FN Thomson Reuters Web of Science™
VR 1.0
PT B
AU Fauci, AS
AF Fauci, AS
BE Knobler, SL
   Mahmoud, AAF
   Pray, LA
TI Role of research in countering bioterrorism
SO BIOLOGICAL THREATS AND TERRORISM, WORKSHOP SUMMARY: ASSESSING THE
   SCIENCE AND RESPONSE CAPABILITIES
LA English
DT Proceedings Paper
CT Workshop of the Forum on Emerging Infections
CY NOV 27-29, 2001
CL WASHINGTON, D.C.
SP US Dept Hlth & Human Serv, NIH, US FDA, US Dept Def, US Dept State, US Dept Vet Affairs, UDSA, Amer Soc Microbiol, Bristol Myers Squibb Co, Burroughs Wellcome Fund, Eli Lilly & Co, Pfizer, GlaxoSmithKline, Wyeth Ayerst Labs
C1 NIAID, Bethesda, MD 20892 USA.
RP Fauci, AS (reprint author), NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 0-309-08253-6
PY 2002
BP 22
EP 27
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA BW72M
UT WOS:000182974100002
ER

PT B
AU Nabel, GJ
AF Nabel, GJ
BE Knobler, SL
   Mahmoud, AAF
   Pray, LA
TI Applications of modern technology to emerging infections and disease
   development: A case study of Ebola virus
SO BIOLOGICAL THREATS AND TERRORISM, WORKSHOP SUMMARY: ASSESSING THE
   SCIENCE AND RESPONSE CAPABILITIES
LA English
DT Proceedings Paper
CT Workshop of the Forum on Emerging Infections
CY NOV 27-29, 2001
CL WASHINGTON, D.C.
SP US Dept Hlth & Human Serv, NIH, US FDA, US Dept Def, US Dept State, US Dept Vet Affairs, UDSA, Amer Soc Microbiol, Bristol Myers Squibb Co, Burroughs Wellcome Fund, Eli Lilly & Co, Pfizer, GlaxoSmithKline, Wyeth Ayerst Labs
C1 NIAID, Vaccine Res Ctr, Bethesda, MD USA.
RP Nabel, GJ (reprint author), NIAID, Vaccine Res Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 0-309-08253-6
PY 2002
BP 101
EP 105
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA BW72M
UT WOS:000182974100018
ER

PT J
AU Koh, CY
   Raziuddin, A
   Welniak, LA
   Blazar, BR
   Bennett, M
   Murphy, WJ
AF Koh, CY
   Raziuddin, A
   Welniak, LA
   Blazar, BR
   Bennett, M
   Murphy, WJ
TI NK inhibitory-receptor blockade for purging of leukemia: Effects on
   hematopoietic reconstitution
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE NK inhibitory-receptor blockade; hematopoietic reconstitution; bone
   marrow cells; BMT; leukemia; purging; LY49 inhibitory receptors;
   engraftment
ID NATURAL-KILLER-CELLS; BONE-MARROW TRANSPLANTATION; CLASS-I MOLECULES;
   BLOOD STEM-CELLS; RECOGNITION; PROGENITORS; INVOLVEMENT; INVITRO;
   LY-49D; BINDS
AB One of the obstacles of BMT that limits its efficacy is failure to eradicate the original tumor. The incidence of tumor relapse is particularly high after autologous BMT. Natural killer (NK) cells comprise various subsets that can express inhibitory receptors for MHC class I determinants. We have recently demonstrated that blockade of NW-cell inhibitory receptors can augment antitumor effects in vitro and in vivo. However, breakdown of tolerance and autoreactivity may occur as a result of the inhibition of NK-cell inactivation to self MHC determinants. We have utilized F(ab)2 fragments of monoclonal antibody, 5E6, against Ly49C/I inhibitory receptors, which are expressed on 35% to 60% of NK cells in H2(b) strains of mice and are specific for H2K(b), to investigate the effect of inhibitory-receptor blockade on syngeneic bone marrow cell (BMC) and tumor cell growth. We show that treatment of interleukin 2-activated C57BL/6 (B6, H2(b)) SCID-mouse NK cells with 5E6 F(ab')(2) fragments during 48-hour coculture resulted in autoreactivity against syngeneic BMCs as demonstrated by suppression of myeloid reconstitution on day 14 post-BMT. However, this suppressive effect was transient and normalized by day 21 post-BMT. In contrast, blockade of inhibitory receptors during 24-hour coculture had no adverse effects on myeloid reconstitution after BMT. Furthermore, under the same coculture conditions, NK cell-mediated purging of C 1498 leukemia cells contaminating syngeneic BMCs was more effective with inhibitory-receptor blockade, leading to a significantly higher proportion of animals with long-term survival compared to the control recipients. These results demonstrate that short-term in vitro blockade of inhibitory receptors can augment antitumor activity without long-term inhibitory effects on BMCs and thus may be of potential use in the purging of contaminating tumor cells prior to autologous BMT.
C1 SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA.
   NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Transplantat Biol Lab, Frederick, MD 21702 USA.
   Univ Minnesota, Ctr Canc, Div Bone Marrow Transplantat, Dept Pediat, Minneapolis, MN 55455 USA.
   Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75230 USA.
RP Murphy, WJ (reprint author), SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA.
RI Koh, Crystal/D-9986-2013
FU NCI NIH HHS [R01 CA 72669, CA 70134, N01-CO-56000]
NR 34
TC 20
Z9 21
U1 0
U2 0
PU CARDEN JENNINGS PUBL CO LTD
PI CHARLOTTESVILLE
PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PY 2002
VL 8
IS 1
BP 17
EP 25
DI 10.1053/bbmt.2002.v8.pm11846352
PG 9
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 517CV
UT WOS:000173594300003
PM 11846352
ER

PT J
AU Hixon, JA
   Anver, MR
   Blazar, BR
   Panoskaltsis-Mortari, A
   Wiltrout, RH
   Murphy, WJ
AF Hixon, JA
   Anver, MR
   Blazar, BR
   Panoskaltsis-Mortari, A
   Wiltrout, RH
   Murphy, WJ
TI Administration of either anti-CD40 or interleukin-12 following lethal
   total body irradiation induces acute lethal toxicity affecting the gut
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE antibodies; transplantation; cytokines; in vivo animal models
ID IFN-GAMMA; INFLAMMATORY RESPONSE; CD40-CD40 LIGAND; IL-12/PULSE IL-2;
   FACTOR RECEPTOR; CD40; CELLS; EXPRESSION; CARCINOMA; CYTOKINE
AB Interleukin (IL)-12 and antibodies against CD40 have demonstrated antitumor effects in a variety of in vivo model systems. However, both agents can also mediate significant toxicities either when used following lethal TBI or when administered in combination with other agents such as IL-2. In this study, we assessed the effects of anti-CD40 monoclonal antibody (MoAb) and IL-12 in lethally irradiated mice. Acute lethal toxicity was observed following the administration of either 10 mug anti-CD40 MoAb (FGK45) or 0.5 mug of recombinant murine (rm)IL-12 that resulted in 100% mortality of all mice within 4 to 6 days. Histological evaluation revealed destruction of the normal gut architecture in both anti-CD40 MoAb- and rmIL-12-treated mice. Analysis of serum cytokine levels in the lethally irradiated mice receiving anti-CD40 MoAb demonstrated a marked increase of interferon (IFN)-gamma and IL-12 p40, whereas mice receiving rmIL-12 demonstrated a marked increase of IFN-gamma. Lethally irradiated IL-12 p40 knock-out mice were resistant to anti-CD40-induced toxicity, suggesting that the lack of IL-12 p40 with no possibility of making functional IL-12 p70 is key for this toxic reaction. Similarly, lethally irradiated IFN-gamma knock-out mice were completely resistant to rmIL-12-induced toxicity, suggesting that IFN-gamma is a major player in IL-12-mediated toxicity. These results suggest that both anti-CD40 MoAb and rmIL-12 induce an acute fatal toxicity characterized by similar intestinal pathology and mediated in part by IFN-gamma.
C1 SAIC Frederick, NCI Frederick, Pathol Histotechnol Lab, Frederick, MD 21702 USA.
   Univ Minnesota, Ctr Canc, Dept Pediat, Div Bone Marrow Transplantat, Minneapolis, MN USA.
   NCI Frederick, Expt Immunol Lab, Frederick, MD USA.
RP Murphy, WJ (reprint author), SAIC Frederick, NCI Frederick, Pathol Histotechnol Lab, Bldg 567,Rm 210, Frederick, MD 21702 USA.
FU NCI NIH HHS [N01-CO-124000]; NHLBI NIH HHS [R37 HL56067, R01 HL63452];
   NIAID NIH HHS [R01 AI34495]
NR 28
TC 16
Z9 16
U1 0
U2 0
PU CARDEN JENNINGS PUBL CO LTD
PI CHARLOTTESVILLE
PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PY 2002
VL 8
IS 6
BP 316
EP 325
DI 10.1053/bbmt.2002.v8.pm12108917
PG 10
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 570LB
UT WOS:000176658800004
PM 12108917
ER

PT J
AU Grochow, LB
AF Grochow, LB
TI Parenteral busulfan: Is therapeutic monitoring still warranted?
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Editorial Material
ID BONE-MARROW TRANSPLANTATION; PHARMACOKINETICS; LEUKEMIA; DISEASE
C1 NCI, Invest Drug Branch, Rockville, MD USA.
RP Grochow, LB (reprint author), NCI, Invest Drug Branch, Rockville, MD USA.
NR 16
TC 8
Z9 15
U1 1
U2 4
PU CARDEN JENNINGS PUBL CO LTD
PI CHARLOTTESVILLE
PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PY 2002
VL 8
IS 9
BP 465
EP 467
DI 10.1053/bbmt.2002.v8.pm12374450
PG 3
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 599UR
UT WOS:000178354000001
PM 12374450
ER

PT J
AU Hennighausen, L
   Miyoshi, K
   Shillingford, J
   Nozawa, M
   Bierie, BW
   Renou, H
   Cui, K
   Shani, M
   Robinson, G
AF Hennighausen, L
   Miyoshi, K
   Shillingford, J
   Nozawa, M
   Bierie, BW
   Renou, H
   Cui, K
   Shani, M
   Robinson, G
TI Genetic pathways controlling cell specification and behavior in the
   mammary gland.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIDDKD, Lab Genet & Physiol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA PS2
BP 71
EP 71
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900007
ER

PT J
AU Parrott, EC
AF Parrott, EC
TI NICHD training and research initiatives in reproductive science.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Natl Inst Child Hlth & Human Dev, Ctr Populat Res, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA MA1
BP 74
EP 74
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900014
ER

PT J
AU Lewandoski, M
   Wilson, C
   Anderson, R
   Mishina, Y
   Williams, T
AF Lewandoski, M
   Wilson, C
   Anderson, R
   Mishina, Y
   Williams, T
TI Using conditional gene inactivation to study signaling pathways during
   limb development.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NCI, Ctr Canc Res, Canc & Dev Biol Lab, NIH, Frederick, MD USA.
   Natl Inst Environm Hlth Sci, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA M19
BP 83
EP 83
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900033
ER

PT J
AU Dean, J
AF Dean, J
TI Targeting oocyte-specific genes: The zona pellucida paradigm.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA M22
BP 84
EP 85
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900036
ER

PT J
AU Korach, KS
   Emmen, JM
   Walker, VB
   Hewitt, SC
   Yates, M
   Hall, JM
   Swope, DL
   Harrell, JC
   Couse, JF
AF Korach, KS
   Emmen, JM
   Walker, VB
   Hewitt, SC
   Yates, M
   Hall, JM
   Swope, DL
   Harrell, JC
   Couse, JF
TI Physiological activity and reproductive phenotypes of estrogen receptor
   knock-out mice.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIEHS, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA M25
BP 85
EP 86
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900039
ER

PT J
AU Couse, JF
   Yates, MM
   Walker, VR
   Korach, KS
AF Couse, JF
   Yates, MM
   Walker, VR
   Korach, KS
TI Characterization of the hypothalamic-pituitary-gonadal (HPG) axis in
   female estrogen receptor knockout mice.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Natl Inst Environm Hlth Sci, Lab Reprod & Dev Toxicol, Receptor Biol Sect, NIH, Res Triangle Pk, NC USA.
   Univ N Carolina, Dept Environm & Mol Toxicol, Raleigh, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 1
BP 98
EP 98
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900061
ER

PT J
AU Burns, KH
   Chen, L
   Haupt, B
   Korach, KS
   Matzuk, MM
AF Burns, KH
   Chen, L
   Haupt, B
   Korach, KS
   Matzuk, MM
TI Growth control in the mammalian gonads and adrenal glands.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA.
   Baylor Coll Med, Dept Mol & Human Genet, Houston, TX USA.
   Baylor Coll Med, Dept Cellular & Mol Biol, Houston, TX USA.
   Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA.
RI Burns, Kathleen/A-3360-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 5
BP 99
EP 100
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900065
ER

PT J
AU Sharan, SK
   Pyle, A
   Benedict, J
   Coppola, V
   Martin, BK
   Tessarollo, L
   Flaws, J
   Handel, MA
AF Sharan, SK
   Pyle, A
   Benedict, J
   Coppola, V
   Martin, BK
   Tessarollo, L
   Flaws, J
   Handel, MA
TI Partial complementation of Brca2 mutation in mice by the human BRCA2
   gene shows a sexually dimorphic meiotic phenotype.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Mouse Canc Genet Program, NCI, Frederick, MD USA.
   Univ Tennessee, Dept Biochem Cellular & Mol Biol, Knoxville, TN USA.
   Univ Baltimore, Dept Epidemiol & Prevent Med, Baltimore, MD USA.
RI Coppola, Vincenzo/E-2917-2011
OI Coppola, Vincenzo/0000-0001-6163-1779
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 27
BP 108
EP 109
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900087
ER

PT J
AU Hild, SA
   Attardi, BJ
   Blye, RP
   Reel, JR
AF Hild, SA
   Attardi, BJ
   Blye, RP
   Reel, JR
TI The ability of a gonadotropin-releasing hormone antagonist, acyline, to
   prevent irreversible infertility induced by the indenopyridine,
   CDB-4022, in adult male rats: The role of testosterone.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 BIOQUAL Inc, Rockville, MD USA.
   NICHD, Contracept & Reprod Hlth Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 105
BP 140
EP 141
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900165
ER

PT J
AU Li, XQ
   Ravindranath, N
   Chan, WY
   Manickam, P
   Dym, M
AF Li, XQ
   Ravindranath, N
   Chan, WY
   Manickam, P
   Dym, M
TI Microarray analysis of spermatogonial responsiveness to stem cell
   factor.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Georgetown Univ, Med Ctr, Dept Cell Biol, Washington, DC 20007 USA.
   NICHD, Lab Clin Genom, Sect Dev Genom, NIH, Bethesda, MD USA.
   NeuroLog Inc, Rockville, MD USA.
   Georgetown Univ, Med Ctr, Dept Pediat, Washington, DC 20007 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 107
BP 141
EP 141
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900167
ER

PT J
AU Miki, M
   Goulding, EH
   Willis, WD
   Bunch, DO
   Eddy, EM
   O'Brien, DA
AF Miki, M
   Goulding, EH
   Willis, WD
   Bunch, DO
   Eddy, EM
   O'Brien, DA
TI Glyceraldehyde 3-phosphate dehydrogenase-S, a germ cell-specific
   glycolytic enzyme, is required for sperm motility.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
   Univ N Carolina, Sch Med, Reprod Biol Lab, Dept Cell & Dev Biol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 173
BP 167
EP 168
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900232
ER

PT J
AU Jefferson, WN
   Couse, JF
   Padilla-Banks, E
   Korach, KS
   Newbold, RR
AF Jefferson, WN
   Couse, JF
   Padilla-Banks, E
   Korach, KS
   Newbold, RR
TI Neonatal exposure to genistein induces estrogen receptor (ER) alpha
   expression, and multi-oocyte follicles in the maturing mouse ovary:
   Evidence for ER beta and nonestrogenic actions.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA.
   NIEHS, Reprod & Dev Toxicol Lab, Receptor Mech Grp, Res Triangle Pk, NC 27709 USA.
   NIEHS, Mol Toxicol Lab, Dev Endocrinol Sect, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 227
BP 189
EP 190
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900286
ER

PT J
AU Walker, VR
   Couse, JF
   Yates, MM
   Korach, KS
AF Walker, VR
   Couse, JF
   Yates, MM
   Korach, KS
TI Evaluation of phase I metabolism of estradiol in estrogen receptor
   (ERKO) mice.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIEHS, Receptor Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 248
BP 197
EP 198
PG 2
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900307
ER

PT J
AU Tilli, MT
   Hruska, KS
   Frech, MS
   Korach, KS
   Lubahn, DB
   Flaws, JA
   Furth, PA
AF Tilli, MT
   Hruska, KS
   Frech, MS
   Korach, KS
   Lubahn, DB
   Flaws, JA
   Furth, PA
TI Characterization of transgenic mice with conditional over-expression of
   estrogen receptor alpha and rescue of reproductive phenotype of estrogen
   receptor a knockout mice.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Univ Maryland, Grad Program Human Genet, Baltimore, MD 21201 USA.
   Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
   Georgetown Univ, Vincent T Lombardi Canc Res Ctr, Washington, DC USA.
   USDA ARS, Beltsville Agr Res Ctr, ANRI, Gene Evaluat & Mapping Lab, Beltsville, MD 20705 USA.
   NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
   Univ Missouri, Dept Biochem, Columbia, MO USA.
   Univ Missouri, Dept Child Hlth, Columbia, MO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 367
BP 247
EP 247
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900426
ER

PT J
AU Brown, PR
   Miki, K
   Willis, WD
   Harper, DA
   Goulding, EH
   Eddy, EM
AF Brown, PR
   Miki, K
   Willis, WD
   Harper, DA
   Goulding, EH
   Eddy, EM
TI Sperm require the AKAP4 scaffold protein for flagellar function.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 NIEHS, Gamete Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 488
BP 296
EP 296
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900547
ER

PT J
AU Newbold, RR
   Padilla-Banks, E
   Jefferson, WN
AF Newbold, RR
   Padilla-Banks, E
   Jefferson, WN
TI Low doses of estrogenic chemicals like diethylstilbestrol (DES) during
   development result in permanent alterations in the reproductive tract.
SO BIOLOGY OF REPRODUCTION
LA English
DT Meeting Abstract
C1 Natl Inst Environm Hlth Sci, Mol Toxicol Lab, Dev Endocrinol Sect, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PY 2002
VL 66
SU 1
MA 543
BP 318
EP 318
PG 1
WC Reproductive Biology
SC Reproductive Biology
GA 568UD
UT WOS:000176561900602
ER

PT J
AU Dylewski, ML
   Mastro, AM
   Picciano, MF
AF Dylewski, ML
   Mastro, AM
   Picciano, MF
TI Maternal selenium nutrition and neonatal immune system development
SO BIOLOGY OF THE NEONATE
LA English
DT Article
DE maternal nutrition; selenium; pregnancy and lactation; neonatal immune
   function; immunodevelopment
ID BREAST-FED INFANTS; HUMAN-MILK; THIOREDOXIN REDUCTASE; SUPPLEMENTATION;
   INFECTION; LYMPHOCYTE; FORMULA; BLOOD; MICE
AB We evaluated the impact of dietary selenium intake on neonatal immune cell differentiation and function. A low selenium intake during pregnancy and lactation produced reductions in maternal plasma selenium (33%, p = 0.0001), milk selenium (36%, p = 0.001), and corresponding neonatal plasma selenium (47%, p = 0.008). Thymocytes from neonates receiving low-selenium milk showed an impaired activation in vitro (p = 0.001). The percentages of CD8 cytotoxic T cells (p = 0.03), CD2 T cells (p = 0.09), panB cells (= 0.02), and natural killer cells (p = 0.07) were all decreased in neonates nursed by mothers fed a low-selenium diet. The results indicate that maternal selenium intake impacts neonatal selenium status which in turn influences the neonatal immune system development. Copyright (C) 2002 S. Karger AG, Basel.
C1 Penn State Univ, Dept Nutr, University Pk, PA USA.
   Penn State Univ, Dept Biochem, University Pk, PA USA.
   Penn State Univ, Dept Mol Biol, University Pk, PA USA.
RP Picciano, MF (reprint author), NIH, Off Dietary Supplements, 31 Ctr Dr,Rm 1B29, Bethesda, MD 20892 USA.
OI Mastro, Andrea/0000-0003-2710-3360
NR 32
TC 14
Z9 18
U1 0
U2 3
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0006-3126
J9 BIOL NEONATE
JI Biol. Neonate
PY 2002
VL 82
IS 2
BP 122
EP 127
DI 10.1159/000063088
PG 6
WC Pediatrics
SC Pediatrics
GA 587FD
UT WOS:000177629100009
PM 12169835
ER

PT S
AU Sollers, JJ
   Ahern, GL
   Merritt, MM
   Thayer, JF
AF Sollers, JJ
   Ahern, GL
   Merritt, MM
   Thayer, JF
BE Sollers, JJ
   Thayer, JF
TI Time frequency analysis of the cardiovascular response during the
   intracarotid amobarbital test
SO BIOMEDICAL SCIENCES INSTRUMENTATION, VOL 38
SE BIOMEDICAL SCIENCES INSTRUMENTATION
LA English
DT Proceedings Paper
CT 39th Annual Rocky Mountain Bioengineering Symposium/39th International
   ISA Biomedical Sciences Instrumentation Symposium
CY APR 12-14, 2002
CL COPPER MT, CO
SP Instrumentat Syst & Automat Soc
DE cardiovascular control; WADA test; time-frequency analysis; vagal
   control; Wigner-Ville distribution
AB Recently, time-frequency analysis has become very popular for examining non-stationary time series and for researching fast changing phenomena. We used the smoothed-pseudo Wigner-Ville distribution to model the underlying dynamic autonomic nervous system changes during the intracarotid sodium amobarbital (ISA) or so-called Wada test. The Wada test involves injecting sodium amobarbitol into the internal carotid artery that results in inactivation of cerebral structures supplied by the ipsilateral anterior and middle cerebral arteries. Electrocardiogram (EKG) data were recorded during the entire procedure and the 10 minutes prior to each injection were used as baseline values for that hemisphere. Interbeat-interval time series were created from these data for a 13 year old patient and were examined using a smoothed-pseudo Wigner-Ville distribution. Inspection of these data indicated that sodium amobarbitol injection to either side produced decreased power in the vagally mediated high frequency band (.14-.40 Hz). Importantly, this decrease was greater when the right hemisphere was inactivated as compared to the left. These results are consistent with the known lateralized innervation of the heart such that right-sided autonomic inputs have greater influence on cardiac chronotropy. The present results also revealed the very rapid changes in autonomic control that characterized the inactivation and subsequent recovery of the cerebral hemispheres. These findings confirm the utility of time-frequency analysis in the investigation of cardiac time series.
C1 NIA, NIH, Baltimore, MD 21224 USA.
RP Sollers, JJ (reprint author), NIA, NIH, Baltimore, MD 21224 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU INSTRUMENT SOC AMER
PI RESEARCH TRIANGLE PARK
PA 67 ALEXANDER DR, PO BOX 12277, RESEARCH TRIANGLE PARK, NC 27709 USA
SN 0067-8856
BN 1-55617-787-9
J9 BIOMED SCI INSTRUM
PY 2002
VL 38
BP 267
EP 271
PG 5
WC Engineering, Biomedical; Instruments & Instrumentation
SC Engineering; Instruments & Instrumentation
GA BX29J
UT WOS:000184842900044
PM 12085614
ER

PT J
AU Zheng, G
AF Zheng, G
TI On the fisher information matrix in type II censored data from the
   exponentiated exponential family
SO BIOMETRICAL JOURNAL
LA English
DT Article
DE asymptotics; exponential distribution; fisher information; hazard
   function; maximum likelihood estimator; type II censoring
AB In this note, we express, in a general setting, the Fisher information matrix under Type II censoring in terms of the hazard function and then obtain the Fisher information matrix under Type II censoring as a single integral for the exponentiated exponential family, which can be easily evaluated. The Fisher information under Type II censoring can also be used to characterize the exponential distribution among the exponentiated exponential family.
C1 NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
NR 8
TC 25
Z9 26
U1 0
U2 3
PU AKADEMIE VERLAG GMBH
PI BERLIN
PA PALISADENSTR 40, D-10243 BERLIN, GERMANY
SN 0323-3847
J9 BIOMETRICAL J
JI Biom. J.
PY 2002
VL 44
IS 3
BP 353
EP 357
DI 10.1002/1521-4036(200204)44:3<353::AID-BIMJ353>3.0.CO;2-7
PG 5
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA 547VR
UT WOS:000175353600006
ER

PT J
AU Nam, JM
AF Nam, JM
TI Testing the intraclass version of kappa coeffcient of agreement with
   binary scale and sample size determination
SO BIOMETRICAL JOURNAL
LA English
DT Article
DE exact evaluation; kappa coefficient; power; sample size; score test
ID INTERVAL ESTIMATION
AB The intraclass version of kappa coefficient has been commonly applied as a measure of agreement for two ratings per subject with binary outcome in reliability studies. We present an efficient statistic for testing the strength of kappa agreement using likelihood scores, and derive asymptotic power and sample size formula. Exact evaluation shows that the score test is generally conservative and more powerful than a method based on a chi-square goodness-of-fit statistic (DONNER and ELIASZIW, 1992, Statistics in Medicine 11, 1511-1519). In particular, when the research question is one directional, the one-sided score test is substantially more powerful and the reduction in sample size is appreciable.
C1 NCI, Biostat Branch, DCEG, Bethesda, MD 20892 USA.
NR 17
TC 6
Z9 6
U1 0
U2 1
PU AKADEMIE VERLAG GMBH
PI BERLIN
PA PALISADENSTR 40, D-10243 BERLIN, GERMANY
SN 0323-3847
J9 BIOMETRICAL J
JI Biom. J.
PY 2002
VL 44
IS 5
BP 558
EP 570
DI 10.1002/1521-4036(200207)44:5<558::AID-BIMJ558>3.0.CO;2-5
PG 13
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA 577NE
UT WOS:000177066600003
ER

PT J
AU Troendle, JF
AF Troendle, JF
TI A likelihood ratio test for the nonparametric Behrens-Fisher problem
SO BIOMETRICAL JOURNAL
LA English
DT Article
DE lagrange multiplier; maximum likelihood; permutation; power; rank;
   simulation
ID SAMPLE
AB The nonparametric Behrens-Fisher hypothesis is the most appropriate null hypothesis for the two-sample comparison when one does not wish to make restrictive assumptions about possible distributions. In this paper, a numerical approach is described by which the likelihood ratio test can be calculated for the nonparametric Behrens-Fisher problem. The approach taken here effectively reduces the number of parameters in the score equations to one by using a recursive formula for the remaining parameters. The resulting single dimensional problem can be solved numerically. The power of the likelihood ratio test is compared by simulation to that of a generalized Wilcoxon test of Brunner and Munzel. The tests have similar power for all alternatives considered when a simulated null distribution is used to generate cutoff values for the tests. The methods are illustrated on data on shoulder pain from a clinical trial.
C1 NICHHD, Div Epidemiol Stat & Prevent Res, Biometry & Math Stat Branch, NIH, Bethesda, MD 20892 USA.
NR 8
TC 15
Z9 15
U1 0
U2 2
PU AKADEMIE VERLAG GMBH
PI BERLIN
PA PALISADENSTR 40, D-10243 BERLIN, GERMANY
SN 0323-3847
J9 BIOMETRICAL J
JI Biom. J.
PY 2002
VL 44
IS 7
BP 813
EP 824
DI 10.1002/1521-4036(200210)44:7<813::AID-BIMJ813>3.0.CO;2-A
PG 12
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA 611LQ
UT WOS:000179019200003
ER

PT J
AU Hsin, LW
   Tian, XR
   Webster, EL
   Coop, A
   Caldwell, TM
   Jacobson, AE
   Chrousos, GP
   Gold, PW
   Habib, KE
   Ayala, A
   Eckelman, WC
   Contoreggi, C
   Rice, KC
AF Hsin, LW
   Tian, XR
   Webster, EL
   Coop, A
   Caldwell, TM
   Jacobson, AE
   Chrousos, GP
   Gold, PW
   Habib, KE
   Ayala, A
   Eckelman, WC
   Contoreggi, C
   Rice, KC
TI CRHR1 receptor binding and lipophilicity of pyrrolopyrimidines,
   potential nonpeptide corticotropin-releasing hormone type 1 receptor
   antagonists
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
ID RAT-BRAIN; FUNCTIONAL EXPRESSION; CRF RECEPTOR; IN-VIVO; PITUITARY;
   CLONING; STRESS; SAUVAGINE; AFFINITY; DESIGN
AB A series of compounds related to N-butyl-N-ethyl[2,5,6-trimethyl-7-(2,4,6-trimethylphenyl)pyrrolo[2,3-d]pyrimidin-4-yl]amine (1, antalarmin, Fig. 1) have been prepared and evaluated for their CRHR1 binding affinity as the initial step in the development of selective high affinity hydrophilic nonpeptide corticotropin-releasing hormone type 1 receptor (CRHR1) antagonists. Calculated log P (Clog P) values were used to evaluate the rank order of hydrophilicity for these analogues. Introducing oxygenated functionalities (delta -hydroxy or bis-beta -ethereal) into 1 gave more hydrophilic compounds, which had good affinity for the receptor. Introducing an amino group or shortening the alkyl side chain was detrimental to CRHR1 affinity. The alcohol 4-[ethyl[2,5,6-trimethyl-7-(2,4,6-trimethylphenyl)pyrrolo[2,3-d pyrimidin-4-yl]amino]butan-1-ol (3), bearing a terminal hydroxyl group on an N-alkyl side-chain, showed the highest CRHR1 binding affinity among these compounds (K-i=0.68 nM), and is one of the highest affinity CRHR1 ligands known. Compounds 3-5, and 8, which are likely to be less lipophilic than 1, have high CRHR1 affinity and may be valuable probes to further study the CRH system. (C) 2001 Elsevier Science Ltd. All rights reserved.
C1 NIDDKD, Med Chem Lab, NIH, Bethesda, MD 20892 USA.
   NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA.
   NICHHD, Pediat Endocrinol Sect, PREB, NIH, Bethesda, MD 20892 USA.
   Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore, MD 21201 USA.
   NIH, PET Dept, Ctr Clin, Bethesda, MD 20892 USA.
   NIDA, Mol Neurobiol Unit, NIH, Baltimore, MD 21224 USA.
RP Rice, KC (reprint author), NIDDKD, Med Chem Lab, NIH, Bldg 8,Room B1-23,8 Ctr Dr MSC 0815, Bethesda, MD 20892 USA.
OI HSIN, LING-WEI/0000-0001-5018-4491
NR 48
TC 34
Z9 35
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD JAN
PY 2002
VL 10
IS 1
BP 175
EP 183
DI 10.1016/S0968-0896(01)00261-9
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
   Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 502HB
UT WOS:000172737000019
PM 11738619
ER

PT J
AU Gawrisch, K
   Eldho, NV
   Mathews, JS
   Lindsay, CC
AF Gawrisch, K
   Eldho, NV
   Mathews, JS
   Lindsay, CC
TI The order parameter profile of docosahexaenoic acid in 18 : 0-22 :
   6(d31) PC
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA, NIH, Rockville, MD 20852 USA.
   Martek Biosci Corp, Columbia, MD 21045 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 13
BP 3A
EP 3A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700015
ER

PT J
AU Polozov, IV
   Hines, KG
   Litman, BJ
   Gawrisch, K
AF Polozov, IV
   Hines, KG
   Litman, BJ
   Gawrisch, K
TI Magic angle spinning NMR reveals formation of gel phase domains upon
   cooling in retinal rod outer segment disk membranes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 17
BP 4A
EP 4A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700019
ER

PT J
AU Burgess, SA
   Walker, ML
   Wang, F
   Sellers, JR
   Knight, PJ
   Trinick, J
AF Burgess, SA
   Walker, ML
   Wang, F
   Sellers, JR
   Knight, PJ
   Trinick, J
TI The pre-power stroke conformation of myosin V
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Leeds, Sch Biomed Sci, Leeds LS2 9JT, W Yorkshire, England.
   NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 69
BP 15A
EP 15A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700071
ER

PT J
AU Jonas, EA
   Hickman, JA
   Zhang, J
   Ivanovska, I
   Basanez, G
   McCarthy, E
   Zimmerberg, J
   Hardwick, JM
   Kaczmarek, LK
AF Jonas, EA
   Hickman, JA
   Zhang, J
   Ivanovska, I
   Basanez, G
   McCarthy, E
   Zimmerberg, J
   Hardwick, JM
   Kaczmarek, LK
TI Actions of Bcl-2 family proteins on mitochondria in synaptic terminals
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Yale Univ, Sch Med, New Haven, CT USA.
   Inst Rech Servier, Paris, France.
   Johns Hopkins Univ, Baltimore, MD 21218 USA.
   NIH, Bethesda, MD 20892 USA.
   Wake Forest Univ, Winston Salem, NC 27109 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 102
BP 22A
EP 22A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700104
ER

PT J
AU Cohen, JA
   Hansen, PL
   Podgornik, R
   Parsegian, VA
AF Cohen, JA
   Hansen, PL
   Podgornik, R
   Parsegian, VA
TI Surface-grafted PEG polymers osmotically compressed between phospholipid
   multilayers obey brush scaling laws
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Pacific, Sch Dent, San Francisco, CA 94115 USA.
   NICHHD, NIH, LPSB, Bethesda, MD USA.
RI Podgornik, Rudolf/C-6209-2008
OI Podgornik, Rudolf/0000-0002-3855-4637
NR 0
TC 0
Z9 0
U1 1
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 154
BP 32A
EP 32A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700157
ER

PT J
AU Bakajin, O
   Schuler, B
   Lipman, EA
   Eaton, WA
AF Bakajin, O
   Schuler, B
   Lipman, EA
   Eaton, WA
TI Microfabricated mixer for time-resolved single molecule protein folding
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Lawrence Livermore Natl Lab, BSSL, Livermore, CA 94550 USA.
   NIH, Bethesda, MD 20892 USA.
RI Schuler, Benjamin/E-7342-2011
OI Schuler, Benjamin/0000-0002-5970-4251
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 220
BP 45A
EP 45A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700223
ER

PT J
AU Lipman, EA
   Bakajin, O
   Schuler, B
   Eaton, WA
AF Lipman, EA
   Bakajin, O
   Schuler, B
   Eaton, WA
TI Instrument calibration for single-molecule FRET measurements in a
   microfabricated laminar flow mixer
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Lawrence Livermore Natl Lab, Livermore, CA USA.
RI Schuler, Benjamin/E-7342-2011
OI Schuler, Benjamin/0000-0002-5970-4251
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 218
BP 45A
EP 45A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700221
ER

PT J
AU Dimitriadis, EK
   Horkay, F
   Bechara, K
   Chadwick, RS
AF Dimitriadis, EK
   Horkay, F
   Bechara, K
   Chadwick, RS
TI Issues concerning the measurement of elastic properties at microscopic
   scales with the AFM
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 OD, NIH, Bethesda, MD 20892 USA.
   NICHHD, NIH, Bethesda, MD 20892 USA.
   NIDCD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 4
U1 2
U2 11
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 277
BP 56A
EP 56A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700280
ER

PT J
AU Chen, YD
   Yan, B
   Rubin, RJ
AF Chen, YD
   Yan, B
   Rubin, RJ
TI Fluctuations and randomness of kinesin movement in a force-clamped
   motility assay are affected by the hydrodynamic parameters of the bead
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 304
BP 62A
EP 62A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700307
ER

PT J
AU Harms, GS
   Kahr, H
   Blab, GA
   Lommerse, PHM
   Zhang, ZG
   Cognet, L
   Ypey, DL
   Soldatov, NM
   Schmidt, T
   Romanin, C
AF Harms, GS
   Kahr, H
   Blab, GA
   Lommerse, PHM
   Zhang, ZG
   Cognet, L
   Ypey, DL
   Soldatov, NM
   Schmidt, T
   Romanin, C
TI Simultaneous FRET microscopy and whole-cell patch clamp monitor
   interactions of fluorescence labeled alpha(1C) and beta subunits of
   L-type Ca2+ channel
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 PNNL, Richland, WA 99352 USA.
   Univ Linz, Inst Biophys, Linz, Austria.
   Leiden Univ, NL-2333 CA Leiden, Netherlands.
   CNRS, CPMOH, F-33405 Talence, France.
   NIA, NIH, Baltimore, MD 21224 USA.
RI Blab, Gerhard/D-2275-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 499
BP 103A
EP 103A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700503
ER

PT J
AU Kobrinsky, E
   Schwartz, E
   Abernethy, DR
   Soldatov, NM
AF Kobrinsky, E
   Schwartz, E
   Abernethy, DR
   Soldatov, NM
TI FRET imaging of state-dependent rearrangements in alpha(1C) subunit of
   human Ca2+ channel
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 498
BP 103A
EP 103A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700502
ER

PT J
AU Soldatov, NM
AF Soldatov, NM
TI Annular determinant and critical components of Ca2+ channel slow
   inactivation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 504
BP 104A
EP 104A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700508
ER

PT J
AU Armstrong, DL
   Ho, MWY
   Erxleben, C
AF Armstrong, DL
   Ho, MWY
   Erxleben, C
TI Phosphorylation-dependence of dihydropyridine action on L-type calcium
   channels in a rat pituitary cell line, GH3
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 511
BP 105A
EP 105A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700515
ER

PT J
AU Roland, G
   Kepplinger, KJF
   Zhu, R
   Maulet, Y
   Groschner, K
   Soldatov, NM
   Hinterdorfer, P
   Romanin, C
AF Roland, G
   Kepplinger, KJF
   Zhu, R
   Maulet, Y
   Groschner, K
   Soldatov, NM
   Hinterdorfer, P
   Romanin, C
TI A combined approach of patch clamp and AFM for studying Ca2+-dependent
   inactivation of class C-type Ca2+ channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Linz, A-4040 Linz, Austria.
   INSERM, U464, F-13916 Marseille, France.
   Karl Franzens Univ Graz, A-8010 Graz, Austria.
   NIA, NIH, Baltimore, MD 21224 USA.
RI Hinterdorfer, Peter/C-4235-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 512
BP 105A
EP 106A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700516
ER

PT J
AU Kahr, H
   Schindl, R
   Groschner, K
   Soldatov, NM
   Romanin, C
AF Kahr, H
   Schindl, R
   Groschner, K
   Soldatov, NM
   Romanin, C
TI Effects of N- and C-terminal lobe of calmodulin on Ca2+-dependent
   inactivation of Cav1.2 channel
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Linz, Inst Biophys, A-4040 Linz, Austria.
   Graz Univ, A-8010 Graz, Austria.
   NIA, NIH, Bethesda, MD 20892 USA.
RI Schindl, Rainer/E-3959-2013
OI Schindl, Rainer/0000-0003-0896-8887
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 514
BP 106A
EP 106A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700518
ER

PT J
AU Mukerji, I
   Augustyn, K
   Wojtuszewski, K
   Hawkins, ME
AF Mukerji, I
   Augustyn, K
   Wojtuszewski, K
   Hawkins, ME
TI Examination of A-tract bending using a fluorescent adenosine analogue
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Wesleyan Univ, Middletown, CT 06459 USA.
   NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 618
BP 127A
EP 127A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700622
ER

PT J
AU Kempner, ES
   Anchordoquy, TJ
   Sluis-Cremer, N
   Parniak, M
AF Kempner, ES
   Anchordoquy, TJ
   Sluis-Cremer, N
   Parniak, M
TI Radiation target analysis of DNA structure
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Univ Colorado, Boulder, CO 80309 USA.
   Univ Pittsburgh, Pittsburgh, PA 15260 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 623
BP 128A
EP 128A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700627
ER

PT J
AU Eldho, NV
   Mathews, JS
   Gawrisch, K
AF Eldho, NV
   Mathews, JS
   Gawrisch, K
TI The influence of docosahexaenoic acid-to-docosapentaenoic acid
   replacement on membrane properties
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 738
BP 151A
EP 152A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700745
ER

PT J
AU Teague, WE
   Fuller, NL
   Rand, RP
   Gawrisch, K
   Sternin, E
AF Teague, WE
   Fuller, NL
   Rand, RP
   Gawrisch, K
   Sternin, E
TI Membrane curvature elasticity of
   1-steroyl-2-docoahexaenoyl-SN-glycero-3-phosphoethanolamine monolayers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA, NIH, LMBB, Rockville, MD 20852 USA.
   Brock Univ, St Catharines, ON L2S 3A1, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 737
BP 151A
EP 151A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700744
ER

PT J
AU Petrache, HI
   Brown, MF
AF Petrache, HI
   Brown, MF
TI Universal features of acyl chain packing in fluid lipid bilayers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Lab Phys & Struct Biol, Bethesda, MD 20892 USA.
   Univ Arizona, Dept Chem, Tucson, AZ 85721 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 741
BP 152A
EP 152A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700748
ER

PT J
AU Niu, SL
   Litman, BJ
AF Niu, SL
   Litman, BJ
TI Lipid dependence of membrane cholesterol partitioning: A direct probe to
   differential cholesterol-lipid interactions
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 745
BP 153A
EP 153A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700752
ER

PT J
AU Tokumasu, F
   Jin, AJ
   Feigenson, GW
   Dvorak, JA
AF Tokumasu, F
   Jin, AJ
   Feigenson, GW
   Dvorak, JA
TI Nanoscopic lipid domain dynamics revealed by Atomic Force Microscopy.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Cornell Univ, Ithaca, NY 14853 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 763
BP 157A
EP 157A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700770
ER

PT J
AU Rostovtseva, TK
   Nestorovich, EM
   Bezrukov, SM
AF Rostovtseva, TK
   Nestorovich, EM
   Bezrukov, SM
TI Partitioning of differently sized poly(ethylene glycol)s into OmpF porin
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID MATRIX PROTEIN PORIN; COLI OUTER MEMBRANES; SINGLE-ION CHANNEL;
   ESCHERICHIA-COLI; FUNCTIONAL-CHARACTERIZATION; TRANSMEMBRANE CHANNELS;
   BACTERIAL PORINS; LIPID BILAYERS; CONDUCTANCE; POLYMER
AB To understand the physics of polymer equilibrium and dynamics in the confines of ion channel pores, we study partitioning of poly(ethylene glycol)s (PEGs) of different molecular weights into the bacterial porin, OmpF. Thermodynamic and kinetic parameters of partitioning are deduced from the effects of polymer addition on ion currents through single OmpF channels reconstituted into planar lipid bilayer membranes. The equilibrium partition coefficient is inferred from the average reduction of channel conductance in the presence of PEG; rates of polymer exchange between the pore and the bulk are estimated from PEG-induced conductance noise. Partition coefficient as a function of polymer weight is best fitted by a "compressed exponential" with the compression factor of 1.65. This finding demonstrates that PEG partitioning into the OmpF channel pore has sharper dependence on polymer molecular weight than predictions of hard-sphere, random-flight, or scaling models. A 1360-Da polymer separates regimes of partitioning and exclusion. Comparison of its characteristic size with the size of a 2200-Da polymer previously found to separate these regimes for the alpha-toxin shows good agreement with the x-ray structural data for these channels. The PEG-induced conductance noise is compatible with the polymer mobility reduced inside the OmpF pore by an order of magnitude relatively to its value in bulk solution.
C1 NICHHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA.
   Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
   St Petersburg Nucl Phys Inst, Gatchina 188350, Russia.
RP Bezrukov, SM (reprint author), NICHHD, Lab Phys & Struct Biol, NIH, Bldg 9,Room 1E-122, Bethesda, MD 20892 USA.
NR 63
TC 84
Z9 86
U1 1
U2 8
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
BP 160
EP 169
PG 10
WC Biophysics
SC Biophysics
GA 511DZ
UT WOS:000173250500016
PM 11751305
ER

PT J
AU Davies, DR
AF Davies, DR
TI The sructure of the nitrogen regulatory fragment of the yeast prion
   protein Ure2p
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 827
BP 169A
EP 169A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700834
ER

PT J
AU Steven, AC
   Ortega, J
   Ishikawa, T
   Lee, H
   Maurizi, MR
AF Steven, AC
   Ortega, J
   Ishikawa, T
   Lee, H
   Maurizi, MR
TI Protein-swallowing proteins: Internalization of substrates by
   energy-dependent proteases
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAMS, NIH, Bethesda, MD 20892 USA.
   NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 871
BP 178A
EP 178A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700878
ER

PT J
AU Cui, CH
   Mayer, ML
AF Cui, CH
   Mayer, ML
TI A glutamate receptor gated by pH and Ca2+
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
RI Mayer, Mark/H-5500-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 888
BP 182A
EP 182A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700895
ER

PT J
AU Horning, M
   Sun, Y
   Olson, R
   Mayer, ML
   Gouaux, E
AF Horning, M
   Sun, Y
   Olson, R
   Mayer, ML
   Gouaux, E
TI Molecular mechanism of glutamate receptor desensitization
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Columbia Univ, Howard Hughes Med Inst, New York, NY 10032 USA.
RI Mayer, Mark/H-5500-2013
NR 0
TC 0
Z9 0
U1 1
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 889
BP 182A
EP 182A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700896
ER

PT J
AU Le Grice, SFJ
   Budihas, SR
   Kvaratskhelia, M
AF Le Grice, SFJ
   Budihas, SR
   Kvaratskhelia, M
TI Pre-existing distortions in nucleic acid structure aid polypurine tract
   selection by HIV-1 reverse transcriptase
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 908
BP 186A
EP 186A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700915
ER

PT J
AU Kullman, L
   Winterhalter, M
   Bezrukov, SM
AF Kullman, L
   Winterhalter, M
   Bezrukov, SM
TI Sugar transport through maltoporin as time-resolved single molecule
   events
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
   CNRS, IPBS, Toulouse, France.
NR 0
TC 5
Z9 5
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 914
BP 187A
EP 187A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700921
ER

PT J
AU Nestorovich, EM
   Rostovtseva, TK
   Bezrukov, SM
AF Nestorovich, EM
   Rostovtseva, TK
   Bezrukov, SM
TI Residue protonation, transport properties, and structural stability of
   OmpF channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
   Univ Maryland, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 2
U2 5
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 915
BP 187A
EP 187A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700922
ER

PT J
AU Tycko, R
   Petkova, A
   Oyler, N
   Chan, CC
   Balbach, J
AF Tycko, R
   Petkova, A
   Oyler, N
   Chan, CC
   Balbach, J
TI Probing the molecular structure of amyloid fibrils with solid state NMR
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 913
BP 187A
EP 187A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700920
ER

PT J
AU Krasilnikov, OV
   Bezrukov, SM
AF Krasilnikov, OV
   Bezrukov, SM
TI Polymer partitioning into a protein cavity modified by solution
   non-ideality
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
   Univ Pernambuco, Recife, Brazil.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 921
BP 188A
EP 188A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700928
ER

PT J
AU Rostovtseva, TK
   Komarov, A
   Bezrukov, SM
   Colombini, M
AF Rostovtseva, TK
   Komarov, A
   Bezrukov, SM
   Colombini, M
TI Dymamics of nucleotides in VDAC channels: Structure-specific noise
   generation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
   NICHHD, NIH, Bethesda, MD USA.
RI Colombini, Marco/A-1540-2014
NR 0
TC 2
Z9 2
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 920
BP 188A
EP 188A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700927
ER

PT J
AU Adhikari, BB
   Dagan, T
   Adelstein, RS
   Wang, K
AF Adhikari, BB
   Dagan, T
   Adelstein, RS
   Wang, K
TI Increased sensitivity of Ca2+ activation of isometric atpase and tension
   in cytoplasmic myosin II-B depleted mice cardiac papillary muscle fibers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAMS, Muscle Biol Lab, NIH, Bethesda, MD 20892 USA.
   NHLBI, Lab Mol Cardiol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 927
BP 190A
EP 190A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252700934
ER

PT J
AU Rostovtseva, TK
   Komarov, A
   Bezrukov, SM
   Colombini, M
AF Rostovtseva, TK
   Komarov, A
   Bezrukov, SM
   Colombini, M
TI Dynamics of Nucleotides in VDAC channels: Structure-specific noise
   generation
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID MITOCHONDRIAL OUTER-MEMBRANE; ION-CHANNEL; ESCHERICHIA-COLI;
   POLYNUCLEOTIDE MOLECULES; ADENINE-NUCLEOTIDES; INTERMEMBRANE SPACE;
   NEUROSPORA-CRASSA; PORE; FLUCTUATIONS; TRANSPORT
AB Nucleotide penetration into the voltage-dependent mitochondrial ion channel (VDAC) reduces single-channel conductance and generates excess current noise through a fully open channel. VDAC channels were reconstituted into planar phospholipid membranes bathed in 1.0 M NaCl. At a given nucleotide concentration, the average decrease in small-ion channel conductance induced by mononucleotides ATP, ADP, AMP, and UTP and dinucleotides beta- and alpha-NADH, NAD, and NADPH are very close. However, the excess current noise is about seven times higher in the presence of NADPH than in the presence of ATP and is about 40 times higher than in the presence of UTP. The nucleotide-generated low-frequency noise obeys the following sequence: beta-NADPH > beta-NADH = alpha-NADH > ATP > ADP > beta-NAD greater than or equal to AMP > UTP. Measurements of bulk-phase diffusion coefficients and of the effective charge of the nucleotides in 1.0 M NaCl suggest that differences in size and charge cannot be the major factors responsible for the ability to generate current noise. Thus, although the ability of nucleotides to partition into the channel's pore, as assessed by the reduction in conductance, is very similar, the ability to generate current noise involves a detailed recognition of the three-dimensional structure of the nucleotide by the VDAC channel. A possible mechanism for this selectivity is two noise-generating processes operating in parallel.
C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
   NICHHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA.
   St Petersburg Nucl Phys Inst, Gatchina 188350, Russia.
RP Colombini, M (reprint author), Univ Maryland, Dept Zool, Cell Biol Lab, College Pk, MD 20742 USA.
RI Colombini, Marco/A-1540-2014
NR 56
TC 55
Z9 56
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
BP 193
EP 205
PG 13
WC Biophysics
SC Biophysics
GA 511DZ
UT WOS:000173250500019
PM 11751308
ER

PT J
AU Erxleben, C
   Everhart, A
   Florance, H
   Shipston, M
   Rossie, S
   Armstrong, DL
AF Erxleben, C
   Everhart, A
   Florance, H
   Shipston, M
   Rossie, S
   Armstrong, DL
TI Full length KCNMA1 channels cannot make heads and tails with STREX
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
   Univ Edinburgh, Sch Med, Edinburgh EH8 9YL, Midlothian, Scotland.
   Purdue Univ, W Lafayette, IN 47907 USA.
RI Shipston, Mike/C-7309-2013
OI Shipston, Mike/0000-0001-7544-582X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 997
BP 204A
EP 204A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701004
ER

PT J
AU Del Negro, CA
   Wilson, CG
   Butera, RJ
   Rigatto, H
   Smith, JC
AF Del Negro, CA
   Wilson, CG
   Butera, RJ
   Rigatto, H
   Smith, JC
TI Periodicity, mixed-mode oscillations, and quasiperiodicity in a
   rhythm-generating neural network
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID PRE-BOTZINGER COMPLEX; RESPIRATORY RHYTHM; PACEMAKER NEURONS;
   PREBOTZINGER COMPLEX; COUPLED BURSTERS; CHEMICAL-SYSTEM; PATTERNS;
   MODULATION; DYNAMICS; MAMMALS
AB We studied patterns of oscillatory neural activity in the network that generates respiratory rhythm in mammals. When isolated in vitro, this network spontaneously generates an inspiratory-related motor rhythm, with stable amplitude from cycle to cycle. We show that progressively elevating neuronal excitability in vitro causes periodic modulation of this inspiratory rhythm, evoking (in order): mixed-mode oscillations, quasiperiodicity, and ultimately disorganized aperiodic activity. Thus, the respiratory network oscillator follows a well defined sequence of behavioral states characterized by dynamical systems theory, which includes discrete stages of periodic and quasiperiodic amplitude modulation and progresses (according to theory) to aperiodic chaos-like behavior. We also observed periodic, mixed-mode periodic, and quasiperiodic breathing patterns in neonatal rodents and human infants in vivo, suggesting that breathing patterns generated by the intact nervous system reflect deterministic neural activity patterns in the underlying rhythm-generating network.
C1 NINCDS, Cellular & Syst Neurobiol Sect, Neural Control Lab, NIH, Bethesda, MD 20892 USA.
   Georgia Inst Technol, Lab Neuroengn, Atlanta, GA 30332 USA.
   Univ Manitoba, Dept Pediat, Winnipeg, MB R3T 2N2, Canada.
   Univ Manitoba, Dept Physiol, Winnipeg, MB R3T 2N2, Canada.
RP Smith, JC (reprint author), NINCDS, Cellular & Syst Neurobiol Sect, Neural Control Lab, NIH, 49 Convent Dr,MSC 4455, Bethesda, MD 20892 USA.
RI Del Negro, Ciro/K-3451-2013; 
OI Butera, Robert/0000-0002-1806-0621
NR 35
TC 53
Z9 54
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
BP 206
EP 214
PG 9
WC Biophysics
SC Biophysics
GA 511DZ
UT WOS:000173250500020
PM 11751309
ER

PT J
AU Komarov, A
   Rostovtseva, T
   Bezrukov, SM
   Colombini, M
AF Komarov, A
   Rostovtseva, T
   Bezrukov, SM
   Colombini, M
TI VDAC channel differentiates between natural metabolites and synthetic
   molecules
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
   NICHHD, NIH, Bethesda, MD USA.
RI Colombini, Marco/A-1540-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1007
BP 206A
EP 207A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701015
ER

PT J
AU Storey, NM
   Gomez-Angelats, M
   Cidlowski, JA
   Armstrong, DL
AF Storey, NM
   Gomez-Angelats, M
   Cidlowski, JA
   Armstrong, DL
TI Activation of potassium channels in Fas-induced apoptosis of Jurkat
   cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1065
BP 219A
EP 219A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701076
ER

PT J
AU Chang, TH
   Swartz, KJ
AF Chang, TH
   Swartz, KJ
TI Cross-linking approaches to examining the interaction between
   voltage-sensing and pore domains in voltage-gated K+ channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS, NIH, Mol Physiol & Biophys Unit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1130
BP 233A
EP 233A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701143
ER

PT J
AU Soler-Llavina, GJ
   Swartz, KJ
AF Soler-Llavina, GJ
   Swartz, KJ
TI Hot spots at the interface between voltage-sensing and pore domains in a
   voltage-gated K channel
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS, NIH, Mol Physiol & Biophys Unit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1131
BP 233A
EP 233A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701144
ER

PT J
AU Sukhareva, M
   Hackos, DH
   Swartz, K
AF Sukhareva, M
   Hackos, DH
   Swartz, K
TI Unitary properties of Shaker K+ channels with mutation in the
   cytoplasmic gate
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1137
BP 234A
EP 234A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701150
ER

PT J
AU Chen, J
   Fananapazir, L
   Sanguinetti, MC
AF Chen, J
   Fananapazir, L
   Sanguinetti, MC
TI Mink variants associated with hypertrophic cardiomyopathy reduce IKs
   function
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Utah, Salt Lake City, UT 84112 USA.
   NHLBI, NIH, Inherited Cardiac Dis Sect, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1157B
BP 239A
EP 239A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701172
ER

PT J
AU Ospeck, MC
   Dong, XX
   Iwasa, KH
AF Ospeck, MC
   Dong, XX
   Iwasa, KH
TI RC time constant paradox of outer hair cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIDCD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1215
BP 251A
EP 251A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701231
ER

PT J
AU Li-Smerin, YY
   Swartz, KJ
AF Li-Smerin, YY
   Swartz, KJ
TI Expression of voltage-gated K+ channels in yeast
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS, Mol Physiol & Biophys Unit, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1229
BP 254A
EP 254A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701245
ER

PT J
AU Sun, Y
   Horning, M
   Olson, R
   Mayer, ML
   Gouaux, E
AF Sun, Y
   Horning, M
   Olson, R
   Mayer, ML
   Gouaux, E
TI Structure of the GluR2 ligand-binding core reveals possible mechanism
   for receptor desensitization
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Columbia Univ, Howard Hughes Med Inst, New York, NY 10032 USA.
   NIH, Bethesda, MD 20892 USA.
RI Mayer, Mark/H-5500-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1238
BP 256A
EP 256A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701254
ER

PT J
AU Froehlich, JP
   Fedorova, O
   Bagrov, A
   Albers, RW
AF Froehlich, JP
   Fedorova, O
   Bagrov, A
   Albers, RW
TI Ligand binding site heterogeneity in Na,K-ATPase revealed by the
   inhibition patterns produced by cardioactive steroids
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, NIH, Baltimore, MD 21224 USA.
   NINCDS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1271
BP 263A
EP 263A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701288
ER

PT J
AU Froehlich, JP
   Mahaney, JE
   Kutchai, HC
   Jones, LR
   Southall, J
   Albers, RW
AF Froehlich, JP
   Mahaney, JE
   Kutchai, HC
   Jones, LR
   Southall, J
   Albers, RW
TI Cardiac Ca-ATPase (SERCA2a) expressed without phospholamban (PLB)
   behaves like SERCA1 with respect to interactions with ATP and ADP in
   transient kinetic experiments
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, NIH, Baltimore, MD 21224 USA.
   W Virginia Univ, Morgantown, WV 26506 USA.
   Univ Virginia, Charlottesville, VA 22903 USA.
   Indiana Univ, Sch Med, Indianapolis, IN 46202 USA.
   NINCDS, NIH, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1275
BP 264A
EP 264A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701292
ER

PT J
AU Anishkin, A
   Gendel, V
   Betanzos, M
   Guy, HR
   Sukharev, S
AF Anishkin, A
   Gendel, V
   Betanzos, M
   Guy, HR
   Sukharev, S
TI On the conformation of the C-terminal domain of the large
   mechanosensitive channel MscL
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Maryland, College Pk, MD 20742 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1304
BP 269A
EP 270A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701320
ER

PT J
AU Betanzos, M
   Chiang, CS
   Guy, HR
   Sukharev, S
AF Betanzos, M
   Chiang, CS
   Guy, HR
   Sukharev, S
TI A large iris-like expansion of MscL protein induced by membrane tension
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Maryland, College Pk, MD 20742 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1300
BP 269A
EP 269A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701316
ER

PT J
AU Woo, SH
   Soldatov, N
   Morad, M
AF Woo, SH
   Soldatov, N
   Morad, M
TI Modulation of spontaneous sparks by fragments of C-terminal tail of
   cardiac Ca2+ channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Georgetown Univ, Washington, DC 20007 USA.
   NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1362
BP 281A
EP 282A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701378
ER

PT J
AU Smith, GD
   Dai, LX
   Miura, RM
   Sherman, A
AF Smith, GD
   Dai, LX
   Miura, RM
   Sherman, A
TI Asymptotic analysis of buffered calcium diffusion near a point source
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Coll William & Mary, Dept Appl Sci, Williamsburg, VA 23197 USA.
   NIDDK, Math Res Branch, NIH, Bethesda, MD 20892 USA.
   New Jersey Inst Technol, Dept Math Sci, Newark, NJ 07102 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1366
BP 282A
EP 282A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701382
ER

PT J
AU Dimitrova, MN
   Szczepanowski, RH
   Ruvinov, SB
   Peterkofsky, A
   Ginsburg, A
AF Dimitrova, MN
   Szczepanowski, RH
   Ruvinov, SB
   Peterkofsky, A
   Ginsburg, A
TI Inter-domain interaction and substrate coupling effects on dimerization
   and conformational stability of enzyme I of the E-coli PEP : sugar
   phosphotransferase system (PTS)
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1429
BP 295A
EP 295A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701445
ER

PT J
AU Henry, ER
   Munoz, V
   Eaton, WA
AF Henry, ER
   Munoz, V
   Eaton, WA
TI Combinatorial modeling of protein folding kinetics.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1466
BP 303A
EP 303A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701482
ER

PT J
AU Schuler, B
   Lipman, EA
   Bakajin, O
   Eaton, WA
AF Schuler, B
   Lipman, EA
   Bakajin, O
   Eaton, WA
TI Single molecule fluorescence studies of protein folding equilibrium and
   kinetics
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Lawrence Livermore Natl Lab, BSSL, Livermore, CA 94550 USA.
RI Schuler, Benjamin/E-7342-2011
OI Schuler, Benjamin/0000-0002-5970-4251
NR 0
TC 0
Z9 0
U1 0
U2 4
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
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MA 1471
BP 304A
EP 304A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701487
ER

PT J
AU Lapidus, LJ
   Steinbach, PJ
   Szabo, A
   Eaton, WA
   Hofrichter, J
AF Lapidus, LJ
   Steinbach, PJ
   Szabo, A
   Eaton, WA
   Hofrichter, J
TI Dynamics of loop formation in disordered polypeptides
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1505
BP 311A
EP 311A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701522
ER

PT J
AU Han, MK
   Lin, P
   Harvey, JJ
   Knutson, JR
AF Han, MK
   Lin, P
   Harvey, JJ
   Knutson, JR
TI Fluoresecnce studies of pyrene maleimide labeled translin
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Georgetown Univ, Washington, DC 20057 USA.
   Natl Inst Hlth, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1514
BP 312A
EP 312A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701531
ER

PT J
AU Keskin, O
   Ji, XH
   Blaszczyk, J
   Covell, DG
AF Keskin, O
   Ji, XH
   Blaszczyk, J
   Covell, DG
TI Ligand binding introduses fluctuation changes in the pyrophosphokinases
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Koc Univ, TR-80910 Istanbul, Turkey.
   NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1549
BP 319A
EP 319A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701566
ER

PT J
AU Gomara, DZ
   Ma, BY
   Nussinov, R
AF Gomara, DZ
   Ma, BY
   Nussinov, R
TI Structural studies of human islet amyloid peptide: Structural models
   based on molecular dinamics simulations
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Frederick, MD 21702 USA.
   Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1553
BP 320A
EP 320A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701570
ER

PT J
AU Gordon, DJ
   Tycko, R
   Meredith, SC
AF Gordon, DJ
   Tycko, R
   Meredith, SC
TI Increasing the amphiphilicity of an amyloidgenic peptide changes the
   beta-strand orientation in the fibril from antiparallel to parallel
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Chicago, Chicago, IL 60637 USA.
   Natl Inst Hlth, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1551
BP 320A
EP 320A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701568
ER

PT J
AU Petkova, AT
   Ishii, Y
   Tycko, R
AF Petkova, AT
   Ishii, Y
   Tycko, R
TI Probing the structure of Alzheimer's beta amyloid fibrils by
   two-dimensional C-13-C-13 and C-13-N-15 solid state NMR methods
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK, Natl Inst Hlth, Chem Phys Lab, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 1
U2 3
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1552
BP 320A
EP 320A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701569
ER

PT J
AU Forster, K
   Groner, F
   Goitzsch, S
   Birnbaumer, L
   Koch, WJ
   Herzig, S
AF Forster, K
   Groner, F
   Goitzsch, S
   Birnbaumer, L
   Koch, WJ
   Herzig, S
TI G-protein Gi-alpha 2 exerts chronic protective effects in cardiac beta
   2-adrenoceptor transgenic mice
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Cologne, D-5000 Cologne 41, Germany.
   NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
   Duke Univ, Durham, NC 27706 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1689
BP 347A
EP 348A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701706
ER

PT J
AU Gu, J
   Xu, SG
   Yu, LPC
AF Gu, J
   Xu, SG
   Yu, LPC
TI What fraction of detached cross-bridges with bound ADP.P-1 can attach
   directly to the actin filament?
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1766
BP 363A
EP 363A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701782
ER

PT J
AU Xu, S
   Offer, G
   Gu, J
   White, H
   Yu, LPC
AF Xu, S
   Offer, G
   Gu, J
   White, H
   Yu, LPC
TI The effect of temperature on myosin conformation: The temperature
   dependence of helical order in mammalian thick filaments with
   non-hydrolyzable ligands.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1775
BP 365A
EP 365A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701791
ER

PT J
AU Rhee, AY
   Adelstein, RS
AF Rhee, AY
   Adelstein, RS
TI NMHC-B and smooth muscle force maintenance
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Case Western Reserve Univ, Dept Physiol & Biophys, Sch Med, Cleveland, OH 44106 USA.
   NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1782
BP 366A
EP 366A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701798
ER

PT J
AU Lewis, MK
   Jia, YW
   Wang, K
AF Lewis, MK
   Jia, YW
   Wang, K
TI Investigation of titin and nebulin using single molecule fluorescence
   microscopy
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1800
BP 370A
EP 370A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701816
ER

PT J
AU Schmitz, S
   Wang, F
   Sellers, JR
   Molloy, J
   Veigel, C
AF Schmitz, S
   Wang, F
   Sellers, JR
   Molloy, J
   Veigel, C
TI The gait of myosin V constructs
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 York Univ, N York, ON M3J 1P3, Canada.
   NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1819
BP 374A
EP 374A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701835
ER

PT J
AU Martyn, DA
   Xu, SG
   Yu, LPC
AF Martyn, DA
   Xu, SG
   Yu, LPC
TI Effects of temperature and ionic strength on equatorial x-ray
   reflections in skinned cardiac muscle
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Washington, Seattle, WA 98195 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1836
BP 377A
EP 377A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701852
ER

PT J
AU Yim, PB
   Jacobs, DT
   Peters, N
   Forbes, JG
   Greer, SC
AF Yim, PB
   Jacobs, DT
   Peters, N
   Forbes, JG
   Greer, SC
TI The polymerization of actin: Volume changes in H2O and D2O buffers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Maryland, College Pk, MD 20742 USA.
   NIH, Bethesda, MD 20892 USA.
   Coll Wooster, Wooster, OH 44691 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1850
BP 380A
EP 380A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701866
ER

PT J
AU Lukoyanova, N
   VanLoock, MS
   Orlova, OA
   Wang, K
   Egelman, EH
AF Lukoyanova, N
   VanLoock, MS
   Orlova, OA
   Wang, K
   Egelman, EH
TI Each actin subunit has three nebulin-binding sites: Implications for
   steric blocking
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Virginia, Charlottesville, VA 22903 USA.
   NIAMS, NIH, Bethesda, MD USA.
RI Egelman, Edward/A-2488-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1854
BP 381A
EP 381A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701870
ER

PT J
AU Yan, B
   Chalovich, JM
   Chen, YD
AF Yan, B
   Chalovich, JM
   Chen, YD
TI Theoretical studies on competitive binding of caldesmon and S1 to actin:
   Prediction of apparent cooperativity for equilibrium measurements and a
   reduced rate of S1 binding by caldesmon
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   E Carolina Univ, Brody Sch Med, Greenville, NC 27858 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1855
BP 381A
EP 381A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701871
ER

PT J
AU Carroll, SL
   Herrera, AH
   Horowits, R
AF Carroll, SL
   Herrera, AH
   Horowits, R
TI A novel model for the initiation of myofibril assembly.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1941
BP 399A
EP 399A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701958
ER

PT J
AU Jin, AJ
   Forbes, JG
   Wang, K
AF Jin, AJ
   Forbes, JG
   Wang, K
TI Modulation of titin PEVK elasticty as studied via atomic force
   spectroscopy
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAMS, LPB, NIH, Bethesda, MD 20892 USA.
   DBEPS, ORS, OD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1943
BP 399A
EP 399A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701960
ER

PT J
AU Zhang, JQ
   Elzey, B
   Williams, G
   Lu, SJ
   Law, DJ
   Horowits, R
AF Zhang, JQ
   Elzey, B
   Williams, G
   Lu, SJ
   Law, DJ
   Horowits, R
TI Ultrastructural and biochemical localization of N-RAP at the interface
   between myofibrils and intercalated disks in the mouse heart.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Univ Missouri, Kansas City, MO 64110 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1942
BP 399A
EP 399A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701959
ER

PT J
AU Ma, K
   Wang, K
AF Ma, K
   Wang, K
TI Nebulin SH3 domain binds to multiple proline-rich peptides of titin PEVK
   and myopalladin: Implications for the targeting pathway of nebulin to
   the IZI assembly
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAMS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1945
BP 400A
EP 400A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701962
ER

PT J
AU Lewis, MK
   Adhikari, B
   Chen, V
   Bass, AH
   Wang, K
AF Lewis, MK
   Adhikari, B
   Chen, V
   Bass, AH
   Wang, K
TI Form and function of desmin filaments in a sound producing muscle from
   the Type I male Midshipman fish
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Cornell Univ, Ithaca, NY 14853 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1951
BP 401A
EP 401A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701968
ER

PT J
AU Ishikawa, T
   Maurizi, MR
   Steven, AC
AF Ishikawa, T
   Maurizi, MR
   Steven, AC
TI ATP-dependent translocation and degradation of a substrate by the ClpAP
   protease complex
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1970
BP 405A
EP 405A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701987
ER

PT J
AU Offer, G
   Yu, LC
   White, H
AF Offer, G
   Yu, LC
   White, H
TI Coupling of ATP hydrolysis to myosin conformation: Van der Waals &
   electrostatic interactions between switch II and ATP or ADP.P-1
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   Univ Bristol, Bristol BS8 1TH, Avon, England.
   Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1977
BP 406A
EP 406A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701994
ER

PT J
AU Hu, AH
   Wang, F
   Sellers, JR
AF Hu, AH
   Wang, F
   Sellers, JR
TI Mutations in human nonmuscle myosin IIA found in patients with
   May-Hegglin Anomaly and Fechtner syndrome result in impaired enzymatic
   function
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 1982
BP 407A
EP 407A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252701999
ER

PT J
AU Boukari, H
   Nossal, RJ
   Sackett, DL
AF Boukari, H
   Nossal, RJ
   Sackett, DL
TI Structure and stability of drug-induced tubulin ring polymers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2018
BP 414A
EP 414A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702034
ER

PT J
AU Hall, DR
AF Hall, DR
TI Tubulin polymerization - The effects of tubulin denaturation on the
   characterization of its polymerization behavior
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIDDK, NIH, Bethesda, MD 20892 USA.
RI Hall, Damien/D-9927-2012
OI Hall, Damien/0000-0003-1538-7618
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2019
BP 414A
EP 415A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702035
ER

PT J
AU Rubin, RJ
AF Rubin, RJ
TI &# 65279 ; Analysis of Hill's model of dynamic instability of
   microtubules.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2024
BP 415A
EP 415A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702040
ER

PT J
AU Xu, JH
   Knutson, JR
AF Xu, JH
   Knutson, JR
TI Femtosecond spectroscopic study of rotation processes of perylene and
   tetracene in hexadecane at different temperatures
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2076
BP 426A
EP 426A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702092
ER

PT J
AU Seibert, E
   Chin, AS
   Pfleiderer, W
   Hawkins, ME
   Laws, WR
   Osman, R
   Ross, JBA
AF Seibert, E
   Chin, AS
   Pfleiderer, W
   Hawkins, ME
   Laws, WR
   Osman, R
   Ross, JBA
TI Spectroscopy and theory of 6-methylisoxanthopterin, a fluorescent
   guanine analog
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Mt Sinai Sch Med, New York, NY 10029 USA.
   Univ Konstanz, D-7750 Constance, Germany.
   NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2109
BP 432A
EP 432A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702125
ER

PT J
AU Joubert, F
   Ferretti, J
   Fales, H
   Wen, H
   Combs, C
   Balaban, R
AF Joubert, F
   Ferretti, J
   Fales, H
   Wen, H
   Combs, C
   Balaban, R
TI Photobleaching of NADH in ED-FRAP: Reaction products and consequences of
   environment
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
RI Wen, Han/G-3081-2010
OI Wen, Han/0000-0001-6844-2997
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2111
BP 433A
EP 433A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702127
ER

PT J
AU Tarasov, SG
   Nelson, C
   Casas-Finet, JR
   Cholody, WM
   Hariprakasha, H
   Michejda, CJ
AF Tarasov, SG
   Nelson, C
   Casas-Finet, JR
   Cholody, WM
   Hariprakasha, H
   Michejda, CJ
TI Spectroscopic characterization and DNA binding properties of the
   naphtylimidoimidazoacridone (NIIA) WMC79 and related compounds
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21702 USA.
   Medimmune Inc, Gaithersburg, MD 20878 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2117
BP 434A
EP 434A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702133
ER

PT J
AU Henry, ER
   Hofrichter, J
   Eaton, WA
AF Henry, ER
   Hofrichter, J
   Eaton, WA
TI A tertiary two-state allosteric model for hemoglobin
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2155
BP 442A
EP 442A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702172
ER

PT J
AU Ramasamy, S
   Nagababu, E
   Alayash, AI
   Dumaswala, UJ
   Rifkind, JM
AF Ramasamy, S
   Nagababu, E
   Alayash, AI
   Dumaswala, UJ
   Rifkind, JM
TI The formation of high-spin rhombic heme during heme degradation of human
   hemoglobin
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, NIH, Baltimore, MD 21224 USA.
   US FDA, Bethesda, MD 20892 USA.
   Univ Cincinnati, Med Ctr, Hoxworth Blood Ctr, Cincinnati, OH 45267 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2158
BP 443A
EP 443A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702175
ER

PT J
AU Mitchell, DC
   Litman, BJ
AF Mitchell, DC
   Litman, BJ
TI Effect of ethanol on receptor-G protein coupling
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIAAA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2204
BP 452A
EP 452A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702221
ER

PT J
AU Hawkins, ME
   Le Grice, S
   Balis, FM
AF Hawkins, ME
   Le Grice, S
   Balis, FM
TI Development of a fluorescence based real time assay for RNase H
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2253
BP 462A
EP 462A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702270
ER

PT J
AU Sidorova, N
   Rau, DC
AF Sidorova, N
   Rau, DC
TI Dehydrating of the EcoRI-noncognate DNA complexes with osmotic stress:
   Dissociation kinetics
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2255
BP 462A
EP 463A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702272
ER

PT J
AU Tolstorukov, M
   Jernigan, RL
   Zhurkin, VB
AF Tolstorukov, M
   Jernigan, RL
   Zhurkin, VB
TI Effect of sugar puckering on protein-DNA interactions in DNA minor
   groove
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, Lab Expt & Computat Biol, NIH, Bethesda, MD 20892 USA.
RI Jernigan, Robert/A-5421-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2265
BP 464A
EP 465A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702282
ER

PT J
AU Ozarowski, A
   Urbaneja, MA
   Henderson, LE
   Casas-Finet, JR
   Maki, AH
AF Ozarowski, A
   Urbaneja, MA
   Henderson, LE
   Casas-Finet, JR
   Maki, AH
TI Optically detected magnetic resonance and luminescence studies of
   stem-loop complexes of Moloney murine leukemia virus nucleocapsid
   protein, NCp10
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Calif Davis, Davis, CA 95616 USA.
   NCI, SAIC Frederick, AIDS Vaccine Program, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2269
BP 465A
EP 465A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702286
ER

PT J
AU Misra, S
   Puertollano, R
   Bonifacino, JS
   Hurley, JH
AF Misra, S
   Puertollano, R
   Bonifacino, JS
   Hurley, JH
TI The structural basis of protein sorting by the VHS domains of CGA
   proteins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2297
BP 471A
EP 471A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702314
ER

PT J
AU Costes, S
   Slobodskaya, O
   Cho, E
   Tsopanomihalu-Nglotsu, M
   Pavlakis, GN
   Lockett, SJ
AF Costes, S
   Slobodskaya, O
   Cho, E
   Tsopanomihalu-Nglotsu, M
   Pavlakis, GN
   Lockett, SJ
TI FRAP model to determine the bi-directional transport rate of proteins
   across the nuclear membrane and the mobile fraction in the cytoplasm and
   nucleus
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, SAIC, Frederick, MD 21701 USA.
RI Costes, Sylvain/D-2522-2013; Cho, Edward/B-3727-2012
OI Costes, Sylvain/0000-0002-8542-2389; Cho, Edward/0000-0002-0278-334X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2366
BP 484A
EP 484A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702383
ER

PT J
AU Ross, JBA
   Osman, R
AF Ross, JBA
   Osman, R
TI Computations of fluorescence properties of nucleotide analogues in DNA
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Mt Sinai Sch Med, New York, NY 10029 USA.
   NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2368
BP 485A
EP 485A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702385
ER

PT J
AU Gunasekaran, K
   Ma, BY
   Ramakrishnan, B
   Qasba, PK
   Nussinov, R
AF Gunasekaran, K
   Ma, BY
   Ramakrishnan, B
   Qasba, PK
   Nussinov, R
TI Molecular dynamics simulations on beta 1, 4-galactosyltransferase-1:
   Flexible regions and conserved positions in the ligand binding mechanism
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, Frederick, MD 21702 USA.
   Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2372
BP 486A
EP 486A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702389
ER

PT J
AU Borgnia, MJ
   Zhang, PJ
   Shi, D
   Akhavannik, H
   Blewis, M
   Subramaniam, S
   Milne, JLS
AF Borgnia, MJ
   Zhang, PJ
   Shi, D
   Akhavannik, H
   Blewis, M
   Subramaniam, S
   Milne, JLS
TI Automation of data collection and single particle analysis of complex
   molecular assemblies by electron cryo-microscopy.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2392
BP 489A
EP 490A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702409
ER

PT J
AU Chen, XB
   Leapman, R
   Petersen, J
   Reeese, T
   Vinade, L
   Dosemeci, A
AF Chen, XB
   Leapman, R
   Petersen, J
   Reeese, T
   Vinade, L
   Dosemeci, A
TI The mass added to postsynatic density
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NINCDS, NIH, Bethesda, MD 20892 USA.
   Marine Biol Lab, Woods Hole, MA 02543 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2396
BP 490A
EP 490A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702413
ER

PT J
AU Heymann, JAW
   Hirai, T
   Shi, D
   Sarker, R
   Maloney, PC
AF Heymann, JAW
   Hirai, T
   Shi, D
   Sarker, R
   Maloney, PC
TI Structure and molecular architecture of OxlT, a bacterial membrane
   carrier
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
   Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
RI Hirai, Teruhisa/G-2105-2015
OI Hirai, Teruhisa/0000-0002-2114-8149
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2395
BP 490A
EP 490A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702412
ER

PT J
AU Milne, JLS
   Shi, D
   Perham, RN
   Subramaniam, S
AF Milne, JLS
   Shi, D
   Perham, RN
   Subramaniam, S
TI Molecular architecture and functional mechanism of pyruvate
   dehydrogenase complexes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
   Univ Cambridge, Cambridge CB2 1TN, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2393
BP 490A
EP 490A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702410
ER

PT J
AU Mooney, PE
   Joyce, DC
   Pan, M
   Shi, D
   Subramaniam, S
AF Mooney, PE
   Joyce, DC
   Pan, M
   Shi, D
   Subramaniam, S
TI Evaluation of the performance of a new 4K CCD camera for imaging
   applications in low-dose, electron cryo-microscopy
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Gatan Inc, Pleasanton, CA 94588 USA.
   NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2394
BP 490A
EP 490A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702411
ER

PT J
AU Patterson, GH
   Lippincott-Schwartz, J
AF Patterson, GH
   Lippincott-Schwartz, J
TI Photoactivatable green fluorescent protein
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, NICHD, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2404
BP 492A
EP 492A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702421
ER

PT J
AU Ma, BY
   Nussinov, R
AF Ma, BY
   Nussinov, R
TI Amyloid-beta peptide beta-sheet oligomers: Insight into amyloid
   formation via MD simulations
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Frederick, MD 21702 USA.
   Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2463
BP 504A
EP 504A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702480
ER

PT J
AU Williams, MC
   Gorelick, RJ
   Musier-Forsyth, K
   Bloomfield, VA
AF Williams, MC
   Gorelick, RJ
   Musier-Forsyth, K
   Bloomfield, VA
TI Role of zinc finger structures in the nucleic acid chaperone activity of
   HIV-1NC proteins investigated by single molecule DNA stretching
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Northeastern Univ, Boston, MA 02115 USA.
   Univ Minnesota, Minneapolis, MN 55455 USA.
   NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2477
BP 507A
EP 507A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702494
ER

PT J
AU Wang, SQ
   Cheng, HP
AF Wang, SQ
   Cheng, HP
TI In situ properties of ryanodine receptors revealed by calcium spark
   analysis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2490E
BP 510A
EP 511A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702512
ER

PT J
AU Forbes, JG
   Wang, K
   Jin, AJ
AF Forbes, JG
   Wang, K
   Jin, AJ
TI AFM investigation of elasticity and conformation maleability of single
   proteins and supramolecular structures
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2495
BP 512A
EP 512A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702520
ER

PT J
AU Turner, GJ
   Martinez, LC
   Voge, GV
   Correia, JJ
   Mitra, A
   Mitchell, DC
AF Turner, GJ
   Martinez, LC
   Voge, GV
   Correia, JJ
   Mitra, A
   Mitchell, DC
TI Roles for the carboxyl-terminal coding region of the bacterio-opsin gene
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Miami, Sch Med, Miami, FL 33101 USA.
   NIAAA, NIH, Bethesda, MD USA.
   Univ Mississippi, Med Ctr, University, MS 38677 USA.
   Scripps Res Inst, La Jolla, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2573
BP 526A
EP 527A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702589
ER

PT J
AU Melikov, KC
   Vives, E
   Lebleu, B
   Chernomordik, LV
AF Melikov, KC
   Vives, E
   Lebleu, B
   Chernomordik, LV
TI Interaction of transducing peptide TAT48-60 with artificial lipid
   bilayer membranes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
   Inst Genet Mol, CNRS, UMR 5535, Montpellier, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2632
BP 539A
EP 539A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702648
ER

PT J
AU Leikina, EA
   Markovic, I
   Ramos, C
   Zimmerberg, J
   Chernomordik, LV
AF Leikina, EA
   Markovic, I
   Ramos, C
   Zimmerberg, J
   Chernomordik, LV
TI Reversible stages of the low pH-triggered conformational change in
   influenza virus hemagglutinin
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2641
BP 540A
EP 541A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702657
ER

PT J
AU Kumar, M
   Kenworthy, AK
   Verma, A
   Roth, MG
   Zimmerberg, J
AF Kumar, M
   Kenworthy, AK
   Verma, A
   Roth, MG
   Zimmerberg, J
TI Role of microdomain-mediated clustering of influenza hemagglutinin in
   viral fusion: The ring raft
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
   Univ Texas, SW Med Ctr, Dallas, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2645
BP 541A
EP 541A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702661
ER

PT J
AU Markovic, I
   Kumar, M
   Zimmerberg, J
   Chernomordik, LV
AF Markovic, I
   Kumar, M
   Zimmerberg, J
   Chernomordik, LV
TI Raft association ensures synchronized unfolding of influenza
   hemagglutinin upon its activation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2644
BP 541A
EP 541A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702660
ER

PT J
AU Zhukovsky, MA
   Bailey, AL
   Leikina, E
   Chernomordik, LV
   Markovic, I
AF Zhukovsky, MA
   Bailey, AL
   Leikina, E
   Chernomordik, LV
   Markovic, I
TI Influenza hemagglutinin-mediated fusion of cells with liposomes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
   NICHHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2650
BP 542A
EP 542A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702666
ER

PT J
AU Kozlov, MM
   Chernomordik, LV
AF Kozlov, MM
   Chernomordik, LV
TI Protein coat in membrane fusion: Lessons from fission
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
   NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2657
BP 543A
EP 544A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702673
ER

PT J
AU Kenworthy, AK
   Lippincott-Schwartz, J
AF Kenworthy, AK
   Lippincott-Schwartz, J
TI Dynamics of lipid rafts measured by large-scale lateral diffusion
   measurements.
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA.
   NICHHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2660
BP 544A
EP 544A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702676
ER

PT J
AU Arie, T
   Jin, AJ
   Dvorak, JA
AF Arie, T
   Jin, AJ
   Dvorak, JA
TI Novel analysis of the flickering of Plasmodium falciparum-infected
   erythrocytes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2698
BP 552A
EP 552A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702714
ER

PT J
AU Jayakumar, R
   Demehin, AA
   Murali, J
   Kusiak, J
   Abugo, OO
   Chrest, J
   Ingram, D
   Rifkind, JM
AF Jayakumar, R
   Demehin, AA
   Murali, J
   Kusiak, J
   Abugo, OO
   Chrest, J
   Ingram, D
   Rifkind, JM
TI Uptake of beta-amyloid by red blood cells: Enhanced oxidative stress and
   modification of red cell function
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Cent Leather Res Inst, Madras 600020, Tamil Nadu, India.
   NIA, NIH, Ctr Gerontol Res, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2704
BP 553A
EP 553A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252702720
ER

PT J
AU Pinz, I
   Wawrousek, E
   Benjamin, IJ
   Ingwall, JS
AF Pinz, I
   Wawrousek, E
   Benjamin, IJ
   Ingwall, JS
TI Deficiency of alpha beta-cristallin and HSPB2 impairs contractile
   function and decreases energetics after myocardial ischemia
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
   NEI, Bethesda, MD 20892 USA.
   Univ Texas, SW Med Ctr, Dallas, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 2988
BP 611A
EP 612A
PN 2
PG 2
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703002
ER

PT J
AU Ramos, C
   Melikov, KC
   Chernomordik, LV
AF Ramos, C
   Melikov, KC
   Chernomordik, LV
TI Cytosol-dependent binding of liposomes to decondensed chromatin in vitro
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NICHHD, NIH, Bethesda, MD 20894 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3064
BP 627A
EP 627A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703078
ER

PT J
AU Shrivastava, IH
   Bright, JN
   Sansom, MSP
   Guy, HR
AF Shrivastava, IH
   Bright, JN
   Sansom, MSP
   Guy, HR
TI Molecular dynamics simulations of the Shaker voltage-gated K+ channel:
   Open vs closed structural model
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Oxford, Oxford OX2 3QU, England.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3069
BP 628A
EP 628A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703083
ER

PT J
AU Durell, SR
   Shafrir, Y
   Guy, HR
AF Durell, SR
   Shafrir, Y
   Guy, HR
TI Structural models of eukaryotic and prokaryotic Kir's
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3072
BP 629A
EP 629A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703086
ER

PT J
AU Guy, HR
   Shafrir, Y
   Durell, SR
AF Guy, HR
   Shafrir, Y
   Durell, SR
TI Structural models of Kv channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3071
BP 629A
EP 629A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703085
ER

PT J
AU Shafrir, Y
   Guy, HR
   Durell, SR
AF Shafrir, Y
   Guy, HR
   Durell, SR
TI Structural models of the transmembrane region of distantly related 6TM
   K+ and Ca2+ channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3073
BP 629A
EP 629A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703087
ER

PT J
AU Pan, Z
   Yang, DM
   Nagaraj, RY
   Nosek, T
   Takeshima, H
   Cheng, HP
   Ma, JJ
AF Pan, Z
   Yang, DM
   Nagaraj, RY
   Nosek, T
   Takeshima, H
   Cheng, HP
   Ma, JJ
TI Deletion of MG29 gene leads to defective function of store-operated Ca2+
   channel in skeletal muscle
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Newark, NJ 07103 USA.
   NIA, Bethesda, MD 20892 USA.
   Case Western Reserve Univ, Cleveland, OH 44106 USA.
   Kurume Univ, Kurume, Fukuoka 830, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3140
BP 643A
EP 643A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703154
ER

PT J
AU Yang, DM
   Pan, Z
   Takeshima, H
   Wu, CH
   Cheng, HP
   Ma, JJ
AF Yang, DM
   Pan, Z
   Takeshima, H
   Wu, CH
   Cheng, HP
   Ma, JJ
TI RyR3 amplifies RyR1-mediated Ca-induced Ca release in neonatal mammalian
   skeletal muscle
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
C1 NIA, Bethesda, MD 20892 USA.
   Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Newark, NJ 07103 USA.
   Kurume Univ, Kurume, Fukuoka 830, Japan.
   Beijing Univ, Beijing 100871, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BIOPHYSICAL SOCIETY
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN
PY 2002
VL 82
IS 1
MA 3141
BP 643A
EP 643A
PN 2
PG 1
WC Biophysics
SC Biophysics
GA 511EY
UT WOS:000173252703155
ER

PT J
AU Hamel, E
AF Hamel, E
TI Interactions of antimitotic peptides and depsipeptides with tubulin
SO BIOPOLYMERS
LA English
DT Review
DE tubulin; antimitotic peptides; depsipeptides; microtubules; spindle
   formation; catharanthus alkaloid binding; GTP hydrolysis; nucleotide
   turnover
ID BOVINE BRAIN TUBULIN; POTENT CYTOTOXIC DEPSIPEPTIDE; SPONGE
   DYSIDEA-ARENARIA; MICROTUBULE-ASSOCIATED PROTEINS;
   GUANINE-NUCLEOTIDE-BINDING; LEUKEMIA-CELL LINES; AMINO-ACID-SEQUENCE; SP
   STRAIN GSV-224; ANTINEOPLASTIC AGENTS; BETA-TUBULIN
AB Tubulin is the target for an ever increasing number of structurally unusual peptides and depsipeptides isolated from a wide range of organisms. Since tubulin is the subunit protein of microtubules, the compounds are usually potently toxic to mammalian cells. Without exception, these (depsi)peptides disrupt cellular microtubules and prevent spindle formation. This causes cells to accumulate at the G2/M phase of the cell cycle through inhibition of mitosis. In biochemical assays, the compounds inhibit microtubule assembly from tubulin and suppress microtubule dynamics at low concentrations. Most of the (depsi)peptides inhibit the binding of Catharanthus alkaloids to tubulin in a noncompetitive manner, GTP hydrolysis by tubulin, and nucleotide turnover at the exchangeable GTP site on beta-tubulin. In general, the (depsi)peptides induce the formation of tubulin oligomers of aberrant morphology. In all cases tubulin rings appear to be formed, but these rings differ in diameter, depending on the (depsi)peptide present during their formation. (C) 2002 Wiley Periodicals, Inc.*.
C1 NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Frederick, MD 21702 USA.
RP Hamel, E (reprint author), NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Bldg 469,Room 104, Frederick, MD 21702 USA.
NR 168
TC 33
Z9 37
U1 2
U2 5
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0006-3525
J9 BIOPOLYMERS
JI Biopolymers
PY 2002
VL 66
IS 3
BP 142
EP 160
DI 10.1002/bip.10255
PG 19
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 612UN
UT WOS:000179094000002
PM 12385035
ER

PT J
AU Longo, DL
AF Longo, DL
TI Gastric lymphoma: a tale of 2 MALTs
SO BLOOD
LA English
DT Editorial Material
C1 Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Longo, DL (reprint author), Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD JAN 1
PY 2002
VL 99
IS 1
BP 1
EP 1
DI 10.1182/blood.V99.1.1
PG 1
WC Hematology
SC Hematology
GA 506PK
UT WOS:000172980800001
ER

PT J
AU Yamano, Y
   Nagai, M
   Brennan, M
   Mora, CA
   Soldan, SS
   Tomaru, U
   Takenouchi, N
   Izumo, S
   Osame, M
   Jacobson, S
AF Yamano, Y
   Nagai, M
   Brennan, M
   Mora, CA
   Soldan, SS
   Tomaru, U
   Takenouchi, N
   Izumo, S
   Osame, M
   Jacobson, S
TI Correlation of human T-cell lymphotropic virus type 1 (HTLV-1) mRNA with
   proviral DNA load, virus-specific CD8(+) T cells, and disease severity
   in HTLV-1-associated myelopathy (HAM/TSP)
SO BLOOD
LA English
DT Article
ID I-ASSOCIATED MYELOPATHY; TROPICAL SPASTIC PARAPARESIS;
   POLYMERASE-CHAIN-REACTION; BLOOD MONONUCLEAR-CELLS; CYTOTOXIC
   LYMPHOCYTES-T; PERIPHERAL-BLOOD; LEUKEMIA-VIRUS; CEREBROSPINAL-FLUID;
   INFECTED INDIVIDUALS; NEUROLOGICAL DISEASE
AB To investigate the role of viral expression in individuals infected with human T-cell lymphotropic virus type 1 (HTLV-1), a real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) of HTLV-1 tax messenger RNA (mRNA) using ABI Prism 7700 Sequence Detection System was developed. Using this system, the HTLV-1 tax mRNA load was compared with HTLV-1 proviral DNA load, HTLV-1 Tax protein expression, HTLV-1 Tax-specific CD8(+) T-cell frequency, and disease severity of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). This approach was a sensitive and specific technique for the precise quantification of HTLV-1 tax mRNA. The total amount of HTLV-1 tax mRNA and mRNA expression level in HTLV-1-infected cells (mRNA/DNA ratio) were higher in HAM/TSP patients than in asymptomatic HTLV-1 carriers. The HTLV-1 tax mRNA load correlated with the HTLV-1 proviral DNA load ex vivo, the Tax protein expression in vitro, and the Tax-specific CD8(+) T-cell frequency ex vivo. The HTLV-1 tax mRNA load also correlated with disease severity in HAM/TSP patients. These data suggest that increased HTLV-1 expression plays an important role In the pathogenesis of HAM/TSP, and the HTLV-1 tax mRNA level could be a useful predictor of disease progression In patients with HAW TSP.
C1 NINCDS, NIH, NIB, Viral Immunol Sect, Bethesda, MD 20892 USA.
   Kagoshima Univ, Fac Med, Ctr Chron Viral Dis, Kagoshima 890, Japan.
   Kagoshima Univ, Fac Med, Dept Internal Med 3, Kagoshima 890, Japan.
RP Jacobson, S (reprint author), NINCDS, NIH, NIB, Viral Immunol Sect, Bldg 10,Rm 5B-16, Bethesda, MD 20892 USA.
NR 51
TC 144
Z9 146
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD JAN 1
PY 2002
VL 99
IS 1
BP 88
EP 94
DI 10.1182/blood.V99.1.88
PG 7
WC Hematology
SC Hematology
GA 506PK
UT WOS:000172980800017
PM 11756157
ER

PT J
AU Kratz, CP
   Emerling, BM
   Bonifas, J
   Wang, W
   Green, ED
   Le Beau, MM
   Shannon, KM
AF Kratz, CP
   Emerling, BM
   Bonifas, J
   Wang, W
   Green, ED
   Le Beau, MM
   Shannon, KM
TI Genomic structure of the PIK3CG gene on chromosome band 7q22 and
   evaluation as a candidate myeloid tumor suppressor
SO BLOOD
LA English
DT Article
ID MICE; DISORDERS; LEUKEMIA; INACTIVATION; DELINEATION; PI3K-GAMMA;
   DELETIONS; DISEASE; CANCER
AB PIK3CG, which encodes the catalytic subunit p110 gamma of phosphoinositide 3-OH-kinase-gamma (PI3K gamma), has been assigned to chromosome band 7q22, a region that is frequently deleted in myeloid malignancies. PI3K gamma -mutant mice have hematologic defects and are predisposed to colon cancer. On the basis of these data, PIK3CG was evaluated as a candidate myeloid tumor suppressor gene (TSG). PIK3CG was mapped by fluorescence in situ hybridization adjacent and telomeric to a commonly deleted segment defined previously in myeloid leukemias with breakpoints within 7q22. PIK3CG contains 10 exons and spans approximately 37 kilobases of genomic DNA. Forty leukemias with monosomy 7 or a del(7q) were screened for PIK3CG mutations. Two patients had missense variations affecting residue 859 in the N-terminal catalytic domain of the protein. This allele was also detected In unaffected parents and in 1 of 60 control alleles; It probably represents a polymorphism. PIK3CG Is unlikely to act as a recessive TSG In myeloid leukemias with monosomy 7. (Blood. 2002;99:372-374) (C) 2002 by The American Society of Hematology.
C1 Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA.
   St Jude Childrens Res Hosp, Dept Hematol Oncol, Memphis, TN 38105 USA.
   NHGRI, Genome Technol Branch, Bethesda, MD 20892 USA.
   Univ Chicago, Dept Med, Hematol Oncol Sect, Chicago, IL 60637 USA.
   Univ Chicago, Canc Res Ctr, Chicago, IL 60637 USA.
RP Shannon, KM (reprint author), Univ Calif San Francisco, Dept Pediat, 513 Parnassus Ave,HSE 302, San Francisco, CA 94143 USA.
EM kevins@itsa.ucsf.edu
FU PHS HHS [P01 40046]
NR 27
TC 24
Z9 24
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD JAN 1
PY 2002
VL 99
IS 1
BP 372
EP 374
DI 10.1182/blood.V99.1.372
PG 3
WC Hematology
SC Hematology
GA 506PK
UT WOS:000172980800054
PM 11756194
ER

PT J
AU Stetler-Stevenson, M
   Rick, M
   Arthur, D
AF Stetler-Stevenson, M
   Rick, M
   Arthur, D
TI Diagnostic flow cytometric immunophenotyping in myelodysplastic
   syndrome: the US-Canadian consensus recommendations on the
   immunophenotypic analysis of hematological neoplasia by flow cytometry
   apply - Response
SO BLOOD
LA English
DT Letter
C1 NCI, Pathol Lab, Bethesda, MD 20895 USA.
RP Stetler-Stevenson, M (reprint author), NCI, Pathol Lab, Bldg 10,Rm 2N-108, Bethesda, MD 20895 USA.
NR 3
TC 2
Z9 3
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD JAN 1
PY 2002
VL 99
IS 1
BP 392
EP 392
PG 1
WC Hematology
SC Hematology
GA 506PK
UT WOS:000172980800064
ER

PT J
AU Rosenbaum, H
   Sidransky, E
AF Rosenbaum, H
   Sidransky, E
TI Cholelithiasis in patients with Gaucher disease
SO BLOOD CELLS MOLECULES AND DISEASES
LA English
DT Article
DE Gaucher diseased; glucocerebrosidase; cholecystectomy; gallbladder;
   cholelithiasis
ID GALLSTONE PREVALENCE; RURAL-POPULATION; NATURAL-HISTORY; ABNORMALITIES;
   SPLENECTOMY; CIRRHOSIS; CHILDREN; TYPE-1
AB Gaucher disease, the inherited deficiency of the lysosomal enzyme glucocerebrosidase, manifests with a continually expanding range of clinical features. Noting that a number of adult patients with type I Gaucher disease also had gallstones, we reviewed the clinical records of 66 adult patients evaluated at the National Institutes of Health with type I Gaucher disease. Twenty-one patients were identified who had either gallstones or a history of cholecystectomy. Of the 21 patients, 6 were male. The age at which stones were noted ranged from 19 to 70 years (mean 39 years). Thirteen of the patients had a cholecystectomy performed. Several different factors may contribute to the development of gallstones in these patients, including anemia, prior splenectomy, and hepatic involvement. Eleven of the patients were found to have chronic anemia. Fifteen of the patients underwent splenectomy. An increased biliary excretion of glucosylceramide could also contribute to cholelithiasis. To determine whether our findings were specific to our referral population, the medical records of a second series of 80 adult patients of Ashkenazi Jewish ancestry with type 1 Gaucher disease followed in Northern Israel were reviewed. Sixteen of these patients (5 male, 11 female) were also noted to have gallstones. Thus, the frequency of gallbladder involvement in patients with Gaucher disease appears to be greater than previously appreciated. (C) 2002 Elsevier Science (USA).
C1 NIMH, Clin Neurosci Branch, NIH, Bethesda, MD 20892 USA.
   Technion Israel Inst Technol, Rambam Med Ctr, Dept Hematol, Haifa, Israel.
   Technion Israel Inst Technol, Bruce Rappaport Fac Med, IL-31096 Haifa, Israel.
RP Sidransky, E (reprint author), NIMH, Clin Neurosci Branch, NIH, 49 Convent Dr,MSC4405,49-B1EE16, Bethesda, MD 20892 USA.
NR 21
TC 19
Z9 21
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 1079-9796
J9 BLOOD CELL MOL DIS
JI Blood Cells Mol. Dis.
PD JAN-FEB
PY 2002
VL 28
IS 1
BP 21
EP 27
DI 10.1006/bcmd.2001.0480
PG 7
WC Hematology
SC Hematology
GA 544TK
UT WOS:000175176700004
PM 11987238
ER

PT J
AU Falardeau, JL
   Kennedy, JC
   Acierno, JS
   Sun, M
   Stahl, S
   Goldin, E
   Slaugenhaupt, SA
AF Falardeau, JL
   Kennedy, JC
   Acierno, JS
   Sun, M
   Stahl, S
   Goldin, E
   Slaugenhaupt, SA
TI Cloning and characterization of the mouse McolnI gene reveals an
   alternatively spliced transcript not seen in humans
SO BMC GENOMICS
LA English
DT Article
ID MUCOLIPIDOSIS TYPE-IV; ABNORMAL TRANSPORT; MUTATIONS; IDENTIFICATION;
   DISEASE; MAP
AB Background: Mucolipidosis type IV (MLIV) is an autosomal recessive lysosomal storage disorder characterized by severe neurologic and ophthalmologic abnormalities. Recently the MLIV gene, NICOLN1, has been identified as a new member of the transient receptor potential (TRP) cation channel superfamily. Here we report the cloning and characterization of the mouse homologue, Mcoln 1, and report a novel splice variant that is not seen in humans.
   Results: The human and mouse genes display a high degree of synteny. Mcoln I shows 91% amino acid and 86% nucleotide identity to NICOLN1. Also, Mcoln I maps to chromosome 8 and contains an open reading frame of 580 amino acids, with a transcript length of approximately 2 kb encoded by 14 exons, similar to its human counterpart. The transcript that results from murine specific alternative splicing encodes a 611 amino acid protein that differs at the c-terminus.
   Conclusions: Mcoln I is highly similar to NICOLN1, especially in the transmembrane domains and ion pore region. Also, the late endosomal/lysosomal targeting signal is conserved, supporting the hypothesis that the protein is localized to these vesicle membranes. To date, there are very few reports describing species-specific splice variants. While identification of Mcoln I is crucial to the development of mouse models for MLIV, the fact that there are two transcripts in mice suggests an additional or alternate function of the gene that may complicate phenotypic assessment.
C1 Harvard Univ, Sch Med, Inst Human Genet, Boston, MA 02115 USA.
   NINDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA.
   Massachusetts Gen Hosp, Mol Neurogenet Unit, Charlestown, MA USA.
RP Slaugenhaupt, SA (reprint author), Harvard Univ, Sch Med, Inst Human Genet, 77 Ave Louis Pasteur, Boston, MA 02115 USA.
FU NINDS NIH HHS [R01 NS039995]
NR 18
TC 8
Z9 9
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2002
VL 3
AR 3
DI 10.1186/1471-2164-3-3
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 654CW
UT WOS:000181477100003
PM 11897010
ER

PT J
AU Iyer, LM
   Aravind, L
AF Iyer, LM
   Aravind, L
TI The catalytic domains of thiamine triphosphatase and CyaB-like adenylyl
   cyclase define a novel superfamily of domains that bind organic
   phosphates
SO BMC GENOMICS
LA English
DT Article
ID POLYPHOSPHATE-AMP PHOSPHOTRANSFERASE; INORGANIC POLYPHOSPHATE; GENOMIC
   CONTEXT; SECONDARY STRUCTURE; P-LOOP; PROTEINS; CLASSIFICATION;
   EVOLUTION; PREDICTION; ALIGNMENT
AB Background: The CyaB protein from Aeromonas hydrophila has been shown to possess adenylyl cyclase activity. While orthologs of this enzyme have been found in some bacteria and archaea, it shows no detectable relationship to the classical nucleotide cyclases. Furthermore, the actual biological functions of these proteins are not clearly understood because they are also present in organisms in which there is no evidence for cyclic nucleotide signaling.
   Results: We show that the CyaB like adenylyl cyclase and the mammalian thiamine triphosphatases define a novel superfamily of catalytic domains called the CYTH domain that is present in all three superkingdoms of life. Using multiple alignments and secondary structure predictions, we define the catalytic core of these enzymes to contain a novel alpha+beta scaffold with 6 conserved acidic residues and 4 basic residues. Using contextual information obtained from the analysis of gene neighborhoods and domain fusions, we predict that members of this superfamily may play a central role in the interface between nucleotide and polyphosphate metabolism. Additionally, based on contextual information, we identify a novel domain (called CHAD) that is predicted to functionally interact with the CYTH domain-containing enzymes in bacteria and archaea. The CHAD is predicted to be an alpha helical domain, and contains conserved histidines that may be critical for its function.
   Conclusions: The phyletic distribution of the CYTH domain suggests that it is an ancient enzymatic domain that was present in the Last Universal Common Ancestor and was involved in nucleotide or organic phosphate metabolism. Based on the conservation of catalytic residues, we predict that CYTH domains are likely to chelate two divalent cations, and exhibit a reaction mechanism that is dependent on two metal ions, analogous to nucleotide cyclases, polymerases and certain phosphoesterases. Our analysis also suggests that the experimentally characterized members of this superfamily, namely adenylyl cyclase and thiamine triphosphatase, are secondary derivatives of proteins that performed an ancient role in polyphosphate and nucleotide metabolism.
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
NR 42
TC 45
Z9 47
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2002
VL 3
AR 33
DI 10.1186/1471-2164-3-33
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 654CW
UT WOS:000181477100033
PM 12456267
ER

PT J
AU Iyer, LM
   Koonin, EV
   Aravind, L
AF Iyer, LM
   Koonin, EV
   Aravind, L
TI Classification and evolutionary history of the single-strand annealing
   proteins, RecT, Red beta, ERF and RAD52
SO BMC GENOMICS
LA English
DT Article
ID SECONDARY STRUCTURE PREDICTION; ESCHERICHIA-COLI RECE;
   BACTERIOPHAGE-LAMBDA; PROMOTES RENATURATION; GENOMIC CONTEXT; DNA;
   RECOMBINATION; PHAGE-P22; SEQUENCE; MULTIPLE
AB Background: The DNA single-strand annealing proteins (SSAPs), such as RecT, Recbeta, ERF and Rad52, function in RecA-dependent and RecA-independent DNA recombination pathways. Recently, they have been shown to form similar helical quaternary superstructures. However, despite the functional similarities between these diverse SSAPs, their actual evolutionary affinities are poorly understood.
   Results: Using sensitive computational sequence analysis, we show that the RecT and Redbeta proteins, along with several other bacterial proteins, form a distinct superfamily. The ERF and Rad52 families show no direct evolutionary relationship to these proteins and define novel superfamilies of their own. We identify several previously unknown members of each of these superfamilies and also report, for the first time, bacterial and viral homologs of Rad52. Additionally, we predict the presence of aberrant HhH modules in RAD52 that are likely to be involved in DNA-binding. Using the contextual information obtained from the analysis of gene neighborhoods, we provide evidence of the interaction of the bacterial members of each of these SSAP superfamilies with a similar set of DNA repair/recombination protein. These include different nucleases or Holliday junction resolvases, the ABC ATPase SbcC and the single-strand-binding protein. We also present evidence of independent assembly of some of the predicted operons encoding SSAPs and in situ displacement of functionally similar genes.
   Conclusions: There are three evolutionarily distinct superfamilies of SSAPs, namely the RecT/ Redbeta, ERF, and RAD52, that have different sequence conservation patterns and predicted folds. All these SSAPs appear to be primarily of bacteriophage origin and have been acquired by numerous phylogenetically distant cellular genomes. They generally occur in predicted operons encoding one or more of a set of conserved DNA recombination proteins that appear to be the principal functional partners of the SSAPs.
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
NR 47
TC 96
Z9 98
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2002
VL 3
AR 8
DI 10.1186/1471-2164-3-8
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 654CW
UT WOS:000181477100008
PM 11914131
ER

PT J
AU Maheshwari, M
   Christian, SL
   Liu, C
   Badner, JA
   Detera-Wadleigh, S
   Gershon, ES
   Gibbs, RA
AF Maheshwari, M
   Christian, SL
   Liu, C
   Badner, JA
   Detera-Wadleigh, S
   Gershon, ES
   Gibbs, RA
TI Mutation screening of two candidate genes from 13q32 in families
   affected with bipolar disorder: human peptide transporter (SLC15A1) and
   human glypican5 (GPC5)
SO BMC GENOMICS
LA English
DT Article
ID GOLABI-BEHMEL-SYNDROME; OLIGOPEPTIDE TRANSPORTER; SUSCEPTIBILITY LOCUS;
   CHROMOSOME 13Q32; NERVOUS-SYSTEM; SCHIZOPHRENIA; LINKAGE; METAANALYSIS;
   GENETICS; IDENTIFICATION
AB Background: Multiple candidate regions as sites for Schizophrenia and Bipolar susceptibility genes have been reported, suggesting heterogeneity of susceptibility genes or oligogenic inheritance. Linkage analysis has suggested chromosome 13q32 as one of the regions with evidence of linkage to Schizophrenia and, separately, to Bipolar disorder (BP). SLC15A1 and GPC5 are two of the candidate genes within an approximately 10-cM region of linkage on chromosome 13q32. In order to identify a possible role for these candidates as susceptibility genes, we performed mutation screening on the coding regions of these two genes in 7 families (n-20) affected with Bipolar disorder showing linkage to 13q32.
   Results: Genomic organization revealed 23 exons in SLC15A1 and 8 exons in GPC5 gene respectively. Sequencing of the exons did not reveal mutations in the GPC5 gene in the 7 families affected with BP. Two polymorphic variants were discovered in the SLC15A1 gene. One was T to C substitution in the third position of codon encoding alanine at 1403 position of mRNA in exon 17, and the other was A to G substitution in the untranslated region at position 2242 of mRNA in exon 23.
   Conclusions: Mutation analysis of 2 candidate genes for Bipolar disorder on chromosome 13q32 did not identify any potentially causative mutations within the coding regions or splice junctions of the SLC15A1 or GPC5 genes in 7 families showing linkage to 13q32. Further studies of the regulatory regions are needed to completely exclude these genes as causative for Bipolar disorder.
C1 Human Genome Sequencing Ctr, Dept Mol & Human Genet, Houston, TX 77030 USA.
   Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA.
   NIMH, NIH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Gibbs, RA (reprint author), Human Genome Sequencing Ctr, Dept Mol & Human Genet, 1 Baylor Plaza,N1519, Houston, TX 77030 USA.
RI Liu, Chunyu/G-7561-2012
OI Liu, Chunyu/0000-0002-5986-4415
FU NIMH NIH HHS [R01 MH065560]
NR 42
TC 6
Z9 6
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2002
VL 3
AR 30
DI 10.1186/1471-2164-3-30
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 654CW
UT WOS:000181477100030
PM 12392603
ER

PT J
AU Xu, LX
   Yang, LH
   Hashimoto, K
   Anderson, M
   Kohlhagen, G
   Pommier, Y
   D'Arpa, P
AF Xu, LX
   Yang, LH
   Hashimoto, K
   Anderson, M
   Kohlhagen, G
   Pommier, Y
   D'Arpa, P
TI Characterization of BTBD1 and BTBD2, two similar BTB-domain-containing
   kelch-like proteins that interact with topoisomerase I
SO BMC GENOMICS
LA English
DT Article
ID N-TERMINAL DOMAIN; LARGE T-ANTIGEN; GENE-EXPRESSION; SPLICING FACTOR;
   DNA; CELLS; CAMPTOTHECIN; LOCALIZATION; PHOSPHORYLATION; REDISTRIBUTION
AB Background: Two-hybrid screening for proteins that interact with the core domain of human topoisomerase I identified two novel proteins, BTBD1 and BTBD2, which share 80% amino acid identities.
   Results: The interactions were confirmed by co-precipitation assays demonstrating the physical interaction of BTBD1 and BTBD2 with 100 kDa topoisomerase I from HeLa cells. Deletion mapping using two-hybrid and GST-pulldown assays demonstrated that less than the C-terminal half of BTBD1 is sufficient for binding topoisomerase 1. The topoisomerase I sequences sufficient to bind BTBD2 were mapped to residues 215 to 329. BTBD2 with an epitope tag localized to cytoplasmic bodies. Using truncated versions that direct BTBD2 and TOP1 to the same cellular compartment, either the nucleus or the cytoplasm, co-localization was demonstrated in cotransfected Hela cells. The supercoil relaxation and DNA cleavage activities of topoisomerase I in vitro were affected little or none by co-incubation with BTBD2. Northern analysis revealed only a single sized mRNA for each BTBD1 and BTBD2 in all human tissues tested. Characterization of BTBD2 mRNA revealed a 255 nucleotide 90% GC-rich region predicted to encode the N-terminus. BTBD1 and BTBD2 are widely if not ubiquitously expressed in human tissues, and have two paralogs as well as putative orthologs in C elegans and D. melanogaster.
   Conclusions: BTBD1 and BTBD2 belong to a small family of uncharacterized proteins that appear to be specific to animals. Epitope-tagged BTBD2 localized to cytoplasmic bodies. The characterization of BTBD1 and BTBD2 and their interaction with TOP1 is underway.
C1 Uniformed Serv Univ Hlth Sci, Dept Biochem & Mol Biol, Bethesda, MD 20814 USA.
   NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA.
   NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP D'Arpa, P (reprint author), Uniformed Serv Univ Hlth Sci, Dept Biochem & Mol Biol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
NR 41
TC 16
Z9 18
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2002
VL 3
AR 1
DI 10.1186/1471-2164-3-1
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 654CW
UT WOS:000181477100001
PM 11818025
ER

PT J
AU Moore, DF
   Altarescu, G
   Herscovitch, P
   Schiffmann, R
AF Moore, David F.
   Altarescu, Gheona
   Herscovitch, Peter
   Schiffmann, Raphael
TI Enzyme replacement reverses abnormal cerebrovascular responses in Fabry
   disease
SO BMC NEUROLOGY
LA English
DT Article
AB Background: Fabry disease is a lysosomal X-linked enzyme deficiency of alpha-galactosidase A associated with an increased mortality and morbidity due to renal failure, cardiac disease and early onset stroke.
   Methods: We examined the functional blood flow response of the brain after visual stimulation (reversing checkerboard pattern), and cerebral vasoreactivity following acetazolamide (15 mg/kg) with [O-15]H2O and positron emission tomography (PET) in Fabry disease. Twenty-six hemizygous patients (age range 19-47 years) were enrolled in a randomized double-blind placebo-controlled 6-month trial of enzyme replacement therapy administered by intravenous infusion every two weeks. Regional cerebral blood flow (rCBF) was measured with PET at the beginning and end of the trial.
   Results: Fabry patients had a significantly greater increase in rCBF following visual stimulation and acetazolamide challenge compared to controls. Visual reactivity was normal. The time for recovery of the cerebral vasculature following acetazolamide was prolonged in Fabry patients compared to controls. The abnormal rCBF response induced by visual stimulation and acetazolamide decreased significantly following enzyme replacement therapy, as did the prolonged recovery of the cerebral vasculature.
   Conclusions: Enzyme replacement therapy reverses the exaggerated cerebrovascular response in Fabry disease.
C1 [Moore, David F.; Altarescu, Gheona; Schiffmann, Raphael] Natl Inst Neurol Disorders & Stroke, Dev & Metab Branch, NIH, Bethesda, MD 20892 USA.
   [Herscovitch, Peter] NIH, PET Dept, Bethesda, MD 20892 USA.
RP Schiffmann, R (reprint author), Natl Inst Neurol Disorders & Stroke, Dev & Metab Branch, NIH, Bethesda, MD 20892 USA.
EM moored@ninds.nih.gov; Altaresg@ninds.nih.gov; PHerscovitch@cc.nih.gov;
   rs4e@nih.gov
FU National Institute of Neurological Disorders and Stroke intra-mural
   program
FX The National Institute of Neurological Disorders and Stroke intra-mural
   program funded this study.
NR 29
TC 67
Z9 67
U1 1
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2377
J9 BMC NEUROL
JI BMC Neurol.
PY 2002
VL 2
AR 4
DI 10.1186/1471-2377-2-4
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA V32RG
UT WOS:000208967700004
PM 12079501
ER

PT S
AU Hoge, R
   Atkinson, J
   Gill, B
   Crelier, G
   Marrett, S
   Pike, B
AF Hoge, R
   Atkinson, J
   Gill, B
   Crelier, G
   Marrett, S
   Pike, B
BE Tomita, M
   Kanno, I
   Hamel, E
TI Flow-metabolism regulation during brain activation and respiratory
   manipulations
SO BRAIN ACTIVATION AND CBF CONTROL, PROCEEDINGS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT International Symposium on Brain Activation and Cerebral Blood Flow
   Control
CY JUN 05-08, 2001
CL TOKYO, JAPAN
DE metabolism; perfusion; brain; MRI; hypercapnia
ID CEREBRAL BLOOD-FLOW; OXIDATIVE-METABOLISM; OXYGEN-CONSUMPTION;
   STIMULATION; CORTEX; MRI
AB Flow-metabolism coupling was examined in awake human volunteers during graded focal brain activation and during graded exposure to CO2, a systemic vasodilator. Data acquired during activation with arterial CO2 levels stabilized to normal values suggest an invariant flow-metabolism coupling relationship, but CO2-related variations in cerebral blood flow combined additively with activation-related flow responses, with negligible interaction between focal and systemic effects. These findings are inconsistent with the existence of a strictly homeostatic feedback scheme for the regulation of cerebral blood flow, and support the existence of multiple independent pathways of cerebrovascular control. (C) 2002 Elsevier Science B.V All rights reserved.
C1 Massachusetts Gen Hosp, NMR Ctr, Charlestown, MA 02129 USA.
   Montreal Neurol Inst, Montreal, PQ, Canada.
   US Natl Inst Hlth, Bethesda, MD USA.
RP Hoge, R (reprint author), Massachusetts Gen Hosp, NMR Ctr, Bldg 149,13th St, Charlestown, MA 02129 USA.
RI Pike, Bruce/K-5562-2014
OI Pike, Bruce/0000-0001-8924-683X
NR 8
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-50874-0
J9 INT CONGR SER
PY 2002
VL 1235
BP 33
EP 38
AR PII S0531-5131(02)00170-X
DI 10.1016/S0531-5131(02)00170-X
PG 6
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA BV28G
UT WOS:000178455900004
ER

PT S
AU Bandettini, PA
   Birn, RM
   Kelley, D
   Saad, ZS
AF Bandettini, PA
   Birn, RM
   Kelley, D
   Saad, ZS
BE Tomita, M
   Kanno, I
   Hamel, E
TI Dynamic nonlinearities in BOLD contrast: neuronal or hemodynamic?
SO BRAIN ACTIVATION AND CBF CONTROL, PROCEEDINGS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT International Symposium on Brain Activation and Cerebral Blood Flow
   Control
CY JUN 05-08, 2001
CL TOKYO, JAPAN
DE BOLD fMRI; linearity; stimulus duration; visual; motor; balloon model
ID BLOOD-FLOW; SIGNAL; FMRI
AB A primary goal of the functional MRI (fMRI) methods development is to characterize the relationship between the blood oxygenation level-dependent (BOLD) signal changes and neuronal activation. Recent studies of blood oxygenation level-dependent (BOLD) signal responses have demonstrated nonlinear behavior with respect to stimulus duration. Specifically, shorter duration stimuli produce larger signal changes than expected from a linear system. The precise reasons for this nonlinearity are not clearly understood. The goal of this study is to further clarify the origin of dynamic BOLD contrast nonlinearities-either neuronal or hemodynamic or both, by a combined approach of task timing modulation, spatial mapping, and modeling/fitting of the BOLD response using the "Balloon model." In this study, we found that (1) in agreement with the literature, the dynamic BOLD "on" response is nonlinear and has significant spatial heterogeneity. Spatial maps of nonlinearity, while highly reproducible, do not correlate with maps of the BOLD response magnitude or latency, but do show some correlation with functional segregation; (2) the dynamic BOLD "off" response is sublinear; and (3) while data fitted with Balloon model hemodynamic parameters, assuming linear neuronal input, generally create nonlinear dynamic BOLD responses, the Balloon model was not able to fit all BOLD contrast response task timing modulations simultaneously. These findings suggest that the dynamic BOLD response may be a linear function of the neuronal input function and that the neuronal input function is not a simple "on/off" boxcar function, but rather a nonlinear function that has an initial overshoot that lasts for approximately 4 s until reaching a steady state. (C) 2002 Elsevier Science B.V All rights reserved.
C1 NIMH, Unit Functional Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Bandettini, PA (reprint author), NIMH, Unit Functional Imaging Methods, Lab Brain & Cognit, NIH, Bldg 10,Rm 1D80,10 Ctr Dr, Bethesda, MD 20892 USA.
NR 14
TC 6
Z9 6
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-50874-0
J9 INT CONGR SER
PY 2002
VL 1235
BP 73
EP 85
AR PII S0531-5131(02)00174-7
DI 10.1016/S0531-5131(02)00174-7
PG 13
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA BV28G
UT WOS:000178455900008
ER

PT S
AU Ruetzler, CA
   Furuya, K
   Takeda, H
   Hallenbeck, JM
AF Ruetzler, CA
   Furuya, K
   Takeda, H
   Hallenbeck, JM
BE Tomita, M
   Kanno, I
   Hamel, E
TI Tumor necrosis factor-alpha, heme oxygenase-1 and manganese superoxide
   dismutase immunostaining of vessels and perivascular brain cells
   provides evidence for cyclic activation and inactivation of brain vessel
   segments
SO BRAIN ACTIVATION AND CBF CONTROL, PROCEEDINGS
SE INTERNATIONAL CONGRESS SERIES
LA English
DT Proceedings Paper
CT International Symposium on Brain Activation and Cerebral Blood Flow
   Control
CY JUN 05-08, 2001
CL TOKYO, JAPAN
DE microvessels; MnSOD; heme oxygenase; TNF-alpha; activation
ID ISCHEMIC STROKE; STRESS
AB The present work explores the possibility that several mediators of local hemostasis, inflammation and reactivity in blood vessels contribute to cyclic activation and inactivation of individual segments of the brain microvascular tree. Immunohistochemistry was performed with anti-manganese superoxide dismutase (MnSOD), anti-heme oxygenase-1 (HO-1), and antitumor necrosis factor-alpha (TNF-alpha) in five different strains of rats and in rats that received lipopolysaccharide to activate their vessels. In both normal and activated brain vessels, immunoreactivity was present as concentric perivascular rings involving vessel wall and surrounding parenchyma that appeared to coincide with one another in serial sections. The ring patterns suggested radial expansion from the vessel lumen into the surrounding parenchyma in cyclic waves. The average number of vessels per high power field (HPF) (mean +/- SD) with perivascular cuffs of immunoreactive MnSOD increased from 51 +/- 28 in Wistar, 72 +/- 46 in Wistar-Kyoto, and 84 +/- 30 in Sprague-Dawley rats (no spontaneous strokes) to 184 +/- 72 in spontaneously hypertensive stroke-prone rats (SHR-SP) (spontaneous strokes). Perivascular immunoreactive cuffs are also increased in spontaneously hypertensive rats (SHR) by the induction of cytokine expression by lipopolysaccharide (64 +/- 15 vs. 131 +/- 32/HPF). The findings are interpreted to indicate that focal hemostatic balance normally fluctuates in brain vessels and influences surrounding parenchymal cells. Perivascular immunoreactive cuffs representing this process are more frequent in animals with LPS-induced endothelial activation or genetic stroke-proneness. (C) 2002 Elsevier Science B.V. All rights reserved.
C1 Natl Inst Neurol Disorders & Stroke, Stroke Branch, NIH, Bethesda, MD 20892 USA.
RP Hallenbeck, JM (reprint author), Natl Inst Neurol Disorders & Stroke, Stroke Branch, NIH, 36 Convent Dr,MSC 4128,Bldg 36,Room 4-A03, Bethesda, MD 20892 USA.
NR 12
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0531-5131
BN 0-444-50874-0
J9 INT CONGR SER
PY 2002
VL 1235
BP 493
EP 500
AR PII S0531-5131(02)00237-6
DI 10.1016/S0531-5131(02)00237-6
PG 8
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA BV28G
UT WOS:000178455900052
ER

PT J
AU Gerald, MS
   Higley, S
   Lussier, ID
   Westergaard, GC
   Suomi, SJ
   Higley, JD
AF Gerald, MS
   Higley, S
   Lussier, ID
   Westergaard, GC
   Suomi, SJ
   Higley, JD
TI Variation in reproductive outcomes for captive male rhesus macaques
   (Macaca mulatta) differing in CSF 5-hydroxyindoleacetic acid
   concentrations
SO BRAIN BEHAVIOR AND EVOLUTION
LA English
DT Article
DE serotonin; cerebrospinal fluid 5-hydroxyindoleacetic acid behavior;
   reproduction; mammals; primates; rhesus macaques
ID MONKEYS CERCOPITHECUS-AETHIOPS; CEREBROSPINAL-FLUID;
   INDIVIDUAL-DIFFERENCES; SEROTONIN; BEHAVIOR; 5-HIAA; FASCICULARIS;
   PRIMATES; AGE; TESTOSTERONE
AB In rhesus macaque males, lower than average cerebrospinal fluid (CSF) concentrations of the principle metabolite of serotonin, 5-hydroxyindoleacetic acid (5-HIAA), have been linked to impulsivity, involvement in escalated aggression, failure to elicit consort relationships, production of fewer sperm plugs, and a relatively early age of mortality. Given these potential fitness costs, we performed two studies aimed at elucidating the effects of CSF 5-HIAA on reproduction. Study 1 retrospectively evaluated over a four-year period, the relative reproductive outcome for pairs of adult male rhesus macaques (n = 15) who lived in social groups and who differed in concentrations of CSF 5-HIAA. Study 2 examined the relationship between CSF 5-HIAA and sperm motility and density (n = 12), as a potential mechanism for maintaining variability in CSF 5-HIAA. For Study 1, an average measure from two CSF 5-HIAA samples was calculated for the two males who were present during the time when conception most likely took place (offspring birth date -165 +/- 14 days). Within-pair comparisons of CSF 5-HIAA concentrations between the sire and the non-successful male were drawn for each of the 72 offspring in the study. We found that while sires were typically the male with relatively higher CSF 5-HIAA within the pair, there were no absolute differences in CSF 5-HIAA between males who sired at least one offspring (sires) and those who failed to reproduce (non-sires). Furthermore, while absolute age was not predictive of reproductive outcome, sires with relatively high CSF 5-HIAA also tended to be also relatively older than their competitors. By contrast, for the males with relatively low CSF 5-HIAA who reproduced, sires were relatively younger than the non-sires. These differences in reproductive outcome for males differing in CSF 5-HIAA could not be explained by variability in sperm quantity or quality as we did not find evidence of a relationship between CSF 5-HIAA and either sperm measure. The results of this study suggest that as serotonergic function affects many aspects of behavior and survivorship, it might also be associated with reproductive outcome and different life-history strategies for males differing in concentrations of CSF 5-HIAA. Copyright (C) 2002 S. Karger AG, Basel.
C1 NICHD, Bethesda, MD USA.
   Primate Unit, NIH Anim Ctr, Poolesville, MD USA.
   Labs Virginia Inc, Yemassee, SC USA.
RP Gerald, MS (reprint author), Caribbean Primate Res Ctr, POB 906, Punta Santiago, PR 00741 USA.
NR 46
TC 10
Z9 10
U1 0
U2 3
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0006-8977
J9 BRAIN BEHAV EVOLUT
JI Brain Behav. Evol.
PY 2002
VL 60
IS 2
BP 117
EP 124
DI 10.1159/000065207
PG 8
WC Behavioral Sciences; Neurosciences; Zoology
SC Behavioral Sciences; Neurosciences & Neurology; Zoology
GA 605CZ
UT WOS:000178659000004
PM 12373062
ER

PT J
AU Smith, GH
AF Smith, GH
TI Mammary cancer and epithelial stem cells: a problem or a solution?
SO BREAST CANCER RESEARCH
LA English
DT Review
DE aging; mammary; neoplasia; stem cell; transplantation
ID ADULT HUMAN BREAST; MYOEPITHELIAL CELLS; DIFFERENTIATION; EXPRESSION;
   CLONOGENS; PROGENY; TISSUE; GLAND
AB The existing paradigms for stem cells in adult tissues include the integument, the alimentary canal, the lung, the liver, skeletal muscle and bone marrow. The mammary gland, by contrast, is the 'new kid on the block'. What little is known about stem cells in the mammary gland indicates that they possess a prodigious capacity for self-renewal. More importantly, in rodents, they persist with undiminished reproductive vigor throughout the organism's lifetime without regard to age or reproductive history. Do these stem cells represent primary targets for mammary neoplasia? If so, what are the implications for prevention/ therapy?
C1 NCI, Basic Res Lab, Canc Res Ctr, Bethesda, MD 20892 USA.
RP Smith, GH (reprint author), NCI, Basic Res Lab, Canc Res Ctr, Bethesda, MD 20892 USA.
NR 26
TC 22
Z9 22
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1465-542X
J9 BREAST CANCER RES
JI Breast Cancer Res.
PY 2002
VL 4
IS 2
BP 47
EP 50
DI 10.1186/bcr420
PG 4
WC Oncology
SC Oncology
GA 564XQ
UT WOS:000176339200001
PM 11879561
ER

PT J
AU McAllister, KA
   Wiseman, RW
AF McAllister, KA
   Wiseman, RW
TI Are Trp53 rescue of Brca1 embryonic lethality and Trp53/Brca1 breast
   cancer association related?
SO BREAST CANCER RESEARCH
LA English
DT Review
DE apoptosis; Brca1; breast cancer; Trp53; tumorigenesis
ID BRCA1-DEFICIENT MICE; TUMOR-FORMATION; CELL-CYCLE; P53; MUTATION;
   TUMORIGENESIS; APOPTOSIS; MOUSE; P21(WAF1/CIP1); PROLIFERATION
AB Brca1 is involved in multiple biological pathways including DNA damage repair, transcriptional regulation, and cell-cycle progression. A complex pattern of interactions of Brca1 with Trp53 has also emerged. Xu and coworkers found that haploid loss of Trp53 significantly reduces the embryonic lethality observed in mice with a homozygous in-frame deletion of Brca1 exon 11. They report that widespread apoptosis correlates with the embryonic lethality resulting from this homozygous 11 Brca1 mutation. A mechanism responsible for Brca1-associated carcinogenesis is proposed. These experiments extend our knowledge of a complex Brca1/Trp53 relationship. However, the precise mechanisms through which Brca1 interacts with Trp53 to suppress mammary tumor formation have yet to be elucidated.
C1 NIEHS, Lab Womens Hlth, NIH, Res Triangle Pk, NC 27709 USA.
RP McAllister, KA (reprint author), NIEHS, Lab Womens Hlth, NIH, MD C4-06,Rall Bldg,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
NR 26
TC 3
Z9 3
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1465-542X
J9 BREAST CANCER RES
JI Breast Cancer Res.
PY 2002
VL 4
IS 2
BP 54
EP 57
DI 10.1186/bcr422
PG 4
WC Oncology
SC Oncology
GA 564XQ
UT WOS:000176339200003
PM 11879563
ER

PT J
AU Sotiriou, C
   Powles, TJ
   Dowsett, M
   Jazaeri, AA
   Feldman, AL
   Assersohn, L
   Gadisetti, C
   Libutti, SK
   Liu, ET
AF Sotiriou, C
   Powles, TJ
   Dowsett, M
   Jazaeri, AA
   Feldman, AL
   Assersohn, L
   Gadisetti, C
   Libutti, SK
   Liu, ET
TI Gene expression profiles derived from fine needle aspiration correlate
   with response to systemic chemotherapy in breast cancer
SO BREAST CANCER RESEARCH
LA English
DT Review
DE breast cancer; cDNA microarray; chemotherapy; fine needle aspiration;
   gene expression
ID CELLS; APOPTOSIS; PATTERNS; OVEREXPRESSION; PREDICTORS; CISPLATIN;
   CARCINOMA
AB Background: Drug resistance in breast cancer is a major obstacle to successful chemotherapy. In this study we used cDNA microarray technology to examine gene expression profiles obtained from fine needle aspiration (FNA) of primary breast tumors before and after systemic chemotherapy. Our goal was to determine the feasibility of obtaining representative expression array profiles from limited amounts of tissue and to identify those expression profiles that correlate with treatment response.
   Methods: Repeat presurgical FNA samples were taken from six patients who were to undergo primary surgical treatment. Additionally, a group of 10 patients who were to receive neoadjuvant chemotherapy underwent two FNAs before chemotherapy (adriamycin 60 mg/m(2) and cyclophosphamide 600 mg/m(2)) followed by another FNA on day 21 after the first cycle. Total RNA was amplified with T7 Eberwine's procedure and labeled cDNA was hybridized onto a 7600-feature glass cDNA microarray.
   Results: We identified candidate gene expression profiles that might distinguish tumors with complete response to chemotherapy from tumors that do not respond, and found that the number of genes that change after one cycle of chemotherapy was 10 times greater in the responding group than in the nonresponding group.
   Conclusion: This study supports the suitability of FNA-derived cDNA microarray expression profiling of breast cancers as a comprehensive genomic approach for studying the mechanisms of drug resistance. Our findings also demonstrate the potential of monitoring post-chemotherapy changes in expression profiles as a measure of pharmacodynamic effect and suggests that these approaches might yield useful results when validated by larger studies.
C1 NCI, Ctr Adv Technol, Div Clin Sci, NIH, Gaithersburg, MD USA.
   Free Univ Brussels, Inst Jules Bordet, Chemotherapy Unit, Microarray Facil, Brussels, Belgium.
   Royal Marsden NHS Trust Hosp, London, England.
   Royal Marsden NHS Trust Hosp, Surrey, England.
   NCI, Surg Branch, NIH, Gaithersburg, MD USA.
   Genome Inst Singapore, Singapore, Singapore.
RP Sotiriou, C (reprint author), NCI, Ctr Adv Technol, Div Clin Sci, NIH, Gaithersburg, MD USA.
RI Jazaeri, Amir/A-2400-2008; Liu, Edison/C-4141-2008; Feldman,
   Andrew/D-5028-2012; Jazaeri, Amir/I-3458-2015
OI Jazaeri, Amir/0000-0003-4335-4151
NR 22
TC 157
Z9 159
U1 1
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND
SN 1465-542X
J9 BREAST CANCER RES
JI Breast Cancer Res.
PY 2002
VL 4
IS 3
AR R3
DI 10.1186/bcr433
PG 8
WC Oncology
SC Oncology
GA 564XV
UT WOS:000176339600001
PM 12052255
ER

PT J
AU Hori, M
   Shimazaki, J
   Inagawa, S
   Itabashi, M
   Hori, M
AF Hori, M
   Shimazaki, J
   Inagawa, S
   Itabashi, M
   Hori, M
TI Overexpression of MDM2 oncoprotein correlates with possession of
   estrogen receptor alpha and lack of MDM2 mRNA splice variants in human
   breast cancer
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE estrogen receptor alpha; human breast cancer MDM2 oncoprotein; MDM2
   oncogene; MDM2 splice variants
ID ONCOGENE OVEREXPRESSION; P53 PROTEIN; EXPRESSION; GENE; CARCINOMAS;
   MUTATIONS; AMPLIFICATION; ASSOCIATION
AB To evaluate the significance of murine double minute 2 (MDM2) oncoprotein in human breast cancer as a nuclear-cytoplasmic shuttling protein, an estrogen receptor (ER) alpha regulator, and a prognostic marker and to study how MDM2 is overexpressed, we investigated its status in tissue samples and examined the correlation between overexpression and MDM2 gene abnormalities, status, and clinicopathological parameters. We detected MDM2 oncoprotein in both nucleus and cytoplasm by frozen-section immunohistochemistry. There was a significant correlation between MDM2 overexpression and low-grade nuclear atypia, absence of lymph node involvement, and increased levels of ER alpha protein. Our molecular assays found no point mutations in Ser(1)7, but there was a correlation between MDM2 overexpression and the lack of splice variant mRNAs. These results suggest that the distribution of MDM2 reflects its nuclear-cytoplasmic shuttling ability; that interaction between p53 and MDM2 for tumor progression is not enhanced by point mutations at codon 17; and that the expression of MDM2 splice variants is a reason for the lack of its overexpression. MDM2 overexpression correlates with favorable prognostic parameters. A decreased level of MDM2 will lead to a deviation from the ER alpha signaling pathway.
C1 Ibaraki Prefectural Cent Hosp & Canc Ctr, Dept Pathol, Tomobe, Ibaraki 3091703, Japan.
   NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA.
RP Hori, M (reprint author), Ibaraki Prefectural Cent Hosp & Canc Ctr, Dept Pathol, 6528 Koibuchi, Tomobe, Ibaraki 3091703, Japan.
EM ms-hori@chubyoin.pref.ibaraki.jp
NR 24
TC 36
Z9 38
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD JAN
PY 2002
VL 71
IS 1
BP 77
EP 83
DI 10.1023/A:1013350419426
PG 7
WC Oncology
SC Oncology
GA 504LZ
UT WOS:000172859300008
PM 11859876
ER

PT J
AU Kuramoto, K
   Sakai, A
   Shigemasa, K
   Takimoto, Y
   Asaoku, H
   Tsujimoto, T
   Oda, K
   Kimura, A
   Uesaka, T
   Watanabe, H
   Katoh, O
AF Kuramoto, K
   Sakai, A
   Shigemasa, K
   Takimoto, Y
   Asaoku, H
   Tsujimoto, T
   Oda, K
   Kimura, A
   Uesaka, T
   Watanabe, H
   Katoh, O
TI High expression of MCL1 gene related to vascular endothelial growth
   factor is associated with poor outcome in non-Hodgkin's lymphoma
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE MCL1; BCL2 family; VEGF; non-Hodgkin's lymphoma; prognosis
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; INHIBITS APOPTOTIC DEATH;
   HEMATOPOIETIC-CELLS; ANGIOGENESIS; VEGF
AB We evaluated the level of MCL1 gene expression using quantitative reverse transcription polymerase chain reaction in lymph nodes of patients with non-Hodgkin lymphoma (NHL). MCL1 expression in patients in complete remission (CR) was significantly lower than in patients with progressive disease (PD, P = 0.0043). The disease-free survival rate was significantly higher in patients with MCL1 levels below the median level (P = 0.007). We also found that the level of expression of MCL1 mRNA was related to that of vascular endothelial growth factor mRNA in NFIL lymph nodes. Our data suggest that the MCL1 expression level could be considered a prognostic factor in NHL.
C1 Hiroshima Univ, RIRBM, Dept Hematol & Oncol, Hiroshima 730, Japan.
   Hiroshima Univ, Sch Med, Dept Gynecol & Obstet, Hiroshima 730, Japan.
   Hiroshima Red Cross Hosp, Hiroshima, Japan.
   Otake Natl Hosp, Hiroshima, Japan.
   Hiroshima City Hosp, Hiroshima, Japan.
   Hiroshima Univ, RIRBM, Dept Environm & Mutat, Hiroshima, Japan.
RP Kuramoto, K (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,7C-210,9000 Rockville Pk, Bethesda, MD 20892 USA.
NR 12
TC 20
Z9 21
U1 0
U2 0
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD JAN
PY 2002
VL 116
IS 1
BP 158
EP 161
DI 10.1046/j.1365-2141.2002.03253.x
PG 4
WC Hematology
SC Hematology
GA 521DQ
UT WOS:000173824000019
PM 11841410
ER

PT J
AU Lau, J
   Michon, JJ
   Chan, WS
   Ellwein, LB
AF Lau, J
   Michon, JJ
   Chan, WS
   Ellwein, LB
TI Visual acuity and quality of life outcomes in cataract surgery patients
   in Hong Kong
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID MADURAI INTRAOCULAR-LENS; OF-LIFE; DOUMEN COUNTY; SHUNYI COUNTY;
   RISK-FACTORS; CHINA; PREVALENCE; OPACITIES; BLINDNESS
AB Background: Visual acuity, visual functioning, and vision related quality of life outcomes after cataract surgery were assessed in a population based study in a suburban area of Hong Kong.
   Methods: A cluster sampling design was used to select apartment buildings within housing estates for enumeration. All enumerated residents 60 years of age or over were invited for an eye examination and visual acuity measurement at a site within each estate. Visual functioning (VF) and vision related quality of life (QOL) questionnaires were administered to interview subjects who had undergone cataract surgery and to unoperated people with presenting visual acuity less than 6/60 in either eye, and a sample of those with normal visual acuity.
   Results: 36.6% of the 3 10 cataract operated individuals had presenting visual acuity 6/18 or better in both eyes, and 40.0% when measured by pinhole. 4.5% were blind, with presenting visual acuity less than 6/60 in both eyes. Of operated eyes, 59.6% presented with visual acuity 6/18 or better. 11.2% of the operated eyes were blind with vision less than 6/60. Visual acuity outcomes 6/18 or better were marginally associated with surgery in private versus public hospitals. Lens status (pseudophakic versus aphakic) and surgical period (within the most recent 3 years versus before) were not significantly related to vision outcomes. Mean VF and QOL scores decreased consistently with decreasing vision status. Spearman correlation with vision status was 0,420 for VF scores and 0.313 for QOL scores. Among VF/QOL subscales, correlation was strongest for visual perception (r = 0.447) among VF subscales and weakest for self care (r = 0. 171) among QOL subscales. Regression adjusted VF and QOL total scores for cataract operated individuals were slightly lower than for those of visually comparable unoperated individuals (p<0.05).
   Conclusions: Cataract operations in Hong Kong did not consistently produce good presenting visual acuity outcomes, suggesting that postoperative monitoring would be useful to minimise visual impairment in this population. Although vision outcomes were consistently correlated with all VF/QOL subscale scores, there was a differential impact with VF subscales usually being affected more by reduced acuity than the more general QOL subscales.
C1 NEI, NIH, Bethesda, MD 20892 USA.
   Chinese Univ Hong Kong, Ctr Clin Trials & Epidemiol Res, Hong Kong, Hong Kong, Peoples R China.
   Chinese Univ Hong Kong, Dept Ophthalmol & Visual Sci, Hong Kong, Hong Kong, Peoples R China.
RP Ellwein, LB (reprint author), NEI, NIH, 31 Ctr Dr, Bethesda, MD 20892 USA.
FU NEI NIH HHS [N01-EY-2103]
NR 14
TC 47
Z9 55
U1 0
U2 2
PU BRITISH MED JOURNAL PUBL GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD JAN
PY 2002
VL 86
IS 1
BP 12
EP 17
DI 10.1136/bjo.86.1.12
PG 6
WC Ophthalmology
SC Ophthalmology
GA 509ZM
UT WOS:000173184300006
PM 11801495
ER

PT J
AU Klein, R
   Marino, EK
   Kuller, LH
   Polak, JF
   Tracy, RP
   Gottdiener, JS
   Burke, GL
   Hubbard, LD
   Boineau, R
AF Klein, R
   Marino, EK
   Kuller, LH
   Polak, JF
   Tracy, RP
   Gottdiener, JS
   Burke, GL
   Hubbard, LD
   Boineau, R
TI The relation of atherosclerotic cardiovascular disease to retinopathy in
   people with diabetes in the Cardiovascular Health Study
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID MICROVASCULAR COMPLICATIONS; HARD EXUDATE; MELLITUS; RISK; ASSOCIATION;
   CHOLESTEROL; PROGRESSION; POPULATION; LIPIDS; OLDER
AB Aims: To describe the association of retinopathy with atherosclerosis and atherosclerotic risk factors in people with diabetes.
   Methods: 296 of the 558 people classified as having diabetes by the American Diabetes Association criteria, from a population based cohort of adults (ranging in age from 69 to 102 years) living in four United States communities (Allegheny County, Pennsylvania; Forsyth County, North Carolina; Sacramento County, California; and Washington County, Maryland) were studied from 1997 to 1998. Lesions typical of diabetic retinopathy were determined by grading a 45degrees colour fundus photograph of one eye of each participant, using a modification of the Airlie House classification system.
   Results: Retinopathy was present in 20% of the diabetic cohort, with the lowest prevalence (16%), in those 80 years of age or older. Retinopathy was detected in 20.3% of the 296 people with diabetes; 2.7% of the 296 had signs of proliferative retinopathy and 2.1% had signs of macular oedema, The prevalence of diabetic retinopathy was higher in black people (35.4%) than white (16,0%). Controlling for age, sex, and blood glucose, retinopathy was more frequent in black people than white (odds ratio (OR) 2.26, 95% confidence interval (Cl) 1.01, 5.05), in those with longer duration of diabetes (OR (per 5 years of diabetes) 1.42, 95% Cl 1.18, 1.70), in those with subclinical cardiovascular disease (OR 1.49, 95% Cl 0.51, 4.31), or coronary heart disease or stroke (OR 3.23, 95% Cl 1.09, 9.56) than those without those diseases, in those with higher plasma low density lipoprotein (LDL) cholesterol (OR (per 10 mg/dl of LDL cholesterol) 1.12, 95% Cl 1.02, 1.23), and in those with gross proteinuria (OR 4.76, 95% Cl 1.53, 14.86).
   Conclusion: Data from this population based study suggest a higher prevalence of retinopathy in black people than white people with diabetes and the association of cardiovascular disease, elevated plasma LDL cholesterol, and gross proteinuria with diabetic retinopathy. However, any conclusions or explanations regarding associations described here must be made with caution because only about one half of those with diabetes mellitus were evaluated.
C1 Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med, Madison, WI 53705 USA.
   Univ Washington, Dept Biostat, CHS Coordinating Ctr, Seattle, WA 98195 USA.
   Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
   Univ Vermont, Lab Clin Biochem Res, Colchester Res Facil, Colchester, VT USA.
   St Francis Hosp, Roslyn, NY USA.
   Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA.
   Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
RP Klein, R (reprint author), Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med, 610 N Walnut St,460 WARF, Madison, WI 53705 USA.
EM kleinr@epi.ophth.wisc.edu
FU NHLBI NIH HHS [HC-97-06]
NR 31
TC 68
Z9 73
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
EI 1468-2079
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD JAN
PY 2002
VL 86
IS 1
BP 84
EP 90
DI 10.1136/bjo.86.1.84
PG 7
WC Ophthalmology
SC Ophthalmology
GA 509ZM
UT WOS:000173184300022
PM 11801510
ER

PT J
AU Foster, JS
   von Boletzky, S
   McFall-Ngai, MJ
AF Foster, JS
   von Boletzky, S
   McFall-Ngai, MJ
TI A comparison of the light organ development of Sepiola robusta Naef and
   Euprymna scolopes Berry (Cephalopoda : Sepiolidae)
SO BULLETIN OF MARINE SCIENCE
LA English
DT Article
ID BACTERIAL SYMBIONTS; VIBRIO-FISCHERI; POSTEMBRYONIC DEVELOPMENT; SQUID;
   MORPHOGENESIS; HOST; MORPHOLOGY; INDUCTION; GROWTH
AB Light organ development was studied in the sepiolid squid Sepiola robusta Naef and compared to that of Euprymna scolopes Berry. Both species form obligate mutualisms with luminous bacteria from the environment. The embryonic period of S. robusta, which is at least double to that of E. scolopes at similar temperatures, produced additional features not reported to occur in the E. scolopes light organ, including an extended ciliated ridge at the base of the light organ, as well as additional crypt spaces to house symbiotic bacteria. Accessory structures, which are used to modify the bacteria-produced light, are not under the induction of symbiotic bacteria and appear in S. robusta before hatching, whereas in E. scolopes these tissues form post-hatching. At hatching the light organs of both species respond to symbiotically competent bacteria and undergo similar developmental remodeling. Specifically, the ciliated epithelial fields on the surface of the light organ undergo a program of cell death and regression that spans 4 to 5 d in E. scolopes, and over 9 d in S. robusta. Although the timing of embryogenesis differs between these two species, the results of these studies demonstrate that the influence of Vibrio fischeri, the specific symbiont, appears to be restricted to the initial stages of post-hatching development of both light organs.
C1 NIDCR, NIH, Bethesda, MD 20892 USA.
   Observ Oceanol Banyuls, CNRS, F-66651 Banyuls sur Mer, France.
RP McFall-Ngai, MJ (reprint author), Univ Hawaii, Pacific Biomed Res Ctr, 41 Ahui St, Honolulu, HI 96813 USA.
NR 36
TC 10
Z9 10
U1 1
U2 3
PU ROSENSTIEL SCH MAR ATMOS SCI
PI MIAMI
PA 4600 RICKENBACKER CAUSEWAY, MIAMI, FL 33149 USA
SN 0007-4977
J9 B MAR SCI
JI Bull. Mar. Sci.
PD JAN
PY 2002
VL 70
IS 1
BP 141
EP 153
PG 13
WC Marine & Freshwater Biology; Oceanography
SC Marine & Freshwater Biology; Oceanography
GA 563RB
UT WOS:000176268400011
ER

PT J
AU Trach, DD
   Cam, PD
   Ke, NT
   Rao, MR
   Dinh, D
   Hang, PV
   Hung, NV
   Canh, DG
   Thiem, VD
   Naficy, A
   Ivanoff, B
   Svennerholm, AM
   Holmgren, J
   Clemens, JD
AF Trach, DD
   Cam, PD
   Ke, NT
   Rao, MR
   Dinh, D
   Hang, PV
   Hung, NV
   Canh, DG
   Thiem, VD
   Naficy, A
   Ivanoff, B
   Svennerholm, AM
   Holmgren, J
   Clemens, JD
TI Investigations into the safety and immunogenicity of a killed oral
   cholera vaccine developed in Viet Nam
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
DE cholera vaccines/immunology/adverse effects; vaccines,
   inactivated/immunology/adverse effects; clinical trials; comparative
   study; Viet Nam (source : MeSH, NLM)
ID WHOLE-CELL; B-SUBUNIT; FIELD TRIAL; IMMUNE-RESPONSES; FOLLOW-UP;
   IMMUNIZATION; BANGLADESH
AB Objective To evaluate a killed oral cholera vaccine produced in Viet Nam, and to compare the Vietnamese vaccine with one that is licensed internationally.
   Method Two-dose regimens of a locally produced, bivalent, anti-O1, anti-O139 killed oral whole-cell cholera vaccine (biv-WC) and of a commercially available, monovalent (anti-O1) oral recombinant B subunit-killed whole-cell cholera vaccine (rBS-WC) were compared in two trials in Viet Nam. In the first trial, 144 adults were randomized to biv-WC with or without buffer, rBS-WC with buffer, or placebo without buffer, In the second, 103 children aged 1-12 years were randomized to biv-WC without buffer, rBS-WC with buffer, or placebo without buffer.
   Findings No regimen was associated with significant side-effects. In adults, ca 60% of recipients of either vaccine exhibited at least fourfold serum anti-O1 vibriocidal antibody responses and ca 40% of recipients of biv-WC demonstrated anti-O139 vibriocidal responses, Both anti-O1 (ca 90% in each vaccine group and anti-O139 (68% in the biv-WC group) vibriocidal responses occurred more frequently in children, The responses to biv-WC were unaffected by the receipt of buffer.
   Conclusion It was concluded that biv-WC was safe and immunogenic, that it could be administered without buffer, and that it could elicit robust immune responses even in children, for whom the risk of endemic cholera is highest.
C1 Int Vaccine Inst, Seoul 151600, South Korea.
   Inst Vaccines & Biol Subst, Nha Trang, Vietnam.
   NICHHD, Bethesda, MD 20892 USA.
   Inst Trop Med, Hanoi, Vietnam.
   World Hlth Org, Geneva, Switzerland.
   Univ Gothenburg, Gothenburg, Sweden.
   Natl Inst Hyg & Epidemiol, Hanoi, Vietnam.
RP Clemens, JD (reprint author), Int Vaccine Inst, Seoul 151600, South Korea.
NR 16
TC 55
Z9 55
U1 0
U2 4
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 1
BP 2
EP 8
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 517LJ
UT WOS:000173611800003
PM 11884967
ER

PT J
AU Williams, HA
   Jones, C
   Alilio, M
   Zimicki, S
   Azevedo, I
   Nyamongo, I
   Sommerfeld, J
   Meek, S
   Diop, S
   Bloland, PB
   Greenwood, B
AF Williams, HA
   Jones, C
   Alilio, M
   Zimicki, S
   Azevedo, I
   Nyamongo, I
   Sommerfeld, J
   Meek, S
   Diop, S
   Bloland, PB
   Greenwood, B
TI The contribution of social science research to malaria prevention and
   control
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
C1 Ctr Dis Control & Prevent, Malaria Epidemiol Branch, Div Parasit Dis, Atlanta, GA USA.
   Univ London London Sch Hyg & Trop Med, DFID Malaria Programme, London WC1E 7HT, England.
   NIH, Multilateral Initiat Malaria, Fogerty Int Ctr, Bethesda, MD 20892 USA.
   Acad Educ Dev, CHANGE Project, Washington, DC USA.
   WHO, Bank WHO Special Programme Res Training Trop Dis, CH-1211 Geneva, Switzerland.
   Univ Nairobi, Nairobi, Kenya.
   Malaria Consortium, London, England.
   Malaria Consortium, Liverpool, Merseyside, England.
RP Williams, HA (reprint author), Ctr Dis Control & Prevent, Malaria Epidemiol Branch, Div Parasit Dis, Atlanta, GA USA.
NR 0
TC 17
Z9 16
U1 0
U2 2
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 3
BP 251
EP 252
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 536EJ
UT WOS:000174687500012
PM 11984613
ER

PT J
AU Fikree, FF
   Azam, SI
   Berendes, HW
AF Fikree, FF
   Azam, SI
   Berendes, HW
TI Time to focus child survival programmes on the newborn: assessment of
   levels and causes of infant mortality in rural Pakistan
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
DE infant, newborn; infant mortality; cause of death; rural population;
   sampling studies; Pakistan
ID VERBAL AUTOPSY; NEONATAL TETANUS; RISK FACTOR; BANGLADESH; PATTERNS;
   DEATHS
AB Objective Population-based surveys were conducted in selected clusters of Pakistan's least developed provinces, Balochistan and North-West Frontier Province (NWFP), including the Federally Administered Tribal Areas (FATA), to assess levels and causes of neonatal and postneonatal mortality.
   Methods Interviews were conducted in a total of 54 834 households: Balochistan, 20 486; NWFP, 26 175; and FATA, 8173. Trained interviewers administered questionnaires after obtaining verbal informed consent from the respondents. Verbal autopsy interviews were conducted for infant deaths reported for the previous year.
   Findings The infant mortality rate based on combined data from the different sites was 99.7 per 1000 live births (range 129.0-70.1). The contribution of neonatal deaths to all infant deaths was much higher for NWFP (67.2%), where the overall rate was lowest, than for Balochistan (50.8%) and FATA (56.8%). Around 70% of all neonatal deaths occurred in the early neonatal period. The three main clinical causes of infant deaths were diarrhoea syndrome (21.6%), tetanus (11.7%) and acute respiratory infections (11.6%). In the neonatal period, however, tetanus (18.3%), small size for gestational age or low birth weight (15.3%), and birth injury (12.0%) accounted for nearly half (45.6%) of all deaths, while the contributions of diarrhoea syndrome (5.1%) and acute respiratory infections (6.0%) were less significant (11.1%). Tetanus was the cause of death for 21.7% and 17.1% of all infant deaths in FATA and NWFP respectively.
   Conclusion The results suggest that there should be a shift in child survival programmes to give greater emphasis to maternal and neonatal health, in particular to maternal tetanus immunization, safe delivery and cord care.
C1 Populat Council, New York, NY 10017 USA.
   Aga Khan Univ, Dept Community Hlth Sci, Karachi, Pakistan.
   NICHHD, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD 20892 USA.
RP Fikree, FF (reprint author), Populat Council, 1 Dag Hammarskjold Plaza, New York, NY 10017 USA.
FU NCI NIH HHS [SFCP -08-024-N]
NR 15
TC 35
Z9 38
U1 0
U2 2
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 4
BP 271
EP 276
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 545MZ
UT WOS:000175222700003
PM 12075362
ER

PT J
AU Ronsmans, C
   Campbell, OMR
   McDermott, J
   Koblinsky, M
AF Ronsmans, C
   Campbell, OMR
   McDermott, J
   Koblinsky, M
TI Questioning the indicators of need for obstetric care
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
DE health care surveys; maternal health services/statistics; health
   services needs and demand/statistics; health services/utilization; data
   collection/methods
ID SAFE MOTHERHOOD PROGRAMS; CESAREAN-SECTION; SOUTH KALIMANTAN;
   SPATIAL-ANALYSIS; HOSPITAL DATA; INTERVENTIONS; COMPLICATIONS;
   COUNTRIES; INDONESIA; ZIMBABWE
AB The difficulties in measuring maternal mortality have led to a shift in emphasis from indicators of health to indicators of use of health care services. Furthermore, the recognition that some women need specialist obstetric care to prevent maternal death has led to the search for indicators measuring the met need for obstetric care. Although intuitively appealing, the conceptualization and definition of the need for obstetric care is far from straightforward, and there is relatively little experience so far in the use and interpretation of indicators of service use or need for obstetric care, In this paper we review indicators of service use and need for obstetric care, and briefly discuss data collection issues.
C1 Univ London London Sch Hyg & Trop Med, Maternal Hlth Programme, Infect Dis Epidemiol Unit, London WC1E 7HT, England.
   Mother Care John Snow Inc, Arlington, VA USA.
   NIH, Fogarty Int Ctr, Div Int Training & Res, Bethesda, MD USA.
RP Ronsmans, C (reprint author), Univ London London Sch Hyg & Trop Med, Maternal Hlth Programme, Infect Dis Epidemiol Unit, Keppel St, London WC1E 7HT, England.
NR 44
TC 33
Z9 35
U1 0
U2 1
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 4
BP 317
EP 324
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 545MZ
UT WOS:000175222700010
PM 12075369
ER

PT J
AU Ginsberg, AM
AF Ginsberg, AM
TI What's new in tuberculosis vaccines?
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
DE BCG vaccine; Mycobacterium bovis, immunology, genetics; Mycobacterium
   tuberculosis, immunology, genetics; drug evaluation; preclinical;
   models, animal; clinical trials, phase I; research
ID MYCOBACTERIUM-TUBERCULOSIS; PROTECTIVE EFFICACY; PUBLISHED LITERATURE;
   CALMETTE-GUERIN; BCG; VACCINATION; PREVENTION; BACILLUS; GENOMICS;
   SEQUENCE
AB Over the past 10 years, tuberculosis (TB) vaccine development has resurged a an active area of investigation. The renewed interest has been stimulated by the recogniton that, although BCG is delivered to approximately 90% of all neonates globally through the Expanded Programme on immunization, Mycobacterium tuberculosis continues to cause over 8 million new cases of TB and over 2 million deaths annually. Over one hundred TB vaccine candidates have been developed, using different approaches to inducing protective immunity. Candidate vaccines are typically screened in small animal models of primary TB disease for their ability to protect against a virulent strain of M. tuberculosis. The most promising are now beginning to enter human safety trials, marking real progress in this field for the first time in 80 years.
C1 NIAID, Resp Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Ginsberg, AM (reprint author), NIAID, Resp Dis Branch, NIH, 6700-B Rockledge Drive,Room 3133, Bethesda, MD 20892 USA.
NR 45
TC 36
Z9 41
U1 0
U2 4
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 6
BP 483
EP 488
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 560AP
UT WOS:000176059300013
PM 12132007
ER

PT J
AU Fisher, M
   Kripke, ML
AF Fisher, M
   Kripke, ML
TI Systemic alteration induced in mice by ultraviolet light irradiation and
   its relationship to ultraviolet carcinogenesis
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
DE immune surveillance; tumor immunology; immunosuppression
ID SKIN TUMORS
AB Chronic irradiation of mice with ultraviolet (UV) light produces a systemic alteration of an immunologic nature. This alteration is detectable in mice long before primary skin cancers induced by UV light begin to appear. The alteration results in the failure of UV-irradiated mice to reject highly antigenic, transplanted UV-induced tumors that are rejected by unirradiated syngeneic recipients. The immunologic aspect of this systemic alteration was demonstrated by transferring lymphoid cells from UV-irradiated mice to lethally x-irradiated recipients. These recipients were unable to resist a later challenge with a syngeneic UV-induced tumor, whereas those given lymphoid cells from normal donors were resistant to tumor growth.
   Parabiosis of normal mice with UV-irradiated mice, followed by tumor challenge of both parabionts with a UV-induced tumor, resulted in the growth of the challenge tumors in both UV-irradiated and unirradiated mice. Splenic lymphocytes from tumor-implanted UV-treated mice were not cytotoxic in vitro against UV-induced tumors, whereas under identical conditions cells from tumor-implanted, unirradiated mice were highly cytotoxic. Our findings suggest that repeated UV irradiation can circumvent an immunologic mechanism that might otherwise destroy nascent UV-induced primary tumors that are strongly antigenic.
C1 NCI, Basic Res Program, Frederick Canc Res Ctr, Frederick, MD 21701 USA.
RP Fisher, M (reprint author), NCI, Basic Res Program, Frederick Canc Res Ctr, POB B, Frederick, MD 21701 USA.
NR 13
TC 17
Z9 18
U1 0
U2 0
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PY 2002
VL 80
IS 11
BP 908
EP 912
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 617DA
UT WOS:000179343900012
PM 12481215
ER

PT J
AU Ho, MWY
   Shears, SB
AF Ho, MWY
   Shears, SB
TI Regulation of calcium-activated chloride channels by inositol
   3,4,5,6-tetrakisphosphate
SO CALCIUM-ACTIVATED CHLORIDE CHANNELS
SE CURRENT TOPICS IN MEMBRANES
LA English
DT Review
ID DEPENDENT PROTEIN-KINASE; MAMMARY-TUMOR CELLS; MYOINOSITOL
   1,3,4,5,6-PENTAKISPHOSPHATE; AVIAN ERYTHROCYTES; TYROSINE
   PHOSPHORYLATION; ENDOTHELIAL-CELLS; APICAL MEMBRANE; BOVINE TRACHEA; CL
   SECRETION; HUMAN CLC-3
C1 NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
RP Ho, MWY (reprint author), NIEHS, Lab Signal Transduct, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 77
TC 13
Z9 13
U1 0
U2 2
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1063-5823
J9 CURR TOP MEMBR
PY 2002
VL 53
BP 345
EP 363
DI 10.1016/S1063-5823(02)53041-6
PG 19
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA BV27Q
UT WOS:000178445000016
ER

PT J
AU Smith, ML
   Fornace, AJ
AF Smith, ML
   Fornace, AJ
TI Chemotherapeutic targeting of p53
SO CANCER BIOLOGY & THERAPY
LA English
DT Editorial Material
ID WILD-TYPE; CYCLIN-G; APOPTOSIS; CONFORMATION; CELLS; MUTATIONS;
   CISPLATIN; PROTEINS; EPITOPE; ARREST
C1 Indiana Univ, Sch Med, Ctr Canc, Dept Microbiol, Indianapolis, IN 46202 USA.
   Indiana Univ, Sch Med, Walther Oncol Ctr, Indianapolis, IN 46202 USA.
   Walther Canc Inst, Indianapolis, IN 46202 USA.
   NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Smith, ML (reprint author), Indiana Univ, Sch Med, Ctr Canc, Dept Microbiol, Indianapolis, IN 46202 USA.
RI Fornace, Albert/A-7407-2008
OI Fornace, Albert/0000-0001-9695-085X
NR 25
TC 9
Z9 10
U1 0
U2 0
PU LANDES BIOSCIENCE
PI GEORGETOWN
PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD JAN-FEB
PY 2002
VL 1
IS 1
BP 56
EP 57
PG 2
WC Oncology
SC Oncology
GA 635DQ
UT WOS:000180383100014
PM 12197484
ER

PT J
AU Egorin, MJ
   Lagattuta, TF
   Hamburger, DR
   Covey, JM
   White, KD
   Musser, SM
   Eiseman, JL
AF Egorin, MJ
   Lagattuta, TF
   Hamburger, DR
   Covey, JM
   White, KD
   Musser, SM
   Eiseman, JL
TI Pharmacokinetics, tissue distribution, and metabolism of
   17-(dimethylaminoethylamino)-17-demethoxygeldanamycin (NSC 707545) in
   CD2F1 mice and Fischer 344 rats
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE geldanamycin; ansamycin; HSP90; pharmacokinetics
ID ANTICANCER DRUG TARGETS; GENE-PRODUCT P185; BENZOQUINOID ANSAMYCINS;
   MUTANT P53; CELL-CYCLE; IN-VIVO; GELDANAMYCIN DERIVATIVES;
   GLUCOCORTICOID RECEPTOR; MOLECULAR CHAPERONE; HSP90-BINDING AGENT
AB Purpose: 17-(Dimethylaminoethylamino)-17-demethoxygeldanamycin (17DMAG) is an analogue of the benzoquinone ansamycin compound 17-(allylamino)-17-demethoxygeldanamycin (17AAG), which is currently being evaluated in clinical trials. Studies were performed in mice and rats to: (1) define the plasma pharmacokinetics, tissue distribution, and urinary excretion of 17DMAG after i.v. delivery; (2) define the bioavailability of 17DMAG after i.p. and oral delivery; (3) characterize the biliary excretion of 17DMAG after i.v. delivery to rats; and (4) characterize, if possible, any metabolites of 17DMAG observed in plasma, tissue, urine, or bile. Materials and methods: Studies were performed in female, CD2F1 mice or male Fischer 344 rats. In preliminary toxicity studies and subsequent i.v. pharmacokinetic studies in mice, 17DMAG i.v. bolus doses of 33.3, 50, and 75 mg/kg were used. In bioavailability studies, i.p. and oral 17DMAG doses of 75 mg/kg were used. In preliminary toxicity studies in rats, i.v. bolus doses of 10 and 20 mg/kg were used, and in i.v. pharmacokinetic studies 10 mg/kg was used. Compartmental and noncompartmental analyses were applied to the plasma concentration versus time data. In mice and rats, concentrations of 17DMAG were determined in multiple tissues. Urine was collected from mice and rats treated with each of the i.v. doses of 17DMAG mentioned above, and drug excretion was calculated until 24 h after treatment. Biliary excretion of 17DMAG and metabolites was studied in bile duct-cannulated rats given a 10 mg/kg i.v. bolus dose of 17DMAG. 17DMAG metabolites were identified with LC/MS. Results: A 75 mg/kg dose of 17DMAG caused no changes in appearance, appetite, waste elimination, or survival of treated mice as compared to vehicle-treated controls. Bolus i.v. delivery of 17DMAG at 75 mg/kg produced "peak" plasma 17DMAG concentrations between 18 and 24.2 mug/ml in mice killed at 5 min after injection. Sequential reduction in the 17DMAG dose to 50 and 33.3 mg/kg resulted in "peak" plasma 17DMAG concentrations between 9.4 and 14.4, and 8.4 and 10.5 mug/ml, respectively. Plasma 17DMAG AUC increased from 362 to 674 and 1150 mug/ml.min when the 17DMAG dose increased from 33.3 to 50 and 75 mg/kg, respectively, corresponding to a decrease in 17DMAG CLtb from 92 ml/min per kg to 75 and 65 ml/min per kg. Plasma 17DMAG concentration versus time data were best fit by a two-compartment open linear model. No potential 17DMAG metabolites were observed in plasma. 17DMAG bioavailability was 100% and 50% after i.p. and oral delivery. respectively. In rats, an i.v. bolus dose of 10 mg/kg produced peak plasma 17DMAG concentrations between 0.88 and 1.74 mug/ml. Plasma 17DMAG concentrations had fallen below the lower limit of quantitation by 180 min and were best fit by a one-compartment open linear model. The plasma 17DMAG AUC was 104 mug/ml.min, corresponding to a 17DMAG CLtb of 96 ml/min per kg. 17DMAG distributed rapidly to all mouse and rat tissues except brain and testes. Only mouse liver contained materials consistent with potential metabolites of 17DMAG, but their concentrations were below the limit of quantitation of the HPLC assay used.
   Within the first 24 h after delivery. urinary excretion of 17DMAG by mice and rats accounted or 10.6-14.8% and 12.5-16%. respectively, of the delivered dose. By 15 min after i.v. delivery of 10 mg/kg of 17DMAG, rat bile contained 11 new materials with absorbance similar to that of 17DMAG. Four of these proposed metabolites had an M, of 633, indicating addition of an oxygen. Two of these proposed metabolites had an M-r of 603. implying the loss of one methyl group, and one had an M-r of 589, implying the loss of two methyl groups. The remaining four proposed metabolites had an M-r of 566, 571, 629, and 645. respectively. Biliary excretion of 17DMAG and metabolites accounted for 4.7 +/- 1.4% of the delivered dose. with 17DMAG accounting for 50.7 +/- 3.4% of the biliary excretion. Conclusions: 17DMAG has excellent bioavailability when given i.p. and good bioavailability when given orally. 17DMAG is widely distributed to tissues and is quantitatively metabolized much less than is 17AAG. The pharmacokinetic and metabolite data generated should prove relevant to the design of additional preclinical studies as well as to contemplated clinical trials of 17DMAG and could be useful in their interpretation.
C1 Univ Pittsburgh, Inst Canc, Mol Therapeut Drug Discovery Program, Pittsburgh, PA 15213 USA.
   Univ Pittsburgh, Sch Med, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15213 USA.
   Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15213 USA.
   NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
   US FDA, Ctr Food Safety & Appl Nutr, Instrumentat & Biophys Branch, Washington, DC 20204 USA.
RP Egorin, MJ (reprint author), Univ Pittsburgh, Inst Canc, Mol Therapeut Drug Discovery Program, Pittsburgh, PA 15213 USA.
EM egorinmj@msx.upmc.edu
FU NCI NIH HHS [2P30 CA47904, N01-CM07106]
NR 71
TC 111
Z9 118
U1 0
U2 15
PU SPRINGER-VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JAN
PY 2002
VL 49
IS 1
BP 7
EP 19
DI 10.1007/s00280-001-0380-8
PG 13
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 521RY
UT WOS:000173856400002
PM 11855755
ER

PT J
AU Iannotti, RJ
   Finney, LJ
   Sander, AA
   De Leon, JM
AF Iannotti, RJ
   Finney, LJ
   Sander, AA
   De Leon, JM
TI Effect of clinical breast examination training on practitioner's
   perceived competence
SO CANCER DETECTION AND PREVENTION
LA English
DT Article
DE CBE experience; self-efficacy; breast lesion detection; prevention and
   control; physical examination; clinical competence; health promotion;
   health education
ID CANCER
AB Effective clinical breast exam (CBE) training should not only improve screening technique but also reduce barriers to performing CBE by increasing perceived competence and self-efficacy. Using the vertical strip technique with silicone breast models and live patients, 4-day CBE training sessions were provided to 34 nurse-practitioners. Trainees perceived a significant decrease in the size of breast lesion they could detect after training (P < 0.0001). The size of the detectable lesion reported prior to training was correlated with the years of CBE experience (P < 0.05); however, the size of the detectable lesion after training was not significantly related to previous CBE experience. Trainees with less CBE experience prior to training reported greater improvement in the ability to detect smaller lesions (P < 0.05). Results indicate a significant CBE training effect on perceived competence, and suggest that nurse practitioners from all levels of experience can benefit significantly from CBE training. (C) 2002 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.
C1 NICHHD, Div Epidemiol, Prevent Res Branch, Bethesda, MD 20892 USA.
   NCI, Div Canc Prevent, Bethesda, MD 20892 USA.
   Mammatech Corp, Gainesville, FL 32601 USA.
RP Iannotti, RJ (reprint author), NICHHD, Div Epidemiol, Prevent Res Branch, 6100 Execut Blvd,7B05, Bethesda, MD 20892 USA.
NR 13
TC 4
Z9 4
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0361-090X
J9 CANCER DETECT PREV
JI Cancer Detect. Prev.
PY 2002
VL 26
IS 2
BP 146
EP 148
AR PII S0361-090X902)00029-6
DI 10.1016/S0361-090X(02)00029-6
PG 3
WC Oncology
SC Oncology
GA 578UP
UT WOS:000177139200007
ER

PT J
AU Michener, CM
   Ardekani, AM
   Petricoin, EF
   Liotta, LA
   Kohn, EC
AF Michener, CM
   Ardekani, AM
   Petricoin, EF
   Liotta, LA
   Kohn, EC
TI Genomics and proteomics: application of novel technology to early
   detection and prevention of cancer
SO CANCER DETECTION AND PREVENTION
LA English
DT Review
DE molecular-targeted therapies; cancer; laser capture microdissection
ID LASER CAPTURE MICRODISSECTION; OVARIAN-CANCER; BREAST-CANCER;
   GENE-EXPRESSION; CELL-LINES; MONOCLONAL-ANTIBODY; ESTROGEN-RECEPTOR;
   CARCINOMA; ONCOGENE; TUMORS
AB Advances in molecular biology over the past decade have helped to enhance our understanding of the complex interplay between genetic, transcriptional and translational alterations in human cancers. These molecular changes are the basis for an evolving field of high-throughput cancer discovery techniques using microscopic amounts of patient-based materials. Laser capture microdissection allows pure populations of cells to be isolated from both the tumor and stroma in order to identify subtle differences in RNA and protein expression. Comparative, analysis of these alterations between normal, pre-invasive, and invasive tissue using powerful bioinformatics programs has allowed us to identify novel tumor markers, profile complex protein pathways, and develop new molecular-based therapies. Continued refinement of such high-throughput microtechnologies will enable us to rapidly query patient specimens to identify novel methods for early detection, treatment, and follow-up of a wide array of human cancers.
   (C) 2002 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.
C1 NCI, FDA Clin Prote Program, Pathol Lab, Mol Signalling Lab,Ctr Canc Res, Bethesda, MD 20892 USA.
   US FDA, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
RP Kohn, EC (reprint author), NCI, FDA Clin Prote Program, Pathol Lab, Mol Signalling Lab,Ctr Canc Res, Bldg 10 Room 2A33, Bethesda, MD 20892 USA.
EM kohne@helix.gov
NR 57
TC 51
Z9 53
U1 1
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0361-090X
J9 CANCER DETECT PREV
JI Cancer Detect. Prev.
PY 2002
VL 26
IS 4
BP 249
EP 255
AR PII S0361-090X(02)00092-2
DI 10.1016/S0361-090X(02)00092-2
PG 7
WC Oncology
SC Oncology
GA 612PN
UT WOS:000179084800001
PM 12430629
ER

PT J
AU Hodge, JW
   Grosenbach, DW
   Schlom, J
AF Hodge, JW
   Grosenbach, DW
   Schlom, J
TI Vector-based delivery of tumor-associated antigens and T-cell
   co-stimulatory molecules in the induction of immune responses and
   anti-tumor immunity
SO CANCER DETECTION AND PREVENTION
LA English
DT Review
DE vaccines; tumor antigens; immunotherapy
ID RECOMBINANT VACCINIA VIRUS; HUMAN CARCINOEMBRYONIC ANTIGEN; DENDRITIC
   CELLS; COSTIMULATORY MOLECULES; ANTITUMOR IMMUNITY; GENE-EXPRESSION;
   PHASE-I; DRIVEN HYPEREXPRESSION; ANTICANCER VACCINES; PRESENTING CELLS
AB It has now been demonstrated in both experimental models and recent clinical trials that certain "self" antigens, which are functionally non-immunogenic in the host, can become immunogenic if presented to the immune system in a certain way. Here, we describe recombinant vaccines and vaccine strategies that have been developed to induce and potentiate T-cell responses of the host to such self-antigens. These strategies include: (a) the use of recombinant poxvirus vectors in which the tumor-associated antigen (TAA) is inserted as a transgene. Recombinant vaccinia vaccines and recombinant avipox (replication-defective) vaccines have been employed to break tolerance to a self-antigen; (b) the use of diversified prime and boost strategies using different vaccines; and (c) the insertion of multiple T-cell co-stimulatory molecules into recombinant poxvirus vectors, along with the TAA gene, to enhance T-cell immune responses to the TAA and induce anti-tumor immunity.
   (C) 2002 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.
C1 NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Schlom, J (reprint author), NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, 10 Ctr Dr,Room 8B09, Bethesda, MD 20892 USA.
RI Hodge, James/D-5518-2015
OI Hodge, James/0000-0001-5282-3154
NR 91
TC 17
Z9 25
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0361-090X
J9 CANCER DETECT PREV
JI Cancer Detect. Prev.
PY 2002
VL 26
IS 4
BP 275
EP 291
AR PII S0361-090X(02)00095-8
DI 10.1016/S0361-090X(02)00095-8
PG 17
WC Oncology
SC Oncology
GA 612PN
UT WOS:000179084800004
PM 12430632
ER

PT J
AU Thigpen, JE
   Haseman, JK
   Saunders, H
   Locklear, J
   Caviness, G
   Grant, M
   Forsythe, D
AF Thigpen, JE
   Haseman, JK
   Saunders, H
   Locklear, J
   Caviness, G
   Grant, M
   Forsythe, D
TI Dietary factors affecting uterine weights of immature CD-1 mice used in
   uterotrophic bioassays
SO CANCER DETECTION AND PREVENTION
LA English
DT Article
DE uterotrophic assays; dietary phytoestrogens; metabolizable energy;
   rodent diets
ID ENDOCRINE-DISRUPTING CHEMICALS; RODENT DIETS; ESTROGENIC ACTIVITY; MOUSE
   BIOASSAY; EDSTAC RECOMMENDATIONS; PREPUBERTAL EXPOSURES; PHYTOESTROGEN
   CONTENT; SOYBEAN ISOFLAVONES; SEXUAL DEVELOPMENT; BREAST-CANCER
AB A study was conducted to determine the effects of dietary factors in natural ingredient and purified diets on uterine weights of immature CD-1 mice used in uterotrophic bioassays. Factors evaluated included body weight gain, dietary phytoestrogen content, total metabolizable energy, and percent crude fiber. Fifteen to 147 mice per group, housed 5 per cage, were randomly assigned to each of the 20 test diets. The test diets were fed for 7 days to 15-day old immature female CD-1 mice and their body weight gain and uterine weights were determined. Analysis of covariance procedures were used to evaluate differences in uterine weights, after adjusting for body weight and time-related trends. Fisher's least significant difference test was used to compare adjusted uterine weights and weight gains among the test diets. Additionally, multiple linear regression procedures were used to identify those characteristics of the rodent diet that were most predictive of the adjusted uterine weights. Total metabolizable energy was significantly (P < 0.01) correlated with and was predictive of uterine weights. The following dietary variables were not significantly predictive of uterine weights: total daidzein and genistein content, percent protein, fat, N-FE (carbohydrates) or percent crude fiber. We concluded that: (1) total metabolizable energy (ME) in natural ingredient or purified diets has a significant (P < 0.01) effect on the uterine weights of immature mice used in 7-day uterotrophic bioassays; (2) a standardized, estrogen-free diet with a constant level of ME should be used for conducting uterotrophic assays when comparing results between different laboratories or when determining the estrogenic or anti-estrogenic activity of endocrine disruptor compounds (3) the mouse uterotrophic assay remains a sensitive bioassay for assessing chemicals for estrogenic activity or for the detection of total estrogenic activity in rodent diets that may be contaminated with estrogenic compounds, and (4) chemical assays should be used to detect or measure low levels of the phytoestrogens in rodent diets. (C) 2002 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.
C1 NIEHS, Comparat Med Branch, Res Triangle Pk, NC 27709 USA.
   NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Thigpen, JE (reprint author), NIEHS, Comparat Med Branch, 111 TW Alexander Dr,POB 12233,Mail Drop C1-06, Res Triangle Pk, NC 27709 USA.
NR 42
TC 27
Z9 28
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0361-090X
J9 CANCER DETECT PREV
JI Cancer Detect. Prev.
PY 2002
VL 26
IS 5
BP 381
EP 393
AR PII S0361-090X(02)00122-8
DI 10.1016/S0361-090X(02)00122-8
PG 13
WC Oncology
SC Oncology
GA 630TP
UT WOS:000180125700007
PM 12518869
ER

PT J
AU Dong, SM
   Pai, SI
   Rha, SH
   Hildesheim, A
   Kurman, RJ
   Schwartz, PE
   Mortel, R
   McGowan, L
   Greenberg, MD
   Barnes, WA
   Sidransky, D
AF Dong, SM
   Pai, SI
   Rha, SH
   Hildesheim, A
   Kurman, RJ
   Schwartz, PE
   Mortel, R
   McGowan, L
   Greenberg, MD
   Barnes, WA
   Sidransky, D
TI Detection and quantitation of human papillomavirus DNA in the plasma of
   patients with cervical carcinoma
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMAS; CIRCULATING TUMOR DNA; NECK-CANCER PATIENTS;
   NESTED CASE-CONTROL; BARR-VIRUS DNA; NASOPHARYNGEAL CARCINOMA;
   MICROSATELLITE ALTERATIONS; VIRAL LOAD; IN-SITU; SERUM
AB Human papillomaviruses (HPVs) play a central role in the development of cervical carcinoma. Plasma DNA from 232 patients taken at diagnosis or after treatment for invasive cervical cancer (n = 175) or carcinoma in situ (n = 57) and 60 normal controls were examined for HPV-16 or HPV-18 E7 DNA by conventional and real-time quantitative PCR assays. We found HPV-16 or HPV-18 E7 DNA in 6.9% (11 of 175) of invasive cervical cancer cases (18.1% of cases positive for HPV-16 or HPV-18 at the genital tract), 1.8% (1 of 57) of carcinoma in situ, and 1.7% (1 of 60) of normal controls by conventional PCR. Quantitative PCR identified the highest concentrations of HPV DNA (copy number of HPV/ml of plasma) in patients with invasive cervical cancer (mean, 11,163; median, 183.5), followed by a level of 8 in the single carcinoma in situ case and 0 copies in the normal control initially positive by conventional PCR. HPV DNA can be detected in the plasma of some patients with HPV-positive cervical tumors. It remains to be demonstrated whether quantitative PCR analysis of HPV DNA in plasma may have utility in patients at high risk of recurrent disease.
C1 Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Div Head & Neck Canc Res, Baltimore, MD 21205 USA.
   Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
   NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   Yale Univ, Sch Med, New Haven, CT USA.
   Milton S Hershey Med Ctr, Hershey, PA USA.
   George Washington Univ, Washington, DC 20052 USA.
   Grad Hosp Philadelphia, Philadelphia, PA 19146 USA.
   Georgetown Univ, Lombardi Canc Ctr, Washington, DC 20007 USA.
RP Sidransky, D (reprint author), Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Div Head & Neck Canc Res, 818 Ross Res Bldg,720 Rutland Ave, Baltimore, MD 21205 USA.
FU NCI NIH HHS [U01-CA-84986]; NIDCR NIH HHS [R01-DE-12588]
NR 28
TC 60
Z9 63
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD JAN
PY 2002
VL 11
IS 1
BP 3
EP 6
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 517WE
UT WOS:000173632800002
PM 11815394
ER

PT J
AU Legler, J
   Meissner, HI
   Coyne, C
   Breen, N
   Chollette, V
   Rimer, BK
AF Legler, J
   Meissner, HI
   Coyne, C
   Breen, N
   Chollette, V
   Rimer, BK
TI The effectiveness of interventions to promote mammography among women
   with historically lower rates of screening
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID RANDOMIZED CONTROLLED TRIAL; LOW-INCOME WOMEN; VIETNAMESE-AMERICAN
   WOMEN; HEALTH INTERVIEW SURVEYS; BREAST-CANCER; INCREASE MAMMOGRAPHY;
   INNER-CITY; TAILORED INTERVENTIONS; EDUCATION-PROGRAM; HISPANIC WOMEN
AB This study examines mammography-enhancing intervention studies that focus on women in groups with historically lower rates of mammography use than the general population. These groups consist of women who are disproportionately older, poorer, of racial-ethnic minorities, have lower levels of formal education, and live in rural areas. We refer to them as diverse populations. The purpose of this report is to determine which types of mammography-enhancing interventions are most effective for these diverse populations. For this report, United States and international studies with concurrent controls that reported actual receipt of mammograms (usually based on self-report) as an outcome were eligible for inclusion. Intervention effects were measured by differences in intervention and control group screening rates postintervention and were weighted to reflect the certainty of each study's contribution. These effects differed significantly (Q = 218, 34 df), and the variation between studies was best explained by indicators of the use of access-enhancing approaches. Combined intervention effects were estimated for different categories of intervention types using random effects models for subgroups of studies. The strongest combination of approaches used access-enhancing and individual-directed strategies and resulted in an estimated 27% increase in mammography use (95% confidence interval, 9.9-43.9, nine studies). Additionally impressive was the access-enhancing and system-directed combination (20% increase and 95% confidence interval, 8.2-30.6, five studies). Access-enhancing strategies are an important complement to individual- and system-directed interventions for women with historically lower rates of screening.
C1 NCI, Appl Canc Screening Res Branch, Behav Res Program, Bethesda, MD 20892 USA.
   NCI, Stat Res & Applicat Branch, Surveillance Res Program, Bethesda, MD 20892 USA.
   NCI, Appl Res Program, Bethesda, MD 20892 USA.
   NCI, Behav Res Program, Appl Canc Screening Res Branch, Bethesda, MD 20892 USA.
   NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   W Virginia Univ, Dept Community Med, Morgantown, WV 26505 USA.
RP Meissner, HI (reprint author), NCI, Appl Canc Screening Res Branch, Behav Res Program, Bethesda, MD 20892 USA.
NR 90
TC 136
Z9 136
U1 5
U2 14
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD JAN
PY 2002
VL 11
IS 1
BP 59
EP 71
PG 13
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 517WE
UT WOS:000173632800010
PM 11815402
ER

PT J
AU Bonovich, M
   Olive, M
   Reed, E
   O'Connell, B
   Vinson, C
AF Bonovich, M
   Olive, M
   Reed, E
   O'Connell, B
   Vinson, C
TI Adenoviral delivery of A-FOS, an AP-1 dominant negative, selectively
   inhibits drug resistance in two human cancer cell lines
SO CANCER GENE THERAPY
LA English
DT Article
DE A-FOS; AP-1; multidrug resistance; KB85; cisplatin; A2780/CP70
ID PROTEIN-KINASE PATHWAY; HUMAN MDR1 GENE; MULTIDRUG-RESISTANCE; C-JUN;
   CARCINOMA-CELLS; BREAST-CANCER; DNA-REPAIR; RAS; EXPRESSION; CISPLATIN
AB Activator protein -1 (AP-1) transcription factor has been I inked to chemotherapeutic resistance. To assess the clinical efficacy of AP-1 inhibition toward reversing drug resistance, we have developed an adenovirus expressing a dominant negative that inhibits AP-1 DNA binding, named AdA-FOS. We examined the consequence of AdA-FOS infection on two paired human cancer cell lines, each pair consisting of a parental cell and the drug-resistant derivative. The first pair of cells is the parental human ovarian cancer cell line A2780 and the cisplatin-resistant A2780/CP70 cell line. The second pair of cells is the parental epidermal carcinoma cell line KB8 and the multidrug-resistant (mdr) KB85 cell line. Because of an association of up-regulated AP-1 activity with their drug resistance, these ceII lines were considered good targets of AdA- FOS therapy. Following infection of the drug-sensitive and drug-resistant cells, we observed a significant decrease in cell viability of KB85 and A2780/CP70 cells at drug (loses normally not lethal to the cell. The parental cell lines, A2780 and KB8 cells, were not similarly affected by AdA-FOS. This decrease in viability was specific to AdA-FOS as an adenovirus control (Advector) did not reverse drug resistance. Although the efficiency of AdA-FOS in therapy would need to be further analyzed with other cisplatin-resistant and mdr cell lines, these results suggest that AP-1 is a therapeutic molecular target and that inhibition of AP-1 DNA binding may be of clinical value in treating chemotherapeutic resistance.
C1 NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
   NCI, Dev Therapeut Dept, Med Branch, NIH, Bethesda, MD 20892 USA.
   Univ Dublin Trinity Coll, Sch Dent Sci, Dublin 2, Ireland.
RP Vinson, C (reprint author), NCI, Lab Metab, NIH, Bldg 37,Room 4D06, Bethesda, MD 20892 USA.
NR 51
TC 33
Z9 35
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0929-1903
J9 CANCER GENE THER
JI Cancer Gene Ther.
PD JAN
PY 2002
VL 9
IS 1
BP 62
EP 70
DI 10.1038/sj/cgt/7700409
PG 9
WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity;
   Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity;
   Research & Experimental Medicine
GA 509CW
UT WOS:000173128200008
PM 11916245
ER

PT J
AU DiPaolo, JA
AF DiPaolo, JA
TI Cancer research in the new millennium - Prologue
SO CANCER INVESTIGATION
LA English
DT Editorial Material
C1 NCI, NIH, Bethesda, MD 20892 USA.
RP DiPaolo, JA (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0735-7907
J9 CANCER INVEST
JI Cancer Invest.
PY 2002
VL 20
IS 1
BP 69
EP 70
PG 2
WC Oncology
SC Oncology
GA 520GG
UT WOS:000173772200010
ER

PT J
AU Mani, S
   Graham, MA
   Bregman, DB
   Ivy, P
   Chaney, SG
AF Mani, S
   Graham, MA
   Bregman, DB
   Ivy, P
   Chaney, SG
TI Oxaliplatin: A review of evolving concepts
SO CANCER INVESTIGATION
LA English
DT Review
ID NUCLEOTIDE EXCISION-REPAIR; HUMAN-BREAST-CANCER; METASTATIC
   COLORECTAL-CANCER; CISPLATIN-DNA-ADDUCTS; HUMAN OVARIAN-CANCER;
   GERM-CELL CANCER; RECEPTOR-ENHANCED CHEMOSENSITIVITY;
   LIQUID-CHROMATOGRAPHIC SEPARATION; CARRIER LIGAND SPECIFICITY;
   ANTICANCER DRUG CISPLATIN
C1 Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10461 USA.
   Weiler Hosp Montefiore Med Ctr, Dept Oncol, Bronx, NY 10461 USA.
   Dept Clin Pharmacokinet, Malvern, PA USA.
   Drug Metab Sanofi Synthelabo, Malvern, PA USA.
   Albert Einstein Coll Med, Dept Pathol, Bronx, NY USA.
   Natl Canc Inst, Canc Therapy Evaluat Program, Bethesda, MD USA.
   Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Biochem & Biophys, Chapel Hill, NC USA.
RP Mani, S (reprint author), Weiler Hosp Montefiore Med Ctr, Dept Oncol, Rm 2S-63 1825 Eastchester Rd, Bronx, NY 10461 USA.
NR 176
TC 40
Z9 41
U1 1
U2 4
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0735-7907
J9 CANCER INVEST
JI Cancer Invest.
PY 2002
VL 20
IS 2
BP 246
EP 263
DI 10.1081/CNV-120001152
PG 18
WC Oncology
SC Oncology
GA 528VM
UT WOS:000174265000012
PM 11901545
ER

PT J
AU Copeland, WC
   Wachsman, JT
   Johnson, FM
   Penta, JS
AF Copeland, WC
   Wachsman, JT
   Johnson, FM
   Penta, JS
TI Mitochondrial DNA alterations in cancer
SO CANCER INVESTIGATION
LA English
DT Review
DE cancer; mitochondrial DNA; mutation; reactive oxygen species
ID RENAL-CELL CARCINOMA; LEUKEMIC HL-60 CELLS; CONTROL REGION DNA;
   OXIDATIVE STRESS; HYDROGEN-PEROXIDE; POLYMERASE-GAMMA; GENE-EXPRESSION;
   GASTRIC TUMORS; HELA-CELLS; MICROSATELLITE INSTABILITY
AB A number of studies have demonstrated the presence of mitochondrial DNA (mtDNA) mutations in cancer cells. In this article, we review mitochondrial genomic aberrations reported in solid tumors of the breast, colon, stomach, liver, kidney, bladder, head/neck, and lung. The tantalizing association of tumors with mDNA mutations implicates these mutations in the process of carcinogenesis. Alterations in expression of mtDNA transcripts in a variety of cancer types are also reviewed. In solid tumors, elevated expression Of mtDNA-genes coding for subunits of the mitochondrial electron respiratory chain may reflect mitochondrial adaptation to perturbations in cellular energy requirements. The role of mtDNA mutations and altered expression of mitochondrial genes in carcinogenesis is discussed. mitochondrial DNA mutations can initiate a cascade of events leading to a continuous increase in the production of reactive oxygen species (persistent oxidative stress), a condition that probably favors tumor development.
C1 NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
   NIEHS, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA.
   NIEHS, Off Clin Res, Res Triangle Pk, NC 27709 USA.
RP Copeland, WC (reprint author), NIEHS, Mol Genet Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 105
TC 139
Z9 145
U1 0
U2 7
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0735-7907
J9 CANCER INVEST
JI Cancer Invest.
PY 2002
VL 20
IS 4
BP 557
EP 569
DI 10.1081/CNV-120002155
PG 13
WC Oncology
SC Oncology
GA 566GE
UT WOS:000176417900013
PM 12094550
ER

PT J
AU Kunschner, LJ
   Fine, H
   Hess, K
   Jaeckle, K
   Kyritsis, AP
   Yung, WKA
AF Kunschner, LJ
   Fine, H
   Hess, K
   Jaeckle, K
   Kyritsis, AP
   Yung, WKA
TI CI-980 for the treatment of recurrent or progressive malignant gliomas:
   National Central Nervous System Consortium Phase I-II Evaluation of
   CI-980
SO CANCER INVESTIGATION
LA English
DT Article
DE CI-980; chemotherapy; malignant gliomas
ID NEUROTOXICITY; PROCARBAZINE; VINCRISTINE; NSC-370147; CARCINOMA; TRIAL
AB Objective: The purpose of this phase I/II trial was to determine the maximal tolerated dose of CI-980, and determine efficacy against malignant glioma.
   Background: The CI-980 is a synthetic mitosis inhibitor that acts via the colchicine binding site on tubulin. Broad in vitro activity has been seen in a variety of human and murine tumor models. Phase I studies have demonstrated schedule dependent toxicity of CI-980. Dose-limiting toxicity was neurologic when CI-980 was given as a 24-hr infusion and hematologic when given over 72 hr at higher doses.
   Methods: Twenty-four patients ages 29-65 entered this study. Six patients were treated on the phase I arm at three escalating dose levels ranging from 10.5 to 13.5 mg/m(2), given over 72 hr. Eighteen patients were then treated at the highest tolerated dose, 13.5 mg/m(2) per cycle. Treatment response was based on serial MRI imaging characteristics.
   Results: The phase II study was stopped at the end of the first stage due to poor treatment response. There were no partial or complete responses, (0/24) 95% CI = 0-14%. Four patients (4/24) had a best treatment response of stable disease/no change. Median time to progression for all patients was 6.4 weeks (95% CI: 6-9 weeks). Dose-limiting toxicity was grade 3-4 granulocytopenia. Three episodes of neurotoxicity manifested by a moderate cerebellar dysfunction were seen.
   Conclusions: These results fail to demonstrate the significant activity of CI-980 against recurrent glioma.
C1 Univ Texas, MD Anderson Canc Ctr, Dept Neurooncol, Houston, TX 77030 USA.
   Univ Texas, MD Anderson Canc Ctr, Dept Biomath, Houston, TX 77030 USA.
   Allegheny Neurol Associates, Pittsburgh, PA USA.
   Dana Farber Canc Inst, Boston, MA 02115 USA.
   NCI, Bethesda, MD 20892 USA.
   Mayo Clin Jacksonville, Jacksonville, FL 32224 USA.
   Univ Ioannina, GR-45110 Ioannina, Greece.
RP Yung, WKA (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Neurooncol, 1515 Holcombe Blvd,Box 431, Houston, TX 77030 USA.
NR 16
TC 4
Z9 5
U1 0
U2 1
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0735-7907
J9 CANCER INVEST
JI Cancer Invest.
PY 2002
VL 20
IS 7-8
BP 948
EP 954
DI 10.1081/CNV-120005910
PG 7
WC Oncology
SC Oncology
GA 614HW
UT WOS:000179183300013
PM 12449727
ER

PT J
AU Strausberg, RL
   Buetow, KH
   Greenhut, SF
   Grouse, LH
   Schaefer, CF
AF Strausberg, RL
   Buetow, KH
   Greenhut, SF
   Grouse, LH
   Schaefer, CF
TI The cancer genome anatomy project: Online resources to reveal the
   molecular signatures of cancer
SO CANCER INVESTIGATION
LA English
DT Article
ID GENE-EXPRESSION; SERIAL ANALYSIS; HUMAN BRAIN; SEQUENCE; DATABASE;
   MARKERS; IDENTIFICATION; DISCOVERY; PROSTATE; ANTIGENS
C1 NCI, Bethesda, MD 20892 USA.
RP Strausberg, RL (reprint author), NCI, Bethesda, MD 20892 USA.
NR 30
TC 19
Z9 19
U1 0
U2 2
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0735-7907
J9 CANCER INVEST
JI Cancer Invest.
PY 2002
VL 20
IS 7-8
BP 1038
EP 1050
DI 10.1081/CNV-120005922
PG 13
WC Oncology
SC Oncology
GA 614HW
UT WOS:000179183300023
PM 12449737
ER

PT J
AU Childs, R
   Srinivasan, R
AF Childs, R
   Srinivasan, R
TI Advances in allogeneic stem cell transplantation: Directing
   graft-versus-leukemia at solid tumors
SO CANCER JOURNAL
LA English
DT Article
DE solid tumors; immunotherapy; allogeneic stem cell transplantation;
   mini-transplant; nonmyeloablative; renal cell carcinoma; melanoma;
   breast carcinoma; graft-vs-tumor (GVT); graft-vs-leukemia (GVL);
   nonmyeloablative stem cell transplant (NST)
ID BONE-MARROW TRANSPLANTATION; MINOR HISTOCOMPATIBILITY ANTIGENS; CHRONIC
   MYELOGENOUS LEUKEMIA; RESTRICTED TISSUE DISTRIBUTION; CHRONIC
   MYELOID-LEUKEMIA; HOST DISEASE; T-CELLS; CANCER-IMMUNOTHERAPY;
   BREAST-CANCER; CARCINOMA
AB Allogeneic stem cell transplantation was originally developed as a method to rescue hematopoietic function following high dose "myeloablative" therapy in the treatment of hematological malignancies. In the first two decades of its use. dose-intensive chemotherapy alone was credited with curing those patients who achieved sustained remission following this procedure. However, more recently investigators have come to recognize that antineoplastic effects mediated by immunocompetent donor T-cells transplanted with the stem cell allograft can be induced against hematological malignancies. Indeed, this graft-vs-leukemia (GVL) or graft-vs-tumor (GVT) effect is now felt to represent the principal modality required to sustain durable remissions of hematological malignancies following this approach. The powerful and potentially curative nature of the GVT effect in hematological cancers has recently lured oncologists into exploring the therapeutic potential of allogeneic stem cell transplantation as an investigational approach for treatment-refractory solid tumors. We review here the development and early clinical results of allogeneic stem cell transplantation as potential immunotherapy for solid tumors.
C1 NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
   NCI, NIH, Bethesda, MD 20892 USA.
RP Childs, R (reprint author), NHLBI, NIH, Hematol Branch, 10-7C103 MSC 1652,9000 Rockville Pike, Bethesda, MD 20892 USA.
RI Ain, Kenneth/A-5179-2012
OI Ain, Kenneth/0000-0002-2668-934X
NR 55
TC 31
Z9 31
U1 0
U2 1
PU JONES AND BARTLETT PUBLISHERS
PI SUDBURY
PA 40 TALL PINE DR, SUDBURY, MA 01776 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD JAN-FEB
PY 2002
VL 8
IS 1
BP 2
EP 11
DI 10.1097/00130404-200201000-00002
PG 10
WC Oncology
SC Oncology
GA 525DD
UT WOS:000174052700002
PM 11895199
ER

PT J
AU Wood, BJ
AF Wood, BJ
TI Feasibility of thermal ablation of lytic vertebral metastases with
   radiofrequency current
SO CANCER JOURNAL
LA English
DT Editorial Material
C1 NIH, Hlth Clin Ctr, Bethesda, MD 20892 USA.
   Georgetown Univ, Washington, DC USA.
   Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Wood, BJ (reprint author), NIH, Hlth Clin Ctr, Bldg 10,Room 1C-660, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 CL999999]
NR 5
TC 4
Z9 4
U1 0
U2 0
PU JONES AND BARTLETT PUBLISHERS
PI SUDBURY
PA 40 TALL PINE DR, SUDBURY, MA 01776 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD JAN-FEB
PY 2002
VL 8
IS 1
BP 26
EP 28
DI 10.1097/00130404-200201000-00004
PG 3
WC Oncology
SC Oncology
GA 525DD
UT WOS:000174052700004
PM 11895200
ER

PT J
AU Filippova, GN
   Qi, CF
   Ulmer, JE
   Moore, JM
   Ward, MD
   Hu, YJ
   Loukinov, DI
   Pugacheva, EM
   Klenova, EM
   Grundy, PE
   Feinberg, AP
   Cleton-Jansen, AM
   Moerland, EW
   Cornelisse, CJ
   Suzuki, H
   Komiya, A
   Lindblom, A
   Dorion-Bonnet, F
   Neiman, PE
   Morse, HC
   Collins, SJ
   Lobanenkov, VV
AF Filippova, GN
   Qi, CF
   Ulmer, JE
   Moore, JM
   Ward, MD
   Hu, YJ
   Loukinov, DI
   Pugacheva, EM
   Klenova, EM
   Grundy, PE
   Feinberg, AP
   Cleton-Jansen, AM
   Moerland, EW
   Cornelisse, CJ
   Suzuki, H
   Komiya, A
   Lindblom, A
   Dorion-Bonnet, F
   Neiman, PE
   Morse, HC
   Collins, SJ
   Lobanenkov, VV
TI Tumor-associated zinc finger mutations in the CTCF transcription factor
   selectively alter its DNA-binding specificity
SO CANCER RESEARCH
LA English
DT Article
ID ENHANCER-BLOCKING ACTIVITY; CHROMOSOME ARM 16Q; C-MYC GENE; PROSTATE
   CANCERS; PROTEIN CTCF; METHYLATION; SEQUENCE; PROMOTER; REGIONS; BREAST
AB CTCF is a widely expressed 11-zinc finger (ZF) transcription factor that is involved in different aspects of gene regulation including promoter activation or repression, hormone-responsive gene silencing, methylation-dependent chromatin insulation, and genomic imprinting. Because CTCF targets include oncogenes and tumor suppressor genes, we screened over 100 human tumor samples for mutations that might disrupt CTCF activity. We did not observe any CTCF mutations leading to truncations/premature stops. Rather, in breast, prostate, and Wilms' tumors, we observed four different CTCF somatic missense mutations involving amino acids within the ZF domain. Each ZF mutation abrogated CTCF binding to a subset of target sites within the promoters/insulators of certain genes involved in regulating cell proliferation but did not alter binding to the regulatory sequences of other genes. These observations suggest that CTCF may represent a novel tumor suppressor gene that displays tumor-specific "change of function" rather than complete "loss of function.".
C1 Fred Hutchinson Canc Res Ctr, Human Biol Div, Seattle, WA 98109 USA.
   NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA.
   Univ Essex, Dept Biol Sci, Colchester CO4 3SQ, Essex, England.
   Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada.
   Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD 21205 USA.
   Leiden Univ, Dept Pathol, NL-2300 RA Leiden, Netherlands.
   Chiba Univ, Sch Med, Dept Urol, Chiba 260, Japan.
   Karolinska Hosp, Dept Clin Genet, S-510401 Stockholm, Sweden.
   Inst Bergonie, Mol Genet Lab, F-33076 Bordeaux, France.
RP Lobanenkov, VV (reprint author), Fred Hutchinson Canc Res Ctr, Human Biol Div, 1100 Fairview Ave N,C2-023,POB 19024, Seattle, WA 98109 USA.
OI Morse, Herbert/0000-0002-9331-3705
FU NCI NIH HHS [R37 CA054358-12, R01 CA68360, R01 CA71732, R37 CA054358]
NR 25
TC 101
Z9 106
U1 0
U2 7
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2002
VL 62
IS 1
BP 48
EP 52
PG 5
WC Oncology
SC Oncology
GA 513MP
UT WOS:000173382600011
PM 11782357
ER

PT J
AU Arnold, JT
   Lessey, BA
   Seppala, M
   Kaufman, DG
AF Arnold, JT
   Lessey, BA
   Seppala, M
   Kaufman, DG
TI Effect of normal endometrial stroma on growth and differentiation in
   Ishikawa endometrial adenocarcinoma cells
SO CANCER RESEARCH
LA English
DT Article
ID EXTRACELLULAR-MATRIX; EPITHELIAL INTERACTIONS; PROGESTERONE-RECEPTOR;
   PLACENTAL PROTEIN-14; ESTROGEN-RECEPTORS; RNA EXPRESSION; LINE ISHIKAWA;
   FACTOR-BETA; CANCER; TISSUE
AB Endometrial cancer is characterized by alterations in the stromal cells and the supporting extracellular matrix in addition to the intrinsic alterations of the malignant epithelia] cells. We have developed a cell culture model that demonstrates the role of stromal cells in the regulation of proliferation, hormone responsiveness, and differentiation of an endometrial adenocarcinoma cell line (Ishikawa). Conditioned medium (CM) was collected from normal primary human endometrial stromal cells grown on plastic or within the basement membrane extract, Matrigel. The CM produced by stromal cells cultured in contact with Matrigel markedly inhibited Ishikawa cell proliferation compared with CM from stromal cells cultured on plastic. Ishikawa cell proliferation varied with steroid hormone treatment in the presence of CM from stromal cells embedded in Matrigel. When the Ishikawa cells were placed in coculture in contact with stromal cells in Matrigel, production of a differentiated epithelial secretory product, glycodelin, was induced. Gene expression of stromal cell hormone receptors, growth factors, and integrins was analyzed, by reverse transcription-PCR in the presence of Matrigel to determine the potential factors involved in stromal regulatory function. These combined studies imply that the phenotype of the Ishikawa cells can be induced to differentiate to more closely resemble normal endometrial epithelium by reintroduction of stromal factors and appropriate extracellular matrix. Additionally, the study shows that basement membrane proteins influence the regulatory function of stromal cells as they mediate epithelial cell growth.
C1 Univ N Carolina, Dept Lab Med & Pathol, Div Reprod Endocrinol & Infertil, Chapel Hill, NC 27599 USA.
   Univ N Carolina, Dept Obstet & Gynecol, Div Reprod Endocrinol & Infertil, Chapel Hill, NC 27599 USA.
   Univ Helsinki, Cent Hosp, Helsinki, Finland.
RP Arnold, JT (reprint author), NIH, Natl Ctr Complementary & Alternat Med, 8 W Dr MSC 2669,Qtrs 15B1, Bethesda, MD 20892 USA.
FU NCI NIH HHS [CA31733]; NICHD NIH HHS [HD 34824, U54 HD-35041]
NR 58
TC 61
Z9 65
U1 1
U2 2
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2002
VL 62
IS 1
BP 79
EP 88
PG 10
WC Oncology
SC Oncology
GA 513MP
UT WOS:000173382600017
PM 11782363
ER

PT J
AU Fan, SJ
   Ma, YX
   Wang, CG
   Yuan, RQ
   Meng, QH
   Wang, JA
   Erdos, M
   Goldberg, ID
   Webb, P
   Kushner, PJ
   Pestell, RG
   Rosen, EM
AF Fan, SJ
   Ma, YX
   Wang, CG
   Yuan, RQ
   Meng, QH
   Wang, JA
   Erdos, M
   Goldberg, ID
   Webb, P
   Kushner, PJ
   Pestell, RG
   Rosen, EM
TI p300 modulates the BRCA1 inhibition of estrogen receptor activity
SO CANCER RESEARCH
LA English
DT Article
ID TUMOR-SUPPRESSOR; TRANSCRIPTIONAL ACTIVATION; HISTONE ACETYLTRANSFERASE;
   NUCLEAR RECEPTORS; OVARIAN-CANCER; BREAST-CANCER; CELL-CYCLE;
   DNA-DAMAGE; COACTIVATOR; BINDING
AB We previously reported that expression of the breast cancer susceptibility gene BRCA1 strongly inhibits the transcriptional activity of the estrogen receptor (ER-alpha) in human breast and prostate cancer cell lines but only weakly inhibits ER-alpha activity in cervical cancer cells (S. Fan et al., Science (Wash. DC), 284: 1354-1356, 1999). We now report that the ability of BRCA1 to repress ER-alpha activity correlates with its ability to induce down-regulation of the cellular levels of the transcriptional coactivator p300 in breast and prostate, but not in cervical cancer cells. On the other hand, BRCA1 failed to alter the expression of the CREB binding protein (CBP), the structural and functional homologue of p300, in any of these eel] types. Ectopic expression of either p300 or CBP "rescued" (i.e., reversed) the BRCA1 inhibition of ER-alpha activity, whereas two other nuclear receptor coactivators, the p300/CBP-associated factor (PCAF) and the glucocorticoid receptor-interacting protein-1 (GRIP1), failed to rescue the ER-alpha activity. The rescue function mapped to the cysteine-histidine rich domain CH3, a region of p300/CBP that we found to interact directly with the conserved COOH-terminal activation domain (AF-2) of ER-alpha. p300 and ER-alpha were also found to interact in vivo and to colocalize within the nucleus in breast cancer cells. These findings suggest that the cofactors p300 and CBP modulate the ability of the BRCA1 protein to inhibit ER-alpha signaling. They further suggest that the BRCA1 inhibition of ER-alpha activity may be attributable, at least in part, to the down-regulation of p300.
C1 Albert Einstein Coll Med, Long Isl Jewish Med Ctr, Dept Radiat Oncol, New Hyde Pk, NY 11040 USA.
   Yeshiva Univ Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10461 USA.
   Yeshiva Univ Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA.
   NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
   Univ Calif San Francisco, Sch Med, Metab Res Unit, San Francisco, CA 94143 USA.
RP Rosen, EM (reprint author), Albert Einstein Coll Med, Long Isl Jewish Med Ctr, Dept Radiat Oncol, Long Isl Campus,270-05 76th Ave, New Hyde Pk, NY 11040 USA.
FU NCI NIH HHS [R01-CA75503, R01-CA70897]; NIEHS NIH HHS [R01-ES09169]; PHS
   HHS [R01-82599, R01-80000]
NR 44
TC 95
Z9 100
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2002
VL 62
IS 1
BP 141
EP 151
PG 11
WC Oncology
SC Oncology
GA 513MP
UT WOS:000173382600025
PM 11782371
ER

PT J
AU Kuppusamy, P
   Li, HQ
   Ilangovan, G
   Cardounel, AJ
   Zweier, JL
   Yamada, K
   Krishna, MC
   Mitchell, JB
AF Kuppusamy, P
   Li, HQ
   Ilangovan, G
   Cardounel, AJ
   Zweier, JL
   Yamada, K
   Krishna, MC
   Mitchell, JB
TI Noninvasive imaging of tumor redox status and its modification by tissue
   glutathione levels
SO CANCER RESEARCH
LA English
DT Article
ID PHASE-I TRIAL; BUTHIONINE SULFOXIMINE; ACCELERATED RADIOTHERAPY;
   POLYNITROXYL-ALBUMIN; FREE-RADICALS; SOLID TUMORS; NITROXIDE; CANCER;
   MODEL; CELL
AB Therapeutic regimens such as radiation or chemotherapy attempt to exploit the physiological differences between normal and malignant tissue. Tissue redox status and pO(2) are two factors that are hypothesized to be different in normal and malignant tissues. Methods that can detect subtle differences in the above physiological parameters would greatly aid in devising appropriate treatment strategies. We have previously used in vivo electron paramagnetic resonance (EPR) spectroscopy and imaging techniques and shown that tumor tissues are highly reducing and hypoxic compared with normal tissues (P. Kuppusamy et aL, Cancer Res., 58: 1562-1568, 1998). The purpose of the present study was to obtain spatially resolved redox data from normal and tumor tissues of radiation-induced fibrosarcoma (RIF-1) tumor-bearing mice and to examine the role of intracellular glutathione (GSH) on the tissue redox status. Experiments were performed using low-frequency (1.3 GHz) in vivo EPR spectroscopy and imaging techniques with a nitroxide redox probe L-buthionine-S,R-sulfoximine (BSO), an inhibitor of GSH synthesis, was used,to deplete tissue GSH levels. The results show the existence of significant heterogeneity of redox status in the tumor tissue compared with normal tissue. The tumor tissues show at least 4-fold higher concentrations of GSH levels compared with normal tissues in the tumor-bearing mice. Also BSO treatment showed a differential depletion of GSH and reducing equivalents in the tumor tissue. Thus, it appears that there is significant heterogeneity of tumor redox status and that manipulation of the tumor redox status may be important in tumor growth and therapy.
C1 Johns Hopkins Univ, Sch Med, EPR Ctr, Baltimore, MD 21224 USA.
   Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21224 USA.
   NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
RP Kuppusamy, P (reprint author), Johns Hopkins Univ, Sch Med, EPR Ctr, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.
RI Yamada, Ken-ichi/E-6318-2012
FU NCI NIH HHS [CA 78886]; NCRR NIH HHS [RR 12190]; NIBIB NIH HHS [R01
   EB000890, R01 EB000890-04]
NR 43
TC 308
Z9 320
U1 9
U2 69
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2002
VL 62
IS 1
BP 307
EP 312
PG 6
WC Oncology
SC Oncology
GA 513MP
UT WOS:000173382600047
PM 11782393
ER

PT J
AU Crawford, KW
   Bowen, WD
AF Crawford, KW
   Bowen, WD
TI Sigma-2 receptor agonists activate a novel apoptotic pathway and
   potentiate antineoplastic drugs in breast tumor cell lines
SO CANCER RESEARCH
LA English
DT Article
ID CANCER CELLS; ANTICANCER DRUG; BINDING-SITE; P53; DEATH; CASPASE-3;
   INHIBITION; EXPRESSION; LIGANDS; PROTEIN
AB We have reported previously that sigma-2 receptors are expressed in high densities in a variety of tumor cell types (B. J. Vilner et al., Cancer Res., 55: 408-413, 1995) and that various sigma ligands have cytotoxic effects (B. J. Vilner et al., J. Neurosci., 15: 117-134, 1995). Other investigators have demonstrated increased expression of sigma-2 receptors in rapidly proliferating tumors (R. H. Mach et al., Cancer Res., 57: 156-161, 1997) and the ability of some sigma ligands to inhibit proliferation (P. J. Brent and G. T. Pang, Eur. J. Pharmacol., 278: 151-160, 1995). We demonstrate here the ability of sigma-2 receptor agonists to induce cell death by a mechanism consistent with apoptosis. In breast tumor cell lines that are sensitive (MCF-7) and resistant (MCF-7/Adr-, T47D, and SKBr3) to antineoplastic agents, incubation with the sigma-2 subtype-selective agonists CB-64D and CB-184 produced dose-dependent cytotoxicity (measured by lactate dehydrogenase release into medium). The EC50 for this response was similar across cell lines, irrespective of p53 genotype and drug-resistance phenotype. CB-64D and the subtype nonselective sigma-2 agonists haloperidol and reduced haloperidol induced terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining in MCF-7 and T47D cells, indicating that cell death occurs via apoptosis. Apoptosis was also indicated by increases in Annexin V binding caused by CB-64D. In MCF-7 cells, cytotoxicity and Annexin V binding induced by the antineoplastics doxorubicin and actinomycin D was partially or completely abrogated by certain specific and general inhibitors of caspases. In contrast, caspase inhibitors had no effect on sigma-2 receptor-mediated (CB-64D and CB-184) cytotoxicity or Annexin V binding. Marked potentiation of cytotoxicity was observed when a subtoxic dose of CB-184 was combined with doxorubicin or actinomycin D, both in drug-sensitive (MCF-7) and drug-resistant (MCF-7/Adr-) cell lines. Haloperidol potentiated doxorubicin only in drug-resistant cells. These findings suggest the involvement of a novel p53- and caspase-independent apoptotic pathway used by sigma-2 receptors, which is distinct from mechanisms used by some DNA-damaging, antineoplastic agents and other apoptotic stimuli. These observations further suggest that sigma-2 receptors may be targets that can be therapeutically exploited in the treatment of both drug-sensitive and drug-resistant metastatic tumors.
C1 NIDDKD, Med Chem Lab, Unit Receptor Biochem & Pharmacol, NIH, Bethesda, MD 20892 USA.
   Howard Univ, Coll Med, Dept Pharmacol, Washington, DC 20059 USA.
RP Bowen, WD (reprint author), NIDDKD, Med Chem Lab, Unit Receptor Biochem & Pharmacol, NIH, Bldg 8,Room B1-23,8 Ctr Dr,MSC 0815, Bethesda, MD 20892 USA.
NR 56
TC 182
Z9 185
U1 0
U2 15
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2002
VL 62
IS 1
BP 313
EP 322
PG 10
WC Oncology
SC Oncology
GA 513MP
UT WOS:000173382600048
PM 11782394
ER

PT J
AU Kamiya, Y
   Puzianowska-Kuznicka, M
   McPhie, P
   Nauman, J
   Cheng, SY
   Nauman, A
AF Kamiya, Y
   Puzianowska-Kuznicka, M
   McPhie, P
   Nauman, J
   Cheng, SY
   Nauman, A
TI Expression of mutant thyroid hormone nuclear receptors is associated
   with human renal clear cell carcinoma
SO CARCINOGENESIS
LA English
DT Article
ID RETINOIC ACID RECEPTORS; TUMOR-SUPPRESSOR GENE; C-ERBA-BETA;
   HEPATOCELLULAR-CARCINOMA; V-ERBA; BREAST-CARCINOMA; ALLELIC LOSS;
   HETEROZYGOSITY; REGION; ONCOGENE
AB Thyroid hormone (T-3) regulates proliferation and differentiation of cells, via its nuclear receptors (TRs). These processes have been shown to be abnormally regulated during carcinogenesis. We have previously found aberrant expression of TRalpha and TRbeta mRNAs in renal clear cell carcinoma (RCCC), suggesting possible involvement of TRs in the carcinogenesis of RCCC. To understand the molecular actions of TRs in RCCC, cDNAs for TRbeta1 and TRalpha1 were cloned from 22 RCCC tissues and 20 surrounding normal tissues. Mutations were found in seven TRbeta1 and three TRalpha1 cDNAs. Two TRbeta1 cDNAs had a single mutation, while five TRbeta1 and three TRalpha1 had two or three mutations. Most of the mutations were localized in the hormone-binding domain. Using the TRs prepared by in vitro transcription/translation, we found that these mutations led to a loss of T-3 binding activity and/or impairment in binding to thyroid hormone response elements (TREs). Furthermore, nuclear extracts from RCCC tissues also exhibited impairment in binding to TREs. These results indicate that the normal functions of TRs in RCCC tissues were impaired. Together with the aberrant expression patterns, these mutated TRs could contribute to the carcinogenesis of RCCC.
C1 Polish Acad Sci, Med Res Ctr, Dept Endocrinol, Warsaw, Poland.
   Med Ctr Postgrad Educ, Dept Biochem, Warsaw, Poland.
   NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Puzianowska-Kuznicka, M (reprint author), Polish Acad Sci, Med Res Ctr, Dept Endocrinol, Warsaw, Poland.
NR 59
TC 67
Z9 69
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD JAN
PY 2002
VL 23
IS 1
BP 25
EP 33
DI 10.1093/carcin/23.1.25
PG 9
WC Oncology
SC Oncology
GA 511NX
UT WOS:000173273400004
PM 11756220
ER

PT J
AU Futaki, M
   Igarashi, T
   Watanabe, S
   Kajigaya, S
   Tatsuguchi, A
   Wang, JX
   Liu, JM
AF Futaki, M
   Igarashi, T
   Watanabe, S
   Kajigaya, S
   Tatsuguchi, A
   Wang, JX
   Liu, JM
TI The FANCG Fanconi anemia protein interacts with CYP2E1: possible role in
   protection against oxidative DNA damage
SO CARCINOGENESIS
LA English
DT Article
ID TRANSCRIPTION-COUPLED REPAIR; NUCLEAR-COMPLEX; MITOMYCIN-C; GENE; CELLS;
   RAT; COMPLEMENTATION; CYTOCHROME-P450; FANCG/XRCC9; EXPRESSION
AB Fanconi anemia (FA) is a genetic disorder that leads to aplastic anemia and birth defects and predisposes to cancer. FA cells exhibit characteristic hypersensitivity to DNA cross-linking agents such as mitomycin C (MMC), and FANCG is one of six known FA gene products. By immunocytochemical analysis of transfected cells, we discovered that although FANCG localized to both the nucleus and cytoplasm, there was an increase in cells with predominantly cytoplasmic staining after treatment with MMC. Concurrently, while searching by two-hybrid analysis for proteins that associate with FANCG, we identified a novel interaction between FANCG and cytochrome P450 2E1 (CYP2E1). A member of the P450 superfamily, CYP2E1 is associated with the production of reactive oxygen intermediates and the bioactivation of carcinogens. High constitutive levels of CYP2E1 were found in a FA-G lymphoblast cell line, whereas complementation of the FA-G line with wild-type FANCG was associated with decreased CYP2E1. These findings suggested that the interaction of FANCG with CYP2E1 might alter redox metabolism and increase DNA oxidation. Using a fluorescent assay, we found a dose-dependent increase in the oxidized DNA base, 8-oxoguanine (8-oxoG), after treatment of mutant FA-G cells with H2O2 or MMC. Conversely, significantly lower levels of 8-oxoG were detected in FANCG-complemented FA-G cells. We conclude that the unknown function of FANCG involves at least transient interaction with cytoplasmic components, possibly including CYP2E1, and propose a role for FANCG in protection against oxidative DNA damage.
C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   NHLBI, Pathol Sect, NIH, Bethesda, MD 20892 USA.
RP Liu, JM (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,Room 7C103, Bethesda, MD 20892 USA.
NR 38
TC 67
Z9 68
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD JAN
PY 2002
VL 23
IS 1
BP 67
EP 72
DI 10.1093/carcin/23.1.67
PG 6
WC Oncology
SC Oncology
GA 511NX
UT WOS:000173273400009
PM 11756225
ER

PT J
AU Alguacil, J
   Porta, M
   Malats, N
   Kauppinen, T
   Kogevinas, M
   Benavides, FG
   Partanen, T
   Carrato, A
AF Alguacil, J
   Porta, M
   Malats, N
   Kauppinen, T
   Kogevinas, M
   Benavides, FG
   Partanen, T
   Carrato, A
CA PANKRAS II Study Grp
TI Occupational exposure to organic solvents and K-ras mutations in
   exocrine pancreatic cancer
SO CARCINOGENESIS
LA English
DT Article
ID VINYL-CHLORIDE; CHEMICAL CARCINOGENESIS; ONCOGENE ACTIVATION; LUNG
   ADENOCARCINOMA; METHYLENE-CHLORIDE; HEALTHY CONTROLS; HUMAN PLASMA; P21
   PROTEIN; IN-VIVO; WORKERS
AB Occupational exposure to hydrocarbon solvents has been found to be associated with an increased risk of exocrine pancreatic cancer (EPC), the human tumor with the highest prevalence of K-ras mutations. Ras genes are critical DNA targets for chemical carcinogens. We analysed the relationship between past occupational exposure to hydrocarbon solvents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational factors and life-style was obtained from personal interviews conducted during hospital stay. Occupational exposure to hydrocarbon solvents (aliphatic, aromatic, chlorinated, benzene, other organic solvents) was examined using two methods: expert assessment and the Finnish job-exposure matrix (Finjem). Exposure among K-ras mutated EPC cases (n = 83) was compared with that of K-ras wild-type EPC cases (n = 24). An association between K-ras mutations and solvent exposure was observed with Finjem but barely so with the expert assessment. Over 7-fold increased odds ratios (OR) were found for every group of solvents evaluated with Finjem (all P < 0.05). On the basis of the expert assessment, K-ras mutations were significantly associated only with exposure to benzene in men (OR = 7.07, P < 0.05). When requiring exposure to have occurred according to both the experts and Finjem, over 4-fold risks were obtained for aromatic, aliphatic, and for `any hydrocarbon solvent'. A significantly higher proportion of cases with a mutation from glycine to valine (GGT-->GTT) or to aspartic acid (GGT-->GAT) were exposed to a hydrocarbon solvent. The results raise the possibility that hydrocarbon solvents might be involved in the pathogenesis of EPC, possibly through indirect modulation of K-ras activation. Since this is only the first study on occupational exposures and K-ras mutations in EPC, studies able to refute or to confirm the findings are required before public health implications, if any, are assessed.
C1 Univ Autonoma Barcelona, Inst Municipal Invest Med, E-08003 Barcelona, Spain.
   NCI, Bethesda, MD 20892 USA.
   Univ Pompeu Fabra, Barcelona, Spain.
   Finnish Inst Occupat Hlth, Helsinki, Finland.
   Univ Nacl, Cent Amer Inst Studies Tox Subst, Heredia, Costa Rica.
   Hosp Gen Elche, Alicante, Spain.
RP Porta, M (reprint author), Univ Autonoma Barcelona, Inst Municipal Invest Med, Carrer Doctor Aiguader 80, E-08003 Barcelona, Spain.
RI Benavides, Fernando/A-5137-2008; Porta, Miquel/B-5787-2008; Kogevinas,
   Manolis/C-3918-2017
OI Benavides, Fernando/0000-0003-0747-2660; Porta,
   Miquel/0000-0003-1684-7428; 
NR 58
TC 33
Z9 37
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD JAN
PY 2002
VL 23
IS 1
BP 101
EP 106
DI 10.1093/carcin/23.1.101
PG 6
WC Oncology
SC Oncology
GA 511NX
UT WOS:000173273400014
PM 11756230
ER

PT J
AU Qu, W
   Bortner, CD
   Sakurai, T
   Hobson, MJ
   Waalkes, MP
AF Qu, W
   Bortner, CD
   Sakurai, T
   Hobson, MJ
   Waalkes, MP
TI Acquisition of apoptotic resistance in arsenic-induced malignant
   transformation: role of the JNK signal transduction pathway
SO CARCINOGENESIS
LA English
DT Article
ID PROTEIN-KINASE PHOSPHATASE-1; ACUTE PROMYELOCYTIC LEUKEMIA; RAT
   MESANGIAL CELLS; ENHANCED EXPRESSION; TRIOXIDE AS2O3; CYTOCHROME-C;
   DNA-DAMAGE; IN-VITRO; BCL-2; INHIBITOR
AB This study examined the role of signal transduction and apoptosis in malignant transformation induced by arsenic. Prior study showed that chronic arsenite exposure (500 nM, greater than or equal to18 weeks) induced malignant transformation in rat liver TRL 1215 cells. In the present work, these transformed cells were compared with passage-matched control cells. In addition, TRL 1215 cells were treated subchronically (up to 6 weeks) with arsenic (termed pre-transformed cells) to define events occurring prior to arsenic-induced transformation. Flow cytometry using annexin/FITC revealed that arsenic-induced apoptosis in transformed cells was markedly suppressed in comparison to control or pre-transformed cells. Ro318220, a strong activator of JNK, enhanced arsenite-induced apoptosis in transformed cells. Densitometric analysis of western blots revealed that the ratios of both Bcl-x(L)/Bax and Bcl-2/Bax were significantly increased (>2.5-fold) in arsenic-transformed cells. Transformed, pre-transformed and control cells were treated with arsenic and levels of phosphorylated extracellular signal-regulated kinases, ERK1/2, JNK1/2 and p38 were determined by western blot analysis. The three mitogen-activated protein kinases (MAPKs) were phosphorylated in a dose-dependent fashion in all cell types. However, the levels of phosphorylated JNK1/2 were markedly decreased in the arsenic-transformed cells, whereas in pre-transformed cells the levels of phosphorylated MAPKs remained the same as in control cells. JNK kinase activity was suppressed in transformed cells whereas Ro318220 enhanced this activity. Thus, during arsenic-induced malignant transformation resistance to apoptosis develops, possibly due to perturbation of the JNK pathway.
C1 NIEHS, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI, Res Triangle Pk, NC 27709 USA.
   NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
RP Waalkes, MP (reprint author), NIEHS, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI, POB 12233,Mail Drop F0-09,111 Alexander Dr, Res Triangle Pk, NC 27709 USA.
NR 40
TC 43
Z9 46
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD JAN
PY 2002
VL 23
IS 1
BP 151
EP 159
DI 10.1093/carcin/23.1.151
PG 9
WC Oncology
SC Oncology
GA 511NX
UT WOS:000173273400020
PM 11756236
ER

PT S
AU Melnick, RL
AF Melnick, RL
BE Mehlman, MA
   Bingham, E
   Landrigan, PJ
   Soffritti, M
   Belpoggi, F
   Melnick, RL
TI Carcinogenicity and mechanistic insights on the behavior of epoxides and
   epoxide-forming chemicals
SO CARCINOGENESIS BIOASSAYS AND PROTECTING PUBLIC HEALTH: COMMEMORATING THE
   LIFEWORK OF CESARE MALTONI AND COLLEAGUES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Carcinogenesis Bioassays and Protecting Public Health
CY APR 29-30, 2002
CL NEW YORK, NEW YORK
SP NY Acad Sci, Collegium Ramazzini, NIEHS
DE vinyl chloride; vinyl halides; butadiene; styrene; ethylene oxide;
   glycidol; epoxides; carcinogenicity; toxicokinetic modeling; DNA
   adducts; etheno adducts; K-ras mutations; cancer risk; human carcinogens
ID MULTIPLE ORGAN CARCINOGENICITY; VINYL-CHLORIDE; INHALATION EXPOSURE;
   FISCHER-344 RATS; B6C3F1 MICE; DNA-ADDUCTS; ONCOGENICITY BIOASSAY;
   MUTATION PATTERN; ETHYLENE-OXIDE; LIVER-TUMORS
AB Many epoxides and their precursors are high production volume chemicals that have major uses in the polymer industry and as intermediates in the manufacture of other chemicals. Several of these chemicals were demonstrated to be carcinogenic in laboratory animal studies conducted by the Ramazzini Foundation (e.g., vinyl chloride, acrylonitrile, styrene, styrene oxide, and benzene) and by the National Toxicology Program (e.g., ethylene oxide, 1,3-butadiene, isoprene, chloroprene, acrylonitrile, glycidol, and benzene). The most common sites of tumor induction were lung, liver, harderian gland, and circulatory system in mice; Zymbal's gland and brain in rats; and mammary gland and forestomach in both species. Differences in cancer outcome among studies of epoxide chemicals may be related to differences in study design (e.g., dose, duration, and route of exposure; observation period; animal strains), as well as biological factors affecting target organ dosimetry of the DNA-reactive epoxide (toxicokinetics) and tissue response (toxicodynamics). N7-Alkylguanine, N1-alkyladenine, and cyclic etheno adducts, as well as K-ras and p53 mutations, have been detected in animals and/or workers exposed to several of these chemicals. The classifications of these chemical carcinogens by IARC and NTP are based on animal and human data and results of mechanistic studies. Reducing occupational and environmental exposures to these chemicals will certainly reduce human cancer risks.
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Melnick, RL (reprint author), NIEHS, POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
NR 40
TC 43
Z9 43
U1 0
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-406-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 982
BP 177
EP 189
PG 13
WC Public, Environmental & Occupational Health; Multidisciplinary Sciences
SC Public, Environmental & Occupational Health; Science & Technology -
   Other Topics
GA BW05K
UT WOS:000180752400011
PM 12562636
ER

PT S
AU Bucher, JR
AF Bucher, JR
BE Mehlman, MA
   Bingham, E
   Landrigan, PJ
   Soffritti, M
   Belpoggi, F
   Melnick, RL
TI The National Toxicology Program rodent bioassay - Designs,
   interpretations, and scientific contributions
SO CARCINOGENESIS BIOASSAYS AND PROTECTING PUBLIC HEALTH: COMMEMORATING THE
   LIFEWORK OF CESARE MALTONI AND COLLEAGUES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Carcinogenesis Bioassays and Protecting Public Health
CY APR 29-30, 2002
CL NEW YORK, NEW YORK
SP NY Acad Sci, Collegium Ramazzini, NIEHS
DE National Toxicology Program; rodent; bioassays; carcinogenesis;
   phototoxicology; photocarcinogenicity; dioxins
ID CARCINOGENIC RISKS; FREQUENCY
AB The National Toxicology Program rodent cancer bioassay program design evolved from that of the National Cancer Institute in the 1970s. Groups of 50 or more mice are assigned to control or treatment groups. Test substances are given at three dose levels by intubation, dietary or drinking water consumption, or dermal or inhalation exposure. Dosing starts at age 5-6 weeks and lasts for 2 years, when surviving animals receive a complete histopathologic examination. Statistical approaches accommodate survival differences and no longer require differentiation between fatal and incidental tumors. Photocarcinogenicity studies, employing SKH-1 hairless mice, evaluate onset of skin papillomas and incidences at 1 year. Top doses are chosen to expose animals to a minimally toxic challenge and lower doses to operate within the linear range of kinetics. This dosing allows comparison of results across studies. Bioassay and ancillary studies successfully identify tumor-causing agents in rodents, provide information on dose-response, and characterize other chemical-related toxicities. NTP and Ramazzini Foundation bioassay designs differ in several aspects, but bioassays at both institutions provide chemical-specific information for predicting human carcinogens, thus providing for protection of public health. Bioassays constitute an essential information reference set for new assay development and further investigations into mechanisms of action. The scientific community and the public owe a huge debt of gratitude to Dr. Cesare Maltoni of the European Foundation of Oncology and Environmental Sciences and to Dr. David P. Rail of the National Institute of Environmental Health Sciences for their foresight and wisdom in creating and nurturing these bioassay programs.
C1 NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Bucher, JR (reprint author), NIEHS, Natl Toxicol Program, 79 TW Alexander Dr,Bldg 4401,POB 12233, Res Triangle Pk, NC 27709 USA.
NR 12
TC 34
Z9 35
U1 0
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-406-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 982
BP 198
EP 207
PG 10
WC Public, Environmental & Occupational Health; Multidisciplinary Sciences
SC Public, Environmental & Occupational Health; Science & Technology -
   Other Topics
GA BW05K
UT WOS:000180752400013
PM 12562638
ER

PT S
AU Huff, J
AF Huff, J
BE Mehlman, MA
   Bingham, E
   Landrigan, PJ
   Soffritti, M
   Belpoggi, F
   Melnick, RL
TI Chemicals studied and evaluated in long-term carcinogenesis bioassays by
   both the Ramazzini Foundation and the National Toxicology Program - In
   tribute to Cesare Maltoni and David Rall
SO CARCINOGENESIS BIOASSAYS AND PROTECTING PUBLIC HEALTH: COMMEMORATING THE
   LIFEWORK OF CESARE MALTONI AND COLLEAGUES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Carcinogenesis Bioassays and Protecting Public Health
CY APR 29-30, 2002
CL NEW YORK, NEW YORK
SP NY Acad Sci, Collegium Ramazzini, NIEHS
DE bioassay; chemical carcinogens; hazard identification; long-term tests;
   Maltoni; National Toxicology Program; Rall; Ramazzini Foundation
ID SPRAGUE-DAWLEY RATS; EXPERIMENTAL MULTIPOTENTIAL CARCINOGEN; HUMAN
   CANCER HAZARDS; B6C3F1 MICE; BOLOGNA-INSTITUTE; F344/N RATS; RODENT
   CARCINOGENICITY; TUMOR-INDUCTION; ANIMAL TESTS; SWISS MICE
AB The Ramazzini Foundation (RF) in Bentivoglio, Italy and the National Toxicology Program (NTP) in Research Triangle Park, North Carolina have carried out several hundred chemical carcinogenesis bioassays: 200 by RF and 500 by NTP. Of these, 21 have been evaluated by both laboratories. The 14 chemicals for which both laboratories have designed, conducted, and reported bioassay results are: acrylonitrile, benzene, chlorine, diesel fuel, ethylbenzene, methylene chloride (dichloromethane), propylene, styrene, styrene oxide, toluene, trichloroethylene, trichloronuoromethane, vinylidene chloride, and xylenes. The other seven chemicals (two are fibers) were evaluated by both laboratories, but results have not vet been published. Results of these 14 interlaboratory studies were compared both to explore consistency of carcinogenic responses and to identify possible factors that may reveal reasons for any differences observed. Individual carcinogenesis results from each laboratory were duplicated and complementary. Of the 14 chemicals compared, 11 (80%) were either carcinogenic (9 chemicals) or noncarcinogenic (2 chemicals) in both studies. Eight of the paired chemicals had at least one carcinogenic target site in common. The other three were carcinogenic in one laboratory but not in the other. Possible explanations for these differences include dose, method of administration, duration of follow-up, and whether or not total tumors are counted. The collaboration between these two pioneering bioassay laboratory programs contributes greatly to our understanding of chemical carcinogenesis and results in better protection of workers and the general population from chemical diseases, especially cancers.
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Huff, J (reprint author), NIEHS, POB 12233,11 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
NR 126
TC 33
Z9 33
U1 2
U2 8
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-406-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 982
BP 208
EP 229
PG 22
WC Public, Environmental & Occupational Health; Multidisciplinary Sciences
SC Public, Environmental & Occupational Health; Science & Technology -
   Other Topics
GA BW05K
UT WOS:000180752400014
PM 12562639
ER

PT B
AU Spooner, PM
AF Spooner, PM
BE Raviele, A
TI Progress in arrhythmia and sudden cardiac death research support
SO CARDIAC ARRHYTHMIAS 2001
LA English
DT Proceedings Paper
CT 7th International Workshop on Cardiac Arrhythmias
CY OCT 07-10, 2001
CL VENICE, ITALY
SP Fdn Giorgio Cini
C1 NHLBI, Div Heart & Vasc Dis, NIH, Bethesda, MD 20892 USA.
RP Spooner, PM (reprint author), NHLBI, Div Heart & Vasc Dis, NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER-VERLAG ITALIA
PI MILAN
PA MILAN, ITALY
BN 88-470-0160-9
PY 2002
BP 3
EP 10
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA BT53M
UT WOS:000173272600001
ER

PT B
AU Summers, RM
AF Summers, RM
BE Lemke, HU
   Vannier, MW
   Inamura, K
   Farman, AG
   Doi, K
   Reiber, JH
TI Current concepts and future directions in computer-aided diagnosis for
   CT colonography
SO CARS 2002: COMPUTER ASSISTED RADIOLOGY AND SURGERY, PROCEEDINGS
LA English
DT Proceedings Paper
CT 16th International Congress and Exhibition on Computer Assisted
   Radiology and Surgery
CY JUN 26-29, 2002
CL PARIS, FRANCE
SP Amer Acad Oral & Maxillofacial Radiol, Bulgarian Assoc Radiol, British Inst Radiol, Czech Radiol Soc, Deutsch Gesell Comp Roboterassistierte Chirurg, Deutsch Gesell Biomed Tech e V, Deutsch Rontgengesell, European Soc Cardiac Radiol
DE colonic polyps; colon cancer; shape detection
ID VIRTUAL BRONCHOSCOPY; COLONIC POLYPS; FEASIBILITY; POPULATION; LESIONS
AB Beginning in approximately 1997, we began an investigation of automated diagnosis for CT bronchography ("virtual bronchoscopy") [1-3]. In our study published in 1998, we found that 100% of airway lesions 5mm in size or larger could be detected using a shape-based detection algorithm [4]. The specificity was 80%. This technology transferred readily to CT colonography, and in association with colleagues at Stanford University, we published a feasibility study showing that colonic polyps could be detected in a phantom model [5]. More recently, we published the first study of computer-aided polyp detection for CT colonography to appear in a peer-reviewed journal, in association with colleagues at Mayo Clinic [6]. These early results showed the feasibility of CT colonography computer-aided diagnosis. In addition, they suggested that computer-aided diagnosis might become an important pail of the radiologist's assessment of CT colonography studies. In this review article, I present a brief overview of the current status of CT colonography computer-aided diagnosis.
C1 NIH, Dept Radiol, Bethesda, MD 20892 USA.
RP NIH, Dept Radiol, Bldg 10,Room 1C660, Bethesda, MD 20892 USA.
NR 20
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
BN 3-540-43655-3
PY 2002
BP 743
EP 748
PG 4
WC Computer Science, Interdisciplinary Applications; Engineering,
   Biomedical; Radiology, Nuclear Medicine & Medical Imaging; Surgery
SC Computer Science; Engineering; Radiology, Nuclear Medicine & Medical
   Imaging; Surgery
GA BV16A
UT WOS:000178013900124
ER

PT S
AU Eiden, LE
   Schutz, B
   Anlauf, M
   Depboylu, C
   Schafer, MKH
   Weihe, E
AF Eiden, LE
   Schutz, B
   Anlauf, M
   Depboylu, C
   Schafer, MKH
   Weihe, E
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI The vesicular monoamine transporters (VMATs): Role in the chemical
   coding of neuronal transmission and monoamine storage in amine-handling
   immune and inflammatory cells
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE Advances in Behavioral Biology
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID DOPAMINE-BETA-HYDROXYLASE; PERIPHERAL NERVOUS-SYSTEM; ACETYLCHOLINE
   TRANSPORTER; SYNAPTIC VESICLES; HOMEODOMAIN PROTEINS; ENDOCRINE-CELLS;
   C-ELEGANS; EXPRESSION; GENE; BRAIN
C1 NIMH, Mol Neurosci Sect, NIH, Bethesda, MD 20892 USA.
RP Eiden, LE (reprint author), NIMH, Mol Neurosci Sect, NIH, Bethesda, MD 20892 USA.
NR 56
TC 5
Z9 5
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
JI Adv. Behav. Biol.
PY 2002
VL 53
BP 23
EP 33
PG 11
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100004
ER

PT S
AU Kopin, IJ
AF Kopin, IJ
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Assessing sympathetic function from dynamics of norepinephrine
   metabolism and false transmitters
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID NEUROTRANSMITTERS
C1 NINDS, NIH, Bethesda, MD 20892 USA.
RP Kopin, IJ (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
NR 13
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 81
EP 86
PG 6
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100016
ER

PT S
AU Sibley, DR
   Gardner, B
   Peters, JD
   Kim, OJ
AF Sibley, DR
   Gardner, B
   Peters, JD
   Kim, OJ
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Structural insights into D-1 dopamine receptor phosphorylation and
   desensitization
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
C1 NINDS, Mol Neuropharmacol Sect, NIH, Bethesda, MD 20892 USA.
RP Sibley, DR (reprint author), NINDS, Mol Neuropharmacol Sect, NIH, Bethesda, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 159
EP 162
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100035
ER

PT S
AU Matsunaga, J
   Riley, PA
   Solano, F
   Hearing, VJ
AF Matsunaga, J
   Riley, PA
   Solano, F
   Hearing, VJ
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Biosynthesis of neuromelanin and melanin: The potential involvement of
   macrophage inhibitory factor and dopachrome tautomerase as rescue
   enzymes
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID HUMAN SUBSTANTIA-NIGRA; PARKINSONS-DISEASE; DOPAMINE-MELANIN; FACTOR
   MIF; CATECHOLAMINES; CELLS
C1 NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Matsunaga, J (reprint author), NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RI Solano, Francisco/G-5001-2013
OI Solano, Francisco/0000-0001-9612-761X
NR 19
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 273
EP 276
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100064
ER

PT S
AU Aguilera, G
   Rabadan-Diehl, C
   Kiss, A
   Ochedalski, T
AF Aguilera, G
   Rabadan-Diehl, C
   Kiss, A
   Ochedalski, T
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Vasoactive hormones and regulation of the hypothalamic-pituitary-adrenal
   axis
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID CORTICOTROPIN-RELEASING HORMONE; ALPHA-1-ADRENERGIC RECEPTORS;
   PARAVENTRICULAR NUCLEUS; MESSENGER-RNA; STRESS; SYSTEM; VASOPRESSIN;
   SECRETION
C1 NICHHD, Sect Endocrine Physiol, NIH, Bethesda, MD 20892 USA.
RP Aguilera, G (reprint author), NICHHD, Sect Endocrine Physiol, NIH, Bethesda, MD 20892 USA.
NR 16
TC 0
Z9 0
U1 0
U2 2
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 281
EP 284
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100066
ER

PT S
AU Armando, I
   Carranza, A
   Nishimura, Y
   Hoe, KL
   Barontini, M
   Saavedra, JM
AF Armando, I
   Carranza, A
   Nishimura, Y
   Hoe, KL
   Barontini, M
   Saavedra, JM
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI The role of angiotensin II AT(1) receptors in the sympathoadrenal
   response to stress
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID RAT-BRAIN; INCREASES
C1 NIMH, Pharmacol Sect, NIH, Bethesda, MD 20892 USA.
RP Armando, I (reprint author), NIMH, Pharmacol Sect, NIH, Bethesda, MD 20892 USA.
NR 14
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 313
EP 316
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100074
ER

PT S
AU Goldstein, DS
   Holmes, CS
   Frank, SM
AF Goldstein, DS
   Holmes, CS
   Frank, SM
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Stressor-specific activation of catecholamine systems in humans
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
C1 NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
RP Goldstein, DS (reprint author), NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
NR 9
TC 0
Z9 0
U1 0
U2 1
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 333
EP 336
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100079
ER

PT S
AU Goldstein, DS
AF Goldstein, DS
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Cardiac sympathetic denervation in Parkinson's disease
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID NEUROCIRCULATORY FAILURE
C1 Natl Inst Neurol Disorders & Stroke, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
RP Goldstein, DS (reprint author), Natl Inst Neurol Disorders & Stroke, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
NR 10
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 443
EP 448
PG 6
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100106
ER

PT S
AU Creveling, CR
AF Creveling, CR
BE Nagatsu, T
   Nabeshima, T
   McCarty, R
   Goldstein, DS
TI Estrogen metabolism: Does the formation of estrogen quinone provide a
   potential pathway to breast carcinogenesis?
SO CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE
SE ADVANCES IN BEHAVIORAL BIOLOGY
LA English
DT Proceedings Paper
CT 9th International Catecholamine Symposium
CY MAR 31-APR 05, 2001
CL KYOTO, JAPAN
ID CATECHOL-O-METHYLTRANSFERASE; MEDIATED METABOLISM; CANCER RISK;
   PHYTOESTROGENS; WOMEN; CELLS; TEA
C1 NIDDK, NIH, Bethesda, MD 20892 USA.
RP Creveling, CR (reprint author), NIDDK, NIH, Bethesda, MD 20892 USA.
NR 23
TC 0
Z9 0
U1 0
U2 0
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0099-9962
BN 0-306-47403-4
J9 ADV BEHAV BIOL
PY 2002
VL 53
BP 533
EP 536
PG 4
WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA BV95A
UT WOS:000180512100127
ER

PT J
AU Koehl, G
   McNally, JG
AF Koehl, G
   McNally, JG
TI Myosin II redistribution during rear retraction and the role of filament
   assembly and disassembly
SO CELL BIOLOGY INTERNATIONAL
LA English
DT Article
DE myosin II; retraction; motility; GFP; time-lapse
ID HEAVY-CHAIN GENE; DICTYOSTELIUM-DISCOIDEUM; CELL MOTILITY; IN-VIVO;
   MORPHOGENESIS; LOCALIZATION; MIGRATION; MOVEMENT
AB The literature to date suggests a role for myosin II in rear retraction, including evidence that myosin undergoes a characteristic 'C'-to-spot redistribution at the cell posterior which is associated with retraction. Here we investigate the mechanism of both retraction and the 'C'-to-spot using Dictyostelium cells containing mutant forms of myosin that affect its polymerization. 3 x Asp-myosin forms few if any filaments. When 3 x Asp cells are added to a wild-type mound, the mutant cells move directionally, but rear retraction is markedly delayed, demonstrating that myosin II filaments are essential for efficient retraction. In addition, using a GFP-tagged 3 x Asp-myosin, we observed a posterior spot pattern associated with retraction, but no cortical 'C' pattern preceding it. This suggests that filamentous myosin is required to produce the 'C', and that its failure to form results in defective rear retraction. In contrast, an alternate mutant myosin that forms filaments constitutively, 3 x Ala-myosin, forms 'Cs' and then spot patterns at the posterior, but in the interim the spots do not disintegrate. This suggests that spot dissolution occurs by filament depolymerization. In summary our data demonstrate a role for myosin II and the 'C'-to-spot in efficient rear retraction, and define filament assembly as critical for formation of the 'C' and filament disassembly as critical for dissolution of the spot. Published by Elsevier Science Ltd.
C1 NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
RP McNally, JG (reprint author), NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
FU NIGMS NIH HHS [GM-47330]
NR 26
TC 10
Z9 10
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1065-6995
J9 CELL BIOL INT
JI Cell Biol. Int.
PY 2002
VL 26
IS 3
BP 287
EP 296
DI 10.1006/cbir.2001.0855
PG 10
WC Cell Biology
SC Cell Biology
GA 556AQ
UT WOS:000175825600009
PM 11991657
ER

PT J
AU Dyer, KD
   Linz-McGillem, LA
   Alliegro, MA
   Alliegro, MC
AF Dyer, KD
   Linz-McGillem, LA
   Alliegro, MA
   Alliegro, MC
TI Receptor-bound uPA is reversibly protected from inhibition by low
   molecular weight inhibitors
SO CELL BIOLOGY INTERNATIONAL
LA English
DT Article
DE angiogenesis; urokinase-type plasminogen activator; uPA; amiloride;
   endothelial cell; urokinase; urokinase receptor
ID PLASMINOGEN-ACTIVATOR INHIBITOR; ENDOMETRIAL STROMAL CELLS; COLLAGEN
   GELS; GROWTH-FACTOR; TUMOR-MODEL; AMILORIDE; UROKINASE; ANGIOGENESIS;
   DEGRADATION; INVITRO
AB Urokinase-type plasminogen activator (uPA) plays a ubiquitous role in cell migration and invasiveness. Amiloride, a competitive inhibitor of uPA, can inhibit endothelial cell (EC) outgrowth during angiogenesis. To address the question of whether amiloride blocked angiogenesis by inhibiting uPA, we undertook a study of uPA expression in sprouting EC in vitro and the effects of amiloride on both enzymatic and morphogenetic activity. As expected, amiloride inhibited soluble uPA (suPA) with an IC50 of 45-85 mum, however, receptor-bound uPA (rbuPA) from the sprouting EC was insensitive to amiloride. Removal of uPA from its receptors confers sensitivity to inhibition by amiloride suggesting that a reversible conformational change may mediate the insensitivity of rbuPA to amiloride and its analogs. In summary, we found no evidence to support the hypothesis that amiloride blocks capillary outgrowth by inhibition of uPA, but were able to successfully demonstrate a functional difference between two physiological forms of this important matrix-degrading enzyme. (C) 2002 Elsevier Science Ltd. All rights reserved.
C1 NIAID, Host Def Lab, Bethesda, MD 20892 USA.
   Louisiana State Univ, Ctr Hlth Sci, Dept Cell Biol & Anat, New Orleans, LA USA.
RP Dyer, KD (reprint author), NIAID, Host Def Lab, 10 Ctr Dr,MSC 1886, Bethesda, MD 20892 USA.
NR 39
TC 4
Z9 4
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1065-6995
J9 CELL BIOL INT
JI Cell Biol. Int.
PY 2002
VL 26
IS 4
BP 327
EP 335
DI 10.1006/cbir.2001.0859
PG 9
WC Cell Biology
SC Cell Biology
GA 559TU
UT WOS:000176042100004
PM 11991662
ER

PT J
AU Blagosklonny, MV
AF Blagosklonny, Mikhail V.
TI Basic Cell Cycle and Cancer Research: Is Harmony Impossible?
SO CELL CYCLE
LA English
DT Editorial Material
C1 [Blagosklonny, Mikhail V.] NCI, Med Branch, Bethesda, MD 20892 USA.
RP Blagosklonny, MV (reprint author), NIH, Med Branch, Bldg 10,Room 12 N 226, Bethesda, MD 20892 USA.
EM mikhailb@box-m.nih.gov
NR 37
TC 5
Z9 5
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD JAN
PY 2002
VL 1
IS 1
BP 3
EP 5
DI 10.4161/cc.1.1.92
PG 3
WC Cell Biology
SC Cell Biology
GA V40OM
UT WOS:000209487900002
PM 12429900
ER

PT J
AU Blagosklonny, MV
   Demidenko, ZN
   Fojo, T
AF Blagosklonny, Mikhail V.
   Demidenko, Zoya N.
   Fojo, Tito
TI Inhibition of Transcription Results in Accumulation of Wt p53 Followed
   by Delayed Outburst of p53-Inducible Proteins: p53 as a Sensor of
   Transcriptional Integrity
SO CELL CYCLE
LA English
DT Article
DE Apoptosis; Growth Arrest; Mdm-2; p21; p53
AB Here we investigate activation of the p53 pathway by inhibition of transcription. Comparison of cells with either mutant p53 or wt p53 indicated that inhibition of p53-dependent transcription is necessary and sufficient for wt p53 accumulation. In addition to Mdm-2, p21 is required for effective p53 degradation. Transient inhibition of transcription resulted in initial downregulation of p21 and Mdm-2 leading to accumulation of wt p53. This was followed by induction of p21 and Mdm-2, normalization of p53 levels, and p21-dependent growth arrest. Although simultaneous induction of p53 and p21 could be detected by immunoblot, levels of p53 and p21 were discordant in individual cells. By inducing p21 and Mdm-2, p53 discriminates between transient and sustained inhibition of transcription. Transient inhibition results in p21-dependent growth, while sustained inhibition of transcription leads to p53-facilitated cell death. One can envision p53 as a physiological sensor of transcriptional integrity. Transient inhibition of p53-stimulated transcription by numerous stimuli including nucleotide depletion, hypoxia, UV light may be an prevalent mechanism of activation of wt p53 and its downstream pathways.
C1 [Blagosklonny, Mikhail V.; Demidenko, Zoya N.; Fojo, Tito] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Blagosklonny, Mikhail V.] New York Med Coll, Dept Med, Valhalla, NY 10595 USA.
RP Blagosklonny, MV (reprint author), NIH, Bldg 10,Room 12 N 226, Bethesda, MD 20892 USA.
EM mikhailb@box-m.nih.gov
NR 47
TC 48
Z9 48
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD JAN
PY 2002
VL 1
IS 1
BP 67
EP 74
DI 10.4161/cc.1.1.102
PG 8
WC Cell Biology
SC Cell Biology
GA V40OM
UT WOS:000209487900013
PM 12429911
ER

PT J
AU Xu, WP
   Mimnaugh, EG
   Kim, JS
   Trepel, JB
   Neckers, LM
AF Xu, WP
   Mimnaugh, EG
   Kim, JS
   Trepel, JB
   Neckers, LM
TI Hsp90, not Grp94, regulates the intracellular trafficking and stability
   of nascent ErbB2
SO CELL STRESS & CHAPERONES
LA English
DT Article
ID FAMILY; GELDANAMYCIN; DEGRADATION; EXPRESSION; CELLS
AB The benzoquinone ansamycin geldanamycin (GA) stimulates proteasome-mediated degradation of plasma membrane-associated ErbB2, a receptor tyrosine kinase. Drug sensitivity is mediated by ErbB2's kinase domain and occurs subsequent to the disruption of Hsp90 interaction with this domain. Full-length ErbB2 is efficiently processed via the endoplasmic reticulum (ER) and Golgi network, so that at steady state most of the detectable protein is plasma membrane associated. However, previous studies have also demonstrated the GA sensitivity of newly synthesized ErbB2, normally a minor component of the total cellular pool of the kinase. Drug sensitivity of nascent ErbB2 is distinguished by 2 characteristics-protein instability and inability to traverse the ER. As nascent ErbB2 can associate with both cytoplasmic Hsp90 and its ER luminal homolog Grp 94, also a GA-binding protein, the purpose of this study was to examine the relative contributions of the cytoplasmic and ER luminal domains of ErbB2 to the GA sensitivity of the nascent kinase. By studying the drug sensitivity of ErbB2/DK, a construct lacking ErbB2's cytoplasmic kinase domain, and by examining the activity of a GA derivative that preferentially binds Hsp90, we conclude that both the stability and the maturation of nascent ErbB2 are regulated by its cytoplasmic, Hsp90-interacting domain.
C1 NCI, Dept Cell & Canc Biol, Med Branch, Rockville, MD 20850 USA.
RP Neckers, LM (reprint author), NCI, Dept Cell & Canc Biol, Med Branch, 9610 Med Ctr Dr,Suite 300, Rockville, MD 20850 USA.
NR 11
TC 55
Z9 58
U1 0
U2 2
PU CELL STRESS SOC INTERNATIONAL
PI STORRS
PA UNIV CONNECTICUT, DEPT M C B, 75 NORTH EAGLEVILLE RD, U-44, STORRS, CT
   06269-3044 USA
SN 1355-8145
J9 CELL STRESS CHAPERON
JI Cell Stress Chaperones
PD JAN
PY 2002
VL 7
IS 1
BP 91
EP 96
DI 10.1379/1466-1268(2002)007<0091:HNGRTI>2.0.CO;2
PG 6
WC Cell Biology
SC Cell Biology
GA 631XT
UT WOS:000180193900010
PM 11892991
ER

PT J
AU McGrath, J
   Lintz, E
   Hoffer, BJ
   Gerhardt, GA
   Quintero, EM
   Granholm, AC
AF McGrath, J
   Lintz, E
   Hoffer, BJ
   Gerhardt, GA
   Quintero, EM
   Granholm, AC
TI Adeno-associated viral delivery of GDNF promotes recovery of
   dopaminergic phenotype following a unilateral 6-hydroxydopamine lesion
SO CELL TRANSPLANTATION
LA English
DT Article; Proceedings Paper
CT 8th Annual Conference of the
   American-Society-for-Neural-Transplantation-and-Repair
CY MAY 03-06, 2001
CL CLEARWATER, FLORIDA
SP Amer Soc Neural Transplantat & Repair
DE glial cell line-derived neurotrophic factor (GDNF); Parkinson's disease;
   adeno-associated viral delivery
ID RECOMBINANT ADENOASSOCIATED VIRUS; NEUROTROPHIC FACTOR;
   PARKINSONS-DISEASE; GENE-THERAPY; IN-VIVO; SUBSTANTIA-NIGRA;
   RHESUS-MONKEYS; RAT MODEL; STEREOLOGICAL METHODS; TYROSINE-HYDROXYLASE
AB Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopamine neurons that has been proposed for use in the treatment of Parkinson's disease (PD). Previous studies using viral vectors to deliver GDNF in rodent models of PD have entailed administering the virus either prior to or immediately after neurotoxin-induced lesions, when the nigrostriatal pathway is largely intact, a paradigm that does not accurately reflect the clinical situation encountered with Parkinson's patients. In this study, recombinant adeno-associated virus carrying the gene encoding GDNF (rAAV-GDNF) was administered to animals bearing a maximal lesion in the nigrostriatal system, more closely resembling fully developed PD. Rats were treated with 6-hydroxydopamine into the medial forebrain bundle and assessed by apomorphine-induced rotational behavior for 5 weeks prior to virus administration. Within 4 weeks of a single intrastriatal injection of rAAV-GDNF, unilaterally lesioned animals exhibited significant behavioral recovery, which correlated with increased expression of dopaminergic markers in the substantia nigra, the medial forebrain bundle, and the striatum. Our findings demonstrate that rAAV-GDNF is capable of rescuing adult dopaminergic neurons from near complete phenotypic loss following a neurotoxic lesion, effectively restoring a functional dopaminergic pathway and diminishing motoric deficits. These data provide further support for the therapeutic potential of rAAV-GDNF-based gene therapy in the treatment of PD.
C1 Med Univ S Carolina, Dept Physiol & Neurosci, Charleston, SC 29425 USA.
   Alkermes Inc, Cambridge, MA USA.
   Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
   NIDA, Intramural Res Program, Baltimore, MD USA.
   Univ Kentucky, Albert B Chandler Med Ctr, Ctr Sensor Technol, Lexington, KY 40536 USA.
   Univ Kentucky, Albert B Chandler Med Ctr, Dept Anat & Neurobiol, Lexington, KY 40536 USA.
   Univ Kentucky, Albert B Chandler Med Ctr, Dept Neurol, Lexington, KY 40536 USA.
   Univ Kentucky, Albert B Chandler Med Ctr, Morris K Udall Parkinsons Dis Res Ctr Excellence, Lexington, KY 40536 USA.
RP Granholm, AC (reprint author), Med Univ S Carolina, Dept Physiol & Neurosci, 173 Ashley Ave, Charleston, SC 29425 USA.
FU NIA NIH HHS [AG00796, AG06434, AG13494, R01 AG015239]; NIMH NIH HHS
   [MH01245]; NINDS NIH HHS [NS39787]
NR 73
TC 29
Z9 30
U1 0
U2 0
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 0963-6897
J9 CELL TRANSPLANT
JI Cell Transplant.
PY 2002
VL 11
IS 3
BP 215
EP 227
PG 13
WC Cell & Tissue Engineering; Medicine, Research & Experimental;
   Transplantation
SC Cell Biology; Research & Experimental Medicine; Transplantation
GA 561LD
UT WOS:000176141400005
PM 12075987
ER

PT J
AU Dillon-Carter, O
   Johnston, RE
   Borlongan, CV
   Truckenmiller, ME
   Coggiano, M
   Freed, WJ
AF Dillon-Carter, O
   Johnston, RE
   Borlongan, CV
   Truckenmiller, ME
   Coggiano, M
   Freed, WJ
TI T155g-immortalized kidney cells produce growth factors and reduce
   sequelae of cerebral ischemia
SO CELL TRANSPLANTATION
LA English
DT Article; Proceedings Paper
CT 8th Annual Conference of the
   American-Society-for-Neural-Transplantation-and-Repair
CY MAY 03-06, 2001
CL CLEARWATER, FLORIDA
SP Amer Soc Neural Transplantat & Repair
DE cell line; transplantation; stroke; neurotrophic factors; behavioral
   recovery
ID LARGE T-ANTIGEN; NEUROTROPHIC FACTOR PROTECTS; SIMIAN-VIRUS-40 LARGE-T;
   ARTERY OCCLUSION; REPLICATIVE SENESCENCE; MESSENGER-RNA; BRAIN INJURY;
   RATS; EXPRESSION; GDNF
AB Fetal rat kidney cells produce high levels of glial-derived neurotrophic factor (GDNF) and exert neuroprotective effects when transplanted into the brain in animal models of Parkinson's disease and stroke. The purpose of the present experiment was to produce kidney cell lines that secrete GDNF. Genes encoding two truncated N-terminal fragments of SV40 large T antigen, T155, and T155c, which does not code for small t antigen, were used. T155g was transduced into E17 cultured fetal Sprague-Dawley rat kidney cortex cells using a plasmid vector, and T155c was transduced with a plasmid and a retroviral vector. Sixteen clones were isolated from cultures transfected with the T155g-expressing plasmid. No cell lines were obtained with T 155c. Four clones produced GDNF at physiological concentrations ranging from 55 to 93 pg/ml of medium. These four clones were transplanted into the ischemic core or penumbra of rats that had undergone middle cerebral artery occlusion (MCAO). Three of the four clones reduced the volume of infarction and the behavioral abnormalities normally resulting from MCAO. Blocking experiments with antibodies to GDNF and platelet-derived growth factor (PDGF) suggested that these growth factors contributed only minimally to the reduction in infarct volume and behavioral abnormality. These cell lines may be useful for intracerebral transplantation in animal models of brain injury, stroke, or Parkinson's disease.
C1 NIDA, Cellular Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Borlongan, CV (reprint author), Med Coll Georgia, Dept Neurol, 1120 15th St, Augusta, GA 30912 USA.
OI Borlongan, Cesar/0000-0002-2966-9782
NR 36
TC 13
Z9 14
U1 0
U2 0
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 0963-6897
J9 CELL TRANSPLANT
JI Cell Transplant.
PY 2002
VL 11
IS 3
BP 251
EP 259
PG 9
WC Cell & Tissue Engineering; Medicine, Research & Experimental;
   Transplantation
SC Cell Biology; Research & Experimental Medicine; Transplantation
GA 561LD
UT WOS:000176141400008
PM 12075990
ER

PT J
AU Bebenek, K
   Kunkel, TA
AF Bebenek, K
   Kunkel, TA
TI Family growth: the eukaryotic DNA polymerase revolution
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article
ID PIGMENTOSUM VARIANT CELLS; XERODERMA-PIGMENTOSUM; EMBRYONIC LETHALITY;
   THYMINE DIMER; IN-VITRO; BYPASS; IOTA; DISRUPTION; KAPPA; ZETA
C1 NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
   NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
RP Bebenek, K (reprint author), NIEHS, Mol Genet Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 48
TC 15
Z9 15
U1 0
U2 0
PU BIRKHAUSER VERLAG AG
PI BASEL
PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD JAN
PY 2002
VL 59
IS 1
BP 54
EP 57
DI 10.1007/s00018-002-8405-y
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 520LA
UT WOS:000173782300007
PM 11846034
ER

PT S
AU Onaivi, ES
   Ali, SF
   Chirwa, SS
   Zwiller, J
   Thiriet, N
   Akinshola, BE
   Ishiguro, H
AF Onaivi, ES
   Ali, SF
   Chirwa, SS
   Zwiller, J
   Thiriet, N
   Akinshola, BE
   Ishiguro, H
BE Ali, SF
TI Ibogaine signals addiction genes and methamphetamine alteration of
   long-term potentiation
SO CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE II: COCAINE,
   SUBSTITUTED AMPHETAMINES, GHB, AND OPIATES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Cellular and Molecular Mechanisms of Drugs of Abuse II -
   Cocaine, Substituted Amphetamines, GHB, and Opiates
CY AUG 22-24, 2001
CL MAR DEL PLATA, ARGENTINA
SP Int Soc Neurochem, Natl Inst Drug Abuse, Argentinian Sectrtary State Prevent Drug Addict & Narcotraffic, Natl Univ Rosario, Sch Biomed & Pharmaceut Sci, SIGMA TAU Hlth Sci, USDA, Natl Ctr Toxicol Res
DE ibogaine; pharmacogenomics; pharmacotherapy; psychostimulant; gene chip;
   addiction; methamphetamine; haplotypes; SNPs; signal transduction;
   animal model
ID IMMEDIATE-EARLY GENES; IN-VIVO; CIGARETTE-SMOKING; HUMAN ALCOHOLISM; CA1
   REGION; EXPRESSION; DOPAMINE; RECEPTOR; COCAINE; DRUGS
AB The mapping of the human genetic code will enable us to identify potential gene products involved in human addictions and diseases that have hereditary components. Thus, large-scale, parallel gene-expression studies, made possible by advances in microarray technologies, have shown insights into the connection between specific genes, or sets of genes, and human diseases. The compulsive use of addictive substances despite adverse consequences continues to affect society, and the science underlying these addictions in general is intensively studied. Pharmacological treatment of drug and alcohol addiction has largely been disappointing, and new therapeutic targets and hypotheses are needed. As the usefulness of the pharmacotherapy of addiction has been limited, an emerging potential, yet controversial, therapeutic agent is the natural alkaloid ibogaine. We have continued to investigate programs of gene expression and the putative signaling molecules used by psychostimulants such as amphetamine in in vivo and in vitro models. Our work and that of others reveal that complex but defined signal transduction pathways are associated with psychostimulant administration and that there is broad-spectrum regulation of these signals by ibogaine. We report that the actions of methamphetamine were similar to those of cocaine, including the propensity to alter long-term potentiation (LTP) in the hippocampus of the rat brain. This action suggests that there may be a "threshold" beyond which the excessive brain stimulation that probably occurs with compulsive psychostimulant use results in the occlusion of LTP. The influence of ibogaine on immediate early genes (IEGs) and other candidate genes possibly regulated by psychostimulants and other abused substances requires further evaluation in compulsive use, reward, relapse, tolerance, craving and withdrawal reactions. It is therefore tempting to suggest that ibogaine signals addiction gene products.
C1 William Paterson Univ, Dept Biol, Wayne, NJ 07470 USA.
   NIDA, NIH, IRP, Mol Neurobiol Branch, Baltimore, MD 21224 USA.
   US FDA, Natl Ctr Toxicol Res, Neurochem Lab, Div Neurotoxicol Res, Jefferson, AR 72079 USA.
   Meharry Med Coll, Dept Anat & Physiol, Nashville, TN 37308 USA.
   INSERM, U338, Ctr Neurochem, Strasbourg, France.
   Howard Univ, Coll Med, Dept Pharmacol, Washington, DC 20059 USA.
RP Onaivi, ES (reprint author), William Paterson Univ, Dept Biol, 300 Pompton Rd, Wayne, NJ 07470 USA.
NR 58
TC 12
Z9 14
U1 1
U2 3
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-408-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 965
BP 28
EP 46
PG 19
WC Cell Biology; Multidisciplinary Sciences; Neurosciences; Pharmacology &
   Pharmacy
SC Cell Biology; Science & Technology - Other Topics; Neurosciences &
   Neurology; Pharmacology & Pharmacy
GA BU83M
UT WOS:000177157600004
PM 12105083
ER

PT S
AU Baumann, MH
   Phillips, JM
   Ayestas, MA
   Ali, SF
   Rice, KC
   Rothman, RB
AF Baumann, MH
   Phillips, JM
   Ayestas, MA
   Ali, SF
   Rice, KC
   Rothman, RB
BE Ali, SF
TI Preclinical evaluation of GBR12909 decanoate as a long-acting medication
   for methamphetamine dependence
SO CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE II: COCAINE,
   SUBSTITUTED AMPHETAMINES, GHB, AND OPIATES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Cellular and Molecular Mechanisms of Drugs of Abuse II -
   Cocaine, Substituted Amphetamines, GHB, and Opiates
CY AUG 22-24, 2001
CL MAR DEL PLATA, ARGENTINA
SP Int Soc Neurochem, Natl Inst Drug Abuse, Argentinian Sectrtary State Prevent Drug Addict & Narcotraffic, Natl Univ Rosario, Sch Biomed & Pharmaceut Sci, SIGMA TAU Hlth Sci, USDA, Natl Ctr Toxicol Res
DE methamphetamine; cocaine; pharmacotherapies; drug addiction; DA
   transporter; GBR-decanoate; GBR12909; psychomotor stimulants
ID BIOGENIC-AMINE TRANSPORTERS; MONOAMINE REUPTAKE INHIBITORS; HUMAN
   DOPAMINE TRANSPORTER; LIGAND-BINDING DOMAINS; ANALOG I-125 RTI-55;
   RHESUS-MONKEYS; COCAINE-ABUSE; D-AMPHETAMINE; GBR-12909; RAT
AB Methamphetamine (METH) abuse is a growing health problem, and no treatments for METH dependence have been identified. The powerful addictive properties of METH are mediated by release of dopamine (DA) from nerve terminals in mesolimbic reward pathways. METH stimulates DA release by acting as a substrate for DA transporter (DAT) proteins, thereby triggering efflux of DA from cells into the synapse. We have shown that blocking DAT activity with high-affinity DA uptake inhibitors, like GBR12909, can substantially reduce METH-evoked DA release in vitro, suggesting GBR12909 may have potential as a pharmacotherapy for METH dependence. The purpose of the present study was to examine the neurobiological effects of a long-acting oil-soluble preparation of GBR12909 (1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-(3-hydroxy-3-phenylpropyl) piperazinyl decanoate, or GBR-decanoate). Male rats received GBR-decanoate (480 mg/kg, i.m.) or its oil vehicle, and were tested using a variety of methods one and two weeks later. Ex vivo autoradiography showed that GBR-decanoate decreases DAT binding in DA-rich brain regions. In vivo microdialysis in the nucleus accumbens revealed that GBR-decanoate elevates baseline levels of extracellular DA and antagonizes the ability of METH to evoke DA release. The dopaminergic effects of GBR-decanoate were sustained, lasting for at least two weeks. Rats pretreated with GBR-decanoate displayed enhanced locomotor responses to novelty at one week, but not two weeks, postinjection. Administration of the D-2/D-3 receptor agonist quinpirole (10 and 100 mug/kg, s.c.) decreased locomotor activity and suppressed plasma prolactin levels; quinpirole-induced responses were not altered by GBR-decanoate. Thus, GBR-decanoate is able to elevate basal synaptic DA levels and block METH-evoked DA release in a persistent manner, without significant perturbation of DA receptor function. The findings suggest that GBR-decanoate, or similar long-acting agents, should be evaluated further as potential treatment adjuncts in the management of METH addiction in humans.
C1 NIDA, IRP, NIH, Clin Psychopharmacol Sect, Baltimore, MD 21224 USA.
   US FDA, Natl Ctr Toxicol Res, Neurochem Lab, Div Neurotoxicol, Jefferson, AR 72079 USA.
   NIDDK, Med Chem Lab, NIH, Bethesda, MD USA.
RP Baumann, MH (reprint author), NIDA, IRP, NIH, Clin Psychopharmacol Sect, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
NR 68
TC 12
Z9 12
U1 1
U2 3
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-408-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 965
BP 92
EP 108
PG 17
WC Cell Biology; Multidisciplinary Sciences; Neurosciences; Pharmacology &
   Pharmacy
SC Cell Biology; Science & Technology - Other Topics; Neurosciences &
   Neurology; Pharmacology & Pharmacy
GA BU83M
UT WOS:000177157600009
PM 12105088
ER

PT S
AU Rothman, RB
   Blough, BE
   Baumann, MH
AF Rothman, RB
   Blough, BE
   Baumann, MH
BE Ali, SF
TI Appetite suppressants as agonist substitution therapies for stimulant
   dependence
SO CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE II: COCAINE,
   SUBSTITUTED AMPHETAMINES, GHB, AND OPIATES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Cellular and Molecular Mechanisms of Drugs of Abuse II -
   Cocaine, Substituted Amphetamines, GHB, and Opiates
CY AUG 22-24, 2001
CL MAR DEL PLATA, ARGENTINA
SP Int Soc Neurochem, Natl Inst Drug Abuse, Argentinian Sectrtary State Prevent Drug Addict & Narcotraffic, Natl Univ Rosario, Sch Biomed & Pharmaceut Sci, SIGMA TAU Hlth Sci, USDA, Natl Ctr Toxicol Res
DE methamphetamine; appetite suppressant; agonist substitution therapy;
   dual-deficit model; stimulant withdrawal
ID BIOGENIC-AMINE TRANSPORTERS; RAT NUCLEUS-ACCUMBENS; COCAINE WITHDRAWAL;
   EXTRACELLULAR DOPAMINE; RHESUS-MONKEYS; DRUG-ABUSE; INTRAVENOUS COCAINE;
   FENFLURAMINE; PHENTERMINE; SEROTONIN
AB Several lines of evidence support a dual-deficit model of stimulant withdrawal in which decreases in synaptic dopamine (DA) and serotonin (5-HT) contribute to withdrawal symptoms, drug craving, and relapse. According to the dual-deficit model, DA dysfunction during withdrawal underlies anhedonia and psychomotor disturbances, whereas 5-HT dysfunction gives rise to depressed mood, obsessive thoughts, and lack of impulse control. The model suggests that medications capable of normalizing stimulant-induced DA and 5-HT deficits should be effective treatment adjuncts. Furthermore, the model may explain why medications targeting only one neurotransmitter system (i.e., DA) have failed to treat cocaine dependence. Amphetamine-type appetite suppressants are logical choices for neurochemical normalization therapy of stimulant dependence, yet few clinical studies have tested anorectics in this regard. The chief purpose of the present work is to profile the activity of various anorectic agents at DA, 5-HT, and NE transporters, in order to identify possible medications for stimulant dependence. Compounds were tested in vitro for their ability to stimulate release and inhibit uptake of [H-3]DA, [H-3]NE, and [H-3]5-HT. Selected compounds were tested in vivo for their ability to elevate extracellular levels of DA and 5-HT in rat nucleus accumbens. The results show that clinically available appetite suppressants display a wide range of activities at monoamine transporters. However, no single medication possesses equal potency at DA and 5-HT transporters, suggesting that none of the anorectics is ideally suited for treatment of stimulant addictions. Future efforts should focus on developing new medications that possess the desired therapeutic activity but lack the adverse effects associated with older amphetamine-type anorectics.
C1 NIDA, IRP, NIH, Clin Psychopharmacol Sect, Baltimore, MD 21224 USA.
   Res Triangle Inst, Res Triangle Pk, NC 27709 USA.
RP Rothman, RB (reprint author), NIDA, IRP, NIH, Clin Psychopharmacol Sect, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
NR 80
TC 31
Z9 32
U1 2
U2 4
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-408-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 965
BP 109
EP 126
PG 18
WC Cell Biology; Multidisciplinary Sciences; Neurosciences; Pharmacology &
   Pharmacy
SC Cell Biology; Science & Technology - Other Topics; Neurosciences &
   Neurology; Pharmacology & Pharmacy
GA BU83M
UT WOS:000177157600010
PM 12105089
ER

PT S
AU Yu, J
   Allison, S
   Ibrahim, D
   Cadet, JL
   Angulo, JA
AF Yu, J
   Allison, S
   Ibrahim, D
   Cadet, JL
   Angulo, JA
BE Ali, SF
TI Ontogeny of neurokinin-1 receptor mediation of methamphetamine
   neurotoxicity in the striatum of the mouse brain
SO CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE II: COCAINE,
   SUBSTITUTED AMPHETAMINES, GHB, AND OPIATES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Cellular and Molecular Mechanisms of Drugs of Abuse II -
   Cocaine, Substituted Amphetamines, GHB, and Opiates
CY AUG 22-24, 2001
CL MAR DEL PLATA, ARGENTINA
SP Int Soc Neurochem, Natl Inst Drug Abuse, Argentinian Sectrtary State Prevent Drug Addict & Narcotraffic, Natl Univ Rosario, Sch Biomed & Pharmaceut Sci, SIGMA TAU Hlth Sci, USDA, Natl Ctr Toxicol Res
DE dopamine transporter; methamphetamine; neurokinin-1 receptor; L-733,060;
   striatum; neurotoxicity; substance P
ID INDUCED DOPAMINERGIC NEUROTOXICITY; SUPEROXIDE-DISMUTASE; MICE LACKING;
   SUBSTANCE-P; AMPHETAMINE; TRANSPORTER; RELEASE
AB We studied the role of the peptide substance P, signaling through the neurokinin-1 (NK-1) receptor, on methamphetamine-induced loss of dopamine transporter sites, a well-documented marker of toxicity in the striatum of the mouse brain, because this peptide is under dynamic regulation by the neurotransmitter dopamine. Methamphetamine is a psychostimulant that induces dopamine overflow from dopamine terminals of the striatum. Mice were given four injections of methamphetamine (7.5 mg/kg of body weight) at two-hour intervals and were sacrificed three days after the treatment. Dopamine transporter levels in the striatum were assessed by receptor autoradiography with [I-125]RTI-121. Exposure to methamphetamine resulted in significant loss of dopamine transporters in the caudate-putamen. This loss was prevented by preexposure (30 min before the first injection of methamphetamine) of the neurokinin-1 receptor antagonist L-733,060. The inactive enantiomer of L-733,060 (L-733,061) failed to protect dopamine transporter sites from methamphetamine, suggesting specificity for the neurokinin-1 receptor. Moreover, the protective effect of L-733,060 was observed in mice that were 10 weeks of age or older (dopamine transporter sites in mice six and eight weeks old were not protected from methamphetamine by the neurokinin-1 receptor antagonist). The results demonstrate that the deleterious effect of methamphetamine on dopamine transporter sites of the striatum is mediated via the neurokinin-1 receptor. The involvement of the NK-1 receptor appears after the eighth week of postnatal life, suggesting that the link between dopamine transporters and the neurokinin-1 receptor becomes functional at approximately the time when the mouse reaches reproductive age.
C1 CUNY Hunter Coll, Dept Biol Sci, New York, NY 10021 USA.
   NIDA, NIH, Mol Neuropsychiat Sect, Div Intramural Res, Baltimore, MD USA.
RP Angulo, JA (reprint author), CUNY Hunter Coll, Dept Biol Sci, 695 Pk Ave,Room 927 N, New York, NY 10021 USA.
NR 19
TC 0
Z9 0
U1 3
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-408-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 965
BP 247
EP 253
PG 7
WC Cell Biology; Multidisciplinary Sciences; Neurosciences; Pharmacology &
   Pharmacy
SC Cell Biology; Science & Technology - Other Topics; Neurosciences &
   Neurology; Pharmacology & Pharmacy
GA BU83M
UT WOS:000177157600021
PM 12105100
ER

PT S
AU Lahiri, DK
   Utsuki, T
   Chen, D
   Farlow, MR
   Shoaib, M
   Ingram, DK
   Greig, NH
AF Lahiri, DK
   Utsuki, T
   Chen, D
   Farlow, MR
   Shoaib, M
   Ingram, DK
   Greig, NH
BE Ali, SF
TI Nicotine reduces the secretion of Alzheimer's beta-amyloid precursor
   protein containing beta-amyloid peptide in the rat without altering
   synaptic proteins
SO CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE II: COCAINE,
   SUBSTITUTED AMPHETAMINES, GHB, AND OPIATES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Cellular and Molecular Mechanisms of Drugs of Abuse II -
   Cocaine, Substituted Amphetamines, GHB, and Opiates
CY AUG 22-24, 2001
CL MAR DEL PLATA, ARGENTINA
SP Int Soc Neurochem, Natl Inst Drug Abuse, Argentinian Sectrtary State Prevent Drug Addict & Narcotraffic, Natl Univ Rosario, Sch Biomed & Pharmaceut Sci, SIGMA TAU Hlth Sci, USDA, Natl Ctr Toxicol Res
DE nicotine; Alzheimer's disease; beta-amyloid precursor protein;
   beta-amyloid peptide; cholinergic system; synaptic proteins
ID ACETYLCHOLINE-RECEPTORS; BINDING-SITES; HUMAN-BRAIN; AGED RATS; DISEASE;
   MODULATION; DEMENTIA; SMOKING; DENSITY; RELEASE
AB Alzheimer's disease (AD) is characterized by cerebrovascular deposition of the amyloid P-peptide (Abeta), which is derived from a larger beta-amyloid precursor protein (betaAPP). Altered metabolism of betaAPP, resulting in increased Abeta production, appears central in the neuropathology of AD. The processing of the holoprotein betaAPP by different "secretase" enzymes results in three major carboxyl-truncated species. One species, which results from the cleavage of betaAPP by gamma-secretase, is secreted into the cerebrospinal fluid (CSF) and is called sAPPgamma as it contains an intact Abeta domain. Moreover, AD is characterized by cholinergic dysfunction and the loss of synaptic proteins. Reports of an inverse relation between nicotine intake, due to cigarette smoking, and the incidence of AD prompted us to investigate the effects of nicotine on betaAPP processing and synaptic proteins in rats and in cell culture. Nicotine, 1 and 8 mg/kg/day, doses commensurate with cigarette smoking, and a higher but well tolerated dose, respectively, was administered over 14 days to rats. Levels of sAPP in the CSF sample were evaluated by Western blot analysis. The higher dose significantly increased levels of total sAPP; however, both doses significantly reduced sAPPgamma, which contains the amyloidogenic portion of Abeta. These actions were blocked by nicotinic receptor antagonism. Nicotinic antagonists alone had no effect on either total sAPP or sAPPgamma levels in CSF. Nicotine did not significantly change the intracellular levels of total betaAPP in rat brain extracts, which is consistent with neuronal cell culture data. Similarly, levels of vesicular protein, such as synaptophysin, and presynaptic terminal protein sNAP-25 were unaffected by nicotine treatment both in vivo and in cell culture experiments. Taken together, these results suggest that nicotine modifies betaAPP processing away from the formation of potentially amyloidogenic products, without altering the levels of synaptic proteins, and that this can potentially offer therapeutic potential for Alzheimer's disease.
C1 Indiana Univ, Sch Med, Inst Psychiat Res, Lab Mol Neurogenet,Dept Psychiat & Neurol, Indianapolis, IN 46202 USA.
   NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Lahiri, DK (reprint author), Indiana Univ, Sch Med, Inst Psychiat Res, Lab Mol Neurogenet,Dept Psychiat & Neurol, Room PR-313,791 Union Dr, Indianapolis, IN 46202 USA.
NR 32
TC 34
Z9 37
U1 1
U2 8
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-408-0
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 965
BP 364
EP 372
PG 9
WC Cell Biology; Multidisciplinary Sciences; Neurosciences; Pharmacology &
   Pharmacy
SC Cell Biology; Science & Technology - Other Topics; Neurosciences &
   Neurology; Pharmacology & Pharmacy
GA BU83M
UT WOS:000177157600033
PM 12105112
ER

PT S
AU Rahamimoff, H
   Ren, XY
   Kimchi-Sarfaty, C
   Ambudkar, S
   Kasir, J
AF Rahamimoff, H
   Ren, XY
   Kimchi-Sarfaty, C
   Ambudkar, S
   Kasir, J
BE Lytton, J
   Schnetkamp, PPM
   Hryshko, LV
   Blaustein, MP
TI NCX1 surface expression - A tool to identify structural elements of
   functional importance
SO CELLULAR AND MOLECULAR PHYSIOLOGY OF SODIUM-CALCIUM EXCHANGE
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 4th International Conference on Cellular and Molecular Physiology of
   Sodium-Calcium Exchange
CY OCT 10-14, 2001
CL BANFF, CANADA
SP Amer Physiol Soc
DE NCX1; Na+/Ca2+ exchange; cysteine mutagenesis; cyclosporin A; PSC833;
   immunophilins
ID CARDIAC SARCOLEMMAL VESICLES; BRAIN NA+-CA2+ EXCHANGER; ADRENAL
   CHROMAFFIN CELLS; CYCLOSPORINE-A; NA+/CA2+ EXCHANGER; CALCIUM RESPONSES;
   QUALITY-CONTROL; PROTEIN; TOPOLOGY; IMMUNOPHILINS
AB The rat Na+/Ca2+ exchanger isoforms of the NCX1 gene have 14 cysteine residues. Each of these cysteines can be mutated individually to alanine or serine without loss of functional expression in transfected HEK293 cells. Yet sequential exchange starting from the amino terminal end of three or more cysteines results in reduced transport activity and surface expression. As more and more cysteines are replaced, transport activity and surface expression decrease in parallel, and the cysteineless mutant exhibits only traces of Na+/Ca2+ exchange activity and surface expression. No significant differences are detected in the amount of total cell exchanger protein between the wildtype exchanger and its functional or nonfunctional cysteine mutants. Reduced surface expression of the Na+/Ca2+ exchanger NCX1 is also observed when HEK293 cells expressing the transporter are treated with cyclosporin A (CsA) or with PSC833. The reductions in transport activity and surface expression are concentration dependent and parallel. No reduction is obtained in the total amount of exchanger protein by CsA or PSC833 treatment, suggesting that the effects of these drugs on NCX1 expression are posttranslational. FK506 and rapamycin treatment of HEK293 cells expressing rat NCX1 isoforms has no effect on transport activity, surface expression, or the total amount of exchanger protein in the transfected cells.
C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Biochem, IL-91120 Jerusalem, Israel.
   NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Rahamimoff, H (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Biochem, Box 12272, IL-91120 Jerusalem, Israel.
RI Ambudkar, Suresh/B-5964-2008
NR 35
TC 3
Z9 3
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-386-6
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 976
BP 176
EP 186
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary
   Sciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics
GA BW14A
UT WOS:000180979900031
PM 12502559
ER

PT S
AU Blaustein, MP
   Juhaszova, M
   Golovina, VA
   Church, PJ
   Stanley, EF
AF Blaustein, MP
   Juhaszova, M
   Golovina, VA
   Church, PJ
   Stanley, EF
BE Lytton, J
   Schnetkamp, PPM
   Hryshko, LV
   Blaustein, MP
TI Na/Ca exchanger and PMCA localization in neurons and astrocytes -
   Functional implications
SO CELLULAR AND MOLECULAR PHYSIOLOGY OF SODIUM-CALCIUM EXCHANGE
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 4th International Conference on Cellular and Molecular Physiology of
   Sodium-Calcium Exchange
CY OCT 10-14, 2001
CL BANFF, CANADA
SP Amer Physiol Soc
DE Na/Ca exchanger; PMCA localization; neurons; astrocytes
ID SODIUM-CALCIUM EXCHANGE; VASCULAR SMOOTH-MUSCLE; ALPHA-SUBUNIT ISOFORMS;
   RETICULUM CA2+ STORES; ENDOPLASMIC-RETICULUM; PHYSIOLOGICAL
   IMPLICATIONS; CARDIAC-MUSCLE; CELLS; NA+; SKELETAL
AB Immunocytochemistry reveals that the Na/Ca exchanger (NCX) in neuronal somata and astrocytes is confined to plasma membrane (PM) microdomains that overlie sub-PM (junctional) endoplasmic reticulum (jER). By contrast, the PM Ca2+ pump (PMCA) is more uniformly distributed in the PM. At presynaptic nerve terminals, the NCX distribution is consistent with that observed in the neuronal somata, but the PMCA is clustered at the active zones. Thus, the PMCA, with high affinity for Ca2+ (K-d approximate to100 nM), may keep active zone Ca2+ very low and thereby "reprime" the vesicular release mechanism following activity. NCX, with lower affinity for Ca2+ (K-d approximate to1,000 nM), on the other hand, may extrude Ca2+ that has diffused away from the active zones and been temporarily sequestered in the endoplasmic reticulum. The PL microdomains that contain the NCX also contain Na+ pump high ouabain affinity alpha2 (astrocytes) or alpha3 (neurons) subunit isoforms (IC50 approximate to5-50 nM ouabain). In constrast, the alpha1 isoform (low ouabain affinity in rodents; IC50 >10,000 nM), like the PMCA, is more uniformly distributed in these cells. The sub-PM endoplasmic reticulum in neurons (and probably glia and other cell types as well) and the adjacent PM form junctions that resemble cardiac muscle dyads. We suggest that the PM microdomains containing NCX and alpha2/alpha3 Na+ pumps, the underlying jER, and the intervening tiny volume of cytosol (<10(-18) 1) form functional units (PLasmERosomes); diffusion of Na+ and Ca2+ between these cytosolic compartments and "bulk" cytosol may be markedly restricted. The activity of the Na+ pumps with alpha2/alpha3 subunits may thus regulate NCX activity and jER Ca2+ content. This view is supported by studies in mice with genetically reduced (by approximate to50%) alpha2 Na+ pumps: evoked Ca2+ transients were augmented in these cells despite normal cytosolic Na+ and resting Ca2+ concentrations ([Na+](CYT) and [Ca2+](CYT)). We conclude that alpha2/alpha3 Na+ pumps control PLasmERosome (local) [Na+](CYT). This, in turn, via NCX; modulates local [Ca2+](CYT), jER Ca2+ storage, Ca2+ signaling, and cell responses.
C1 Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
   NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA.
   CUNY Mt Sinai Sch Med, Dept Physiol & Biophys, New York, NY 10029 USA.
   Toronto Western Res Inst, Cellular & Mol Biol Sect, Toronto, ON MST 258, Canada.
RP Blaustein, MP (reprint author), Univ Maryland, Sch Med, Dept Physiol, 655 W Baltimore St, Baltimore, MD 21201 USA.
FU NINDS NIH HHS [NS-16106]
NR 29
TC 78
Z9 81
U1 2
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-386-6
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 976
BP 356
EP 366
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary
   Sciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics
GA BW14A
UT WOS:000180979900054
PM 12502582
ER

PT S
AU Murphy, E
   Cross, HR
   Steenbergen, C
AF Murphy, E
   Cross, HR
   Steenbergen, C
BE Lytton, J
   Schnetkamp, PPM
   Hryshko, LV
   Blaustein, MP
TI Is Na/Ca exchange during ischemia and reperfusion beneficial or
   detrimental?
SO CELLULAR AND MOLECULAR PHYSIOLOGY OF SODIUM-CALCIUM EXCHANGE
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 4th International Conference on Cellular and Molecular Physiology of
   Sodium-Calcium Exchange
CY OCT 10-14, 2001
CL BANFF, CANADA
SP Amer Physiol Soc
DE cytosolic calcium; ischemia; Na/Ca exchanger
ID CYTOSOLIC FREE CALCIUM; PERFUSED RAT-HEART; NA+-H+ EXCHANGE;
   INTRACELLULAR SODIUM; VENTRICULAR MYOCYTES; MYOCARDIAL-ISCHEMIA;
   NA+-CA2+ EXCHANGER; STUNNED MYOCARDIUM; TRANSGENIC MICE; GLOBAL-ISCHEMIA
AB Cytosolic calcium increases to approximately 3 muM after 15 min of global ischemia. Manipulations that attenuate this increase in cytosolic Ca2+ reduce myocyte death and dysfunction. The increase in cytosolic Ca2+ during ischemia is dependent on an increase in intracellular Na+, suggesting a role for Na/Ca exchange. Typical ischemic values for ionized intra- and extracellular N+, Ca2+, and membrane potential are consistent with the Na/Ca exchanger operating near equilibrium during ischernia. Studies were undertaken using hearts from mice that overexpress the Na/Ca exchanger to determine if Na/Ca exchanger overexpression enhances or reduces ischemic injury. These studies suggest that overexpression of the Na/Ca exchanger enhances injury in males, but females are protected by a gender-related mechanism.
C1 NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
   Duke Univ, Dept Pathol, Durham, NC 27706 USA.
RP Murphy, E (reprint author), NIEHS, Lab Signal Transduct, 111 Alexander Dr,Bldg 101, Res Triangle Pk, NC 27709 USA.
FU NHLBI NIH HHS [R01 HL039752]
NR 39
TC 19
Z9 20
U1 0
U2 4
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-386-6
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 976
BP 421
EP 430
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary
   Sciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics
GA BW14A
UT WOS:000180979900063
PM 12502591
ER

PT J
AU Deng, HY
   Kowalczyk, D
   O, I
   Blaszczyk-Thurin, M
   Xiang, ZQ
   Giles-Davis, W
   Ertl, HCJ
AF Deng, HY
   Kowalczyk, D
   O, I
   Blaszczyk-Thurin, M
   Xiang, ZQ
   Giles-Davis, W
   Ertl, HCJ
TI A modified DNA vaccine to p53 induces protective immunity to challenge
   with a chemically induced sarcoma cell line
SO CELLULAR IMMUNOLOGY
LA English
DT Article
ID CYTOTOXIC T-LYMPHOCYTES; WILD-TYPE; TETRAMERIZATION DOMAIN;
   BETA-GALACTOSIDASE; ANTITUMOR IMMUNITY; SURFACE-ANTIGEN; TUMOR-ANTIGEN;
   RABIES VIRUS; IMMUNIZATION; RESPONSES
AB Different vaccine constructs based on DNA vaccines and viral recombinant vaccines expressing mouse p53 were compared for induction of protective immune responses to challenge with a sarcoma cell line that expresses high levels of mutated p53 protein. Viral recombinant vaccines based on E1-deleted adenovirus or vaccinia virus recombinants expressing p53 with wild-type sequences in the mutational hotspot domain and a single mutation in the tetramerization domain (p53(mu338)) failed to induce protection against progression of this tumor cell line. A DNA vaccine expressing a form of p53 carrying the same point mutations as the tumor cell line showed low efficacy that was comparable to that of a DNA vaccine expressing p53(mu338). Efficacy of the DNA vaccine was augmented upon expressing p53(mu338) as a fusion protein linked to a viral leader sequence. Other modifications such as fusion to the signal sequence of the lysosome-associated membrane protein (LAMP) or ubiquitin failed to improve the efficacy of the vaccine to p53. Protection mediated by CD4(+) and CD8(+) T cells was specific for p53. (C) 2002 Elsevier Science (USA). All rights reserved.
C1 Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
   Univ Penn, Howard Hughes Med Inst, Philadelphia, PA 19104 USA.
   Great Poland Canc Ctr, PL-61866 Poznan, Poland.
   NCI, EPN, Rockville, MD 20852 USA.
RP Ertl, HCJ (reprint author), Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA.
NR 38
TC 14
Z9 15
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 0008-8749
J9 CELL IMMUNOL
JI Cell. Immunol.
PD JAN
PY 2002
VL 215
IS 1
BP 20
EP 31
AR PII S0008-8749(02)00004-7
DI 10.1016/S0008-8749(02)00004-7
PG 12
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA 585JM
UT WOS:000177521700003
PM 12142033
ER

PT J
AU Steele-Mortimer, O
   Brumell, JH
   Knodler, LA
   Meresse, S
   Lopez, A
   Finlay, BB
AF Steele-Mortimer, O
   Brumell, JH
   Knodler, LA
   Meresse, S
   Lopez, A
   Finlay, BB
TI The invasion-associated type III secretion system of Salmonella enterica
   serovar Typhimurium is necessary for intracellular proliferation and
   vacuole biogenesis in epithelial cells
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID LYSOSOMAL MEMBRANE-GLYCOPROTEINS; PATHOGENICITY ISLAND 2;
   PHOSPHATIDYLINOSITOL 3-KINASE; PHOSPHOINOSITIDE 3-KINASE; BACTERIAL
   INVASION; ENDOCYTIC PATHWAY; HOST-CELL; MOLECULAR CHARACTERIZATION;
   NUCLEAR RESPONSES; MAMMALIAN-CELLS
AB Type III secretion systems (TTSS) are used by Gram-negative pathogens to translocate proteins into eukaryotic host cells. Salmonella enterica serovar Typhimurium (S. Typhimurium) has two of these specialized systems, which are encoded on separate Salmonella pathogenicity islands (SPI-1 and SPI-2) and translocate unique sets of effectors. The specific roles of these systems in Salmonella pathogenesis remain undefined, although SPI-1 is required for bacterial invasion of epithelial cells and SPI-2 for survival/replication in phagocytic cells. However, because SPI-1 TTSS mutants are invasion-incompetent, the role of this TTSS in post-invasion processes has not been investigated. In this study, we have used two distinct methods to internalize a non-invasive SPI-1 TTSS mutant (invA) into cultured epithelial cells: (i) co-internalization with wild-type S. Typhimurium (SPI-1-dependent) and (ii) complementation with the Yersinia pseudotuberculosis invasin (inv) gene (SPI-1-independent). In both cases, internalized invA mutants were unable to replicate intracellularly, indicating that SPI-1 effectors are essential for this process and cannot be complemented by wild-type bacteria In the same cell. Analysis of the biogenesis of SCVs showed that vacuoles containing mutant bacteria displayed abnormal maturation that was dependent on the mechanism of entry. Manipulation of Salmonella-containing vacuole (SCV) biogenesis by pharmacologically perturbing membrane trafficking in the host cell increased intracellular replication of wild-type but not mutant S. Typhimurium This demonstrates a previously unknown role for SPI-1 in vacuole biogenesis and intracellular survival in non-phagocytic cells.
C1 Univ British Columbia, Biotechnol Lab, Vancouver, BC V6T 1Z3, Canada.
   NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT 59840 USA.
   CNRS Univ Med, INSERM, Ctr Immunol Marseille Luminy, Marseille, France.
RP Steele-Mortimer, O (reprint author), NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT 59840 USA.
RI Meresse, Stephane/E-2192-2012
OI Meresse, Stephane/0000-0001-6578-5177
NR 58
TC 138
Z9 139
U1 0
U2 5
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 1462-5814
J9 CELL MICROBIOL
JI Cell Microbiol.
PD JAN
PY 2002
VL 4
IS 1
BP 43
EP 54
DI 10.1046/j.1462-5822.2002.00170.x
PG 12
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA 519YV
UT WOS:000173753800005
PM 11856172
ER

PT J
AU Teague, WE
   Fuller, NL
   Rand, RP
   Gawrisch, K
AF Teague, WE
   Fuller, NL
   Rand, RP
   Gawrisch, K
TI Polyunsaturated lipids in membrane fusion events
SO CELLULAR & MOLECULAR BIOLOGY LETTERS
LA English
DT Article; Proceedings Paper
CT Conference on Liposomes: from Models to Applications
CY MAY 26-29, 2002
CL WROCLAW, POLAND
ID PHASE-TRANSITION; DIOLEOYLPHOSPHATIDYLETHANOLAMINE; CURVATURE; ACID
C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA.
   Brock Univ, Dept Biol Sci, St Catharines, ON L2S 3A1, Canada.
RP Teague, WE (reprint author), NIAAA, Lab Membrane Biochem & Biophys, NIH, 12420 Parklawn Dr, Rockville, MD 20852 USA.
NR 10
TC 20
Z9 20
U1 2
U2 4
PU CELLULAR & MOLECULAR BIOLOGY LETTERS
PI WROCLAW
PA UNIV WROCLAW, INST BIOCHEM, DEPT GENETIC BIOCHEMISTRY, PRZBYSZEWSKIEGO
   63/77, 51-148 WROCLAW, POLAND
SN 1425-8153
J9 CELL MOL BIOL LETT
JI Cell. Mol. Biol. Lett.
PY 2002
VL 7
IS 2
BP 262
EP 264
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 570NF
UT WOS:000176663800024
PM 12097942
ER

PT J
AU Summers, RM
   Aggarwal, NR
   Sneller, MC
   Cowan, MJ
   Wood, BJ
   Langford, CA
   Shelhamer, JH
AF Summers, RM
   Aggarwal, NR
   Sneller, MC
   Cowan, MJ
   Wood, BJ
   Langford, CA
   Shelhamer, JH
TI CT virtual bronchoscopy of the central airways in patients with
   Wegener's granulomatosis
SO CHEST
LA English
DT Article
DE bronchoscopy; CT; endobronchial stenosis; Wegener's granulomatosis
ID SPIRAL-CT; TRACHEOBRONCHIAL TREE; FIBEROPTIC BRONCHOSCOPY; SUBGLOTTIC
   STENOSIS; ENDOSCOPY; FEATURES; MANIFESTATIONS; PERSPECTIVE; SIMULATIONS;
   EXPERIENCE
AB Objectives: To compare CT virtual bronchoscopy (VB) to CT alone and to conventional bronchoscopy for evaluation of central airway stenoses in patients with Wegener's granulomatosis.
   Design: Prospective observer study, in which 18 thin-section helical CT scans of the trachea and bronchi of 11 patients with Wegener's granulomatosis were obtained. VB was performed using surface rendering and was evaluated by one bronchoscopist and one radiologist in a blinded fashion. Bronchoscopic correlation within an average of 1.8 days of CT was available.
   Measurements and results: VB displayed 188 of 198 bronchi (95%). Thirty-two of 40 stenoses (80%) were detected by VB by at least one of two physicians (double reading), and 22 of 40 stenoses (55%) were detected by a third physician reading only the CT.
   Conclusions: VB depicts bronchi to the segmental level and detects the majority of central airway stenoses in patients with Wegener's granulomatosis. A team approach is useful to attain optimal clinical benefit from VB for these patients.
C1 NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
   NIH, Warren Grant Magnuson Clin Ctr, Div Crit Care Med, Bethesda, MD 20892 USA.
   NIAID, NIH, Bethesda, MD 20892 USA.
RP Summers, RM (reprint author), NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bldg 10,Room 1C660,10 Ctr Dr,MSC 1182, Bethesda, MD 20892 USA.
NR 31
TC 37
Z9 40
U1 0
U2 0
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD JAN
PY 2002
VL 121
IS 1
BP 242
EP 250
DI 10.1378/chest.121.1.242
PG 9
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 514GU
UT WOS:000173431400039
PM 11796457
ER

PT S
AU Hill, RM
   Coates, LC
   Parmar, PK
   Mezey, E
   Pearson, JF
   Birch, NP
AF Hill, RM
   Coates, LC
   Parmar, PK
   Mezey, E
   Pearson, JF
   Birch, NP
BE OConnor, DT
   Eiden, LE
TI Expression and functional characterization of the serine protease
   inhibitor neuroserpin in endocrine cells
SO CHROMAFFIN CELL: TRANSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS,
   AND INFORMATICS
SE Annals of the New York Academy of Sciences
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE neuroserpin; endocrine cells; serine protease; serpin
ID TISSUE-PLASMINOGEN ACTIVATOR; NERVE GROWTH-FACTOR; GLIA-DERIVED NEXIN;
   NEXIN/PROTEASE NEXIN-1; CATECHOLAMINE RELEASE; EXTRACELLULAR-MATRIX;
   NEURITE OUTGROWTH; CHROMOGRANIN-A; NEURONAL DEATH; ATT-20 CELLS
AB Serine proteases play essential roles in a wide variety of cellular processes in endocrine cells. There is a growing interest in the roles of serine protease inhibitors, or serpins, as key regulators of their activity. We have cloned two neuroserpin cDNAs from a rat pituitary cDNA library and confirmed tissue plasminogen activator as a potential target for this inhibitor. We show that neuroserpin transcripts are expressed by endocrine cells in the adrenal and pituitary glands and that immunoreactive neuroserpin is stored in densely cored secretory granules in these cells. Overexpression of neuroserpin in an anterior pituitary corticotroph cell line results in the extension of neurite-like processes, suggesting that neuroserpin may play a role in cell communication, cell adhesion, and/or cell migration.
C1 Univ Auckland, Sch Biol Sci, Mol Neuroendocrinol Lab, Auckland, New Zealand.
   NINDS, Basic Neurosci Program, NIH, Bethesda, MD 20892 USA.
   Univ Auckland, Sch Math & Informat Sci, Dept Stat, Auckland, New Zealand.
RP Birch, NP (reprint author), Univ Auckland, Sch Biol Sci, Mol Neuroendocrinol Lab, Private Bag 92019,Level 4,Thomas Bldg, Auckland, New Zealand.
EM n.birch@auckland.ac.nz
RI Birch, Nigel/H-2498-2011; Pearson, John/B-4376-2012; 
OI Birch, Nigel/0000-0002-8417-3587; Pearson, John/0000-0001-5607-4517
NR 55
TC 13
Z9 13
U1 3
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-391-2
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 406
EP 415
PG 10
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100078
PM 12438159
ER

PT S
AU Turquier, V
   Vaudry, H
   Yon, L
   Hsu, CM
   Ait-Ali, D
   Grumolato, L
   Eiden, LE
   Anouar, Y
AF Turquier, V
   Vaudry, H
   Yon, L
   Hsu, CM
   Ait-Ali, D
   Grumolato, L
   Eiden, LE
   Anouar, Y
BE OConnor, DT
   Eiden, LE
TI Proinflammatory cytokines TNF-alpha and IL-1 alpha stimulate
   neuropeptide gene expression in adrenochromaffin cells
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE chromaffin cells; cytokines; neuropeptides; secretion; gene expression;
   inflammation
ID TRANSCRIPTION; PATHWAYS
C1 Univ Rouen, European Inst Peptide Res, Lab Cellular & Mol Neuroendocrinol, INSERM,U413,UA CNRS, F-76821 Mont St Aignan, France.
   NIMH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
RP Anouar, Y (reprint author), Univ Rouen, European Inst Peptide Res, Lab Cellular & Mol Neuroendocrinol, INSERM,U413,UA CNRS, IFRMP 23, F-76821 Mont St Aignan, France.
RI Grumolato, Luca/A-1697-2015; 
OI Grumolato, Luca/0000-0001-8231-3032; Eiden, Lee/0000-0001-7524-944X
NR 5
TC 3
Z9 3
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 45
EP 48
PG 4
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100006
PM 12438087
ER

PT S
AU Kim, T
   Tao-Cheng, JH
   Eiden, LE
   Loh, YP
AF Kim, T
   Tao-Cheng, JH
   Eiden, LE
   Loh, YP
BE OConnor, DT
   Eiden, LE
TI Large dense-core secretory granule biogenesis is under the control of
   chromogranin A in neuroendocrine cells
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE chromogranin A; dense-core secretory granule; secretory granule
   biogenesis; regulated secretion; PC12 cells
ID REGULATED SECRETION; SECRETOGRANIN-II; PROTEINS; EXPRESSION; VESICLES;
   GONADOTROPES; PEPTIDES; PATHWAY; ATT-20; LINE
AB The large dense-core secretory granule is an organelle in neuroendocrine/endocrine cells, where prohormones and proneuropeptides are stored, processed, and secreted in a regulated manner. Here we present evidence that chromogranin A (CgA), one of the most abundant acidic glycoproteins ubiquitously present in neuroendocrine/endocrine cells, regulates dense-core secretory granule biogenesis. Specific depletion of CgA expression by antisense RNAs in PC12 cells led to a profound loss of secretory granule formation. An exogenously expressed prohormone, pro-opiomelanocortin, was neither stored nor secreted in a regulated manner in CgA-deficient PC12 cells. Overexpression of bovine CgA into CgA-deficient PC12 cells rescued regulated secretion. Other secretory granule proteins, such as chromogranin B (CgB), carboxypeptidase E, and synaptotagmin, were rapidly degraded, whereas nongranule proteins were not affected in CgA-deficient PC12 cells. Unlike CgA, another granin protein CgB could not substitute for the role of CgA in secretory granule biogenesis. Thus, we conclude that CgA is a master "on/off" switch regulating the formation of the dense-core secretory granule in neuroendocrine cells.
C1 NICHHD, Dev Neurobiol Lab, Sect Cellular Neurobiol, NIH, Bethesda, MD 20892 USA.
   NIH, NIMH, NINDS, EM Facil, Bethesda, MD 20892 USA.
   NIH, Natl Inst Mental Hlth, Lab Cellular & Mol Regulat, Sect Mol Neurosci, Bethesda, MD 20892 USA.
RP Kim, T (reprint author), NICHHD, Dev Neurobiol Lab, Sect Cellular Neurobiol, NIH, Bethesda, MD 20892 USA.
OI Eiden, Lee/0000-0001-7524-944X
NR 27
TC 11
Z9 12
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 323
EP 331
PG 9
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100062
PM 12438143
ER

PT S
AU Loh, YP
   Maldonado, A
   Zhang, CF
   Tam, WH
   Cawley, N
AF Loh, YP
   Maldonado, A
   Zhang, CF
   Tam, WH
   Cawley, N
BE OConnor, DT
   Eiden, LE
TI Mechanism of sorting proopiomelanocortin and proenkephalin to the
   regulated secretory pathway of neuroendocrine cells
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE proopiomelanocortin; proenkephalin; carboxypeptidase E; prohormone
   trafficking; sorting signals
ID CARBOXYPEPTIDASE-E MUTATION; GRANULE BIOGENESIS; ENZYME-ACTIVITY;
   CHROMOGRANIN-A; CPE(FAT) MICE; RECEPTOR; SIGNAL; BINDING;
   IDENTIFICATION; PROHORMONES
AB Proopiomelanocortin (POMC) and proenkephalin (PE) are synthesized at the endoplasmic reticulum and transported to the trans-Golgi network (TGN) where they are sorted and packaged into dense-core granules of the regulated secretory pathway (RSP). The mechanism of sorting POMC and PE to the RSP in neuroendocrine cells was investigated. Consensus sorting signals comprising two acidic residues and two hydrophobic residues exposed on the surface of N-POMC1-26 and N-PE1-32 were identified and shown to be sufficient and necessary for targeting POMC and PE to the RSP in PC12, Neuro2a, and AtT-20 cells. The acidic residues of these sorting signals bind specifically to basic residues on the sorting receptor membrane, carboxypeptidase E (CPE), to effect sorting to the RSP. Analysis of POMC and PE sorting in Neuro2a cells depleted of CPE by CPE antisense RNA, and Cpe(fat/fat) mouse pituitary cells lacking CPE showed missorting of both these molecules to the constitutive pathway in vivo. Thus, POMC and PE are sorted to the RSP at the TGN by a mechanism involving the interaction of a specific sorting signal on these molecules with the sorting receptor, CPE.
C1 NICHHD, Dev Biol Lab, Cellular Neurobiol Sect, NIH, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), NICHHD, Dev Biol Lab, Cellular Neurobiol Sect, NIH, 49 Convent Dr,Rm 5A38, Bethesda, MD 20892 USA.
NR 24
TC 49
Z9 50
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 416
EP 425
PG 10
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100079
PM 12438160
ER

PT S
AU Vaudry, D
   Taupenot, L
AF Vaudry, D
   Taupenot, L
BE OConnor, DT
   Eiden, LE
TI Fast-breaking results on the PACAP/VIP/secretin peptide family in
   chromaffin cells
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE PACAP; VIP; secretin; peptides; chromaffin
ID CYCLASE-ACTIVATING POLYPEPTIDE; VASOACTIVE-INTESTINAL-PEPTIDE; NERVE
   GROWTH-FACTOR; ADENYLATE-CYCLASE; PC12 CELLS; TYROSINE-HYDROXYLASE;
   GENE-TRANSCRIPTION; NEURITE OUTGROWTH; PACAP RECEPTOR; PITUITARY
AB The neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP) has been reported to be a potent regulator of chromaffin cell activity. In particular, PACAP stimulates catecholamine biosynthesis as well as the expression of various genes, including chromogranin A, neuropeptide Y, enkephalins, vasoactive intestinal polypeptide, and PACAP itself. The mechanisms involved in the effects of PACAP on chromaffin cells have been investigated using rat pheochromocytoma PC 12 cells. This cell line turned out to be a suitable model in which to study the neurotrophic activities of PACAP. Recent studies using transgenic mice have shown that in the sympathoadrenal system, PACAP acts as an "emergency response" cotransmitter involved in the regulation of insulin-induced hypoglycemia.
C1 NIMH, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA.
   Univ Calif San Diego, Dept Med 0838, La Jolla, CA 92093 USA.
   Univ Calif San Diego, VA San Diego Healthcare Syst, La Jolla, CA 92093 USA.
RP Vaudry, D (reprint author), NIMH, Lab Cellular & Mol Regulat, 36 Convent Dr, Bethesda, MD 20892 USA.
NR 26
TC 3
Z9 3
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 460
EP 466
PG 7
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100084
PM 12438165
ER

PT S
AU Hamelink, C
   Lee, HW
   Hsu, CM
   Eiden, LE
AF Hamelink, C
   Lee, HW
   Hsu, CM
   Eiden, LE
BE OConnor, DT
   Eiden, LE
TI Role of protein kinases in neuropeptide gene regulation by PACAP in
   chromaffin cells - A pharmacological and bioinformatic analysis
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE calcium/calmodulin kinase; cyclic AMP; mitogen-activated protein kinase;
   pituitary adenylate cyclase-activating polypeptide; phorbol myristate
   acetate; proenkephalin; protein kinase A; protein kinase C; vasoactive
   intestinal polypeptide
ID CYCLASE-ACTIVATING POLYPEPTIDE; VASOACTIVE-INTESTINAL-PEPTIDE;
   ADRENAL-MEDULLARY CELLS; CYTOKINE RESPONSE ELEMENT; PROENKEPHALIN-A
   GENE; SIGNAL-TRANSDUCTION PATHWAYS; PHORBOL ESTER TREATMENT; CYCLIC-AMP;
   CATECHOLAMINE SECRETION; MESSENGER-RNA
AB Pituitary adenylate cyclase-activating polypeptide (PACAP) is an adrenomedullary cotransmitter that along with acetylcholine is responsible for driving catecholamine and neuropeptide biosynthesis and secretion from chromaffin cells in response to stimulation of the splanchnic nerve. Two neuropeptides whose biosynthesis is regulated by PACAP include enkephalin and vasoactive intestinal polypeptide (VIP). Occupancy of PAC1 PACAP receptors on chromaffin cells can result in elevation of cyclic AMP, inositol phosphates, and intracellular calcium. The proenkephalin A and VIP genes are transcriptionally responsive to signals generated within all three pathways, and potentially by combinatorial activation of these pathways as well. The characteristics of PACAP regulation of enkephalin and VIP biosynthesis were examined pharmacologically for evidence of involvement of several serine/threonine protein kinases activated by cAMP, IP3, and/or calcium, including calmodulin kinase II, protein kinase A, and protein kinase C. Evidence is presented for the differential involvement of these protein kinases in regulation of enkephalin and VIP biosynthesis in chromaffin cells, and for a prominent role of the mixed-function (tyrosine and serine/threonine) MAP kinase family in mediating transcriptional activation of neuropeptide genes by PACAP.
C1 NIMH, Mol Neurosci Sect, Intramural Res Program, Bethesda, MD 20892 USA.
RP Hamelink, C (reprint author), NIMH, Mol Neurosci Sect, Intramural Res Program, Bethesda, MD 20892 USA.
OI Eiden, Lee/0000-0001-7524-944X
NR 67
TC 8
Z9 8
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 474
EP 490
PG 17
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100087
PM 12438168
ER

PT S
AU Vaudry, D
   Chen, Y
   Hsu, CM
   Eiden, LE
AF Vaudry, D
   Chen, Y
   Hsu, CM
   Eiden, LE
BE OConnor, DT
   Eiden, LE
TI PC12 cells as a model to study the neurotrophic activities of PACAP
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE PC12; PACAP; neurotrophic factor; apoptosis; neurite formation
ID CYCLASE-ACTIVATING POLYPEPTIDE; NERVE GROWTH-FACTOR; CEREBELLAR GRANULE
   CELLS; PROTEIN-KINASE; GENE-EXPRESSION; CANCER CELLS; TRANSCRIPTION
   FACTOR; NEURITE OUTGROWTH; VIP RECEPTORS; MAP KINASE
C1 NIMH, Mol Neurosci Sect, Intramural Res Program, Bethesda, MD 20892 USA.
RP Eiden, LE (reprint author), NIMH, Mol Neurosci Sect, Intramural Res Program, Bethesda, MD 20892 USA.
OI Eiden, Lee/0000-0001-7524-944X
NR 33
TC 30
Z9 30
U1 0
U2 4
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 491
EP 496
PG 6
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100088
PM 12438169
ER

PT S
AU Rao, FW
   Keiser, HR
   O'Connor, DT
AF Rao, FW
   Keiser, HR
   O'Connor, DT
BE OConnor, DT
   Eiden, LE
TI Malignant and benign pheochromocytoma - Chromaffin granule transmitters
   and the response to medical and surgical treatment
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE plasma chromogranin A; norepinephrine; epinephrine
ID CHROMOGRANIN-A; STORAGE; PLASMA; RADIOIMMUNOASSAY; CATECHOLAMINES;
   SECRETION; RELEASE
C1 Univ Calif San Diego, Dept Med, San Diego, CA 92161 USA.
   Univ Calif San Diego, Ctr Mol Genet, San Diego, CA 92161 USA.
   NHLBI, Bethesda, MD 20892 USA.
   VA San Diego Healthcare Syst, San Diego, CA USA.
RP O'Connor, DT (reprint author), Univ Calif San Diego, Dept Med, 9111H,3350 La Jolla Village Dr, San Diego, CA 92161 USA.
NR 18
TC 13
Z9 13
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 530
EP 532
PG 3
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100094
PM 12438175
ER

PT S
AU Eiden, LE
   Hirsch, MD
AF Eiden, LE
   Hirsch, MD
BE OConnor, DT
   Eiden, LE
TI Computing the chromaffin cell - A research-community curator/user
   approach to biocomputation for chromaffin cell biology
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE computational biology; proteomics; genomics; biocomputation; signaling
   pathways; bioinformatics
AB Exocytosis, stimulus-secretion coupling, real-time measurements of neurosecretion, and stimulus-secretion-synthesis coupling (stimulus-transcription coupling) were all initially proposed and verified in the chromaffin cell. Detailed analysis of the molecules and pathways responsible for secretion and transsynaptic regulation of gene expression patterns in neuroendoccrine cells have been very fruitfully explored in chromaffin cells and the related PC12 pheochromocytoma cell line, using modern molecular biologcal, cellular imaging, and expression profiling techniques. The time is clearly at hand for a concerted bioinformatics approach to acquiring and synthesizing electrophysiological, biochemical, and proteomic/genomic data on the chromaffin cell. Accelerating this process will fully realize the unique attributes of the chromaffin cell as a homogeneous, accessible, fully functional model of the posttmitotic neuroendocrine cell.
C1 NIMH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Intramural Res Program, Bethesda, MD 20892 USA.
   NIMH, Off Neuroinformat, Extramural Res Program, Bethesda, MD 20892 USA.
RP Eiden, LE (reprint author), NIMH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Intramural Res Program, Bethesda, MD 20892 USA.
OI Eiden, Lee/0000-0001-7524-944X
NR 1
TC 0
Z9 0
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 576
EP 583
PG 8
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100105
PM 12438186
ER

PT S
AU Hirsch, MD
AF Hirsch, MD
BE OConnor, DT
   Eiden, LE
TI A neuroscience knowledge management systems approach - Application to
   functional proteomics/genomics of the chromaffin cell
SO CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND
   INFORMATICS
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 11th International Symposium on Chromaffin Cell Biology
CY SEP 03-08, 2001
CL SAN DIEGO, CALIFORNIA
SP NIH, Univ Calif Biotechnol Program, Univ Calif Life Sci Informat Program, Int Union Biochem & Molec Biol, Merck Co, Aventis Pharmaceut, Sankyo Pharmaceut
DE chromaffin cell biology; neuroscience knowledge management
C1 NIMH, Off Neuroinformat, Bethesda, MD 20892 USA.
RP Hirsch, MD (reprint author), NIMH, Off Neuroinformat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-390-4
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 971
BP 615
EP 616
PG 2
WC Biochemical Research Methods; Cell Biology; Multidisciplinary Sciences;
   Neurosciences
SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology -
   Other Topics; Neurosciences & Neurology
GA BV61K
UT WOS:000179509100113
PM 12438194
ER

PT J
AU Vasan, RS
   Massaro, JM
   Wilson, PWF
   Seshadri, S
   Wolf, PA
   Levy, D
   D'Agostino, RB
AF Vasan, RS
   Massaro, JM
   Wilson, PWF
   Seshadri, S
   Wolf, PA
   Levy, D
   D'Agostino, RB
TI Antecedent blood pressure and risk of cardiovascular disease - The
   framingham heart study
SO CIRCULATION
LA English
DT Article
DE blood pressure; cardiovascular diseases; epidemiology; risk factors
ID FOLLOW-UP; TERM; ATHEROSCLEROSIS; ASSOCIATIONS; CHOLESTEROL; PREVENTION;
   PREDICTION
AB Background-Casual blood pressure (BP) is a powerful predictor of risk of cardiovascular disease (CVD), but a single BP determination may not accurately reflect the residual impact of antecedent BP levels on vascular risk. It is unclear whether time-averaged past BP measures incrementally improve CVD risk assessment.
   Methods and Results-We used sex- and age-specific multivariable Cox regression to evaluate the association of current BP (at baseline), recent antecedent BP (average of readings for all available examinations I to 10 years before baseline), and remote antecedent BP (average for all available examinations I I to 20 years before baseline) with the 10-year risk of CVD in 2313 Framingham Study subjects (910 men, 1403 women) free of CVD at baseline. During follow-up, 899 incident initial CVD events were observed (479 in women). In multivariable models incorporating established CVD risk factors, recent and remote antecedent BP predicted CVD risk incrementally over current BP. This effect was consistent in multiple subgroups: men and women, older and younger age groups, and lower and higher BP groups. The relations of antecedent BP to CVD risk were consistent for systolic BP, diastolic BP, and pulse pressure.
   Conclusions-Antecedent BP is an important determinant of future risk of CVD events above and beyond current BP. When available, use of long-term average BP may improve the prognostic utility of conventional CVD risk prediction that is based on current BP. Our findings suggest that effective prevention of CVD requires adequate control of BP throughout life.
C1 Framingham Heart Dis Epidemiol Study, Natl Heart Lung & Blood Inst, Framingham, MA 01702 USA.
   Boston Univ, Sch Med, Cardiol Sect, Boston, MA 02215 USA.
   Boston Univ, Sch Med, Endocrinol Sect, Boston, MA 02215 USA.
   Boston Univ, Sch Med, Dept Neurol, Boston, MA 02215 USA.
   Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiol, Cambridge, MA 02138 USA.
   Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Clin Epidemiol, Cambridge, MA 02138 USA.
   Boston Univ, Dept Epidemiol & Biostat, Boston, MA USA.
   Boston Univ, Dept Math & Stat, Boston, MA USA.
   Natl Heart Lung & Blood Inst, Bethesda, MD USA.
RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, Natl Heart Lung & Blood Inst, 5 Thurber, Framingham, MA 01702 USA.
OI Ramachandran, Vasan/0000-0001-7357-5970
FU NHLBI NIH HHS [K24-HL-04334-01A1, N01-HC-38038]; NINDS NIH HHS [NS
   17950]
NR 28
TC 69
Z9 70
U1 2
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD JAN 1
PY 2002
VL 105
IS 1
BP 48
EP 53
DI 10.1161/hc0102.101774
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 509GF
UT WOS:000173137400011
PM 11772875
ER

PT J
AU Kim, M
   Turnquist, H
   Jackson, J
   Sgagias, M
   Yan, Y
   Gong, M
   Dean, M
   Sharp, JG
   Cowan, K
AF Kim, M
   Turnquist, H
   Jackson, J
   Sgagias, M
   Yan, Y
   Gong, M
   Dean, M
   Sharp, JG
   Cowan, K
TI The multidrug resistance transporter ABCG2 (breast cancer resistance
   protein 1) effluxes Hoechst 33342 and is overexpressed in hematopoietic
   stem cells
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID P-GLYCOPROTEIN; DRUG ACCUMULATION; IN-VIVO; GENES; EXPRESSION; LINES;
   INDUCTION; APOPTOSIS; PUMP
AB The human ATP-binding cassette superfamily G (White) member 2 (ABCG2) gene and its murine homologue breast cancer resistance protein 1 (Bcrp1) are recently described ATP-binding cassette transporters associated with drug resistance in tumor cell lines, including the MCF-7 cell line, selected for its resistance to mitoxantrone (MCF-7/ MitoR). Infection of MCF-7 cells with the retroviral vector containing ABCG2 cDNA (G1-ABCG2) resulted in cells (MCF-7/ABCG2) that were resistant to mitoxantrone at levels similar to those observed in MCF-7/MitoR cells. Previous studies have shown that pluripotent hematopoietic stem cells overexpress the multidrug-resistant transport (MDR1) gene and efflux rhodamine, a substrate for the MDR1 transporter. Other studies have identified a primitive hematopoietic stem cell population, or side population (SP) cells, which are identified by their efflux of the fluorescent dye, Hoechst 33342. In an attempt to identify the transport genes responsible for this phenotype, we examined the uptake of Hoechst 33342 into MCF-7, MCF-7/MitoR, and MCF-7 cells infected with a retroviral vector expressing the ABCG2 gene (MCF-7/ABCG2). MCF-7/MitoR cells as well as MCF-7/ABCG2 cells demonstrated lower levels of Hoechst 33342 uptake compared with the parental MCF-7 cells. We also examined the level of the mouse Bcrp1 RNA in SP cells and non-SP cells isolated from mouse hematopoietic cells. Mouse SP cells expressed relatively high levels of Bcrp1 mRNA relative to non-SP cells. These results suggest that Hoechst 33342 is a substrate for the ABCG2 transporter and that ABCG2/Bcrp1 expression may serve as a marker for hematopoietic stem cells in hematopoietic cells.
C1 Univ Nebraska, Med Ctr, Eppley Inst Res Canc, Dept Pathol, Omaha, NE 68198 USA.
   NCI, Bethesda, MD 20892 USA.
   Univ Nebraska, Med Ctr, Eppley Inst Res Canc, Dept Cell Biol, Omaha, NE 68198 USA.
RP Cowan, K (reprint author), Univ Nebraska, Med Ctr, Eppley Inst Res Canc, Dept Pathol, Room 2016, Omaha, NE 68198 USA.
RI Dean, Michael/G-8172-2012; Turnquist, Heth/L-2319-2016
OI Dean, Michael/0000-0003-2234-0631; Turnquist, Heth/0000-0002-4173-4014
NR 24
TC 279
Z9 304
U1 0
U2 16
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN
PY 2002
VL 8
IS 1
BP 22
EP 28
PG 7
WC Oncology
SC Oncology
GA 515WM
UT WOS:000173519700006
PM 11801536
ER

PT J
AU Terasawa, H
   Tsang, KY
   Gulley, J
   Arlen, P
   Schlom, J
AF Terasawa, H
   Tsang, KY
   Gulley, J
   Arlen, P
   Schlom, J
TI Identification and characterization of a human agonist cytotoxic
   T-lymphocyte epitope of human prostate-specific antigen
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID RECOMBINANT VACCINIA VIRUS; HUMAN CARCINOEMBRYONIC ANTIGEN;
   TUMOR-REACTIVE CTL; DIVERSIFIED PRIME; IMMUNE-RESPONSES; PEPTIDE
   ANALOGS; DENDRITIC CELLS; FLT3 LIGAND; PHASE-I; MHC
AB One potential target of vaccine therapy for human prostate cancer Is the prostate-specific antigen (PSA). One strategy to enhance the immunogenicity of a self-antigen such as PSA is to develop agonist epitopes that are potentially more immunogenic. The studies described here report the design and analysis of an agonist epitope designated PSA-3A ("A" for agonist) of the PSA-3 CTL epitope. Studies demonstrate that when compared with the native PSA-3 epitope, the PSA-3A agonist demonstrates enhanced binding to the MHC class I A2 allele as well as enhanced stability of the peptide-MHC complex. T-cell lines generated with either the PSA-3 or the PSA-3A peptide showed higher levels of lysis of targets pulsed with the PSA-3A peptide than those targets pulsed with the PSA-3 peptide; this was observed when both the concentration of peptide and the ratio of effector to target cells were titrated. T cells stimulated with dendritic cells (DCs) pulsed with PSA-3A peptide produced higher levels of IFN-gamma than did DCs pulsed with PSA-3 peptide; however, no increase in apoptosis was seen in T cells stimulated with the PSA-3A agonist compared with those stimulated with PSA-3. Human T-cell lines generated with the PSA-3A agonist had the ability to lyse human prostate carcinoma cells expressing native PSA in an NHC-restricted manner. Recombinant vaccinia viruses were also constructed that contained the entire PSA transgene with and without the single amino acid change that constitutes the PSA-3A epitope; DCs infected with the recombinant vector containing the agonist amino acid change within the entire PSA gene (designated rV-PSA-3A) were more effective than DCs infected with the rV-PSA vector in enhancing IFN-gamma production by T cells. Finally, the PSA-3A agonist was shown to induce higher levels of T-cell activation, compared with the PSA-3 peptide, in an in vivo model using HLA-A2.1/K-b transgenic mice. These studies thus demonstrate the potential use of the PSA-3A agonist epitope in both peptide- and vector-mediated immunotherapy protocols for prostate cancer.
C1 NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Schlom, J (reprint author), NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, 10 Ctr Dr,Room 8B09, Bethesda, MD 20892 USA.
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
NR 54
TC 59
Z9 69
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN
PY 2002
VL 8
IS 1
BP 41
EP 53
PG 13
WC Oncology
SC Oncology
GA 515WM
UT WOS:000173519700009
PM 11801539
ER

PT J
AU Berlin, J
   Tutsch, KD
   Arzoomanian, RZ
   Alberti, D
   Binger, K
   Feierabend, C
   Dresen, A
   Marnocha, RA
   Pluda, J
   Wilding, G
AF Berlin, J
   Tutsch, KD
   Arzoomanian, RZ
   Alberti, D
   Binger, K
   Feierabend, C
   Dresen, A
   Marnocha, RA
   Pluda, J
   Wilding, G
TI Phase I and pharmacokinetic study of a micronized formulation of
   carboxyamidotriazole, a calcium signal transduction inhibitor: Toxicity,
   bioavailability and the effect of food
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID INFLUX INHIBITOR; CELL-LINES; TRIAZOLE; CANCER; THERAPY; TRIALS
AB Purpose: This Phase I study was conducted to evaluate the toxicity profile and determine the maximum tolerated dose (MTD) of an oral micronized formulation of the signal transduction inhibitor carboxyamidotriazole (CAI). Bioavailability of the micronized formulation relative to a gelatin capsule (gelcap) formulation was assessed. The effects of food intake and timing on CAI steady-state plasma concentrations (C-ss) were also investigated.
   Experimental Design: Patients received continuous daily CAI (28-day cycles). Starting dose was 150 mg/m(2) daily and escalations were by 50 mg/m(2) increments. The first three patients enrolled were given test doses of the original gelcap formulation and two different micronized formulations to determine relative bioavailability. Toxicity and pharmacokinetic assessments were performed weekly. Additional cohorts were added after MTD) determination to assess the effect of food intake and duration of fast on CAI C-ss.
   Results: The micronized formulation was absorbed more slowly than the gelcap formulation. Twenty-nine patients were enrolled in the dose-escalation portion of the study. After dose escalation to 300 mg/m(2), dose-limiting neurotoxicities occurred including reversible vision loss in two patients. Other toxicities were mild. The final MTD was 150 mg/m(2). Pharmacokinetics appeared linear with significant inter- and intrapatient variability. Patients with C-ss of greater than or equal to 4.0 mg/liter were more likely to have neurotoxicity. Nine patients with renal cell cancer and one with hepatocellular cancer had prolonged stable disease. CAI plasma concentrations were higher when taken with food.
   Conclusions: Micronized CAI was well tolerated at the MTD of 150 mg/m(2). Higher doses were limited by significant neurotoxicity. The variability in CAI pharmacokinetics may be partially attributable to concomitant food intake and timing of the dose.
C1 Univ Wisconsin, Sch Med, Ctr Comprehens Canc, Div Med Oncol, Madison, WI 53792 USA.
   NCI, Med Branch, Div Clin Sci, NIH, Bethesda, MD 20892 USA.
RP Wilding, G (reprint author), Univ Wisconsin, Sch Med, Ctr Comprehens Canc, Div Med Oncol, 600 Highland Ave,Room K6-550, Madison, WI 53792 USA.
FU NCI NIH HHS [UO1-CA62491, U01 CA062491, P30CA14520]; NCRR NIH HHS
   [MO1-RR01386]
NR 16
TC 17
Z9 17
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN
PY 2002
VL 8
IS 1
BP 86
EP 94
PG 9
WC Oncology
SC Oncology
GA 515WM
UT WOS:000173519700013
PM 11801543
ER

PT J
AU Kawakami, K
   Kawakami, M
   Leland, P
   Puri, RK
AF Kawakami, K
   Kawakami, M
   Leland, P
   Puri, RK
TI Internalization property of interleukin-4 receptor a chain increases
   cytotoxic effect of interleukin-4 receptor-targeted cytotoxin in cancer
   cells
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CIRCULARLY PERMUTED INTERLEUKIN-4; BREAST-CARCINOMA CELLS; COMMON
   GAMMA-CHAIN; PSEUDOMONAS EXOTOXIN; CHIMERIC PROTEIN; KAPOSIS-SARCOMA;
   CYTOSINE DEAMINASE; RECOMBINANT TOXINS; MALIGNANT-CELLS; ALPHA CHAIN
AB Although the receptor for interleukin-4 (IL-4R) is highly expressed on solid human cancer cells, its significance and internalization function is still unclear. To address these issues, we reconstituted Chinese hamster ovarian (CHO-K1) cells with various components of the IL-4R by transient transfection and performed internalization assays using radiolabeled IL-4. Radiolabeled IL-4 internalized through the IL-4Ralpha chain in a time-dependent manner. When the IL-4Ralpha chain was cotransfected with the IL-13Ralpha1 or -gamma(c) chain, the IL-4 internalization level was identical to IL-4Ralpha transfectants, suggesting that the IL-4Ralpha chain plays a major role in IL-4 internalization. These results were confirmed by determining the cytotoxicity of a chimeric protein composed of IL-4 and a mutated form of Pseudomonas exotoxin [IL4(38-37)-PE38KDEL] in CHO-K1 cells transfected with increasing concentrations of IL-4Ralpha cDNA. To use the internalization property of the IL-4Ralpha chain in the context of IL-4R-targeted cytotoxin therapy, we transiently transfected pancreatic and brain tumor cells with IL-4Ralpha chain. Surprisingly, these tumor cells acquired 4-75-fold higher binding activity to IL-4 compared with control cells. Consequently, the cytotoxic activity of IL-4 toxin to these cancer cells was enhanced 5-13-fold compared with control cells as assessed by protein synthesis inhibition and clonogenic assays. Taken together, a combination approach that involves transfer of the IL-4Ra, gene and IL-4R-targeted cytotoxin therapy may serve as a novel approach for cancer therapy.
C1 US FDA, Ctr Biol Evaluat & Res, Div Cellular & Gene Therapies, Lab Mol Tumor Biol, Bethesda, MD 20892 USA.
RP Puri, RK (reprint author), US FDA, Ctr Biol Evaluat & Res, Div Cellular & Gene Therapies, Lab Mol Tumor Biol, NIH Bldg 29B,Room 2NN10,29 Lincoln Dr MSC 4555, Bethesda, MD 20892 USA.
NR 59
TC 14
Z9 15
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI BIRMINGHAM
PA PO BOX 11806, BIRMINGHAM, AL 35202 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN
PY 2002
VL 8
IS 1
BP 258
EP 266
PG 9
WC Oncology
SC Oncology
GA 515WM
UT WOS:000173519700037
PM 11801567
ER

PT J
AU Robbins, J
AF Robbins, J
TI Transthyretin from discovery to now
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article; Proceedings Paper
CT 1st International Congress on Transthyretin in Health and Disease
CY APR 22-25, 2002
CL STRASBOURG, FRANCE
DE prealbumin; thyroxine; choroid plexus; retinol; vitamin A; amyloidopathy
ID HUMAN-SERUM PREALBUMIN; TRANSPORTING PROTEIN; BINDING; THYROXINE;
   COMPLEX; GENE
AB As introduction to the First International Congress on Transthyretin in Health and Disease, this lecture traces the origin of the subject from the discovery in the 1950s that a serum protein migrating ahead of albumin in an electrical field binds the thyroid hormone, thyroxine. Early work defined the molecular and biological properties of thyroxinebinding prealbumin (TBPA). Its tetrameric structure, first recognized from a polymorphism in monkeys, was later elaborated by crystallographic studies, and the very different affinity of its two identical thyroxinebinding sites was explained by an allosteric effect upon occupation of the first site. The far higher concentration of TBPA in cerebrospinal fluid compared to blood was explained by the discovery, 30 years later, that TBPA is synthesized by cells of the choroid plexus, and its rapid turnover in the body made TBPA a convenient marker of malnutrition and chronic disease. Late in the 1960s it was learned that TBPA also carries vitamin A in the circulation by interacting with retinolbinding protein (RBP). TBPA then was renamed transthyretin (TTR), in recognition of its dual transport function, and it was shown that retinolRBPTTR interactions are mutually enhancing. Investigation of the molecular genetics of TTR began in 1980 and a large number of inherited variants were discovered in the ensuing years. Some affect thyroxine and/or RBP binding but the majority are associated with familial amyloidotic polyneuropathy. Seizing on this discovery, structural biologists are now investigating why mutated TTR changes from a compact, soluble molecule into a fibrillar, insoluble polymer, and how this pathological transformation might be prevented.
C1 NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
RP Robbins, J (reprint author), NIDDKD, Genet & Biochem Branch, NIH, Bldg 10,Room 7C432B, Bethesda, MD 20892 USA.
NR 27
TC 19
Z9 19
U1 0
U2 4
PU WALTER DE GRUYTER & CO
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PY 2002
VL 40
IS 12
BP 1183
EP 1190
DI 10.1515/CCLM.2002.208
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 624LJ
UT WOS:000179760900002
PM 12553418
ER

PT J
AU Ouatas, T
   Clare, SE
   Hartsough, MT
   De La Rosa, A
   Steeg, PS
AF Ouatas, T
   Clare, SE
   Hartsough, MT
   De La Rosa, A
   Steeg, PS
TI MMTV-associated transcription factor binding sites increase nm23-H1
   metastasis suppressor gene expression in human breast carcinoma cell
   lines
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE breast; cancer; metastasis; MMTV; nmm23
ID NM23/NUCLEOSIDE DIPHOSPHATE KINASE; ADENOCARCINOMA CELLS;
   BASEMENT-MEMBRANE; MELANOMA-CELLS; ALPHA-ISOFORM; GROWTH-FACTOR; 2
   ISOTYPES; IN-VIVO; CANCER; OVEREXPRESSION
AB We hypothesize that elevation of nm23-H1 metastasis suppressor gene expression in micrometastatic tumor cells may reduce their subsequent colonization and invasion, and induce differentiation, with a clinical benefit. This report presents the first analysis of the nm23-H1 promoter to identify sites which can increase its transcription. Deletion mapping of a 2.1 kb nm23-H1 promoter fragment tethered to a reporter gene identified three regions involved in its differential expression levels among a panel of human breast carcinoma cell lines: a 195 bp NheI-XbaI fragment responsible for basal expression levels, a 248 bp AvrII-NheI fragment which contributed to the elevated nm23-H1 expression observed in the high expressing cell lines, and a 544 bp AvrII fragment containing an inhibitory element. Examination of the 248 bp AvrII-NheI fragment revealed the unexpected presence of three transcription factor binding sites (MAF/Ets, CTF/NF1 half site and ACAAAG enhancer) previously identified in the MMTV-LTR, and in WAP and milk gene promoters, proposed to mediate mammary-specific gene expression. Mutation of the three sites, individually or together, resulted in two-fold reductions in reporter gene expression. As controls, the same panel of mutations caused a different pattern of reporter gene expression in a non-mammary cell line, and mutation of another nearby site was without effect on nm23-H1. Our data identify a complex regulatory pattern for nm23-H1 transcription, and suggest that a mammary-specific cassette of transcription factors contribute to its elevated expression
C1 NCI, Womens Canc Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Ouatas, T (reprint author), NCI, Womens Canc Sect, Pathol Lab, NIH, Bldg 10,Room 2A33, Bethesda, MD 20892 USA.
NR 33
TC 32
Z9 33
U1 0
U2 2
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PY 2002
VL 19
IS 1
BP 35
EP 42
DI 10.1023/A:1013897022827
PG 8
WC Oncology
SC Oncology
GA 514XM
UT WOS:000173466400005
PM 11918081
ER

PT J
AU Schrayer, DP
   Kouttab, N
   Hearing, VJ
   Wanebo, HJ
AF Schrayer, DP
   Kouttab, N
   Hearing, VJ
   Wanebo, HJ
TI Synergistic effect of interleukin-2 and a vaccine of irradiated melanoma
   cells transfected to secrete staphylococcal enterotoxin A
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE IL-2; irradiated melanoma vaccine; lymphokines; melanoma; metastasis
ID FORMALINIZED EXTRACELLULAR ANTIGENS; MURINE MELANOMA; BACTERIAL
   SUPERANTIGENS; T-CELLS; MONOCLONAL-ANTIBODIES; INVIVO; TUMOR; MODEL;
   GENE; MICE
AB We have previously reported that immunization of mice with melanoma cells transfected to secrete the superantigen, Staphylococcal enterotoxin A (SEA), increased the production of antibodies to the B700 melanoma antigen, stimulated the production of endogenous interleukin 2 (IL-2), activated the expression of CD4, CD8 and CD25 T cell markers and enhanced NK cell activity. Now we show that immunization of mice with a vaccine of irradiated sea-transfected melanoma cells coupled with IL-2 therapy was even more effective in inhibiting the growth of primary melanoma tumors and the development of lung metastases than was the irradiated melanoma cell vaccine alone or IL-2 alone. The morphological and immunological effectiveness of the therapy was dose-dependent on IL-2.
C1 Boston Univ, Sch Med, Roger Williams Med Ctr, Univ Med Grp,Dept Surg,Surg Oncol Res Lab, Providence, RI 02908 USA.
   Boston Univ, Sch Med, Roger Williams Med Ctr, Univ Med Grp,Dept Pathol, Providence, RI 02908 USA.
   NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Schrayer, DP (reprint author), Boston Univ, Sch Med, Roger Williams Med Ctr, Univ Med Grp,Dept Surg,Surg Oncol Res Lab, 825 Chalkstone Ave, Providence, RI 02908 USA.
NR 53
TC 3
Z9 4
U1 0
U2 1
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PY 2002
VL 19
IS 1
BP 43
EP 53
DI 10.1023/A:1013875104326
PG 11
WC Oncology
SC Oncology
GA 514XM
UT WOS:000173466400006
PM 11918082
ER

PT J
AU Seftor, EA
   Meltzer, PS
   Kirschmann, DA
   Pe'er, J
   Maniotis, AJ
   Trent, JM
   Folberg, R
   Hendrix, MJC
AF Seftor, EA
   Meltzer, PS
   Kirschmann, DA
   Pe'er, J
   Maniotis, AJ
   Trent, JM
   Folberg, R
   Hendrix, MJC
TI Molecular determinants of human uveal melanoma invasion and metastasis
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE invasion; metastasis; microarray; tumor plasticity; uveal melanoma;
   vasculogenic mimicry
ID TISSUE GROWTH-FACTOR; BLOOD-VESSEL FORMATION; GENE-EXPRESSION;
   VASCULOGENIC MIMICRY; CHOROIDAL MELANOMA; PROGNOSTIC FACTORS;
   CELL-LINES; ANTIGEN PRESENTATION; DOWN-REGULATION; IN-VITRO
AB The molecular analysis of cancer has benefited tremendously from the sequencing of the human genome integrated with the science of bioinformatics. Microarray analysis technology has the potential to classify tumors based on the differential expression of genes. In the current study, a collaborative, multidisciplinary approach was utilized to study the molecular determinants of human uveal melanoma invasion and metastasis. Uveal melanoma is considered the most common primary intraocular cancer in adults, resulting in the death of approximately 50% of patients affected. Unfortunately, at the time of diagnosis, many patients already harbor microscopic metastases, thus underscoring a critical need to identify prognostic markers indicative of metastatic potential. The investigative strategy consisted of isolating highly invasive vs. poorly invasive uveal melanoma cells from a heterogeneous tumor derived from cells that had metastasized from the eye to the liver. The heterogeneous tissue explant MUM-2 led to the derivation of two clonal cell lines: MUM-2B and MUM-2C. Further morphological and functional analyses revealed that the MUM-2B cells were epithelioid, interconverted (expressing mesenchymal and epithelial phenotypes) highly invasive, and demonstrated vasculogenic mimicry. The MUM-2C cells were spindle-like, expressed only a vimentin mesenchymal phenotype, poorly invasive, and were incapable of vasculogenic mimicry. The molecular analysis of the MUM-2B vs. the MUM-2C clones resulted in the differential expression of 210 known genes. Overall, the molecular signature of the MUM-2B cells resembled that of multiple phenotypes - similar to a pluripotent, embryonic-like genotype. Validation of select genes that were upregulated and down-regulated was conducted by semiquantitative RT-PCR measurement. This study provides a molecular profile that will hopefully lead to the development of new molecular targets for therapeutic intervention and possible diagnostic markers to predict the clinical outcome of patients with uveal melanoma.
C1 Univ Iowa, Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA.
   Univ Iowa, Holden Comprehens Canc Ctr, Iowa City, IA USA.
   NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
   Hadassah Hebrew Univ Hosp, Dept Ophthalmol, Jerusalem, Israel.
   Univ Illinois, Dept Pathol, Chicago, IL 60612 USA.
RP Hendrix, MJC (reprint author), Univ Iowa, Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA.
FU NCI NIH HHS [CA59702, CA80318]; NEI NIH HHS [EY10457]
NR 69
TC 111
Z9 130
U1 0
U2 2
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PY 2002
VL 19
IS 3
BP 233
EP 246
DI 10.1023/A:1015591624171
PG 14
WC Oncology
SC Oncology
GA 554CZ
UT WOS:000175717200006
PM 12067204
ER

PT J
AU Alessandro, R
   Kohn, EC
AF Alessandro, R
   Kohn, EC
TI Signal transduction targets in invasion
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE signal transduction; invasion; integrins; pathways; motility; tyrosine
   kinase
ID FOCAL ADHESION KINASE; ACTIVATED PROTEIN-KINASE; HEPATOCYTE
   GROWTH-FACTOR; PDGF BETA-RECEPTOR; EGF RECEPTOR; PHOSPHATIDYLINOSITOL
   3-KINASE; CELL-MIGRATION; EXTRACELLULAR-MATRIX; CANCER INVASION; IV
   COLLAGEN
AB The processes of physiologic and malignant invasion use the same cellular pathways, albeit under differential regulation. Critical signaling messages can be initiated through cell-cell and cell-substratum contact, as well as using autocrine and paracrine activation. Cancer cells are known for their flexibility and autocrine functions, however, they still rely on a battery of important signaling events. The interaction between the tumor cell and the stroma provides an important signaling milieu and target zone for molecular therapeutic intervention. It is now recognized that malignant invasion requires that interaction for optimal signaling and function. New technologies are now available to allow more rapid dissection of these pathways and characterization of unique regulatory sites for therapeutic gain.
C1 NCI, Mol Signaling Sect, Pathol Lab, Canc Res Ctr, Bethesda, MD 20892 USA.
   Univ Palermo, Dept Biopathol & Biomed Methodol, Palermo, Italy.
RP Kohn, EC (reprint author), NCI, Mol Signaling Sect, Pathol Lab, Canc Res Ctr, 10 Ctr Dr MSC 1500, Bethesda, MD 20892 USA.
NR 80
TC 27
Z9 28
U1 0
U2 0
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PY 2002
VL 19
IS 3
BP 265
EP 273
DI 10.1023/A:1015547804511
PG 9
WC Oncology
SC Oncology
GA 554CZ
UT WOS:000175717200009
PM 12067207
ER

PT J
AU Park, JK
   Tauebi, N
   Stubblefield, BK
   LaMarca, ME
   MacKenzie, JJ
   Stone, DL
   Sidransky, E
AF Park, JK
   Tauebi, N
   Stubblefield, BK
   LaMarca, ME
   MacKenzie, JJ
   Stone, DL
   Sidransky, E
TI The E326K mutation and Gaucher disease: mutation or polymorphism?
SO CLINICAL GENETICS
LA English
DT Article
DE Gaucher disease; glucocerebrosidase; lysosomal storage disease;
   mutation; polymorphism
ID GLUCOCEREBROSIDASE GENE; PSEUDOGENE; TYPE-1
AB Gaucher disease is caused by mutations in the gene for human glucocerebrosidase, a lysosomal enzyme involved in the intracellular hydrolysis of glucosylceramide. While over 150 different glucocerebrosidase mutations have been identified in patients with Gaucher disease, not all reported mutations have been fully characterized as being causative. One such mutation is the E326K mutation, which results from a G to A nucleotide substitution at genomic position 6195 and has been identified in patients with type 1, type 2 and type 3 Gaucher disease. However, in each instance, the E326K mutation was found on the same allele with another glucocerebrosidase mutation. Utilizing polymerase chain reaction (PCR) screening and restriction digestions of both patients with Gaucher disease and normal controls, we identified the E326K allele in both groups. Of the 310 alleles screened from patients with Gaucher disease, the E326K mutation was detected in four alleles (1.3%). In addition, screening for the E326K mutation among normal controls from a random population revealed that three alleles among 316 screened (0.9%) also carried the E326K mutation. In the normal controls with the E326K allele, the glucocerebrosidase gene was completely sequenced, but no additional mutations were found, Because the E326K mutation may be a polymorphism, we caution that a careful examination of any allele with this mutation should be performed to check for the presence of other glucocerebrosidase mutations.
C1 NIMH, Sect Mol Neurogenet, Bethesda, MD 20892 USA.
   Queens Univ, Med Genet Unit, Kingston, ON, Canada.
RP Sidransky, E (reprint author), NIMH, Sect Mol Neurogenet, 49 Convent Dr MSC 4405,49-B1EE16, Bethesda, MD 20892 USA.
NR 16
TC 26
Z9 26
U1 0
U2 0
PU BLACKWELL MUNKSGAARD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 0009-9163
J9 CLIN GENET
JI Clin. Genet.
PD JAN
PY 2002
VL 61
IS 1
BP 32
EP 34
DI 10.1034/j.1399-0004.2002.610106.x
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 538RK
UT WOS:000174828700009
PM 11903352
ER

PT J
AU Rosenzweig, S
   Dorman, SE
   Roesler, J
   Palacios, J
   Zelazko, M
   Holland, SM
AF Rosenzweig, S
   Dorman, SE
   Roesler, J
   Palacios, J
   Zelazko, M
   Holland, SM
TI 561 del4 defines a novel small deletion hotspot in the interferon-gamma
   receptor 1 chain
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE interferon-gamma receptor 1; mycobacteria; BCG; hotspot; small deletion;
   autosomal recessive; single nucleotide polymorphism; single nucleotide
   deletion
ID CALMETTE-GUERIN INFECTION; MYCOBACTERIAL INFECTION; DEFICIENCY;
   SUSCEPTIBILITY; DISEASE; CHILD; GENE
AB Patients with a dominant small deletion (818del4, hotspot) in the interferon-gamma receptor 1 (IFNGR1) gene (6q23-q24) and increased susceptibility to mycobacterial infections have been recently reported. We describe a female patient homozygous for a 4-bp deletion in exon 5 of IFNGR1 (561del4) who developed postvaccinal disseminated Bacille Calmette-Guerin infection. She was born to unrelated Argentinean parents, each of whom was heterozygous for this mutation. 561del4 has been previously described as a maternally inherited mutation in a compound heterozygous German patient. By single nucleotide polymorphism analysis of the areas surrounding the deletion, we showed the independent inheritance of 561del4 in three heterozygous carriers. Polypurine runs and "direct repeats," previously shown to be associated with areas of recurrent small deletions, were found in the flanking region of 561del4. The independent inheritance of three identical mutational events defines 561del4 as a new hotspot in the IFNGR1 gene. (C) 2001 Elsevier Science.
C1 Hosp Garrahan, Buenos Aires, DF, Argentina.
   Univ Dresden, Dresden, Germany.
   NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
   Hosp Navarro, San Juan, Argentina.
RP Rosenzweig, S (reprint author), Hosp Garrahan, Buenos Aires, DF, Argentina.
NR 9
TC 29
Z9 29
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 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD JAN
PY 2002
VL 102
IS 1
BP 25
EP 27
DI 10.1006/clim.2001.5135
PG 3
WC Immunology
SC Immunology
GA 513NJ
UT WOS:000173384400005
PM 11781064
ER

PT J
AU Ascioglu, S
   Rex, JH
   de Pauw, B
   Bennett, JE
   Bille, J
   Crokaert, F
   Denning, DW
   Donnelly, JP
   Edwards, JE
   Erjavec, Z
   Fiere, D
   Lortholary, O
   Maertens, J
   Meis, JF
   Patterson, TF
   Ritter, J
   Selleslag, D
   Shah, PM
   Stevens, DA
   Walsh, TJ
AF Ascioglu, S
   Rex, JH
   de Pauw, B
   Bennett, JE
   Bille, J
   Crokaert, F
   Denning, DW
   Donnelly, JP
   Edwards, JE
   Erjavec, Z
   Fiere, D
   Lortholary, O
   Maertens, J
   Meis, JF
   Patterson, TF
   Ritter, J
   Selleslag, D
   Shah, PM
   Stevens, DA
   Walsh, TJ
CA Invasive Fungal Infections Coopera
TI Defining opportunistic invasive fungal infections in immunocompromised
   patients with cancer and hematopoietic stem cell transplants: An
   international consensus
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID CRYPTOCOCCAL ANTIGEN; PULMONARY ASPERGILLOSIS; LATEX AGGLUTINATION;
   RISK-FACTORS; CRITERIA; CLASSIFICATION; DIAGNOSIS; CANDIDEMIA;
   GALACTOMANNAN; PROBABILITY
AB During the past several decades, there has been a steady increase in the frequency of opportunistic invasive fungal infections (IFIs) in immunocompromised patients. However, there is substantial controversy concerning optimal diagnostic criteria for these IFIs. Therefore, members of the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group formed a consensus committee to develop standard definitions for IFIs for clinical research. On the basis of a review of literature and an international consensus, a set of research-oriented definitions for the IFIs most often seen and studied in immunocompromised patients with cancer is proposed. Three levels of probability are proposed: "proven," "probable," and "possible." The definitions are intended for use in the context of clinical and/or epidemiological research, not for clinical decision making.
C1 European Org Res Treatment Canc, Invas Infect Cooperat Grp, Brussels, Belgium.
   NIAID, Mycoses Study Grp, NIH, Bethesda, MD 20892 USA.
RP Walsh, TJ (reprint author), NCI, 9000 Rockville Pike,Bldg 10,Rm 13N240, Bethesda, MD 20892 USA.
RI Meis, Jacques/A-9241-2010; Ascioglu, Sibel /I-9043-2013; 
OI Meis, Jacques/0000-0003-3253-6080; Ascioglu, Sibel /0000-0002-6052-029X;
   Denning, David/0000-0001-5626-2251
NR 35
TC 1631
Z9 1761
U1 5
U2 63
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JAN 1
PY 2002
VL 34
IS 1
BP 7
EP 14
DI 10.1086/323335
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 498ZM
UT WOS:000172543800007
PM 11731939
ER

PT J
AU Becker, BN
   Jacobson, LM
   Hullett, DA
   Radke, NA
   Oberley, TD
   Brazy, PC
   Kirk, AD
AF Becker, BN
   Jacobson, LM
   Hullett, DA
   Radke, NA
   Oberley, TD
   Brazy, PC
   Kirk, AD
TI Type 2 angiotensin II receptor expression in human renal allografts: an
   association with chronic allograft nephropathy
SO CLINICAL NEPHROLOGY
LA English
DT Article
DE angiotension II; type 2 angiotensin II receptor; renal transplantation;
   chronic allograft nephropathy
ID GENE-TRANSFER; HUMAN KIDNEY; CELL-DEATH; RENIN; SUBTYPES; FIBROSIS;
   TRANSCRIPTION; HYPERTENSION; CYCLOSPORINE; ANTAGONIZES
AB Aims: The renin-angiotensin system (RAS) has been implicated in renal fibrosis through activation of the type 1 angio, tensin II (Ang II) receptor (AT(1)R). Whether the other predominant Ang II receptor, the type 2 Ang II receptor (AT(2)R), has a fibrotic or sparing role in adult human renal tissue is unknown. Materials and methods: We used the reverse-transcription polymerase chain reaction (RT-PCR) to assess intragraft AT(2)R mRNA expression in biopsy samples from 23 renal transplant recipients. Potential correlations between intragraft AT(2)R mRNA, matrix-modulating genes and histologic evidence of chronic rejection were assessed. Results: AT(2)R mRNA was confirmed by sequence analysis of the RT-PCR product. AT(2)R mRNA expression directly correlated with angiotensinogen (Spearman correlation coefficient (r(s)) 0.72; p = 0.0011) mRNA expression, and interestingly, AT(2)R mRNA inversely correlated with inflammatory gene expression in the biopsy samples. However, AT(2)R mRNA directly correlated with transforming growth factor-beta(TGF-beta) (r(s) 0.59; p = 0.044), matrix metalloproteinase-I (MMP- 1) (r(s) 0.83; p = 0.001), tissue inhibitor of metalloproteinase-2 (TIMP-2) (r(s) 0.74; p = 0.001) and TIMP-3 (r(s) 0.80; p = 0.001) mRNA expression. Moreover, AT(2)R mRNA and protein expression was significantly greater in the patients with biopsy-proven chronic allograft nephropathy (n = 9; p = 0.045 vs. no chronic allograft nephropathy and donor biopsy samples for mRNA analyses). Conclusions: These data demonstrate that AT(2)R mRNA is expressed in adult human renal tissue in the setting of renal transplantation. Its apparent association with matrix-modulating genes raises the hypothesis that AT(2)R mRNA expression may be linked with extracellular matrix regulation in the setting of chronic allograft nephropathy.
C1 Univ Wisconsin, Dept Vet Affairs Hosp, Dept Med, Div Nephrol, Madison, WI USA.
   Univ Wisconsin, Dept Vet Affairs Hosp, Dept Surg, Div Transplantat, Madison, WI USA.
   Univ Wisconsin, Dept Vet Affairs Hosp, Dept Pathol & Lab Med, Madison, WI USA.
   USN, NIDDK, Transplantat & Autoimmun Branch, Natl Med Ctr, Bethesda, MD 20084 USA.
RP Becker, BN (reprint author), Univ Wisconsin, Dept Med, Div Nephrol, B 3063 Nephrol,2500 Overlook Terrace, Madison, WI 53705 USA.
RI Kirk, Allan/B-6905-2012
FU NIAID NIH HHS [R01 AI-49285-01]; NIDDK NIH HHS [KO8 DK-02420-05]
NR 32
TC 7
Z9 7
U1 0
U2 0
PU DUSTRI-VERLAG DR KARL FEISTLE
PI OBERHACHING
PA BAJUWARENRING 4, D-82041 OBERHACHING, GERMANY
SN 0301-0430
J9 CLIN NEPHROL
JI Clin. Nephrol.
PD JAN
PY 2002
VL 57
IS 1
BP 19
EP 26
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 514HG
UT WOS:000173432700003
PM 11837798
ER

PT J
AU Robbins, JH
   Kraemer, KH
   Merchant, SN
   Brumback, RA
AF Robbins, JH
   Kraemer, KH
   Merchant, SN
   Brumback, RA
TI Adult-onset xeroderma pigmentosum neurological disease - observations in
   an autopsy case
SO CLINICAL NEUROPATHOLOGY
LA English
DT Article
DE xeroderma pigmentosum; DNA repair; primary neuronal degeneration;
   sensorineural hearing loss; cochlea
ID DEFECTIVE-DNA REPAIR; CACCHIONE SYNDROME; GROUP-C; NEURODEGENERATION;
   ABNORMALITIES; PATHWAY; CELLS
AB Xeroderma pigmentosum (XP) is an inherited disease with defective DNA repair. Patients develop skin cancer because of unrepaired DNA damage produced by the ultraviolet radiation (UV) in sunlight. Many XP children also develop XP neurological disease (ND), consisting of sensorineural hearing loss (SNHL) and a primary neuronal degeneration of the central and peripheral nervous systems. Since the harmful UV in sunlight cannot reach the nervous system, the cause of the death of XP neurons has been hypothesized to result from the inability to repair their DNA that has been damaged by endogenous metabolites. Progressive XP ND originating in an adult has been identified in only a single case. Although clinically asymptomatic at the age of 47 years, the patient had audiometric evidence of a developing mild SNHL together with elicited signs and electrophysiologic evidence of a peripheral neuropathy. She died of metastatic endocervical adenocarcinoma at 49 years of age. We describe here the neuropathological findings in this patient, including examination of the inner ear. Despite clinical evidence of SNHL, there were no anatomic abnormalities of the inner ear. However, the dorsal root ganglia (DRG) showed ongoing neuronal loss. Our findings indicate that XP ND originating in this adult is, like XP ND in children, a primary neuronal degeneration that manifests first in the peripheral nervous system.
C1 NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Basic Res Lab, NIH, Bethesda, MD 20892 USA.
   Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otol & Laryngol, Boston, MA USA.
   Creighton Univ, St Joseph Hosp, Sch Med, Dept Pathol, Omaha, NE USA.
RP Robbins, JH (reprint author), NCI, Dermatol Branch, NIH, Bldg 10,Room 12N238,9000 Rockville Pike, Bethesda, MD 20892 USA.
RI Brumback, Roger/A-2404-2008
FU Intramural NIH HHS [Z01 BC004517-31]
NR 37
TC 19
Z9 19
U1 0
U2 0
PU DUSTRI-VERLAG DR KARL FEISTLE
PI OBERHACHING
PA BAJUWARENRING 4, D-82041 OBERHACHING, GERMANY
SN 0722-5091
J9 CLIN NEUROPATHOL
JI Clin. Neuropathol.
PD JAN-FEB
PY 2002
VL 21
IS 1
BP 18
EP 23
PG 6
WC Clinical Neurology; Pathology
SC Neurosciences & Neurology; Pathology
GA 518FY
UT WOS:000173657000005
PM 11846040
ER

PT J
AU Frank, SM
   Cattaneo, CG
   Wieneke-Brady, MB
   El-Rahmany, H
   Gupta, N
   Lima, JAC
   Goldstein, DS
AF Frank, SM
   Cattaneo, CG
   Wieneke-Brady, MB
   El-Rahmany, H
   Gupta, N
   Lima, JAC
   Goldstein, DS
TI Threshold for adrenomedullary activation and increased cardiac work
   during mild core hypothermia
SO CLINICAL SCIENCE
LA English
DT Article
DE body temperature; catecholamines; echocardiography
ID RANDOMIZED CLINICAL-TRIAL; ISCHEMIC HEART-DISEASE; PERIOPERATIVE
   HYPOTHERMIA; HUMANS; CATECHOLAMINE; RESPONSES; THERMOREGULATION;
   CORTISOL
AB Postoperative hypothermia increases the incidence of ischaemic cardiac events in patients at risk, but the underlying mechanism is unclear. One possibility is increased cardiac work related to the sympathoneural or adrenomedullary hormonal responses. In awake human volunteers, the present study assessed the effects of mild core hypothermia on these responses, and on the associated changes in indices of cardiac work. A total of 11 healthy men were studied on two separate days. On one day, core temperature (T-c) was decreased by the intravenous infusion of cold normal saline (4 degreesC; 60 ml/kg over 30 min) through a central venous catheter. On the other day (normothermic control), warm normal saline (37 degreesC; 60 ml/kg over 30 min) was given intravenously. Transthoracic echocardiograms, the sympathoneural response (noradrenaline) and the adrenomedullary response (adrenaline) were evaluated before, during and after the intravenous infusions. Echocardiography was used to measure left ventricular function and cardiac output. Compared with the normothermic control treatment, core cooling of 0.7 degreesC was associated with increased plasma noradrenaline (220% increase; P = 0.001), whereas adrenaline, cardiac output, heart rate and the rate-pressure product were unchanged. After core cooling of 1.0 degreesC, increases in noradrenaline (by 230%; P = 0.001), adrenaline (by 68%; P = 0.05), cardiac output (by 23%; P = 0.04), heart rate (by 16%; P = 0.04) and rate-pressure product (by 25%; P = 0.007) were all significant compared with the normothermic control treatment. In conclusion, there is a T, threshold, below which an adrenomedullary (adrenaline) response is triggered in addition to the sympathoneural (noradrenaline) response. This T-c threshold (1 degreesC below the normothermic baseline) is also associated with an increase in haemodynamic indices of cardiac work. Mild core hypothermia therefore constitutes a catecholamine-mediated cardiovascular 'stress test'.
C1 Johns Hopkins Med Inst, Dept Anesthesia & Crit Care Med, Baltimore, MD 21287 USA.
   Johns Hopkins Med Inst, Div Cardiol, Baltimore, MD 21287 USA.
   NINCDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
RP Frank, SM (reprint author), Johns Hopkins Med Inst, Dept Anesthesia & Crit Care Med, Carnegie 280,600 N Wolfe St, Baltimore, MD 21287 USA.
NR 35
TC 17
Z9 18
U1 0
U2 15
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON W1N 3AJ, ENGLAND
SN 0143-5221
J9 CLIN SCI
JI Clin. Sci.
PD JAN
PY 2002
VL 102
IS 1
BP 119
EP 125
DI 10.1042/CS20010073
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 525PW
UT WOS:000174081000016
PM 11749669
ER

PT J
AU Sloan, JA
   Aaronson, NK
   Cappelleri, JC
   Fairclough, DL
   Varricchio, C
AF Sloan, JA
   Aaronson, NK
   Cappelleri, JC
   Fairclough, DL
   Varricchio, C
CA Clin Significance Consensus Me
TI Assessing the clinical significance of single items relative to summated
   scores
SO CLINICAL THERAPEUTICS
LA English
DT Meeting Abstract
C1 Netherlands Canc Inst, Amsterdam, Netherlands.
   Pfizer Inc, Groton, CT 06340 USA.
   Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
   NCI, Bethesda, MD 20892 USA.
   Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA
SN 0149-2918
J9 CLIN THER
JI Clin. Ther.
PY 2002
VL 24
SU B
MA 3
BP 6
EP 7
DI 10.1016/S0149-2918(02)85090-1
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 550CF
UT WOS:000175485500005
ER

PT J
AU Bezjak, A
   Dancey, J
   Tu, DS
   Pater, JL
   Seymour, L
   Moore, M
AF Bezjak, A
   Dancey, J
   Tu, DS
   Pater, JL
   Seymour, L
   Moore, M
CA Qual Life Comm Natl Canc Inst C
TI Clinical benefit in patients with cancer of the pancreas: How does it
   compare with clinically significant changes in quality-of-life scores?
SO CLINICAL THERAPEUTICS
LA English
DT Meeting Abstract
C1 Queens Univ, Kingston, ON, Canada.
   Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
   NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA
SN 0149-2918
J9 CLIN THER
JI Clin. Ther.
PY 2002
VL 24
SU B
MA 9
BP 12
EP 14
DI 10.1016/S0149-2918(02)85096-2
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 550CF
UT WOS:000175485500011
ER

PT J
AU Snyder, C
   Gotay, CC
   Lipscomb, J
AF Snyder, C
   Gotay, CC
   Lipscomb, J
TI The Cancer Outcomes Measurement Working Group: Evaluating the state of
   the science and developing recommendations for improving outcomes
   assessment in cancer
SO CLINICAL THERAPEUTICS
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
   Univ Hawaii, Honolulu, HI 96822 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA
SN 0149-2918
J9 CLIN THER
JI Clin. Ther.
PY 2002
VL 24
SU B
MA 14
BP 21
EP 21
DI 10.1016/S0149-2918(02)85101-3
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 550CF
UT WOS:000175485500016
ER

PT J
AU Costantino, J
AF Costantino, J
TI The impact of hormonal treatments on quality of life of patients with
   metastatic breast cancer
SO CLINICAL THERAPEUTICS
LA English
DT Article
DE estrogen receptor antagonists; endocrine therapy; advanced breast
   cancer; quality of life
ID FIRST-LINE THERAPY; RANDOMIZED DOUBLE-BLIND; PHASE-III; POSTMENOPAUSAL
   WOMEN; OF-LIFE; MEGESTROL-ACETATE; AROMATASE INHIBITOR;
   EUROPEAN-ORGANIZATION; FUNCTIONAL ASSESSMENT; TAMOXIFEN
AB Background: The concept of quality of life (QOL) increasingly has been used to assess health-related outcomes associated with a specific disease or its treatment, especially in patients with incurable tumors, such as metastatic breast cancer (MBC). Hormonal therapy (HT) is often used to treat hormone receptor-positive MBC, with the primary treatment goal of reducing both disease burden and patient suffering.
   Objective: This article reviews the instruments used to assess QOL in patients with breast cancer, the adverse effects of HTs, and the clinical trials that assess QOL in patients with MBC receiving various HTs.
   Methods: Articles were identified for inclusion in this manuscript through the following searches, limited to English-language publications: MEDLINE (mid 1960s to January 2002), American Society of Oncology abstracts (1997-2001), and San Antonio Breast Cancer Symposium abstracts (2001 and 2002). The following search terms were used: quality of life, breast cancer, hormonal therapies, tamoxifen, toremifine, letrozole, anastrozole, exemestane, and megestrol acetate.
   Conclusions: QOL assessment following MBC treatment has become an important indicator of treatment effectiveness, and numerous clinical trials have studied the impact of HT on QOL. In general, the older HTs, such as the progestins and selective estrogen receptor modulators (SERMs), produce more adverse effects than do the newer HTs, such as the aromatase inhibitors (AIs) and estrogen receptor (ER) antagonists. QOL data regarding tamoxifen, a SERM associated with a high incidence of vasomotor symptoms and vaginal discharge, are limited, although tamoxifen has not been associated with significant psychological distress when administered as a chemopreventive or adjuvant MBC therapy in clinical trials. QOL studies comparing the third-generation AIs with tamoxifen or megestrol acetate show that the AIs produce a more favorable QOL, probably because these agents target the aromatase enzyme, which results in a lower incidence of thromboembolism and vaginal bleeding. Although QOL studies of the ER antagonist fulvestrant have not been conducted, several attributes of this new HT may contribute to the retention of a good QOL in patients with MBC. A variety of QOL-assessment tools to measure the impact of HTs on patients with MBC are available. Clinical trial data regarding QOL in patients with MBC receiving HT will be useful for both clinicians and patients in evaluating treatment options and developing treatment strategies.
C1 Univ Pittsburgh, Grad Sch Publ Hlth, NSABP, Ctr Biostat, Pittsburgh, PA 15261 USA.
   Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
RP Costantino, J (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, NSABP, Ctr Biostat, 316 Parran Hall,130 DeSoto St, Pittsburgh, PA 15261 USA.
NR 31
TC 8
Z9 8
U1 0
U2 5
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA
SN 0149-2918
J9 CLIN THER
JI Clin. Ther.
PY 2002
VL 24
SU C
BP C26
EP C42
DI 10.1016/S0149-2918(02)85159-1
PG 17
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 571DW
UT WOS:000176700400003
PM 12117073
ER

PT J
AU Weinstein, BM
   Lawson, ND
AF Weinstein, BM
   Lawson, ND
TI Arteries, veins, notch, and VEGF
SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Cold Spring Harbor Symposium on Quantitiative Biology
CY 2002
CL COLD SPRING HARBOR, NEW YORK
SP Aventis Pharma AG, Bristol Mayers Squibb Co, Eli Lilly & Co, GlaxoSmithKline, Novartis Pharma AG, Pfizer Inc, Abbott Lab, Amersham Biosci Inc, Amgen Inc, Appl Biosyst, Bio Ventures Inc, Chugai Pharmaceut Co Ltd, Cogene Bio Tech Ventures Ltd, Diagnost Products Corp, Forest Lab, Genentech Inc, Hoffmann Rache Inc, Johnson & Johnson Pharmaceut, Res & Dev L L C, Kyowa Hakko Kogyo Co Ltd, Merck Res Lab, New England BioLab Inc, OSI Pharmaceut Inc, Pall Corp, Pharmacia Corp, ResGen Inc, Schering Plough Res Inst, Wyeth Genet Inst
ID ENDOTHELIAL-GROWTH-FACTOR; VASCULAR MORPHOGENESIS; CARDIOVASCULAR
   DEVELOPMENT; VENOUS DIFFERENTIATION; EMBRYONIC LETHALITY; SMOOTH-MUSCLE;
   CHICK-EMBRYO; ZEBRAFISH; EXPRESSION; ANGIOGENESIS
C1 NICHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA.
RP Weinstein, BM (reprint author), NICHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA.
FU NICHD NIH HHS [ZO1-HD-01011]
NR 58
TC 37
Z9 37
U1 2
U2 4
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 0091-7451
J9 COLD SPRING HARB SYM
JI Cold Spring Harbor Symp. Quant. Biol.
PY 2002
VL 67
BP 155
EP 162
DI 10.1101/sqb.2002.67.155
PG 8
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA 694NM
UT WOS:000183780700021
PM 12858536
ER

PT J
AU Nabel, EG
   Boehm, M
   Akyurek, LM
   Yoshimoto, T
   Crook, MF
   Olive, M
   San, H
   Qu, X
AF Nabel, EG
   Boehm, M
   Akyurek, LM
   Yoshimoto, T
   Crook, MF
   Olive, M
   San, H
   Qu, X
TI Cell cycle signaling and cardiovascular disease
SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Cold Spring Harbor Symposium on Quantitiative Biology
CY 2002
CL COLD SPRING HARBOR, NEW YORK
SP Aventis Pharma AG, Bristol Mayers Squibb Co, Eli Lilly & Co, GlaxoSmithKline, Novartis Pharma AG, Pfizer Inc, Abbott Lab, Amersham Biosci Inc, Amgen Inc, Appl Biosyst, Bio Ventures Inc, Chugai Pharmaceut Co Ltd, Cogene Bio Tech Ventures Ltd, Diagnost Products Corp, Forest Lab, Genentech Inc, Hoffmann Rache Inc, Johnson & Johnson Pharmaceut, Res & Dev L L C, Kyowa Hakko Kogyo Co Ltd, Merck Res Lab, New England BioLab Inc, OSI Pharmaceut Inc, Pall Corp, Pharmacia Corp, ResGen Inc, Schering Plough Res Inst, Wyeth Genet Inst
ID DEPENDENT KINASE INHIBITOR; MICE LACKING; GROWTH-FACTOR; F-BOX;
   P27(KIP1); P21; EXPRESSION; MUSCLE; G1; PROLIFERATION
C1 NHLBI, Cardiovasc Branch, Bethesda, MD 20892 USA.
RP Nabel, EG (reprint author), NHLBI, Cardiovasc Branch, Bldg 10, Bethesda, MD 20892 USA.
NR 45
TC 3
Z9 3
U1 0
U2 1
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 0091-7451
J9 COLD SPRING HARB SYM
JI Cold Spring Harbor Symp. Quant. Biol.
PY 2002
VL 67
BP 163
EP 170
DI 10.1101/sqb.2002.67.163
PG 8
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA 694NM
UT WOS:000183780700022
PM 12858537
ER

PT J
AU Davis, JS
   Hassanzadeh, S
   Winitsky, S
   Wen, H
   Aletras, A
   Epstein, ND
AF Davis, JS
   Hassanzadeh, S
   Winitsky, S
   Wen, H
   Aletras, A
   Epstein, ND
TI A gradient of myosin regulatory light-chain phosphorylation across the
   ventricular wall supports cardiac torsion
SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Cold Spring Harbor Symposium on Quantitiative Biology
CY 2002
CL COLD SPRING HARBOR, NEW YORK
SP Aventis Pharma AG, Bristol Mayers Squibb Co, Eli Lilly & Co, GlaxoSmithKline, Novartis Pharma AG, Pfizer Inc, Abbott Lab, Amersham Biosci Inc, Amgen Inc, Appl Biosyst, Bio Ventures Inc, Chugai Pharmaceut Co Ltd, Cogene Bio Tech Ventures Ltd, Diagnost Products Corp, Forest Lab, Genentech Inc, Hoffmann Rache Inc, Johnson & Johnson Pharmaceut, Res & Dev L L C, Kyowa Hakko Kogyo Co Ltd, Merck Res Lab, New England BioLab Inc, OSI Pharmaceut Inc, Pall Corp, Pharmacia Corp, ResGen Inc, Schering Plough Res Inst, Wyeth Genet Inst
ID FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; SKELETAL-MUSCLE; BETA-MYOSIN;
   STRETCH-ACTIVATION; MUTATIONS; CONTRACTION; DEPENDS; FIBERS; HEART
C1 Cardiol Branch, Mol Physiol Sect, Bethesda, MD 20892 USA.
   NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
RP Davis, JS (reprint author), Cardiol Branch, Mol Physiol Sect, Bethesda, MD 20892 USA.
RI Wen, Han/G-3081-2010; 
OI Wen, Han/0000-0001-6844-2997; Aletras, Anthony/0000-0002-3786-3817
NR 20
TC 13
Z9 13
U1 0
U2 0
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 0091-7451
J9 COLD SPRING HARB SYM
JI Cold Spring Harbor Symp. Quant. Biol.
PY 2002
VL 67
BP 345
EP 352
DI 10.1101/sqb.2002.67.345
PG 8
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA 694NM
UT WOS:000183780700044
PM 12858559
ER

PT J
AU Dolensky, B
   Kirk, KL
AF Dolensky, B
   Kirk, KL
TI Preparation of (fluoromethyl)- and (difluoromethyl) imidazoles
SO COLLECTION OF CZECHOSLOVAK CHEMICAL COMMUNICATIONS
LA English
DT Article
DE fluorinated imidazoles; deoxyfluorination; fluorinated heterocycles;
   Deoxo-Fluor; fluorinations; aldehydes; alcohols
ID ACTIVE ANTIINFLAMMATORY AGENTS; HETEROARYL-N-DIFLUOROMETHYL; FACILE
   SYNTHESIS; 1,2-DIARYLIMIDAZOLES; INHIBITORS; HISTAMINE; ANIONS; POTENT
AB 2-(Fluoromethyl)- and 2-(difluoromethyl)imidazoles, and 4-(fluoromethyl)- and 4-( difluoromethyl) imidazoles have been prepared by deoxyfluorination of (hydroxymethyl) imidazole or formylimidazole precursors.
C1 NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Kirk, KL (reprint author), NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM BohumilD@intra.niddk.nih.gov; KennethK@bdg8.niddk.nih.gov
NR 31
TC 7
Z9 7
U1 0
U2 1
PU INST ORGANIC CHEM AND BIOCHEM
PI PRAGUE 6
PA ACAD SCI CZECH REPUBLIC, FLEMINGOVO NAM 2, PRAGUE 6 166 10, CZECH
   REPUBLIC
SN 0010-0765
J9 COLLECT CZECH CHEM C
JI Collect. Czech. Chem. Commun.
PY 2002
VL 67
IS 9
BP 1335
EP 1344
DI 10.1135/cccc20021335
PG 10
WC Chemistry, Multidisciplinary
SC Chemistry
GA 600NY
UT WOS:000178398300010
ER

PT J
AU Bons, N
   Lehmann, S
   Nishida, N
   Mestre-Frances, N
   Dormont, D
   Belli, P
   Delacourte, A
   Grassi, J
   Brown, P
AF Bons, N
   Lehmann, S
   Nishida, N
   Mestre-Frances, N
   Dormont, D
   Belli, P
   Delacourte, A
   Grassi, J
   Brown, P
TI BSE infection of the small short-lived primate Microcebus marinus
SO COMPTES RENDUS BIOLOGIES
LA English
DT Article; Proceedings Paper
CT Conference on Transmissible Spongiform Encephalopathies
CY MAR 14-16, 2001
CL PARIS, FRANCE
DE BSE; primate; prion protein; immunohistochemistry; Western blot;
   neurodegeneration
ID CREUTZFELDT-JAKOB-DISEASE; ABNORMAL PRION PROTEIN; SPONGIFORM
   ENCEPHALOPATHY; RETINAL DEGENERATION; VARIANT CJD; TRANSMISSION; AGENT;
   MICE; ANTIBODIES; STRAINS
AB Eleven Microcebus murinus (lemur) primates were intracerebrally or orally infected by bovine spongiform encephalopathy (BSE) or macaque-adapted BSE (MBSE) brain homogenates. In many BSE and MBSE infected lemurs, but not in animals inoculated with normal bovine brain, persistent behavioral changes occurred as early as 3 months, and neurological signs as early as 13 months after infection. Immunohistochemical examination of animals sacrificed during the incubation period revealed an abnormal accumulation of 'prion' protein (PrP) in the intestinal wall, intestinal nervous plexus, mesenteric lymph nodes and spleen, and in the clinical stage, also in the brain. In MBSE-inoculated animals, proteinase K resistance of the PrP (PrPres) was confirmed by Western blot in the spleen and the brain. Obvious signs of neurodegeneration were observed in all infected animals characterized by hyperaggregated and paired-helical filaments-immunoreactive Tau proteins, beta42-amyloid plaques and astrogliosis. Additionally, PrPres was present in the ganglion cells of the retina in diseased animals after either intracerebrally or oral infection by the BSE or MBSE agent. These results show that the microcebe is susceptible to the BSE infectious agent via intracerebral and oral routes with comparatively short incubation periods compared to simians, and could be a useful animal model to study the pathophysiology of disease transmission in primates. To cite this article: N. Bons et al., C. R. Biologies 325 (2002) 67-74. (C) 2002 Academie des Sciences/Editions scientifiques et medicales Elsevier SAS.
C1 Univ Montpellier 2, EPHE, Lab Neuromorphol Fonctionnelle, F-34095 Montpellier 5, France.
   CNRS, UPR 1142, IGH, F-34396 Montpellier, France.
   CEA, CRSSA, EPHE, F-92265 Fontenay Aux Roses, France.
   CNEVA, Pathol Bovine, F-69342 Lyon 7, France.
   INSERM, U422, F-59045 Lille, France.
   CEA, F-91191 Gif Sur Yvette, France.
   NINCDS, Cent Nervous Syst Studies Lab, NIH, Bethesda, MD 20892 USA.
RP Bons, N (reprint author), Univ Montpellier 2, EPHE, Lab Neuromorphol Fonctionnelle, F-34095 Montpellier 5, France.
NR 23
TC 11
Z9 12
U1 1
U2 7
PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS CEDEX 15
PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE
SN 1631-0691
J9 CR BIOL
JI C. R. Biol.
PD JAN
PY 2002
VL 325
IS 1
BP 67
EP 74
DI 10.1016/S1631-0691(02)01390-2
PG 8
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 546UB
UT WOS:000175291900011
PM 11862624
ER

PT S
AU Felts, AK
   Wallqvist, A
   Gallicchio, E
   Bassolino, D
   Krystek, SR
   Levy, RM
AF Felts, AK
   Wallqvist, A
   Gallicchio, E
   Bassolino, D
   Krystek, SR
   Levy, RM
BE Schlick, T
   Gan, HH
TI Fold recognition using the OPLS all-atom potential and the surface
   generalized born solvent model
SO COMPUTATIONAL METHODS FOR MACROMOLECULES: CHALLENGES AND APPLICATIONS
SE LECTURE NOTES IN COMPUTATIONAL SCIENCE AND ENGINEERING
LA English
DT Proceedings Paper
CT 3rd International Workshop on Algorithms for Macromolecular Modeling
CY OCT 12-14, 2000
CL NYU, NEW YORK, NY
HO NYU
ID SOLVATION FREE-ENERGIES; MOLECULAR-DYNAMICS SIMULATIONS; PANCREATIC
   TRYPSIN-INHIBITOR; PROTEIN-STRUCTURE PREDICTION; POISSON-BOLTZMANN
   EQUATION; CONFORMATIONAL FREE-ENERGY; NEAR-NATIVE FOLDS; EXPLICIT
   SOLVENT; CONTINUUM MODEL; ELECTROSTATIC CONTRIBUTIONS
AB Protein decoy data sets provide a benchmark for testing scoring functions designed for fold recognition and protein homology modeling problems. It is commonly believed that statistical potentials based on reduced atomic models are better able to discriminate native-like from misfolded decoys than scoring functions based on more detailed molecular mechanics models. Recent benchmark tests, however, suggest otherwise. Further analysis of the effectiveness of all atom molecular mechanics scoring functions for detecting misfolded decoys and direct comparison with results obtained using a statistical potential derived for a reduced atomic model are presented in this report. The OPLS all-atom force field is used as a scoring function to detect native protein folds among the Park & Levitt large decoy sets. Solvent electrostatic effects are included through the Surface Generalized Born (SGB) model. The OPLS potential with SGB solvation (OPLS-AA/SGB) provides good discrimination between native-like structures and non-native decoys. Rom an analysis of the individual energy components of the OPLS-AA/SGB potential for the native and the best-ranked decoy, it is determined that a roughly even balance of the terms of the potential is responsible for distinguishing the native from the misfolded conformations. Different combinations of individual energy terms provide less discrimination than the total energy. The effects of scoring decoys using several dielectric models are compared also. With the SGB solvation model, close to 100% of the structures with energies within 100 kcal/mol of the native state minimum are native-like. In contrast, only 20% of the low energy structures are found to be native-like when a distance dependent dielectric is used instead of SGB to model solvent electrostatic effects. The results are consistent with observations that all-atom molecular potentials coupled with intermediate level solvent dielectric models are competitive with knowledge-based potentials for decoy detection and protein modeling problems such as fold recognition.
C1 NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
RP Wallqvist, A (reprint author), NCI, Frederick Canc Res & Dev Ctr, SAIC Bldg 430,POB B, Frederick, MD 21702 USA.
NR 80
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 1439-7358
BN 3-540-43756-8
J9 LECT NOTES COMP SCI
PY 2002
VL 24
BP 445
EP 476
PG 32
WC Biochemistry & Molecular Biology; Mathematics, Applied; Physics, Atomic,
   Molecular & Chemical
SC Biochemistry & Molecular Biology; Mathematics; Physics
GA BV88U
UT WOS:000180302400018
ER

PT B
AU Cohen, JI
AF Cohen, JI
BE Knobler, S
   Lederberg, J
   Pray, LA
TI Vaccine-associated cases due to immunization with live virus vaccines
SO CONSIDERATIONS FOR VIRAL DISEASE ERADICATION, WORKSHOP SUMMARY: LESSONS
   LEARNED AND FUTURE STRATEGIES
LA English
DT Proceedings Paper
CT Workshop on the Consequences of Viral Disease Eradication
CY FEB 01-02, 2001
CL INST MED, FORUM EMERGING INFECT, WASHINGTON, D.C.
SP US Dept HHS, NIH, Ctr Dis Control & Prevent, US FDA, US Dept Def, US Dept State, US Agcy Int Dev, US Dept Vet Affairs, Abbott Labs, Amer Soc Microbiol, Bristol Myers Squibb Co, Burroughs Wellcome Fund, Eli Lilly Co, Ellison Med Fdn, Glaxo Wellcome, F Hoffmann La Roche AG, Pfizer, SmithKline Beecham Corp, Wyeth Ayerst Labs
HO INST MED, FORUM EMERGING INFECT
C1 NIH, Med Virol Sect, Clin Invest Lab, Bethesda, MD 20892 USA.
RP Cohen, JI (reprint author), NIH, Med Virol Sect, Clin Invest Lab, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU NATL ACADEMIES PRESS
PI WASHINGTON
PA 2101 CONSTITUTION AVE, WASHINGTON, DC 20418 USA
BN 0-309-08414-8
PY 2002
BP 90
EP 97
PG 8
WC Public, Environmental & Occupational Health; Infectious Diseases;
   Virology
SC Public, Environmental & Occupational Health; Infectious Diseases;
   Virology
GA BX26B
UT WOS:000184775800010
ER

PT S
AU Hirano, T
   Watanabe, D
   Kawaguchi, SY
   Pastan, I
   Nakanishi, S
AF Hirano, T
   Watanabe, D
   Kawaguchi, SY
   Pastan, I
   Nakanishi, S
BE Highstein, TM
   Thach, WT
TI Roles of inhibitory interneurons in the cerebellar cortex
SO CREBELLUM: RECENT DEVELOPMENTS IN CEREBELLAR RESEARCH
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Conference on Recent Developments in Cerebellar Research
CY NOV 15-18, 2001
CL ST LOUIS, MISSOURI
SP McDonnell Ctr Higher Brain Funct, NIH, Natl Sci Fdn, Washington Univ Continuing Educ, Washington Univ Dept Anatomy & Neurobiol, Neurol, Otolaryngol
DE cerebellum; interneuron; Golgi cell; transgenic mouse; GABA; synaptic
   plasticity
ID LONG-TERM DEPRESSION; REBOUND POTENTIATION; SYNAPTIC EXCITATION; CELLS;
   PLASTICITY; RECEPTORS; LOCALIZATION; HIPPOCAMPUS; DISRUPTION; ACTIVATION
AB The roles of inhibitory interneurons in the cerebellar cortex were investigated. First, Golgi cells were specifically eliminated in transgenic mice in which Golgi cells expressed human interleukin-2 receptor alpha subunit (IL2Ralpha). Injection of exotoxin coupled to anti-IL2Ralpha antibody in the cerebellum of the transgenic mouse eliminated Golgi cells and abolished GABA and synaptic inhibition in the granular layer. After elimination of Golgi cells, acute severe ataxia and subsequent mild motor discoordination were observed. In the latter chronic phase, NMDA receptor-mediated synaptic response was reduced in granule cells. Our findings indicate that elimination of GABAergic inhibition in the granular layer caused overexcitation of granule cells resulting in severe ataxia, and then NMDA receptors in granule cells were downregulated, compensating for the reduction of GABAergic inhibition and improving motor control. In the second part, we report on the regulation mechanism of synaptic plasticity at inhibitory synapses on Purkinje cells (PCs). Inhibitory synaptic transmission on a PC is potentiated after repetitive PC depolarization. This synaptic plasticity (rebound potentiation, RP) was suppressed when a presynaptic neuron was activated during the PC depolarization. This synaptic regulation is unique in the sense that the homosynaptic activity suppresses the induction of synaptic plasticity. The mechanism of how presynaptic activity suppresses RP was examined. GABA released from the presynaptic terminal activated not only GABA(A) receptor but also GABA(B) receptor. The latter was coupled to Gi/o proteins, which downregulated adenylyl cyclase reducing cAMP and inactivated cAMP-dependent protein kinase (PKA). Downregulation of PKA suppressed RP induction.
C1 Kyoto Univ, Dept Biophys, Grad Sch Sci, Sakyo Ku, Kyoto 6068502, Japan.
   Japan Sci & Technol Corp, CREST, Kawaguchi, Saitama 3320012, Japan.
   Kyoto Univ, Grad Sch Biostudies, Dept Mol & Syst Biol, Sakyo Ku, Kyoto 6068501, Japan.
   Kyoto Univ, Fac Med, Dept Biol Sci, Sakyo Ku, Kyoto 6068501, Japan.
   NCI, Mol Biol Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA.
RP Hirano, T (reprint author), Kyoto Univ, Dept Biophys, Grad Sch Sci, Sakyo Ku, Kyoto 6068502, Japan.
NR 23
TC 19
Z9 20
U1 1
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-436-6
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 978
BP 405
EP 412
DI 10.1111/j.1749-6632.2002.tb07583.x
PG 8
WC Multidisciplinary Sciences; Neurosciences
SC Science & Technology - Other Topics; Neurosciences & Neurology
GA BW14B
UT WOS:000180980000033
PM 12582069
ER

PT J
AU Tsai, CJ
   Maizel, JV
   Nussinov, R
AF Tsai, CJ
   Maizel, JV
   Nussinov, R
TI The hydrophobic effect: A new insight from cold denaturation and a
   two-state water structure
SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Review
DE cold denaturation; hydrophobic effect; entropy; water structure; molten
   globule; alpha-lactalbumin; molecular simulations
ID MOLTEN GLOBULE STATE; ALPHA-LACTALBUMIN; PROTEIN; STABILITY; ORIGIN;
   MODEL
AB Herein we provide a new insight into the hydrophobic effect in protein folding. Our proposition explains the molecular basis of cold denaturation, and of intermediate states in heat and their absence in cold denaturation. The exposure of non-polar surface reduces the entropy and enthalpy of the system, at low and at high temperatures. At low temperatures the favorable reduction in enthalpy overcomes the unfavorable reduction in entropy, leading to cold denaturation. At high temperatures, folding/unfolding is a two-step process: in the first, the entropy gain leads to hydrophobic collapse, in the second, the reduction in enthalpy due to protein-protein interactions leads to the native state. The different entropy and enthalpy contributions to the Gibbs energy change at each step at high, and at low, temperatures can be conveniently explained by a two-state model of the water structure. The model provides a clear view of the dominant factors in protein folding and stability. Consequently, it appears to provide a microscopic view of the hydrophobic effect and is consistently linked to macroscopic thermodynamic parameters.
C1 NCI, Intramural Res Support Program, SAIC, Lab Expt & Computat Biol, Frederick, MD 21702 USA.
   Tel Aviv Univ, Sackler Fac Med, Dept Human Genet & Mol Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel.
RP Tsai, CJ (reprint author), NCI, Intramural Res Support Program, SAIC, Lab Expt & Computat Biol, Bldg 469,Rm 151, Frederick, MD 21702 USA.
FU NCI NIH HHS [N01-CO-12400]
NR 22
TC 78
Z9 79
U1 4
U2 19
PU CRC PRESS LLC
PI BOCA RATON
PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431
   USA
SN 1040-9238
J9 CRIT REV BIOCHEM MOL
JI Crit. Rev. Biochem. Mol. Biol.
PY 2002
VL 37
IS 2
BP 55
EP 69
DI 10.1080/10409230290771456
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 548TW
UT WOS:000175406800001
PM 12027264
ER

PT J
AU Milner, JA
AF Milner, JA
TI Foods and health promotion: The case for cranberry
SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION
LA English
DT Article; Proceedings Paper
CT Workshop on Cranberries and Health
CY SEP, 2000
CL HOUSTON, TEXAS
SP Ocean Spray Cranberries Inc
C1 NCI, Nutr Sci Res Grp, Div Canc Prevent, Rockville, MD 20854 USA.
RP Milner, JA (reprint author), NCI, Nutr Sci Res Grp, Div Canc Prevent, Rockville, MD 20854 USA.
NR 8
TC 6
Z9 7
U1 0
U2 0
PU CRC PRESS LLC
PI BOCA RATON
PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431
   USA
SN 1040-8398
J9 CRIT REV FOOD SCI
JI Crit. Rev. Food Sci. Nutr.
PY 2002
VL 42
IS 3
SU S
BP 265
EP 266
DI 10.1080/10408390209351913
PG 2
WC Food Science & Technology; Nutrition & Dietetics
SC Food Science & Technology; Nutrition & Dietetics
GA 559KB
UT WOS:000176024400002
PM 12058983
ER

PT J
AU Nagorsen, D
   Wang, E
   Marincola, FM
   Even, J
AF Nagorsen, D
   Wang, E
   Marincola, FM
   Even, J
TI Transcriptional analysis of tumor-specific T-cell responses in cancer
   patients
SO CRITICAL REVIEWS IN IMMUNOLOGY
LA English
DT Review
DE specific T cells; qRT-PCR; cDNA microarrays; TCR repertoire analysis
ID MESSENGER-RNA AMPLIFICATION; GENE-EXPRESSION PATTERNS; IFN-GAMMA;
   METASTATIC MELANOMA; ELISPOT ASSAY; RT-PCR; DENDRITIC CELLS; IMMUNE
   RESPONSIVENESS; CYTOKINE EXPRESSION; PEPTIDE VACCINATION
AB Over the last decade, tumor immunology in general and tumor immunotherapy in particular have made important progress. Thanks to the discovery of tumor-associated antigens (TAA) and the consequent development of active-specific immunization protocols, TAA-specific T-cell responses can now be induced reproducibly in cancer patients. However, clinical responses directly ascribable to TAA-specific T cells occur only occasionally. It is not clear why TAA-specific T cells do not eliminate tumor cells in vivo. This paradoxical coexistence of antigen-bearing tumor cells and antigen-specific T cells constitutes a critical point of current investigation. In recent years, protein-ligand interaction-based methods aimed at the identification and characterization of T cells using antibodies (cell surface phenotyping, intracellular and secreted cytokine detection), or HLA-peptide multimers, have significantly improved the analysis of TAA-specific T cells. These methods, however, seem to have reached the limit of their usefulness. Transcriptional analysis may add sensitivity and resolution and may provide global pictures of the multifactorial. requirements for an efficient immune response against tumors. In this review, we describe the use of molecular genetic methods, such as real time qRT-PCR, cDNA microarrays, and TCR repertoire analysis. In addition, we describe techniques for high-fidelity messenger RNA amplification that allow high-throughput analysis of samples obtained from minimal sources, such as HLA/peptide tetramer sorted antigen-specific T cells, laser capture dissection, or fine needle aspirates. Recent work discussed in this review summarizes the complementarity of transcriptional analysis as an essential tool that, in addition to conventional methods, may deepen and broaden the characterization of tumor-specific T cells.
C1 NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Marincola, FM (reprint author), NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bldg 10,Room 1C711,10 Ctr Dr, Bethesda, MD 20892 USA.
NR 106
TC 9
Z9 10
U1 0
U2 1
PU BEGELL HOUSE INC
PI NEW YORK
PA 145 MADISON AVE, NEW YORK, NY 10016 USA
SN 1040-8401
J9 CRIT REV IMMUNOL
JI Crit. Rev. Immunol.
PY 2002
VL 22
IS 5-6
BP 449
EP 462
PG 14
WC Immunology
SC Immunology
GA 676WV
UT WOS:000182776300006
PM 12803321
ER

PT J
AU Weinberg, WC
   Denning, MF
AF Weinberg, WC
   Denning, MF
TI p21(waf1) control of epithelial cell cycle and cell fate
SO CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE
LA English
DT Review
DE p21(WAF1); cell cycle; keratinocytes; cyclin-dependent kinase; cell
   transformation
ID DEPENDENT KINASE INHIBITOR; GROWTH-FACTOR-BETA; SQUAMOUS
   CARCINOMA-CELLS; FAS-MEDIATED APOPTOSIS; PCNA BINDING DOMAINS;
   HUMAN-MELANOMA CELLS; NF-KAPPA-B; TERMINAL DIFFERENTIATION; HUMAN
   KERATINOCYTES; SKIN CARCINOGENESIS
AB As a broad-acting cyclin-dependent kinase inhibitor, p21(WAF1) occupies a central position in the cell cycle regulation of self-renewing tissues such as oral mucosa and skin. In addition to regulating normal cell cycle progression decisions, p21(WAF1) integrates genotoxic insults into growth arrest and apoptotic signaling pathways that ultimately determine cell fate. As a result of its complex interactions with cell cycle machinery and response to mutagenic agents, p21(WAF1) also has stage-specific roles in epithelial carcinogenesis. Finally, a view is emerging of p21(WAF1) as not merely a cyclin-dependent kinase inhibitor, but also as a direct participant in regulating genes involved in growth arrest, senescence, and aging, thus providing an additional layer of control over matters of the cell cycle. This review discusses these various roles played by p21(WAF1) in cell cycle control, and attempts to relate these to epithelial cell biology, with special emphasis on keratinocytes. (Abbreviations used include the following: Brdu, 5-Bromo-2'-deoxyuridine; cdk, cyclin-dependent kinase; EGF, epidermal growth factor; KIP, kinase inhibitor protein; PCNA, proliferating cell nuclear antigen; and TPA, 12-O-tetradecanoylphorbol-13-acetate.)
C1 US FDA, CBER, DMA, Immunobiol Lab, Bethesda, MD 20892 USA.
   Loyola Univ, Med Ctr, Dept Pathol, Maywood, IL 60153 USA.
   Loyola Univ, Med Ctr, Cardinal Bernardin Canc Ctr, Maywood, IL 60153 USA.
RP Weinberg, WC (reprint author), US FDA, CBER, DMA, Immunobiol Lab, 29 Lincoln Dr,NIH Bldg 29B,Room 3NN04,HFM-564, Bethesda, MD 20892 USA.
RI Weinberg, Wendy/A-8920-2009
NR 142
TC 106
Z9 115
U1 0
U2 4
PU INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R
PI ALEXANDRIA
PA 1619 DUKE ST, ALEXANDRIA, VA 22314-3406 USA
SN 1045-4411
J9 CRIT REV ORAL BIOL M
JI Crit. Rev. Oral Biol. Med.
PY 2002
VL 13
IS 6
BP 453
EP 464
PG 12
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 677PC
UT WOS:000182815900001
PM 12499239
ER

PT J
AU Newman, DJ
   Cragg, GM
   Holbeck, S
   Sausville, EA
AF Newman, David J.
   Cragg, Gordon M.
   Holbeck, Susan
   Sausville, Edward A.
TI Natural Products and Derivatives as Leads to Cell Cycle Pathway Targets
   in Cancer Chemotherapy
SO CURRENT CANCER DRUG TARGETS
LA English
DT Article
AB The influence of natural products upon drug discovery in general has been quite impressive; one only has to look at the number of clinically active drugs that are in use in cancer therapy to see how many either are natural products or have a natural product pharmacophore. What is now becoming quite apparent is that materials from natural sources are excellent probes (indicators) for cellular targets that when modulated, may well have a deleterious effect upon the cycling of a tumor cell through the conventional cell cycle. If the particular target is not expressed in normal cell cycling, then a directed "perturbation" of the tumor cell's cycle may well lead to a novel method of treatment for specific tumor types. In this review we have not attempted to be exhaustive but have given a current overview of how natural products from marine, microbial and plant sources have permitted in-depth analyses of various parts of the cell cycle under varying conditions with the ultimate aims of attempting to "control or perturb" the cycling of tumor cells in a fashion that permits their ultimate removal via cellular death, with a minimum of trauma to the host.
C1 [Newman, David J.; Cragg, Gordon M.] NCI, Nat Prod Branch, Bethesda, MD 20892 USA.
   [Holbeck, Susan] NCI, Informat Technol Branch, Bethesda, MD 20892 USA.
   [Sausville, Edward A.] NCI, Off Associate Director, Dev Therapeut Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Newman, DJ (reprint author), NCI, Nat Prod Branch, Fairview Ctr, Suite 206,POB B, Frederick, MD 21702 USA.
EM newmand@mail.nih.gov
NR 195
TC 91
Z9 96
U1 0
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2002
VL 2
IS 4
BP 279
EP 308
DI 10.2174/1568009023333791
PG 30
WC Oncology
SC Oncology
GA V33XX
UT WOS:000209052600001
PM 12470208
ER

PT J
AU Williams, ML
   Wainer, IW
AF Williams, ML
   Wainer, IW
TI Genotype/phenotype comparisons: A probe for the effect of disease
   progression on drug metabolism
SO CURRENT OPINION IN DRUG DISCOVERY & DEVELOPMENT
LA English
DT Review
DE advanced disease; cancer; CYP2C19; genotype; HIV plus /AIDS;
   N-acetyltransferase-2; phenotype
ID CANCER CACHECTIC FACTOR; CYTOCHROME-P-450 ENZYMES; NUTRITIONAL SUPPORT;
   POSITIVE PATIENTS; HUMAN LIVER; PHENOTYPE; CYTOCHROMES-P450;
   ACETYLATION; INFECTION; CACHEXIA
AB The effect of disease state on drug metabolism has been investigated using the relationship between genotype and metabolic phenotype. The two polymorphic probes, N-acetyltransferases-2 (NAT2) and cytochrome P450 2C19 (CYP2C19), were respectively used in HIV+/AIDS patients and patients with advanced cancer. The results of the studies suggest that advanced disease produces discordances between genotype and phenotype, indicating a reduction in the metabolic capabilities of these individuals. Thus, polymorphic enzymes such as CYP2C19 and NAT2 can be used to probe changes in drug-metabolizing enzyme capacities. The development of genotype/phenotype discordances should reflect general changes in metabolic capabilities and, thus, alterations in the activities of other important enzymes such as CYP3A. The data also suggest that the genotype/phenotype probes can be used to optimize the clinical treatment of patients with advanced disease states.
C1 Univ Leicester, Dept Oncol, Leicester LE1 9HN, Leics, England.
   NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Williams, ML (reprint author), Univ Leicester, Dept Oncol, Hodgkin Bldg,POB 138,Lancaster Rd, Leicester LE1 9HN, Leics, England.
NR 34
TC 4
Z9 4
U1 0
U2 1
PU CURRENT DRUGS LTD
PI LONDON
PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1P 6LB, ENGLAND
SN 1367-6733
J9 CURR OPIN DRUG DI DE
JI Curr. Opin. Drug Discov. Dev.
PD JAN
PY 2002
VL 5
IS 1
BP 144
EP 149
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 646TC
UT WOS:000181049500015
PM 11865668
ER

PT J
AU Langford, CA
AF Langford, CA
TI Systemic vasculitis: new insights and emerging issues
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Editorial Material
C1 NIAID, Immunol Dis Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Langford, CA (reprint author), NIAID, Immunol Dis Sect, Immunoregulat Lab, NIH, Bldg 10,Room 11B-13, Bethesda, MD 20892 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8711
J9 CURR OPIN RHEUMATOL
JI CURR. OPIN. RHEUMATOL.
PD JAN
PY 2002
VL 14
IS 1
BP 1
EP 2
DI 10.1097/00002281-200201000-00001
PG 2
WC Rheumatology
SC Rheumatology
GA 507PE
UT WOS:000173036200001
ER

PT J
AU Langford, CA
   Kerr, GS
AF Langford, CA
   Kerr, GS
TI Pregnancy in vasculitis
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Review
ID HENOCH-SCHONLEIN PURPURA; CHURG-STRAUSS-SYNDROME;
   WEGENERS-GRANULOMATOSIS; TAKAYASUS-DISEASE; IMMUNOSUPPRESSIVE DRUGS;
   POLYARTERITIS-NODOSA; MANAGEMENT; ARTERITIS; STENOSIS; HISTORY
AB Little is known about pregnancy in patients with vasculitis because of the nature of these diseases and the potential for infertility to occur from effective treatments. However, with the expanding armamentarium of therapeutic options that do not affect reproductive function, it is anticipated that more vasculitis patients will entertain the possibility of conception and consider the outcomes of pregnancy. Relevant issues include the effects of the vasculitis on pregnancy, the effects of the pregnancy on vasculitic disease activity, and the impact of medications used during the peripartum period. Although available data are limited and fall short in many regards, there is support for successful outcomes of pregnancy when conception occurs in disease remission. Maternal and fetal outcome is optimized by the establishment of a multidisciplinary team that can provide preconception evaluation and counseling followed by frequent monitoring throughout the pregnancy and the postpartum period. Curr Opin Rheumatol 2002, 14:36-41 (C) 2002 Lippincott Williams & Wilkins, Inc.
C1 NIAID, Immunol Dis Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
   Georgetown Univ Hosp, Washington, DC 20007 USA.
   Vet Adm Med Ctr, Dept Rheumatol, Washington, DC 20422 USA.
RP Langford, CA (reprint author), NIAID, Immunol Dis Sect, Immunoregulat Lab, NIH, Bldg 10,Room 11B-13, Bethesda, MD 20892 USA.
NR 42
TC 16
Z9 16
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8711
J9 CURR OPIN RHEUMATOL
JI CURR. OPIN. RHEUMATOL.
PD JAN
PY 2002
VL 14
IS 1
BP 36
EP 41
DI 10.1097/00002281-200201000-00007
PG 6
WC Rheumatology
SC Rheumatology
GA 507PE
UT WOS:000173036200007
PM 11790994
ER

PT J
AU Anderson, WF
   Umar, A
   Viner, JL
   Hawk, ET
AF Anderson, WF
   Umar, A
   Viner, JL
   Hawk, ET
TI The role of cyclooxygenase inhibitors in cancer prevention
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; FAMILIAL ADENOMATOUS POLYPOSIS;
   HUMAN COLON-CANCER; RANDOMIZED CONTROLLED TRIAL; SQUAMOUS-CELL
   CARCINOMA; HUMAN GASTRIC-CARCINOMA; ABERRANT CRYPT FOCI; FEMALE A/J
   MICE; PROLIFERATOR-ACTIVATED RECEPTORS; SPORADIC COLORECTAL ADENOMAS
AB Carcinogenesis results from the long-term accumulation of genetic and epigenetic aberrations at the molecular level, which are under constant selection pressure for growth advantage. Recognizing that cancer is the result of this long-term, multi-step process provides opportunities for molecularly targeted cancer prevention. Ideally, chemopreventive agents should be low in toxicity, morbidity, and cost. Several individual agents and agent combinations are currently under evaluation in the U.S. National Cancer Institute's (NCI) chemoprevention agent development program. Nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX) -1 and -2 are among the most promising classes of agents for targeted molecular prevention.
C1 NCI, Div Canc Prevent, Gastrointestinal & Other Canc Res Grp, EPN, Bethesda, MD 20892 USA.
RP Hawk, ET (reprint author), NCI, Div Canc Prevent, Gastrointestinal & Other Canc Res Grp, EPN, Room 2141,6130 Execut Blvd, Bethesda, MD 20892 USA.
NR 338
TC 51
Z9 52
U1 0
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 12
BP 1035
EP 1062
DI 10.2174/1381612023394935
PG 28
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 546HV
UT WOS:000175269400003
PM 11945150
ER

PT J
AU Altaha, R
   Fojo, T
   Reed, E
   Abraham, J
AF Altaha, R
   Fojo, T
   Reed, E
   Abraham, J
TI Epothilones: A novel class of non-taxane microtubule-stabilizing agents
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID CYCLE-DEPENDENT CHANGES; PHASE-II TRIAL; DYNAMIC INSTABILITY; PACLITAXEL
   TAXOL(R); INDIVIDUAL MICROTUBULES; BIOLOGICAL EVALUATION;
   SORANGIUM-CELLULOSUM; DESOXYEPOTHILONE-B; ANTITUMOR AGENT;
   OVARIAN-CANCER
AB The epothilones are a novel class of non-taxane microtubuic-stabilizing agents obtained from the fermentation of the cellulose degrading myxobacteria, Sorangium cellulosum. Preclinical studies have shown that the epothilones are more potent than the taxanes and active in some taxane-resistant models. Similar to paclitaxel and other taxanes, the epothilones block cells in mitosis, resulting in cell death. The chief components of the fermentation process are epothilones A and B, with epothilones C and D found in smaller amounts. Trace amounts of other epothilones have also been detected. Pre-clinical studies have shown that epothilone B is the most active form, exhibiting significantly higher antitumor activity than paclitaxel and docetaxel. Several phase I and phase It clinical trials are ongoing with epothilone B and BMS 247550, an epothilone B analog. Preliminary reports indicate these agents are active against human cancers in heavily pretreated patients. The epothilones appear to be well tolerated, with a side effect profile that is similar to that reported with the taxanes. This article will review some basic aspects of epothilone chemistry and biology, and pre-clinical and preliminary clinical experience with epothilone B and its analog, BMS 247550.
C1 W Virginia Univ, Robert C Byrd Hlth Sci Ctr, Mary Babb Randolph Canc Ctr, Hematol Oncol Sect, Morgantown, WV 26506 USA.
   NCI, Med Branch, Bethesda, MD 20892 USA.
RP Abraham, J (reprint author), W Virginia Univ, Robert C Byrd Hlth Sci Ctr, Mary Babb Randolph Canc Ctr, Hematol Oncol Sect, POB 9162, Morgantown, WV 26506 USA.
NR 51
TC 44
Z9 48
U1 0
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 19
BP 1707
EP 1712
DI 10.2174/1381612023394043
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 578EF
UT WOS:000177103900004
PM 12171542
ER

PT J
AU Milenic, DE
AF Milenic, DE
TI Monoclonal antibody-based therapy strategies: Providing options for the
   cancer patient
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID ENZYME PRODRUG THERAPY; METASTATIC BREAST-CANCER;
   ALPHA-PARTICLE-EMITTER; PHASE-II TRIAL; COLON-CARCINOMA XENOGRAFTS;
   STEM-CELL TRANSPLANTATION; ACTIVATED KILLER-CELLS;
   NON-HODGKINS-LYMPHOMA; SITE-SPECIFIC LINKAGE; LONG-TERM SURVIVAL
AB Treatment of patients with unconjugated MAb such as rituximab (Rituxan) the anti-CD20 MAb or trastuzumab (Herceptin) the anti-Her2 MAb, have shown efficacy in clinical trials and have gained approval from the Food and Drug Administration (FDA) has a result. Likewise, an anti-CD33 MAb conjugated with the antibiotic calicheamicin (Mylotarg) has proven efficacious in the treatment of patients with acute myeloid leukemia and has also been approved by the FDA. This overview presents some of the monoclonal antibody (MAb)-guided strategies with a focus on some of the experiences reported for MAb evaluated in clinical trials.
C1 NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Milenic, DE (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, NIH, 10 Ctr Dr MSC-1002,Bldg 10,Rm B3B69, Bethesda, MD 20892 USA.
NR 162
TC 37
Z9 40
U1 1
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 19
BP 1749
EP 1764
DI 10.2174/1381612023393963
PG 16
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 578EF
UT WOS:000177103900008
PM 12171546
ER

PT J
AU Friedman, EJ
AF Friedman, EJ
TI Immune modulation by ionizing radiation and its implications for cancer
   immunotherapy
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID INTERCELLULAR-ADHESION MOLECULE-1; T-CELL TOLERANCE; ANTIGEN-PRESENTING
   CELLS; LOCAL TUMOR-IRRADIATION; HUMAN ENDOTHELIAL-CELLS; HUMAN
   CERVICAL-CANCER; DOUBLE-STRANDED-RNA; HISTOCOMPATIBILITY
   COMPLEX-MOLECULES; VECTOR-DRIVEN HYPEREXPRESSION; DAMAGE-INDUCED
   APOPTOSIS
AB Ionizing radiation exhibits immunomodulatory properties, which could portend a future collaboration of cancer immunotherapy with radiation therapy. The "danger" model of immunity describes antigen-specific cellular immunity engendered by an inflammatory milieu. Dendritic cells (DCs) are attracted to this microenvironment, undergoing maturation after internalizing apoptotic and necrotic cellular debris. Mature DCs mediate antigen-specific cellular immunity via presentation of processed antigen to T cells. Administration of radiation has been utilized in vitro and in vivo to create an inflammatory setting, via induction of apoptosis, necrosis, cell surface molecules, and secretory molecules. Caspase-mediated cellular apoptosis is induced by radiation through multiple signaling pathways. Radiation upregulates expression of immunomodulatory surface molecules (MHC, costimulatory molecules, adhesion molecules, death receptors, heat shock proteins) and secretory molecules (cytokines, inflammatory mediators) in tumor, stromal, and vascular endothelial cells. Results of animal studies indicate possible radiation-mediated modulation of tumor antigen-specific immunity. Experimental data could indicate that the radiation-induced "danger" microenvironment engenders a DC-mediated antigen-specific immune response. Further enhancement of radiation-mediated inflammation and cell death can be achieved via administration of radiosensitizing pharmaceuticals. Radiation-mediated immune modulation currently remains unquantified and poorly understood. A major research effort will be required to elucidate mechanisms of action. With a thorough understanding of this phenomenon, we believe that ionizing radiation could be optimized for use with cancer vaccines and generate turner antigen-specific cellular immunity.
C1 NCI, Radiat Oncol Branch, Radiat Oncol Sci Program, NIH, Bethesda, MD 20892 USA.
RP Friedman, EJ (reprint author), NCI, Radiat Oncol Branch, Radiat Oncol Sci Program, NIH, Bldg 10,Rm B3b69, Bethesda, MD 20892 USA.
EM EF68K@NIH.GOV
NR 227
TC 152
Z9 164
U1 1
U2 6
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 19
BP 1765
EP 1780
DI 10.2174/1381612023394089
PG 16
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 578EF
UT WOS:000177103900009
PM 12171547
ER

PT J
AU Dancey, JE
AF Dancey, JE
TI Agents targeting Ras signaling pathway
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Ras pathway; inhibitors; oligonucleotides; farnesyl transferase
ID FARNESYL-PROTEIN TRANSFERASE; PHASE-I TRIAL; PRECLINICAL
   ANTITUMOR-ACTIVITY; FARNESYLTRANSFERASE INHIBITOR SCH66336; CONTINUOUS
   INTRAVENOUS-INFUSION; ADVANCED SOLID TUMORS; ISIS-5132 CGP 69846A; MAP
   KINASE PATHWAY; ANTISENSE OLIGONUCLEOTIDE; ADVANCED CANCER
AB Ras genes encode proteins that activate in an intracellular signaling network controlling differentiation, proliferation and cell survival. Mutated Ras oncogenes encoding proteins that are constitutively active can induce malignancies in a variety of laboratory models. In human malignancies, Ras mutations are common, having been identified in approximately 30% of cancers. Given the importance of Ras and downstream targets Raf and MEK in the development of malignancies and their frequent expression in human cancers, it is not surprising that a variety of agents disrupting signaling through Ras and downstream proteins are under development. These agents can be broadly classified structurally as small molecules and anti-sense oligonucleotides. They can be characterized functionally as those inhibiting Ras protein expression such as the oligodeoxynucleotide ISIS 2503, those inhibiting Ras processing, in particular the farnesyl transferase inhibitors R1 15777, SCH 66336 and BMS 214662, and those inhibiting downstream effectors Raf, such as ISIS 5132 and MEK, which is inhibited by CI-1040. The purpose of this review is to highlight recent advances in the development of these agents.
C1 NCI, Canc Therapy Evaluat Program, Rockville, MD 20852 USA.
RP Dancey, JE (reprint author), NCI, Canc Therapy Evaluat Program, 6130 Execut blvd,EPN 7131, Rockville, MD 20852 USA.
NR 63
TC 28
Z9 29
U1 0
U2 1
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 25
BP 2259
EP 2267
DI 10.2174/1381612023393071
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 602GY
UT WOS:000178498600006
PM 12369854
ER

PT J
AU Moro, S
   Jacobson, KA
AF Moro, S
   Jacobson, KA
TI Molecular modeling as a tool to investigate molecular recognition in P2Y
   receptors
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID PROTEIN-COUPLED RECEPTORS; SITE-DIRECTED MUTAGENESIS;
   THYROTROPIN-RELEASING-HORMONE; EXTRACELLULAR LOOPS; LIGAND RECOGNITION;
   ANTAGONIST BINDING; ADENYLYL-CYCLASE; PHOSPHOLIPASE-C; AMINO-ACIDS;
   NUCLEOTIDE DERIVATIVES
AB Nucleotides are emerging as an ubiquitous family of extracellular signaling molecules. These effects are mediated through a specific class of plasma membrane receptors called P2 receptors that, according to the molecular structure, are further subdivided into two subfamilies: P2Y and P2X. Specifically, P2X-receptors are ligand-gated ion channels, whereas P2Y-receptors belong to the superfamily of G-protein-coupled receptors. In this review, we focus our attention to GPCRs molecular architecture, with the special emphasis on our work on the human P2Y(1) receptor. In fact, despite an enormous amount of research on the structure and function of these receptors, fundamental understanding of the molecular details of ligand/GPCR interactions remains very rudimentary. How agonist binding transforms a resting GPCR into its active form and the microscopic basis of binding site blockade by an antagonist are generally still unclear. In the absence of high-resolution structural knowledge of GPCRs, such questions only can be addressed by building models, which are tested through pharmacological and biochemical studies. In this review, we underline how different molecular modeling approaches can help the investigation of both receptor architecture and ligand/receptor molecular recognition.
C1 Univ Padua, Dept Pharmaceut Sci, Mol Modeling Sect, I-35131 Padua, Italy.
   NIDDK, Mol Recognit Sect, LBC, NIH, Bethesda, MD USA.
RP Moro, S (reprint author), Univ Padua, Dept Pharmaceut Sci, Mol Modeling Sect, Via Marzolo 5, I-35131 Padua, Italy.
RI Moro, Stefano/A-2979-2012; Jacobson, Kenneth/A-1530-2009
OI Moro, Stefano/0000-0002-7514-3802; Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [Z01 DK031126-01]
NR 68
TC 18
Z9 18
U1 0
U2 0
PU BENTHAM SCIENCE PUBL LTD
PI HILVERSUM
PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2002
VL 8
IS 26
BP 2401
EP 2413
DI 10.2174/1381612023392892
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 612EP
UT WOS:000179061800008
PM 12369952
ER

PT J
AU Sueyoshi, T
   Moore, R
   Pascussi, JM
   Negishi, M
AF Sueyoshi, T
   Moore, R
   Pascussi, JM
   Negishi, M
TI Direct expression of fluorescent protein-tagged nuclear receptor CAR in
   mouse liver
SO CYTOCHROME P450, PT C
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID CYTOCHROME-P450 GENES; CYP2B GENE; TRANSLOCATION; INDUCTION
C1 NIEHS, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Sueyoshi, T (reprint author), NIEHS, Lab Reprod & Dev Toxicol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
RI pascussi, jean marc/F-9311-2013
NR 10
TC 15
Z9 16
U1 0
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 357
BP 205
EP 213
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BV53H
UT WOS:000179269200021
PM 12424912
ER

PT J
AU Prades, C
   Arnould, I
   Annilo, T
   Shulenin, S
   Chen, ZQ
   Orosco, L
   Triunfol, M
   Devaud, C
   Maintoux-Larois, C
   Lafargue, C
   Lemoine, C
   Denefle, P
   Rosier, M
   Dean, M
AF Prades, C
   Arnould, I
   Annilo, T
   Shulenin, S
   Chen, ZQ
   Orosco, L
   Triunfol, M
   Devaud, C
   Maintoux-Larois, C
   Lafargue, C
   Lemoine, C
   Denefle, P
   Rosier, M
   Dean, M
TI The human ATP binding cassette gene ABCA13, located on chromosome
   7p12.3, encodes a 5058 amino acid protein with an extracellular domain
   encoded in part by a 4.8-kb conserved exon
SO CYTOGENETIC AND GENOME RESEARCH
LA English
DT Article
ID RECESSIVE RETINITIS-PIGMENTOSA; STARGARDT-DISEASE; TANGIER-DISEASE;
   TRANSPORTER GENE; ABCR; MUTATIONS; SEQUENCE; IDENTIFICATION;
   SUPERFAMILY; DEFICIENCY
AB The ABCA subfamily of ATP-binding cassette (ABC) transporters includes eleven members to date. In this study, we describe a new, unusually large gene on chromosome 7p12.3, ABCA13. This gene spans over 450 kb and is split into 62 exons. The predicted ABCA13 protein consists of 5,058 amino acid residues making it the largest ABC protein described to date. Like the other ABCA subfamily members, ABCA13 contains a hydrophobic, predicted transmembrane segment at the N-terminus, followed by a large hydrophilic region. In the case of ABCA13, the hydrophilic region is unexpectedly large, more than 3,500 amino acids, encoded by 30 exons, two of which are 4.8 and 1.7 kb in length. These two large exons are adjacent to each other and are conserved in the mouse Abca13 gene. Tissue profiling of the major transcript reveals the highest expression in human trachea, testis, and bone marrow. The expression of the gene was also determined in 60 tumor cell lines and the highest expression was detected in the SR leukemia, SNB-19 CNS tumor and DU-145 prostate tumor cell lines. ABCA13 has high similarity with other ABCA subfamily genes which are associated with human inherited diseases: ABCA 1 with the cholesterol transport disorders Tangier disease and familial hypoalphalipoproteinemia, and ABCA4 with several retinal degeneration disorders. The ABCA 13 gene maps to chromosome 7p12.3, a region that contains an inherited disorder affecting the pancreas (Shwachman-Diamond syndrome) as well as a locus involved in T-cell tumor invasion and metastasis (INM7), and therefore is a positional candidate for these pathologies. Copyright (C) 2002 S. Karger AG, Basel.
C1 NCI Frederick, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA.
   NCI Frederick, Intramural Res & Support Program, SAIC Frederick, Frederick, MD 21702 USA.
   Aventis Pharma SA, Funct Genom, Vitry Sur Seine, France.
   Ist Pediat, Mexico City, DF, Mexico.
   Aventis Pharmaceut, Evry, France.
RP Dean, M (reprint author), NCI Frederick, Human Genet Sect, Lab Genom Divers, Bld 560,Rm 21-18, Frederick, MD 21702 USA.
RI Dean, Michael/G-8172-2012; Annilo, Tarmo/J-2900-2013
OI Dean, Michael/0000-0003-2234-0631; Annilo, Tarmo/0000-0002-9588-3058
FU NCI NIH HHS [N01-CO-12400]
NR 26
TC 18
Z9 21
U1 1
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1424-8581
J9 CYTOGENET GENOME RES
JI Cytogenet. Genome Res.
PY 2002
VL 98
IS 2-3
BP 160
EP 168
DI 10.1159/000069852
PG 9
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 671PD
UT WOS:000182472500006
PM 12697998
ER

PT J
AU Annilo, T
   Shulenin, S
   Chen, ZQ
   Arnould, I
   Prades, C
   Lemoine, C
   Maintoux-Larois, C
   Devaud, C
   Dean, M
   Denefle, P
   Rosier, M
AF Annilo, T
   Shulenin, S
   Chen, ZQ
   Arnould, I
   Prades, C
   Lemoine, C
   Maintoux-Larois, C
   Devaud, C
   Dean, M
   Denefle, P
   Rosier, M
TI Identification and characterization of a novel ABCA subfamily member,
   ABCA12, located in the lamellar ichthyosis region on 2q34
SO CYTOGENETIC AND GENOME RESEARCH
LA English
DT Article
ID BINDING CASSETTE TRANSPORTER-1; CAUSE PSEUDOXANTHOMA ELASTICUM; DISEASE
   GENE ABCR; TANGIER-DISEASE; STARGARDT-DISEASE; CHROMOSOME 2Q33-35;
   MEMBRANE-PROTEIN; II CELLS; MUTATIONS; SEQUENCE
AB The ABCA subfamily of ABC transporters includes ten members to date. In this study, we describe an additional gene, ABCA12. Four full-length cDNA sequences have been obtained from human placenta that contain two different polyadenylation sites and two splicing forms, coding for ABCA12 isoforms of 2,595 and 2,516 amino acid residues. Both isoforms are predicted to have two ATP-binding domains (nucleotide binding domain, NBD) and two transmembrane (TM) domains, features shared by all other ABCA subfamily proteins. ABCA12 is most closely related to ABCA1, with an amino acid similarity of 47%. Northern blot analysis demonstrates that a 9.5-kb transcript is mainly expressed in the stomach. ABCA12 was mapped to human chromosome 2q34. Two other genes from ABCA subfamily are associated with human inherited diseases, ABCA1 with the cholesterol transport disorders Tangier disease and familial hypoalphalipoproteinemia, and ABCA4 with several retinal degeneration disorders. The ABCA12 gene is located in a region of chromosome 2q34 that harbors the genes for lamellar ichthyosis, polymorphic congenital cataract, and insulin-dependent diabetes mellitus (IDDM 13), and therefore is a positional candidate for these pathologies. Copyright (C) 2002 S. Karger AG, Basel.
C1 NCI Frederick, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA.
   NCI Frederick, Intramural Res & Support Program, SAIC Frederick, Frederick, MD 21702 USA.
   Aventis Pharma SA, Funct Genom, Vitry Sur Seine, France.
RP Dean, M (reprint author), NCI Frederick, Human Genet Sect, Lab Genom Divers, Bld 560,Rm 21-18, Frederick, MD 21702 USA.
RI Dean, Michael/G-8172-2012; Annilo, Tarmo/J-2900-2013
OI Dean, Michael/0000-0003-2234-0631; Annilo, Tarmo/0000-0002-9588-3058
FU NCI NIH HHS [N01-CO-12400]
NR 43
TC 41
Z9 45
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1424-8581
J9 CYTOGENET GENOME RES
JI Cytogenet. Genome Res.
PY 2002
VL 98
IS 2-3
BP 169
EP 176
DI 10.1159/000069811
PG 8
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 671PD
UT WOS:000182472500007
PM 12697999
ER

PT J
AU Karkera, JD
   Izraeli, S
   Roessler, E
   Dutra, A
   Kirsch, I
   Muenke, M
AF Karkera, JD
   Izraeli, S
   Roessler, E
   Dutra, A
   Kirsch, I
   Muenke, M
TI The genomic structure, chromosomal localization, and analysis of SIL as
   a candidate gene for holoprosencephaly
SO CYTOGENETIC AND GENOME RESEARCH
LA English
DT Article
ID LEFT-RIGHT ASYMMETRY; MOUSE; PATHWAYS; HEDGEHOG; SHH; HEART; ROLES
AB Holoprosencephaly (HPE) is the most common congenital malformation of the brain and face in humans. In this study we report the analysis of SIL (SCL interrupting locus) as a candidate gene for HPE. Fluorescent in situ hybridization (FISH) analysis using a BAC 246e16 confirmed the assignment of SIL to 1p32. Computational analysis of SIL at the protein level revealed a 73% overall identity between the human and murine proteins. Denaturing high performance liquid chromatography (dHPLC) techniques were used to screen for mutations and these studies identified several common polymorphisms but no disease-associated mutations, suggesting that SIL is not a common factor in HPE pathogenesis in humans. Copyright (C) 2002 S. Karger AG, Basel.
C1 NHGRI, Mol Genet Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   NHGRI, Cytogenet & Confocal Microscopy Core, NIH, Bethesda, MD 20892 USA.
RP Muenke, M (reprint author), NHGRI, Mol Genet Branch, NIH, Bldg 10-C103, Bethesda, MD 20892 USA.
NR 22
TC 16
Z9 19
U1 4
U2 5
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1424-8581
J9 CYTOGENET GENOME RES
JI Cytogenet. Genome Res.
PY 2002
VL 97
IS 1-2
BP 62
EP 67
DI 10.1159/000064057
PG 6
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 607BW
UT WOS:000178771400012
PM 12438740
ER

PT J
AU Niimi, T
   Copeland, NG
   Gilbert, DJ
   Jenkins, NA
   Srisodsai, A
   Zimonjic, DB
   Keck-Waggoner, CL
   Popescu, NC
   Kimura, S
AF Niimi, T
   Copeland, NG
   Gilbert, DJ
   Jenkins, NA
   Srisodsai, A
   Zimonjic, DB
   Keck-Waggoner, CL
   Popescu, NC
   Kimura, S
TI Cloning, expression, and chromosomal localization of the mouse gene
   (Scgb3a1, alias Ugrp2) that encodes a member of the novel
   uteroglobin-related protein gene family
SO CYTOGENETIC AND GENOME RESEARCH
LA English
DT Article
ID THYROID TRANSCRIPTION FACTOR-1; CELL-SPECIFIC EXPRESSION; LUNG
   DEVELOPMENT; LINKAGE MAP; B GENE; ASTHMA; PROMOTER; SUSCEPTIBILITY;
   TARGET
AB The mouse UGRP gene family consists of two genes, Ugrp1 and Ugrp2. In this study, the genomic structure and expression patterns of Ugrp2 and its alternative spliced form were characterized. The authentic Ugrp2 gene has three exons and two introns, similar to the Ugrp1 gene, which produces a secreted protein. The Ugrp2 variant uses a sequence located between authentic exons 1 and 2, resulting in a cytoplasmic form due to a termination codon within the inserted sequence. Both mouse and human UGRP2 mRNAs are expressed in lung. In the case of human, the mRNA is expressed at the highest level in trachea, followed by salivary gland at a level similar to lung. Weak expression was also found in fetal lung and mammary gland. Ugrp2 was mapped by fluorescence in situ hybridization to mouse chromosome 11A5-B1 and human chromosome 5q35. These regions are known to be homologous. Interspecific mouse backcross mapping was also performed to obtain further detailed localization of mouse Ugrp1 and Ugrp2.
C1 NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
   NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
   NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
RP Kimura, S (reprint author), NCI, Lab Metab, NIH, Bldg 37,Rm 3E-24, Bethesda, MD 20892 USA.
NR 29
TC 16
Z9 17
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1424-8581
J9 CYTOGENET GENOME RES
JI Cytogenet. Genome Res.
PY 2002
VL 97
IS 1-2
BP 120
EP 127
DI 10.1159/000064067
PG 8
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 607BW
UT WOS:000178771400022
PM 12438750
ER

PT B
AU Wahl, SM
   Chan, J
   Burstein, H
   Song, XY
AF Wahl, SM
   Chan, J
   Burstein, H
   Song, XY
BE Gressner, AM
   Heinrich, PC
   Matern, S
TI Cytokine modulation in the therapy of hepatic immunopathology and
   fibrosis
SO CYTOKINES IN LIVER INJURY AND REPAIR
SE FALK SYMPOSIUM
LA English
DT Proceedings Paper
CT Falk Symposium 125 on Cytokines in Liver Injury and Repair
CY SEP 30-OCT 01, 2001
CL HANNOVER, GERMANY
SP Falk Fdn
ID GROWTH-FACTOR-BETA; TNF-ALPHA THERAPY; TGF-BETA; RHEUMATOID-ARTHRITIS;
   TRANSFORMING GROWTH-FACTOR-BETA-1; GENE-TRANSFER; FIBROGENESIS;
   INHIBITION; INDUCTION; DISEASES
C1 NIDCR, NIH, Bethesda, MD 20892 USA.
RP Wahl, SM (reprint author), NIDCR, NIH, 30 Convent Dr,Blvd 30,Room 332, Bethesda, MD 20892 USA.
NR 25
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
BN 0-7923-8775-9
J9 FALK SYMP
PY 2002
VL 125
BP 279
EP 285
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA BU95H
UT WOS:000177475800023
ER

PT J
AU Weinstein, JN
   Scherf, U
   Lee, JK
   Nishizuka, S
   Gwadry, F
   Ajay
   Bussey, K
   Kim, S
   Smith, LH
   Tanabe, L
   Richman, S
   Alexander, J
   Kouros-Mehr, H
   Maunakea, A
   Reinhold, WC
AF Weinstein, JN
   Scherf, U
   Lee, JK
   Nishizuka, S
   Gwadry, F
   Ajay
   Bussey, K
   Kim, S
   Smith, LH
   Tanabe, L
   Richman, S
   Alexander, J
   Kouros-Mehr, H
   Maunakea, A
   Reinhold, WC
TI The bioinformatics of microarray gene expression profiling
SO CYTOMETRY
LA English
DT Article; Proceedings Paper
CT 3rd Samuel A Latt Conference on Genomics and Proteomics in Cancer
CY MAY 01-04, 2001
CL DETROIT, MICHIGAN
DE gene expression profiling; microarray; biochip; cDNA; oligonucleotide;
   clustering; clustered image map
ID MOLECULAR PHARMACOLOGY; DRUG-DISCOVERY; CELL-LINES; CANCER; PATTERNS;
   INFORMATION; DATABASE; DISPLAY
C1 NCI, Genom & Bioinformat Grp, Mol Pharmacol Lab, Bethesda, MD 20892 USA.
RP Weinstein, JN (reprint author), NIH, Bldg 37,Rm 4F-28,9000 Rockville Pike, Bethesda, MD 20892 USA.
OI Kim, Sohyoung/0000-0002-6140-7918; Pillai, Ajay/0000-0002-9789-7189
NR 19
TC 10
Z9 11
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PD JAN 1
PY 2002
VL 47
IS 1
BP 46
EP 49
DI 10.1002/cyto.10041
PG 4
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 507GZ
UT WOS:000173019800007
PM 11774349
ER

PT J
AU Perfetto, S
   De Rosa, S
   Koup, R
   Brittain, N
   Roederer, M
AF Perfetto, S
   De Rosa, S
   Koup, R
   Brittain, N
   Roederer, M
TI Functional characterization of hyperfine T cell subsets: Calcium
   mobilization
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 32
EP 32
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400046
ER

PT J
AU Bigos, M
   Roederer, M
   Parks, DR
AF Bigos, M
   Roederer, M
   Parks, DR
TI Methodologies for measuring absolute light collection and comparing
   sensitivities for different fluorochromes on flow cytometers
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 Gladstone Inst Virol & Immunol, San Francisco, CA USA.
   NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 46
EP 46
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400084
ER

PT J
AU Perfetto, S
   Ambrozak, D
   Koup, R
   Roederer, M
AF Perfetto, S
   Ambrozak, D
   Koup, R
   Roederer, M
TI Safety protocol for high speed sorting of viable infectious cells using
   the Aerosol Management System (AMS)
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 66
EP 66
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400144
ER

PT J
AU Scoltock, AB
   Cidlowski, JA
AF Scoltock, AB
   Cidlowski, JA
TI Evidence for protease dependent and independent signaling during UV-C
   induced apoptosis of Jurkat cells
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 75
EP 75
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400169
ER

PT J
AU Bortner, C
   Cidlowski, JA
AF Bortner, C
   Cidlowski, JA
TI Sodium uptake is required for apoptotic cell shrinkage during anti-Fas
   induced apoptosis
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIEHS, Natl Inst Hlth Signal Transduct, Res Triangle Pk, NC 27709 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 78
EP 78
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400176
ER

PT J
AU Fischer, RT
   Lipsky, PE
   Grammer, AC
AF Fischer, RT
   Lipsky, PE
   Grammer, AC
TI Activation of signaling cascades and expression of cytokines in
   tonsillar B cell subsets
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAMS, NIH, AB, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 86
EP 87
PG 2
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400203
ER

PT J
AU Marti, G
   Luning, M
   Dreyfuss, R
   Zenger, VE
   Stetler-Stevenson, M
   Rick, ME
AF Marti, G
   Luning, M
   Dreyfuss, R
   Zenger, VE
   Stetler-Stevenson, M
   Rick, ME
TI Morphometric image analysis in CLL
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 US FDA, CBER, Rockville, MD 20857 USA.
   Gustavus Adolphus Coll, St Peter, MN 56082 USA.
   NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 107
EP 107
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400267
ER

PT J
AU Roederer, M
   De Rosa, S
   Bigos, M
   Parks, DR
   Baumgarth, N
   Herzenberg, LA
   Herzenberg, LA
AF Roederer, M
   De Rosa, S
   Bigos, M
   Parks, DR
   Baumgarth, N
   Herzenberg, LA
   Herzenberg, LA
TI The state of polychromatic flow cytometry
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   Univ Calif San Francisco, Gladstone Inst Virol & Immunol, San Francisco, CA 94143 USA.
   Stanford Univ, Stanford, CA 94305 USA.
   Univ Calif Davis, Davis, CA 95616 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 122
EP 123
PG 2
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400314
ER

PT J
AU Roederer, M
AF Roederer, M
TI Spectral compensation for flow cytometry: Visualization artifacts,
   limitations, and caveats
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 122
EP 122
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400312
ER

PT J
AU Roederer, M
   Sasaki, D
   Stall, A
AF Roederer, M
   Sasaki, D
   Stall, A
TI Positive or negative? It's not just black or white
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   PharMingen Inc, Res ImmunoCytometry, San Diego, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 123
EP 123
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400315
ER

PT J
AU Telford, W
   Hawley, TS
   Hawley, RG
AF Telford, W
   Hawley, TS
   Hawley, RG
TI Analysis of violet-excited fluorochromes by flow cytometry using a
   violet diode laser
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NCI, Bethesda, MD 20892 USA.
   Amer Red Cross, Holland Lab, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 123
EP 123
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400317
ER

PT J
AU Roederer, M
   Hardy, RR
AF Roederer, M
   Hardy, RR
TI Frequency difference gating: A multivariate method for identifying
   subsets that differ between samples
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 134
EP 135
PG 2
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400352
ER

PT J
AU Roederer, M
AF Roederer, M
TI A new, highly efficient algorithm for cluster analysis
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 135
EP 135
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400354
ER

PT J
AU Roederer, M
   Moore, WA
   Treister, AS
   Hardy, RR
   Herzenberg, LA
AF Roederer, M
   Moore, WA
   Treister, AS
   Hardy, RR
   Herzenberg, LA
TI Probability binning comparison: A metric for comparing univariate or
   multivariate distributions
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAID, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   Stanford Univ, Stanford, CA 94305 USA.
   Tree State Inc, Redwood City, CA USA.
   Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 135
EP 135
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400353
ER

PT J
AU He, LS
   Wu, XL
   Fischer, RT
   Grammer, AC
   Peter, LE
AF He, LS
   Wu, XL
   Fischer, RT
   Grammer, AC
   Peter, LE
TI Flow cytometric measurement of fluorescence resonance energy transfer
   from cyan fluorescent protein to yellow fluorescent protein using
   single-laser excitation at 458 nm
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 136
EP 138
PG 3
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400358
ER

PT J
AU Lamoreaux, L
   Perfetto, S
   Koup, R
   Roederer, M
AF Lamoreaux, L
   Perfetto, S
   Koup, R
   Roederer, M
TI The reproducibility, sensitivity, carry-over, speed and ergonomic
   function of the multiwell autosampler system (MAS) using either a 96 or
   384 well format
SO CYTOMETRY
LA English
DT Meeting Abstract
C1 NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0196-4763
J9 CYTOMETRY
JI Cytometry
PY 2002
SU 11
BP 141
EP 141
PG 1
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 544VM
UT WOS:000175182400367
ER

PT J
AU van Rhee, F
   Barrett, J
AF van Rhee, F
   Barrett, J
TI Adoptive transfer of Ag-specific T cells to prevent CMV disease after
   allogeneic stem-cell transplantation
SO CYTOTHERAPY
LA English
DT Review
DE management of CMV post-allo-SCT; CMV specific T cells; adoptive
   immunotherapy
ID HUMAN CYTOMEGALOVIRUS-INFECTION; BONE-MARROW TRANSPLANTATION; LYMPHOCYTE
   CTL RESPONSE; DENDRITIC CELLS; GANCICLOVIR PROPHYLAXIS;
   PERIPHERAL-BLOOD; PROTEIN PP65; RISK-FACTORS; IMMUNODEFICIENCY-VIRUS;
   ENDOPLASMIC-RETICULUM
AB Background
   Cytomegalovirus is a major cause of infectious morbidity and mortality after allogeneic stem-cell transplantation (allo-SCT). Farmacotherapy to prevent or treat CMV reaction and infection is only partially effective, and has considerable toxicity. Adoptive transfer of ex vivo generated CMV specific T cells is a new approach to the management of Of CMV post-allo-SCT
   Methods
   A comprehensive review, of the published literature describing 1) the recovery of CMV immunity post-allo-SCT and 2) new strategies for the production of Of V specific T cells for adoptive immunotherapy.
   Results
   CMV specific T cells can be generated using a variety of systems comprising different antigen presenting cells and antigens.
   Discussion
   The ability to raise CMV specific T cells on a clinical scale will have a major impact on the management of CMV post-allo-SCT, but will have to be compared to current pharmacological approaches. Further the raising of CMV specific T cells may serve as a model, to generate other antigen specific T cells including other anti-viral and anti-tumor T cells.
C1 Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
   NHLBI, Hematol Branch, NIH, Bethesda, MD USA.
RP van Rhee, F (reprint author), Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, 4301 W Markham,Slot 776, Little Rock, AR 72205 USA.
NR 62
TC 6
Z9 6
U1 0
U2 0
PU TAYLOR & FRANCIS AS
PI OSLO
PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY
SN 1465-3249
J9 CYTOTHERAPY
JI Cytotherapy
PY 2002
VL 4
IS 1
BP 3
EP 10
PG 8
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
   Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
   & Experimental Medicine
GA 541MJ
UT WOS:000174988100002
PM 11953036
ER

PT J
AU Hensel, N
   Melenhorst, JJ
   Bradstock, K
   Schwarer, AP
   Eniafe, R
   Nakamura, R
   Barrett, AJ
AF Hensel, N
   Melenhorst, JJ
   Bradstock, K
   Schwarer, AP
   Eniafe, R
   Nakamura, R
   Barrett, AJ
TI Flow cytometric quantitation and characterization of the T-lymphocyte
   memory response to CMV in healthy donors
SO CYTOTHERAPY
LA English
DT Article
DE cytomegalovirus; CMV; intracellular cytokine; TNF-alpha;
   interferon-gamma; lymphocyte
ID MARROW TRANSPLANTATION; CYTOKINE EXPRESSION; CYTOMEGALOVIRUS; CELL;
   ANTIGEN; FREQUENCIES; BLOOD; VIRUS; INFECTION; IMMUNITY
AB Background
   Levels of circulating Of V Ag-specific lymphocytes determine CMV reactivation risk in immunocompromised individuals.
   Methods
   Frequencies of T cells producing cytokines after stimulation by CMV Ag were measured in hematopoietic stem-cell donors using flow cytometry.
   Results
   In seropositive individuals (n = 75) the mean number of CD8(+) (CD8(bright), CD8(dim)) and CD4(+) cells producing IFN-gamma was respectively 3.1% (12.6 /muL) and 0.38% (3.2/muL), over 10-fold higher than in seronegative subjects (n = 22). CMV stimulation induced tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in both CD4(+) and CD8(+) cells (usually together), with a shift from memory- to effector-cell phenotype, while only a small proportion of CD4(+) cells produced IL-4. Although the normal range was wide, neither age, sex nor HLA type affected the frequency.
   Discussion
   These quantitative studies and the recognition of CD4(+) cells as potential effectors of CMV immunity are of relevance for immunotherapeutic approaches to prevent CMV disease after stem-cell transplantation.
C1 NHLBI, Hematol Branch, Stem Cell Transplantat Sect, NIH, Bethesda, MD 20892 USA.
   Westmead Hosp, Dept Haematol, Blood & Marrow Transplant Serv, Westmead, NSW, Australia.
   Alfred Hosp, Bone Marrow Transplant Programme, Melbourne, Vic, Australia.
RP Hensel, N (reprint author), NHLBI, Hematol Branch, Stem Cell Transplantat Sect, NIH, Bldg 10,Room 7C103,9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 24
TC 17
Z9 17
U1 0
U2 0
PU TAYLOR & FRANCIS AS
PI OSLO
PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY
SN 1465-3249
J9 CYTOTHERAPY
JI Cytotherapy
PY 2002
VL 4
IS 1
BP 29
EP 40
DI 10.1080/146532402317251509
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
   Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
   & Experimental Medicine
GA 541MJ
UT WOS:000174988100005
PM 11953039
ER

PT J
AU Wong, ECC
   Lee, SM
   Hines, K
   Lee, J
   Carter, CS
   Kopp, W
   Bender, J
   Read, EJ
AF Wong, ECC
   Lee, SM
   Hines, K
   Lee, J
   Carter, CS
   Kopp, W
   Bender, J
   Read, EJ
TI Development of a closed-system process for clinical-scale generation of
   DCs: evaluation of two monocyte-enrichment methods and two culture
   containers
SO CYTOTHERAPY
LA English
DT Article
DE dendritic cells; cancer immunotherapy; elutriation; immunomagnetic
   selection
ID FUNCTIONAL DENDRITIC CELLS; PERIPHERAL-BLOOD MONOCYTES;
   ANTIGEN-PRESENTING CELLS; EX-VIVO GENERATION; IN-VITRO;
   INTERFERON-ALPHA; LARGE NUMBERS; VACCINATION; LEUKAPHERESIS; IMMUNITY
AB Background
   Clinical immunotherapy trials using DCs depend on large-scale methods for DC generation that fulfil current good manufacturing practice requirements. Our goal was to develop data on two variables monocyte-enrichment method and culture container, which could be used to design a closed-system process for ex vivo generation of immature DCs.
   Methods
   Mononuclear cells were collected by leukapheresis and enriched for monocytes by either counterflow centrifugal elutriation, or immunomagnetic selection using Isolex, an automated closed-system device. Monocytes were cultured for 7 days in serum-free medium with GM-CSF and IL-4, using either plastic flasks or gas-permeable Stericell bags. Monocytes and cultured DCs were evaluated for yield flow cytometric phenotype, and in vitro function in MLR, and autologous recall responses to tetanus toxoid and influenza virus.
   Results
   Enriched monocyte products from elutriation and immunomagnetic selection were equivalent in yield and purity, and were capable of generating immature DCs in either flasks or bags. DCs from all jour culture conditions were equivalent in yield, phenotype, and in vitro function. Mean DC yield was 67-80% per seeding monocyte, and 11-13% per starting mononuclear cell (MNC). A leukapheresis product containing 5 x 10(9) MNCs processed by this method could therefore yield approximately 5 x 10(8) immature DCs.
   Discussion
   In this manufacturing process, the Isolex system was equivalent to elutriation,and Stericell bags were equivalent to flasks. Together, the Isolex system and Stericell bags can be incorporated into a closed-system process to generate immature DCs.
C1 NIH, Warren G Magnuson Clin Ctr, Dept Transfus Med, Bethesda, MD 20892 USA.
   Nexell Therapeut Inc, Irvine, CA USA.
   SAIC, Frederick, MD USA.
RP Read, EJ (reprint author), NIH, Warren G Magnuson Clin Ctr, Dept Transfus Med, Bldg 10,Rm 1C711, Bethesda, MD 20892 USA.
FU NCI NIH HHS [N01-CO-56000]
NR 23
TC 31
Z9 32
U1 0
U2 0
PU TAYLOR & FRANCIS AS
PI OSLO
PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY
SN 1465-3249
J9 CYTOTHERAPY
JI Cytotherapy
PY 2002
VL 4
IS 1
BP 65
EP 76
DI 10.1080/146532402317251545
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
   Biology; Hematology; Medicine, Research & Experimental
SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research
   & Experimental Medicine
GA 541MJ
UT WOS:000174988100009
PM 11953043
ER

PT J
AU Edwards, E
   Kitt, C
   Oliver, E
   Finkelstein, J
   Wagster, M
   McDonald, WM
AF Edwards, E
   Kitt, C
   Oliver, E
   Finkelstein, J
   Wagster, M
   McDonald, WM
TI Depression and Parkinson's disease: A new look at an old problem
SO DEPRESSION AND ANXIETY
LA English
DT Article
ID BASAL GANGLIA; IMPAIRMENT; DEMENTIA; DISABILITY; CIRCUITRY; FEATURES;
   SYMPTOMS
AB A National Institutes of Health (National Institute of Neurological Disorders and Stroke; National Institute of Mental Health; National Institute on Aging) working group meeting focused on the non-motor aspects of Parkinson's disease (PD). Below is the summary of the meeting presentations and recommendations for a research agenda on the epidemiology, assessment, circuitry, therapeutic approaches, and clinical trials of Parkinson's disease co-morbid with depression. A second summary will focus on PD and dementia. (C) 2002 Wiley-Liss, Inc.
C1 Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30329 USA.
   NINDS, Bethesda, MD 20892 USA.
   NIA, Bethesda, MD 20892 USA.
RP McDonald, WM (reprint author), Emory Univ, Dept Psychiat & Behav Sci, 1841 Clifton Rd NE, Atlanta, GA 30329 USA.
NR 40
TC 22
Z9 23
U1 0
U2 2
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PY 2002
VL 16
IS 1
BP 39
EP 48
DI 10.1002/da.10057
PG 10
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 588LQ
UT WOS:000177703300004
PM 12203670
ER

PT J
AU Denicoff, KD
   Ali, SO
   Sollinger, AB
   Smith-Jackson, EE
   Leverich, GS
   Post, RM
AF Denicoff, KD
   Ali, SO
   Sollinger, AB
   Smith-Jackson, EE
   Leverich, GS
   Post, RM
TI Utility of the daily prospective National Institute of Mental Health
   Life-Chart Method (NIMH-LCM-p) ratings in clinical trials of bipolar
   disorder
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE bipolar disorder; clinical global impressions scale; Life Chart Method;
   global ratings
ID AFFECTIVE-ILLNESS; WORKSHOP REPORT; SCALE; CARBAMAZEPINE; RELIABILITY;
   TOLERANCE; VALIDITY; LITHIUM
AB This study investigated the assets of the daily prospective National Institute of Mental Health Life-Chart Method (NIMH-LCM-p or LCM-p) for use in clinical trials in bipolar disorder. Fifty-two outpatients, who met DSM-III-R criteria for bipolar disorder, were randomly assigned in a double-blind design to an intended 1 year of treatment with lithium or carbamazepine, a crossover to the opposite drug in the second year; and theca to a combination of both agents in the third year. For each patient, the LCM-p was initiated upon admission and was continued on a daily basis. Overall therapeutic effect for each phase (intended year) was assessed by using the Clinical Global Impressions-Bipolar Version (CGI-BP) scale. Kruskal-Wallis analysis of variance was used to examine the detailed course-of-illness variables derived from the LCM-p (e.g., percentage of time ill, average severity of illness, episodes per year, and mood switches per year) in relation to the global assessments of treatment response (CGI-BP). Most of the individual LCM-p-derived illness variables varied significantly (P < .05) as a function of global treatment response. Since global ratings of the degree of improvement can represent very different proportions of improvement in percentage of time ill, average severity of mania or depression, or. frequency of manic and depressive episodes, the LCM-p provides the basis for a comprehensive description of both the illness course and the response to treatment. The LCM-p appears to have considerable utility in clinical trials of pharmacological and other interventions of bipolar disorder. It provides a detailed characterization of the severity, frequency, and duration of manic and depressive episodes, which facilitates the assessment of global improvement and allows for the quantification of separate components of the illness, which are or are not responsive to a given treatment. (C) 2002 Wiley-Liss, Inc.
C1 NIMH, Sect Psychobiol, Biol Psychiat Branch, NIH, Bethesda, MD 20892 USA.
RP Denicoff, KD (reprint author), NIMH, Sect Psychobiol, Biol Psychiat Branch, NIH, Bldg 10,Room 3S239,9000 Rockville Pike, Bethesda, MD 20892 USA.
OI Ali, Syed/0000-0003-3131-3299
NR 33
TC 26
Z9 26
U1 2
U2 5
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PY 2002
VL 15
IS 1
BP 1
EP 9
DI 10.1002/da.1078
PG 9
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 522TC
UT WOS:000173912200001
PM 11816046
ER

PT J
AU Goodwin, RD
   Hamilton, SP
   Milne, BJ
   Pine, DS
AF Goodwin, RD
   Hamilton, SP
   Milne, BJ
   Pine, DS
TI Generalizability and correlates of clinically derived panic subtypes in
   the population
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE panic attacks; epidemiology; comorbidity; anxiety; prevalence; subtype;
   psychopathology; dyspnea; early-onset; agoraphobia
ID NATIONAL-COMORBIDITY-SURVEY; EARLY-ONSET; DEPRESSION COMORBIDITY;
   PSYCHIATRIC-DISORDERS; FAMILIAL AGGREGATION; SOCIAL MORBIDITY;
   UNITED-STATES; CO-MORBIDITY; ATTACKS; LIFETIME
AB To determine the generalizability and population-based correlates of clinically derived panic attack subtypes among adults in the community. Data were drawn from the National Comorbidity Survey (n = 8,098), a representative sample of adults of age 18-54 years in the United States. Sociodemographic characteristics, psychiatric comorbidity, and panic symptomotology associated with three clinically derived panic subtypes (early-onset, agoraphobia, and dyspnea) were compared using two-way ANOVA and multivariate logistic regression analyses. Among those with panic attacks in the community, 51.2% bad early-onset, 32.6% bad agoraphobia, and 64.4% bad dysthymia. Significant differences in sociodemographic characteristics, psychiatric comorbidity, and panic symptomotology emerged between the three groups. Early-onset panic was associated with significantly increased likelihood of bipolar disorder and substance dependence but was not distinguished from the other two subtypes by panic symptoms. Panic attack with agoraphobia was associated with significantly higher odds of several comorbid anxiety disorders, and panic with dyspnea was more common among married females with less education and high levels of comorbid alcohol and depressive disorders. These data suggest that clinically derived panic subtypes are generalizable and may be associated with several unique sociodemographic and psychiatric correlates in the general population. Observed differences between these subtypes may influence results from clinical samples. (C) 2002 Wiley-Liss, Inc.
C1 Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA.
   Columbia Univ, Coll Phys & Surg, Dept Epidemiol, New York, NY USA.
   Dunedin Sch Med, Dept Social & Prevent Med, Dunedin, New Zealand.
   Natl Inst Mental Hlth, Bethesda, MD USA.
RP Goodwin, RD (reprint author), 1051 Riverside Dr,Unit 43, New York, NY 10032 USA.
OI Hamilton, Steven/0000-0001-8106-6260
NR 33
TC 18
Z9 19
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PY 2002
VL 15
IS 2
BP 69
EP 74
DI 10.1002/da.10023
PG 6
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 532PQ
UT WOS:000174484600004
PM 11891996
ER

PT J
AU Yu, XB
   Shacka, JJ
   Eells, JB
   Suarez-Quian, C
   Przygodzki, RM
   Beleslin-Cokic, B
   Lin, CS
   Nikodem, VM
   Hempstead, B
   Flanders, KC
   Costantini, F
   Noguchi, CT
AF Yu, XB
   Shacka, JJ
   Eells, JB
   Suarez-Quian, C
   Przygodzki, RM
   Beleslin-Cokic, B
   Lin, CS
   Nikodem, VM
   Hempstead, B
   Flanders, KC
   Costantini, F
   Noguchi, CT
TI Erythropoietin receptor signalling is required for normal brain
   development
SO DEVELOPMENT
LA English
DT Article
DE erythropoietin; receptor; brain; heart; development; neural progenitor
   cells; mouse
ID CELL-DEATH; ENDOTHELIAL-CELLS; IN-VIVO; BCL-X; DEPENDENT PRODUCTION;
   GENE-EXPRESSION; NERVOUS-SYSTEM; MESSENGER-RNA; MOUSE EMBRYOS; C-KIT
AB Erythropoietin, known for its role in erythroid differentiation, has been shown to be neuroprotective during brain ischaemia in adult animal models. Although high levels of erythropoietin receptor are produced in embryonic brain, the role of erythropoietin during brain development is uncertain. We now provide evidence that erythropoietin acts to stimulate neural progenitor cells and to prevent apoptosis in the embryonic brain. Mice lacking the erythropoietin receptor exhibit severe anaemia and defective cardiac development, and die at embryonic day 13.5 (E13.5). By E12.5, in addition to apoptosis in foetal liver, endocardium and myocardium, the erythropoietin receptor null mouse shows extensive apoptosis in foetal brain. Lack of erythropoietin receptor affects brain development as early as E10.5, resulting in a reduction in the number of neural progenitor cells and increased apoptosis. Corresponding in vitro cultures of cortical cells from Epor(-/-) mice also exhibited decreases in neuron generation compared with normal controls and increased sensitivity to low oxygen tension with no surviving neurons in Epor(-/-) cortical cultures after 24 hour exposure to hypoxia. The viability of primary Epor(+/+) rodent embryonic cortical neurons was further increased by erythropoietin stimulation. Exposure of these cultures to hypoxia induced erythropoietin expression and a tenfold increase in erythropoietin receptor expression, increased cell survival and decreased apoptosis. Cultures of neuronal progenitor cells also exhibited a proliferative response to erythropoietin stimulation. These data demonstrate that the neuroprotective activity of erythropoietin is observed as early as E10.5 in the developing brain, and that induction of erythropoietin and its receptor by hypoxia may contribute to selective cell survival in the brain.
C1 NIDDK, Biol Chem Lab, NIH, Bethesda, MD 20892 USA.
   NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Lab Cell Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA.
   Georgetown Univ, Sch Med, Dept Cell Biol, Washington, DC 20007 USA.
   Armed Forces Inst Pathol, Washington, DC 20306 USA.
   Columbia Univ, Dept Genet & Dev, New York, NY 10032 USA.
   Cornell Univ, Coll Med, New York, NY 10021 USA.
RP Noguchi, CT (reprint author), NIDDK, Biol Chem Lab, NIH, Bethesda, MD 20892 USA.
OI Eells, Jeffrey/0000-0002-6381-1666; Przygodzki,
   Ronald/0000-0002-1238-262X
NR 54
TC 220
Z9 237
U1 1
U2 6
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
   CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD JAN
PY 2002
VL 129
IS 2
BP 505
EP 516
PG 12
WC Developmental Biology
SC Developmental Biology
GA 520BB
UT WOS:000173759100021
PM 11807041
ER

PT J
AU Morton, DG
   Shakes, DC
   Nugent, S
   Dichoso, D
   Wang, WF
   Golden, A
   Kemphues, KJ
AF Morton, DG
   Shakes, DC
   Nugent, S
   Dichoso, D
   Wang, WF
   Golden, A
   Kemphues, KJ
TI The Caenorhabditis elegans par-5 gene encodes a 14-3-3 protein required
   for cellular asymmetry in the early embryo
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE par-5; 14-3-3; Caenorhabditis elegans; asymmetry; polarity
ID ANTERIOR-POSTERIOR AXIS; C-ELEGANS; KINASE-C; CYTOPLASMIC LOCALIZATION;
   GERMLINE SPECIFICATION; ANTEROPOSTERIOR AXIS; MAMMALIAN HOMOLOG;
   POLARITY; POLARIZATION; GRANULES
AB The establishment of anterior-posterior polarity in the Caenorhabditis elegans embryo requires the activity of the maternally expressed par genes. We report the identification and analysis of a new par gene, par-5. We show that par-5 is required for asynchrony and asymmetry in the first embryonic cell divisions, normal pseudocleavage, normal cleavage spindle orientation at the two-cell stage, and localization of P granules and MEX-5 during the first and subsequent cell cycles. Furthermore, par-5 activity is required in the first cell cycle for the asymmetric cortical localization of PAR-1 and PAR-2 to the posterior, and PAR-3, PAR-6, and PKC-3 to the anterior. When PAR-5 is reduced by mutation or by RNA interference, these proteins spread around the cortex of the one-cell embryo and partially overlap. We have shown by sequence analysis of par-5 mutants and by RNA interference that the par-5 gene is the same as the ftt-1 gene, and encodes a 14-3-3 protein. The PAR-5 14-3-3 protein is present in,gonads, oocytes, and early embryos, but is not asymmetrically distributed. Our analysis indicates that the par-5 14-3-3 gene plays a crucial role in the early events leading to polarization of the C. elegans zygote. (C) 2001 Elsevier Science.
C1 Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
   Univ Houston, Dept Biol, Houston, TX 77204 USA.
   Coll William & Mary, Dept Biol, Williamsburg, VA 23187 USA.
   NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Kemphues, KJ (reprint author), Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
FU NICHD NIH HHS [HD27689]; NIGMS NIH HHS [GM33763]
NR 65
TC 108
Z9 129
U1 0
U2 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD JAN 1
PY 2002
VL 241
IS 1
BP 47
EP 58
DI 10.1006/dbio.2001.0489
PG 12
WC Developmental Biology
SC Developmental Biology
GA 513YV
UT WOS:000173409600004
PM 11784094
ER

PT J
AU Bonifacino, JS
AF Bonifacino, JS
TI Quality control of receptor-kinase signaling complexes
SO DEVELOPMENTAL CELL
LA English
DT Editorial Material
ID ERYTHROPOIETIN RECEPTOR; ACTIVATION
AB The erythropoietin receptor transduces signals leading to the growth, differentiation, and survival of red blood cell precursors via interaction with Janus kinase 2 (JAK2). This interaction was thought to occur only at the plasma membrane. Recent evidence, however, shows that JAK2 assembles with newly synthesized erythropoietin receptors in the endoplasmic reticulum, and that this assembly is essential for efficient expression of the receptors at the cell surface.
C1 NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA.
RP Bonifacino, JS (reprint author), NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA.
OI Bonifacino, Juan S./0000-0002-5673-6370
NR 6
TC 8
Z9 8
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 1100 MASSACHUSETTS AVE,, CAMBRIDGE, MA 02138 USA
SN 1534-5807
J9 DEV CELL
JI Dev. Cell
PD JAN
PY 2002
VL 2
IS 1
BP 1
EP 2
DI 10.1016/S1534-5807(01)00114-9
PG 2
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 546XP
UT WOS:000175301900001
PM 11782306
ER

PT J
AU Bhanumathy, CD
   Tang, Y
   Monga, SPS
   Katuri, V
   Cox, JA
   Mishra, B
   Mishra, L
AF Bhanumathy, CD
   Tang, Y
   Monga, SPS
   Katuri, V
   Cox, JA
   Mishra, B
   Mishra, L
TI Itih-4, a serine protease inhibitor regulated in interleukin-6-dependent
   liver formation: Role in liver development and regeneration
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE ITIH-4; hyaluronic acid binding; ontogeny; liver regeneration; IL-6
ID ALPHA-TRYPSIN INHIBITOR; CHAIN-RELATED PROTEIN; HEPATOCYTE
   GROWTH-FACTOR; HUMAN-PLASMA; HEAVY-CHAIN; EXTRACELLULAR-MATRIX;
   DNA-SYNTHESIS; IN-VITRO; FAMILY; CELLS
AB Inter-alpha -trypsin inhibitor-4 (Itih-4) is a liver-restricted member of the serine protease inhibitor family with diverse functions as an anti-apoptotic and matrix stabilizing molecule that are important throughout development. We investigate the functional role of Itih-4 in liver formation, regeneration (LR) and examine its role in calcium and hyaluronic acid binding. Itih-4 expression is prominent in early liver development at E9 and later at E16 being restricted to hepatoblasts, immature hepatocytes, and differentiated hepatocytes. We note a marked and differential increase in Itih-4 labeling in proliferating hepatocytes, compared with bile duct cells in liver explant cultures treated with interleukin-6 (IL-6). After partial hepatectomy, maximal Itih-4 expression occurs in a bimodal manner at 30 min and at 12 hr, with a predominant centrizonal distribution. There is no detectable binding of glutathione transferase-fusion Itih-4 protein to calcium and hyaluronic acid, indicating a possible requirement for posttranslational modifications for these functions. These results suggest that in LR, Itih-4 expression corresponds to that of immediate early genes and may contribute to the entry of normally quiescent hepatocytes into the early stages of the cell cycle. The markedly high expression of Itih-4 in early liver development and in explants treated with IL-6 suggests a prominent role for Itih-4 at key points in liver formation. (C) 2002 Wiley-Liss, Inc.
C1 Temple Univ, Fels Inst Canc Res & Mol Biol, Lab Gastrointestinal Dev Mol Biol, Philadelphia, PA 19140 USA.
   DVAMC, Washington, DC USA.
   Univ Geneva, Dept Biochem, CH-1211 Geneva, Switzerland.
   NHGRI, Clin Gene Therapy Branch, NIH, Bethesda, MD 20892 USA.
RP Mishra, L (reprint author), Temple Univ, Fels Inst Canc Res & Mol Biol, Lab Gastrointestinal Dev Mol Biol, 3307 N Broad St, Philadelphia, PA 19140 USA.
FU NIDDK NIH HHS [1R01DK58637, 1R01 DK56111, 1R03 DK53861]
NR 60
TC 21
Z9 23
U1 0
U2 4
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD JAN
PY 2002
VL 223
IS 1
BP 59
EP 69
DI 10.1002/dvdy.1235
PG 11
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 507PP
UT WOS:000173037100019
PM 11803570
ER

PT J
AU Lee, ET
   Welty, TK
   Cowan, LD
   Wang, WY
   Rhoades, DA
   Devereux, R
   Go, O
   Fabsitz, R
   Howard, BV
AF Lee, ET
   Welty, TK
   Cowan, LD
   Wang, WY
   Rhoades, DA
   Devereux, R
   Go, O
   Fabsitz, R
   Howard, BV
TI Incidence of diabetes in American Indians of three geographic areas -
   The Strong Heart Study
SO DIABETES CARE
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; PIMA-INDIANS; RISK-FACTORS; MELLITUS; NIDDM;
   PREVALENCE; ADULTS; PROGRESSION; NAURUANS; WEIGHT
AB OBJECTIVE - To estimate incidence rates of diabetes and associated risk factors among participants of the Strong Heart Study.
   RESEARCH DESIGN AND METHODS - Of the 4,549 Strong Heart Study participants examined at baseline, 3,638 returned for a similar examination after an average of 4 years. The 1985 World Health Organization criteria for diabetes were used to identify new diabetes cases. Rates of diabetes among participants who did not have diabetes at baseline examination were determined. The relationships between the incidence rates of diabetes and a number of risk factors measured at baseline examination were studied.
   RESULTS - Significant variables associated with the development of diabetes included triglycerides, obesity, fasting plasma glucose, insulin, and degree of American Indian blood among participants With NGT at baseline. For those with IGT at baseline, significant predictors included fasting plasma glucose, 2-h glucose, BMI, degree of American Indian blood, and albuminuria.
   CONCLUSIONS - The high incidence rates found in this study were alarming. To slow down the rapid increase of this disease in the American Indian population, preventive programs must be designed and implemented. Patients with IGT should be treated with diabetes medication or put on a rigid weight-reduction program to reduce the risk of progression to diabetes.
C1 Univ Oklahoma, Hlth Sci Ctr, Coll Publ Hlth, Ctr Amer Indian Hlth Res, Oklahoma City, OK 73190 USA.
   Aberdeen Area Tribal Chairmens Hlth Board, Aberdeen, SD USA.
   Univ Oklahoma, Hlth Sci Ctr, Dept Biostat & Epidemiol, Coll Publ Hlth, Norman, OK 73019 USA.
   Univ Colorado, Boulder, CO 80309 USA.
   Cornell Univ, Med Ctr, New York, NY 14853 USA.
   NHLBI, Bethesda, MD 20892 USA.
   MedStar Res Inst, Washington, DC USA.
RP Lee, ET (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Publ Hlth, Ctr Amer Indian Hlth Res, POB 26901, Oklahoma City, OK 73190 USA.
FU NHLBI NIH HHS [U01 HL-41642, U01 HL-41652, U01 HL-41654]
NR 27
TC 52
Z9 54
U1 0
U2 3
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD JAN
PY 2002
VL 25
IS 1
BP 49
EP 54
DI 10.2337/diacare.25.1.49
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 507PM
UT WOS:000173036900009
PM 11772900
ER

PT J
AU Dolan, NC
   Liu, K
   Criqui, MH
   Greenland, P
   Guralnik, JM
   Chan, CL
   Schneider, JR
   Mandapat, AL
   Martin, G
   McDermott, MM
AF Dolan, NC
   Liu, K
   Criqui, MH
   Greenland, P
   Guralnik, JM
   Chan, CL
   Schneider, JR
   Mandapat, AL
   Martin, G
   McDermott, MM
TI Peripheral artery disease, diabetes, and reduced lower extremity
   functioning
SO DIABETES CARE
LA English
DT Article
ID ANKLE-BRACHIAL INDEX; SUBSEQUENT DISABILITY; PHYSICAL-DISABILITY;
   CALCIFICATION; ASSOCIATION; PREDICTOR; PRESSURES; MELLITUS; HEALTH; FOOT
AB OBJECTIVE - To characterize lower extremity function and dysfunction in peripheral artery disease (PAD) patients with and without diabetes.
   RESEARCH DESIGN AND METHODS - in this cross-sectional study, 460 men and women with PAD (147 with diabetes) were recruited from three academic medical centers. Assessments included ankle brachial index (ABI), neuropathy score, 6-min walk distance 4-m walking velocity, Walking Impairment Questionnaire (0-100 scale, 100 = best), and summary performance score (SPS) (0-12 scale, 12 = best).
   RESULTS - The mean ABI was similar in PAD patients with and without diabetes. PAD patients with diabetes were younger, had a higher BMI, had a worse neuropathy score, and had a greater number of cardiovascular comorbidities compared with those without diabetes. Participants with diabetes were less likely to report classical symptoms of intermittent claudication and more likely to report exertional leg pain, which sometimes started at rest. After adjusting for age, those with diabetes had a shorter mean 6-min walk distance (1,040 vs. 1,168 feet, P < 0.001), slower fast-pace 4-m walk velocity (0.83 vs. 0.90 m/sec, P < 0.001), and a lower SPS (7.3 vs. 8.6, P < 0.001) than those without diabetes. Patients with diet-controlled diabetes performed better than those on diabetes medications. Differences in lower extremity functioning between patients with and without diabetes were largely attenuated but not abolished for SPS and fast-pace 4-m walk velocity after adjustment for type of exertional leg pain, neuropathy score, and number of cardiovascular comorbidities.
   CONCLUSIONS - Subjects with PAD and diabetes have poorer lower extremity function than those with PAD alone. This difference in functioning appears to be largely explained by diabetes-associated neuropathy, differences in exertional leg symptoms, and greater cardiovascular disease in patients with diabetes.
C1 Northwestern Univ, Sch Med, Dept Med, Chicago, IL 60611 USA.
   Northwestern Univ, Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
   Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
   NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA.
   Northwestern Univ, Sch Med, Div Vasc Surg, Dept Surg, Chicago, IL 60611 USA.
   Northwestern Univ, Evanston Hosp, Dept Surg, Div Vasc Surg, Evanston, IL 60201 USA.
RP Dolan, NC (reprint author), Northwestern Univ, Sch Med, Dept Med, 675 N St Clair,Suite 18-200, Chicago, IL 60611 USA.
FU NCRR NIH HHS [RR-00048]; PHS HHS [R01-58099]
NR 31
TC 86
Z9 96
U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD JAN
PY 2002
VL 25
IS 1
BP 113
EP 120
DI 10.2337/diacare.25.1.113
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 507PM
UT WOS:000173036900020
PM 11772911
ER

PT J
AU Fetsch, PA
   Simsir, A
   Brosky, K
   Abati, A
AF Fetsch, PA
   Simsir, A
   Brosky, K
   Abati, A
TI Comparison of three commonly used cytologic preparations in effusion
   immunocytochemistry
SO DIAGNOSTIC CYTOPATHOLOGY
LA English
DT Article; Proceedings Paper
CT 90th Annual Meeting of the
   United-States-and-Canadian-Academy-of-Pathology
CY MAR 03-09, 2001
CL ATLANTA, GEORGIA
SP US & Canadian Acad Pathol
DE effusion; immunocytochemistry; cell block; cytospin; ThinPrep
ID MALIGNANT MESOTHELIOMA; E-CADHERIN; DIFFERENTIAL-DIAGNOSIS; SEROUS
   EFFUSIONS; N-CADHERIN; ADENOCARCINOMA; THINPREP(R); CALRETININ; CELLS;
   SPECIMENS
AB Discrepant results in effusion immunocytochemistry are often, the result of specimen processing. Smears, cytospins, cell blocks, and, monolayer preparations have all been used in various published studies; thus, there is no consistency in the immunostaining process for cytology to compare with the surgical pathology "gold standard" results.
   We sought to evaluate optimal specimen preparation for the immunostaining of effusion samples. Fourteen reactive,and 15 malignant effusion samples (various epithelial/inesothelial neoplasms) were each prepared in three forms: air-dried cytospins (postfixed in ethanol), formalin -fixed, paraffin -embedded cell blocks, and liquid-based thin-layer (ThinPrep(TM), CYTYC, Boxborough, MA) processing. All slides were immunostained with antibodies commonly used in effusion cytology: HBME-1, calretinin, E-cadherin, BerEP4, B72.3, LeuM1, and CA19-9.
   Cytospin and ThinPrep samples performed in a similar manner: high background staining it-as encountered in 66% of cases, most evident in three-dimensional clusters of cells. In addition, membrane staining patterns were difficult to interpret. Cell blocks provided the best milieu for morphologic interpretation, with less background staining (only 17% of Cases) and results that most closely approximated those reported in the surgical pathology literature. The cost per test for cell block immunocytochemistry was also the most economical for our laboratory. Published 2002 Wiley-Liss. Inc.(dagger).
C1 NCI, Cytopathol Sect, NIH, Bethesda, MD 20892 USA.
RP Abati, A (reprint author), NCI, Cytopathol Sect, NIH, Bldg 10,Room 2A19, Bethesda, MD 20892 USA.
NR 31
TC 50
Z9 65
U1 1
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 8755-1039
J9 DIAGN CYTOPATHOL
JI Diagn. Cytopathol.
PD JAN
PY 2002
VL 26
IS 1
BP 61
EP 66
DI 10.1002/dc.10039
PG 6
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA 507ZT
UT WOS:000173062100015
PM 11782091
ER

PT J
AU Preiss, JC
   Faiss, S
   Loddenkemper, C
   Zeitz, M
   Duchmann, R
AF Preiss, JC
   Faiss, S
   Loddenkemper, C
   Zeitz, M
   Duchmann, R
TI Pancreatic panniculitis in an 88-year-old man with neuroendocrine
   carcinoma
SO DIGESTION
LA English
DT Article
DE case report; panniculitis; pancreas; neuroendocrine carcinoma;
   histology; pathophysiology; octreotide
ID FAT NECROSIS; SYSTEMIC LUPUS; PATIENT
AB Pancreatic panniculitis is a rare complication that occurs in 0.3-3% of patients with pancreatic diseases. Most of the cases reported to date were associated with adenocarcinoma and acute or chronic pancreatitis. We here present an 88-year-old man who was admitted to our institution with a nonfunctional neuroendocrine carcinoma of the pancreas. He subsequently developed pancreatic panniculitis and arthritis. Treatment with octreotide did not have an effect neither on progression of the carcinoma nor on development of new skin lesions. Two months after the diagnosis of pancreatic panniculitis had been made, the patient died from progressing carcinoma. A review of the literature shows that there is no congruent hypothesis for the pathogenesis of pancreatic panniculitis. Vascular damage seems to induce lipolysis by pancreatic enzymes. This eventually leads to fat necrosis. The diversity of disorders that can go along with pancreatic panniculitis suggests an unspecific damage of pancreatic tissue as a first step in the chain of events. Copyright (C) 2002 S. Karger AG, Basel.
C1 NIAID, Mucosal Immun Sect, Clin Invest Lab, NIH, Bethesda, MD 20892 USA.
   Free Univ Berlin, Med Dept Gastroenterol Infect Dis & Rheumatol 1, Klinikum Benjamin Franklin, D-1000 Berlin, Germany.
   Free Univ Berlin, Inst Pathol, Klinikum Benjamin Franklin, D-1000 Berlin, Germany.
RP Preiss, JC (reprint author), NIAID, Mucosal Immun Sect, Clin Invest Lab, NIH, Bldg 10,Room 11N238, Bethesda, MD 20892 USA.
NR 23
TC 24
Z9 24
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0012-2823
J9 DIGESTION
JI Digestion
PY 2002
VL 66
IS 3
BP 193
EP 196
DI 10.1159/000066758
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 637UY
UT WOS:000180533200008
PM 12481166
ER

PT J
AU Srivastava, S
AF Srivastava, S
TI The Early Detection Research Network Second Annual Scientific Workshop -
   14-16 October 2001, Seattle, Washington, USA - Foreword
SO DISEASE MARKERS
LA English
DT Editorial Material
C1 NCI, Div Canc Prevent, Canc Biomarkers Res Grp, NIH, Bethesda, MD 20892 USA.
RP Srivastava, S (reprint author), NCI, Div Canc Prevent, Canc Biomarkers Res Grp, NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0278-0240
J9 DIS MARKERS
JI Dis. Markers
PY 2002
VL 18
IS 1
BP 1
EP 1
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA 549GD
UT WOS:000175435400001
ER

PT J
AU Srivastava, S
   Wagner, JA
AF Srivastava, S
   Wagner, JA
TI Surrogate endpoints in medicine - Foreword
SO DISEASE MARKERS
LA English
DT Editorial Material
C1 NCI, Div Canc Prevent, Canc Biomarkers Res Grp, Bethesda, MD 20892 USA.
   Merck Res Labs, Dept Clin Pharmacol, Rahway, NJ USA.
RP Srivastava, S (reprint author), NCI, Div Canc Prevent, Canc Biomarkers Res Grp, 6130 Execut Plaza N,Suite 3142, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0278-0240
J9 DIS MARKERS
JI Dis. Markers
PY 2002
VL 18
IS 2
BP 39
EP 40
PG 2
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA 612CH
UT WOS:000179056300001
ER

PT J
AU Zullo, SJ
   Srivastava, S
   Looney, JP
   Barker, PE
AF Zullo, SJ
   Srivastava, S
   Looney, JP
   Barker, PE
TI Nanotechnology: Emerging developments and early detection of cancer - A
   two-day workshop sponsored by the National Cancer Institute and the
   National Institute of Standards and Technology, August 30-31 2001, on
   the National Institute of Standards and Technology Campus, Gaithersburg,
   MD, USA
SO DISEASE MARKERS
LA English
DT Editorial Material
DE biomarker; cancer detection; nanotechnology; high throughput;
   microarray; mitochondria
AB A recent meeting jointly sponsored by the National Cancer Institute (NCI) and National Institute of Standards and Technology (NIST) brought together researchers active in nanotechnology and cancer molecular biology to discuss and evaluate the interface between disciplines.', Emerging areas where nanotechnologies may impact cancer prevention and early cancer detection were elaborated by key researchers who catalyzed interdisciplinary dialogue aimed at fostering. cross-discipline communications and future collaboration.
C1 NIST, Chem & Life Sci Div, Adv Technol Program, Gaithersburg, MD 20899 USA.
   NCI, Canc Biomarkers Res Grp, Div Canc Prevent, Bethesda, MD 20892 USA.
   NIST, Program Off, Gaithersburg, MD 20899 USA.
   NIST, NCI, Biomarkers Validat Lab, DNA Technol Grp,Biotechnol Div, Gaithersburg, MD 20899 USA.
RP Zullo, SJ (reprint author), NIST, Chem & Life Sci Div, Adv Technol Program, Gaithersburg, MD 20899 USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0278-0240
J9 DIS MARKERS
JI Dis. Markers
PY 2002
VL 18
IS 4
BP 153
EP 158
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA 666LN
UT WOS:000182178900001
PM 12590168
ER

PT J
AU Croft, BY
AF Croft, BY
TI Special issue: Functional Imaging of Early Markers of Disease - Forword
SO DISEASE MARKERS
LA English
DT Editorial Material
C1 NCI, Biomed Imaging Program, NIH, Rockville, MD 20852 USA.
RP Croft, BY (reprint author), NCI, Biomed Imaging Program, NIH, Rockville, MD 20852 USA.
RI Croft, Barbara/D-1248-2013
OI Croft, Barbara/0000-0003-2544-150X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0278-0240
J9 DIS MARKERS
JI Dis. Markers
PY 2002
VL 18
IS 5-6
BP 207
EP 209
PG 3
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA 761QP
UT WOS:000187919700001
ER

PT J
AU Croft, BY
AF Croft, BY
TI Animal models for imaging
SO DISEASE MARKERS
LA English
DT Article
ID GREEN FLUORESCENT PROTEIN; IN-VIVO; COMPUTED-TOMOGRAPHY;
   GENE-EXPRESSION; CONTRAST AGENT; TUMOR-GROWTH; MRI; MICE; ANGIOGENESIS;
   METASTASIS
AB Animal models can be used in the study of disease. This chapter discusses imaging animal models to elucidate the process of human disease. The mouse is used as the primary model. Though this choice simplifies many research choices, it necessitates compromises for in vivo imaging. In the future, we can expect improvements in both animal models and imaging techniques.
C1 NCI, Biomed Imaging Program, NIH, Bethesda, MD 20892 USA.
RP Croft, BY (reprint author), NCI, Biomed Imaging Program, NIH, 6130 Execut Blvd,EPN 6064, Bethesda, MD 20892 USA.
EM croftb@mail.nih.gov
RI Croft, Barbara/D-1248-2013
OI Croft, Barbara/0000-0003-2544-150X
NR 33
TC 11
Z9 11
U1 0
U2 0
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 0278-0240
J9 DIS MARKERS
JI Dis. Markers
PY 2002
VL 18
IS 5-6
BP 365
EP 374
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA 761QP
UT WOS:000187919700008
PM 14646045
ER

PT J
AU Kitanaka, J
   Kitanaka, N
   Takemura, M
   Wang, XB
   Hembree, CM
   Goodman, NL
   Uhl, GR
AF Kitanaka, J
   Kitanaka, N
   Takemura, M
   Wang, XB
   Hembree, CM
   Goodman, NL
   Uhl, GR
TI Isolation and Sequencing of a putative promoter region of the murine G
   protein beta 1 subunit (GNB1) gene
SO DNA SEQUENCE
LA English
DT Article
DE GTP-binding protein beta 1 subunit gene; psychostimulation;
   pschostimulant-regulated gene; promoter sequence
ID NF-KAPPA-B; PREFRONTAL CORTEX; RAT-BRAIN; EXPRESSION; COCAINE;
   SENSITIZATION; AMPHETAMINE; CDNA
AB The expression of the heterotrimeric GTP-binding protein beta1 subunit gene (GNB1) is regulated by psychostimulants such as cocaine and amphetamines. Since the up-regulation appears to be one of the candidate processes of sensitization, it is necessary to elucidate the cellular and molecular mechanism of the GNB1 gene regulation for a better understanding the establishment of sensitization. In the present study, we describe the isolation and nucleotide sequence analysis of the GNB1 gene promoter region. We have isolated approximately 10kb of the 5'-flanking region of the mouse of GNB1 gene and found potential elements involved in putative transcriptional control of the GNB1 such as AP1, AP2, Sp1, cyclic AMP response element, and nuclear factor kappaB recognition sites, within the sequences 0.3 kb upstream from the putative transcription start site. This region was highly rich in G + C content, but lacked TATA or CATT boxes. Comparing the nucleotide sequence of the cDNA clone with the human genome databases using the BLAST program a region containing putative exon 1 and promoter of the human GNB1 gene in chromosome 1 was found. The cloning and sequence analysis of an extensive portion of the 5-flanking regulatory region of the GNB1 gene provides new insights into the factors involved in the regulation by psychostimulants of GNB1 expression.
C1 Hyogo Med Univ, Dept Pharmacol, Nishinomiya, Hyogo 6638501, Japan.
   NIDA, Mol Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
   Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
RP Kitanaka, J (reprint author), Hyogo Med Univ, Dept Pharmacol, 1-1 Mukogawa Cho, Nishinomiya, Hyogo 6638501, Japan.
NR 22
TC 6
Z9 6
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1042-5179
J9 DNA SEQUENCE
JI DNA Seq.
PY 2002
VL 13
IS 1
BP 39
EP 45
DI 10.1080/10425170290019883
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 559CW
UT WOS:000176008400006
PM 12180136
ER

PT S
AU Theodore, WH
   Gaillard, WD
AF Theodore, WH
   Gaillard, WD
BE Sutula, T
   Pitkanen, A
TI Neuroirnaging and the progression of epilepsy
SO DO SEIZURES DAMAGE THE BRAIN
SE PERSPECTIVES IN ANALYTICAL PHILOSOPHY
LA English
DT Article; Proceedings Paper
CT Workshop on Do Seizures Damage the Brain
CY JUN 27-JUL 01, 2001
CL ROVANIEMI, FINLAND
ID TEMPORAL-LOBE EPILEPSY; COMPLEX PARTIAL SEIZURES; POSITRON EMISSION
   TOMOGRAPHY; RESONANCE-IMAGING EVIDENCE; DIAGNOSED PARTIAL SEIZURES;
   FEBRILE SEIZURES; HIPPOCAMPAL ATROPHY; FOLLOW-UP; GLUCOSE-METABOLISM;
   KAINIC ACID
AB Several lines of evidence can be used to try to answer the question of whether epilepsy is a progressive disease, and whether persistent seizures, or the underlying process itself, cause neuronal injury. The results of clinical studies have been inconclusive. Neuroimaging studies offer a quantitative approach. In patients with temporal lobe epilepsy, structural magnetic resonance imaging (MRI) has shown volume reductions ipsilateral to the epileptic focus in hippocampal and extrahippocampal regions; the former, in cross-sectional studies, increase with increasing epilepsy duration. Other factors associated with increasing hippocampal atrophy include a history of complex or prolonged febrile seizures, and generalized tonic-clonic seizure number. Positron emission tomography (PET) has shown supporting results. However, these studies have been cross-sectional rather than longitudinal. Preliminary results from prospective imaging studies using fluorodeoxyglucose PET and volumetric MRI show that patients with more recent seizure onset are less likely to have hypometabolism or volume loss than those with a long history of epilepsy. Alternate interpretations of these data include a possible progressive effect of epilepsy, or a tendency for patients with structural or functional findings at seizure onset to be more likely to develop uncontrolled epilepsy. In addition to the human studies that have been performed, parallel investigations in animal models using some of the same imaging techniques may help to unravel the factors associated with neuronal injury due to seizures, and aid in interpreting results of clinical studies.
C1 NIH, Clin Epidemiol Sect, Bethesda, MD 20892 USA.
RP Theodore, WH (reprint author), NIH, Clin Epidemiol Sect, Bldg 10,Room 5N-250, Bethesda, MD 20892 USA.
NR 58
TC 28
Z9 29
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0079-6123
BN 0-444-50814-7
J9 PROG BRAIN RES
PY 2002
VL 135
BP 305
EP 313
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA BW09B
UT WOS:000180831700026
PM 12143351
ER

PT S
AU Thoma, GR
   Ford, G
   Le, D
   Li, ZR
AF Thoma, GR
   Ford, G
   Le, D
   Li, ZR
BE Lopresti, EP
   Hu, J
   Kashi, R
TI Text verification in an automated system for the extraction of
   bibliographic data
SO DOCUMENT ANALYSIS SYSTEM V, PROCEEDINGS
SE LECTURE NOTES IN COMPUTER SCIENCE
LA English
DT Article; Proceedings Paper
CT 5th International Workshop on Document Analysis Systems
CY AUG 19-21, 2002
CL PRINCETON, NEW JERSEY
SP Avaya Inc
ID DOCUMENT IMAGES
AB An essential stage in any text extraction system is the manual verification of the printed material converted by OCR. This proves to be the most labor-intensive step in the process. In a system built and deployed at the National Library of Medicine to automatically extract bibliographic data from scanned biomedical journals, alternative means were considered to validate the text. This paper describes two approaches and gives preliminary performance data.
C1 Natl Lib Med, Bethesda, MD 20894 USA.
RP Thoma, GR (reprint author), Natl Lib Med, Bethesda, MD 20894 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0302-9743
BN 3-540-44068-2
J9 LECT NOTES COMPUT SC
PY 2002
VL 2423
BP 423
EP 432
PG 10
WC Computer Science, Information Systems; Computer Science,
   Interdisciplinary Applications; Computer Science, Theory & Methods
SC Computer Science
GA BY01S
UT WOS:000187252700046
ER

PT S
AU Thoma, GR
   Ford, G
AF Thoma, GR
   Ford, G
BE Kantor, PB
   Kanungo, T
   Zhou, J
TI Automated data entry system: performance issues
SO DOCUMENT RECOGNITION AND RETRIEVAL IX
SE Proceedings of SPIE
LA English
DT Proceedings Paper
CT Conference on Document Recognition and Retrieval IX
CY JAN 21-22, 2002
CL SAN JOSE, CA
SP SPIE, Soc Imaging Sci & Technol
DE automated data entry; MEDLINE; system performance; scanning; document
   image analysis
AB This paper discusses the performance of a system for extracting bibliographic fields from scanned pages in biomedical journals to populate MEDLINES(R), the flagship database of the National Library of Medicine (NLM), and heavily used worldwide. This system consists of automated processes to extract the article title, author names, affiliations and abstract, and manual workstations for the entry of other required fields such as pagination, grant support information, databank accession numbers and others needed for a completed bibliographic record in MEDLINE. Labor and time data are given for (1) a wholly manual keyboarding process to create the records, (2) an OCR-based system that requires all fields except the abstract to be manually input, and (3) a more automated system that relies on document image analysis and understanding techniques for the extraction of several fields. It is shown that this last, most automated, approach requires less than 25% of the labor effort in the first, manual, process.
C1 Natl Lib Med, Bethesda, MD 20894 USA.
RP Natl Lib Med, Bethesda, MD 20894 USA.
NR 11
TC 1
Z9 2
U1 0
U2 0
PU SPIE-INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA
SN 0277-786X
BN 0-8194-4410-3
J9 PROC SPIE
PY 2002
VL 4670
BP 181
EP 190
PG 10
WC Computer Science, Artificial Intelligence; Imaging Science &
   Photographic Technology
SC Computer Science; Imaging Science & Photographic Technology
GA BU25H
UT WOS:000175476600020
ER

PT J
AU Herning, RI
   Tate, K
   Better, W
   Cadet, JL
AF Herning, RI
   Tate, K
   Better, W
   Cadet, JL
TI Cerebral blood flow pulsatility deficits in HIV plus poly substance
   abusers: differences associated with antiviral medications
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE cocaine abuse; transcranial Doppler sonography; perfusion deficits; HIV;
   antiviral medications
ID AIDS DEMENTIA COMPLEX; IMMUNODEFICIENCY-VIRUS-INFECTION; EMISSION
   COMPUTED-TOMOGRAPHY; NITRIC-OXIDE; ANTIRETROVIRAL THERAPY; COGNITIVE
   IMPAIRMENT; OXIDATIVE STRESS; BRAIN PERFUSION; COCAINE ABUSE;
   ABNORMALITIES
AB This Study examines the influence of HIV-seropositivity and antiviral medications on cerebral blood flow in cocaine abusers. Forty-five HIV negative (HIV-) cocaine abusers, 36 HIV positive (HIV+) cocaine abusers (CD4; mean 378, +/-229) and 27 control HIV- subjects were studied. Blood flow velocity and pulsatility were determined for the anterior and middle cerebral arteries using transcranial Doppler sonography (TCD). Psychological assessments, which included the psychiatric symptom checklist (SCL-90R), hopelessness (Beck) and well-being (Ellison) questionnaires revealed greater psychiatric distress in HIV+ cocaine abusers than the other groups. HIV - cocaine abusers and HIV+ cocaine abusers not receiving antiviral medications (n = 25 of 36) had elevated pulsatility values, indicating increased resistance in the cerebral blood vessels in comparison to control subjects. HIV+ cocaine abusers using antiviral medications (n = 11 of 36) had pulsatility values similar to HIV- control subjects, Interestingly, there was no significant relationship between intensity of psychiatric distress reported by HIV+ cocaine abusers and perfusion deficits. Our findings suggest that unmedicated HIV+ cocaine abusers have cerebrovascular deficits, which are similar to HIV- cocaine abusers. In addition, the use of antiviral medications appears to be associated with a reduction of these deficits in HIV+ cocaine abusers. Nevertheless, more studies will be needed before any conclusion can be reached regarding possible beneficial effects of these agents on the cerebral vasculature. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
C1 NIDA, Mol Neuropsychiat Sect, Div Intramural Res, NIH, Baltimore, MD 21224 USA.
RP Herning, RI (reprint author), NIDA, Mol Neuropsychiat Sect, Div Intramural Res, NIH, POB 5180, Baltimore, MD 21224 USA.
NR 53
TC 3
Z9 3
U1 0
U2 5
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD JAN 1
PY 2002
VL 65
IS 2
BP 129
EP 135
DI 10.1016/S0376-8716(01)00158-2
PG 7
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 515UK
UT WOS:000173514900003
PM 11772474
ER

PT J
AU King, VL
   Stoller, KB
   Hayes, M
   Umbricht, A
   Currens, M
   Kidorf, MS
   Carter, JA
   Schwartz, R
   Brooner, RK
AF King, VL
   Stoller, KB
   Hayes, M
   Umbricht, A
   Currens, M
   Kidorf, MS
   Carter, JA
   Schwartz, R
   Brooner, RK
TI A multicenter randomized evaluation of methadone medical maintenance
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE methadone; medical maintenance; stepped care; opioid dependence
ID OPIOID ABUSERS; STEPPED CARE; FOLLOW-UP; DEPENDENCE; OUTCOMES
AB Methadone medical maintenance (MMM) is a rational, cost-effective method to match treatment intensity to level of needed services. In the present study, 73 highly stable methadone maintenance patients were randomly assigned to either a routine methadone treatment, MMM - a once monthly reporting schedule - at the methadone maintenance program or MMM at a physician office. A 'stepped care' intensified treatment approach was used for patients who had drug-positive urine specimens or failed the medication recall procedure. Patients left two urine specimens for analysis each month (at least one on a random basis) and responded to one medication recall each month. Results are presented for the first 6 months of the 1-year trial. Only 1% of urine specimens were positive for illicit drugs, there was no evidence of methadone diversion and there were very low rates of medication misuse, with no between group differences. MMM patients initiated more new employment or family/social activities than the routine care patients. MMM patients were more satisfied with their treatment than the routine treatment patients, but all patients rated themselves satisfied or very satisfied with their treatment. Stepped care was well-tolerated and helped match patients to an appropriate intensity of service. The good outcomes observed with the present sample suggest that MMM can be implemented effectively as part of a continuum of care in clinic and office-based sites. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved,
C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Behav Biol Res Ctr, Baltimore, MD 21224 USA.
   Ctr Addict Med, Baltimore, MD 21201 USA.
   NIDA, Intramural Res Program, Baltimore, MD 21224 USA.
   Friends Res Inst, Baltimore, MD 21204 USA.
   Open Soc Inst, Baltimore, MD 21201 USA.
RP King, VL (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Behav Biol Res Ctr, 5510 Nathan Shock Dr,Ste 1500, Baltimore, MD 21224 USA.
FU NIDA NIH HHS [P50 DA05273]
NR 28
TC 34
Z9 35
U1 2
U2 2
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD JAN 1
PY 2002
VL 65
IS 2
BP 137
EP 148
DI 10.1016/S0376-8716(01)00155-7
PG 12
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 515UK
UT WOS:000173514900004
PM 11772475
ER

PT J
AU Goldstein, JA
AF Goldstein, JA
TI Polymorphisms in the human CYP2C subfamily
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 9
Z9 9
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 9
BP 5
EP 5
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200009
ER

PT J
AU Gorokhov, A
   Negishi, M
   Johnson, EF
   Pedersen, LC
   Perera, L
   Darden, TA
   Pedersen, LG
AF Gorokhov, A
   Negishi, M
   Johnson, EF
   Pedersen, LC
   Perera, L
   Darden, TA
   Pedersen, LG
TI Explicit water near the catalytic I-helix THR in the predicted solution
   structure of CYP2A4
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
   NIEHS, Res Triangle Pk, NC 27709 USA.
   Scripps Res Inst, La Jolla, CA 92037 USA.
RI perera, Lalith/B-6879-2012; Pedersen, Lee/E-3405-2013
OI perera, Lalith/0000-0003-0823-1631; Pedersen, Lee/0000-0003-1262-9861
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 16
BP 8
EP 8
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200016
ER

PT J
AU Kobayashi, K
   Sueyoshi, T
   Negishi, M
AF Kobayashi, K
   Sueyoshi, T
   Negishi, M
TI Tetratricopeptide repeat (TPR)-containing protein retains car in the
   cytoplasm of HEPG2 cells
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 36
BP 18
EP 18
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200036
ER

PT J
AU Eling, T
   Baek, SJ
AF Eling, T
   Baek, SJ
TI Altered gene expression by Cox inhibitors: A novel pathway to
   anti-carcinogenesis
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 54
BP 27
EP 27
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200054
ER

PT J
AU Zeldin, DC
   Bradbury, JA
   Graves, J
   Miller, L
   DeGraff, J
   Yang, BC
   Ma, JX
AF Zeldin, DC
   Bradbury, JA
   Graves, J
   Miller, L
   DeGraff, J
   Yang, BC
   Ma, JX
TI P450 epoxygenase pathways of arachidonic acid metabolism - Information
   gleaned from transgenic and knockout mice
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 63
BP 32
EP 32
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200063
ER

PT J
AU Wang, DW
   Wang, H
   Lin, L
   Zeldin, DC
AF Wang, DW
   Wang, H
   Lin, L
   Zeldin, DC
TI Cytochrome P450 epoxygenase-eNOS interactions
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 HUST, Tongji Med Coll, Tongji Hosp, Dept Internal Med, Wuhan 430030, Peoples R China.
   NIEHS, Lab Pulm Pathol, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 66
BP 33
EP 33
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200066
ER

PT J
AU Reilly, TP
AF Reilly, TP
TI In search of susceptibility factors for idiosyncratic drug-induced liver
   injury
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NHLBI, Mol & Cellular Toxicol Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 87
BP 44
EP 44
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200087
ER

PT J
AU Bleasby, K
   Mohrenweiser, HW
   Pritchard, JB
AF Bleasby, K
   Mohrenweiser, HW
   Pritchard, JB
TI Identification of single nucleotide polymorphisms in the human organic
   anion transporter hOAT1
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
   Lawrence Livermore Natl Lab, Livermore, CA 94551 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 165
BP 83
EP 83
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200165
ER

PT J
AU Soars, MG
   Gelboin, HV
   Krausz, KW
   Riley, RJ
AF Soars, MG
   Gelboin, HV
   Krausz, KW
   Riley, RJ
TI A comparison of relative abundance, activity factor and inhibitory
   monoclonal antibody approaches in the identification of human CYP
   enzymology
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 AstraZeneca Charnwood, Dept Phys & Metab Sci, Loughborough, Leics, England.
   NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 211
BP 106
EP 106
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200211
ER

PT J
AU Ferguson, SS
   LeCluyse, E
   Negishi, M
   Goldstein, J
AF Ferguson, SS
   LeCluyse, E
   Negishi, M
   Goldstein, J
TI Induction of CYP2C8 by rifampicin is mediated via a novel pregnane X
   receptor (PXR) binding site in the CYP2C8 promoter
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
   Univ N Carolina, Sch Pharm, Chapel Hill, NC 27599 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 222
BP 111
EP 111
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200222
ER

PT J
AU Ferguson, SS
   Chen, YP
   Negishi, M
   Goldstein, J
AF Ferguson, SS
   Chen, YP
   Negishi, M
   Goldstein, J
TI Identification of a constitutive androstane receptor (CAR) binding site
   in the promoter region of CYP2C19
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 221
BP 111
EP 111
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200221
ER

PT J
AU Nukaya, M
   Takahashi, Y
   Gonzalez, FJ
   Kamatakia, T
AF Nukaya, M
   Takahashi, Y
   Gonzalez, FJ
   Kamatakia, T
TI Aryl hydrocarbon receptor mediated suppression of PPAR alpha signal
   caused by polycyclic aromatic hydrocarbons
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 Hokkaido Univ, Grad Sch Pharmaceut Sci, Lab Drug Metab, Sapporo, Hokkaido 0600812, Japan.
   NCI, Lab Metab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 228
BP 114
EP 114
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200228
ER

PT J
AU Wang, HB
   Faucette, S
   Sueyoshi, T
   Ferguson, S
   Negishi, M
   LeCluyse, EL
AF Wang, HB
   Faucette, S
   Sueyoshi, T
   Ferguson, S
   Negishi, M
   LeCluyse, EL
TI Identification of a distal nuclear receptor response element involved in
   the transcriptional regulation of CYP2B6 gene expression
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 Univ N Carolina, Sch Pharm, Div Drug Delivery & Disposit, Chapel Hill, NC 27599 USA.
   NIEHS, LRDT, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 231
BP 116
EP 116
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200231
ER

PT J
AU Desta, Z
   Takada, K
   Arefayene, M
   Yarboro, C
   Carrero, H
   Illei, G
   Flockhart, D
AF Desta, Z
   Takada, K
   Arefayene, M
   Yarboro, C
   Carrero, H
   Illei, G
   Flockhart, D
TI Cytochrome P450 genetic polymorphism as predictor of response to
   cyclophosphamide in lupus nephritis
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 Indiana Univ, Sch Med, Indianapolis, IN USA.
   NIAMS, Off Clin Director, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 300
BP 150
EP 150
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200299
ER

PT J
AU Krausz, KW
   Gelboin, HV
AF Krausz, KW
   Gelboin, HV
TI Specific inhibitory monoclonal antibodies to cytochrome P450 quantitate
   their role in the metabolism of a drug in HLM
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 11th North-American-International-Society-for-the-Study-of-Xenobiotics
   Meeting
CY OCT 27-31, 2002
CL ORLANDO, FLORIDA
SP N Amer Int Soc Study Xenobiot
C1 NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PY 2002
VL 34
SU 1
MA 346
BP 173
EP 173
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 609WC
UT WOS:000178927200343
ER

PT J
AU Schiffmann, R
   Brady, RO
AF Schiffmann, R
   Brady, RO
TI New prospects for the treatment of lysosomal storage diseases
SO DRUGS
LA English
DT Article
ID ENZYME-REPLACEMENT THERAPY; BONE-MARROW TRANSPLANTATION;
   ALPHA-GALACTOSIDASE-A; MUCOPOLYSACCHARIDOSIS TYPE-VII; I
   GAUCHER-DISEASE; FABRY-DISEASE; N-BUTYLDEOXYNOJIRIMYCIN; GENE-TRANSFER;
   GLYCOSPHINGOLIPID BIOSYNTHESIS; SUBSTRATE DEPRIVATION
AB Although individually rare, lysosomal storage disorders constitute a significant burden on society. To date, enzyme replacement therapy (ERT) has been the most successful therapeutic approach for lysosomal storage disorders.
   ERT reverses systemic manifestations of Gaucher disease but does not effectively treat the neurological complications. Recently, ERT produced a reduction of severe neuropathic pain, stabilisation of renal disease, and improved vascular function and structure in short-term, placebo-controlled trials in patients with Fabry's disease. Long-term studies are necessary to evaluate the full potential of ERT in this disease. In patients with Pompe disease, a fatal cardiac and skeletal muscle disorder, ERT improved cardiac function and structure, and increased overall muscle strength. It has already increased survival in a small number of affected infants. ERT also decreased liver and spleen size, joint mobility and quality of life in patients with mucopolysaccharidosis type I, but when the therapeutic protein is administered intravenously, it is unlikely to modify the neurological outcome in this or in other similar disorders.
   Bone marrow transplantation continues to be effective in Gaucher disease, in some forms of mucopolysaccharidosis and in mild forms of Krabbe disease, but it has high morbidity and mortality that limits its use in lysosomal storage disorders. Drugs that slow the rate of formation of accumulating glycolipids are being developed and one of them, OGT-918 (N-butyldeoxynojirimycin), is showing promise in patients with Gaucher disease. Gene therapy for lysosomal storage disorders holds promise as a replacement for the other therapies described here but requires much more development before clinical efficacy trials.
C1 NINCDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Schiffmann, R (reprint author), NINCDS, Dev & Metab Neurol Branch, NIH, 9000 Rockville Pike,Bldg 10,Room 3D03, Bethesda, MD 20892 USA.
NR 65
TC 57
Z9 70
U1 0
U2 1
PU ADIS INTERNATIONAL LTD
PI AUCKLAND
PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW
   ZEALAND
SN 0012-6667
J9 DRUGS
JI Drugs
PY 2002
VL 62
IS 5
BP 733
EP 742
DI 10.2165/00003495-200262050-00002
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 549FW
UT WOS:000175434700002
PM 11929328
ER

PT S
AU Hsi, LC
   Angerman-Stewart, J
   Eling, TE
AF Hsi, LC
   Angerman-Stewart, J
   Eling, TE
BE Honn, KV
   Marnett, LJ
   Nigam, S
   Dennis, E
   Serhan, C
TI Modulation of cyclooxygenase-2 expression by APC in HT-29 human
   colorectal carcinoma cells
SO EICOSANOIDS AND OTHER BIOACTIVE LIPIDS IN CANCER, INFLAMMATION, AND
   RADIATION INJURY, 5
SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
LA English
DT Article; Proceedings Paper
CT 6th International Conference on Eicosanoids and Other Bioactive Lipids
   in Cancer, Inflammation and Related Diseases
CY SEP 12-15, 1999
CL BOSTON, MASSACHUSETTS
ID BETA-CATENIN; COLON-CANCER; GENE-PRODUCT; ASSOCIATION; SYNTHASE-1;
   ACTIVATION; APOPTOSIS; PROTEIN; MICE
C1 NIEHS, Eicosanoid Biochem Sect, Lab Mol Carcinogenesis, Res Triangle Pk, NC 27709 USA.
RP Hsi, LC (reprint author), NIEHS, Eicosanoid Biochem Sect, Lab Mol Carcinogenesis, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 15
TC 1
Z9 1
U1 0
U2 2
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-47283-X
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2002
VL 507
BP 127
EP 131
PG 5
WC Medicine, Research & Experimental; Physiology
SC Research & Experimental Medicine; Physiology
GA BW31F
UT WOS:000181518300021
PM 12664576
ER

PT J
AU Hart, MK
   Del Giudice, RA
   Korch, GW
AF Hart, MK
   Del Giudice, RA
   Korch, GW
TI Absence of mycoplasma contamination in the anthrax vaccine
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID STRAINS
AB Mycoplasma contamination of the licensed anthrax vaccine administered to military personnel has been suggested as a possible cause of Persian Gulf illness. Vaccine samples tested by nonmilitary laboratories were negative for viable mycoplasma and mycoplasma DNA and did not support its survival. Mycoplasma contamination of anthrax vaccine should not be considered a possible cause of illness.
C1 USAMRIID, Frederick, MD 21702 USA.
   Natl Canc Inst, Frederick Canc Res & Dev Ctr, Frederick, MD USA.
RP Korch, GW (reprint author), USAMRIID, 1425 Porter St, Frederick, MD 21702 USA.
NR 9
TC 4
Z9 4
U1 0
U2 0
PU CENTER DISEASE CONTROL
PI ATLANTA
PA ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD JAN
PY 2002
VL 8
IS 1
BP 94
EP 96
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 513ZL
UT WOS:000173411200021
PM 11840996
ER

PT B
AU Elahi, D
   Muller, DC
   Egan, JM
   Andres, R
   Veldhuis, J
   Meneilly, GS
AF Elahi, D
   Muller, DC
   Egan, JM
   Andres, R
   Veldhuis, J
   Meneilly, GS
BE Chadwick, D
TI Glucose tolerance, glucose utilization and insulin secretion in ageing
SO ENDOCRINE FACETS OF AGEING
SE NOVARTIS FOUNDATION SYMPOSIUM
LA English
DT Article; Proceedings Paper
CT Novartis Foundation Symposium on Endocrine Facets of Ageing
CY JAN 30-FEB 01, 2001
CL NOVARTIS FDN, LONDON, ENGLAND
HO NOVARTIS FDN
ID GLUCAGON-LIKE PEPTIDE-1(7-37); DEPENDENT DIABETES-MELLITUS; BETA-CELL;
   CARBOHYDRATE-METABOLISM; HEALTHY CENTENARIANS; NONDIABETIC SUBJECTS;
   PERIPHERAL TISSUE; BODY-FAT; RESISTANCE; INDIVIDUALS
AB Ageing is associated with an increased incidence of hypertension, macrovascular disease and type 2 diabetes (non-insulin-dependent diabetes). It has been suggested that a common mechanism may be responsible for all of these pathological states since all of these conditions often cluster in the same individual. Epidemiological and clinical data have consistently demonstrated an association between insulin resistance and/or hyperinsulinaemia and glucose intolerance, dyslipidaemia and elevated systolic blood pressures. Therefore, insulin resistance and hyperinsulinaemia have been proposed as the causal link among the elements of the clusters. The elderly are more glucose intolerant and insulin resistant, but it remains controversial whether this decrease in function is due to an inevitable consequence of 'biological ageing' or due to environmental or lifestyle variables, noticeably increased adiposity/altered fat distribution and physical inactivity. An increase of these modifiable factors has been shown to result in increases in insulin resistance and hyperinsulinaemia and vice versa. However, insulin secretion appears to decrease with age even after adjustments for differences in adiposity, fat distribution and physical activity. The glucose intolerance of ageing may be due, in part, to decreased insulin sensitivity of pancreatic beta cells to insulinotropic gut hormones (GLP1/GIP) and in part to alterations of hepatic glucose production.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA.
   NIA, Gerontol Res Ctr, Lab Clin Physiol, NIH, Baltimore, MD 21224 USA.
   Univ Virginia, Div Endocrinol & Metab, Charlottesville, VA 22908 USA.
   Univ British Columbia, Dept Med, Vancouver, BC V6T 1Z3, Canada.
RP Muller, DC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA.
FU NIA NIH HHS [AG-00599]
NR 64
TC 32
Z9 33
U1 0
U2 7
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND
BN 0-471-48636-1
J9 NOVART FDN SYMP
PY 2002
VL 242
BP 222
EP 242
PG 21
WC Endocrinology & Metabolism; Geriatrics & Gerontology; Medicine, General
   & Internal
SC Endocrinology & Metabolism; Geriatrics & Gerontology; General & Internal
   Medicine
GA BU35C
UT WOS:000175745900013
PM 11855690
ER

PT S
AU Koch, CA
   Vortmeyer, AO
   Zhuang, ZP
   Brouwers, FM
   Pacak, K
AF Koch, CA
   Vortmeyer, AO
   Zhuang, ZP
   Brouwers, FM
   Pacak, K
BE Pacak, K
   Eisenhofer, G
TI New insights into the genetics of familial chromaffin cell tumors
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE RET; VHL; NF1; SDHD; SDHC; SDHB; multiple endocrine neoplasia type 2;
   paraganglioma; pheochromocytoma; tumor formation; second hit
ID VON-HIPPEL-LINDAU; MULTIPLE ENDOCRINE NEOPLASIA; MEDULLARY-THYROID
   CARCINOMA; NEUROFIBROMATOSIS TYPE-I; RET PROTOONCOGENE; SPORADIC
   PHEOCHROMOCYTOMAS; GERMLINE MUTATIONS; SUPPRESSOR GENE; CAROTID-BODY;
   HIRSCHSPRUNGS-DISEASE
AB We review genetic aspects and recent advances in our understanding of the molecular pathogenesis of familial chromaffin cell tumors (pheochromocytoma, paraganglioma). About 10 percent of pheochromocytomas are familial and occur as part of multiple endocrine neoplasia type 2 (MEN 2), von Hippel-Lindau (VHL) disease, and neurofibromatosis type 1 (NF 1). A subset of paragangliomas, tumors that can also produce and secrete catecholamines, are also familial and occur in patients with germline mutations in genes that encode subunits of the mitochondrial complex II. The precise molecular mechanisms underlying the pathogenesis of chromaffin cell tumors remain widely unknown, although recent studies in hereditary tumors help elucidate their development. In MEN 2, overrepresentation of mutant RET in selected adrenomedullary cells may be an important mechanism in initiating the formation of a pheochromocytoma. In VHL disease, pheochromocytoma development appears to occur according to Knudson's two-hit model, a VHL germline mutation and wildlype allelic deletion. Tumorigenesis of NF1-associated pheochromocytomas remains unknown, as does tumor formation (i.e., carotid body tumor) in patients with germline mutations in SDHB, SDHC, and SDHD, genes that encode subunits of the mitochondrial complex 11, the smallest complex in the respiratory chain. Many genetic alterations have been found in sporadic chromaffin cell tumors. However, at present such genetic changes are difficult to place into context with regard to tumor formation and progression.
C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Koch, CA (reprint author), Dept Med 3, Endocrinol Uniklin, Phil Rosenthalstr 27, D-04103 Leipzig, Germany.
RI Koch, Christian/A-4699-2008; 
OI Koch, Christian/0000-0003-3127-5739; Koch, Christian/0000-0003-0678-1242
NR 112
TC 32
Z9 32
U1 1
U2 4
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 11
EP 28
PG 18
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600002
PM 12381538
ER

PT S
AU Lenders, JWM
   Pacak, K
   Eisenhofer, G
AF Lenders, JWM
   Pacak, K
   Eisenhofer, G
BE Pacak, K
   Eisenhofer, G
TI New advances in the biochemical diagnosis of pheochromocytoma - Moving
   beyond catecholamines
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE pheochromocytoma; normetanephrine; metanephrine; norepinephrine;
   epinephrine; diagnosis, adrenal incidentaloma, von Hippel-Lindau
   disease; multiple endocrine neoplasia type 2
ID ENDOCRINE NEOPLASIA TYPE-2; HIPPEL-LINDAU-DISEASE; PLASMA METANEPHRINES;
   URINARY; METABOLISM; TESTS
AB Pheochromocytomas are dangerous tumors that, although a rare cause of hypertension, require consideration among large numbers of patients. The resulting low prevalence of the tumor among tested populations and the inadequacies of commonly used biochemical tests make excluding or confirming the tumor an often difficult and time-consuming task. Recognition that catecholamines are metabolized to free metanephrines within pheochromocytoma tumor cells, and that this process is independent of catecholamine release, provides a rationale for use of these metabolites in the biochemical diagnosis of pheochromocytoma. Here we briefly review the history of biochemical diagnosis of pheochromocytoma in relation to recent data about the diagnostic utility of plasma free metanephrines for detection of these tumors. Measurements of urinary or plasma catecholamines have reasonable sensitivity for detection of most pheochromocytomas, particularly those in patients with sustained hypertension. False-negative test results can, however, occur in asymptomatic patients tested because of an adrenal incidentaloma or a familial predisposition for pheochromocytoma, or when sampling is carried out between episodes of paroxysmal hypertension. Measurements of urinary total metanephrines or vanillylmandelic acid are less reliable and are of little value as initial screening tests. In contrast, measurements of plasma concentrations or free metanephrines or 24-hour urinary outputs of fractionated normetanephrine and metanephrine almost always reveal the tumor. Although, both tests have similarly high sensitivity, the relatively low specificity of urinary fractionated metanephrines means that pheochromocytomas can be more efficiently excluded or confirmed using measurements of plasma free metanephrines.
C1 NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
   NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   St Radboud Univ, Med Ctr, Dept Internal Med, Nijmegen, Netherlands.
RP Eisenhofer, G (reprint author), NINDS, Clin Neurocardiol Sect, NIH, Bldg 10,Room 6N252,10 Ctr Dr,MSC-1620, Bethesda, MD 20892 USA.
RI Lenders, J.W.M./L-4487-2015
NR 38
TC 35
Z9 38
U1 0
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 29
EP 40
PG 12
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600003
PM 12381539
ER

PT S
AU Walther, MM
AF Walther, MM
BE Pacak, K
   Eisenhofer, G
TI New therapeutic and surgical approaches for sporadic and hereditary
   pheochromocytoma
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE pheochromocytoma; diagnosis; surgery; hereditary disorders
ID ENDOCRINE NEOPLASIA TYPE-2; HIPPEL-LINDAU-DISEASE; LAPAROSCOPIC
   ADRENALECTOMY; BILATERAL ADRENALECTOMY; FAMILIAL PHEOCHROMOCYTOMA;
   MULTIPLE; MANAGEMENT; 2A; PARAGANGLIOMAS; CHEMODECTOMA
AB Pheochromocytoma is a rare, surgically correctable cause of hypertension. Modern medical blockade has significantly improved patient survival and morbidity. The last decade has seen the identification of the genes responsible for several hereditary causes of pheochromocytoma. Evaluation of these patients has demonstrated different catecholamine profiles associated with the different syndromes. Genetic testing and new, more sensitive catecholamine tests are allowing better, earlier diagnosis of affected patients. Some patients with small tumors deemed nonfunctional by traditional methods may be safely observed until function is demonstrated. Laparoscopic surgery has supplanted the use of open surgery in the management of these tumors. Adrenocortical-sparing surgery may be performed using laparoscopy in patients with hereditary forms of pheochromocytoma.
C1 NCI, Urol Oncol Branch, DCS, NIH, Bethesda, MD 20892 USA.
RP Walther, MM (reprint author), NCI, Urol Oncol Branch, DCS, NIH, Bldg 10,Room 2B-43,10 Ctr Dr,MSC 1502, Bethesda, MD 20892 USA.
NR 54
TC 8
Z9 8
U1 0
U2 3
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 41
EP 53
PG 13
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600004
PM 12381540
ER

PT S
AU Kino, T
   Vottero, A
   Charmandari, E
   Chrousos, GP
AF Kino, T
   Vottero, A
   Charmandari, E
   Chrousos, GP
BE Pacak, K
   Eisenhofer, G
TI Familial/sporadic glucocorticoid resistance syndrome and hypertension
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE glucocorticoid receptor; tissue sensitivity to glucocorticoids;
   mutation; nuclear translocation; p160 coactivators
ID PRIMARY CORTISOL RESISTANCE; BINDING DOMAIN; RECEPTOR; MUTATION;
   ANTAGONISM; COMPLEX; DISEASE
AB Glucocorticoids regulate diverse functions important for the maintenance of central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by the specific intracellular glucocorticoid receptors (GRs). Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial/sporadic glucocorticoid resistance is characterized by hypercortisolism without Cushing syndrome stigmata. Many of the patients present with hypertension, with or without hypokalemic alkalosis, as a result of elevated concentrations of cortisol and other salt-retaining steroids. The molecular defects of 4 kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of the GR. In two patients in whom the GR was mutated at amino acid isoleucine 559 to aspartic acid (GRalphaI559N) and isoleucine 747 to methionine (GRalphaI747M), respectively, glucocorticoid resistance developed at the heterozygous state, with transdominant negative activity of each of the mutant receptors upon the wild-type protein. Retention of the wild-type receptor in the cytoplasm by the mutant receptor was found in the former, while inappropriate accumulation of p160-type coactivators on the promoter region of glucocorticoid-responsive genes, because of a defective interaction between the AF2 region of the mutant receptor and the LXXLL motif of the coactivators, was determined in the latter. These results suggest that the pathologic mechanisms of glucocorticoid resistance is quite broad, and this is reflected in the wide variability of the clinical picture in patients with the syndrome.
C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
RP Kino, T (reprint author), NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bldg 10,Room 9D42,10 Ctr Dr MSC 1583, Bethesda, MD 20892 USA.
RI Charmandari, Evangelia/B-6701-2011
NR 31
TC 31
Z9 32
U1 0
U2 3
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 101
EP 111
PG 11
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600009
PM 12381545
ER

PT S
AU Nieman, LK
AF Nieman, LK
BE Pacak, K
   Eisenhofer, G
TI Diagnostic tests for Cushing's syndrome
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE cortisol; ACTH; Cushing's syndrome
ID CORTISOL MEASUREMENT; SALIVARY CORTISOL; SCREENING-TEST; STATES
AB The diagnosis of Cushing's syndrome rests on the demonstration of clinical features and biochemical abnormalities that reflect hypercortisolism. If a patient presents with typical clinical features such as weight gain with truncal obesity and supraclavicular fat deposition, wide purple striae, and proximal muscle weakness, the diagnosis is clear-cut and is nearly always substantiated by a 24-hour urine free cortisol excretion value more than four times the normal level. However, many patients present with signs and symptoms that are common in the general population, such as hypertension, generalized weight gain, reproductive abnormalities, and depression. Many of these patients have normal cortisol excretion and do not have Cushing's syndrome. Others have mild hypercortisolism caused by psychiatric disorders, obligate exercise, morbid obesity, sleep apnea, or uncontrolled diabetes mellitus. These patients may be confused with those with the true Cushing's syndrome, and thus are considered to have a "pseudo-Cushing" state. Additional observation over time, and testing with midnight cortisol measurements, the 2-day-2-mg dexamethasone suppression test, or the dexamethasone suppression-CRH stimulation test may be useful to identify true Cushing's syndrome in these patients.
C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
RP Nieman, LK (reprint author), Bldg 10,Room 9D42,MSC 1583,10 Ctr Dr, Bethesda, MD 20892 USA.
NR 16
TC 38
Z9 39
U1 0
U2 5
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 112
EP 118
PG 7
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600010
PM 12381546
ER

PT S
AU Torpy, DJ
   Mullen, N
   Ilias, A
   Nieman, LK
AF Torpy, DJ
   Mullen, N
   Ilias, A
   Nieman, LK
BE Pacak, K
   Eisenhofer, G
TI Association of hypertension and hypokalemia with Cushing's syndrome
   caused by ectopic ACTH secretion - A series of 58 cases
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE corticotropin; hypertension; hypokalemia; 11
   beta-hydroxysteroid-dehydrogenase
ID APPARENT MINERALOCORTICOID EXCESS; VASCULAR SMOOTH-MUSCLE;
   11-BETA-HYDROXYSTEROID DEHYDROGENASE; ADRENOCORTICOTROPIN SYNDROME;
   ENDOTHELIAL-CELLS; DISEASE; GLUCOCORTICOIDS; PATHOGENESIS; DEFICIENCY;
   DIAGNOSIS
AB Cushing's syndrome is associated with hypertension in approximately 80% of cases. Hypertension contributes to the marked increased mortality risk of past or current Cushing's syndrome, largely because of increased cardiovascular risk. Observation of the pathophysiological effect of chronically elevated ACTH and cortisol values in patients with ectopic ACTH secretion complements the available data from acute studies of the effects of ACTH and glucocorticoid infusions in normal volunteers. In a retrospective case review, we identified 58 patients with Cushing's syndrome caused by ectopic ACTH secretion, who were treated at the National Institutes of Health between 1983-1997. The diagnosis of an ectopic ACTH cause was confirmed by inferior petrosal sinus sampling and/or pathologic examination of tumor. The commonest causes were bronchial carcinoid (40%) and thymic carcinoid (10%), but 18 of 58 (31%) patients had an unknown source of ectopic ACTH. Hypertension (systolic blood pressure >140 mmHg and/or diastolic blood pressure >90 mmHg in adults) was noted in 45 of 58 (78%) ectopic Cushing's patients, a prevalence similar to that noted in other endogenous Cushing's syndrome etiologies. Hypertension was severe, deemed to require 3 or more drugs by the treating physicians, in 26 of 58 (45%) patients. Hypokalemia was much more prevalent than in patients with other causes of Cushing's syndrome, affecting 33 of 58 (57%) patients. The range of plasma ACTH (17-1557 pg/mL, normal <60) and 24-hour urine cortisol (UC) excretion (192-1600 mcg/24 hr, normal <90) allowed analysis of the influence of these hormones on blood pressure and plasma potassium. There was a significant relationship between 24-hour UC excretion and the presence of hypokalemia (P = 0.003). Eight of nine patients with a UC >6000 mcg/24 hr had hypokalemia. There was no relation between ACTH level and hypokalemia. In addition, we did not find blood pressure severity to be related to UC excretion or ACTH levels. Urine and plasma cortisol and cortisol metabolite measurements suggest that cortisol may act as a mineralocorticoid when in excess, perhaps by saturating the 11beta-hydroxysteroid-dehydrogenase (11beta-HSD2 enzyme) that inactivates cortisol at the renal tubule. The current data suggest that high cortisol levels may be the principal cause of hypokalemic alkalosis in Cushing's syndrome, rather than inhibition of the 11betaHSD2 enzyme by ACTH or the effects of adrenal steroid biosynthetic intermediaries with mineralococorticoid activity.
C1 Univ Queensland, Dept Med, Greenslope Hosp, Brisbane, Qld 4120, Australia.
   NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   NIH, Dept Nursing, Ctr Clin, Bethesda, MD 20892 USA.
RP Torpy, DJ (reprint author), Univ Queensland, Dept Med, Greenslope Hosp, Newegate St, Brisbane, Qld 4120, Australia.
NR 36
TC 66
Z9 68
U1 0
U2 4
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 134
EP 144
PG 11
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600012
PM 12381548
ER

PT S
AU Pacak, K
   Eisenhofer, G
   Carrasquillo, JA
   Chen, CC
   Whatley, M
   Goldstein, DS
AF Pacak, K
   Eisenhofer, G
   Carrasquillo, JA
   Chen, CC
   Whatley, M
   Goldstein, DS
BE Pacak, K
   Eisenhofer, G
TI Diagnostic localization of pheochromocytoma - The coming of age of
   positron emission tomography
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE pheochromocytoma; positron emission tomography; metaiodobenzylguanidine
   scintigraphy; Octreoscan
ID CARDIAC SYMPATHETIC INNERVATION; MALIGNANT PHEOCHROMOCYTOMA;
   SCINTIGRAPHY; PET; METAIODOBENZYLGUANIDINE; 6-<F-18>FLUORODOPAMINE;
   OCTREOTIDE; HUMANS
AB Pheochromocytoma is a rare but clinically important tumor of catecholamine-secreting chromaffin cells. This tumor constitutes a surgically curable cause of hypertension. Therefore, correct localization of pheochromocytoma is essential for effective management of this tumor. Several conventional and nuclear imaging modalities are currently available to localize pheochromocytoma. Computed tomography (CT) and magnetic resonance imaging (MRI) have good sensitivity but poor specificity for detecting pheochromocytoma, and nuclear imaging approaches such as I-131-metaiodobenzylguanidine scintigraphy or [In-111]-DTPA-D-Phe-pentetreotide (Octreoscan) have limited sensitivity. However, specificity of I-131-metaiodobenzylguanidine scintigraphy is very good and this means of imaging provides a method for confirming that a tumor is a pheochromocytoma and rules out metastatic disease. Recently, we introduced a new imaging method, 6-[F-18] fluorodopamine positron emission tomography, that can be used successfully for the detection of solitary and metastatic pheochromocytomas. Our preliminary data suggest that this method is superior to other nuclear imaging methods including metaiodobenzylguanidine and octreotide scintigraphy. In this report we provide an update regarding nuclear imaging of primary and metastatic pheochromocytoma, particularly using 6-[F-18]fluorodopamine positron emission tomographic scanning.
C1 NIH, Dept Nucl Med, Ctr Clin, Bethesda, MD 20892 USA.
   NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
   NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
RP Pacak, K (reprint author), NICHD, PREB, NIH, Bldg 10,Room 9D42,10 Ctr Dr, Bethesda, MD 20892 USA.
RI Carrasquillo, Jorge/E-7120-2010; 
OI Carrasquillo, Jorge/0000-0002-8513-5734
NR 23
TC 31
Z9 31
U1 0
U2 3
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 170
EP 176
PG 7
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600016
PM 12381552
ER

PT S
AU Alesci, S
   Chrousos, GP
   Pacak, K
AF Alesci, S
   Chrousos, GP
   Pacak, K
BE Pacak, K
   Eisenhofer, G
TI Genomic medicine - Exploring the basis of a new approach to endocrine
   hypertension
SO ENDOCRINE HYPERTENSION
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT 1st International Workshop on Endocrine Hypertension
CY NOV   16, 2001
CL BETHESDA, MARYLAND
SP NIH, Off Rare Dis, NICHHD
DE endocrine hypertension; gene therapy; adrenal gland; adrenal cancer;
   adrenocortical carcinoma; pheochromocytoma; congenital adrenal
   hyperplasia; hyperaldosteronism; Cushing's syndrome
ID MEDIATED GENE-TRANSFER; ANTERIOR-PITUITARY-CELLS; ADENOASSOCIATED VIRUS;
   IN-VIVO; RECOMBINANT ADENOVIRUS; HORMONE-SECRETION; LENTIVIRAL VECTOR;
   THERAPY VECTORS; IMMUNE-RESPONSE; DNA INJECTION
AB Recent improvements in defining the molecular basis of disease have encouraged scientists worldwide to develop new therapeutic strategies based on engineered genes and cells. Genomic medicine has the potential to revolutionize diagnosis and therapy of a variety of human diseases, including endocrine disorders. Hypertension is the presenting feature of some of these disorders, such as congenital adrenal diseases, and adrenal and pituitary tumors. Preclinical data indicate that gene transfer to both the adrenal gland and the pituitary is not only feasible but also quite efficient. Research in this field is only in its infancy, but with the ever-increasing advances in DNA technologies, genomic therapies for endocrine hypertension may become available within the next few decades.
C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   Univ Messina, Dipartimento Clin Sperimentale Med & Farmacol, Sezione Endocrinol, I-98100 Messina, Italy.
RP Alesci, S (reprint author), NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bldg 10,Room 9D42,10 Ctr Dr MSC 1583, Bethesda, MD 20892 USA.
NR 84
TC 3
Z9 3
U1 0
U2 2
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-418-8
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 970
BP 177
EP 192
PG 16
WC Endocrinology & Metabolism; Multidisciplinary Sciences; Peripheral
   Vascular Disease
SC Endocrinology & Metabolism; Science & Technology - Other Topics;
   Cardiovascular System & Cardiology
GA BV61J
UT WOS:000179508600017
PM 12381553
ER

PT J
AU Kirschner, LS
   Stratakis, CA
AF Kirschner, LS
   Stratakis, CA
TI Protein kinase A and tumorigenicity: The example of micronodular
   adrenocortical hyperplasia and Carney complex
SO ENDOCRINE RESEARCH
LA English
DT Article; Proceedings Paper
CT 10th Conference on the Adrenal Cortex
CY JUN 15-18, 2002
CL SAN FRANCISCO, CALIFORNIA
SP Marcel Dekker Inc, Dekker Fdn, Eli Lilly Corp, Invitrogen Life Technol, Adrenal 2000, Univ toronto, Univ Buffalo, Dept Biochem, Univ Cal San Francisco, Dept Biochem
C1 NICHD, Unit Genet & Endocrinol, DEB, NIH, Bethesda, MD 20892 USA.
RP Stratakis, CA (reprint author), NICHD, Unit Genet & Endocrinol, DEB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARCEL DEKKER INC
PI NEW YORK
PA 270 MADISON AVE, NEW YORK, NY 10016 USA
SN 0743-5800
J9 ENDOCR RES
JI Endocr. Res.
PY 2002
VL 28
IS 4
BP 749
EP 750
DI 10.1081/ERC-120017000
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 632FU
UT WOS:000180213900076
PM 12530691
ER

PT S
AU Yoshinaga, K
   Parrott, EC
AF Yoshinaga, K
   Parrott, EC
BE Yoshinaga, K
   Parrott, EC
TI Summary of future research directions and recommendations
SO ENDOMETRIOSIS: EMERGING RESEARCH AND INTERVENTION STRATEGIES
SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article; Proceedings Paper
CT Workshop on Endometriosis - Emerging Research and Intervention
   Strategies
CY APR 09-10, 2001
CL NIH, BETHESDA, MARYLAND
SP NICHHD, NIEHS, Off Res Womens Hlth
HO NIH
C1 NICHHD, Reprod Sci Branch, Ctr Populat Res, NIH, Bethesda, MD 20892 USA.
RP Yoshinaga, K (reprint author), NICHHD, Reprod Sci Branch, Ctr Populat Res, NIH, 6100 Execut Blvd,Room 8B-01, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
BN 1-57331-380-7
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PY 2002
VL 955
BP 394
EP 406
PG 13
WC Multidisciplinary Sciences; Obstetrics & Gynecology
SC Science & Technology - Other Topics; Obstetrics & Gynecology
GA BU39N
UT WOS:000175883100032
ER

PT J
AU Hein, DW
   Leff, MA
   Ishibe, N
   Sinha, R
   Frazier, HA
   Doll, MA
   Xiao, GH
   Weinrich, MC
   Caporaso, NE
AF Hein, DW
   Leff, MA
   Ishibe, N
   Sinha, R
   Frazier, HA
   Doll, MA
   Xiao, GH
   Weinrich, MC
   Caporaso, NE
TI Association of prostate cancer with rapid N-acetyltransferase 1
   (NAT1*10) in combination with slow N-acetyltransferase 2 acetylator
   genotypes in a pilot case-control study
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE prostate cancer; N-acetyltransferase 1; N-acetyltransferase 2;
   acetylator genotype
ID ARYLAMINE N-ACETYLTRANSFERASE-1 NAT1; CARCINOGEN-METABOLIZING ENZYMES;
   DNA ADDUCT FORMATION; BLADDER-CANCER;
   2-AMINO-1-METHYL-6-PHENYLIMIDAZO<4,5-B>PYRIDINE PHIP; COLORECTAL-CANCER;
   FUNCTIONAL-CHARACTERIZATION; NUCLEOTIDE POLYMORPHISMS; GENETIC
   POLYMORPHISMS; HETEROCYCLIC AMINES
AB N-acetyltransferase-1 (NAT1) and N-acetyltransferase-2 (NAT2) are important in the metabolism of aromatic and heterocyclic amine carcinogens that induce prostate tumors in the rat. We investigated the association of genetic polymorphisms in NAT1 and NAT2, alone and in combination, with human prostate cancer. Incident prostate cancer cases and controls in a hospital-based case-control study were frequency-matched for age, race, and referral pattern. The frequency of slow acetylator NAT1 genotypes (NAT1 * 14, * 15, * 17) was 5.8% in controls but absent in cases. In contrast, in comparison with all other NAT1 genotypes the putative rapid acetylator NAT1 genotype (NAT1 * 10) was significantly higher in prostate cancer cases than controls (OR, 2.17; 95% Cl, 1.08-4.33; P = 0.03). Combinations of NAT1 * 10 with NAT2 slow acetylator genotypes (OR, 5.08; 95% Cl, 1.56-16.5; P = 0.008) or with NAT2 very slow (homozygous NAT2 * 5) acetylator genotypes (OR, 7.50; 95% Cl, 1.55-15.4; P = 0.016) further increased prostate cancer risk. The results of this small pilot study suggest increased susceptibility to prostate cancer for subjects with combinations of NAT1 * 10 and slow (particularly very slow) NAT2 acetylator genotypes. This finding should be investigated further in larger cohorts and in other ethnic populations. (C) 2002 Wiley-Liss, Inc.
C1 Univ Louisville, Sch Med, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA.
   NCI, Natl Epidemiol Branch, Bethesda, MD 20892 USA.
   Natl Naval Med Res Inst, Bethesda, MD USA.
   Univ Louisville, Sch Med, Dept Med, Louisville, KY 40292 USA.
RP Hein, DW (reprint author), Univ Louisville, Sch Med, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA.
EM d.hein@louisville.edu
RI Hein, David/A-9707-2008; Sinha, Rashmi/G-7446-2015
OI Sinha, Rashmi/0000-0002-2466-7462
FU NCI NIH HHS [CA-34627, R01 CA034627, R01 CA034627-17]
NR 69
TC 42
Z9 43
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 40
IS 3
BP 161
EP 167
DI 10.1002/em.10103
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 600WB
UT WOS:000178413800002
PM 12355549
ER

PT J
AU Barnett, LB
   Tyl, RW
   Shane, BS
   Shelby, MD
   Lewis, SE
AF Barnett, LB
   Tyl, RW
   Shane, BS
   Shelby, MD
   Lewis, SE
TI Transmission of mutations in the lacl transgene to the offspring of
   ENU-Treated big Blue (R) male mice
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE N-ethyl-N-nitrosourea; locl transgenic mice; germ cell mutagenesis;
   specific-locus test
ID GERM-CELLS; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; BENZO<A>PYRENE
   TREATMENT; MOUSE SPERMATOGONIA; LOCUS MUTATIONS; ETHYLNITROSOUREA;
   MUTAGENESIS; FREQUENCY; SPECTRA; INVIVO
AB The purpose of the study was to determine: 1) if male germ cells of Big Blue(R) mice carrying newly induced mutations in the lacI transgene were effective in fertilization; 2) if offspring arising from such mutant sperm had the mutation in germ cells and multiple somatic tissues; and 3) how the frequency of mutants induced in the loci transgene compared to the frequency induced in endogenous genes traditionally employed to study germ cell mutagenesis in mice. Male B6C3F(1) mice hemizygous for the lambda/lacI transgene were treated weekly with 100 mg/kg body weight of the mammalian germ cell mutagen N-ethyl-N-nitrosourea (ENU). The cumulative dose for each treated animal was 300 mg ENU/kg body weight. Ten weeks later the treated mice were mated to T stock females and the resulting offspring were screened for specific-locus mutations at six loci affecting external appearance, as well as for mutations in the loci transgene in multiple somatic tissues and germ cells. Five offspring carrying recessive specific-locus mutations were observed among 597 offspring screened (mutant frequency = 139.6 x per locus). Four offspring carrying lacI mutations were observed among 280 offspring screened (mutant frequency = 35.7 x 10(-5) per locus (assuming 40 target loci)). Each of the four lacI mutant offspring carried a different mutation. Three of the mutations were A:T-->G:C transitions and one a G:C -->A:T transition. Consistent with the expectation that a mutation induced in a parental germ cell and transmitted to a conceptus would exist in every cell of the offspring, each mutant mouse had identical mutations in all somatic tissues sampled, as well as in its germ cells. These data provide preliminary evidence for the biological validity of assessing induced, heritable mutations using transgenic mice, without the need for generating an F-1 generation.
C1 Integrated Syst Lab, Res Triangle Pk, NC USA.
   NIEHS, Res Triangle Pk, NC 27709 USA.
   Durham Tech Community Coll, Durham, NC USA.
   RTI Int, Res Triangle Pk, NC USA.
RP Barnett, LB (reprint author), 1012 Stonehedge Ave, Durham, NC 27707 USA.
FU NIEHS NIH HHS [R01 ES 06339]
NR 38
TC 20
Z9 20
U1 0
U2 2
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 40
IS 4
BP 251
EP 257
DI 10.1002/em.10114
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 632GC
UT WOS:000180214700004
PM 12489115
ER

PT J
AU Valentine, CR
   Montgomery, BA
   Miller, SG
   Delongchamp, RR
   Fane, BA
   Malling, HV
AF Valentine, CR
   Montgomery, BA
   Miller, SG
   Delongchamp, RR
   Fane, BA
   Malling, HV
TI Characterization of mutant spectra generated by a forward mutational
   assay for gene A of Phi X174 from ENU-treated transgenic mouse embryonic
   cell line PX-2
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE phiX174; transgenic; ENU; mouse cell; gene A
ID ETHYLNITROSOUREA-INDUCED MUTATION; ESCHERICHIA-COLI; ETHYLATING AGENTS;
   POINT MUTATIONS; SHUTTLE VECTOR; DNA-ADDUCTS; MICE; MUTAGENESIS; SINGLE;
   BACTERIOPHAGE-PHI-X174
AB The sensitivity of in vivo transgenic mutation assays benefits from the sequencing of mutations, although the large number of possible mutations hinders high throughput sequencing. A forward mutational assay exists for PhiX174 that requires an altered, Functional PhiX174 protein and therefore should have fewer targets (sense, base-pair substitutions) than forward assays that inactivate a protein. We investigated this assay to determine the number of targets and their suitability for detecting a known mutagen, N-ethyl-N-nitrosourea (ENU). We identified 25 target sites and 33 different mutations in PhiX174 gene A after sequencing over 350 spontaneous and ENU-induced mutants, mostly from mouse embryonic cell line PX-2 isolated from mice transgenic for PhiX174 am3, cs70 (line 54). All six types of base-pair substitution were represented among both the spontaneous and ENU-treated mutant spectra. The mutant spectra from cells treated with 200 and 400 mug/ml ENU were both highly different from the spontaneous spectrum (P < 0.000001) but not from each other. The dose trend was significant (P < 0.0001) fora linear regression of mutant Frequencies (R-2 = 0.79), with a ninefold increase in mutant frequency at the 400 mug/ml dose. The spontaneous mutant frequency was 1.9 X 10(-5) and the spontaneous spectrum occurred at 11 target base pairs with 15 different mutations. Thirteen mutations at 12 targets were identified only from ENU-treated cells. Seven mutations had highly significant increases with ENU treatment (P < 0.0001) and 15 showed significant increases. The results suggest that the PhiX174 forward assay might be developed into a sensitive, inexpensive in vivo mutagenicity assay. Published 2002 Wiley-Liss, Inc.
C1 US FDA, Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, Jefferson, AR 72079 USA.
   US FDA, Div Biometry & Risk Assessment, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
   Univ Arizona, Dept Vet Sci & Microbiol, Tucson, AZ 85721 USA.
   NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Valentine, CR (reprint author), US FDA, Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, 3900 NCTR Rd,HFT-120, Jefferson, AR 72079 USA.
NR 67
TC 8
Z9 8
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 1
BP 55
EP 68
DI 10.1002/em.10043
PG 14
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 522EY
UT WOS:000173883800008
PM 11813297
ER

PT J
AU Johnson, FM
AF Johnson, FM
TI How many food additives are rodent carcinogens?
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE food additives; carcinogens; National Toxicology Program rodent
   bioassay; 1958 Food Additives Amendment; Food and Drug Administration
ID NATIONAL-TOXICOLOGY-PROGRAM; HUMAN CANCER HAZARDS; CENTER-DOT-AC;
   TRANSGENIC MOUSE; CHEMICAL CARCINOGENESIS; MICE; BIOASSAYS; PREVENTION;
   SUSCEPTIBILITY; STRAINS
AB One generally assumes that chemical agents added to foods are reasonably free of risks to human health, and practically everyone consumes some additives in his or her food daily throughout life. In the United States, the 1958 Food Additives Amendment to the Federal Food, Drug and Cosmetic Act of 1938 requires food manufacturers to demonstrate the safety of food additives to the Food and Drug Administration (FDA). The Amendment contains a provision that prohibits approval of an additive if it is found to cause cancer in humans or animals. In the present study, data from the National Toxicology Program rodent bioassay (NTPRB) were used to identify a sample of approximately 50 rodent-tested additives and other chemicals added to food that had been evaluated independently of the FDA/food industry. Surprisingly, the sample shows more than 40% of these food chemicals to be carcinogenic in one or more rodent groups. If this percentage is extrapolated to all substances added to food in the United States, it would imply that more than 1000 of such substances are potential rodent carcinogens. The NTP and FDA test guidelines use similar, though not necessarily identical, rodent test procedures, including near lifetime exposures to the maximum tolerated dose. The FDA specifies that test chemicals should be administered by the oral route. However, the oral route includes three methods of delivering chemicals, that is, mixed in the food or water or delivered by stomach tube (gavage). The NTP data show only I of 18 food chemicals mixed in the food are rodent carcinogens, but 16 of 23 govage-administered food chemicals are carcinogenic to rodents. The distribution suggests that among orally delivered chemicals, those administered in the feed will more likely prove to be noncarcinogens than chemicals given by gavage. The rodent data also reveal that effects may vary according to dose and genotype, as well as by route of administration, to further complicate extrapolation to humans. Human experience with known carcinogens such as tobacco, asbestos, and benzidine convinces us that environmental carcinogens constitute a real threat to human health, although predicting human carcinogens from rodent tests involves a number of uncertainties. These uncertainties do not mean that we should simply ignore the presence of carcinogens. Rather, in the interests of public safety, a serious effort should be made to resolve the questions surrounding the presence of chemicals identified as rodent carcinogens in our food. Published 2002 Wiley-Liss, Inc.
C1 NIEHS, Toxicol Operat Branch EC31, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Johnson, FM (reprint author), NIEHS, Toxicol Operat Branch EC31, Environm Toxicol Program, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 71
TC 12
Z9 12
U1 2
U2 9
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 1
BP 69
EP 80
DI 10.1002/em.10037
PG 12
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 522EY
UT WOS:000173883800009
PM 11813298
ER

PT J
AU Lacey, JV
   Devesa, SS
   Brinton, LA
AF Lacey, JV
   Devesa, SS
   Brinton, LA
TI Recent trends in breast cancer incidence and mortality
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NORTH CAROLINA
SP Environm Mutagen Soc
DE epidemiology; age-period-cohort analyses; incidence rates; mortality
   rates; breast neoplasms
ID PERIOD-COHORT ANALYSIS; UNITED-STATES; GEOGRAPHIC-VARIATION;
   AMERICAN-WOMEN; WHITE WOMEN; RISK; RATES; PATTERNS
AB Breast cancer accounts for one-third of cancer diagnoses and 15% of cancer deaths in U.S. women. Its 192,000 cases and 40,000 deaths in 2001 make it the most common incident cancer (excluding superficial skin cancers) and second leading cause of cancer death. Over one-half of the 300,000 breast cancer deaths worldwide in 1990 (the latest year with such data) occurred in developed countries, but annual mortality rates ranged from 27/100,000 women in northern Europe to 41100,000 women in Asia. Incidence data are less complete, although 1988-1992 rates varied threefold: low in Asia, intermediate in South America and Eastern Europe, and high in North America and Western Europe. Migrant studies suggest that lifestyle factors largely explain these international differences. U.S. incidence rates are generally 20%-40% higher in white women than in non-white women, but are higher in young (under age 40) black women than in young white women. Incidence rates rose in the 1970s, leveled off in the 1990s, and are declining for young women. Women in some areas of the northeast U.S. have twofold higher mortality than that of other U.S. women, but reproductive and socioeconomic characteristics explain much of that difference. In the 1970s and 1980s, mortality rates held steady in developed countries but rose in developing countries. Since 1987 mortality rates fell by 25% as a result of earlier detection and improved treatment. Age-period-cohort analyses indicate that changes in recognized risk factors may affect mortality patterns. Continued analysis of international and intranational trends may reveal targets for multidisciplinary intervention and prevention efforts. Published 2002 Wiley-Liss, Inc.
C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
RP Lacey, JV (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC 7234, Rockville, MD 20852 USA.
RI Brinton, Louise/G-7486-2015
OI Brinton, Louise/0000-0003-3853-8562
NR 34
TC 157
Z9 162
U1 2
U2 7
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 82
EP 88
DI 10.1002/em.10062
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000002
PM 11921173
ER

PT J
AU Bennett, LM
   Davis, BJ
AF Bennett, LM
   Davis, BJ
TI Identification of mammary carcinogens in rodent bioassays
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NC
SP Environm Mutagen Soc
DE mammary; carcinogen; National Toxicology Program; bioassay; rodent;
   exposure
ID TRANSGENIC MOUSE MODELS; BREAST-CANCER; CHLOROPRENE
   2-CHLORO-1,3-BUTADIENE; MICE; DIETHYLSTILBESTROL; GLAND; 1,3-BUTADIENE;
   INDUCTION; MUTATION; TISSUE
AB Results from chemical carcinogenesis studies in rodents are useful to identify substances in our environment that may contribute to cancer development. The National Toxicology Program (NTP) was established in 1978 to coordinate research and testing of potential human carcinogens and to publish the Report on Carcinogens, which lists human carcinogens. The results for over 500 chemicals tested in the NTP 2-year bioassays have been published in Technical Reports and include data for chemical, agent, or complex mixture exposures. The bioassays have identified 42 chemicals that induce tumors in the rodent mammary gland. The physical and chemical characteristics of the carcinogens vary, but epoxides (including chemicals metabolized to epoxides) and nitro-containing compounds are well represented. The 9th Report on Carcinogens, issued in 2000, lists 21 of the 42 chemicals as human carcinogens including benzene, ethylene oxide, 1,3-butadiene, isoprene, chloroprene, C.I. basic red 9, and C.I. acid red 114. Ethylene oxide was associated with increased breast cancer risk in an epidemiologic study, whereas other listed chemicals, for which human data are available display different target organ specificity. Bioassays other than those conducted by the NTP also provide information about rodent mammary gland carcinogens. Several carcinogen exposures are associated with breast tumor induction in both humans and rodents including radiation, diethylstilbestrol, and estrogens. These studies demonstrate that route, timing and frequency of exposure, and genetic factors contribute to the overall susceptibility to breast cancer development. More information is needed on the effects of chemicals to which humans are exposed and the manner by which they influence breast cancer risks. Published 2002 Wiley-Liss, Inc.(dagger)
C1 Lawrence Livermore Natl Lab, Genet Canc Grp, Biol & Biotechnol Res Program, Livermore, CA 94551 USA.
   NIEHS, Lab Womens Hlth, NIH, Res Triangle Pk, NC 27709 USA.
RP Bennett, LM (reprint author), Lawrence Livermore Natl Lab, Genet Canc Grp, Biol & Biotechnol Res Program, BBRP-L-448,7000 E Ave, Livermore, CA 94551 USA.
EM lmbennett@llnl.gov
NR 50
TC 12
Z9 13
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 150
EP 157
DI 10.1002/em.10068
PG 8
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000012
PM 11921183
ER

PT J
AU Snyderwine, EG
AF Snyderwine, EG
TI Mammary gland carcinogenesis by food-derived heterocyclic amines:
   Metabolism and additional factors influencing carcinogenesis by
   2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NORTH CAROLINA
SP Environm Mutagen Soc
DE mammary gland; carcinogenesis; heterocyclic amines; PhIP; metabolism;
   DNA adduct
ID SPRAGUE-DAWLEY RATS; BREAST-CANCER; DNA-ADDUCTS; LIVER-MICROSOMES;
   IN-VITRO; HIGH-FAT; ACTIVATION; RISK; 7,12-DIMETHYLBENZ<A>ANTHRACENE;
   GLUCURONIDATION
AB The heterocyclic amines (HCAs) are a family of mutagenic/carcinogenic compounds found in cooked meats. Several HCAs are mammary gland carcinogens in rats. Of these compounds, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the major one present in the human diet. This report reviews the studies on rat mammary gland carcinogenesis by HCAs; discusses what is currently known regarding mechanisms of mammary gland carcinogenesis of PhlP, especially the significance of metabolic processing; and further highlights the evidence for the possible role of PhIP in human breast cancer. Published 2002 Wiley-Liss, lnc.(dagger)
C1 NCI, Chem Carcinogenesis Sect, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Snyderwine, EG (reprint author), NCI, Chem Carcinogenesis Sect, Expt Carcinogenesis Lab, Ctr Canc Res, Bldg 37,Room 3C28,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA.
NR 45
TC 18
Z9 20
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 165
EP 170
DI 10.1002/em.10053
PG 6
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000014
PM 11921185
ER

PT J
AU Deng, CX
AF Deng, CX
TI Tumor formation in Brca1 conditional mutant mice
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NORTH CAROLINA
SP Environm Mutagen Soc
DE Brca1; p53; cyclin D1; C-neu; tumorigenesis
ID FAMILIAL BREAST-CANCER; GENETIC INSTABILITY; MOUSE; CELLS; P53;
   MORPHOGENESIS; MUTATIONS; DEFICIENT
AB BRCA1 is the first breast cancer-associated gene, whose mutation predisposes women to breast and ovarian cancers. Targeted mutations of Brca1 in the mouse result in embryonic lethality primarily attributed to cellular proliferation defects, raising questions about the mechanisms by which Brca1 represses tumor formation. To overcome the early lethality, we engineered Brca1 by flanking its exon 11 with loxP sites. We showed that deletion of the exon by EIIA-Cre, which expresses Cre in the germline, causes p53-dependent lethality at late gestation. On the other hand, MMTV-Cre, which expresses Cre in mammary epithelium, resulted in tumorigenesis at low frequency after a long latency, accompanied by increased epithelial cell apoptosis and abnormal ductal development. Mammary tumor formation was significantly accelerated in a p53(+/-) genetic background; however, it still appeared in a stochastic fashion, suggesting the involvement of additional factors. Notably, the tumors were highly diverse in histopathology and displayed extensive genetic/molecular alterations, including overexpression of ErbB2, c-Myc, p27, and Cyclin D1, and downregulation of p16 in the majority of tumors. This observation suggests roles for these proteins in Brca1-associated tumorigenesis. Published 2002 Wiley-Liss, Inc.
C1 NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Deng, CX (reprint author), NIDDK, Genet Dev & Dis Branch, NIH, 10-9N105,10 Ctr Dr, Bethesda, MD 20892 USA.
RI deng, chuxia/N-6713-2016
NR 30
TC 41
Z9 42
U1 0
U2 2
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 171
EP 177
DI 10.1002/em.10069
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000015
PM 11921186
ER

PT J
AU Medina, D
   Ullrich, R
   Meyn, R
   Wiseman, R
   Donehower, L
AF Medina, D
   Ullrich, R
   Meyn, R
   Wiseman, R
   Donehower, L
TI Environmental carcinogens and p53 tumor-suppressor gene interactions in
   a transgenic mouse model for mammary carcinogenesis
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NORTH CAROLINA
SP Environm Mutagen Soc
DE p53; mammary; environmental agents; hormones
ID BREAST-CANCER; MICE; BALB/C; INSTABILITY; APOPTOSIS; PROMOTES
AB Mouse mammary tumorigenesis is greatly influenced by a variety of exogenous agents, such as MMTV, chemical carcinogens (i.e., polycyclic aromatic hydrocarbons), and radiation, as well as by endogenous/physiological factors, such as steroid hormones, tumor-suppressor genes (i.e., Brca1/2, p53), and gene products of modifier genes. In the mouse model, the most frequently used chemical carcinogen has been 7,12-dimethylbenz[a]anthracene (DMBA), which activates the Ha-ras gene but does not alter the p53 tumor-suppressor gene. However, on an existing background of p53 gene alteration, low doses of DMBA are strongly cocarcinogenic. Using a transgenic model system, in which the p53 gene was deleted in the mammary gland, we examined the carcinogenic effects of a variety of external agents and internal factors given at either low doses or physiological doses. These agents/factors included DMBA, gamma-radiation, Brca2 heterozygosity, and steroid hormones. All agents/factors increased the tumorigenic response of the p53 null mammary cells, even under conditions where no tumorigenic response was observed in the p53 wildtype mammary cell. The strongest cocarcinogenic effect was observed with the steroid hormone progesterone. The majority of tumors were highly aneuploid and composed of nuclear igh-grade cells. The mechanism for the aneuploidy and secondary events associated with high tumorigenicity were examined using array technology, These results demonstrate that, on a background of underlying genetic instability, very low doses of environmental mutagens and mitogens can produce strong cocarcinogenic effects. (C) 2002 Wiley-Liss, Inc.
C1 Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA.
   Colorado State Univ, Ft Collins, CO 80523 USA.
   Univ Texas, MD Anderson Canc Ctr, Dept Expt Radiat Oncol, Houston, TX 77030 USA.
   NIEHS, Res Triangle Pk, NC 27709 USA.
   Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA.
RP Medina, D (reprint author), Baylor Coll Med, Dept Mol & Cellular Biol, 1 Baylor Plaza, Houston, TX 77030 USA.
FU NCI NIH HHS [U01CA84243, R01CA84320]
NR 28
TC 17
Z9 17
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 178
EP 183
DI 10.1002/em.10064
PG 6
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000016
PM 11921187
ER

PT J
AU Zujewski, J
AF Zujewski, J
TI Selective estrogen receptor modulators (SERMs) and retinoids in breast
   cancer chemoprevention
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article; Proceedings Paper
CT Conference on Breast Cancer and Environmental Mutagens
CY SEP 22-25, 2001
CL RES TRIANGLE PK, NORTH CAROLINA
SP Environm Mutagen Soc
DE chemoprevention; tamoxifen; selective estrogen receptor modulator;
   raloxifene; fenretinide; insulin-like growth factor 1
ID BONE-MINERAL DENSITY; CARCINOMA CELL-PROLIFERATION; CARDIOVASCULAR
   RISK-FACTORS; POSTMENOPAUSAL WOMEN; MAMMARY-CARCINOMA;
   N-(4-HYDROXYPHENYL) RETINAMIDE; HEPATOCELLULAR-CARCINOMA; MAMMOGRAPHIC
   DENSITIES; SERUM-CHOLESTEROL; RANDOMIZED TRIAL
AB Tamoxifen has been shown to decrease the risk of invasive breast cancer by 49% and noninvasive breast cancer by 50%. Tamoxifen is also associated with a threefold increased risk of endometrial cancer. Raloxifene, a second-generation selective estrogen receptor modulator (SERM), has not been associated with endometrial cancer risk, and is currently study in a large, multi-institutional, randomized of Tamoxifen and Raloxifene (STAR) for breast cancer prevention in postmenopausal women. A pilot trial of raloxifene in premenopausal women to assess the safety, tolerability, effects on bone mineral density, mammographic density, and other biological end-points is ongoing. The retinoids have been shown to decrease mammary tumors in rodent carcinogenesis models. The Italian trial of fenretinide (4-HPR) in women with stage I breast cancer randomized women to fenretinide or no intervention. This study did not show an overall effect of decreasing the risk of contralateral breast cancer. However, a protective effect was suggested in premenopausal women. It has been suggested that this effect may be related to insulin-like growth factor 1 (IGF-1), which has been shown to be modulated by fenretinide in premenopausal but not postmenopausal women. Pilot studies of SERMs alone and in combination with refinoids or other agents provide a model for testing the safety and tolerability, pharmacokinetics and pharmacodynamics, and biomarker modulation in high-risk women. These studies can provide information as to both the pathophysiology of carcinogenesis and the mechanism of action of chemopreventive agents, and help select agents and doses for testing in large randomized studies. Published 2002 Wiley-Liss, Inc.(dagger).
C1 NCI, Ctr Canc Res, Med Oncol Clin Res Unit, Bethesda, MD 20892 USA.
RP Zujewski, J (reprint author), NCI, Ctr Canc Res, Med Oncol Clin Res Unit, Bldg 10,Room 12N 226,9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 70
TC 9
Z9 9
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 2-3
BP 264
EP 270
DI 10.1002/em.10054
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 532UT
UT WOS:000174494000026
PM 11921197
ER

PT J
AU Vermeulen, R
   Talaska, G
   Schumann, B
   Bos, RP
   Rothman, N
   Kromhout, H
AF Vermeulen, R
   Talaska, G
   Schumann, B
   Bos, RP
   Rothman, N
   Kromhout, H
TI Urothelial cell DNA adducts in rubber workers
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE rubber industry; urothelial cells; DNA adducts; aryldiamine; NAT2
ID BLADDER-CANCER; MANUFACTURING-INDUSTRY; LIQUID-CHROMATOGRAPHY;
   N-ACETYLATION; CARBON-BLACK; EXPOSURE; MORTALITY; RISK; URINE;
   MUTAGENICITY
AB Workers employed in the rubber industry appear to have a significant excess cancer risk in a variety of sites, including cancer of the urinary bladder. In this cross-sectional study, we investigated the occurrence of DNA adducts in exfoliated bladder cells of currently exposed, nonsmoking rubber workers (n = 52) and their relationship with occupational exposure estimates and acetylation phenotype (NAT2). Four DNA adducts were identified, with the proportion of positive samples (e.g., DNA samples with quantifiable levels of a specific DNA adduct) ranging from 3.8 to 79%. The highest proportion of positive samples and the highest relative adduct labeling levels were in workers involved in the production functions "mixing" and "curing," areas with potential for substantial exposure to a wide range of chemical compounds used in rubber manufacturing (P < 0.05 for adducts 2 and/or 3, compared to all other departments). No statistically significant relationships were found between identified DNA adducts and urinary mutagenicity or personal inhalable and dermal exposure estimates. Interestingly, subjects with a fast NAT2 acetylation phenotype tended to have higher levels of DNA adducts. This study suggests that rubber workers engaged in mixing and curing may be exposed to compounds that can form DNA adducts in urothelial cells. Larger studies among rubber workers should be conducted to study in more detail the potential carcinogenicity of exposures encountered in these work areas. Published 2002 Wiley-Liss, Inc.(dagger)
C1 NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
   Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Grp, Utrecht, Netherlands.
   Univ Nijmegen, Dept Pharmacol & Toxicol, Nijmegen, Netherlands.
   Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH USA.
RP Vermeulen, R (reprint author), NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Rockville, MD 20852 USA.
RI Kromhout, Hans/A-9159-2008; Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
FU PHS HHS [263-MQ-001469, 263-MQ-004907]
NR 47
TC 17
Z9 17
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PY 2002
VL 39
IS 4
BP 306
EP 313
DI 10.1002/em.10078
PG 8
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 570VA
UT WOS:000176678200003
PM 12112382
ER

PT J
AU Tennant, RW
AF Tennant, RW
TI The national center for toxicogenomics: Using new technologies to inform
   mechanistic toxicology
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
ID COMPLEMENTARY-DNA MICROARRAY; GENE-EXPRESSION; PATTERNS; IDENTIFICATION;
   GENOME; ARRAYS; CHIPS
C1 NIEHS, Natl Ctr Toxicogenom, Res Triangle Pk, NC 27709 USA.
RP Tennant, RW (reprint author), NIEHS, Natl Ctr Toxicogenom, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 30
TC 60
Z9 67
U1 1
U2 8
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
   RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD JAN
PY 2002
VL 110
IS 1
BP A8
EP A10
DI 10.1289/ehp.110-a8
PG 3
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Toxicology
GA 521WH
UT WOS:000173864000001
PM 11781174
ER

PT J
AU Johnson, CC
   Ownby, DR
   Zoratti, EM
   Alford, SH
   Williams, LK
   Joseph, CLM
AF Johnson, CC
   Ownby, DR
   Zoratti, EM
   Alford, SH
   Williams, LK
   Joseph, CLM
TI Environmental epidemiology of pediatric asthma and allergy
SO EPIDEMIOLOGIC REVIEWS
LA English
DT Review
ID SKIN-TEST REACTIVITY; BODY-MASS INDEX; HOUSE-DUST MITE; CORD SERUM IGE;
   LOWER RESPIRATORY ILLNESS; PROSPECTIVE BIRTH COHORT; NEW-ZEALAND
   CHILDREN; DAY-CARE ATTENDANCE; T-CELL ACTIVATION; AGE 4 YEARS
C1 Henry Ford Hlth Sci Ctr, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA.
   Wayne State Univ, NIEHS, Ctr Mol & Cellular Toxicol Human Applicat, Detroit, MI USA.
   Med Coll Georgia, Sect Allergy Immunol, Augusta, GA USA.
   Henry Ford Hlth Syst, Sect Allergy & Immunol, Div Pulm Crit Care Allergy Immunol & Sleep Med, Detroit, MI USA.
   Henry Ford Hlth Syst, Dept Med, Detroit, MI USA.
RP Johnson, CC (reprint author), Henry Ford Hlth Sci Ctr, Dept Biostat & Res Epidemiol, 1 Ford Pl,5C, Detroit, MI 48202 USA.
OI Johnson, Christine Cole/0000-0002-6864-6604
FU NHLBI NIH HHS [HL67462, HL68971, HL68245, HL67427]; NIAID NIH HHS
   [AI50681]; NIEHS NIH HHS [P03ES06639]
NR 228
TC 46
Z9 47
U1 1
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0193-936X
J9 EPIDEMIOL REV
JI Epidemiol. Rev.
PY 2002
VL 24
IS 2
BP 154
EP 175
DI 10.1093/epirev/mxf013
PG 22
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 675AA
UT WOS:000182669700006
PM 12762090
ER

PT J
AU Veld, BAIT
   Launer, LJ
   Breteler, MMB
   Hofman, A
   Stricker, BHC
AF Veld, BAIT
   Launer, LJ
   Breteler, MMB
   Hofman, A
   Stricker, BHC
TI Pharmacologic agents associated with a preventive effect on Alzheimer's
   disease: A review of the epidemiologic evidence
SO EPIDEMIOLOGIC REVIEWS
LA English
DT Review
ID ESTROGEN-REPLACEMENT THERAPY; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
   RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL;
   ANTIHYPERTENSIVE-MEDICATION-USE; HISTAMINE-H2 BLOCKING-DRUGS;
   POPULATION-BASED COHORT; CORONARY-HEART-DISEASE; EXTRACT EGB 761;
   POSTMENOPAUSAL WOMEN
C1 Erasmus MC, Dept Epidemiol & Biostat, NL-3000 DR Rotterdam, Netherlands.
   Drug Safety Unit, The Hague, Netherlands.
   Leiden Univ, Ctr Med, Dept Anesthesiol, Leiden, Netherlands.
   NIA, Epidemiol Demog & Biometry Program, Bethesda, MD USA.
RP Stricker, BHC (reprint author), Erasmus MC, Dept Epidemiol & Biostat, POB 1738, NL-3000 DR Rotterdam, Netherlands.
EM b.stricker@erasmusmc.nl
RI Breteler, Monique /J-5058-2014
NR 187
TC 6
Z9 7
U1 4
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0193-936X
EI 1478-6729
J9 EPIDEMIOL REV
JI Epidemiol. Rev.
PY 2002
VL 24
IS 2
BP 248
EP 268
DI 10.1093/epirev/mxf001
PG 21
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 675AA
UT WOS:000182669700012
ER

PT J
AU Lee, GM
   Neutra, RR
   Hristova, L
   Yost, M
   Hiatt, RA
AF Lee, GM
   Neutra, RR
   Hristova, L
   Yost, M
   Hiatt, RA
TI A nested case-control study of residential and personal magnetic field
   measures and miscarriages
SO EPIDEMIOLOGY
LA English
DT Article
DE miscarriage; spontaneous abortion; magnetic fields; electromagnetic
   fields; maternal exposure; wire codes
ID VIDEO DISPLAY TERMINALS; SPONTANEOUS-ABORTION; ELECTRIC BLANKETS;
   EARLY-PREGNANCY; CHICK-EMBRYOS; EXPOSURE; CANCER; RISK
AB We conducted a nested case-control study (177 cases, 550 controls) to assess the relation between retrospective magnetic field measures and clinical miscarriage among members of the northern California Kaiser Permanente medical care system. We also conducted a prospective substudy of 219 participants of the same parent cohort to determine whether 12-week and 30-week exposure assessments were similar. We evaluated wire codes, area measures, and three personal meter metrics: (1) the average difference between consecutive levels (a rate,of-change metric), (2) the maximum level, and (3) the time-weighted average. For wire codes and area measures we found little association. For the personal metrics (30 weeks after last menstrual period), we found positive associations. Each exposure was divided into quartiles, with the lowest quartile as referent. Starting with the highest quartile, adjusted odds ratios and 95% confidence intervals were 3.1 (95% CI = 1.6-6.0), 2.3 (95% CI = 1.2-4.4), and 1.5 (95% CI = 0.8-3.1) for the rate-ofchange metric; 2.3 (95% CI = 1.24-4), 1.9 (95% CI = 1.0-3.5), and 1.4 (95% CI = 0.7-2.8) for the maximum value; and 1.7 (95% CI = 0.9-3.3), 1.7 (95% CI = 0.9-3.3), and 1.7 (95% CI = 0.9-3.3) for the time-weighted average. The odds ratio conveyed by being above a 24-hour time-weighted average of 2 milligauss was 1.0 (95% Cl = 0.5-2.1). Exposure assessment measurements at 12 weeks were poorly correlated with those taken at 30 weeks. Nonetheless, the prospective substudy results regarding miscarriage risk were consistent with the nested study results.
C1 Calif Dept Hlth Serv, Environm Hlth Invest Branch, Oakland, CA 94612 USA.
   Univ Washington, Dept Environm Hlth, Seattle, WA 98195 USA.
   NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Neutra, RR (reprint author), Calif Dept Hlth Serv, Environm Hlth Invest Branch, 1515 Clay St,17th Floor, Oakland, CA 94612 USA.
NR 21
TC 67
Z9 72
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD JAN
PY 2002
VL 13
IS 1
BP 21
EP 31
DI 10.1097/00001648-200201000-00005
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 505HY
UT WOS:000172908400005
PM 11805582
ER

PT J
AU Hemila, H
   Kaprio, J
   Albanes, D
   Heinonen, OP
   Virtamo, J
AF Hemila, H
   Kaprio, J
   Albanes, D
   Heinonen, OP
   Virtamo, J
TI Vitamin C, vitamin E, and beta-carotene in relation to common cold
   incidence in male smokers
SO EPIDEMIOLOGY
LA English
DT Article
DE alcohol; alpha-tocopherol; ascorbic acid; beta carotene; fruits;
   smoking; upper respiratory infections; vegetables
ID HEALTHY ELDERLY SUBJECTS; CONTROLLED TRIAL; IMMUNE-RESPONSE; E
   SUPPLEMENTATION; INFECTIONS; FOOD; SUSCEPTIBILITY; SYMPTOMS; ILLNESS;
   DIETARY
AB We evaluated the role of dietary vitamin C, vitamin E, and beta,carotene, as well as long-term vitamin E and beta-carotene supplementation, on the incidence of common ci,td episodes. A cohort of 21,796 male smokers was drawn from the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study, which examined the effects of 50 mg per day vitamin E and 20 mg per day beta-carotene on lung cancer, Diet and background characteristics were recorded at the study entry, and subjects were queried three times per year on common cold episodes. We modeled the total number of colds during a 4-year follow-up period with Poisson regression, adjusting for covariates of dietary intake. Dietary vitamins C and E and beta,carotene had no meaningful association with common cold incidence. Long-term vitamin E and beta-carotene supplementation had no overall effect. Among subjects 65 years of age or older, the incidence of colds was slighty tower in the vitamin E group (RR = 0.95; 95% CI = 0.90-1.00); this reduction was greatest among, older city dwellers who smoked fewer than 15 cigarettes per day (RR = 0.72; 95% CI = 0.62-0.83). In this male smoking population, vitamins C and E and beta-carotene had no overall association with the incidence of common cold episodes.
C1 Univ Helsinki, Dept Publ Hlth, FIN-00014 Helsinki, Finland.
   Natl Publ Hlth Inst, Helsinki, Finland.
   NCI, Bethesda, MD 20892 USA.
RP Hemila, H (reprint author), Univ Helsinki, Dept Publ Hlth, POB 41, FIN-00014 Helsinki, Finland.
RI Kaprio, Jaakko/A-1820-2008; Albanes, Demetrius/B-9749-2015; 
OI Hemila, Harri/0000-0002-4710-307X; Kaprio, Jaakko/0000-0002-3716-2455
FU NCI NIH HHS [N01-CN-45165]
NR 39
TC 30
Z9 32
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD JAN
PY 2002
VL 13
IS 1
BP 32
EP 37
DI 10.1097/00001648-200201000-00006
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 505HY
UT WOS:000172908400006
PM 11805583
ER

PT J
AU Vachon, CM
   Mink, PJ
   Janney, CA
   Sellers, TA
   Cerhan, JR
   Hartmann, L
   Folsom, AR
AF Vachon, CM
   Mink, PJ
   Janney, CA
   Sellers, TA
   Cerhan, JR
   Hartmann, L
   Folsom, AR
TI Association of parity and ovarian cancer risk by family history of
   breast or ovarian cancer in a population-based study of postmenopausal
   women
SO EPIDEMIOLOGY
LA English
DT Article
DE ovarian cancer; parity; family history; risk factors; prospective cohort
   study
ID FOLLOW-UP; REPRODUCTIVE FACTORS; FERTILITY DRUGS; OLDER WOMEN; BRCA1;
   ACCURACY; OVULATION; DATABASE; CARRIERS
AB Although parity is associated with a decreased risk of ovarian cancer in the general population, this association among women with a family history is less clear. We examined this question in a prospective cohort of 31,377 Iowa women 55-69 years of age at baseline. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated through Cox regression. We identified 181 incident epithelial ovarian cancers through 13 years of follow-up. At baseline, 14% of the women reported breast or ovarian cancer in a first-degree relative, and an additional 12% reported a family history in a second-degree relative. Among women without a family history of breast or ovarian cancer in a first-degree relative, nulliparous women were at slightly increased risk of ovarian cancer (RR = 1.4, 95% CI = 0.9-2.4) compared with parous women, whereas among women with a family history, nulliparous women were at a much higher risk (RR = 2.7, 95% CI = 1.1-6.6) than parous women. Similar results were seen when family history included first- or second-degree relatives with breast or ovarian cancer or a first- or second degree relative with ovarian cancer only. Nulliparity may be more strongly associated with an increased risk of ovarian cancer among women with a family history of breast or ovarian cancer, compared with women who do not have a family history of those cancers.
C1 Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, Rochester, MN 55905 USA.
   Mayo Clin & Mayo Fdn, Dept Oncol, Rochester, MN 55905 USA.
   Mayo Clin & Mayo Fdn, Ctr Canc, Rochester, MN 55905 USA.
   NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
   Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA.
RP Vachon, CM (reprint author), Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, 200 1st St SW, Rochester, MN 55905 USA.
FU PHS HHS [A39742]
NR 33
TC 19
Z9 19
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD JAN
PY 2002
VL 13
IS 1
BP 66
EP 71
DI 10.1097/00001648-200201000-00011
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 505HY
UT WOS:000172908400011
PM 11805588
ER

PT J
AU Blair, A
   Tarone, R
   Sandler, D
   Lynch, CF
   Rowland, A
   Wintersteen, W
   Steen, WC
   Samanic, C
   Dosemeci, M
   ALavanja, MCR
AF Blair, A
   Tarone, R
   Sandler, D
   Lynch, CF
   Rowland, A
   Wintersteen, W
   Steen, WC
   Samanic, C
   Dosemeci, M
   ALavanja, MCR
TI Reliability of reporting on life-style and agricultural factors by a
   sample of participants in the agricultural health study from Iowa
SO EPIDEMIOLOGY
LA English
DT Article
DE pesticides; reliability; agriculture
ID PROXY RESPONDENTS; PESTICIDE USE; EXPOSURE; SELF; MISCLASSIFICATION;
   REPEATABILITY; QUESTIONNAIRE; INFORMATION; FARMERS; CANCER
AB Repeat interviews from 4,088 Iowa pesticide applicators participating in the Agricultural Health Study provided the opportunity to evaluate the reliability of self-reported information on pesticide use and various demographic and lifestyle factors. Self-completed questionnaires were administered 1 year apart when participants returned to county agricultural extension offices for pesticide certification or training. Percentage agreement for ever-/never-use of specific pesticides and application practices was quite high, generally ranging from 70% to more than 90%, and did not vary by age, educational level, or farm size. Agreement was lower (typically 50-60%) for duration, frequency, or decade of first use of specific pesticides. Level of agreement regarding pesticide use in this population is similar to that generally found for factors typically used in epidemiologic studies such as tobacco use and higher than typically reported for diet, physical activity, and medical conditions.
C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
   Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
   Iowa State Univ, Extens Serv, Ames, IA USA.
   US EPA, Athens, GA USA.
RP Blair, A (reprint author), NCI, Div Canc Epidemiol & Genet, EPS Room 8118, Bethesda, MD 20892 USA.
NR 23
TC 125
Z9 128
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD JAN
PY 2002
VL 13
IS 1
BP 94
EP 99
DI 10.1097/00001648-200201000-00015
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 505HY
UT WOS:000172908400015
PM 11805592
ER

PT J
AU Hikosaka, O
AF Hikosaka, O
TI A new approach to the functional systems of the brain
SO EPILEPSIA
LA English
DT Article; Proceedings Paper
CT 34th Congress of the Japan-Epilepsy-Society
CY SEP 21-22, 2000
CL TOKYO, JAPAN
SP Japan Epilepsy Soc
DE visuomotor sequence learning; procedural memory; learned action; basal
   ganglia; premotor cortex; cerebellum
ID PRESUPPLEMENTARY MOTOR AREA; MEDIAL FRONTAL-CORTEX;
   SEQUENTIAL-PROCEDURES; NEURONAL-ACTIVITY; MONKEY; MEMORY; ACTIVATION;
   RETENTION; MOVEMENTS; SUPERIOR
AB Action is the means by which animals survive. It consists of a complex combination of movements that are either innately endowed or acquired by learning. Innate and learned actions are controlled by different levels of neural networks: innate actions are controlled by reflex mechanisms and pattern generators in the spinal cord and brainstem, whereas learned actions are controlled by the cerebral cortex, basal ganglia, and cerebellum. However, these mechanisms are by no means independent. Recent studies have shown that multiple brain areas contribute to the implementation of learned actions. Based on a series of studies using a sequenced learning task with trial and error, we propose a hypothetical scheme in which a sequential procedure is acquired independently by two cortical systems, one using spatial coordinates, and the other using motor coordinates. They are active preferentially in the early and late stages of learning, respectively. Both of the systems are supported by loop circuits formed with the basal ganglia and the cerebellum, the former for reward-based evaluation and the latter for processing of timing. The proposed neural architecture would operate in a flexible manner to acquire and execute multiple sequential procedures.
C1 Juntendo Univ, Sch Med, Dept Physiol, Tokyo 113, Japan.
RP Hikosaka, O (reprint author), NEI, Sensorimotor Res Lab, NIH, Bldg 49,Rm 2A50, Bethesda, MD 20892 USA.
NR 17
TC 2
Z9 2
U1 0
U2 0
PU BLACKWELL PUBLISHING INC
PI MALDEN
PA 350 MAIN ST, MALDEN, MA 02148 USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PY 2002
VL 43
SU 9
BP 9
EP 15
DI 10.1046/j.1528-1157.43.s.9.4.x
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 617HV
UT WOS:000179357000004
PM 12383273
ER

PT J
AU Binder, JR
   Achten, E
   Constable, RT
   Detre, JA
   Gaillard, WD
   Jack, CR
   Loring, DW
AF Binder, JR
   Achten, E
   Constable, RT
   Detre, JA
   Gaillard, WD
   Jack, CR
   Loring, DW
TI Functional MRI in epilepsy
SO EPILEPSIA
LA English
DT Article; Proceedings Paper
CT 3rd International Magnetic Resonance and Epilepsy Symposium
CY OCT 20-21, 2000
CL UNIV BIRMINGHAM, BIRMINGHAM, ALABAMA
HO UNIV BIRMINGHAM
ID ANTERIOR TEMPORAL LOBECTOMY; PRIMARY MOTOR CORTEX; INTRACAROTID
   AMOBARBITAL TEST; REGIONAL BRAIN ACTIVITY; CEREBRAL BLOOD-FLOW; LANGUAGE
   DOMINANCE; GRADIENT-ECHO; LOBE EPILEPSY; FIELD INHOMOGENEITIES; HAND
   AREA
C1 Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA.
   Med Coll Georgia, Dept Neurol, Augusta, GA 30912 USA.
   Mayo Clin, Dept Radiol, Rochester, MN USA.
   NIH, Clin Epilepsy Sect, Bethesda, MD 20892 USA.
   Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA.
   Yale Univ, Dept Neurosurg, New Haven, CT USA.
   Yale Univ, Dept Diagnost Radiol, New Haven, CT USA.
   State Univ Ghent Hosp, B-9000 Ghent, Belgium.
RP Binder, JR (reprint author), Med Coll Wisconsin, Dept Neurol, 9200 W Wisconsin Ave, Milwaukee, WI 53226 USA.
RI Jack, Clifford/F-2508-2010; 
OI Jack, Clifford/0000-0001-7916-622X; Binder, Jeffrey/0000-0002-2233-5640
NR 127
TC 14
Z9 14
U1 0
U2 0
PU BLACKWELL PUBLISHING INC
PI MALDEN
PA 350 MAIN ST, MALDEN, MA 02148 USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PY 2002
VL 43
SU 1
BP 51
EP 63
DI 10.1046/j.1528-1157.2002.043s1051.x
PG 13
WC Clinical Neurology
SC Neurosciences & Neurology
GA 528DL
UT WOS:000174229100008
ER

PT J
AU Alsop, DC
   Connelly, A
   Duncan, JS
   Hufnagel, A
   Pierpaoli, C
   Rugg-Gunn, FJ
AF Alsop, DC
   Connelly, A
   Duncan, JS
   Hufnagel, A
   Pierpaoli, C
   Rugg-Gunn, FJ
TI Diffusion and perfusion MRI in epilepsy
SO EPILEPSIA
LA English
DT Article; Proceedings Paper
CT 3rd International Magnetic Resonance and Epilepsy Symposium
CY OCT 20-21, 2000
CL UNIV BIRMINGHAM, BIRMINGHAM, AL
HO UNIV BIRMINGHAM
ID CEREBRAL-BLOOD-FLOW; PARTIAL STATUS EPILEPTICUS; ACUTE HUMAN STROKE;
   WATER DIFFUSION; HUMAN BRAIN; LOBE EPILEPSY; NAVIGATOR ECHOES;
   NERVOUS-SYSTEM; SELF-DIFFUSION; TENSOR MRI
C1 UCL, Inst Child Hlth, Radiol & Phys Unit, London WC1N 1EH, England.
   Harvard Univ, Sch Med, Boston, MA USA.
   Natl Soc Epilepsy, MR Unit, London, England.
   Univ Hosp, Dept Neurol, Essen, Germany.
   NICHHD, NIH, Bethesda, MD USA.
RP Connelly, A (reprint author), UCL, Inst Child Hlth, Radiol & Phys Unit, 30 Guilford St, London WC1N 1EH, England.
EM aconnell@ich.ucl.ac.uk
RI Pierpaoli, Carlo/E-1672-2011; Connelly, Alan/A-9065-2013; Alsop,
   David/J-5764-2013
OI Alsop, David/0000-0002-8206-1995
NR 58
TC 14
Z9 15
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PY 2002
VL 43
SU 1
BP 69
EP 77
DI 10.1046/j.1528-1157.2002.043s1069.x
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 528DL
UT WOS:000174229100010
ER

PT J
AU Rogawski, MA
   Reddy, DS
AF Rogawski, MA
   Reddy, DS
TI Neurosteroids and infantile spasms: The deoxycorticosterone hypothesis
SO EPILEPSY, INFANTILE SPASMS, AND DEVELOPMENTAL ENCEPHALOPATHY
SE INTERNATIONAL REVIEW OF NEUROBIOLOGY
LA English
DT Review
ID CORTICOTROPIN-RELEASING HORMONE; AMINOBUTYRIC ACID(A) RECEPTOR;
   NEUROACTIVE STEROIDS; ANTICONVULSANT ACTIVITY; RAT-BRAIN; SWIM STRESS;
   ADRENOCORTICOTROPIC HORMONE; GABA RECEPTOR; KAINIC ACID; ACTH
C1 NINCDS, Epilepsy Res Sect, NIH, Bethesda, MD 20892 USA.
RP Rogawski, MA (reprint author), NINCDS, Epilepsy Res Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
OI Reddy, Samba/0000-0003-2735-9550
NR 112
TC 32
Z9 33
U1 0
U2 3
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0074-7742
J9 INT REV NEUROBIOL
PY 2002
VL 49
BP 199
EP 219
PG 21
WC Neurosciences
SC Neurosciences & Neurology
GA BU48D
UT WOS:000176124400012
PM 12040893
ER

PT J
AU Street, LL
   Luoma, JB
AF Street, LL
   Luoma, JB
TI Control groups in psychosocial intervention research: Ethical and
   methodological issues
SO ETHICS & BEHAVIOR
LA English
DT Article
DE psychosocial interventions; control groups; placebo; research ethics
ID PSYCHOTHERAPY; CONSENT; THERAPY
AB This article summarizes a National Institute of Mental Health (NIMH) workshop that was convened to address the ethical and methodological issues that arise when conducting controlled psychosocial interventions research and introduces 6 thoughtful and inspiring papers prepared by workshop participants. These papers, on topics ranging from informed consent to ethnic minority issues, reflect the depth and breadth of expertise represented by the multidisciplinary group of scientists and ethicists present at the meeting. More extensive follow-up, particularly from federal research applications and publications, of how investigators balance the need for strong research design with ethical considerations may help advance the science of psychosocial intervention research.
C1 NIMH, Bethesda, MD 20892 USA.
   Catholic Univ Amer, Washington, DC 20064 USA.
RP Street, LL (reprint author), NIMH, 6001 Execut Blvd,Room 7160,MSC 9635, Bethesda, MD 20892 USA.
NR 22
TC 21
Z9 22
U1 1
U2 9
PU LAWRENCE ERLBAUM ASSOC INC
PI MAHWAH
PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA
SN 1050-8422
J9 ETHICS BEHAV
JI Ethics Behav.
PY 2002
VL 12
IS 1
BP 1
EP 30
DI 10.1207/S15327019EB1201_1
PG 30
WC Ethics; Psychology, Multidisciplinary
SC Social Sciences - Other Topics; Psychology
GA 541PH
UT WOS:000174992600001
PM 12171079
ER

PT B
AU Schairer, C
AF Schairer, C
TI Risk and prognostic factors for breast cancer in young women
SO EUROCANCER 2002
LA English
DT Proceedings Paper
CT 15th Congress of the Eurocancer
CY JUN 04-05, 2002
CL PARIS, FRANCE
C1 NCI, Bethesda, MD 20892 USA.
RP Schairer, C (reprint author), NCI, Bethesda, MD 20892 USA.
NR 7
TC 0
Z9 0
U1 0
U2 0
PU JOHN LIBBEY EUROTEXT
PI MONTROUGE
PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE
BN 2-7420-0433-5
PY 2002
BP 45
EP 46
PG 2
WC Oncology
SC Oncology
GA BX45B
UT WOS:000185329900013
ER

PT J
AU Maeda, T
   Kitazoe, M
   Tada, H
   de Llorens, R
   Salomon, DS
   Ueda, M
   Yamada, H
   Seno, M
AF Maeda, T
   Kitazoe, M
   Tada, H
   de Llorens, R
   Salomon, DS
   Ueda, M
   Yamada, H
   Seno, M
TI Growth inhibition of mammalian cells by eosinophil cationic protein
SO EUROPEAN JOURNAL OF BIOCHEMISTRY
LA English
DT Article
DE cell cycle; colony formation; cytostatic effect; eosinophil cationic
   protein (ECP); growth inhibition
ID HUMAN PANCREATIC RIBONUCLEASE; HUMAN IMMUNOTOXIN ANALOG;
   SCHISTOSOMA-MANSONI; COMPARATIVE TOXICITY; ANGSTROM RESOLUTION; TERMINAL
   SEQUENCE; CRYSTAL-STRUCTURE; GRANULE PROTEINS; NEUROTOXIN; INVITRO
AB Eosinophil cationic protein (ECP), one of the major components of basic granules of eosinophils, is cytotoxic to tracheal epithelium. However, the extent of this effect on other cell types has not been evaluated in vitro. In this study, we evaluated the effect of ECP on 13 mammalian cell lines. ECP inhibited the growth of several cell lines including those derived from carcinoma and leukemia in a dose-dependent manner. The IC50 values on A431 cells, MDA-MB-453 cells, HL-60 cells and K562 cells were estimated to be approximate to1-5 muM. ECP significantly suppressed the size of colonies of A431 cells, and decreased K562 cells in G(1)/G(0) phase. However, there was little evidence that ECP killed cells in either cell line. These effects of ECP were not enhanced by extending its N-terminus. Rhodamine B isothiocyanate-labeled ECP started to bind to A431 cells after 0.5 h and accumulated for up to 24 h, indicating that specific affinity for the cell surface may be important. ne affinity of ECP for heparin was assessed and found to be reduced when tryptophan residues, one of which is located at a position in the catalytic subsite of ribonuclease in ECP, were modified. The growth-inhibitory effect was also attenuated by this modification. These results suggest that growth inhibition by ECP is dependent on cell type and is cytostatic.
C1 Okayama Univ, Grad Sch Nat Sci & Technol, Fac Engn, Dept Biosci & Biotechnol, Okayama 7008530, Japan.
   Univ Girona, Fac Sci, Dept Biol, Girona, Spain.
   NCI, Tumor Growth Factor Sect, Basic Res Lab, NIH, Bethesda, MD 20892 USA.
   Keio Univ, Sch Med, Dept Surg, Tokyo 160, Japan.
RP Seno, M (reprint author), Okayama Univ, Grad Sch Nat Sci & Technol, Fac Engn, Dept Biosci & Biotechnol, 3-1-1 Tsushima Naka, Okayama 7008530, Japan.
RI YAMADA, Hidenori/B-2639-2011; SENO, Masaharu /B-2092-2011
OI SENO, Masaharu /0000-0001-8547-6259
NR 57
TC 48
Z9 48
U1 2
U2 5
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0014-2956
J9 EUR J BIOCHEM
JI Eur. J. Biochem.
PD JAN
PY 2002
VL 269
IS 1
BP 307
EP 316
DI 10.1046/j.0014-2956.2001.02653.x
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 513UP
UT WOS:000173398100034
PM 11784325
ER

PT J
AU Bodor, J
   Bodorova, J
   Bare, C
   Hodge, DL
   Young, HA
   Gress, RE
AF Bodor, J
   Bodorova, J
   Bare, C
   Hodge, DL
   Young, HA
   Gress, RE
TI Differential inducibility of the transcriptional repressor ICER and its
   role in modulation of Fas ligand expression in T and NK lymphocytes
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE transcription factor; apoptosis; T lymphocyte; NK cell
ID CYTOKINE GENE-EXPRESSION; POTENTIAL ROLE; CELL-DEATH; MICE; NFAT;
   APOPTOSIS; FAMILY; INVOLVEMENT; PROMOTER; PROTEIN
AB The engagement of antigen receptor can initiate apoptosis of T lymphocytes through the induced expression of Fas ligand (FasL). Forskolin, an activator of the cAMP/PKA pathway, results in antagonism of Fas-dependent, activation-induced cell death (AICD) by suppressed expression of the FasL. We report that forskolin-mediated induction of inducible cAMP early repressor (ICER) correlates with transcriptional attenuation of FasL expression in the AICD model 2134 T cell hybridoma. ICER is inducible in human peripheral blood CD3(+) T cells, but in CD19(+) B cells, its induction is less responsive to forskolin treatment. Increased expression of ICER correlates with decreased FasL expression in both T and NK cells. ICER binds specifically to the proximal DNA binding site of the nuclear factor of activated T cells (NFAT) in the FasL promoter and in the presence of the minimal NFAT DNA-binding domain, the proximal NFAT motif allows ICER and NFAT to form an NFAT/ICER ternary complex in vitro. Moreover, in the activated 2B4 T cell hybridoma, the proximal INFAT motif participates in the down-regulation of the FasL promoter mediated by ICER. These findings provide further insight into the mechanism involved in cAMP-mediated transcriptional attenuation of FasL expression in T and INK lymphocytes.
C1 NCI, Expt Immunol Branch, Div Basic Sci, NIH, Bethesda, MD 20892 USA.
   NCI, Transplantat Therapy Sect, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Frederick Canc Res & Dev Ctr, Biol Response Modifiers Program, Expt Immunol Lab, Frederick, MD 21701 USA.
RP Gress, RE (reprint author), NCI, Expt Immunol Branch, Div Basic Sci, NIH, Bldg 10,Rm 4B14,10 Ctr Dr, Bethesda, MD 20892 USA.
NR 35
TC 16
Z9 19
U1 0
U2 0
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD JAN
PY 2002
VL 32
IS 1
BP 203
EP 212
DI 10.1002/1521-4141(200201)32:1<203::AID-IMMU203>3.0.CO;2-C
PG 10
WC Immunology
SC Immunology
GA 515ZV
UT WOS:000173527400023
PM 11754361
ER

PT J
AU Dimmock, JR
   Jha, A
   Kumar, P
   Zello, GA
   Quail, JW
   Oloo, EO
   Oucharek, JJ
   Pasha, MK
   Seitz, D
   Sharma, RK
   Allen, TM
   Santos, CL
   Manavathu, EK
   De Clercq, E
   Balzarini, J
   Stables, JP
AF Dimmock, JR
   Jha, A
   Kumar, P
   Zello, GA
   Quail, JW
   Oloo, EO
   Oucharek, JJ
   Pasha, MK
   Seitz, D
   Sharma, RK
   Allen, TM
   Santos, CL
   Manavathu, EK
   De Clercq, E
   Balzarini, J
   Stables, JP
TI Cytotoxic 1,4-bis(2-oxo-1-cycloalkylmethylene)benzenes and related
   compounds
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE cytotoxicity; alpha,beta-unsaturated ketones; Mannich bases;
   N-myristoyltransferase; X-ray crystallography
ID CONJUGATED STYRYL KETONES; HUMAN-COLON-CARCINOMA;
   N-MYRISTOYLTRANSFERASE; MANNICH-BASES; IN-VITRO; INHIBITION; ANTICANCER;
   KINASE; GROWTH; POTENTIATION
AB A series of 1,4-bis(2-oxo-1-cycloalkylmethylene)benzenes 2a-c and 4 and a related acyclic analogue 6a were synthesised and converted to the corresponding Mannich bases 3a-c, 5 and 6b. Evaluation of these compounds against murine P388 and L1210 cells as well as human Molt 4/C8 and CEM T-lymphocytes revealed that the Mannich bases were more cytotoxic than the corresponding unsaturated ketones. 1,4-bis(3-Dimethylaminomethyl-2-oxo-1-cyclohexylmethylene) benzene dihydrochloride (3a) had lower IC(50) values than melphalan against the four cell lines and was 15 times more potent than this drug when examined against a panel of human tumours. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved.
C1 Univ Saskatchewan, Coll Phar & Nutr, Saskatoon, SK S7N 5C9, Canada.
   Univ Saskatchewan, Saskatchewan Canc Agcy, Coll Med, Dept Pathol, Saskatoon, SK S7N 4H4, Canada.
   Univ Alberta, Dept Pharmacol, Edmonton, AB T6G 2H7, Canada.
   Wayne State Univ, Dept Med, Detroit, MI 48201 USA.
   Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium.
   NINCDS, NIH, Bethesda, MD 20892 USA.
   Univ Saskatchewan, Dept Chem, Saskatoon, SK S7N 5C9, Canada.
   Univ Saskatchewan, Canc Res Unit, Hlth Res Div, Saskatoon, SK S7N 5C9, Canada.
RP Dimmock, JR (reprint author), Univ Saskatchewan, Coll Phar & Nutr, 110 Sci Pl, Saskatoon, SK S7N 5C9, Canada.
EM dimmock@skyway.usask.ca
RI Jha, Amitabh/B-5452-2010
OI Jha, Amitabh/0000-0002-6305-0721
NR 46
TC 21
Z9 21
U1 0
U2 1
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0223-5234
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD JAN
PY 2002
VL 37
IS 1
BP 35
EP 44
AR PII S0223-5234(01)01294-6
DI 10.1016/S0223-5234(01)01294-6
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 533LZ
UT WOS:000174532700004
PM 11841873
ER

PT J
AU Leenders, AGM
   van den Maagdenberg, AMJM
   da Silva, FHL
   Sheng, ZH
   Molenaar, PC
   Ghijsen, WEJM
AF Leenders, AGM
   van den Maagdenberg, AMJM
   da Silva, FHL
   Sheng, ZH
   Molenaar, PC
   Ghijsen, WEJM
TI Neurotransmitter release from tottering mice nerve terminals with
   reduced expression of mutated P- and Q-type Ca2+-channels
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE amino acid release; cholecystokinin release; Ca2+-channels; presynaptic
   terminal
ID CALCIUM CHANNELS; N-TYPE; SYNAPTIC TRANSMISSION; MUTANT MOUSE;
   SUBCELLULAR-DISTRIBUTION; ABSENCE EPILEPSY; PURKINJE-CELLS; CA2+
   CHANNELS; MUTATIONS; SUBUNIT
AB Neurotransmitter release is triggered by Ca2+-influx through multiple sub-types of high voltage-activated Ca2+-channels, Tottering mice have a mutation in the alpha1A pore-forming subunit of P- and Q-type Ca2+-channels, two prominent sub-types that regulate transmitter release from central nerve terminals. Immunoblotting analysis of purified forebrain terminals from tottering mice revealed an 85% reduction in the protein expression level of the mutated alpha1A subunit compared to expression of the alpha1A subunit in wild-type terminals, In contrast, the expression of the alpha1B subunit of the N-type Ca2+-channels was unchanged. Release of the amino acids glutamate and GABA and of the neuropeptide cholecystokinin (CCK) induced by a short (100 ms) depolarization pulse was unchanged in the terminals of tottering mice. Studies using specific blockers of Ca2+-channels however, revealed a reduced contribution of P- and Q-type Ca2+-channels to glutamate and cholecystokinin release, whereas a greater reliance on N-type Ca2+-channels for release of these transmitters was observed. In contrast, the contribution of the P-, Q- and N-type Ca2+-channels to the release of GABA was not altered in tottering mice. These results indicate that the expression of the alpha1A subunit was decreased in terminals from tottering mice, and that a decreased contribution of P- and Q-type Ca2+-channels to the release of glutamate and cholecystokinin was functionally compensated by an increased contribution of N-type Ca2+-channels.
C1 Univ Amsterdam, Fac Sci, Neurobiol Sect, Swammerdam Inst Life Sci, NL-1090 GB Amsterdam, Netherlands.
   Leiden Univ, Med Ctr, Dept Human & Clin Genet & Neurol, NL-2300 RA Leiden, Netherlands.
   NINCDS, Synapt Funct Unit, NIH, Bethesda, MD 20892 USA.
   Leiden Univ, Med Ctr, Dept Physiol, NL-2300 RA Leiden, Netherlands.
RP Ghijsen, WEJM (reprint author), Univ Amsterdam, Fac Sci, Neurobiol Sect, Swammerdam Inst Life Sci, Kruislaan 320, NL-1090 GB Amsterdam, Netherlands.
NR 31
TC 27
Z9 27
U1 1
U2 3
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD JAN
PY 2002
VL 15
IS 1
BP 13
EP 18
DI 10.1046/j.0953-816x.2001.01839.x
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 525FH
UT WOS:000174057800003
PM 11860502
ER

PT J
AU Romanczyk, TB
   Weickert, CS
   Webster, MJ
   Herman, MM
   Akil, M
   Kleinman, JE
AF Romanczyk, TB
   Weickert, CS
   Webster, MJ
   Herman, MM
   Akil, M
   Kleinman, JE
TI Alterations in trkB mRNA in the human prefrontal cortex throughout the
   lifespan
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE ageing; BDNF receptor; development; gene expression; growth factor;
   neurotrophin; postmortem; puberty; senescence; truncated trkB
ID TYROSINE PROTEIN-KINASE; CENTRAL-NERVOUS-SYSTEM; CORTICAL DENDRITIC
   GROWTH; HUMAN CEREBRAL-CORTEX; NEUROTROPHIC FACTOR; FULL-LENGTH;
   MESSENGER-RNA; SYNAPTIC TRANSMISSION; SIGNAL-TRANSDUCTION;
   HIPPOCAMPAL-NEURONS
AB Signalling through tyrosine kinase receptor B (trkB) influences neuronal survival, differentiation and synaptogenesis. trkB exists in a full-length form (trkB(TK+)), which contains a catalytic tyrosine kinase (TK) domain, and a truncated form (trkB(TK-)), which lacks this domain. In the rodent brain, expression of trkB(TK+) decreases and trkB(TK-) increases during postnatal life. We hypothesized that both forms of trkB receptor mRNA would be present in the human neocortex and that the developmental profile of trkB gene expression in human may be distinct from that in rodent. We detected both trkB(TK+) and trkB(TK-) mRNA in RNA extracted from multiple human brain regions by Northern blot. Using in situ hybridization, we found trkB(TK+) mRNA in all cortical layers, with highest expression in layer IV and intermediate-to-high expression in layers III and V of the human dorsolateral prefrontal cortex. trkB(TK+) mRNA was present in neurons with both pyramidal and nonpyramidal shapes in the dorsolateral prefrontal cortex. trkB(TK+) mRNA levels were significantly increased in layer III in young adults as compared with infants and the elderly. In the elderly, trkB(TK+) mRNA levels were reduced markedly in all cortical layers. Unlike the mRNA encoding the full-length form of trkB, trkB(TK-) mRNA was distributed homogeneously across the grey matter, and trkB(TK-) mRNA levels increased only slightly during postnatal life. The results suggest that neurons in the human dorsolateral prefrontal cortex are responsive to neurotrophins throughout postnatal life and that this responsiveness may be modulated during the human lifespan.
C1 NIMH, Clin Brain Disorders Branch, IRP, NIH, Bethesda, MD 20892 USA.
   Uniformed Serv Univ Hlth Sci, Dept Psychiat, Stanley Lab Brain Res, Bethesda, MD 20814 USA.
RP Weickert, CS (reprint author), NIMH, Clin Brain Disorders Branch, IRP, NIH, Bldg 10-4,N312,MSC 1385, Bethesda, MD 20892 USA.
RI Shannon Weickert, Cynthia/G-3171-2011
NR 72
TC 61
Z9 63
U1 1
U2 2
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD JAN
PY 2002
VL 15
IS 2
BP 269
EP 280
DI 10.1046/j.0953-816x.2001.01858.x
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 526XH
UT WOS:000174154800005
PM 11849294
ER

PT J
AU Bussey, TJ
   Saksida, LM
AF Bussey, TJ
   Saksida, LM
TI The organization of visual object representations: a connectionist model
   of effects of lesions in perirhinal cortex
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE configural learning; discrimination learning; inferotemporal cortex;
   object recognition; rhesus macaque monkey; ventral visual stream
ID MEMORY IMPAIRMENT; RHESUS-MONKEYS; TEMPORAL-LOBE; PLACE MEMORY; AREA TE;
   PARAHIPPOCAMPAL CORTICES; HIPPOCAMPAL-FORMATION; INTERTRIAL INTERVALS;
   RECOGNITION MEMORY; FORNIX TRANSECTION
AB We have developed a simple connectionist model based on the idea that perirhinal cortex has properties similar to other regions in the ventral visual stream, or 'what' pathway. The model is based on the assumption that representations in the ventral visual stream are organized hierarchically, such that representations of simple features of objects are stored in caudal regions of the ventral visual stream, and representations of the conjunctions of these features are stored in more rostral regions. We propose that a function of these feature conjunction representations is to help to resolve 'feature ambiguity', a property of visual discrimination problems that can emerge when features of an object predict a given outcome (e.g. reward) when part of one object, but predict a different outcome when part of another object. Several recently reported effects of lesions of perirhinal cortex in monkeys have provided key insights into the functions of this region. In the present study these effects were simulated by comparing the performance of connectionist networks before and after removal of a layer of units corresponding to perirhinal cortex. The results of these simulations suggest that effects of lesions in perirhinal cortex on visual discrimination may be due not to the impairment of a specific type of learning or memory, such as declarative or procedural, but to compromising the representations of visual stimuli. Furthermore, we propose that attempting to classify perirhinal cortex function as either 'perceptual' or 'mnemonic' may be misguided, as it seems unlikely that these broad constructs will map neatly onto anatomically defined regions of the brain.
C1 NIMH, Sect Neurobiol Learning & Memory, Neuropsychol Lab, Bethesda, MD 20892 USA.
RP Bussey, TJ (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England.
RI Saksida, Lisa/M-2753-2016; Bussey, Timothy/M-2758-2016
OI Saksida, Lisa/0000-0002-8416-8171; Bussey, Timothy/0000-0001-7518-4041
NR 58
TC 146
Z9 148
U1 4
U2 11
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD JAN
PY 2002
VL 15
IS 2
BP 355
EP 364
DI 10.1046/j.0953-816x.2001.01850.x
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 526XH
UT WOS:000174154800012
PM 11849301
ER

PT J
AU Bussey, TJ
   Saksida, LM
   Murray, EA
AF Bussey, TJ
   Saksida, LM
   Murray, EA
TI Perirhinal cortex resolves feature ambiguity in complex visual
   discriminations
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE configural learning; discrimination learning; inferotemporal cortex;
   object recognition; rhesus monkey; ventral visual stream
ID RHESUS-MONKEYS; OBJECT-DISCRIMINATION; RECOGNITION MEMORY;
   HIPPOCAMPAL-FORMATION; TEMPORAL-LOBE; LESIONS; IDENTIFICATION; ABLATION;
   RATS; ASSOCIATION
AB The present experiment tested predictions of a 'perceptual-mnemonic/feature conjunction' (PMFC) model of perirhinal cortex function. The model predicts that lesions of perirhinal cortex should disrupt complex visual discriminations with a high degree of 'feature ambiguity', a property of visual discrimination problems that can emerge when features of an object are rewarded when they are part of one object, but not when part of another. As feature ambiguity is thought to be the critical factor, such effects should be independent of the number of objects to be discriminated. This was tested directly, by assessing performance of control monkeys and monkeys with aspiration lesions of perirhinal cortex on a series of concurrent discriminations in which the number of object pairs was held constant, but the degree of feature ambiguity was varied systematically. Monkeys were tested in three conditions: Maximum Feature Ambiguity, in which all features were explicitly ambiguous (AB+, CD+, BC-, AD-; the biconditional problem); Minimum Feature Ambiguity, in which no features were explicitly ambiguous (AB+, CD+, EF-, GH-); and Intermediate Feature Ambiguity, in which half the features were explicitly ambiguous (AB+, CD+, CE-, AF-). The pattern of results closely matched that predicted by simulations using a connectionist network: monkeys with perirhinal cortex lesions were unimpaired in the Minimum Feature Ambiguity condition, mildly impaired in the Intermediate Feature Ambiguity condition and severely impaired in the Maximum Feature Ambiguity condition. These results confirm the predictions of the PMFC model, and force a reconsideration of prevailing views regarding perirhinal cortex function.
C1 NIMH, Sect Neurobiol Learning & Memory, Neuropsychol Lab, Bethesda, MD 20892 USA.
RP Bussey, TJ (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England.
RI Saksida, Lisa/M-2753-2016; Bussey, Timothy/M-2758-2016; 
OI Saksida, Lisa/0000-0002-8416-8171; Bussey, Timothy/0000-0001-7518-4041;
   Murray, Elisabeth/0000-0003-1450-1642
NR 41
TC 212
Z9 212
U1 1
U2 5
PU BLACKWELL PUBLISHING LTD
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD JAN
PY 2002
VL 15
IS 2
BP 365
EP 374
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 526XH
UT WOS:000174154800013
PM 11849302
ER

PT J
AU Kornyshev, AA
   Leikin, S
   Malinin, SV
AF Kornyshev, AA
   Leikin, S
   Malinin, SV
TI Chiral electrostatic interaction and cholesteric liquid crystals of DNA
SO EUROPEAN PHYSICAL JOURNAL E
LA English
DT Article
ID HELICAL MACROMOLECULES; PHASES; MOLECULES; FORCES; STATE; PITCH
AB Explicit expressions for electrostatic interaction between stiff DNA duplexes of finite length are obtained. These expressions allow for the helical symmetry of charge distribution on DNA molecules and reveal chiral and non-chiral interaction terms. Asymptotic expressions at small twist angles axe applied to evaluate the cholesteric pitch and the twist elastic constant and their dependence on the length of DNA fragments. These estimates suggest an explanation for the large value of the cholesteric pitch and its nonmonotonic variation with the density of the liquid crystal. An analysis of biaxial correlations rationalizes the driving force of the transition from the cholesteric to hexagonal phase upon dehydration.
C1 Forschungszentrum Julich, D-52425 Julich, Germany.
   NICHHD, NIH, Bethesda, MD 20892 USA.
   RAS, LD Landau Theoret Phys Inst, Moscow 117940, Russia.
RP Leikin, S (reprint author), Forschungszentrum Julich, Postfach 1913, D-52425 Julich, Germany.
EM leikin@helix.nih.gov; s.malinin@fz-juelich.de
RI Leikin, Sergey/A-5518-2008; Kornyshev, Alexei/C-3404-2008
OI Leikin, Sergey/0000-0001-7095-0739; 
NR 30
TC 53
Z9 58
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0253-2786
J9 EUR PHYS J E
JI Eur. Phys. J. E
PD JAN
PY 2002
VL 7
IS 1
BP 83
EP 93
DI 10.1140/epje/i200101159
PG 11
WC Chemistry, Physical; Materials Science, Multidisciplinary; Physics,
   Applied; Polymer Science
SC Chemistry; Materials Science; Physics; Polymer Science
GA 536KJ
UT WOS:000174699000010
ER

PT J
AU Ring, J
   Brockow, K
AF Ring, J
   Brockow, K
TI Adverse drug reactions: Mechanisms and assessment
SO EUROPEAN SURGICAL RESEARCH
LA English
DT Article
DE adverse drug reaction; drug allergy; pseudo-allergy; IgE; anaphylactoid
   reaction; drug metabolism; exanthematous drug eruption
ID BETA-LACTAM ANTIBIOTICS; ALLERGIC REACTIONS; ANAPHYLACTOID REACTIONS;
   CUTANEOUS REACTIONS; T-CELLS; IDIOSYNCRATIC TOXICITY; RADIOCONTRAST
   MEDIUM; TRYPTASE; SULFONAMIDES; ACTIVATION
AB Adverse drug reactions (ADR) are an important clinical problem. They account for about 5% of all hospital admissions and cause death in approximately 0.01% of surgical patients. The mechanisms leading to ADR beyond IgE-mediated allergy are still poorly understood. The importance of chemically reactive drug metabolites and the involvement of T-lymphocytes in many drug hypersensitivity reactions have been highlighted in recent years. ADR are diagnosed on clinical grounds and the temporal relation between drug intake and the appearance of the symptoms. Allergy tests are required in the further assessment of the reaction. By means of skin tests, in vitro tests and provocation tests information about the culprit drug, the mechanism involved and possible alternatives can be obtained. Copyright (C) 2002 S. Karger AG, Basel.
C1 Tech Univ Munich, Dept Dermatol & Allergy Biederstein, D-80802 Munich, Germany.
   NIAID, Allerg Dis Sect, NIH, Bethesda, MD 20892 USA.
RP Ring, J (reprint author), Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Biedersteinerstr 29, D-80802 Munich, Germany.
NR 47
TC 11
Z9 11
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0014-312X
J9 EUR SURG RES
JI Eur. Surg. Res.
PD JAN-APR
PY 2002
VL 34
IS 1-2
BP 170
EP 175
DI 10.1159/000048905
PG 6
WC Surgery
SC Surgery
GA 535QQ
UT WOS:000174655900027
PM 11867919
ER

PT J
AU Datiles, MB
   Ansari, RR
   Reed, GF
AF Datiles, MB
   Ansari, RR
   Reed, GF
TI A clinical study of the human lens with a dynamic light scattering
   device
SO EXPERIMENTAL EYE RESEARCH
LA English
DT Article
DE cataract; lens; dynamic light scattering; corneal topography; clinical
   study
ID PHOTON-CORRELATION SPECTROSCOPY; LIVING HUMAN LENS; CATARACT; SYSTEM;
   EYE; AGE
AB A study was conducted to determine the potential usefulness and repeatability of a new dynamic light scattering (DLS) device for clinical studies of the human lens and early cataract. Studies using the cold cataract model showed this new device to be more sensitive than the Scheimpflug cataract imaging system in detecting the earliest cataractous changes. A miniaturized clinical DLS device developed by NASA using fiber optic probes was mounted on a Keratoscope (Optikon 2000), which has a 3-dimensional aiming system for accurate repeated sampling of the same area of the lens. A test/retest study was then conducted on the nuclear region of the lenses of 12 normal eyes. After a full, dilated eye examination, DLS data were obtained using the new device on the same eyes twice, 30-60 min apart. Particle size distributions and mean log particle size data were obtained. The mean percent differences between the larger and smaller of the test-retest pairs was 6.4 % (range 0.05-10.8 %); the between-test S.D. was 0.116. Actual numerical margin of error was +/-0.023. In addition, the mean coefficient of variation was 4.2 % (range 0.3-7.3 %), A useful clinical end point obtained from data produced by the device was the mean log particle size. These results suggest that the DLS will be useful in the detection and study of the beginning and earliest stages of cataract formation in humans.
C1 NEI, Cataract Sect, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
   NASA, Glenn Res Ctr, Cleveland, OH 44135 USA.
   NEI, Biometry Branch, Div Epidemiol & Clin Res, Bethesda, MD 20892 USA.
RP Datiles, MB (reprint author), NEI, Cataract Sect, Ophthalm Genet & Visual Funct Branch, NIH, Bldg 10,Rm 10N226,MSC 1860, Bethesda, MD 20892 USA.
OI Datiles, Manuel III B./0000-0003-4660-1664
NR 23
TC 19
Z9 19
U1 1
U2 3
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0014-4835
J9 EXP EYE RES
JI Exp. Eye Res.
PD JAN
PY 2002
VL 74
IS 1
BP 93
EP 102
DI 10.1006/exer.2001.1106
PG 10
WC Ophthalmology
SC Ophthalmology
GA 542JX
UT WOS:000175040700010
PM 11878822
ER

PT J
AU Childs, RW
   Igarashi, T
AF Childs, RW
   Igarashi, T
TI The identification of renal cell carcinoma as a target for allogeneic
   based cancer immunotherapy
SO EXPERIMENTAL NEPHROLOGY
LA English
DT Article
DE renal cell carcinoma; immunotherapy; nonmyeloablative; allogeneic stem
   cell transplantation
ID BONE-MARROW TRANSPLANTATION; MYELOABLATIVE THERAPY; BREAST-CANCER; HOST
   DISEASE; GRAFT; CHEMOTHERAPY; ENGRAFTMENT; REGRESSION; CHIMERISM;
   INDUCTION
AB Renal cell carcinoma tumor cells are intrinsically resistant to chemotherapy, but unlike most solid tumors, may be susceptible to immune-based therapy. Because powerful immune effects can be generated against hematological malignancies following allogeneic stem cell transplantation, we investigated for similar anti-tumor responses in patients with metastatic renal cell carcinoma following the transplantation of an allogeneic immune system from a healthy HLA-matched family donor. Early laboratory and clinical results have demonstrated that following a reduced-intensity allogeneic stem cell transplant, donor T-cell mediated anti-tumor effects, resulting in sustained and sometimes complete tumor regression, can be generated against renal cell carcinoma (RCC) refractory to conventional cytokine-based therapy. Early data indicate that cytotoxic T cells of donor origin are the mediators of these anti-tumor effects. These preliminary studies provide additional evidence supporting the susceptibility of RCC to immune attack and lay the foundation for future targeted allo-immune-based cancer strategies. Copyright (C) 2002 S. Karger AG, Basel.
C1 NHLBI, NIH, Bethesda, MD 20892 USA.
RP Childs, RW (reprint author), NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 22
TC 6
Z9 6
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1018-7782
J9 EXP NEPHROL
JI Exp. Nephrol.
PY 2002
VL 10
IS 3
BP 227
EP 234
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 563LZ
UT WOS:000176258300007
PM 12053124
ER

PT J
AU Banu, N
   Mozes, MM
   Kopp, JB
   Ziyadeh, FN
   Meyers, CM
AF Banu, N
   Mozes, MM
   Kopp, JB
   Ziyadeh, FN
   Meyers, CM
TI Regulation of inducible class II MHC, costimulatory molecules, and
   cytokine expression in TGF-beta 1 knockout renal epithelial cells:
   Effect of exogenous TGF-beta 1
SO EXPERIMENTAL NEPHROLOGY
LA English
DT Article
DE major histocompatibility complex; costimulatory molecules; cytokines;
   immunomodulators; transgenic/knockout mice
ID TRANSFORMING GROWTH FACTOR-BETA-1; CD4(+) T-CELLS; MAJOR
   HISTOCOMPATIBILITY COMPLEX; BETA TRANSGENIC MICE; KIDNEY TUBULE CELLS;
   TGF-BETA; IFN-GAMMA; MESSENGER-RNA; ANTIGEN EXPRESSION; TNF-ALPHA
AB As reports of mice genetically deficient for TGF-beta1 demonstrated aberrant renal class II MHC expression, we investigated inducible class 11 MHC expression on renal tubular epithelial cells derived from TGF-beta1 knockout (-/-) and wild-type (+/+) mice. IFN-gamma markedly upregulated class 11 MHC (I-Ab) expression in both (-/-) and (+/+) tubular epithelial cells. Coincubation studies of (+/+) and (-/-) tubular epithelial cells with IFN-gamma+LPS, or pretreatment of these cells with TGF-beta1, revealed inhibition of IFN-gamma-induced I-A(b) mRNA and cell surface expression that occurred via a decrease in class 11 transactivator gene expression in both (+/+) and (-/-) tubular epithelial cells. In addition, ICAM-1 was constitutively expressed on both (+/+) and (-/-) tubular epithelial cells and was upregulated by IFN-gamma or IFN-gamma+LPS. ICAM-1 expression in (+/+) and (-/-) tubular epithelial cells, however, was decreased by TGF-beta1. Parallel analysis evaluating B7-1 expression detected low levels of B7-1 in unstimulated (+/+) and (-/-) tubular epithelial cells that were increased by IFN-gamma, LPS, and IFN-gamma+LPS. IFN-gamma+LPS-mediated upregulation of B7-1 was also blocked by pretreatment with TGF-beta1. Cytokine analysis detected significantly higher levels of TNF-alpha and MIP-1alpha mRNA in all treated (-/-) preparations than in (+/+) tubular epithelial cell controls. These studies demonstrate normal patterns of class 11 MHC, ICAM-1, and B7 expression in TGF-beta1 (-/-) tubular epithelial cells in response to IFN-gamma, LPS, and TGF-beta1. Upregulated cytokine expression at baseline and in response to proinflammatory mediators is apparent in (-/-) tubular epithelial cells, however, and suggests that dysregulation of cytokine expression in inflammatory responses may be a primary event in multifocal inflammation observed in TGF-beta1-deficient animals. Copyright (C) 2002 S. Karger AG, Basel.
C1 NIDDK, KUH Div, NIH, Kidney Dis Sect, Bethesda, MD 20892 USA.
   Univ Penn, Sch Med, Penn Ctr Mol Studies Kidney Dis, Dept Med,Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA.
RP Meyers, CM (reprint author), NIDDK, KUH Div, NIH, Kidney Dis Sect, 6707 Democracy Blvd,Suite 601,2 Democracy Plaza, Bethesda, MD 20892 USA.
RI Mozes, Miklos/E-9003-2011
FU NIDDK NIH HHS [DK-07006, DK-49724]
NR 49
TC 7
Z9 7
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1018-7782
J9 EXP NEPHROL
JI Exp. Nephrol.
PY 2002
VL 10
IS 5-6
BP 320
EP 331
DI 10.1159/00065295
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 608RX
UT WOS:000178861400006
PM 12381916
ER

PT J
AU Cheson, BD
AF Cheson, BD
TI Rituximab: clinical development and future directions
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Review
DE antibody; CD20; CLL lymphoma; monoclonal; rituximab
ID ANTI-CD20 MONOCLONAL-ANTIBODY; NON-HODGKINS-LYMPHOMA; B-CELL LYMPHOMA;
   BONE-MARROW TRANSPLANTATION; MULTICENTER PHASE-II; REFRACTORY LOW-GRADE;
   LYMPHOPROLIFERATIVE DISORDERS; FOLLICULAR LYMPHOMA; INDOLENT LYMPHOMA;
   THERAPY
AB The availability of effective monoclonal antibodies (mAbs) has revolutionised the management of patients with B-cell malignancies. The most widely studied of these agents is rituximab (Rituxan(TM), IDEC Pharmaceuticals, San Diego, CA), a chimeric anti-CD20 antibody. Using the standard 4-weekly administration schedule, rituximab induces responses in almost half of patients with relapsed follicular/low-grade (F/LG) non-Hodgkin's lymphoma (NHL) with complete remissions in 6%. Lower response rates (RRs) have been noted in chronic lymphocytic leukaemia (CLL) using the standard dose and schedule. The drug has been well tolerated in most patients with common adverse events including mild to moderate fevers and chills and rare occurrences of a serious syndrome related to cytokine release and rapid tumour clearance. This antibody is also active against aggressive NHL, mantle cell NHL, post-transplant lymphoproliferative disorder (PTLD), lymphoplasmacytic NHL and hairy cell leukaemia and is also being evaluated in autoimmune disorders. Combinations of rituximab with chemotherapy regimens such as CHOP (cyclophosphamide, adriamycin, vincristine, predinisone) may alter the therapeutic paradigm for these diseases. The future promise of this antibody is a foundation on which to develop new strategies to increase the cure of patients with lymphoid malignancies.
C1 NCI, Bethesda, MD 20892 USA.
RP Cheson, BD (reprint author), NCI, Execut Pl N Rm 7026, Bethesda, MD 20892 USA.
NR 107
TC 21
Z9 22
U1 0
U2 2
PU ASHLEY PUBLICATIONS LTD
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
   ENGLAND
SN 1471-2598
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD JAN
PY 2002
VL 2
IS 1
BP 97
EP 110
DI 10.1517/14712598.2.1.97
PG 14
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 511PM
UT WOS:000173274800011
PM 11772344
ER

PT J
AU Marrazzo, A
   Prezzavento, O
   Pappalardo, MS
   Bousquet, E
   Iadanza, M
   Pike, VW
   Ronsisvalle, G
AF Marrazzo, A
   Prezzavento, O
   Pappalardo, MS
   Bousquet, E
   Iadanza, M
   Pike, VW
   Ronsisvalle, G
TI Synthesis of (+)- and
   (-)-cis-2-[(1-adamantylamino)-methyl]-1-phenylcyclopropane derivatives
   as high affinity probes for sigma(1) and sigma(2) binding sites
SO FARMACO
LA English
DT Article
DE sigma; receptors; ligands; stereoselectivity; PET
ID GUINEA-PIG BRAIN; BREAST-CANCER; RECEPTOR; NEUROSTEROIDS; LOCALIZATION;
   EXPRESSION; CLONING; SUGGEST; LIGAND
AB Selective ligands for either sigma(1) (sigma(1)) or sigma(2) binding sites are potentially useful for gaining a better understanding of the physiological functions of these proteins. Moreover, potent and selective homochiral sigma(1) and sigma(2) binding site ligands represent leads to potential radioligands for tumour imaging with positron emission tomography (PET). On the basis of their structural similarity to previous leads, new (+)- and (-)-cis-2-[(1-adamantylamino)-methyl]-1-phenylcyclopropane derivatives were synthesised and their binding affinities for sigma(1) and sigma(2) binding sites were determined. Each enantiomer showed high affinity for both sigma(1) and sigma(2) binding sites, but only (-)-cis-methyl-2-{[1-adamantyl(methyl)amino]methyl}-1-phenylcyclopropane-carboxylate, (-)-4, showed appreciable selectivity for binding to sigma(1) versus sigma(2) sites. The enantiomers of cis-(2-{[1-adamantyl(methyl)amino]methyl}-1-phenylcyclopropyl)methanol, 6, expressed the highest affinity for sigma(1) and sigma(2) binding sites. Ligands (-)-4, (+)-6 and (-)-6 might be rapidly labelled in their N-methyl groups by methylation of the N-desmethyl analogues with [C-11]iodomethane to provide prospective radioligands for PET. The N-desmethyl analogues, which are also high affinity ligands, were prepared and shown to undergo satisfactory methylation with iodomethane. (C) 2002 Elsevier Science S.A. All rights reserved.
C1 Univ Catania, Dept Pharmaceut Sci, I-95125 Catania, Italy.
   NIMH, Mol Imaging Branch, Bethesda, MD 20852 USA.
RP Ronsisvalle, G (reprint author), Univ Catania, Dept Pharmaceut Sci, Viale Andrea Doria,6 Citta Univ, I-95125 Catania, Italy.
NR 34
TC 23
Z9 24
U1 0
U2 3
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0014-827X
J9 FARMACO
JI Farmaco
PD JAN
PY 2002
VL 57
IS 1
BP 45
EP 53
AR PII S0014-827X(01)01170-3
DI 10.1016/S0014-827X(01)01170-3
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 587AY
UT WOS:000177619400007
PM 11902645
ER

PT J
AU Galon, J
   Franchimont, D
   Hiroi, N
   Frey, G
   Boettner, A
   Ehrhart-Bornstein, M
   O'Shea, JJ
   Chrousos, GP
   Bornstein, SR
AF Galon, J
   Franchimont, D
   Hiroi, N
   Frey, G
   Boettner, A
   Ehrhart-Bornstein, M
   O'Shea, JJ
   Chrousos, GP
   Bornstein, SR
TI Gene profiling reveals unknown enhancing and suppressive actions of
   glucocorticoids on immune cells
SO FASEB JOURNAL
LA English
DT Article
DE DNA microarray; clinical medicine; immune system
ID RESPIRATORY-DISTRESS SYNDROME; HUMAN MONOCYTES; T-LYMPHOCYTES; RECEPTOR;
   DEXAMETHASONE; EXPRESSION; INFLAMMATION; INDUCTION; PROTEIN; FAMILY
AB Glucocorticoids continue to be the major immunomodulatory agents used in clinical medicine today. However, their actions as anti-inflammatory and immunosuppressive drugs are both beneficial and deleterious. We analyzed the effect of glucocorticoids on the gene expression profile of peripheral blood mononuclear cells from healthy donors. DNA microarray analysis combined with quantitative TaqMan PCR and flow cytometry revealed that glucocorticoids induced the expression of chemokine, cytokine, and complement family members as well as of newly discovered innate immune-related genes, including scavenger and Toll-like receptors. In contrast, glucocorticoids repressed the expression of adaptive immune-related genes. Simultaneous inhibitory and stimulatory effects of glucocorticoids were found on inflammatory T helper subsets and apoptosis-related gene clusters. In cells activated by T cell receptor cross-linking, glucocorticoids down-regulated the expression of specific genes that were previously up-regulated in resting cells, suggesting a potential new mechanism by which they exert positive and negative effects. Considering the broad and continuously renewed interest in glucocorticoid therapy, the profiles we describe here will be useful in designing more specific and efficient treatment strategies.
C1 NIAMS, Lymphocyte Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
   NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   Inst Curie, INSERM, U255, Paris, France.
   Free Univ Brussels, Erasme Hosp, Dept Gastroenterol, B-1050 Brussels, Belgium.
   Univ Leipzig, Dept Pediat, D-04103 Leipzig, Germany.
   Univ Dusseldorf, Dept Endocrinol, D-40225 Dusseldorf, Germany.
RP Galon, J (reprint author), Ctr Rech Biomed Cordeliers, INSERM, U255, Lab Immunol Cellulaire & Clin, 15 Rue Ecole Med, F-75270 Paris 06, France.
EM jerome.galon@u255.bhdc.jussieu.fr
RI Korner, Antje/B-3988-2015
OI Korner, Antje/0000-0001-6001-0356
NR 42
TC 324
Z9 343
U1 3
U2 11
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD JAN
PY 2002
VL 16
IS 1
BP 61
EP 71
DI 10.1096/fj.01-0245com
PG 11
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Cell Biology
GA 518FU
UT WOS:000173656600008
PM 11772937
ER

PT S
AU Jacobson, KA
   Moro, S
   Manthey, JA
   West, PL
   Ji, XD
AF Jacobson, KA
   Moro, S
   Manthey, JA
   West, PL
   Ji, XD
BE Buslig, BS
   Manthey, JA
TI Interactions of flavones and other phytochemicals with adenosine
   receptors
SO FLAVONOIDS IN CELL FUNCTION
SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
LA English
DT Article; Proceedings Paper
CT Symposium on Flavonoids in Cell Function
CY MAR 29-30, 2000
CL SAN FRANCISCO, CALIFORNIA
SP Cargill Foods Inc, Amer Chem Soc, Div Agr & Food Chem
ID BIOLOGICAL PROPERTIES; ANTAGONISTS; DERIVATIVES; GENISTEIN; BINDING;
   ALPHA; CELLS; BETA
AB Dietary flavonoids have varied effects on animal cells, such as inhibition of platelet binding and aggregation, inhibition of inflammation, and anticancer properties, but the mechanisms of these effects remain largely unexplained. Adenosine receptors are involved in the homeostasis of the immune, cardiovascular, and central nervous systems, and adenosine agonists/antagonists; exert many similar effects. The affinity of flavonoids and other phytochemicals to adenosine receptors suggests that a wide range of natural substances in the diet may potentially block the effects of endogenous adenosine. We used competitive radioligand binding assays to screen flavonoid libraries for affinity and a computational CoMFA analysis of flavonoids to compare steric and electrostatic requirements for ligand recognition at three subtypes of adenosine receptors. Flavone derivatives, such as galangin, were found to bind to three subtypes of adenosine receptors in the gM range. Pentamethylmorin (K-i 2.65 muM) was 14- to 17-fold selective for human A(1) receptors than for A(1) and A(2A) receptors. An isoflavone, genistein, was found to bind to A(1) receptors. Aurones, such as hispidol (K-i 350 nM) are selective A(1) receptor antagonists, and, like genistein, are present in soy. The flavones, chemically optimized for receptor binding, have led to the antagonist, MRS 1067 (3,6-dichloro-2'.(isopropoxy)-4'-methylflavone), which is 200-fold more selective for human A(3) than A(1) receptors. Adenosine receptor antagonism, therefore, may be important in the spectrum of biological activities reported for the flavonoids.
C1 NIDDK, Mol Recognit Sect, LBC, NIH, Bethesda, MD 20892 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, LBC, NIH, Bldg 8A,Room B1A-19, Bethesda, MD 20892 USA.
RI Moro, Stefano/A-2979-2012; Jacobson, Kenneth/A-1530-2009
OI Moro, Stefano/0000-0002-7514-3802; Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999]
NR 26
TC 36
Z9 37
U1 0
U2 1
PU KLUWER ACADEMIC/PLENUM PUBL
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0065-2598
BN 0-306-47254-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2002
VL 505
BP 163
EP 171
PG 9
WC Chemistry, Applied; Food Science & Technology; Medicine, Research &
   Experimental
SC Chemistry; Food Science & Technology; Research & Experimental Medicine
GA BU35G
UT WOS:000175746500015
PM 12083460
ER

PT J
AU Laurenzana, EM
   Weis, CC
   Bryant, CW
   Newbold, R
   Delclos, KB
AF Laurenzana, EM
   Weis, CC
   Bryant, CW
   Newbold, R
   Delclos, KB
TI Effect of dietary administration of genistein, nonylphenol or ethinyl
   estradiol on hepatic testosterone metabolism, cytochrome P-450 enzymes,
   and estrogen receptor alpha expression
SO FOOD AND CHEMICAL TOXICOLOGY
LA English
DT Article
DE genistein; nonylphenol; ethinyl estradiol; cytochromes P450;
   testosterone metabolism
ID SPRAGUE-DAWLEY RATS; HORMONAL-REGULATION; GROWTH-HORMONE; MESSENGER-RNA;
   TISSUE DISTRIBUTION; MAMMALIAN LIVER; SEX DIFFERENCE; FEMALE RATS;
   IGF-I; MECHANISMS
AB The objective of this study was to examine effects of estrogenic agents of varying potencies (genistein, p-nonylphenol, and ethinyl estradiol) on hepatic testosterone metabolism, cytochrome P-450 (CYP450) enzymes, and ER alpha expression. These endpoints were examined as potential biomarkers of, and contributors to, endocrine disruptive activity. Exposure occurred during critical developmental periods, from gestational day 7 through weaning via the mothers' diet. Thereafter, rats were exposed via their diet to the compounds until puberty (postnatal day 50). Testosterone hydroxylase and 5 alpha -reductase activities, CYP2C and CYP3A levels were determined. In general, the compounds were more active in male rats than female rats. The only effect observed in female rats was at the 250 ppm genistein dose, in which an approximately 40% increase in 5 alpha -reductase activity was observed. In male rats, genistein treatment had mixed effects on testosterone metabolism. The 1250 ppm dose decreased both CYP2C and CYP3A protein levels. Nonylphenol had the most profound effects on testosterone metabolism and CYP450 expression in male rats, with effects occurring at doses as low as 25 ppm. An increase in 5 alpha -reductase activity and a decrease in the formation of 16 alpha -OH-, 2 alpha -OH-testosterone metabolites, CYP2C and CYP3A protein were observed. EE2 decreased the formation of several testosterone metabolites and CYP2C protein. All compounds had some effect on hepatic ERa expression, although a consistent effect was not observed. This study demonstrates that the test compounds can influence hepatic testosterone hydroxylase activity and CYP450 expression, as well as ER alpha expression, although these activities cannot be directly related to estrogenic activity. Published by Elsevier Science Ltd.
C1 Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA.
   NIEHS, Res Triangle Pk, NC 27709 USA.
RP Delclos, KB (reprint author), Natl Ctr Toxicol Res, Div Biochem Toxicol, HFT-110,3900 NCTR Rd, Jefferson, AR 72079 USA.
NR 47
TC 46
Z9 49
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-6915
J9 FOOD CHEM TOXICOL
JI Food Chem. Toxicol.
PD JAN
PY 2002
VL 40
IS 1
BP 53
EP 63
DI 10.1016/S0278-6915(01)00095-3
PG 11
WC Food Science & Technology; Toxicology
SC Food Science & Technology; Toxicology
GA 506CM
UT WOS:000172952400007
PM 11731036
ER

PT J
AU Fauci, AS
AF Fauci, AS
TI Bioterrorism: Defining a research agenda
SO FOOD AND DRUG LAW JOURNAL
LA English
DT Article
C1 NIAID, NIH, Bethesda, MD 20205 USA.
RP Fauci, AS (reprint author), NIAID, NIH, Bethesda, MD 20205 USA.
NR 3
TC 7
Z9 7
U1 0
U2 0
PU FOOD DRUG LAW INST
PI WASHINGTON
PA 1000 VERMONT AVE NW, SUITE 1200, WASHINGTON, DC 20005-4903 USA
SN 1064-590X
J9 FOOD DRUG LAW J
JI Food Drug Law J.
PY 2002
VL 57
IS 3
BP 413
EP 421
PG 9
WC Food Science & Technology; Law; Nutrition & Dietetics; Pharmacology &
   Pharmacy
SC Food Science & Technology; Government & Law; Nutrition & Dietetics;
   Pharmacology & Pharmacy
GA 653AR
UT WOS:000181413500001
PM 12703508
ER

PT J
AU Arimoto, T
   Sato, K
   Kadiiska, MB
   Corbett, J
   Mason, RP
AF Arimoto, T
   Sato, K
   Kadiiska, MB
   Corbett, J
   Mason, RP
TI In vivo direct evidence of free radical generation in diesel exhaust
   particle-induced lung injury in rats
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 113
BP S343
EP S343
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600131
ER

PT J
AU Chiueh, CC
   Andoh, T
   Chock, PB
AF Chiueh, CC
   Andoh, T
   Chock, PB
TI The roles of CGMP-dependent thioredoxin (TRX) expression in
   preconditioning induction of hormesis.
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 NIMH, Bethesda, MD 20892 USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
   Toyama Med & Pharmaceut Univ, Toyama 9300194, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 248
BP S95
EP S95
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300248
ER

PT J
AU English, S
   Cook, J
   Subramanian, S
   Mitchell, J
   Krishna, M
AF English, S
   Cook, J
   Subramanian, S
   Mitchell, J
   Krishna, M
TI Imaging oxygen and perfusion in tumor bearing animals using Overhauser
   enhanced MRI.
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 374
BP S428
EP S428
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600393
ER

PT J
AU Espey, MG
   Sinha, B
AF Espey, MG
   Sinha, B
TI No2 mediated detoxification of etoposide (VP-16)
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 408
BP S440
EP S440
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600427
ER

PT J
AU Espey, MG
   Gladwin, M
   Wink, D
   Thomas, D
AF Espey, MG
   Gladwin, M
   Wink, D
   Thomas, D
TI NO2 and lightning bugs
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 356
BP S420
EP S420
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600375
ER

PT J
AU Gladwin, MT
AF Gladwin, MT
TI Role of nitric oxide in the pathogenesis and therapy of sickle cell
   disease
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIDDK, Dept Crit Care Med, Ctr Clin, Bethesda, MD USA.
   NIDDK, Biol Chem Lab, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA P4
BP S299
EP S299
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600005
ER

PT J
AU Guo, Q
   Qian, SY
   Mason, RP
AF Guo, Q
   Qian, SY
   Mason, RP
TI Separation and identification of DMPO radical adducts formed from
   organic hydroperoxides
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, LPC, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 367
BP S424
EP S424
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600386
ER

PT J
AU Hodara, R
   Mason, R
   Cassina, A
   Radi, R
AF Hodara, R
   Mason, R
   Cassina, A
   Radi, R
TI Peroxynitrite and protein radical formation during superoxide-nitric
   oxide interaction in mitochondria.
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 Fac Med, Dept Bioquim, Montevideo, Uruguay.
   NIH, Lab Pharmacol & Chem, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 47
BP S323
EP S323
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600065
ER

PT J
AU Holbrook, NJ
   Ikeyama, S
   Li, J
   Kokkonen, T
AF Holbrook, NJ
   Ikeyama, S
   Li, J
   Kokkonen, T
TI Cellular response to oxidants: Links to proliferation and alterations
   with aging.
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 Natl Inst Aging, Baltimore, MD USA.
   Yale Univ, New Haven, CT 06520 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 151
BP S60
EP S60
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300151
ER

PT J
AU Jaszewski, AR
   Fann, Y
   Chen, YR
   Sato, K
   Corbett, J
   Mason, R
AF Jaszewski, AR
   Fann, Y
   Chen, YR
   Sato, K
   Corbett, J
   Mason, R
TI EPR spectroscopy studies on the structural transition of nitrosyl
   hemoglobin in the arterial-venous cycle of DEANO-treated rats
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 225
BP S377
EP S377
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600243
ER

PT J
AU Kadiiska, MB
   Augusto, O
AF Kadiiska, MB
   Augusto, O
TI Generation of free radical metabolites by ketones in rats with
   endotoxemia
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
   Univ Sao Paulo, Inst Chem, Sao Paulo, Brazil.
RI Augusto, Ohara/D-3839-2012
OI Augusto, Ohara/0000-0002-7220-4286
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 32
BP S319
EP S320
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600050
ER

PT J
AU Kennedy, C
   Pass, H
   Mitchell, J
AF Kennedy, C
   Pass, H
   Mitchell, J
TI Overexpression of human mutt homologue (hMTH1) protein as a marker of
   persistent oxidative stress in primary non-small cell lung tumors
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NCI, Dept Canc Prevent, Radiat Biol Branch, Bethesda, MD 20892 USA.
   Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 412
BP S441
EP S441
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600431
ER

PT J
AU Kubota, S
   Oroszlan, S
AF Kubota, S
   Oroszlan, S
TI The role of redox signaling in the processing of Gag polyprotein in
   immature retrovirus.
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 NCI, HIV Drug Resistance Program, Ft Detrick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 180
BP S70
EP S70
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300180
ER

PT J
AU Lam, S
   MacAuley, C
   le Riche, J
   Dyacgjiva, Y
   Coldman, A
   Guillaud, M
   Hawk, E
   Christen, MO
   Gazdar, A
AF Lam, S
   MacAuley, C
   le Riche, J
   Dyacgjiva, Y
   Coldman, A
   Guillaud, M
   Hawk, E
   Christen, MO
   Gazdar, A
TI Anethole dithiolethione (Sulfarlem (R), Sialor (R)): A radical scavenger
   beneficial in bronchial dysplasia in smokers
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
   British Columbia Canc Agcy, Vancouver, BC, Canada.
   NCI, DCP, GI, Bethesda, MD USA.
   Other Canc Res Grp, Bethesda, MD USA.
   Univ Texas, SW Med Ctr, Hamon Ctr Therapeut Oncol, Dallas, TX USA.
   Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 429
BP S163
EP S164
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300428
ER

PT J
AU Mason, R
   Deterding, L
   Tomer, K
   Detweiler, C
AF Mason, R
   Deterding, L
   Tomer, K
   Detweiler, C
TI Immunological identification of the myoglobin radical formed by hydrogen
   peroxide
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, DIR, LPC, FRM, Res Triangle Pk, NC 27709 USA.
   NIEHS, DIR, LSB, MS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 368
BP S424
EP S424
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600387
ER

PT J
AU Qian, SY
   Kadiiska, MB
   Mason, RP
AF Qian, SY
   Kadiiska, MB
   Mason, RP
TI Identification of prostaglandin-like radicals formed in in vitro & in
   vivo AA-derived lipid peroxidations
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 262
BP S388
EP S388
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600280
ER

PT J
AU Ramirez, DC
   Chen, YR
   Corbett, J
   Mason, RP
AF Ramirez, DC
   Chen, YR
   Corbett, J
   Mason, RP
TI Detection of hemoglobin-tyrosyl-radical derived nitrone adducts by
   immuno-spin trapping. A first application to in vivo toxicology
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 434
BP S449
EP S449
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600453
ER

PT J
AU Reiter, CD
   Hogg, N
   Wang, XD
   Tanus-Santos, JE
   Smith, RD
   Gladwin, MT
AF Reiter, CD
   Hogg, N
   Wang, XD
   Tanus-Santos, JE
   Smith, RD
   Gladwin, MT
TI Hemoglobin-haptoglobin multimers consume NO and limit NO bioavailability
   and S-nitrosation in human plasma
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIH, Bethesda, MD 20892 USA.
   Med Coll Wisconsin, Milwaukee, WI 53226 USA.
RI Tanus-Santos, Jose/A-4451-2008
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 210
BP S371
EP S372
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600228
ER

PT J
AU Ridnour, LA
   Dennery, P
   Goswami, P
   Spitz, D
AF Ridnour, LA
   Dennery, P
   Goswami, P
   Spitz, D
TI Stimulation of proteolysis by nitric oxide
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NCI, Bethesda, MD 20892 USA.
   Stanford Univ, Dept Pediat, Stanford, CA 94305 USA.
   Univ Iowa, Free Rad & Radiat Biol Program, Iowa City, IA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 186
BP S365
EP S365
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600204
ER

PT J
AU Romero, N
   Radi, R
   Linares, E
   Mason, R
   Augusto, O
   Denicola, A
AF Romero, N
   Radi, R
   Linares, E
   Mason, R
   Augusto, O
   Denicola, A
TI Reaction of human hemoglobin and peroxynitrite: Involvement of protein
   radicals on the reaction mechanism
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 Univ Republica, Fac Med, Dept Bioquim, Montevideo, Uruguay.
   Univ Republica, Fac Ciencias, Inst Quim Biol, Montevideo, Uruguay.
   Univ Sao Paulo, Inst Quim, Dept Bioquim, BR-01498 Sao Paulo, Brazil.
   NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
RI Augusto, Ohara/D-3839-2012
OI Augusto, Ohara/0000-0002-7220-4286
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 121
BP S48
EP S48
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300122
ER

PT J
AU Sato, K
   Arimoto, T
   Kadiiska, MB
   Corbett, J
   Qian, SY
   Mason, RP
AF Sato, K
   Arimoto, T
   Kadiiska, MB
   Corbett, J
   Qian, SY
   Mason, RP
TI Mechanism of in vivo lipid-derived free radical formation in acute lung
   injury caused by LPS
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 122
BP S345
EP S345
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600140
ER

PT J
AU Shvedova, A
   Kisin, E
   Murray, A
   Mason, R
   Kadiiska, M
   Castranova, V
   Gunther, M
AF Shvedova, A
   Kisin, E
   Murray, A
   Mason, R
   Kadiiska, M
   Castranova, V
   Gunther, M
TI In vivo detection of vitamin E-dependent protection against free radical
   formation and oxidative stress in skin treated with cumene hydroperoxide
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 NIOSH, HELD, Morgantown, WV USA.
   NIEHS, Res Triangle Pk, NC 27709 USA.
   W Virginia Univ, Morgantown, WV 26506 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 104
BP S339
EP S339
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600122
ER

PT J
AU Spencer, NY
   Xu, XL
   Gladwin, MT
   Kim-Shapiro, DB
   Hogg, N
AF Spencer, NY
   Xu, XL
   Gladwin, MT
   Kim-Shapiro, DB
   Hogg, N
TI Reoxygenation/deoxygenation cycles of nitrosylhemoglobin
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   Wake Forest Univ, Winston Salem, NC 27109 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 240
BP S381
EP S381
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600258
ER

PT J
AU Stadtman, TC
AF Stadtman, TC
TI Biosynthesis of specific selenocysteine-containing enzymes: Delivery
   protein systems provide selenium for synthesis of selenophosphate, a key
   intermediate
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 1
MA 242
BP S93
EP S93
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 578AY
UT WOS:000177096300242
ER

PT J
AU Zhao, YF
   Colburn, N
   St Clair, D
AF Zhao, YF
   Colburn, N
   St Clair, D
TI Tumor promoter induced p53 migration to mitochondria is an early event
   in apoptosis of skin epidermal cells
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 9th Annual Meeting of the Oxygen-Society
CY NOV 20-24, 2002
CL SAN ANTONIO, TEXAS
SP Oxygen Soc
C1 Univ Kentucky, Grad Ctr Toxicol, Lexington, KY USA.
   NCI, Gene Regulat Sect, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PY 2002
VL 33
SU 2
MA 427
BP S444
EP S445
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 614PY
UT WOS:000179199600446
ER

PT J
AU Kadiiska, MB
   Gladen, BC
   Baird, DB
   Germolec, D
   Graham, LB
   Parker, CE
   Ames, BN
   Basu, S
   Brot, N
   Fitzgerald, GA
   Floyd, RA
   George, M
   Hatch, GH
   Heineke, JW
   Hensley, K
   Lawson, JA
   Marnett, LJ
   Morrow, JD
   Murray, DM
   Plastaras, J
   Roberts, LJ
   Shigenaga, MK
   Sohal, RS
   Sun, J
   Tice, RR
   Van Thiel, DH
   Wellner, D
   Walter, PB
   Tomer, KB
   Mason, RP
   Barrett, JC
AF Kadiiska, MB
   Gladen, BC
   Baird, DB
   Germolec, D
   Graham, LB
   Parker, CE
   Ames, BN
   Basu, S
   Brot, N
   Fitzgerald, GA
   Floyd, RA
   George, M
   Hatch, GH
   Heineke, JW
   Hensley, K
   Lawson, JA
   Marnett, LJ
   Morrow, JD
   Murray, DM
   Plastaras, J
   Roberts, LJ
   Shigenaga, MK
   Sohal, RS
   Sun, J
   Tice, RR
   Van Thiel, DH
   Wellner, D
   Walter, PB
   Tomer, KB
   Mason, RP
   Barrett, JC
TI Biomarkers of oxidative stress: Experimental studies in animal models
SO FREE RADICAL RESEARCH
LA English
DT Meeting Abstract
CT Conference on European Research on Functional Effects of Dietary
   Antioxidants - Benefits and Risks
CY SEP 25-28, 2002
CL CHURCHILL COLL, CAMBRIDGE, ENGLAND
HO CHURCHILL COLL
DE CCl4; rat; antioxidants; oxidation products of lipids; proteins; DNA
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
   Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA.
   Univ Uppsala, S-75105 Uppsala, Sweden.
   Hosp Special Surg, New York, NY 10021 USA.
   Univ Penn, Ctr Expt Therapeut, Philadelphia, PA 19104 USA.
   Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
   Loyola Univ, Med Ctr, Maywood, IL 60153 USA.
   US EPA, Res Triangle Pk, NC 27711 USA.
   Washington Univ, Sch Med, St Louis, MO 63130 USA.
   Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
   Oxis Int Inc, Portland, OR USA.
   So Methodist Univ, Dallas, TX 75275 USA.
   Integrated Lab Syst Inc, Res Triangle Pk, NC USA.
   Cornell Univ, Weill Med Coll, New York, NY USA.
RI Walter, Patrick/A-4117-2011
NR 1
TC 1
Z9 1
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1071-5762
J9 FREE RADICAL RES
JI Free Radic. Res.
PY 2002
VL 36
SU S
BP 1
EP 1
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 611VQ
UT WOS:000179038800002
ER

PT J
AU Neuveut, C
   Jeang, KT
AF Neuveut, C
   Jeang, KT
TI Cell cycle dysregulation by HTLV-I: Role of the tax oncoprotein
SO FRONTIERS IN BIOSCIENCE
LA English
DT Review
DE cell cycle regulation; cellular transformation; HTLV-I; adult T-cell
   leukemia; tax oncoprotein; MAD1; p53; review
ID VIRUS TYPE-I; DEPENDENT KINASE INHIBITORS; RETINOBLASTOMA GENE-PRODUCT;
   WILD-TYPE P53; LEUKEMIA-VIRUS; S-PHASE; KAPPA-B; E7 PROTEIN;
   TRANSCRIPTIONAL ACTIVATION; MYOGENIC DIFFERENTIATION
AB HTLV-I is a human retrovirus which is the etiological agent for adult T-cell leukemia. The virus encodes a 40 kDa oncoprotein, Tax, which has no cellular counterpart. Findings from several laboratories over the past decade have shown that over-expression of the Tax oncoprotein is wholly sufficient to transform animal cells. Emerging evidence supports that Tax transforms cells through dysregulation of several cell cycle checkpoints. Here, we review extant data on how Tax targets cyclins, inhibitors of cyclin dependant kinase, as well as cellular sentries for DNA-damage.
C1 NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   Inst Pasteur, Lab Recombinaison & Express Genet, F-75724 Paris 15, France.
RP Jeang, KT (reprint author), NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bldg 4,Room 306,9000 Rockville Pike, Bethesda, MD 20892 USA.
RI Jeang, Kuan-Teh/A-2424-2008
NR 97
TC 34
Z9 34
U1 0
U2 3
PU FRONTIERS IN BIOSCIENCE INC
PI MANHASSET
PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY
   DR, MANHASSET, NY 11030 USA
SN 1093-9946
J9 FRONT BIOSCI
JI Front. Biosci.
PD JAN
PY 2002
VL 7
BP D157
EP D163
DI 10.2741/neuveut
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 509ZK
UT WOS:000173184100013
PM 11779707
ER

PT S
AU Bushel, PR
   Bennett, L
   Hamadeh, H
   Green, J
   Ableson, A
   Misener, S
   Paules, R
   Afshari, C
AF Bushel, PR
   Bennett, L
   Hamadeh, H
   Green, J
   Ableson, A
   Misener, S
   Paules, R
   Afshari, C
BE Kessler, MD
   Muller, GJ
TI Gene expression pattern recognition algorithm inferences to classify
   samples exposed to chemical agents
SO FUNCTIONAL MONITORING AND DRUG-TISSUE INTERACTION
SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
   (SPIE)
LA English
DT Proceedings Paper
CT Conference on Functional Monitoring and Drug-Tissue Interaction
CY JAN 21-24, 2002
CL SAN JOSE, CA
SP SPIE
DE microarray; gene expression; classification; toxicogenomics; toxicants;
   pattern recognition
ID CLASSIFICATION
AB We present an analysis of pattern recognition procedures used to predict the classes of samples exposed to pharmacologic agents by comparing gene expression patterns from samples treated with two classes of compounds. Rat liver mRNA samples following exposure for 24 hours with phenobarbital or peroxisome proliferators were analyzed using a 1700 rat cDNA microarray platform. Sets of genes that were consistently differentially expressed in the rat liver samples following treatment were stored in the MicroArray Project System (MAPS) database. MAPS identified 238 genes in common that possessed a low probability (P < 0.01) of being randomly detected as differentially expressed at the 95% confidence level. Hierarchical cluster analysis on the 238 genes clustered specific gene expression profiles that separated samples based on exposure to a particular class of compound.
C1 Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
RP Bushel, PR (reprint author), Natl Inst Environm Hlth Sci, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 21
TC 1
Z9 1
U1 0
U2 0
PU SPIE-INT SOC OPTICAL ENGINEERING
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA
SN 0277-786X
BN 0-8194-4362-X
J9 P SOC PHOTO-OPT INS
PY 2002
VL 4623
BP 85
EP 93
DI 10.1117/12.469471
PG 9
WC Engineering, Biomedical; Instruments & Instrumentation; Optics;
   Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Instruments & Instrumentation; Optics; Radiology, Nuclear
   Medicine & Medical Imaging
GA BU92S
UT WOS:000177418700009
ER

PT J
AU Rebois, RV
   Schuck, P
   Northup, JK
AF Rebois, RV
   Schuck, P
   Northup, JK
TI Elucidating kinetic and thermodynamic constants for interaction of G
   protein subunits and receptors by surface plasmon resonance spectroscopy
SO G PROTEIN PATHWAYS PART B: G PROTEINS AND THEIR REGULATORS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID BETA-GAMMA-SUBUNITS; GTP-BINDING PROTEINS; ALPHA-SUBUNITS;
   BIOLOGICAL-ACTIVITIES; ADP-RIBOSYLATION; PERTUSSIS TOXIN; RHODOPSIN;
   TRANSDUCIN; MEMBRANES; AFFINITY
C1 NINCDS, Lab Mol & Cellular Neurobiol & Biol, NIH, Bethesda, MD 20892 USA.
   Off Res Serv, Div Bioeng & Phys Sci, Mol Interact Resource, NIH, Bethesda, MD 20892 USA.
   Natl Inst Deafness & Other Commun Disorders, Lab Cellular Biol, NIH, Rockville, MD 20850 USA.
RP Rebois, RV (reprint author), NINCDS, Lab Mol & Cellular Neurobiol & Biol, NIH, Bethesda, MD 20892 USA.
NR 37
TC 9
Z9 9
U1 0
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 344
BP 15
EP 42
PG 28
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT54H
UT WOS:000173312300002
PM 11771379
ER

PT S
AU Cismowski, MJ
   Takesono, A
   Ma, CL
   Lanier, SM
   Duzic, E
AF Cismowski, MJ
   Takesono, A
   Ma, CL
   Lanier, SM
   Duzic, E
BE Iyengar, R
   Hildebrandt, JD
TI Identification of modulators of mammalian G-protein signaling by
   functional screens in the yeast Saccharomyces cerevisiae
SO G PROTEIN PATHWAYS PART B: G PROTEINS AND THEIR REGULATORS
SE Methods in Enzymology
LA English
DT Review
ID PHEROMONE RESPONSE PATHWAY; COUPLED RECEPTORS; KINASE CASCADES;
   ALZHEIMERS-DISEASE; TRANSDUCTION; GENE; ACTIVATION; TRANSFORMATION;
   EXPRESSION; HOMOLOG
C1 Neurocrine Biosci Incorp, San Diego, CA 92121 USA.
   Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA.
   OSI Pharmaceut Incorp, Tarrytown, NY 10591 USA.
   Louisiana State Univ, Ctr Hlth Sci, Dept Pharmacol, New Orleans, LA 70118 USA.
   Millennium Pharmaceut Incorp, Cambridge, MA 02139 USA.
RP Neurocrine Biosci Incorp, San Diego, CA 92121 USA.
RI Cismowski, Mary/E-2897-2011
FU NINDS NIH HHS [R01-NS24821]
NR 41
TC 8
Z9 8
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182245-1
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 344
BP 153
EP 168
PG 16
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT54H
UT WOS:000173312300011
PM 11771380
ER

PT J
AU Dermott, JM
   Dhanasekaran, N
AF Dermott, JM
   Dhanasekaran, N
TI Determining cellular role of G alpha(12)
SO G PROTEIN PATHWAYS PART B: G PROTEINS AND THEIR REGULATORS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID ACTIVATED PROTEIN-KINASE; GENE-EXPRESSION; TERMINAL KINASE; CELLS;
   RECEPTORS; TRANSFORMATION; FIBROBLASTS; FAMILY; MUTANT
C1 Natl Canc Inst Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA.
   Temple Univ, Sch Med, Fels Inst Canc Res & Mol Biol, Dept Biochem, Philadelphia, PA 19140 USA.
RP Dermott, JM (reprint author), Natl Canc Inst Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA.
FU NIGMS NIH HHS [GM 49897]
NR 25
TC 8
Z9 8
U1 0
U2 2
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 344
BP 298
EP 309
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT54H
UT WOS:000173312300021
PM 11771390
ER

PT J
AU Weinstein, LS
   Yu, SH
   Liu, J
AF Weinstein, LS
   Yu, SH
   Liu, J
TI Analysis of genomic imprinting of G(s)alpha gene
SO G PROTEIN PATHWAYS PART B: G PROTEINS AND THEIR REGULATORS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID ALBRIGHT HEREDITARY OSTEODYSTROPHY; NUCLEOTIDE-BINDING PROTEIN; CYCLASE
   COUPLING PROTEIN; HUMAN GNAS1 GENE; GS-ALPHA GENE; DNA METHYLATION;
   MAMMALIAN DEVELOPMENT; DEFICIENT ACTIVITY; CANDIDATE GENE;
   PSEUDOHYPOPARATHYROIDISM
C1 NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
   NHLBI, Lab Biochem Genet, NIH, Bethesda, MD 20892 USA.
RP Weinstein, LS (reprint author), NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
RI Weinstein, Lee/I-5575-2015
NR 41
TC 5
Z9 5
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 344
BP 369
EP 383
PG 15
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT54H
UT WOS:000173312300027
PM 11771397
ER

PT S
AU Wess, J
AF Wess, J
BE Iyengar, R
   Hildebrandt, JD
TI Considerations in the design and use of chimeric G protein-coupled
   receptors
SO G PROTEIN PATHWAYS, PT A, RECEPTORS
SE Methods in Enzymology
LA English
DT Review
ID MUSCARINIC ACETYLCHOLINE-RECEPTORS; V2 VASOPRESSIN RECEPTORS;
   PHOSPHOLIPASE-C; MOLECULAR-BASIS; INTRAMOLECULAR INTERACTIONS;
   ADRENERGIC-RECEPTORS; FUNCTIONAL RESCUE; EXPRESSION; ARRANGEMENT;
   SELECTIVITY
C1 NIDDKD, Bioorgan Chem Lab, Bethesda, MD 20892 USA.
RP NIDDKD, Bioorgan Chem Lab, Bethesda, MD 20892 USA.
NR 32
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182244-3
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 343
BP 295
EP 312
PG 18
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT07A
UT WOS:000171866900020
PM 11665575
ER

PT J
AU Pacheco-Rodriguez, G
   Moss, J
   Vaughan, M
AF Pacheco-Rodriguez, G
   Moss, J
   Vaughan, M
TI BIG1 and BIG2: Brefeldin A-inhibited guanine nucleotide-exchange
   proteins for ADP-ribosylation factors
SO G PROTEIN PATHWAYS: PT C, EFFECTOR MECHANISMS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID SEC7 DOMAIN; BOVINE BRAIN; ARF; GOLGI; TRANSPORT; IDENTIFICATION;
   COMPLEX; P200; GTP
C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA.
RP Pacheco-Rodriguez, G (reprint author), NHLBI, Pulm Crit Care Med Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 23
TC 8
Z9 8
U1 2
U2 3
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 345
BP 397
EP 404
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT06Z
UT WOS:000171866300030
PM 11665623
ER

PT J
AU Chiariello, M
   Gutkind, JS
AF Chiariello, M
   Gutkind, JS
TI Regulation of mitogen-activated protein kinases by G-protein-coupled
   receptors
SO G PROTEIN PATHWAYS: PT C, EFFECTOR MECHANISMS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID BETA-GAMMA-SUBUNITS; JUN KINASE; PATHWAY; CASCADE; RAS
C1 Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Chiariello, M (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RI Gutkind, J. Silvio/A-1053-2009; Chiariello, Mario/O-3642-2014
OI Chiariello, Mario/0000-0001-8434-5177
NR 13
TC 3
Z9 3
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 345
BP 437
EP 447
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT06Z
UT WOS:000171866300034
PM 11665627
ER

PT J
AU Muller, J
   Morrison, DK
AF Muller, J
   Morrison, DK
TI Assay of Raf-1 activity
SO G PROTEIN PATHWAYS: PT C, EFFECTOR MECHANISMS
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID PROTEIN-KINASE; MAP KINASE; PLASMA-MEMBRANE; PHOSPHATIDIC-ACID; RAS;
   PHOSPHORYLATION; IDENTIFICATION; ACTIVATION; RESIDUES; SERINE
C1 NCI, Regulat Cell Growth Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
   NCI, Regulat Cell Growth Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Muller, J (reprint author), NCI, Regulat Cell Growth Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
NR 28
TC 4
Z9 4
U1 0
U2 0
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 345
BP 490
EP 498
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BT06Z
UT WOS:000171866300038
PM 11665631
ER

PT J
AU Maraia, RJ
   Intine, RV
AF Maraia, RJ
   Intine, RV
TI La protein and its associated small nuclear and nucleolar precursor RNAs
SO GENE EXPRESSION
LA English
DT Review
DE tRNA processing; RNA modification; RNase P; RNA recognition motif (RRM);
   protein structure modeling; transcription; nucleolus; autoantigen; 5
   '-ppp; Walker A motif; Lhpl; Sla1
ID POLYMERASE-III TRANSCRIPTS; SS-B AUTOANTIGEN; LUPUS ANTIGEN-LA; 5S
   RIBOSOMAL-RNA; SUPPRESSOR TRANSFER-RNA; METHIONYL-TRANSFER-RNA;
   TRACT-BINDING-PROTEIN; TERMINATION FACTOR LA; U6 SPLICEOSOMAL RNA;
   SACCHAROMYCES-CEREVISIAE
AB After transcription by RNA polymerase (pol) III, nascent Pot III transcripts pass through RNA processing, modification, and transport machineries as part of their posttranscriptional maturation process. The first factor to interact with Pot III transcripts is La protein, which binds principally via its conserved N-terminal domain (NTD), to the UUU-OH motif that results from transcription termination. This review includes a sequence Logo of the most conserved region of La and its refined modeling as an RNA recognition motif (RRM). La protects RNAs from 3' exonucleolytic digestion and also contributes to their nuclear retention. The variety of modifications found on La-associated RNAs is reviewed in detail and considered in the contexts of how La may bind the termini of structured RNAs without interfering with recognition by modification enzymes, and its ability to chaperone RNAs through multiple parts of their maturation pathways. The CTD of human La recognizes the 5' end region of nascent RNA in a manner that is sensitive to serine 366 phosphorylation. Although the CTD can control pre-tRNA cleavage by RNase P, a rate-limiting step in tRNA(UGA)(Ser) maturation, the extent to which it acts in the maturation pathway(s) of other transcripts is unknown but considered here. Evidence that a fraction of La resides in the nucleolus together with recent findings that several Pot III transcripts pass through the nucleolus is also reviewed. An imminent goal is to understand how the bipartite RNA binding, intracellular trafficking, and signal transduction activities of La are integrated with the maturation pathways of the various RNAs with which it associates.
C1 NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA.
RP Maraia, RJ (reprint author), NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA.
NR 146
TC 38
Z9 44
U1 0
U2 2
PU COGNIZANT COMMUNICATION CORP
PI ELMSFORD
PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA
SN 1052-2166
J9 GENE EXPRESSION
JI Gene Expr.
PY 2002
VL 10
IS 1-2
BP 41
EP 57
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 523LL
UT WOS:000173955300004
PM 11868987
ER

PT J
AU Holmes, A
   Wrenn, CC
   Harris, AP
   Thayer, KE
   Crawley, JN
AF Holmes, A
   Wrenn, CC
   Harris, AP
   Thayer, KE
   Crawley, JN
TI Behavioral profiles of inbred strains on novel olfactory, spatial and
   emotional tests for reference memory in mice
SO GENES BRAIN AND BEHAVIOR
LA English
DT Review
DE Barnes maze; genetic background; inbred strains; learning and memory;
   social transmission of food preference; trace fear conditioning
ID LONG-TERM POTENTIATION; PROTEIN-KINASE-C; TRAIT LOCI ANALYSES; ELEVATED
   PLUS-MAZE; CONTEXTUAL FEAR; MOUSE STRAINS; MUTANT MICE;
   ALZHEIMERS-DISEASE; TRANSGENIC MICE; PREPULSE INHIBITION
AB Studying the behavior of genetic background strains provides important information for the design and interpretation of cognitive phenotypes in mutant mice. Our experiments examined the performance of three commonly used strains (C57BL/6J, 129S6, DBA/2J) on three behavioral tests for learning and memory that measure very different forms of memory, and for which there is a lack of data on strain differences. In the social transmission of food preference test (STFP) all three strains demonstrated intact memory for an odorcued food that had been sampled on the breath of a cagemate 24 hours previously. While C57BL/6J and 129S6 mice showed good trace fear conditioning, DBA/2J mice showed a profound deficit on trace fear conditioning. In the Barnes maze test for spatial memory, the 129S6 strain showed poor probe trial performance, relative to C57BL/6J mice. Comparison of strains for open field exploratory activity and anxiety-like behavior suggests that poor Barnes maze performance reflects low exploratory behavior, rather than a true spatial memory deficit, in 129S6 mice. This interpretation is supported by good Morris water maze performance in 129S6 mice. These data support the use of a C57BL/6J background for studying memory deficits in mutant mice using any of these tasks, and the use of a 129S6 background in all but the Barnes maze. A DBA/2J background may be particularly useful for investigating the genetic basis of emotional memory using fear conditioning.
C1 NIMH, Sect Behav Genomics, NIH, Bethesda, MD 20892 USA.
RP Holmes, A (reprint author), NIMH, Sect Behav Genomics, NIH, Bldg 10,Room 4D11, Bethesda, MD 20892 USA.
NR 111
TC 169
Z9 170
U1 3
U2 13
PU BLACKWELL MUNKSGAARD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD JAN
PY 2002
VL 1
IS 1
BP 55
EP 69
DI 10.1046/j.1601-1848.2001.00005.x
PG 15
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 608UY
UT WOS:000178866100008
PM 12886950
ER

PT J
AU Rosen, ED
   Hsu, CH
   Wang, XZ
   Sakai, S
   Freeman, MW
   Gonzalez, FJ
   Spiegelman, BM
AF Rosen, ED
   Hsu, CH
   Wang, XZ
   Sakai, S
   Freeman, MW
   Gonzalez, FJ
   Spiegelman, BM
TI C/EBP alpha induces adipogenesis through PPAR gamma: a unified pathway
SO GENES & DEVELOPMENT
LA English
DT Article
DE adipogenesis; PPAR gamma; C/EBP alpha; PPAR gamma null fibroblasts
ID EMBRYONIC STEM-CELLS; ADIPOSE-TISSUE; ADIPOCYTE DIFFERENTIATION;
   PROMOTER ACTIVITY; IN-VITRO; EXPRESSION; PROTEINS
AB PPARgamma and C/EBPalpha are critical transcription factors in adipogenesis, but the precise role of these proteins has been difficult to ascertain because they positively regulate each other's expression. Questions remain about whether these factors operate independently in separate, parallel pathways of differentiation, or whether a single pathway exists. PPARgamma can promote adipogenesis in C/EBPalpha-deficient cells, but the converse has not been tested. We have created an immortalized line of fibroblasts lacking PPARgamma, which we use to show that C/EBPalpha has no ability to promote adipogenesis in the absence of PPARgamma. These results indicate that C/EBPalpha and PPARgamma participate in a single pathway of fat cell development with PPARgamma being the proximal effector of adipogenesis.
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
   Massachusetts Gen Hosp, Lipid Unit, Boston, MA 02114 USA.
   NCI, Lab Metab, Bethesda, MD 20892 USA.
   Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Spiegelman, BM (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
FU NIDDK NIH HHS [DK02535, R37 DK031405, R37DK31405]
NR 20
TC 629
Z9 663
U1 4
U2 34
PU COLD SPRING HARBOR LAB PRESS
PI PLAINVIEW
PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD JAN 1
PY 2002
VL 16
IS 1
BP 22
EP 26
DI 10.1101/gad.948702
PG 5
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 510BD
UT WOS:000173188100003
PM 11782441
ER

PT J
AU Pfeiffer, RM
   Rutter, JL
   Gail, MH
   Struewing, J
   Gastwirth, JL
AF Pfeiffer, RM
   Rutter, JL
   Gail, MH
   Struewing, J
   Gastwirth, JL
TI Efficiency of DNA pooling to estimate joint allele frequencies and
   measure linkage disequilibrium
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE joint prevalence estimation; risk modification; population genetics;
   association studies
ID DISEASE GENES; PREVALENCE; MUTATIONS; SAMPLES
AB Pooling DNA samples can yield efficient estimates of the prevalence of genetic variants. We extend methods of analyzing pooled DNA samples to estimate the joint prevalence of variants at two or more loci. If one has a sample from the general population, one can adapt the method for joint prevalence estimation to estimate allele frequencies and D, the measure of linkage disequilibrium. The parameter D is fundamental in population genetics and in determining the power of association studies. fn addition, joint allelic prevalences can be used in case-control studies to estimate the relative risks of disease from joint exposures to the genetic variants. Our methods allow for imperfect assay sensitivity and specificity. The expected savings in numbers of assays required when pooling is utilized compared to individual testing are quantified. (C) 2002 Wiley-Liss, Inc.
C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   George Washington Univ, Dept Stat, Washington, DC 20052 USA.
RP Pfeiffer, RM (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS-8030, Bethesda, MD 20892 USA.
RI Struewing, Jeffery/C-3221-2008; Pfeiffer, Ruth /F-4748-2011; Struewing,
   Jeffery/I-7502-2013; 
OI Struewing, Jeffery/0000-0002-4848-3334; Rutter, Joni/0000-0002-6502-2361
NR 16
TC 24
Z9 26
U1 1
U2 4
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD JAN
PY 2002
VL 22
IS 1
BP 94
EP 102
DI 10.1002/gepi.1046
PG 9
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 504YV
UT WOS:000172884700008
PM 11754476
ER

PT J
AU Lewis, LK
   Karthikeyan, G
   Westmoreland, JW
   Resnick, MA
AF Lewis, LK
   Karthikeyan, G
   Westmoreland, JW
   Resnick, MA
TI Differential suppression of DNA repair deficiencies of yeast rad50,
   mre11 and xrs2 mutants by EXO1 and TLC1 (the RNA component of
   telomerase)
SO GENETICS
LA English
DT Article
ID DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE; HOMOLOGOUS
   RECOMBINATION; IN-VITRO; INTRACHROMOSOMAL RECOMBINATION; MEIOTIC
   RECOMBINATION; ENDONUCLEASE CLEAVAGE; SILENCING PROTEIN; MULTIPLE
   PATHWAYS; BUDDING YEAST
AB Rad50, Mre11, and Xrs2 form a nuclease complex that functions in both nonhomologous end joining (NHEJ) and recombinational repair of DNA double-strand breaks (DSBs). A search for highly expressed cDNAs that suppress the DNA repair deficiency of rad50 mutants yielded multiple isolates of two genes: EXO1 and TLC1. Overexpression of EXO1 or TLC1 increased the resistance of rad50, mre11, and xrs2 mutants to ionizing radiation and MINIS, but did not increase resistance in strains defective in recombination (rad51, rad52, rad54, rad59) or NHEJ only (yku70, sir4). Increased Exo1 or TLC1 RNA did not alter checkpoint responses or restore NHEJ proficiency, but DNA repair defects of yku70 and rad27 (fen) mutants were differentially suppressed by the two genes. Overexpression of Exo1, but not mutant proteins containing substitutions in the conserved nuclease domain, increased recombination and suppressed HO and EcoRI enclonuclease-induced killing of rad50 strains. exo1 rad50 mutants lacking both nuclease activities exhibited a high proportion of enlarged, G2-arrested cells and displayed a synergistic decrease in DSB-induced plasmid:chromosome recombination. These results support a model in which the nuclease activity of the Rad50/Mre11/Xrs2 complex is required for recombinational repair, but not NHEJ. We suggest that the 5'-3' exo activity of Exol is able to substitute for Rad50/Mre11/Xrs2 in rescission of specific classes of DSB end structures. Gene-specific suppression by TLC1, which encodes the RNA subunit of the yeast telomerase complex, demonstrates that components of telomerase can also impact on DSB repair pathways.
C1 NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Resnick, MA (reprint author), NIEHS, Genet Mol Lab, NIH, 111 Alexander Dr, Res Triangle Pk, NC 27709 USA.
NR 95
TC 74
Z9 74
U1 0
U2 0
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD JAN
PY 2002
VL 160
IS 1
BP 49
EP 62
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 516TY
UT WOS:000173573900006
PM 11805044
ER

PT J
AU Siriaco, GM
   Cenci, G
   Haoudi, A
   Champion, LE
   Zhou, C
   Gatti, M
   Mason, JM
AF Siriaco, GM
   Cenci, G
   Haoudi, A
   Champion, LE
   Zhou, C
   Gatti, M
   Mason, JM
TI Telomere elongation (Tel), a new mutation in Drosophila melanogaster
   that produces long telomeres
SO GENETICS
LA English
DT Article
ID POSITION EFFECT VARIEGATION; HUMAN-CELLS; DNA-SEQUENCES; TRANSPOSABLE
   ELEMENTS; CATALYTIC SUBUNIT; CHROMOSOME ENDS; HETEROCHROMATIN; REPEATS;
   LENGTH; PROTEIN
AB In most eukaryotes telomeres are extended by telomerase. Drosophila melanogaster; however, lacks telomerase, and telomere-specific non-LTR retrotransposons, HeT-A and TART, transpose specifically to chromosome ends. A Drosophila strain, Gaiano, that has long telomeres has been identified. We extracted the major Gaiano chromosomes into an Oregon-R genetic background and examined the resulting stocks after 60 generations. In situ hybridization using HeT-A and TART sequences showed that, in stocks carrying either the X or the second chromosome from Gaiano, only the Gaiano-derived chromosomes display long telomeres. However, in stocks carrying the Gaiano third chromosome, all telomeres are substantially elongated, indicating that the Gaiano chromosome 3 carries a factor that increases HeT-A and TART addition to the telomeres. We show that this factor, termed Telomere elongation (Tel), is dominant and localizes as a single unit to 69 on the genetic map. The long telomeres tend to associate with each other in both polytene and mitotic cells. These associations depend on telomere length rather than the presence of Tel. Associations between metaphase chromosomes are resolved during anaphase, suggesting that they are mediated by either proteinaceous links or DNA hydrogen bonding, rather than covalent DNA-DNA bonds.
C1 NIEHS, Lab Mol Genet, Res Triangle Pk, NC 27709 USA.
   NIEHS, Lab Environm Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA.
   Univ Roma La Sapienza, Dipartimento Genet & Biol Mol, Ist Pasteur Fondaz Cenci Bolognetti, I-00185 Rome, Italy.
RP Mason, JM (reprint author), NIEHS, Lab Mol Genet, POB 12233, Res Triangle Pk, NC 27709 USA.
OI Gatti, Maurizio/0000-0003-3777-300X
NR 58
TC 58
Z9 59
U1 0
U2 4
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD JAN
PY 2002
VL 160
IS 1
BP 235
EP 245
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 516TY
UT WOS:000173573900021
PM 11805059
ER

PT J
AU Anantharaman, V
   Aravind, L
AF Anantharaman, Vivek
   Aravind, L.
TI The PRC-barrel: a widespread, conserved domain shared by photosynthetic
   reaction center subunits and proteins of RNA metabolism
SO GENOME BIOLOGY
LA English
DT Article
AB Background: The H subunit of the purple bacterial photosynthetic reaction center (PRC-H) is important for the assembly of the photosynthetic reaction center and appears to regulate electron transfer during the reduction of the secondary quinone. It contains a distinct cytoplasmic beta-barrel domain whose fold has no close structural relationship to any other well known beta-barrel domain.
   Results: We show that the PRC-H beta-barrel domain is the prototype of a novel superfamily of protein domains, the PRC-barrels, approximately 80 residues long, which is widely represented in bacteria, archaea and plants. This domain is also present at the carboxyl terminus of the pan-bacterial protein RimM, which is involved in ribosomal maturation and processing of 16S rRNA. A family of small proteins conserved in all known euryarchaea are composed entirely of a single stand-alone copy of the domain. Versions of this domain from photosynthetic proteobacteria contain a conserved acidic residue that is thought to regulate the reduction of quinones in the light-induced electron-transfer reaction. Closely related forms containing this acidic residue are also found in several non-photosynthetic bacteria, as well as in cyanobacteria, which have reaction centers with a different organization. We also show that the domain contains several determinants that could mediate specific protein-protein interactions.
   Conclusions: The PRC-barrel is a widespread, ancient domain that appears to have been recruited to a variety of biological systems, ranging from RNA processing to photosynthesis. Identification of this versatile domain in numerous proteins could aid investigation of unexplored aspects of their biology.
C1 [Anantharaman, Vivek; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM aravind@ncbi.nlm.nih.gov
NR 46
TC 1
Z9 1
U1 1
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 11
AR 0061.1
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EJ
UT WOS:000207582200013
ER

PT J
AU Anantharaman, V
   Aravind, L
AF Anantharaman, Vivek
   Aravind, L.
TI The GOLD domain, a novel protein module involved in Golgi function and
   secretion
SO GENOME BIOLOGY
LA English
DT Article
AB Background: Members of the p24 (p24/gp25L/emp24/Erp) family of proteins have been shown to be critical components of the coated vesicles that are involved in the transportation of cargo molecules from the endoplasmic reticulum to the Golgi complex. The p24 proteins form hetero-oligomeric complexes and are believed to function as receptors for specific secretory cargo.
   Results: Using sensitive sequence-profile analysis methods, we identified a novel beta-strand-rich domain, the GOLD (Golgi dynamics) domain, in the p24 proteins and several other proteins with roles in Golgi dynamics and secretion. This domain is predicted to mediate diverse protein-protein interactions. Other than in the p24 proteins, the GOLD domain is always found combined with lipid-or membrane-association domains such as the pleckstrin homology (PH), Sec14p and FYVE domains.
   Conclusions: The identification of the GOLD domain could aid in directed investigation of the role of the p24 proteins in the secretion process. The newly detected group of GOLD-domain proteins, which might simultaneously bind membranes and other proteins, point to the existence of a novel class of adaptors that could have a role in the assembly of membrane-associated complexes or in regulating assembly of cargo into membranous vesicles.
C1 [Anantharaman, Vivek; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM aravind@ncbi.nlm.nih.gov
NR 38
TC 9
Z9 9
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 5
AR 0023.1
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DX
UT WOS:000207581000013
ER

PT J
AU Aravind, L
   Iyer, LM
AF Aravind, L.
   Iyer, Lakshminarayan M.
TI The SWIRM domain: a conserved module found in chromosomal proteins
   points to novel chromatin-modifying activities
SO GENOME BIOLOGY
LA English
DT Article
AB Background: Eukaryotic chromosomal components, especially histones, are subject to a wide array of covalent modifications and catalytic reorganization. These modifications have an important role in the regulation of chromatin structure and are mediated by large multisubunit complexes that contain modular proteins with several conserved catalytic and noncatalytic adaptor domains.
   Results: Using computational sequence-profile analysis methods, we identified a previously uncharacterized, predicted alpha-helical domain of about 85 residues in chromosomal proteins such as Swi3p, Rsc8p, Moira and several other uncharacterized proteins. This module, termed the SWIRM domain, is predicted to mediate specific protein-protein interactions in the assembly of chromatin-protein complexes. In one group of proteins, which are highly conserved throughout the crown-group eukaryotes, the SWIRM domain is linked to a catalytic domain related to the monoamine and polyamine oxidases. Another human protein has the SWIRM domain linked to a JAB domain that is involved in protein degradation through the ubiquitin pathway.
   Conclusions: Identification of the SWIRM domain could help in directed experimental analysis of specific interactions in chromosomal proteins. We predict that the proteins in which it is combined with an amino-oxidase domain define a novel class of chromatin-modifying enzymes, which are likely to oxidize either the amino group of basic residues in histones and other chromosomal proteins or the polyamines in chromatin, and thereby alter the charge distribution. Other forms, such as KIAA1915, may link chromatin modification to ubiquitin-dependent protein degradation.
C1 [Aravind, L.; Iyer, Lakshminarayan M.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM aravind@ncbi.nlm.nih.gov
NR 52
TC 1
Z9 2
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 8
AR 0039.1
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EA
UT WOS:000207581300009
ER

PT J
AU Banerjee-Basu, S
   Baxevanis, AD
AF Banerjee-Basu, Sharmila
   Baxevanis, Andreas D.
TI The DNA-binding region of RAG1 is not a homeodomain
SO GENOME BIOLOGY
LA English
DT Letter
C1 [Banerjee-Basu, Sharmila; Baxevanis, Andreas D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
RP Baxevanis, AD (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
EM andy@nhgri.nih.gov
NR 22
TC 1
Z9 1
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 8
AR 1004.1
PG 4
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EA
UT WOS:000207581300015
ER

PT J
AU Chaussabel, D
   Sher, A
AF Chaussabel, Damien
   Sher, Alan
TI Mining microarray expression data by literature profiling
SO GENOME BIOLOGY
LA English
DT Article
AB Background: The rapidly expanding fields of genomics and proteomics have prompted the development of computational methods for managing, analyzing and visualizing expression data derived from microarray screening. Nevertheless, the lack of efficient techniques for assessing the biological implications of gene-expression data remains an important obstacle in exploiting this information.
   Results: To address this need, we have developed a mining technique based on the analysis of literature profiles generated by extracting the frequencies of certain terms from thousands of abstracts stored in the Medline literature database. Terms are then filtered on the basis of both repetitive occurrence and co-occurrence among multiple gene entries. Finally, clustering analysis is performed on the retained frequency values, shaping a coherent picture of the functional relationship among large and heterogeneous lists of genes. Such data treatment also provides information on the nature and pertinence of the associations that were formed.
   Conclusions: The analysis of patterns of term occurrence in abstracts constitutes a means of exploring the biological significance of large and heterogeneous lists of genes. This approach should contribute to optimizing the exploitation of microarray technologies by providing investigators with an interface between complex expression data and large literature resources.
C1 [Chaussabel, Damien; Sher, Alan] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Chaussabel, D (reprint author), NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM dchaussabel@niaid.nih.gov
NR 37
TC 27
Z9 30
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 10
AR 0055.1
PG 16
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EK
UT WOS:000207582300010
ER

PT J
AU Dunn, BM
   Goodenow, MM
   Gustchina, A
   Wlodawer, A
AF Dunn, Ben M.
   Goodenow, Maureen M.
   Gustchina, Alla
   Wlodawer, Alexander
TI Retroviral proteases
SO GENOME BIOLOGY
LA English
DT Review
AB The proteases of retroviruses, such as leukemia viruses, immunodeficiency viruses (including the human immunodeficiency virus, HIV), infectious anemia viruses, and mammary tumor viruses, form a family with the proteases encoded by several retrotransposons in Drosophila and yeast and endogenous viral sequences in primates. Retroviral proteases are key enzymes in viral propagation and are initially synthesized with other viral proteins as polyprotein precursors that are subsequently cleaved by the viral protease activity at specific sites to produce mature, functional units. Active retroviral proteases are homodimers, with each dimer structurally related to the larger class of single-chain aspartic peptidases. Each monomer has four structural elements: two distinct hairpin loops, a wide loop containing the catalytic aspartic acid and an alpha helix. Retroviral gene sequences can vary between infected individuals, and mutations affecting the binding cleft of the protease or the substrate cleavage sites can alter the response of the virus to therapeutic drugs. The need to develop new drugs against HIV will continue to be, to a large extent, the driving force behind further characterization of retroviral proteases.
C1 [Dunn, Ben M.] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
   [Goodenow, Maureen M.] Univ Florida, Dept Pathol & Expt Med, Gainesville, FL 32610 USA.
   [Gustchina, Alla; Wlodawer, Alexander] Natl Canc Inst, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RP Dunn, BM (reprint author), Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
EM bdunn@college.med.ufl.edu
NR 19
TC 7
Z9 7
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 4
AR 3006.1
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DW
UT WOS:000207580900005
ER

PT J
AU Iyer, LM
   Koonin, EV
   Aravind, L
AF Iyer, Lakshminarayan M.
   Koonin, Eugene V.
   Aravind, L.
TI Extensive domain shuffling in transcription regulators of DNA viruses
   and implications for the origin of fungal APSES transcription factors
SO GENOME BIOLOGY
LA English
DT Article
AB Background: Viral DNA-binding proteins have served as good models to study the biochemistry of transcription regulation and chromatin dynamics. Computational analysis of viral DNA-binding regulatory proteins and identification of their previously undetected homologs encoded by cellular genomes might lead to a better understanding of their function and evolution in both viral and cellular systems.
   Results: The phyletic range and the conserved DNA-binding domains of the viral regulatory proteins of the poxvirus D6R/N1R and baculoviral Bro protein families have not been previously defined. Using computational analysis, we show that the amino-terminal module of the D6R/N1R proteins defines a novel, conserved DNA-binding domain (the KilA-N domain) that is found in a wide range of proteins of large bacterial and eukaryotic DNA viruses. The KilA-N domain is suggested to be homologous to the fungal DNA-binding APSES domain. We provide evidence for the KilA-N and APSES domains sharing a common fold with the nucleic acid-binding modules of the LAGLIDADG nucleases and the amino-terminal domains of the tRNA endonuclease. The amino-terminal module of the Bro proteins is another, distinct DNA-binding domain (the Bro-N domain) that is present in proteins whose domain architectures parallel those of the KilA-N domain-containing proteins. A detailed analysis of the KilA-N and Bro-N domains and the associated domains points to extensive domain shuffling and lineage-specific gene family expansion within DNA virus genomes.
   Conclusions: We define a large class of novel viral DNA-binding proteins and their cellular homologs and identify their domain architectures. On the basis of phyletic pattern analysis we present evidence for a probable viral origin of the fungus-specific cell-cycle regulatory transcription factors containing the APSES DNA-binding domain. We also demonstrate the extensive role of lineage-specific gene expansion and domain shuffling, within a limited set of approximately 24 domains, in the generation of the diversity of virus-specific regulatory proteins.
C1 [Iyer, Lakshminarayan M.; Koonin, Eugene V.; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Aravind, L (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM aravind@ncbi.nlm.nih.gov
NR 49
TC 13
Z9 14
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 3
AR 0012.1
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DV
UT WOS:000207580800009
ER

PT J
AU Kondrashov, FA
   Rogozin, IB
   Wolf, YI
   Koonin, EV
AF Kondrashov, Fyodor A.
   Rogozin, Igor B.
   Wolf, Yuri I.
   Koonin, Eugene V.
TI Selection in the evolution of gene duplications
SO GENOME BIOLOGY
LA English
DT Article
ID AMINO-ACID SUBSTITUTIONS; DROSOPHILA-MELANOGASTER; METALLOTHIONEIN GENE;
   ESCHERICHIA-COLI; COMPLETE GENOMES; CULEX-PIPIENS; RATE VARIES;
   AMPLIFICATION; RESISTANCE; YEAST
AB Background: Gene duplications have a major role in the evolution of new biological functions. Theoretical studies often assume that a duplication per se is selectively neutral and that, following a duplication, one of the gene copies is freed from purifying (stabilizing) selection, which creates the potential for evolution of a new function.
   Results: In search of systematic evidence of accelerated evolution after duplication, we used data from 26 bacterial, six archaeal, and seven eukaryotic genomes to compare the mode and strength of selection acting on recently duplicated genes (paralogs) and on similarly diverged, unduplicated orthologous genes in different species. We find that the ratio of nonsynonymous to synonymous substitutions (K(n)/K(s)) in most paralogous pairs is <<1 and that paralogs typically evolve at similar rates, without significant asymmetry, indicating that both paralogs produced by a duplication are subject to purifying selection. This selection is, however, substantially weaker than the purifying selection affecting unduplicated orthologs that have diverged to the same extent as the analyzed paralogs. Most of the recently duplicated genes appear to be involved in various forms of environmental response; in particular, many of them encode membrane and secreted proteins.
   Conclusions: The results of this analysis indicate that recently duplicated paralogs evolve faster than orthologs with the same level of divergence and similar functions, but apparently do not experience a phase of neutral evolution. We hypothesize that gene duplications that persist in an evolving lineage are beneficial from the time of their origin, due primarily to a protein dosage effect in response to variable environmental conditions; duplications are likely to give rise to new functions at a later phase of their evolution once a higher level of divergence is reached.
C1 [Kondrashov, Fyodor A.; Rogozin, Igor B.; Wolf, Yuri I.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RP Kondrashov, FA (reprint author), NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
EM fkondras@ncbi.nlm.nih.gov
RI Kondrashov, Fyodor Alexeevich/H-6331-2015
OI Kondrashov, Fyodor Alexeevich/0000-0001-8243-4694
NR 89
TC 111
Z9 113
U1 3
U2 26
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 2
AR 0008.1
DI 10.1186/gb-2002-3-2-research0008
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DU
UT WOS:000207580700009
ER

PT J
AU Koonin, EV
   Makarova, KS
   Davidovic, L
   Pellegrini, L
AF Koonin, Eugene V.
   Makarova, Kira S.
   Davidovic, Laetitia
   Pellegrini, Luca
TI The rhomboids: a near ubiquitous family of intramembrane serine
   proteases evolved via multiple horizontal gene transfers
SO GENOME BIOLOGY
LA English
DT Article
AB Background. The rhomboid family consists of polytopic membrane proteins, which show a level of evolutionary conservation that is unique among membrane proteins. The rhomboids are present in nearly all sequenced genomes of archaea, bacteria and eukaryotes, with the exception of several species with small genomes. On the basis of experimental studies with the developmental regulator Rhomboid from Drosophila and the AarA protein from the bacterium Providencia stuartii, the rhomboids are thought to be intramembrane serine proteases whose signaling function is conserved in eukaryotes and prokaryotes.
   Results. Phylogenetic tree analysis suggests that, despite the broad distribution in all three kingdoms of life, the rhomboid family was not present in the last universal common ancestor of the extant life forms, but instead evolved in bacteria and has been acquired by archaea and eukaryotes via several independent horizontal gene transfer events. In eukaryotes, two distinct, ancient horizontal acquisitions apparently gave rise to the two major subfamilies typified by Rhomboid and PARL (presenilin-associated Rhomboid-like protein), respectively. The subsequent evolution of the rhomboid family in eukaryotes proceeded via multiple duplications and functional diversification through the addition of extra transmembrane helices and other domains in different orientations relative to the conserved core that harbors the protease activity. Conclusions. Although the near universal presence of the rhomboid family in bacteria, archaea and eukaryotes appears to suggest that this protein is part of the heritage of the last universal common ancestor, phylogenetic tree analysis indicates bacterial origin with subsequent dissemination via horizontal gene transfer. This emphasizes the importance of explicit phylogenetic analysis for the reconstruction of ancestral life forms. A hypothetical scenario of origin of intracellular membrane proteases from membrane transporters is proposed.
C1 [Davidovic, Laetitia; Pellegrini, Luca] Univ Laval, CRULRG, Mol Neurobiol Lab, Quebec City, PQ G1J 2G3, Canada.
   [Koonin, Eugene V.; Makarova, Kira S.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Pellegrini, L (reprint author), Univ Laval, CRULRG, Mol Neurobiol Lab, Rm F-5519,2601 Chemin Canardiere, Quebec City, PQ G1J 2G3, Canada.
EM Luca.Pellegrini@crulrg.ulaval.ca
NR 36
TC 0
Z9 0
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 11
AR 0010.3
PG 25
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EJ
UT WOS:000207582200010
ER

PT J
AU Panelli, MC
   Wang, E
   Phan, G
   Puhlmann, M
   Miller, L
   Ohnmacht, GA
   Klein, HG
   Marincola, FM
AF Panelli, Monica C.
   Wang, Ena
   Phan, Giao
   Puhlmann, Markus
   Miller, Lance
   Ohnmacht, Galen A.
   Klein, Harvey G.
   Marincola, Francesco M.
TI Gene-expression profiling of the response of peripheral blood
   mononuclear cells and melanoma metastases to systemic IL-2
   administration
SO GENOME BIOLOGY
LA English
DT Article
AB Background: Interleukin-2 (IL-2) has direct pluripotent effects on cells with immune and inflammatory function. Which of these effects has a critical role in mediating tumor regression remains enigmatic. In this study, we compared early changes in transcriptional profiles of circulating mononuclear cells with those occurring within the microenvironment of melanoma metastases following systemic IL-2 administration.
   Results: The results suggest that the immediate effects of IL-2 administration on the tumor microenvironment is transcriptional activation of genes predominantly associated with monocyte cell function; minimal effects were noted on migration, activation and proliferation of T cells. However, production of chemokines and markers of adhesion and migration within few hours of IL-2 administration may be responsible for a secondary recruitment of immune cells to the tumor site later.
   Conclusion: Our results suggest that IL-2 induces inflammation at tumor sites with three predominant secondary effects: activation of antigen-presenting monocytes; massive production of chemoattractants that may recruit other immune cells to the tumor (including MIG and PARC, which are specific for T cells); and activation of cytolytic mechanisms in monocytes (calgranulin, grancalcin) and NK cells (NKG5, NK4).
C1 [Panelli, Monica C.; Wang, Ena; Klein, Harvey G.; Marincola, Francesco M.] NCI, Immunogenet Sect, Dept Transfus Med, Ctr Clin,NIH, Bethesda, MD 20892 USA.
   [Phan, Giao; Puhlmann, Markus; Miller, Lance; Ohnmacht, Galen A.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Marincola, FM (reprint author), NCI, Immunogenet Sect, Dept Transfus Med, Ctr Clin,NIH, Bethesda, MD 20892 USA.
EM marincola@mail.cc.nih.gov
NR 30
TC 16
Z9 16
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 7
AR 0035.1
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DZ
UT WOS:000207581200011
ER

PT J
AU Szak, ST
   Pickeral, OK
   Makalowski, W
   Boguski, MS
   Landsman, D
   Boeke, JD
AF Szak, Suzanne T.
   Pickeral, Oxana K.
   Makalowski, Wojciech
   Boguski, Mark S.
   Landsman, David
   Boeke, Jef D.
TI Molecular archeology of L1 insertions in the human genome
SO GENOME BIOLOGY
LA English
DT Article
AB Background: As the rough draft of the human genome sequence nears a finished product and other genome-sequencing projects accumulate sequence data exponentially, bioinformatics is emerging as an important tool for studies of transposon biology. In particular, L1 elements exhibit a variety of sequence structures after insertion into the human genome that are amenable to computational analysis. We carried out a detailed analysis of the anatomy and distribution of L1 elements in the human genome using a new computer program, TSDfinder, designed to identify transposon boundaries precisely.
   Results: Structural variants of L1 elements shared similar trends in the length and quality of their target site duplications (TSDs) and poly(A) tails. Furthermore, we found no correlation between the composition and genomic location of the pre-insertion locus and the resulting anatomy of the L1 insertion. We verified that L1 insertions with TSDs have the 5'-TTAAAA-3' cleavage site associated with L1 endonuclease activity. In addition, the second target DNA cut required for L1 insertion weakly matches the consensus pattern TTAAAA. On the other hand, the L1-internal breakpoints of deleted and inverted L1 elements do not resemble L1 endonuclease cleavage sites. Finally, the genome sequence data indicate that whereas singly inverted elements are common, doubly inverted elements are almost never found.
   Conclusions: The sequence data give no indication that the creation of L1 structural variants depends on characteristics of the insertion locus. In addition, the formation of 5' truncated and 5' inverted L1s are probably not due to the action of the L1 endonuclease.
C1 [Pickeral, Oxana K.; Boguski, Mark S.; Boeke, Jef D.] Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA.
   [Szak, Suzanne T.; Pickeral, Oxana K.; Makalowski, Wojciech; Boguski, Mark S.; Landsman, David] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Boeke, JD (reprint author), Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, 725 N Wolfe St, Baltimore, MD 21205 USA.
EM jboeke@jhmi.edu
RI Makalowski, Wojciech/I-2843-2016
FU NIH [CA16519]
FX We are grateful to members of the Boeke lab and Landsman group for
   helpful discussions during the preparation of this manuscript,
   especially Liora Strichman-Almashanu, John S.J. Anderson, Wataru
   Fujibuchi, David Symer, and Greg Cost. We thank Qing Liu for work on
   Figure 3a. We also acknowledge Joana Silva for critical reading of the
   manuscript. This work was supported by NIH grant CA16519 to J.D.B.
NR 58
TC 16
Z9 16
U1 1
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 10
AR 0052.1
PG 18
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12EK
UT WOS:000207582300012
ER

PT J
AU Yanai, I
   Wolf, YI
   Koonin, EV
AF Yanai, Itai
   Wolf, Yuri I.
   Koonin, Eugene V.
TI Evolution of gene fusions: horizontal transfer versus independent events
SO GENOME BIOLOGY
LA English
DT Article
ID BACTERIAL HYPERTHERMOPHILES; COMPARATIVE GENOMICS; PROTEIN SEQUENCES;
   ARCHAEA; CLASSIFICATION; ALIGNMENT; EXCHANGE; CONTEXT; ORIGIN; TREES
AB Background: Gene fusions can be used as tools for functional prediction and also as evolutionary markers. Fused genes often show a scattered phyletic distribution, which suggests a role for processes other than vertical inheritance in their evolution.
   Results: The evolutionary history of gene fusions was studied by phylogenetic analysis of the domains in the fused proteins and the orthologous domains that form stand-alone proteins. Clustering of fusion components from phylogenetically distant species was construed as evidence of dissemination of the fused genes by horizontal transfer. Of the 51 examined gene fusions that are represented in at least two of the three primary kingdoms (Bacteria, Archaea and Eukaryota), 31 were most probably disseminated by cross-kingdom horizontal gene transfer, whereas 14 appeared to have evolved independently in different kingdoms and two were probably inherited from the common ancestor of modern life forms. On many occasions, the evolutionary scenario also involves one or more secondary fissions of the fusion gene. For approximately half of the fusions, stand-alone forms of the fusion components are encoded by juxtaposed genes, which are known or predicted to belong to the same operon in some of the prokaryotic genomes. This indicates that evolution of gene fusions often, if not always, involves an intermediate stage, during which the future fusion components exist as juxtaposed and co-regulated, but still distinct, genes within operons.
   Conclusion: These findings suggest a major role for horizontal transfer of gene fusions in the evolution of protein-domain architectures, but also indicate that independent fusions of the same pair of domains in distant species is not uncommon, which suggests positive selection for the multidomain architectures.
C1 [Wolf, Yuri I.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
   [Yanai, Itai] Boston Univ, Bioinformat Grad Program, Boston, MA 02215 USA.
   [Yanai, Itai] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
NR 33
TC 1
Z9 1
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PY 2002
VL 3
IS 5
AR 0024.1
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA V12DX
UT WOS:000207581000014
ER

PT J
AU DeSilva, U
   Elnitski, L
   Idol, JR
   Doyle, JL
   Gan, WN
   Thomas, JW
   Schwartz, S
   Dietrich, NL
   Beckstrom-Sternberg, SM
   McDowell, JC
   Blakesley, RW
   Bouffard, GG
   Thomas, PJ
   Touchman, JW
   Miller, W
   Green, ED
AF DeSilva, U
   Elnitski, L
   Idol, JR
   Doyle, JL
   Gan, WN
   Thomas, JW
   Schwartz, S
   Dietrich, NL
   Beckstrom-Sternberg, SM
   McDowell, JC
   Blakesley, RW
   Bouffard, GG
   Thomas, PJ
   Touchman, JW
   Miller, W
   Green, ED
TI Generation and comparative analysis of similar to 3.3 Mb of mouse
   genomic sequence orthologous to the region of human chromosome 7q11.23
   implicated in Williams syndrome
SO GENOME RESEARCH
LA English
DT Review
ID BEUREN-SYNDROME-DELETION; PUTATIVE TRANSCRIPTION FACTOR; CHRONIC
   GRANULOMATOUS-DISEASE; REGULATORY ELEMENTS; HUMAN GENE; TFII-I;
   HEMIZYGOTIC DELETION; NONCODING SEQUENCES; CONSERVED SYNTENY; COMMON
   DELETION
AB Williams syndrome is a complex developmental disorder that results from the heterozygous deletion of a similar to1.6-Mb segment of human chromosome 7q11.23. These deletions are mediated by large (similar to300 kb) duplicated blocks of DNA of near-identical sequence. Previously, we showed that the orthologous region of the mouse genome is devoid of such duplicated segments. Here, we extend our studies to include the generation of similar to3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is Finished to high accuracy. Comparative analyses of the mouse and human sequences within and immediately flanking the interval commonly deleted in Williams syndrome have facilitated the identification of nine previously unreported genes, provided detailed sequence-based information regarding 30 genes residing in the region, and revealed a number of potentially interesting conserved noncoding sequences. Finally, to facilitate comparative sequence analysis, we implemented several enhancements to the program Pipmaker, including the addition of links from annotated features within a generated percent-identity plot to specific records in public databases. Taken together, the results reported here provide all important comparative sequence resource that should catalyze additional studies of Williams syndrome, including those that aim to characterize genes within the commonly deleted interval and to develop mouse models of the disorder.
C1 NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
   NIH, Intramural Sequencing Ctr, Bethesda, MD 20892 USA.
   Penn State Univ, Dept Comp Sci & Engn, University Pk, PA 16802 USA.
RP Green, ED (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
EM egreen@nhgri.nih.gov
FU NHGRI NIH HHS [F32 HG002325, HG02238, HG02325-01, R01 HG002238]
NR 120
TC 66
Z9 67
U1 0
U2 1
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
J9 GENOME RES
JI Genome Res.
PD JAN
PY 2002
VL 12
IS 1
BP 3
EP 15
DI 10.1101/gr.214802
PG 13
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
GA 508AN
UT WOS:000173064900002
PM 11779826
ER

PT J
AU Jia, L
   Young, MF
   Powell, J
   Yang, LM
   Ho, NC
   Hotchkiss, R
   Robey, PG
   Francomano, CA
AF Jia, L
   Young, MF
   Powell, J
   Yang, LM
   Ho, NC
   Hotchkiss, R
   Robey, PG
   Francomano, CA
TI Gene expression profile of human bone marrow stromal cells:
   High-throughput expressed sequence tag sequencing analysis
SO GENOMICS
LA English
DT Article
DE human bone marrow stromal cells; EST sequencing analysis; novel genes;
   gene expression profile; data mining
ID FORMATION IN-VITRO; CAENORHABDITIS-ELEGANS; HUMAN BRAIN; STEM-CELLS;
   IDENTIFICATION; DATABASE; CDNAS; TRANSCRIPTS; PRECURSORS; DIVERSITY
AB Human bone marrow stromal cells (HBMSC) are pluripotent cells with the potential to differentiate into osteoblasts, chondrocytes, myelosupportive stroma, and marrow adipocytes. We used high-throughput DNA sequencing analysis to generate 4258 single-pass sequencing reactions (known as expressed sequence tags, or ESTs) obtained from the 5' (97) and 3' (4161) ends of human cDNA clones from a HBMSC cDNA library. Our goal was to obtain tag sequences from the maximum number of possible genes and to deposit them in the publicly accessible database for ESTs (dbEST of the National Center for Biotechnology Information). Comparisons of our EST sequencing data with nonredundant human mRNA and protein databases showed that the ESTs represent 1860 gene clusters. The EST sequencing data analysis showed 60 novel genes found only in this cDNA library after BLAST analysis against 3.0 million ESTs in NCBI's dbEST database. The BLAST search also showed the identified ESTs that have close homology to known genes, which suggests that these may be newly recognized members of known gene families. The gene expression profile of this cell type is revealed by analyzing both the frequency with which a message is encountered and the functional categorization of expressed sequences. Comparing an EST sequence with the human genomic sequence database enables assignment of an EST to a specific chromosomal region (a process called digital gene localization) and often enables immediate partial determination of intron/exon boundaries within the genomic structure. It is expected that high-throughput EST sequencing and data mining analysis will greatly promote our understanding of gene expression in these cells and of growth and development of the skeleton.
C1 NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
   NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
   NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Ctr Informat Technol, Bioinformat & Mol Anal Sect, Bethesda, MD 20892 USA.
   Hosp Special Surg, New York, NY 10021 USA.
RP Francomano, CA (reprint author), NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
NR 40
TC 36
Z9 41
U1 2
U2 6
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 JAN
PY 2002
VL 79
IS 1
BP 7
EP 17
DI 10.1006/geno.2001.6683
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 511ZL
UT WOS:000173296600003
PM 11827452
ER

PT J
AU Stephan, DA
   Howell, GR
   Teslovich, TM
   Coffey, AJ
   Smith, L
   Bailey-Wilson, JE
   Malechek, L
   Gildea, D
   Smith, JR
   Gillanders, EM
   Schleutker, J
   Hu, P
   Steingruber, HE
   Dhami, P
   Robbins, CM
   Makalowska, I
   Carpten, JD
   Sood, R
   Mumm, S
   Reinbold, R
   Bonner, TI
   Baffoe-Bonnie, A
   Bubendorf, L
   Heiskanen, M
   Kallioneimi, OP
   Baxevanis, AD
   Joseph, SS
   Zucchi, I
   Burk, RD
   Isaacs, W
   Ross, MT
   Trent, JM
AF Stephan, DA
   Howell, GR
   Teslovich, TM
   Coffey, AJ
   Smith, L
   Bailey-Wilson, JE
   Malechek, L
   Gildea, D
   Smith, JR
   Gillanders, EM
   Schleutker, J
   Hu, P
   Steingruber, HE
   Dhami, P
   Robbins, CM
   Makalowska, I
   Carpten, JD
   Sood, R
   Mumm, S
   Reinbold, R
   Bonner, TI
   Baffoe-Bonnie, A
   Bubendorf, L
   Heiskanen, M
   Kallioneimi, OP
   Baxevanis, AD
   Joseph, SS
   Zucchi, I
   Burk, RD
   Isaacs, W
   Ross, MT
   Trent, JM
TI Physical and transcript map of the hereditary prostate cancer region at
   Xq27
SO GENOMICS
LA English
DT Article
DE physical mapping; genome mapping; genome sequencing; contig mapping;
   bacterial artificial chromosomes; P1 artificial chromosomes; prostate
   cancer; Xq26.3-q27.3; sequence annotation; repetitive elements
ID ALBINISM-DEAFNESS SYNDROME; SUSCEPTIBILITY LOCUS; LINKAGE ANALYSIS;
   GENE; CHROMOSOME; GENOME; IDENTIFICATION; LOCALIZATION; ANOPHTHALMOS;
   SEARCH
AB We have recently mapped a locus for hereditary prostate cancer (termed HPCX) to the long arm of the X chromosome (Xq25-q27) through a genome-wide linkage study. Here we report the construction of an similar to 9-Mb sequence-ready bacterial clone contig map of Xq26.3-q27.3. The contig was constructed by screening BAC/PAC libraries with markers spaced at similar to 85-kb intervals. We identified overlapping clones by end-sequencing framework clones to generate 407 new sequence-tagged sites, followed by PCR verification of overlaps. Contig assembly was based on clone restriction fingerprinting and the landmark information. We identified a minimal overlap contig for genomic sequencing, which has yielded 7.7 Mb of finished sequence and 1.5 Mb of draft sequence. The transcriptional mapping effort localized 57 known and predicted genes by database searching, STS content mapping, and sequencing, followed by sequence annotation. These transcriptional units represent candidate genes for HPCX and multiple other hereditary diseases at Xq26.3-q27.3.
C1 NHGRI, Canc Genet Brach, NIH, Bethesda, MD 20892 USA.
   Sanger Ctr, Cambridge CB10 1SA, England.
   Albert Einstein Coll Med, Bronx, NY 10461 USA.
   NHGRI, Inherited Dis Res Branch, NIH, Baltimore, MD 21224 USA.
   Vanderbilt Univ, Med Ctr, Dept Med, Div Med Genet, Nashville, TN 37232 USA.
   Tampere Univ Hosp, Canc Genet Lab, Tampere 33521, Finland.
   NHGRI, Gene Technol Branch, NIH, Bethesda, MD 20892 USA.
   CNR, Ist Tecnol Biomed, I-20090 Milan, Italy.
   NIMH, Genet Lab, NIH, Bethesda, MD 20892 USA.
   Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
   Johns Hopkins Univ Hosp, Dept Urol, Baltimore, MD 21287 USA.
RP Stephan, DA (reprint author), NHGRI, Canc Genet Brach, NIH, Bethesda, MD 20892 USA.
EM dstephan@cnmcresearch.org
RI Bubendorfl, Lukas/H-5880-2011; Smith, Jeff/C-3484-2012; 
OI Bailey-Wilson, Joan/0000-0002-9153-2920
NR 30
TC 16
Z9 16
U1 1
U2 4
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 JAN
PY 2002
VL 79
IS 1
BP 41
EP 50
DI 10.1006/geno.2001.6681
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 511ZL
UT WOS:000173296600007
PM 11827456
ER

PT J
AU Bondy, CA
   Cheng, CM
AF Bondy, CA
   Cheng, CM
TI Insulin-like growth factor-1 promotes neuronal glucose utilization
   during brain development and repair processes
SO GLUCOSE METABOLISM IN THE BRAIN
SE INTERNATIONAL REVIEW OF NEUROBIOLOGY
LA English
DT Review
ID CENTRAL-NERVOUS-SYSTEM; I IGF-I; RECEPTOR GENE-EXPRESSION;
   GLYCOGEN-SYNTHASE KINASE-3-BETA; MESSENGER-RIBONUCLEIC-ACID; RAT-BRAIN;
   TRANSGENIC MICE; POSTNATAL-GROWTH; LIGAND-BINDING; AUTORADIOGRAPHIC
   LOCALIZATION
C1 NICHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
RP Bondy, CA (reprint author), NICHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
NR 115
TC 27
Z9 27
U1 6
U2 9
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0074-7742
J9 INT REV NEUROBIOL
PY 2002
VL 51
BP 189
EP 217
PG 33
WC Neurosciences
SC Neurosciences & Neurology
GA BV51T
UT WOS:000179204300004
PM 12420360
ER

PT J
AU Lipkowitz, MS
   Leal-Pinto, E
   Cohen, BE
   Abramson, RG
AF Lipkowitz, MS
   Leal-Pinto, E
   Cohen, BE
   Abramson, RG
TI Galectin 9 is the sugar-regulated urate transporter/channel UAT
SO GLYCOCONJUGATE JOURNAL
LA English
DT Article
DE ion channel; transmembrane protein; hyperuricemia; isoforms
ID SERUM URIC-ACID; MICROVILLUS MEMBRANE-VESICLES; GALACTOSIDE-BINDING
   LECTINS; JUVENILE GOUTY NEPHROPATHY; CARDIOVASCULAR-DISEASE;
   RENAL-DISEASE; FOLLOW-UP; EOSINOPHIL CHEMOATTRACTANT; FUNCTIONAL
   RECONSTITUTION; JAPANESE FAMILY
AB UAT, also designated galectin 9, is a multifunctional protein that can function as a urate channel/transporter, a regulator of thymocyte-epithelial cell interactions, a tumor antigen, an eosinophil chemotactic factor, and a mediator of apoptosis. We review the evidence that UAT is a transmembrane protein that transports urate, describe our molecular model for this protein, and discuss the evidence from epitope tag and lipid bilayer studies that support this model of the transporter. The properties of recombinant UAT are compared with those of urate transport into membrane vesicles derived from proximal tubule cells in rat kidney cortex. In addition, we review channel functions predicted by our molecular model that resulted in the novel finding that the urate channel activity is regulated by sugars and adenosine. Finally, the presence and possible functions of at least 4 isoforms of UAT and a closely related gene hUAT2 are discussed.
C1 Mt Sinai Sch Med, Dept Med, Div Nephrol, New York, NY 10029 USA.
   NIAID, Div Extramural Act, NIH, Bethesda, MD 20892 USA.
RP Lipkowitz, MS (reprint author), Mt Sinai Sch Med, Dept Med, Div Nephrol, 1 Gustave L Levy Pl,Box 1243, New York, NY 10029 USA.
EM mike.lipkowitz@mssm.edu
NR 57
TC 0
Z9 0
U1 2
U2 5
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0282-0080
J9 GLYCOCONJUGATE J
JI Glycoconjugate J.
PY 2002
VL 19
IS 7-9
BP 491
EP 498
DI 10.1023/B:GLYC.0000014078.65610.2f
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 769UE
UT WOS:000188667500007
ER

PT S
AU Sutton-Smith, M
   Morris, HR
   Grewal, PK
   Hewitt, JE
   Bittner, RE
   Goldin, E
   Schiffmann, R
   Dell, A
AF Sutton-Smith, M
   Morris, HR
   Grewal, PK
   Hewitt, JE
   Bittner, RE
   Goldin, E
   Schiffmann, R
   Dell, A
BE Drickamer, K
   Dell, A
TI MS screening strategies: investigating the glycomes of knockout and
   myodystrophic mice and leukodystrophic human brains
SO GLYCOGENOMICS: THE IMPACT OF GENOMICS AND INFORMATICS ON GLYCOBIOLOGY
SE BIOCHEMICAL SOCIETY SYMPOSIUM
LA English
DT Article; Proceedings Paper
CT Annual Symposium of the Biochemistry-Society
CY DEC, 2001
CL UNIV YORK, YORK, ENGLAND
SP Biochem Soc
HO UNIV YORK
ID ALPHA-DYSTROGLYCAN; GLYCOSYLATION; GLYCOSYLTRANSFERASE; LAMININ;
   DISEASE; GLYCANS; MUTANT; GENE
AB The implementation of highly sensitive and rapid mass spectrometric screening strategies for defining the glycosylation repertoires of organs in knockout mice is helping to reveal the roles that glycans play in health and disease. Thus novel glycosylation pathways have been uncovered in two such knockouts, namely alpha-mannosidase II null mice and UDP-N-acetylglucosamine:alpha-D-mannoside beta1,2-N-acetylglucosaminyltransferase II null mice. This chapter documents the glycosylation profiles of a wide range of organs from the normal mouse which should facilitate future glycomics studies of knockout mice. Furthermore, we report applications of our screening technology in studies of the myodystrophy mouse and a human leukodystrophy.
C1 Univ London Imperial Coll Sci Technol & Med, Dept Biol Sci, London SW7 2AY, England.
   Univ Nottingham, Queens Med Ctr, Inst Genet, Nottingham NG7 2UH, England.
   Univ Vienna, Inst Anat, Neuromuscular Res Dept, A-1090 Vienna, Austria.
   NIH, Bethesda, MD 20892 USA.
RP Dell, A (reprint author), Univ London Imperial Coll Sci Technol & Med, Dept Biol Sci, London SW7 2AY, England.
NR 30
TC 7
Z9 7
U1 1
U2 1
PU PORTLAND PRESS LTD
PI LONDON
PA 59 PORTLAND PL, LONDON W1N 3AJ, ENGLAND
SN 0067-8694
BN 1-85578-154-9
J9 BIOCHEM SOC SYMP
PY 2002
IS 69
BP 105
EP 115
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BV88X
UT WOS:000180303400009
PM 12655778
ER

PT J
AU Basrai, MA
   Hieter, P
AF Basrai, MA
   Hieter, P
TI Transcriptome analysis of Saccharomyces cerevisiae using serial analysis
   of gene expression
SO GUIDE TO YEAST GENETICS AND MOLECULAR AND CELL BIOLOGY, PT B
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID LARGE-SCALE ANALYSIS; MESSENGER-RNA; ALPHA-FACTOR; DNA-DAMAGE;
   RIBONUCLEOTIDE REDUCTASE; CHECKPOINT PATHWAYS; FACTOR PHEROMONE; YEAST;
   SEQUENCE; REPLICATION
C1 NCI, Genet Branch, Bethesda, MD 20889 USA.
   Univ British Columbia, Dept Med Genet, Ctr Mol Med & Therapeut, Vancouver, BC V5Z 4H4, Canada.
RP Basrai, MA (reprint author), NCI, Genet Branch, Bethesda, MD 20889 USA.
NR 47
TC 8
Z9 9
U1 1
U2 7
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 350
BP 414
EP 444
PN B
PG 31
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BU60A
UT WOS:000176466300024
PM 12073327
ER

PT S
AU Asano, K
   Phan, L
   Krishnamoorthy, T
   Pavitt, GD
   Gomez, E
   Hannig, EM
   Nika, J
   Donahue, TF
   Huang, HK
   Hinnebusch, AG
AF Asano, K
   Phan, L
   Krishnamoorthy, T
   Pavitt, GD
   Gomez, E
   Hannig, EM
   Nika, J
   Donahue, TF
   Huang, HK
   Hinnebusch, AG
BE Guthrie, C
   Fink, GR
TI Analysis and reconstitution of translation initiation in vitro
SO GUIDE TO YEAST GENETICS AND MOLECULAR AND CELL BIOLOGY, PT C
SE Methods in Enzymology
LA English
DT Review
ID GUANINE-NUCLEOTIDE-EXCHANGE; YEAST SACCHAROMYCES-CEREVISIAE;
   TRANSFER-RNA FORMYLTRANSFERASE; ACID INSERTION MODULE; FACTOR-II;
   PROTEIN COMPLEX; MESSENGER-RNA; EIF5; BINDING; PRT1
C1 Kansas State Univ, Dept Biol, Manhattan, KS 66506 USA.
   NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
   NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
   Univ Manchester, Inst Sci & Technol, Dept Biomol Sci, Manchester M60 1QD, Lancs, England.
   Univ Dundee, Sch Life Sci, Dundee DD1 5EH, Scotland.
   Univ Texas, Dept Mol & Cell Biol, Richardson, TX 75083 USA.
   Indiana Univ, Dept Biol, Bloomington, IN 47405 USA.
   Salk Inst Biol Studies, Mol Biol & Virol Lab, La Jolla, CA 92037 USA.
RP Kansas State Univ, Dept Biol, Manhattan, KS 66506 USA.
RI Pavitt, Graham/A-1363-2010
OI Pavitt, Graham/0000-0002-8593-2418
FU NIGMS NIH HHS [GM32263]
NR 34
TC 15
Z9 15
U1 0
U2 0
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
BN 0-12-182254-0
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 351
BP 221
EP 247
PN C
PG 27
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BU60B
UT WOS:000176466400013
PM 12073347
ER

PT J
AU Searfoss, AM
   Masison, DC
   Wickner, RB
AF Searfoss, AM
   Masison, DC
   Wickner, RB
TI Protein synthesis assayed by electroporation of mRNA in Saccharomyces
   cerevisiae
SO GUIDE TO YEAST GENETICS AND MOLECULAR AND CELL BIOLOGY, PT C
SE METHODS IN ENZYMOLOGY
LA English
DT Review
ID MESSENGER-RNA; TRANSLATION; EXPRESSION; 3'-POLY(A); HOMOLOG; YEAST;
   TAIL; CAP
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
   NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Searfoss, AM (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
NR 16
TC 2
Z9 2
U1 0
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0076-6879
J9 METHOD ENZYMOL
JI Methods Enzymol.
PY 2002
VL 351
BP 631
EP 639
PN C
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA BU60B
UT WOS:000176466400036
PM 12073373
ER

PT J
AU Bingham, R
AF Bingham, R
TI Leaving nursing
SO HEALTH AFFAIRS
LA English
DT Editorial Material
C1 NINR, NIH, Bethesda, MD 20892 USA.
RP Bingham, R (reprint author), NINR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 5
Z9 5
U1 0
U2 0
PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD JAN-FEB
PY 2002
VL 21
IS 1
BP 211
EP 217
DI 10.1377/hlthaff.21.1.211
PG 7
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 511LC
UT WOS:000173264500029
PM 11900079
ER

PT S
AU Knox, SS
   Viigmaa, M
   Unden, AL
   Elofsson, S
   Johansson, J
AF Knox, SS
   Viigmaa, M
   Unden, AL
   Elofsson, S
   Johansson, J
BE Weidner, G
   Kopp, M
   Kristenson, M
TI Psychosocial factors and cardiovascular risk in the East-West divide:
   The Swestonia study
SO HEART DISEASE: ENVIRONMENT, STRESS AND GENDER
SE NATO SCIENCE SERIES, SUB-SERIES I: LIFE AND BEHAVIOURAL SCIENCES
LA English
DT Proceedings Paper
CT NATO Advanced Research Workshop on Increase in Coronary Heart Disease in
   Central and Eastern Europe
CY MAY 20-24, 2000
CL BUDAPEST, HUNGARY
SP NATO, Natl Inst Hlth, Off Behav & Social Sci Res, Wellcome Trust, Hungarian Minist Hlth, Hungarian/Amer TET
DE cardiovascular risk; morbidity; mortality; behavior; smoking;
   neuroendocrine processes
ID CORONARY HEART-DISEASE; FEMALE CYNOMOLGUS MONKEYS; SWEDISH MEN; SOCIAL
   SUPPORT; BLOOD-PRESSURE; YOUNG-ADULTS; ATHEROSCLEROSIS; DETERMINANTS;
   MORTALITY; HOSTILITY
AB Swedes have one of the highest and Estonians one of the lowest life expectancies in Europe. The mortality rates for heart disease and stroke are also significantly greater in Estonia than Sweden. In a study comparing cardiovascular risk factors of Swedish and Estonian men and women, we found a significantly better psychosocial profile in Swedes than in Estonians. Some of the factors that were worse in Estonians also correlated with higher heart rate, a factor that may be causally associated with coronary artery disease. There were no consistent cultural differences in traditional risk factors except for a much higher smoking rate in Estonians, especially among women. These data indicate that psychosocial factors may play an important part in the risk factor profile of Estonians through their influence on health behaviors and neuroendocrine factors.
C1 NHLBI, Bethesda, MD 20892 USA.
RP Knox, SS (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA.
NR 43
TC 1
Z9 1
U1 2
U2 2
PU I O S PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1566-7693
BN 1-58603-082-5
J9 NATO SCI SER I LIFE
PY 2002
VL 327
BP 138
EP 152
PG 15
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA BV45D
UT WOS:000179014800012
ER

PT S
AU Solomon, SD
AF Solomon, SD
BE Weidner, G
   Kopp, M
   Kristenson, M
TI Gender differences in response to disaster
SO HEART DISEASE: ENVIRONMENT, STRESS AND GENDER
SE NATO SCIENCE SERIES, SUB-SERIES I: LIFE AND BEHAVIOURAL SCIENCES
LA English
DT Proceedings Paper
CT NATO Advanced Research Workshop on Increase in Coronary Heart Disease in
   Central and Eastern Europe
CY MAY 20-24, 2000
CL BUDAPEST, HUNGARY
SP NATO, Natl Inst Hlth, Off Behav & Social Sci Res, Wellcome Trust, Hungarian Minist Hlth, Hungarian/Amer TET
DE alcohol; anxiety; coping; depression; disaster; family role; gender
   differences; nurturer; post-traumatic stress disorder; provider; sex
   differences; social support; stress; traumatic stress
ID SEXUAL ASSAULT HISTORY; MENTAL-HEALTH-SERVICES; SOCIAL SUPPORT; STRESS;
   DISTRESS; EVENTS
AB A series of studies of individuals exposed to flooding and chemical contamination found men to be more adversely affected than women. Women coped well with the direct effects of disaster exposure. However, women with excellent spousal relationships were found to have worse outcomes following disaster than those with weaker spousal ties. This finding was in direct contrast to that for disaster-exposed males, whose outcomes were positively related to the strength of their spouse relationship. Findings are explained in terms of gender role expectations: Disaster primarily disrupts the role of the provider, a role traditionally assigned to men. Only when disaster exposure is accompanied by high expectations for nurturance - an obligation traditionally associated with the female role - does it have a negative impact on women's mental health. Similarities between the experiences of disaster and economic collapse are noted.
C1 NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Solomon, SD (reprint author), NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
NR 34
TC 4
Z9 4
U1 1
U2 3
PU I O S PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1566-7693
BN 1-58603-082-5
J9 NATO SCI SER I LIFE
PY 2002
VL 327
BP 267
EP 274
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA BV45D
UT WOS:000179014800022
ER

PT J
AU Rao, MS
   Peters, JM
   Gonzalez, FJ
   Reddy, JK
AF Rao, MS
   Peters, JM
   Gonzalez, FJ
   Reddy, JK
TI Hepatic regeneration in peroxisome proliferator-activated receptor
   alpha-null mice after partial hepatectomy
SO HEPATOLOGY RESEARCH
LA English
DT Article
DE liver regeneration; peroxisome proliferator-activated receptors
   peroxisome proliferators; bromodeoxyuridine; partial hepatectomy
ID INDUCED CELL-PROLIFERATION; LIVER-REGENERATION; RAT-LIVER; PPAR-ALPHA;
   MOUSE-LIVER; EXPRESSION; HEPATOCARCINOGENESIS; HYPERPLASIA; HEPATOCYTES;
   INDUCTION
AB Peroxisome proliferator activated receptor alpha (PPARalpha), a member of the nuclear hormone receptor superfamily, is essential for hepatic pleiotropic effects induced by peroxisome proliferators including cell proliferation. In a previous study, we have shown that PPARalpha null mice do not show increased hepatocyte proliferation after administration of peroxisome proliferators, confirming that PPARalpha is necessary for peroxisome proliferator-induced cell proliferation. However. the role of PPARalpha. if any. in compensatory lifer cell hyperplasia is not known. Therefore, we examined the role of PPARa in modulating compensatory liver cell proliferation occurring after partial hepatectomy (PH). Replicative DNA synthesis, as measured by bromodeoxyuridine labeling of liver cell nuclei. was significantly higher after 48 h post-hepatectomy in both wild type and PPARalpha-null mouse livers, as compared to sham-operated control mice. Interestingly. in PPARa-null mice labeling index was significantly higher at 60 h after hepatectomy compared to wild-type mice: however, at 72 and 84 h the values were comparable in both the groups. Hepatic levels of mRNAs encoding CDK1, CDK2, CDK4, cyclin B1, cyclin D1 and PCNA were all elevated at 60 and 72 h post-hepatectomy and this effect was similar in both PPARalpha genotypes. Similarly, CDK2, CDK4. cyclin B1, cyclin D1 and PCNA proteins also showed comparable increase in both the groups. These results show that PPARalpha receptor is not essential for increased expression of CDKs, cyclins, PCNA and enhanced cell proliferation that Occur after PH. This strongly suggests that the signaling for increased cell proliferation in response to PH is distinctly different from that observed after administration of peroxisome proliferators. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
C1 Northwestern Univ, Sch Med, Dept Pathol, Chicago, IL 60611 USA.
   Penn State Univ, Dept Vet Sci, University Pk, PA 16802 USA.
   Penn State Univ, Ctr Mol Toxicol, University Pk, PA 16802 USA.
   NCI, Met Lab, Div Basic Sci, Bethesda, MD 20892 USA.
RP Rao, MS (reprint author), Northwestern Univ, Sch Med, Dept Pathol, 303 E Chicago Ave, Chicago, IL 60611 USA.
RI Peters, Jeffrey/D-8847-2011
NR 33
TC 21
Z9 21
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 1386-6346
J9 HEPATOL RES
JI Hepatol. Res.
PD JAN
PY 2002
VL 22
IS 1
BP 52
EP 57
AR PII S1386-6346(01)00119-X
DI 10.1016/S1386-6346(01)00119-X
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 530LC
UT WOS:000174358300007
ER

PT J
AU Tansey, EP
   Chow, A
   Rudy, B
   McBain, CJ
AF Tansey, EP
   Chow, A
   Rudy, B
   McBain, CJ
TI Developmental expression of potassium-channel subunit Kv3.2 within
   subpopulations of mouse hippocampal inhibitory interneurons
SO HIPPOCAMPUS
LA English
DT Article
DE GABAergic; somatostatin; parvalbumin; immunohistochemistry; Western
   blot; fast spiking
ID GATED K+ CHANNELS; RAT HIPPOCAMPUS; NEOCORTICAL INTERNEURONS;
   DIFFERENTIAL EXPRESSION; PYRAMIDAL NEURONS; ACTION-POTENTIALS;
   PARVALBUMIN; CURRENTS; CELLS; IMMUNOREACTIVITY
AB The developmental expression of the voltage-gated potassium channel subunit, Kv3.2, and its localization within specific mouse hippocampal inhibitory interneuron populations were determined using immunoblotting and immunohistochemical techniques. Using immunoblotting techniques, the Kv3.2 protein was weakly detected at postnatal age day 7 (P7), and full expression was attained at P21 in tissue extracts from homogenized hippocampal preparations. A similar developmental profile was observed using immunohistochemical techniques in hippocampal tissue sections. Kv3.2 protein expression was clustered on the somata and proximal dendrites of presumed inhibitory interneurons. Using double immunofluorescence, Kv3.2 subunit expression was detected on subpopulations of GABAergic inhibitory interneurons. Kv3.2 was detected in similar to100% of parvalbumin-positive interneurons, 86% of interneurons expressing nitric oxide synthase, and similar to50% of somatostatin-immunoreactive cells. Kv3.2 expression was absent from both calbindin- and calretinin-containing interneurons. Using immunoprecipitation, we further demonstrate that Kv3.2 and its related subunit Kv3.1b are coexpressed within the same protein complexes in the hippocampus. These data demonstrate that potassium channel subunit Kv3.2 expression is developmentally regulated in a specific set of interneurons. The vast majority of these interneuron subpopulations possess a "fast-spiking" phenotype, consistent with a role for currents through Kv3.2 containing channels in determining action potential kinetics in these cells. Published 2002 Wiley-Liss, lnc.(dagger)
C1 NICHHD, NIH, Lab Cellular & Synapt Neurophysiol, Bethesda, MD USA.
   NYU, Sch Med, Dept Physiol & Neurosci, New York, NY USA.
   NYU, Sch Med, Dept Biochem, New York, NY 10016 USA.
RP McBain, CJ (reprint author), NICHHD, NIH, LCSN, Rm 5A72,Bldg 49,Convent Dr, Bethesda, MD 20892 USA.
OI Rudy, Bernardo/0000-0001-5748-6900
FU NINDS NIH HHS [NS30989]
NR 39
TC 44
Z9 45
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1050-9631
J9 HIPPOCAMPUS
JI Hippocampus
PY 2002
VL 12
IS 2
BP 137
EP 148
DI 10.1002/hipo.1104
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 540RP
UT WOS:000174942500003
PM 12000114
ER

PT J
AU Morales, M
   Backman, C
AF Morales, M
   Backman, C
TI Coexistence of serotonin 3 (5-HT3) and CB1 cannabinoid receptors in
   interneurons of hippocampus and dentate gyrus
SO HIPPOCAMPUS
LA English
DT Article
DE GABA; CCK; hippocampus; basket cells
ID LONG-TERM POTENTIATION; CENTRAL-NERVOUS-SYSTEM; RAT-BRAIN; RECOGNITION
   SITES; GABAERGIC INTERNEURONS; FUNCTIONAL EXPRESSION; RADIOLIGAND
   BINDING; H-3 ZACOPRIDE; CA1 REGION; NEURONS
AB Using in situ hybridization histochemistry, a high degree of coexpression of the functional 5-HT3A Subunit of the 5-HT3 receptor and the central CB1 cannabinoid receptor was detected in all subfields of the hippocampus and subgranular layer of the dentate gyrus (DG). Semi-quantitative analysis demonstrated that, depending on the hippocampal layer, 72-88% of CB1-expressing interneurons coexpress the 5-HT3A subunit. Within the DG, 5-HT3A/CB1 double-labeled neurons were confined to the subgranular layer, where close to 80% of all CB1 -expressing basket neurons were found to contain 5-HT3A subunit transcripts. These results provide the first evidence indicating that the only ion channel receptor for serotonin and central CB1 cannabinoid receptor coexist in neurons containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). These findings suggest possible interactions between the cannabinoid and serotonergic systems at the level of GABA neurotransmission. However, activation of 5-HT3- or CB1-receptors are likely to have opposing regulatory effects on GABA neurotransmission, as 5-HT3 receptor activation by serotonin results in the release of GABA, while CB1 activation by cannabinoids results in inhibition of GABA release. Hippocampus 2002;12:756-764. Published 2002 Wiley-Liss, Inc.
C1 NIDA, Baltimore, MD 21224 USA.
RP Morales, M (reprint author), NIDA, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
RI backman, cristina/C-1276-2013
NR 61
TC 21
Z9 24
U1 0
U2 1
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1050-9631
J9 HIPPOCAMPUS
JI Hippocampus
PY 2002
VL 12
IS 6
BP 756
EP 764
DI 10.1002/hipo.10025
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 632UY
UT WOS:000180242900005
PM 12542227
ER

PT J
AU Quan, N
   Herkenham, M
AF Quan, N
   Herkenham, M
TI Connecting cytokines and brain: A review of current issues
SO HISTOLOGY AND HISTOPATHOLOGY
LA English
DT Review
DE IL-1; TNF; neuroimmune communication; neurodegeneration
ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1 RECEPTOR ANTAGONIST;
   CENTRAL-NERVOUS-SYSTEM; LIPOPOLYSACCHARIDE-INDUCED FEVER;
   CORTICOTROPIN-RELEASING-FACTOR; CEREBRAL-ARTERY OCCLUSION; MESSENGER-RNA
   EXPRESSION; LONG-TERM POTENTIATION; FUNCTIONAL ANATOMICAL ANALYSIS;
   PRECURSOR PROTEIN EXPRESSION
AB Cytokines have been a multi-disciplinary research focus for over 2 decades. To date, there have been more than 15000 articles published concerning the relationship between cytokines and the central nervous system (CNS). Over half of these articles have been published in the last 5 years. From such vast number of studies, two major topics emerge as the critical issues: 1) how do cytokines modulate the functions of the CNS? 2) what is the role of cytokines in the pathogenesis of neurological diseases? Thus far, it has been clearly established that cytokines can alter the functions of the CNS in specific manners, invoking CNS-controlled autonomic, neuroendocrine, and behavioral responses. Induced expression of cytokines has also been found in the CNS during brain injury and infection, contributing to the immunological processes at this "immunologically privileged" site. Furthermore, increasing evidence points to the potential involvement of cytokines in the induction and modulation of an array of neurological diseases ranging from Alzheimer's disease to chronic fatigue syndrome. Despite such progress, however, substantial obstacles remain for both the basic understanding and the potential clinical exploitation of how cytokines interact with CNS. In this review, we will attempt to synopsize the current theories and evidence regarding the answers to the above-mentioned critical questions. These issues will be reviewed not only in isolation, as most of the original reports focused on only one of the questions, but also in parallel such that inter-issue insights may be gained.
C1 Ohio State Univ, Dept Oral Biol, Columbus, OH 43210 USA.
   NIMH, Funct Neuroanat Sect, Bethesda, MD 20892 USA.
RP Quan, N (reprint author), Ohio State Univ, Dept Oral Biol, 2214 Postle Hall,305 W 12th Ave, Columbus, OH 43210 USA.
EM quan.14@osu.edu
OI Herkenham, Miles/0000-0003-2228-4238
NR 227
TC 70
Z9 73
U1 0
U2 2
PU F HERNANDEZ
PI MURCIA
PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN
SN 0213-3911
J9 HISTOL HISTOPATHOL
JI Histol. Histopath.
PY 2002
VL 17
IS 1
BP 273
EP 288
PG 16
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 512ME
UT WOS:000173327500029
PM 11813877
ER

PT J
AU Kennison, JA
   Southworth, JW
AF Kennison, JA
   Southworth, JW
TI Transvection in Drosophila
SO HOMOLOGY EFFECTS
SE ADVANCES IN GENETICS INCORPORATING MOLECULAR GENETIC MEDICINE
LA English
DT Review
ID ZESTE-WHITE INTERACTION; CIS-REGULATORY ELEMENTS; BITHORAX COMPLEX;
   GENETIC-ANALYSIS; MOLECULAR ANALYSIS; DECAPENTAPLEGIC GENE; IMAGINAL
   DISKS; TRANSCRIPTIONAL ENHANCERS; ALLELIC COMPLEMENTATION; POLYTENE
   CHROMOSOMES
C1 NICHHD, Sect Drosophila Gene Regulat, Genet Mol Lab, NIH, Bethesda, MD 20892 USA.
RP Kennison, JA (reprint author), NICHHD, Sect Drosophila Gene Regulat, Genet Mol Lab, NIH, Bethesda, MD 20892 USA.
NR 144
TC 40
Z9 40
U1 0
U2 6
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-2660
J9 ADV GENET
PY 2002
VL 46
BP 399
EP 420
PG 22
WC Genetics & Heredity
SC Genetics & Heredity
GA BX64G
UT WOS:000185944200013
PM 11931232
ER

PT J
AU Kassis, JA
AF Kassis, JA
TI Pairing-sensitive silencing, polycomb group response elements, and
   transposon homing in Drosophila
SO HOMOLOGY EFFECTS
SE ADVANCES IN GENETICS INCORPORATING MOLECULAR GENETIC MEDICINE
LA English
DT Review
ID HOMEOTIC GENE PROBOSCIPEDIA; CHROMOSOME-BINDING-SITES; BITHORAX COMPLEX;
   GROUP PROTEINS; POLYTENE CHROMOSOMES; REGULATORY SEQUENCES;
   FUNCTIONAL-ANALYSIS; CHROMATIN PROTEIN; TARGET GENES; ABDOMINAL-B
C1 NICHHD, NIH, Bethesda, MD 20892 USA.
RP Kassis, JA (reprint author), NICHHD, NIH, Bethesda, MD 20892 USA.
NR 74
TC 76
Z9 77
U1 1
U2 5
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-2660
J9 ADV GENET
PY 2002
VL 46
BP 421
EP 438
PG 18
WC Genetics & Heredity
SC Genetics & Heredity
GA BX64G
UT WOS:000185944200014
PM 11931233
ER

PT J
AU Wickner, RB
   Edskes, HK
   Roberts, BT
   Pierce, M
   Baxa, U
AF Wickner, RB
   Edskes, HK
   Roberts, BT
   Pierce, M
   Baxa, U
TI Prions of yeast as epigenetic phenomena: High protein "copy number"
   inducing protein "silencing"
SO HOMOLOGY EFFECTS
SE ADVANCES IN GENETICS INCORPORATING MOLECULAR GENETIC MEDICINE
LA English
DT Review
ID DE-NOVO APPEARANCE; FUNGUS PODOSPORA-ANSERINA; SACCHAROMYCES-CEREVISIAE;
   SUP35 PROTEIN; SCRAPIE PRION; IN-VITRO; GENE-EXPRESSION; PSI+ PRION;
   HETEROKARYON INCOMPATIBILITY; VEGETATIVE INCOMPATIBILITY
C1 NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Wickner, RB (reprint author), NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
NR 131
TC 13
Z9 15
U1 1
U2 1
PU ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-2660
J9 ADV GENET
PY 2002
VL 46
BP 485
EP 525
PG 41
WC Genetics & Heredity
SC Genetics & Heredity
GA BX64G
UT WOS:000185944200017
PM 11931236
ER

PT J
AU Wildner, O
   Morris, JC
AF Wildner, O
   Morris, JC
TI Subcutaneous administration of a replication-competent adenovirus
   expressing HSV-tk to cotton rats: Dissemination, persistence, shedding,
   and pathogenicity
SO HUMAN GENE THERAPY
LA English
DT Article
ID VIRUS THYMIDINE KINASE; GENE-THERAPY; P53 STATUS; RECOMBINANT
   ADENOVIRUSES; ONCOLYTIC ADENOVIRUS; SIGMODON-HISPIDUS; CANCER-CELLS;
   SUICIDE GENE; ANIMAL-MODEL; COLON-CANCER
AB Since human adenoviruses replicate only in human cells, toxicology studies with adenoviral vectors are hampered by the lack of a permissive nonhuman host. Before a replication-competent adenoviral vector expressing HSV-tk (Ad.OW34) can be used in clinical studies for intratumoral injections in patients with cutaneous lesions of head and neck cancer or intralesional injection for in situ vaccination strategy in advanced metastatic melanoma patients, risks have to be estimated in animal studies. In an attempt to assess potential toxicology, dissemination, persistence and shedding, we injected Ad.OW34 subcutaneously into cotton rats. (Sigmodon hispidus), which are considered a semipermissive host for human adenoviruses. The animals underwent one or two subcutaneous injection cycles with 2.3 x 10(12) viral particles/kg each or a single course with 6.9 x 10(13) viral particles/kg and were analyzed at defined time points for histopathological changes in the brain, heart, lungs, spleen, liver, kidneys, ovaries, and skin. Additionally, these tissues as well as urine, feces, mouth, and skin swabs were analyzed at multiple time points by real-time quantitative polymerase chain reaction for the presence of vector sequences. The only significant treatment-related histopathologic finding was dermatitis with mild acanthosis at the site of vector injection. All other tissues evaluated were within normal limits or showed changes that were most likely incidental or spontaneous in nature. Vector sequences were detected in the skin at the injection site and to a lesser extent in the liver, spleen, and lungs. In addition, small amounts of vector DNA were detected in the ovaries. The vector sequences were rapidly cleared and the absence of viral sequences in the excreta and swabs of the majority of animals suggest that there was no significant replication of the vector in this host. The administration of Ad.OW34 was also associated with mild hyperamylasemia, lymphocytosis, and granulocytosis; however, we did not observe any clinical signs of illness or death in the experimental animals over the course of the study.
C1 NHGRI, Clin Gene Therapy Branch, NIH, Bethesda, MD 20892 USA.
   NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Wildner, O (reprint author), Ruhr Univ Bochum, Abt Mol & Med Virol, D-44780 Bochum, Germany.
NR 60
TC 22
Z9 26
U1 0
U2 1
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD JAN
PY 2002
VL 13
IS 1
BP 101
EP 112
DI 10.1089/10430340152712656
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA 508ED
UT WOS:000173075000005
PM 11779414
ER

PT J
AU Lozier, JN
   Csako, G
   Mondoro, TH
   Krizek, DM
   Metzger, ME
   Costello, R
   Vostal, JG
   Rick, ME
   Donahue, RE
   Morgan, RA
AF Lozier, JN
   Csako, G
   Mondoro, TH
   Krizek, DM
   Metzger, ME
   Costello, R
   Vostal, JG
   Rick, ME
   Donahue, RE
   Morgan, RA
TI Toxicity of a first-generation adenoviral vector in rhesus Macaques
SO HUMAN GENE THERAPY
LA English
DT Article
ID NONHUMAN PRIMATE LUNGS; HUMAN FACTOR-IX; GENE-THERAPY; ESCHERICHIA-COLI;
   HEMOPHILIA-B; IN-VIVO; MEDIATED EXPRESSION; IMMUNE-RESPONSES;
   VIRAL-ANTIGENS; TISSUE FACTOR
AB We constructed a first-generation adenovirus vector (AVC3FIX5) that we used to assess the rhesus macaque as a nonhuman primate model for preclinical testing of hemophilia B gene therapy vectors. Although we succeeded in our primary objective of demonstrating expression of human factor IX we encountered numerous toxic side effects that proved to be dose limiting. Following intravenous administration of AVC3FIX5 at doses of 3.4 x 10(11) vector particles/kg to 3.8 x 10(12) vector particles/kg, the animals in our study developed antibodies against human factor IX, and dose-dependent elevations of enzymes specific for liver, muscle, and lung injury. In addition, these animals showed dose-dependent prolongation of clotting times as well as acute, dose-dependent decreases in platelet counts and concomitant elevation of fibrinogen and von Willebrand factor. These abnormalities may be caused by the direct toxic effects of the adenovirus vector itself, or may result indirectly from the accompanying acute inflammatory response marked by elevations in IL-6, a key regulator of the acute inflammatory response. The rhesus macaque may be a useful animal model in which to evaluate mechanisms of adenovirus toxicities that have been encountered during clinical gene therapy trials.
C1 US FDA, Lab Hemostasis, Div Hematol, Off Blood Res & Review,Ctr Biol Evaluat & Res, Rockville, MD 20852 USA.
   NHGRI, Bethesda, MD 20892 USA.
   NIH, Dept Clin Pathol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
   NIH, Hematol Serv, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
   NHLBI, Rockville, MD USA.
   NCI, Surg Branch, Bethesda, MD 20892 USA.
RP Lozier, JN (reprint author), US FDA, Lab Hemostasis, Div Hematol, Off Blood Res & Review,Ctr Biol Evaluat & Res, 1401 Rockville Pike, Rockville, MD 20852 USA.
NR 39
TC 78
Z9 79
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD JAN
PY 2002
VL 13
IS 1
BP 113
EP 124
DI 10.1089/10430340152712665
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA 508ED
UT WOS:000173075000006
PM 11779415
ER

PT J
AU Higginbotham, JN
   Seth, P
   Blaese, RM
   Ramsey, WJ
AF Higginbotham, JN
   Seth, P
   Blaese, RM
   Ramsey, WJ
TI The release of inflammatory Cytokines from human peripheral blood
   mononuclear cells in vitro following exposure to adenovirus variants and
   capsid
SO HUMAN GENE THERAPY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; MEDIATED GENE-TRANSFER; REPLICATION-DEFICIENT
   ADENOVIRUS; RECOMBINANT ADENOVIRUS; NONHUMAN-PRIMATES; CYSTIC-FIBROSIS;
   FACTOR-ALPHA; CFTR GENE; PHASE-I; IMMUNE-RESPONSES
AB Preclinical and clinical studies with adenoviral vectors have clearly illustrated the potential advantages of this gene transfer system. However, many studies have also demonstrated potent immune responses directed at both vector and transduced cells. We examined in vitro responses of human peripheral blood mononuclear cells (PBMC) to virus exposure as a model for this host response. PBMC were isolated from normal donors and incubated with wild-type adenovirus (Ad5), Ad5 variants deleted for segments of E1 and/or E3, and empty viral capsids. Proinflammatory cytokine release was monitored for 96 hr. Induction of TNF-alpha by intact virions was low although stimulation by empty capsid gave a significant and sustained response. Induction of IL-6, GM-CSF, and a panel alpha- and beta-chemokines by intact virions was prominent, often approaching results obtained with 2.5 mg/ml of lipopolysaccharide (LPS). Responses were generally independent of virion genetic composition and were only partially blunted when UV-inactivated virus was used. Dose-response data showed 100-fold increases in virion concentration produced a maximum 3-fold increase in cytokine release, suggesting saturation. Surprisingly, prominent stimulation occurred after addition of empty capsid, which typically provoked responses equivalent to those seen with LPS stimulation. We present arguments that cellular signal transduction mechanisms activated by binding of virions/capsids stimulate transcription of proinflammatory cytokine genes.
C1 NHGRI, Clin Gene Therapy Branch, NIH, Bethesda, MD 20892 USA.
RP Higginbotham, JN (reprint author), NewLink Genet, Flow Cytometry, 3900 S Loop Dr, Ames, IA 50010 USA.
NR 69
TC 90
Z9 91
U1 0
U2 2
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD JAN
PY 2002
VL 13
IS 1
BP 129
EP 141
DI 10.1089/10430340152712683
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA 508ED
UT WOS:000173075000008
PM 11779417
ER

PT J
AU Yamano, S
   Huang, LY
   Ding, CT
   Chiorini, JA
   Goldsmith, CM
   Wellner, RB
   Golding, B
   Kotin, RM
   Scott, DE
   Baum, BJ
AF Yamano, S
   Huang, LY
   Ding, CT
   Chiorini, JA
   Goldsmith, CM
   Wellner, RB
   Golding, B
   Kotin, RM
   Scott, DE
   Baum, BJ
TI Recombinant adeno-associated virus serotype 2 vectors mediate stable
   interleukin 10 secretion from salivary glands into the bloodstream
SO HUMAN GENE THERAPY
LA English
DT Article
ID ADENOASSOCIATED VIRUS; GENE-TRANSFER; IN-VIVO; TRANSGENE PRODUCTS;
   AUTOIMMUNE-DISEASE; NONDIVIDING CELLS; SYSTEMIC DELIVERY;
   HIGH-EFFICIENCY; GROWTH-HORMONE; AAV VECTORS
AB We have constructed a recombinant adeno-associated virus serotype 2 vector encoding human interleukin 10 (rAAVhIL10). IL-10 is a potent antiinflammatory/immune cytokine, which has received growing attention for its therapeutic potential. Human IL-10 (hIL-10) production was virus dose dependent after in vitro infection of HSG cells, a human submandibular gland cell line. The vector-derived hIL-10 produced was biologically active, as the medium from rAAVhIL10-infected HSG cells caused a dose-dependent blockade of IL-12 secretion from spleen cells of IL-10 knockout mice challenged with heat-killed Brucella abortus. Administration of rAAVhIL10 (10(10) genomes per gland) to both mouse submandibular glands led to hIL-10 secretion into the bloodstream (similar to1-5 pg/ml), that is, in an endocrine manner, which was stable for similar to2 months. Salivary gland administration of rAAVhIL10 under experimental conditions was more efficacious than intravenous administration (similar to0.5-0.7 pg/ml). Also, hIL-10 was readily secreted in vitro from organ cultures of minced submandibular glands infected with rAAVhIL10, 6 or 8 weeks earlier. Consistent with these results, hIL-10 mRNA was detected by reverse transcription-polymerase chain reaction in submandibular glands of mice infected with rAAVhIL10 but not from control mice. At these doses, little to no hIL-10 was detected in mouse saliva. Using a rAAV serotype 2 vector encoding beta-galactosidase, we observed that the primary parenchymal target cells were ductal. These findings represent the first report of rAAV use to target exocrine glands for systemic secretion of a therapeutic protein, and support the notion that rAAV serotype 2 vectors may be useful in salivary glands for local (periglandular) and systemic gene-based protein therapeutics.
C1 NIDCR, GTTB, NIH, Bethesda, MD 20892 USA.
   US FDA, Div Hematol, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
   NHLBI, Lab Biochem Genet, NIH, Bethesda, MD 20892 USA.
RP Baum, BJ (reprint author), NIDCR, GTTB, NIH, 10 Ctr Dr,MSC 1190,Bldg 10,Room 1N113, Bethesda, MD 20892 USA.
RI kotin, robert/B-8954-2008; 
OI Yamano, Seiichi/0000-0003-2056-4359
NR 57
TC 27
Z9 28
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD JAN
PY 2002
VL 13
IS 2
BP 287
EP 298
DI 10.1089/10430340252769806
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA 515ML
UT WOS:000173499600010
PM 11812284
ER

PT J
AU Kimchi-Sarfaty, C
   Ben-Nun-Shaul, O
   Rund, D
   Oppenheim, A
   Gottesman, MM
AF Kimchi-Sarfaty, C
   Ben-Nun-Shaul, O
   Rund, D
   Oppenheim, A
   Gottesman, MM
TI In vitro-packaged SV40 pseudovirions as highly efficient vectors for
   gene transfer
SO HUMAN GENE THERAPY
LA English
DT Article
ID HUMAN HEMATOPOIETIC-CELLS; CLASS-I MOLECULES; EXPRESSION; THERAPY;
   PROMOTER; ELEMENTS; SIMIAN-VIRUS-40; ENCAPSIDATION; RETROVIRUS;
   SEQUENCES
AB A procedure for in vitro packaging of plasmid DNA in recombinant SV40 capsid proteins was developed by Sandalon et al. (1997). Here, we report the highly efficient transduction into different human, murine and monkey cell lines using a scaled-up protocol for producing SV40 pseudovirions, packaged in vitro, carrying the human multidrug-resistance gene MDR1 encoding P-glycoprotein (P-gp) or the green fluorescent protein reporter gene (GFP) under control of SV40 and cytomegalovirus (CMV) promoters. The percentage of expressing cells was proportional to the number of transducing particles, with close to 100% of cells transduced at optimal ratios of transducing particles to cells. The ability to confer multidrug resistance was evaluated by measuring dye efflux and cell-surface expression in infected cells. The relative level of expression of P-gp driven by the different promoters varied among different cell lines. In human lymphoblastoid cells, which express high levels of major histocompatibility complex (MHC) class I (a surface receptor for SV40), constructs that carry an intron yield the highest expression. Our experiments further demonstrate that MDR1 and GFP expression driven by these promoters is transient; however, transduced cells remain MDR1-positive if selected in colchicine. Thus, the SV40 vectors are well suited to situations in which only short-term expression is required or expression is selected, such as for bone marrow protection during chemotherapy.
C1 NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
   Hebrew Univ Jerusalem, Hadassah Med Sch, IL-91120 Jerusalem, Israel.
   Hadassah Univ Hosp, IL-91120 Jerusalem, Israel.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37,Room 1A09,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA.
NR 34
TC 25
Z9 26
U1 0
U2 2
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD JAN
PY 2002
VL 13
IS 2
BP 299
EP 310
DI 10.1089/10430340252769815
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA 515ML
UT WOS:000173499600011
PM 11812285
ER

PT J
AU Luka, Z
   Cerone, R
   Phillips, JA
   Mudd, SH
   Wagner, C
AF Luka, Z
   Cerone, R
   Phillips, JA
   Mudd, SH
   Wagner, C
TI Mutations in human glycine N-methyltransferase give insights into its
   role in methionine metabolism
SO HUMAN GENETICS
LA English
DT Article
ID CRYSTAL-STRUCTURE; RAT-LIVER; PROTEIN; INHIBITION; BALANCES; ENZYMES;
   GENE
AB Methylation is an essential process in the body. Methyl groups in the form of S-adenosylmethionine are used for the synthesis of many essential compounds (e.g., creatine, phosphatidylcholine, and the methylation of DNA in gene expression). Glycine N-methyltransferase (GNMT) is an abundant enzyme in liver. It catalyzes the methylation of glycine by using S-adenosylmethionine (AdoMet) to form N-methylglycine (sarcosine) with the concommitant production of S-adenosylhomocysteine (AdoHcy). It plays an important role in the economy of methyl groups in the body. The function of GNMT has been hypothesized to provide an alternative route for the conversion of excess AdoMet to AdoHcy in order to preserve the AdoMet/AdoHcy ratio. GNMT is also inhibited by a specific form of folate, 5-methyltetrahydrofolate pentaglutamate. As such, GNMT participates in a regulatory scheme that links the de novo synthesis of methyl groups to the availability of dietary methionine. This hypothesis can now be tested in man. We report here for the first time two Italian sibs who are compound heterzygotes in the gene that encodes GNMT. Both have evidence of mild liver disease. Each bears the same two missense mutations, one in exon 1 (Leu49Pro) and the second in exon 4 (His176Asn). Restriction enzyme analysis of panels of diverse DNA samples indicates that these mutations are not attributable to a common polymorphism.
C1 Vanderbilt Univ, Med Ctr, Dept Biochem, Nashville, TN 37232 USA.
   Univ Genoa, Dept Pediat, G Gaslini Inst, I-16145 Genoa, Italy.
   Dept Vet Affairs, Med Ctr, Nashville, TN USA.
   NIMH, Mol Biol Lab, Bethesda, MD 20892 USA.
   Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37212 USA.
RP Wagner, C (reprint author), Vanderbilt Univ, Med Ctr, Dept Biochem, 620 Light Hall, Nashville, TN 37232 USA.
FU NCRR NIH HHS [RR0095]; NIDDK NIH HHS [DK35592]; NIGMS NIH HHS
   [T32GM62758]; PHS HHS [54859, 15289]
NR 26
TC 43
Z9 44
U1 1
U2 7
PU SPRINGER-VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD JAN
PY 2002
VL 110
IS 1
BP 68
EP 74
DI 10.1007/s00439-001-0648-4
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 521NB
UT WOS:000173845900011
PM 11810299
ER

PT J
AU Malley, JD
   Naiman, DQ
   Bailey-Wilson, JE
AF Malley, JD
   Naiman, DQ
   Bailey-Wilson, JE
TI A comprehensive method for genome scans
SO HUMAN HEREDITY
LA English
DT Article
DE linkage; affected sib pair; bonferroni adjustment; Gaussian process;
   importance sampling
ID FALSE-POSITIVE PEAKS; LINKAGE; TRUE
AB In applications involving the use of genome scans the problem of correcting for multiple testing figures prominently. A frequently used approach is the Bonferroni adjustment, but this is known to be often severely conservative. As an alternative we use the method of importance sampling to accurately and efficiently obtain required exceedance probabilities. This method is comprehensive in the sense that it has application to exceedance probabilities for other classes of test statistics, such as those for linkage disequilibrium or Hardy-Weinberg equilibrium at multiple loci. We illustrate the importance sampling technique by focusing on affected sib pair tests done at a large number of fully informative markers. We demonstrate how our approach can be used to obtain exceedance probabilities for arbitrary marker spacings, and we compare our approach with that of Feingold et al. [1993], which uses the method of large deviations and does not provide the means for adjusting for unequal marker spacing. Copyright (C) 2002 S. Karger AG, Basel.
C1 Johns Hopkins Univ, Dept Math Sci, Baltimore, MD 21218 USA.
   NHGRI, NIH, Bethesda, MD 20892 USA.
   NIH, Ctr Informat Technol Technol, Bethesda, MD 20892 USA.
RP Naiman, DQ (reprint author), Johns Hopkins Univ, Dept Math Sci, Baltimore, MD 21218 USA.
RI Naiman, Daniel/A-3304-2010; 
OI Naiman, Daniel/0000-0001-6504-9081; Bailey-Wilson,
   Joan/0000-0002-9153-2920; Malley, James/0000-0002-9895-7454
NR 22
TC 11
Z9 12
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0001-5652
J9 HUM HERED
JI Hum. Hered.
PY 2002
VL 54
IS 4
BP 174
EP 185
DI 10.1159/000070663
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 690DX
UT WOS:000183533100003
PM 12771550
ER

PT J
AU Li, ZH
   Gail, MH
   Pee, D
   Gastwirth, JL
AF Li, ZH
   Gail, MH
   Pee, D
   Gastwirth, JL
TI Statistical properties of Teng and Risch's sibship type tests for
   detecting an association between disease and a candidate allele
SO HUMAN HEREDITY
LA English
DT Article
DE family-based case-control design; TDT-like tests; partial ascertainment
   approximation; full ascertainment correction
ID FAMILY-BASED ASSOCIATION; QUANTITATIVE TRAIT LOCI; HAPLOTYPE RELATIVE
   RISK; COMPLEX HUMAN-DISEASES; DISCORDANT SIB PAIRS; TRANSMISSION
   DISEQUILIBRIUM; LINKAGE DISEQUILIBRIUM; GENES; DESIGNS; POWER
AB Risch and Teng [Genome Res 1998;8:1273-1288] and Teng and Risch [Genome Res 1999;9:234-241] proposed a class of transmission/disequilibrium test-like statistical tests based on the difference between the estimated allele frequencies in the affected and control populations. They evaluated the power of a variety of family-based and nonfamily-based designs for detecting an association between a candidate allele and disease. Because they were concerned with diseases with low penetrances, their power calculations assumed that unaffected individuals can be treated as a random sample from the population. They predicted that this assumption rendered their sample size calculations slightly conservative. We generalize their partial ascertainment conditioning by including the status of the unaffected sibs in the calculations of the distribution and power of the statistic used to compare the allele frequency in affected offspring to the estimated frequency in the parents, based on sibships with genotyped affected and unaffected sibs. Sample size formulas for our full ascertainment methods are presented. The sample sizes for our procedure are compared to those of Teng and Risch. The numerical results and simulations indicate that the simplifying assumption used in Teng and Risch can produce both conservative and anticonservative results. The magnitude of the difference between the sample sizes needed by their partial ascertainment approximation and the full ascertainment is small in the circumstances they focused on but can be appreciable in others, especially when the baseline penetrances are moderate. Two other statistics, using different estimators for the variance of the basic statistic comparing the allele frequencies in the affected and unaffected sibs are introduced. One of them incorporates an estimate of the null variance obtained from an auxiliary sample and appears to noticeably decrease the sample sizes required to achieve a prespecified power. Copyright (C) 2002 S. Karger AG, Basel.
C1 George Washington Univ, Ctr Biostat, Dept Stat, Rockville, MD 20852 USA.
   NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   Informat Management Serv Inc, Rockville, MD USA.
   George Washington Univ, Dept Stat, Washington, DC 20052 USA.
RP Li, ZH (reprint author), George Washington Univ, Ctr Biostat, Dept Stat, Rockville, MD 20852 USA.
FU NCI NIH HHS [CA 64363]
NR 30
TC 2
Z9 2
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0001-5652
J9 HUM HERED
JI Hum. Hered.
PY 2002
VL 53
IS 3
BP 114
EP 129
DI 10.1159/000064974
PG 16
WC Genetics & Heredity
SC Genetics & Heredity
GA 583EV
UT WOS:000177394400002
PM 12145548
ER

PT J
AU Freidlin, B
   Zheng, G
   Li, ZH
   Gastwirth, JL
AF Freidlin, B
   Zheng, G
   Li, ZH
   Gastwirth, JL
TI Trend tests for case-control studies of genetic markers: Power, sample
   size and robustness
SO HUMAN HEREDITY
LA English
DT Article
DE candidate gene associations; Cochran-Armitage trend test; MAX test;
   maximin efficiency robust test; power approximation; sample size
ID CONTINGENCY-TABLES; SURVIVAL
AB The Cochran-Armitage trend test is commonly used as a genotype-based test for candidate gene association. Corresponding to each underlying genetic model there is a particular set of scores assigned to the genotypes that maximizes its power. When the variance of the test statistic is known, the formulas for approximate power and associated sample size are readily obtained. In practice, however, the variance of the test statistic needs to be estimated. We present formulas for the required sample size to achieve a prespecified power that account for the need to estimate the variance of the test statistic. When the underlying genetic model is unknown one can incur a substantial loss of power when a test suitable for one mode of inheritance is used where another mode is the true one. Thus, tests having good power properties relative to the optimal tests for each model are useful. These tests are called efficiency robust and we study two of them: the maximin efficiency robust test is a linear combination of the standardized optimal tests that has high efficiency and the MAX test, the maximum of the standardized optimal tests. Simulation results of the robustness of these two tests indicate that the more computationally involved MAX test is preferable. Copyright (C) 2002 S. Karger AG, Basel.
C1 NCI, Biometr Res Branch, Rockville, MD USA.
   NCI, Biostat Branch, Rockville, MD USA.
   NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
   George Washington Univ, Ctr Biostat, Rockville, MD USA.
   George Washington Univ, Dept Stat, Washington, DC 20052 USA.
RP Freidlin, B (reprint author), NCI, Biometr Res Branch, MSC 7434, Bethesda, MD 20892 USA.
FU NEI NIH HHS [EY14478]
NR 13
TC 208
Z9 213
U1 1
U2 15
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0001-5652
J9 HUM HERED
JI Hum. Hered.
PY 2002
VL 53
IS 3
BP 146
EP 152
DI 10.1159/000064976
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 583EV
UT WOS:000177394400004
PM 12145550
ER

PT J
AU Ravnik-Glavac, M
   Atkinson, A
   Glavac, D
   Dean, M
AF Ravnik-Glavac, M
   Atkinson, A
   Glavac, D
   Dean, M
TI DHPLC screening of cystic fibrosis gene mutations
SO HUMAN MUTATION
LA English
DT Article
DE DHPLC; mutation detection; cystic fibrosis; CF; CFTR; ABCC7; mutation
   screening; sensitivity
ID PERFORMANCE LIQUID-CHROMATOGRAPHY; SINGLE-STRANDED CONFORMATION;
   GRADIENT GEL-ELECTROPHORESIS; CFTR GENE; POINT MUTATIONS; DENATURING
   HPLC; IDENTIFICATION; DNA; POLYMORPHISMS; DISEASE
AB Denaturing high performance liquid chromatography (DHPLC) using ion-pairing reverse phase chromatography (IPRPC) columns is a technique for the screening of gene mutations. In order to evaluate the potential utility of this assay method in a clinical laboratory setting, we subjected the PCR products of 73 CF patients known to bear CFTR mutations to this analytic technique. We used thermal denaturation profile parameters specified by the MELT program tool, made available by Stanford University. Using this strategy, we determined an initial analytic sensitivity of 90.4% for any of 73 known CFTR mutations. Most of the mutations not detected by DHPLC under these conditions are cc-substitutions. This information may eventually help to improve the MELT algorithm. Increasing column denaturation temperatures for one or two degrees above those recommended by the MELT program allowed 100% detection of CFTR mutations tested. By comparing DHPLC methodology used in this study with the recently reported study based on Wavemaker 3.4.4 software (Transgenomic, Omaha, NE) [Le Marechal et al., 2001) and with previous SSCP analysis of CFTR mutations [Ravnik-Glavac et al., 19941 we emphasized differences and similarities in order to refine the DHPLC system and discuss the relationship to the alternative approaches. We conclude that the DHPLC method, under optimized conditions, is highly accurate, rapid, and efficient in detecting mutations in the CFTR gene and may find high utility in screening individuals for CFTR mutations. Hum Mutat 19:374-383, 2002. Published 2002 Wiley-Liss, Inc.(dagger).
C1 NCI, Lab Genome Divers, Human Genet Sect, Frederick, MD 21702 USA.
   Univ Ljubljana, Fac Med, Inst Biochem, Ljubljana 61000, Slovenia.
   NCI, SAIC Frederick, Frederick, MD 21702 USA.
   Univ Ljubljana, Inst Pathol, Dept Mol Genet, Ljubljana, Slovenia.
RP Dean, M (reprint author), NCI, Lab Genome Divers, Human Genet Sect, Frederick, MD 21702 USA.
RI Dean, Michael/G-8172-2012
OI Dean, Michael/0000-0003-2234-0631
NR 34
TC 36
Z9 40
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PY 2002
VL 19
IS 4
BP 374
EP 383
DI 10.1002/humu.10065
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 534QY
UT WOS:000174599300007
PM 11933191
ER

PT J
AU Olivier, M
   Eeles, R
   Hollstein, M
   Khan, MA
   Harris, CC
   Hainaut, P
AF Olivier, M
   Eeles, R
   Hollstein, M
   Khan, MA
   Harris, CC
   Hainaut, P
TI The IARC TP53 database: New Online mutation analysis and recommendations
   to users
SO HUMAN MUTATION
LA English
DT Article
DE TP53; p53; mutation analysis; database; Li-Fraumeni syndrome; LFS;
   cancer; tumor suppressor
ID LI-FRAUMENI-SYNDROME; P53 MUTATIONS; HUMAN CANCER; HUMAN TUMORS;
   CELL-LINES; FAMILIES; GENE; CHK2
AB Mutations in the tumor suppressor gene TP53 are frequent in most human cancers. Comparison of the mutation patterns in different cancers may reveal clues on the natural history of the disease. Over the past 10 years, several databases of TP53 mutations have been developed. The most extensive of these databases is maintained and developed at the International Agency for Research on Cancer. The database compiles all mutations (somatic and inherited), as well as polymorphisms, that have been reported in the published literature since 1989. The IARC TP53 mutation dataset is the largest dataset available on the variations of any human gene. The database is avail, able at wwwdarc.fr/P53/. In this paper, we describe recent developments of the database. These developments include restructuring of the database, which is now patient-centered, with more detailed annotations on the patient (carcinogen exposure, virus infection, genetic background). In addition, a new on,line application to retrieve somatic mutation data and analyze mutation patterns is now available. We also discuss limitations on the use of the database and provide recommendations to users.
C1 Int Agcy Res Canc, Mol Carcinogenesis Grp, WHO, F-69372 Lyon, France.
   Inst Canc Res, Canc Genet Team, Surrey, England.
   German Canc Res Ctr, D-6900 Heidelberg, Germany.
   NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Hainaut, P (reprint author), Int Agcy Res Canc, Mol Carcinogenesis Grp, WHO, 150 Cours Albert Thomas, F-69372 Lyon, France.
RI Olivier, Magali/G-3728-2010; Hainaut, Pierre /B-6018-2012; 
OI Olivier, Magali/0000-0002-8202-342X; Hainaut, Pierre
   /0000-0002-1303-1610; Eeles, Rosalind/0000-0002-3698-6241
NR 13
TC 775
Z9 792
U1 2
U2 22
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PY 2002
VL 19
IS 6
BP 607
EP 614
DI 10.1002/humu.10081
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 556HR
UT WOS:000175843800002
PM 12007217
ER

PT J
AU Orvisky, E
   Park, JK
   Parker, A
   Walker, JM
   Martin, BM
   Stubblefield, BK
   Uyama, E
   Tayebi, N
   Sidransky, E
AF Orvisky, E.
   Park, J. K.
   Parker, A.
   Walker, J. M.
   Martin, B. M.
   Stubblefield, B. K.
   Uyama, E.
   Tayebi, N.
   Sidransky, E.
TI The Identification of Eight Novel Glucocerebrosidase (GBA) Mutations in
   Patients with Gaucher Disease
SO HUMAN MUTATION
LA English
DT Article
DE glucocerebrosidase; glucosidase; beta; acid; GBA; Gaucher disease;
   mutation analysis
AB Mutations in the gene encoding for the lysosomal enzyme glucocerebrosidase (GBA) result in Gaucher disease. In this study, seven novel missense mutations in the glucocerebrosidase gene (A136E, H162P, K198E, Y205C, F251L, Q350X and I402F) and a splice site mutation (IVS10+2T -> A) were identified by direct sequencing of three amplified segments of the glucocerebrosidase gene. Five of the novel mutations were found in patients with neuronopathic forms of Gaucher disease, two of which, K198E and F251L, appear to be associated with type 2 Gaucher disease. (C) 2002 Wiley-Liss, Inc.
C1 [Orvisky, E.; Park, J. K.; Parker, A.; Walker, J. M.; Martin, B. M.; Stubblefield, B. K.; Tayebi, N.; Sidransky, E.] NIMH, Clin Neurosci Branch, Sect Mol Neurogenet, NIH, Bethesda, MD 20892 USA.
   [Uyama, E.] Kumamoto Univ, Sch Med, Dept Neurol, Kumamoto 860, Japan.
RP Sidransky, E (reprint author), NIMH, Clin Neurosci Branch, Sect Mol Neurogenet, NIH, 49 Convent Dr MSC4405,49-B1EE16, Bethesda, MD 20892 USA.
EM sidranse@irp.nimh.nih.gov
NR 18
TC 12
Z9 13
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PY 2002
VL 19
IS 4
DI 10.1002/humu.9024
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA V16XC
UT WOS:000207901300002
PM 11933202
ER

PT J
AU Staebler, A
   Heselmeyer-haddad, K
   Bell, K
   Riopel, M
   Perlman, E
   Reid, T
   Kurman, RJ
AF Staebler, A
   Heselmeyer-haddad, K
   Bell, K
   Riopel, M
   Perlman, E
   Reid, T
   Kurman, RJ
TI Micropapillary serous carcinoma of the ovary has distinct patterns of
   chromosomal imbalances by comparative genomic hybridization compared
   with atypical proliferative serous tumors and serous carcinomas
SO HUMAN PATHOLOGY
LA English
DT Article
DE chromosomal imbalances; micropapillary serous carcinoma of the ovary
ID IN-SITU HYBRIDIZATION; BORDERLINE TUMORS; CYTOGENETIC ANALYSIS;
   LOW-GRADE; CANCER; OVERREPRESENTATION; FREQUENT; GENESIS; BENIGN; LOSSES
AB Recent studies have subdivided serous borderline tumors into 2 categories: atypical proliferative serous tumors (APSTs), which have a relatively benign course, and micropapillary serous carcinomas (MPSCs), which behave like low-grade carcinoma. This study was undertaken to determine, using comparative genomic hybridization (CGH), whether cytogenetic changes support this hypothesis. Nine cases of APST, 10 of MPSC, and 11 of invasive serous carcinoma (SC) were analyzed by CGH. Tumor DNA was extracted from frozen or paraffin-embedded tissue from the primary ovarian tumor, using either sections with at least 70% tumor cells or tissue after relative enrichment by microdissection. Chromosomal imbalances were identified in 3 of 9 APST, 6 of 10 MPSC, and 11 of 11 SC. Three or more chromosomal imbalances were found in 0 of 9 APST, 4 of 10 MPSC, and 9 of 11 SC. Recurrent copy number alterations were grouped into 4 classes correlating with the different tumor types. Class I changes were present in APST and in MPSC or SC and included +8q (7 of 11 SC, 2 of 10 MPSC, 2 of 9 APST), -9p (5 of 11 SC, 0 of 10 MPSC, 1 of 9 APST), and +12 (+12p in 3/11 SC, +12 in 2 of 10 MPSC, +12 in 1 of 9 APST). Class II changes were found only in MPSC and SC, but not in APST. The most frequent examples were +3q (10 of 11 SC, 1 of 10 MPSC), -4q (5 of 11 SC, 1 of 10 MPSC), and -17p (5 of 11 SC, 1 of 10 MPSC). Class III changes were limited to SC, like -16q (7 of 11 SC) and -18q (6 of 11 SC). Class VI changes were unique to MPSC. Gain of 16p (3 of 10 MPSC) was the only aberration in this group. This aberration was not only unique to MPSC but was also the most frequent finding in MPSC. These data support the hypothesis that noninvasive serous tumors of fine ovary can be subdivided into 2 categories: APST and MPSC. The number of imbalances in MPSC is substantially higher than in APST and lower than in SC. Some changes in MPSC are shared with SC and APST and others with SC only, suggesting that a subset of MPSC may represent a stage in progression from APST to SC. Other cases of MPSC with independent genetic alterations may represent another subset of tumors that are a distinct entity from APST and SC. Copyright (C) 2002 by W.B. Saunders Company.
C1 Johns Hopkins Univ Hosp, Dept Pathol, Baltimore, MD 21231 USA.
   Johns Hopkins Univ Hosp, Dept Gynecol & Obstet, Baltimore, MD 21231 USA.
   Natl Canc Inst, Bethesda, MD USA.
   Univ Munster, Gerhard Domagk Inst Pathol, D-4400 Munster, Germany.
RP Kurman, RJ (reprint author), Johns Hopkins Univ Hosp, Dept Pathol, Weinberg Bldg,Room 2242,401 N Broadway, Baltimore, MD 21231 USA.
NR 24
TC 43
Z9 45
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399 USA
SN 0046-8177
J9 HUM PATHOL
JI Hum. Pathol.
PD JAN
PY 2002
VL 33
IS 1
BP 47
EP 59
DI 10.1053/hupa.2002.30212
PG 13
WC Pathology
SC Pathology
GA 516GV
UT WOS:000173546300008
PM 11823973
ER

PT B
AU Hummer, G
   Rasaiah, JC
   Noworyta, JP
AF Hummer, G.
   Rasaiah, J. C.
   Noworyta, J. P.
BE Laudon, M
   Romanowicz, B
TI Water conduction through carbon nanotubes
SO ICCN 2002: INTERNATIONAL CONFERENCE ON COMPUTATIONAL NANOSCIENCE AND
   NANOTECHNOLOGY
LA English
DT Proceedings Paper
CT 2nd International Conference on Computational Nanoscience and
   Nanotechnology
CY APR 21-25, 2002
CL San Juan, PR
SP Appl Computat Res Soc, DARPA, Amer Phys Soc, Soc Ind & Appl Math, IEEE Electron Devices Soc, Swiss Fed Inst Technol Lausanne, TIMA CMP Lab, Univ Calif Davis, Dept Appl Sci, Coll Engn, Int Assoc Math & Comp Modeling, Accelrys Inc, Mintz Levin Cohn Ferris Glovsky & Popeo PC, Motorola, ANSYS Inc
DE carbon nanotubes; water transport; onedimensional fluids
ID CYTOCHROME-C-OXIDASE; HEME-COPPER OXIDASES; PROTON TRANSLOCATION;
   PROTEIN; SIMULATION; MOLECULES; MECHANISM; TRANSPORT; CHANNELS; PATHWAY
AB In molecular dynamics simulations we found that water can form hydrogen-bonded water chains in the interior of carbon nanotubes. Water penetration is sensitive to details of thermodynamic conditions and interaction potentials, resulting in sharp, first-order like transitions between filled and empty states. Under wetting conditions, water molecules are transported efficiently through nanotubes. Implications on the design of nanotube channels for small molecules and protons will be discussed.
C1 NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Hummer, G (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
NR 27
TC 0
Z9 0
U1 1
U2 2
PU COMPUTATIONAL PUBLICATIONS
PI CAMBRIDGE
PA PUBISHING OFFICE, 308 ONE KENDALL SQ BLDG 600, CAMBRIDGE, MA 02139 USA
BN 0-9708275-6-3
PY 2002
BP 124
EP 127
PG 4
WC Nanoscience & Nanotechnology
SC Science & Technology - Other Topics
GA BEY39
UT WOS:000240119600034
ER

EF