on gene expression and secretion of PW. In conscious dogs, PYY release in response to oral food was inhibited (P < 0.05) by pharmacologic inhibition of gastric acid secretion (omeprazole, famotidine). In rats, omeprazole treatment resulted in a significant elevation in serum gastrin concentrations and a simultaneous decrease in PYY messenger RNA (mRNA) and peptide levels in the colon; administration of a gastrin receptor antagonist (L365, 260) prevented the inhibitory actions of omeprazole on colonic PYY mRNA levels. In athymic-nude mice, implantation of a human gastrinoma resulted in an elevation of serum gastrin concentrations and a concomitant depression of colonic PYY mRNA levels. We conclude that endogenous gastric acid secretion up-regulates PYY release and PYY mRNA expression. Circulating gastrin acts to down-regulate PYY release and PYY mRNA expression. This study provides evidence that foregut functions (i.e., gastric acid secretion and gastrin release) exert control over an antiacid signal (e.g. PYY release) emanating from the hindgut.
C1 UNIV TEXAS, MED BRANCH, DEPT SURG, GALVESTON, TX 77555 USA.
NCI, MOLEC ASPECTS DRUG DESIGRN SECT, FREDERICK, MD 21702 USA.
LUND UNIV, DEPT MED CELL RES, S-22362 LUND, SWEDEN.
FU NIDDK NIH HHS [DK-15241]
NR 24
TC 12
Z9 12
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD APR
PY 1996
VL 137
IS 4
BP 1365
EP 1369
DI 10.1210/en.137.4.1365
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB891
UT WOS:A1996UB89100031
PM 8625912
ER
PT J
AU Malik, KF
Young, WS
AF Malik, KF
Young, WS
TI Localization of binding sites in the central nervous system for leptin
(OB protein) in normal, obese (ob/ob), and diabetic (db/db) C57BL/6J
mice.
SO ENDOCRINOLOGY
LA English
DT Article
ID RECEPTORS; BRAIN
AB Leptin (OB protein) fused to the FLAG epitope and a kinase recognition site was expressed in bacteria, immunopurified, and phosphorylated using [gamma-(33)p] ATP. The resulting probe was used to characterize the distribution of leptin binding sites within brain sections of normal, ob/ob, and db/db C57BL/6J male mice. Leptin binding sites were found in leptomeninges and choroid plexus. Leptin binding within the choroid plexus is slightly elevated in ob/ob mice when compared to normal males (p<0.05). Binding of leptin by the choroid plexus of db/db male mice is lower than in normal males (p<0.05), but normally distributed. Based on the association and dissociation rates of leptin binding on tissue sections, we estimate the KD of the choroid plexus site at 0.25x10(-9) M. From our results, we hypothesize that the binding of leptin to its site may cause the release or transport of uncharacterized factor(s) into the cerebral spinal fluid (CSF) to affect neuronal populations controlling feeding and metabolism.
RP Malik, KF (reprint author), NIMH, CELL BIOL LAB, NIH, BETHESDA, MD 20892 USA.
RI Young, W Scott/A-9333-2009
OI Young, W Scott/0000-0001-6614-5112
NR 11
TC 98
Z9 99
U1 0
U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD APR
PY 1996
VL 137
IS 4
BP 1497
EP 1500
DI 10.1210/en.137.4.1497
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA UB891
UT WOS:A1996UB89100048
PM 8625929
ER
PT J
AU Hattis, D
Glowa, J
Tilson, H
Ulbrich, B
AF Hattis, D
Glowa, J
Tilson, H
Ulbrich, B
TI Risk assessment for neurobehavioral toxicity: SGOMSEC Joint Report
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article; Proceedings Paper
CT 11th SGOMSEC Workshop/19th Rochester International Conference on
Environmental Toxicity - Risk Assessment for Neurobehavioral Toxicity
CY JUN 12-17, 1994
CL ROCHESTER, NY
SP Sci Grp Methodol Safety Evaluat Chem, Sci Comm Problems Environm, Int Programme Chem Safety, WHO, NIEHS, Univ Rochester
DE benchmark dose; effect levels; identification of neurotoxicity;
interindividual variability; quantitative models; reference doses;
regulatory activity; reversibility
ID NEUROTOXICOLOGY; CHEMICALS; HAIR; TIME
AB Behavioral end points for neurotoxicity risk assessment have been developed and examined over the past three decades. They are now ready to move from simple qualitative guidelines, such as exemplified by reference doses, to more quantitative models, such as benchmark doses, based on dose-response information. Risk assessors, confronted by a wider array of methodologies and data than in the past, should be offered guidance in interpretation because now they have to deal with unaccustomed questions and problems. These include reversibility, susceptible populations, multiple end points, and the details of dose-response and dose-effect distributions.
C1 NIDDKD,LMC,NIH,BETHESDA,MD 20892.
US EPA,RES TRIANGLE PK,NC 27711.
BUNDESGESUNDHEITSAMT,INST ARZBEUNUTTEK,W-1000 BERLIN,GERMANY.
RP Hattis, D (reprint author), CLARK UNIV,MARSH INST CTR TECHNOL ENVIRONM & DEV,950 MAIN ST,WORCESTER,MA 01610, USA.
NR 44
TC 4
Z9 4
U1 0
U2 1
PU NATL INST ENVIRON HEALTH SCI
PI RES TRIANGLE PK
PA PO BOX 12233, RES TRIANGLE PK, NC 27709
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD APR
PY 1996
VL 104
SU 2
BP 217
EP 226
DI 10.2307/3432643
PG 10
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA UL607
UT WOS:A1996UL60700006
PM 8860324
ER
PT J
AU Alavanja, MCR
Sandler, DP
McMaster, SB
Zahm, SH
McDonnell, CJ
Lynch, CF
Pennybacker, M
Rothman, N
Dosemeci, M
Bond, AE
Blair, A
AF Alavanja, MCR
Sandler, DP
McMaster, SB
Zahm, SH
McDonnell, CJ
Lynch, CF
Pennybacker, M
Rothman, N
Dosemeci, M
Bond, AE
Blair, A
TI The agricultural health study
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE cancers; exposure assessment; farmers; lymphoma; noncancer toxicity;
pesticides; prospective cohort
ID CANCER MORTALITY; FARMERS; CANADA; RISKS
AB The Agricultural Health Study, a large prospective cohort study, has been initiated in North Carolina and Iowa. The objectives of this study are to: 1) identify and quantify cancer risks among men, women, whites, and minorities associated with direct exposure to pesticides and other agricultural agents; 2) evaluate noncancer heath risks including neurotoxicity, reproductive effects, immunologic effects, nonmalignant respiratory disease, kidney disease, and growth and development among children; 3) evaluate disease risks among spouses and children of farmers that may arise from direct contact with pesticides and agricultural chemicals used in the home, lawns and gardens, and from indirect contact, such as spray drift, laundering work clothes, or contaminated food or water; 4) assess current and past occupational and nonoccupational agricultural exposures using periodic interviews and environmental and biologic monitoring, 5) study the relationship between agricultural exposures, biomarkers of exposure, biologic effect, and genetic susceptibility factors relevant to carcinogenesis; and 6) identify and quantify cancer and other disease risks associated with lifestyle factors such as diet, cooking practices, physical activity, smoking and alcohol consumption, and hair dye use. In the first year of a 3-year enrollment period, 26,235 people have been enrolled in the study including 19,776 registered pesticide applicators and 6,459 spouses of registered farmer applicators. It is estimated that when the total cohort is assembled in 1997 it will include approximately 75,000 adult study subjects. Farmers, the largest group of registered pesticide applicators, comprise 77% of the target population enrolled in the study. This experience compares favorably with enrollment rates of previous prospective studies.
C1 NIEHS,RES TRIANGLE PK,NC 27709.
SRA TECHNOL INC,FALLS CHURCH,VA 22042.
UNIV IOWA,IOWA CITY,IA 52242.
SURVEY RES ASSOCIATES,DURHAM,NC 27713.
US EPA,RES TRIANGLE PK,NC 27711.
RP Alavanja, MCR (reprint author), NCI,DIV CANC EPIDEMIOL & GENET,EPN-418,6130 EXECUT BLVD,BETHESDA,MD 20892, USA.
RI Zahm, Shelia/B-5025-2015;
OI Sandler, Dale/0000-0002-6776-0018
FU NCI NIH HHS [N01-CP-21095, N01-CP-33047, N01-CP-33048]
NR 40
TC 288
Z9 292
U1 6
U2 41
PU NATL INST ENVIRON HEALTH SCI
PI RES TRIANGLE PK
PA PO BOX 12233, RES TRIANGLE PK, NC 27709
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD APR
PY 1996
VL 104
IS 4
BP 362
EP 369
DI 10.2307/3432672
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA UH994
UT WOS:A1996UH99400008
PM 8732939
ER
PT J
AU Glowa, JR
AF Glowa, JR
TI Dose-response analysis in risk assessment: Evaluation of behavioral
specificity
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article; Proceedings Paper
CT 11th SGOMSEC Workshop/19th Rochester International Conference on
Environmental Toxicity - Risk Assessment for Neurobehavioral Toxicity
CY JUN 12-17, 1994
CL ROCHESTER, NY
SP Sci Grp Methodol Safety Evaluat Chem, Sci Comm Problems Environm, Int Programme Chem Safety, WHO, NIEHS, Univ Rochester
DE risk assessment; drug abuse; rhesus monkeys; GBR 12909;
schedule-controlled behavior; neurotoxicology
ID MOLECULAR MECHANISMS; RHESUS-MONKEYS; COCAINE; INHIBITORS; FOOD
AB Several methods of quantitative risk assessment that have been described recently are particularly applicable to neurotoxic end points. These methods can be broadly divided into two types of approaches based on their treatment of dose-response data to estimate risks. Benchmark approaches estimate risks using variability in response to a fixed dose level in comparison with background control variability. Probabilistic approaches estimate risks using the variability in the dose to produce a small effect in the sample population. The current report seeks to extend the development of probabilistic approaches for neurotoxic end points. Because behavioral data are often used to assess therapeutic efficacy as well as toxicity (unwanted effects), this analysis focused on the relative risks of producing these effects with the same agent. The therapeutic potential of GBR 12909 was determined by its ability to decrease cocaine-maintained responding in monkeys. The effects of this agent were also assessed in the same monkeys using food-maintained responding to provide an indication of behavioral toxicity. GBR 12909 decreased both behaviors, with complete decreases on drug-seeking behavior occurring al doses that had minimal effects on food-maintained responding. The difference in the estimates of doses to decrease drug-seeking and food-maintained behavior suggested that specific therapeutic effects could be obtained in the absence of unwanted side effects for a definable proportion of the population. These results also suggest that multiple behavioral end points can be useful for identifying specific effects of chemicals for the purposes of risk assessment.
RP Glowa, JR (reprint author), NIDDK, NIH,LMC,BEHAV PHARMACOL UNIT,BLDG 14D, ROOM 311, BETHESDA, MD 20892 USA.
FU ONDIEH CDC HHS [RA-ND-94-24]
NR 36
TC 4
Z9 4
U1 1
U2 1
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD APR
PY 1996
VL 104
SU 2
BP 391
EP 396
DI 10.2307/3432659
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA UL607
UT WOS:A1996UL60700022
PM 9182046
ER
PT J
AU Ford, PA
Arbuck, SG
Minniti, C
Miller, LL
DeMaria, D
ODwyer, PJ
AF Ford, PA
Arbuck, SG
Minniti, C
Miller, LL
DeMaria, D
ODwyer, PJ
TI Phase I trial of etoposide, doxorubicin and cisplatin (EAP) in
combination with GM-CSF
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE phase I trial; GM-CSF; etoposide; doxorubicin; cisplatin
ID COLONY-STIMULATING FACTOR; HIGH-DOSE CHEMOTHERAPY;
NON-HODGKINS-LYMPHOMA; GASTRIC-CANCER; BREAST-CANCER; GRANULOCYTE
AB The aim of this study was to ameliorate the toxicity of the etoposide, doxorubicin and cisplatin (EAP) regimen and to investigate the feasibility of dose escalation, using the molgramostim form of granulocyte macrophage-colony stimulating factor (GM-CSF) 10 mu g/kg/day s.c. into the regimen. The design of the trial allowed for amended scheduling of the agents in the event of suboptimal results. Initially the regimen comprised etoposide 120 mg/m(2), days 1-3, doxorubicin 40 mg/m(2), day 1, and cisplatin 40 mg/m(2), days 2 and 8. GM-CSF was begun on day 4 and continued until recovery of granulocyte counts. Courses were repeated every 21 days. 3 patients were treated at these doses. 5 patients received escalated doses (etoposide 180 mg/m(2); doxorubicin 60 mg/m(2) cisplatin 60 mg/m(2)) on this schedule; 4 out of 5 had intolerable myelosuppression (grade IV neutropenia or thrombocytopenia lasting greater than or equal to 7 days). These results prompted the administration of the day 8 cisplatin dose on day 3, with GM-CSF beginning on day 4. At the lowest doses of each agent (etoposide 120-doxorubicin 40-cisplatin 40), 3 of 6 patients had intolerable myelosuppression, and 3 patients had febrile neutropenia. Dose escalation of all of the drugs to etoposide 180 mg/m(2), doxorubicin 60 mg/m(2), cisplatin 60 mg/m(2) resulted in documented infections in 4 out of 4 patients. GM-CSF toxicity included rash, dyspnoea, arrhythmias and pericardial effusions. The conclusion was that the use of GM-CSF does not permit escalation of drug doses on either schedule of EAP administration, and that these results do not support the combined use of GM-CSF and EAP. (C) 1996 Elsevier Science Ltd
C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111.
ROSWELL PK MEM INST,BUFFALO,NY.
NCI,BETHESDA,MD 20892.
FU NCI NIH HHS [CA 06972, CA 49820]
NR 33
TC 3
Z9 3
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD APR
PY 1996
VL 32A
IS 4
BP 631
EP 635
DI 10.1016/0959-8049(95)00602-8
PG 5
WC Oncology
SC Oncology
GA UJ370
UT WOS:A1996UJ37000018
PM 8695266
ER
PT J
AU Mannisto, S
Pietinen, P
Haukka, J
Ovaskainen, ML
Albanes, D
Virtamo, J
AF Mannisto, S
Pietinen, P
Haukka, J
Ovaskainen, ML
Albanes, D
Virtamo, J
TI Reported alcohol intake, diet and body mass index in male smokers
SO EUROPEAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID UNITED-STATES ADULTS; DRINKING PATTERN; NUTRIENT INTAKE; SMOKING-HABITS;
CONSUMPTION; MEN; POPULATION; PREVALENCE; DISEASE; ETHANOL
AB Objective: The study was carried out to determine associations of reported alcohol intake with diet and body mass index. Type and frequency of consumed alcohol were also considered.
Design: A cross-sectional study.
Setting: The baseline examination of the participants of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in 1985-1988.
Subjects: 27 215 middle-aged Finnish male smokers.
Interventions: The diet was assessed by a self-administered food use questionnaire: Subject's habitual diet and alcohol intake over the previous 12 months were asked. Body mass index was used as the measure of adiposity.
Results: Energy intake from food was not related to alcohol intake. Although alcohol consumption was associated with food selection (eg berry and coffee consumption), this only slightly influenced daily nutrient intakes. Intake of spirits was more consistently related to higher body mass index than that of other alcoholic beverages. Daily alcohol intake had a much smaller association with body mass index than less frequent use, independently of the total consumption.
Conclusions: The differences in nutrient intake between abstainers, light and moderate alcohol consumers were small although the consumption of many foods varied with alcohol consumption. Even if alcohol consumption is one noteworthy factor associated with weight, the energy from alcohol increases body weight less than expected; both the type and frequency of consumed alcohol may explain why energy from alcohol is utilized less efficiently than nonalcoholic energy.
C1 NATL PUBL HLTH INST,CANC PREVENT UNIT,HELSINKI,FINLAND.
NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892.
RP Mannisto, S (reprint author), NATL PUBL HLTH INST,DEPT NUTR,HELSINKI,FINLAND.
RI Albanes, Demetrius/B-9749-2015; Haukka, Jari/G-1484-2014
OI Haukka, Jari/0000-0003-1450-6208
FU NCI NIH HHS [N01-CN-45165]
NR 33
TC 15
Z9 15
U1 0
U2 2
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0954-3007
J9 EUR J CLIN NUTR
JI Eur. J. Clin. Nutr.
PD APR
PY 1996
VL 50
IS 4
BP 239
EP 245
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA UD595
UT WOS:A1996UD59500007
PM 8730611
ER
PT J
AU Newmann, RD
AF Newmann, RD
TI Findings of the Advisory Committee on human radiation experiments
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE
LA English
DT Editorial Material
RP Newmann, RD (reprint author), NIH,BLDG 10,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
SN 0340-6997
J9 EUR J NUCL MED
JI Eur. J. Nucl. Med.
PD APR
PY 1996
VL 23
IS 4
BP 476
EP 477
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA UE802
UT WOS:A1996UE80200022
ER
PT J
AU Wassermann, EM
Samii, A
Mercuri, B
Ikoma, K
Oddo, D
Grill, SE
Hallett, M
AF Wassermann, EM
Samii, A
Mercuri, B
Ikoma, K
Oddo, D
Grill, SE
Hallett, M
TI Responses to paired transcranial magnetic stimuli in resting, active,
and recently activated muscles
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Article
DE motor cortex; exercise; transcranial magnetic stimulation; inhibition;
paired stimuli; human
ID MOTOR CORTEX; BRAIN-STIMULATION; CORTICAL STIMULI; SILENT PERIOD;
POTENTIALS
AB Transcranial magnetic stimulation (TMS) causes the corticospinal system to become refractory to subsequent stimuli for up to 200 ms. We examined the phenomenon of paired pulse inhibition with TMS under conditions of rest, ongoing voluntary activation (isometric force generation), and at variable delays following activation (postactivation) of the wrist extensors of seven normal subjects, Paired stimuli were delivered to the motor cortex with a circular coil at 1.1 times motor evoked potential (MEP) threshold, with various interstimulus intervals. Voluntary activation caused a marked decrease in the variability of the ratio of the amplitude of the MEP evoked by the test pulse to that of the MEP evoked by the conditioning pulse. Marked inhibition of the MEP evoked by the test pulse was still present. Postactivation, however, caused a dramatic reversal of the inhibitory effect of the conditioning pulse in all subjects at interstimulus intervals ranging from 40 to 120 ms. This effect lasted for up to 10 s following the cessation of activation. MEPs to transcranial electrical stimulation were also inhibited by conditioning TMS, but postactivation did not reverse this inhibition, indicating that the reversal of paired pulse inhibition is intracortical. We conjecture that paired pulse inhibition reflects activity of inhibitory interneurons or inhibitory connections between cortical output cells that are inactivated in the postactivation state.
C1 NINCDS,NIH,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892.
RI Ikoma, Katsunori/D-8158-2012
NR 21
TC 120
Z9 121
U1 1
U2 9
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0014-4819
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD APR
PY 1996
VL 109
IS 1
BP 158
EP 163
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA UG931
UT WOS:A1996UG93100019
PM 8740220
ER
PT J
AU Heindel, JJ
Bates, HK
Price, CJ
Marr, MC
Myers, CB
Schwetz, BA
AF Heindel, JJ
Bates, HK
Price, CJ
Marr, MC
Myers, CB
Schwetz, BA
TI Developmental toxicity evaluation of sodium fluoride administered to
rats and rabbits in drinking water
SO FUNDAMENTAL AND APPLIED TOXICOLOGY
LA English
DT Article
ID ZERO DOSE CONTROL; ENAMEL FLUORIDE; ETHYLENE-GLYCOL; REPRODUCTION;
EXPOSURE; PLASMA; MICE; CORD
AB Sodium fluoride (NaF; Cas No. 7681-49-4) is used in fluoridating municipal water supplies, resulting in chronic exposure of millions of people worldwide. Because of a lack of pertinent developmental toxicity studies in the literature, sodium fluoride was administered ad libitum in deionized/filtered drinking water (to mimic human exposure) to Sprague-Dawley-derived rats (26/group) on Gestation Days (GD) 6 through 15 at levels of 0, 50, 150, or 300 ppm and New Zealand White rabbits (26/group) on GD 6 through 19 at levels of 0, 100, 200, or 400 ppm. Higher concentrations via drinking water were not practicable due to the poor palatability of sodium fluoride. Drinking water (vehicle) contained less than 0.6 ppm sodium fluoride (limit of detection) and sodium fluoride content of the feed was 12.4 ppm fluoride (rats) and 15.6 ppm fluoride (rabbits). Maternal food, water, body weights, and clinical signs were recorded at regular intervals throughout these studies. Animals were killed on GD 20 (rats) or 30 (rabbits) and examined for implant status, fetal weight, sex, and morphological development. In the high-dose group of both studies there was an initial decreased maternal body weight gain which recovered over time and a decreased water consumption-attributed to decreased palatability. No clear clinical signs of toxicity were observed. Maternal exposure to sodium fluoride during organogenesis did not significantly affect the frequency of postimplantation loss, mean fetal body weight/litter, or external, visceral or skeletal malformations in either the rat or the rabbit. The NOAEL for maternal toxicity was 150 ppm sodium fluoride in drinking water (similar to 18 mg/kg/day) for rats, and 200 ppm (similar to 18 mg/kg/day) for rabbits. The NOAEL for developmental toxicity was greater than or equal to 300 ppm sodium fluoride (similar to 27 mg/kg/day) for rats and greater than or equal to 400 ppm (similar to 29 mg/kg/day) for rabbits administered during organogenesis in drinking water. The total exposure to fluoride (mg F/kg body weight/day from food and drinking water combined) in the mid- and high-dose groups for both species was >100-fold higher than the range at 0.014-0.08 mg F/kg/day estimated for a 70-kg person from food and fluoridated (1 ppm) drinking water. (C) 1996 Society of Toxicology
C1 NIEHS, NATL TOXICOL PROGRAM, RES TRIANGLE PK, NC 27709 USA.
RP Heindel, JJ (reprint author), RES TRIANGLE INST, CTR LIFE SCI & TOXICOL, RES TRIANGLE PK, NC 27709 USA.
FU NIEHS NIH HHS [N01-ES-95255]
NR 56
TC 23
Z9 24
U1 2
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0272-0590
J9 FUND APPL TOXICOL
JI Fundam. Appl. Toxicol.
PD APR
PY 1996
VL 30
IS 2
BP 162
EP 177
DI 10.1006/faat.1996.0053
PG 16
WC Toxicology
SC Toxicology
GA UF098
UT WOS:A1996UF09800002
PM 8812262
ER
PT J
AU Zenilman, ME
Magnuson, TH
Swinson, K
Egan, J
Perfetti, R
Shuldiner, AR
AF Zenilman, ME
Magnuson, TH
Swinson, K
Egan, J
Perfetti, R
Shuldiner, AR
TI Pancreatic thread protein is mitogenic to pancreatic-derived cells in
culture
SO GASTROENTEROLOGY
LA English
DT Article
ID CHRONIC CALCIFYING PANCREATITIS; MESSENGER-RNA; STONE PROTEIN;
REGENERATING ISLETS; ENDOCRINE PANCREAS; EXPRESSION; SEQUENCE; EXOCRINE;
GENE; ACINAR
AB Background & Aims: Pancreatic thread proteins (PTPs) ave acinar cell products and members of the regenerating gene (reg) family. reg expression increases during islet regeneration, is depressed during aging-related islet dysfunction, and may be important in p-cell growth and maintenance. The aim of this study was to examine the genetic expression of reg in pancreatic-derived cells in vitro and the mitogenic effect of PTP/reg protein on these cells. Methods: reg gene expression was measured by Northern analysis in three rat pancreatic cell lines: ARIP (ductal), AR42J (acinar), and RIN (beta-cell). PTP/reg protein was isolated from bovine and human pancreas. Cells were cultured with PTP/reg for 72 hours, and thymidine incorporation was measured. Results: reg messenger RNA was detected in AR42J but not in ARIP or RIN. PTP/reg protein was mitogenic to RIN and ARIP in a dose-related fashion but not to AR42J. It was not mitogenic to cultured mature rat islets. Conclusions: reg messenger RNA is expressed in acinar but not in beta-cell or ductal pancreatic cell lines. PTP/reg protein was mitogenic to both beta-cell and ductal cell lines but not to mature, nondividing islets. This supports the hypothesis that PTP/reg protein is an acinar cell-derived mediator of beta-cell growth and may be involved in modulating the duct-to-islet axis.
C1 NIA,NIH,LAB CLIN PHYSIOL,BALTIMORE,MD 21224.
JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,BALTIMORE,MD 21205.
JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205.
NR 39
TC 58
Z9 59
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
19106-3399
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
BP 1208
EP 1214
DI 10.1053/gast.1996.v110.pm8613011
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UD846
UT WOS:A1996UD84600029
PM 8613011
ER
PT J
AU Carethers, JM
Koi, M
Chauhan, DP
Boland, CR
AF Carethers, JM
Koi, M
Chauhan, DP
Boland, CR
TI The human mismatch repair system recognizes the O-6-methylguanine
(O-6-meG) mispair after the first S phase to cause G2/M cell cycle
arrest
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA.
VAMC, SAN DIEGO, CA USA.
NIEHS, RES TRIANGLE PK, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A498
EP A498
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73701979
ER
PT J
AU Corleto, VD
Jensen, RT
Weber, HC
AF Corleto, VD
Jensen, RT
Weber, HC
TI Somatostatin receptor subtype expression in guinea pig colonic smooth
muscle cells.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A650
EP A650
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73702584
ER
PT J
AU Dickson, RC
Everhart, JE
AF Dickson, RC
Everhart, JE
TI Transmission of hepatitis B by transplantation of livers from donors
positive for antibody to hepatitis B core antigen.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIDDK, LIVER TRANSPLANTAT DATABASE, GAINESVILLE, FL USA.
UNIV FLORIDA, GAINESVILLE, FL 32611 USA.
NIDDKD, BETHESDA, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1182
EP A1182
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704706
ER
PT J
AU Everhart, JE
AF Everhart, JE
TI Incidence of self-reported peptic ulcer in the United States.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV NEW MEXICO, ALBUQUERQUE, NM 87131 USA.
NIDDKD, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A105
EP A105
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73700414
ER
PT J
AU Felley, CP
Saraga, E
Ambs, S
Friess, H
Diezi, J
Blum, AL
FelleyBosco, E
AF Felley, CP
Saraga, E
Ambs, S
Friess, H
Diezi, J
Blum, AL
FelleyBosco, E
TI Nitric oxide synthases and oxidant stress in human stomach cancer and
peritumoral tissue
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NATL CANC INST, BETHESDA, MD USA.
UNIV HOSP BERN, DEPT SURG, CH-3010 BERN, SWITZERLAND.
UNIV LAUSANNE HOSP, DEPT GASTROENTEROL & PATHOL, LAUSANNE, SWITZERLAND.
UNIV LAUSANNE, INST PHARMACOL & TOXICOL, CH-1015 LAUSANNE, SWITZERLAND.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A511
EP A511
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73702032
ER
PT J
AU Ferrin, LJ
CameriniOtero, RD
Fleischer, D
Tio, L
AF Ferrin, LJ
CameriniOtero, RD
Fleischer, D
Tio, L
TI An integrated approach to the rapid analysis of DNA rearrangements in GI
malignancies.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIDDK, GENET & BIOCHEM BRANCH, BETHESDA, MD USA.
GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC 20007 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1190
EP A1190
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704736
ER
PT J
AU Fuss, I
Kelsall, B
Strober, W
Neurath, M
AF Fuss, I
Kelsall, B
Strober, W
Neurath, M
TI TNBS-induced experimental granulomatous colitis in mice is abrogated by
the induction of TGF-beta mediated oral tolerance.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIH, MUCOSAL IMMUN SECT, BETHESDA, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A912
EP A912
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73703628
ER
PT J
AU Garcia, LJ
Rosado, JA
Tsuda, T
Jensen, RT
AF Garcia, LJ
Rosado, JA
Tsuda, T
Jensen, RT
TI Both low and high affinity CCK receptor states mediate CCK stimulation
of p125 focal adhesion kinase and paxillin tyrosine phosphorylation in
rat pancreatic acinar cells
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV EXTREMADURA, DEPT PHYSIOL, E-10080 CACERES, SPAIN.
NIDDK, NIH, DIGEST DIS BRANCH, BETHESDA, MD USA.
RI rosado, juan/H-3488-2015
OI rosado, juan/0000-0002-9749-2325
NR 0
TC 3
Z9 3
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A390
EP A390
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73701553
ER
PT J
AU Gibril, F
Termanini, B
Stewart, CA
Sutliff, VE
Jensen, RT
AF Gibril, F
Termanini, B
Stewart, CA
Sutliff, VE
Jensen, RT
TI Prospective study of the occurrence of metastases to bone in patients
with Zollinger-Ellison syndrome (ZES).
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1073
EP A1073
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704272
ER
PT J
AU Gibril, F
Fraker, DL
Alexander, HR
Termanini, B
Stewart, CA
Sutliff, VE
Jensen, RT
AF Gibril, F
Fraker, DL
Alexander, HR
Termanini, B
Stewart, CA
Sutliff, VE
Jensen, RT
TI Does the use of preoperative somatostatin receptor scintigraphy (SRS)
have an impact in improving postoperative cure rate in patients
undergoing surgery with Zollinger Ellison syndrome (ZES): A prospective
study
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NIH, BETHESDA, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A391
EP A391
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73701556
ER
PT J
AU Guo, YS
Evers, BM
Ives, K
Battey, JF
Thompson, JC
Townsend, CM
AF Guo, YS
Evers, BM
Ives, K
Battey, JF
Thompson, JC
Townsend, CM
TI Effect of transfection of gastrin releasing peptide-receptors (GRP-R) on
the expression of neurotensin receptors (NT-R) in BON cells.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UTMB, DEPT SURG, GALVESTON, TX USA.
NIDOCD, ROCKVILLE, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1076
EP A1076
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704286
ER
PT J
AU Harris, PR
Weber, HC
Wilcox, CM
Kawabata, S
Kiyono, H
Jensen, RT
Smith, PD
AF Harris, PR
Weber, HC
Wilcox, CM
Kawabata, S
Kiyono, H
Jensen, RT
Smith, PD
TI Cytokine profile in gastric tissue from patients with Helicobacter
pylori infection and Zollinger-Ellison syndrome by quantitative PCR.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV ALABAMA, DEPT PEDIAT, BIRMINGHAM, AL USA.
UNIV ALABAMA, DEPT MICROBIOL, BIRMINGHAM, AL 35294 USA.
UNIV ALABAMA, DEPT MED, BIRMINGHAM, AL 35294 USA.
NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A922
EP A922
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73703668
ER
PT J
AU Hirayama, T
Miyake, M
Wada, A
Nagata, H
Makiyama, K
Moss, J
Noda, M
AF Hirayama, T
Miyake, M
Wada, A
Nagata, H
Makiyama, K
Moss, J
Noda, M
TI ADP-ribosyltransferase activin of Helicobacter pylori
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NAGASAKI UNIV, INST TROP MED, DEPT BACTERIOL, NAGASAKI, JAPAN.
CHIBA UNIV, SCH MED, DEPT MICROBIOL 2, CHIBA 260, JAPAN.
NAGASAKI UNIV, SCH MED, DEPT MED 2, NAGASAKI, JAPAN.
NHLBI, PULM CRIT CARE MED BRANCH, NIH, BETHESDA, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A134
EP A134
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73700529
ER
PT J
AU Hong, MK
Montgomery, EA
Lewis, JH
Sobin, LH
Allegra, CJ
Johnston, PG
AF Hong, MK
Montgomery, EA
Lewis, JH
Sobin, LH
Allegra, CJ
Johnston, PG
TI Correlation of Ki-67 staining pattern, p53 staining, flow cytometry with
routine histologic assessment for dysplasia in Barrett's esophagus (BE)
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 GEORGETOWN UNIV, DEPT MED, WASHINGTON, DC USA.
GEORGETOWN UNIV, DEPT PATHOL, WASHINGTON, DC USA.
ARMED FORCES INST PATHOL, WASHINGTON, DC 20306 USA.
NCI, NMOB, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A531
EP A531
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73702110
ER
PT J
AU Jacoby, RF
Marshall, DJ
Newton, M
Tutsch, K
Cole, CE
Lubet, RA
Kelloff, GJ
Verma, A
Moser, AR
Dove, WF
AF Jacoby, RF
Marshall, DJ
Newton, M
Tutsch, K
Cole, CE
Lubet, RA
Kelloff, GJ
Verma, A
Moser, AR
Dove, WF
TI Chemoprevention of spontaneous intestinal adenomas in the Apc mutant Min
mouse model by the nonsteroidal anti-inflammatory drug piroxicam.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV WISCONSIN, DEPT MED, MADISON, WI 53706 USA.
UNIV WISCONSIN, DEPT BIOSTAT, MADISON, WI 53706 USA.
UNIV WISCONSIN, DEPT ONCOL, MADISON, WI 53706 USA.
UNIV WISCONSIN, DEPT GENET, MADISON, WI 53706 USA.
WM S MIDDLETON MEM VET HOSP, MADISON, WI USA.
NCI, DIV CANC PREVENT & CONTROL, CHEMOPREVENT BRANCH, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A535
EP A535
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73702127
ER
PT J
AU Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
AF Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
TI CCK-8 regulates the distribution of its own receptor affinity states in
COS cells transfected with the CCK-A receptor.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 ST LOUIS UNIV, ST LOUIS, MO 63104 USA.
NATL INST HLTH, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1085
EP A1085
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704321
ER
PT J
AU Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
AF Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
TI Differential biochemical regulation of CCK-A and CCK-B receptors is
accompanied by differential coupling of the receptors to signal
transduction mechanisms.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 ST LOUIS UNIV, ST LOUIS, MO 63104 USA.
NATL INST HLTH, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1085
EP A1085
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704320
ER
PT J
AU Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
AF Joshi, SN
Xu, ZQ
Wank, SA
Gardner, JD
TI CCK-8 activation of individual signal transduction mechanisms is
mediated by specific affinity states of the CCK-A receptor.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NATL INST HLTH, BETHESDA, MD 20892 USA.
ST LOUIS UNIV, ST LOUIS, MO 63104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1085
EP A1085
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704319
ER
PT J
AU Josovitz, KN
Holland, SM
Malech, HL
Lewis, JH
Gallin, JI
AF Josovitz, KN
Holland, SM
Malech, HL
Lewis, JH
Gallin, JI
TI Endoscopic findings in chronic granulomatous disease
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC 20007 USA.
NIAID, NIH, HOST DEF LAB, BETHESDA, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A933
EP A933
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73703715
ER
PT J
AU Josoyitz, KN
Herion, DW
Weber, HC
Lewis, JH
Hoofnagle, JH
AF Josoyitz, KN
Herion, DW
Weber, HC
Lewis, JH
Hoofnagle, JH
TI Prospective evaluation of routine endoscopy in patients with primary
biliary cirrhosis
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC USA.
NIDDK, LIVER DIS SECT, BETHESDA, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A1224
EP A1224
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73704873
ER
PT J
AU Krishnamurthy, S
Dayal, Y
Termanini, B
Gibril, F
Jensen, RT
AF Krishnamurthy, S
Dayal, Y
Termanini, B
Gibril, F
Jensen, RT
TI Correlation of gastric mucosal changes with disease activity and
treatment in patients with Zollinger-Ellison syndrome (ZES): A
prospective study
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 NEMCH, DEPT PATHOL, BOSTON, MA USA.
NIH, BETHESDA, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A162
EP A162
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73700644
ER
PT J
AU Kronenberg, SA
Hyde, TM
Mulberg, AE
AF Kronenberg, SA
Hyde, TM
Mulberg, AE
TI Expression of the cystic fibrosis transmembrane conductance regulator
mRNA in human hypothalamus.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 CHILDRENS HOSP PHILADELPHIA, DEPT PEDIAT, DIV PEDIAT GASTROENTEROL & NUTR, PHILADELPHIA, PA 19104 USA.
NIMH, CTR NEUROSCI, NIH, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A814
EP A814
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73703237
ER
PT J
AU Laghi, L
Chauhan, DP
Marra, G
Major, EO
Neel, JV
Boland, CR
AF Laghi, L
Chauhan, DP
Marra, G
Major, EO
Neel, JV
Boland, CR
TI Amplification of JC virus (JCV) sequences from human colorectal cancers.
SO GASTROENTEROLOGY
LA English
DT Meeting Abstract
C1 UNIV CALIF SAN DIEGO, LA JOLLA, CA 92093 USA.
NIH, BETHESDA, MD 20892 USA.
UNIV MICHIGAN, ANN ARBOR, MI USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD APR
PY 1996
VL 110
IS 4
SU S
BP A548
EP A548
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA UF737
UT WOS:A1996UF73702181
ER
EF