FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Brotman, MA
Skup, M
Rich, BA
Blair, KS
Pine, DS
Blair, JR
Leibenluft, E
AF Brotman, Melissa A.
Skup, Martha
Rich, Brendan A.
Blair, Karina S.
Pine, Daniel S.
Blair, James R.
Leibenluft, Ellen
TI Risk for Bipolar Disorder Is Associated With Face-Processing Deficits
Across Emotions
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE bipolar disorder; endophenotype; face emotion labeling; at risk
ID LABELING DEFICITS; RATING-SCALE; CHILDREN; ENDOPHENOTYPES;
PSYCHOPATHOLOGY; ADOLESCENTS; RELIABILITY; VALIDITY; PARENTS;
SCHIZOPHRENIA
AB Objective: Youths with euthymic bipolar disorder (BD) have a deficit in face-emotion labeling that is present across multiple emotions. Recent research indicates that youths at familial risk for BD, but without a history of mood disorder, also have a deficit in face-emotion labeling, suggesting that such impairments may be an endophenotype for BD. It is unclear whether this deficit in at-risk youths is present across all emotions or if the impairment presents initially as an emotion-specific dysfunction that then generalizes to other emotions as the symptoms of BID become manifest. Method; Thirty-seven patients with pediatric BD, 25 unaffected children with a first-degree relative with BD, and 36 typically developing youths were administered the Emotional Expression Multimorph Task, a computerized behavioral task, which presents gradations of facial emotions from 100% neutrality to 100% emotional expression (happiness, surprise, fear, sadness, anger, and disgust). Results: Repeated-measures analysis of covariance revealed that, compared with the control youths, the patients and the at-risk youths required significantly more intense emotional information to identify and correctly label face emotions. The patients with BD and the at-risk youths did not differ from each other. Group-by-emotion interactions were not significant, indicating that the group effects did not differ based on the facial emotion. Conclusions: The youths at risk for BD demonstrate nonspecific deficits in face-emotion recognition, similar to patients with the illness. Further research is needed to determine whether such deficits meet all the criteria for an endophenotype. J. Am. Acad. Child Adolesc. Psychiatty, 2008;47(12):1455-1461.
C1 [Brotman, Melissa A.; Skup, Martha; Rich, Brendan A.; Blair, Karina S.; Pine, Daniel S.; Blair, James R.; Leibenluft, Ellen] NIMH, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Brotman, MA (reprint author), 15K N Dr,Room 208, Bethesda, MD 20892 USA.
EM brotman@mail.nih.gov
RI Brotman, Melissa/H-7409-2013
FU Intramural NIH HHS [Z01 MH002778-08]
NR 36
TC 58
Z9 59
U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD DEC
PY 2008
VL 47
IS 12
BP 1455
EP 1461
DI 10.1097/CHI.0b013e318188832e
PG 7
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 375KI
UT WOS:000261112200013
PM 19034190
ER
PT J
AU Patel, AR
Avila, D
Malech, HL
Pavletic, SZ
Yao, L
Cowen, EW
AF Patel, Asha R.
Avila, Daniele
Malech, Harry L.
Pavletic, Steven Z.
Yao, Larry
Cowen, Edward W.
TI Rippled skin, fasciitis, and joint contractures
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Editorial Material
ID VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION; MONOCLONAL-ANTIBODY;
RITUXIMAB; MANIFESTATIONS; DIAGNOSIS; THERAPY; GVHD
C1 [Patel, Asha R.; Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Avila, Daniele; Pavletic, Steven Z.] NCI, Dermatol Branch, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Malech, Harry L.] NIAID, Host Def Lab, Bethesda, MD 20892 USA.
[Yao, Larry] Natl Inst Hlth, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
RP Cowen, EW (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10 Room 12N238,10 Ctr Dr MSC 1908, Bethesda, MD 20892 USA.
EM cowene@mail.nih.gov
OI Malech, Harry/0000-0001-5874-5775
FU Intramural NIH HHS [Z99 CA999999]
NR 34
TC 5
Z9 7
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD DEC
PY 2008
VL 59
IS 6
BP 1070
EP 1074
DI 10.1016/j.jaad.2008.08.023
PG 5
WC Dermatology
SC Dermatology
GA 375VJ
UT WOS:000261141600023
PM 19022104
ER
PT J
AU Huang, LM
Jeang, KT
AF Huang, Li-Min
Jeang, Kuan-Teh
TI HIV-1 at Age 25: Some Thoughts for Taiwan and China
SO JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID AIDS; PERSPECTIVE
C1 [Jeang, Kuan-Teh] NIAID, NIH, Bethesda, MD 20892 USA.
[Huang, Li-Min] Natl Taiwan Univ, Sch Med, Taipei 10764, Taiwan.
RP Jeang, KT (reprint author), NIAID, NIH, 9000 Rockville Pike,Bldg 4, Bethesda, MD 20892 USA.
EM KJEANG@niaid.nih.gov
RI Jeang, Kuan-Teh/A-2424-2008;
OI Huang, Li-Min/0000-0002-9291-260X
NR 10
TC 4
Z9 5
U1 0
U2 1
PU ELSEVIER SINGAPORE PTE LTD
PI SINGAPORE
PA 3 KILLINEY ROAD 08-01, WINSLAND HOUSE 1, SINGAPORE, 239519, SINGAPORE
SN 0929-6646
J9 J FORMOS MED ASSOC
JI J. Formos. Med. Assoc.
PD DEC
PY 2008
VL 107
IS 12
BP 907
EP 908
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 392TW
UT WOS:000262326100001
PM 19129049
ER
PT J
AU Gill, J
Vythilingam, M
Page, GG
AF Gill, Jessica
Vythilingam, Meena
Page, Gayle G.
TI Low Cortisol, High DHEA, and High Levels of Stimulated TNF-alpha, and
IL-6 in Women With PTSD
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; INTIMATE PARTNER VIOLENCE; MAJOR
DEPRESSION; RHEUMATOID-ARTHRITIS; COMBAT VETERANS; INNATE IMMUNITY;
PLASMA-LEVELS; RECEPTOR; DEHYDROEPIANDROSTERONE; PATHOPHYSIOLOGY
AB Posttraumatic stress disorder (PTSD) has been associated with hypothalamic-pituitary-adrenal (HPA) axis and immune function alterations; however, few studies have simultaneously investigated these systems in participants with PTSD. In this study, HPA axis and immune function in 26 women with PTSD with and without major depressive disorder was compared to 24 traumatized controls and to 21 nontraumatized controls. Posttraumatic stress disorder was associated with low cortisol and higher levels of DHEA and greater production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) compared to traumatized and healthy controls. Women with PTSD and depression exhibited greater production IL-6 and higher levels of dehydroepiandrosterone (DHEA) than those with PTSD, but without depression. These findings suggest dysregulated HPA axis and immune function in women with PTSD, and that comorbid depression may contribute to these abnormalities.
C1 [Gill, Jessica] NINR, NIH, Bethesda, MD 20892 USA.
[Vythilingam, Meena] NIMH, Bethesda, MD 20892 USA.
[Page, Gayle G.] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
RP Gill, J (reprint author), NINR, NIH, 10 Ctr Dr,10 CRC 2-1339, Bethesda, MD 20892 USA.
EM jgill@mail.nih.gov
FU NINR NIH HHS [F31 NR009166, F31 NR009166-01A1, T32 NR 07968, T32
NR007968]; PHS HHS [8326927]
NR 61
TC 95
Z9 98
U1 4
U2 10
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD DEC
PY 2008
VL 21
IS 6
BP 530
EP 539
DI 10.1002/jts.20372
PG 10
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 391ZD
UT WOS:000262271800006
PM 19107725
ER
PT J
AU Rogers, CG
Metwalli, A
Blatt, AM
Bratslavsky, G
Menon, M
Linehan, WM
Pinto, PA
AF Rogers, Craig G.
Metwalli, Adam
Blatt, Adam M.
Bratslavsky, Gennady
Menon, Mani
Linehan, W. Marston
Pinto, Peter A.
TI Robotic Partial Nephrectomy for Renal Hilar Tumors: A
Multi-Institutional Analysis
SO JOURNAL OF UROLOGY
LA English
DT Article
DE kidney neoplasms; laparoscopy; nephrectomy; robotics
ID LAPAROSCOPIC PARTIAL NEPHRECTOMY; CHRONIC KIDNEY-DISEASE; EXPERIENCE
AB Purpose: Laparoscopic partial nephrectomy is an advanced surgical procedure requiring technical skill in minimally invasive techniques. Tumors located adjacent to the renal hilum pose an additional challenge. We report a multi-institutional study of robotic partial nephrectomy for renal hilar tumors and describe our results.
Materials and Methods: We evaluated patients from 2 institutions who underwent robotic partial nephrectomy for renal hilar tumors. Renal hilar tumors were defined as tumors abutting the renal artery and/or renal vein on preoperative imaging. After clamping the renal hilar vessels tumors were excised with fine dissection from the renal vessels followed by sutured renal reconstruction.
Results: Robotic partial nephrectomy was successfully performed on 11 patients (mean age 56.4 years, range 30 to 76). Mean tumor size was 3.8 cm (range 2.3 to 6.4). Mean warm ischemia time was 28.9 minutes (range 20 to 39) and mean operating time was 202 minutes (range 154 to 253). Mean blood loss was 220 ml (range 50 to 750). Mean hospital stay was 2.6 days (range 1 to 4). Histopathological evaluation confirmed 8 cases of clear cell renal cell carcinoma, 1 of papillary renal cell carcinoma and 2 of chromophobe renal cell carcinoma. Surgical margins were negative for malignancy in all cases.
Conclusions: Robotic partial nephrectomy is a safe and feasible approach for select patients with renal hilar tumors. Robotic assistance may facilitate tumor resection and renal reconstruction for challenging renal hilar tumors, offering a minimally invasive and nephron sparing surgical option for select patients who might otherwise require open surgery or total nephrectomy.
C1 [Rogers, Craig G.; Menon, Mani] Henry Ford Hosp, Vattikuti Urol Inst, Detroit, MI 48202 USA.
[Rogers, Craig G.; Metwalli, Adam; Blatt, Adam M.; Bratslavsky, Gennady; Linehan, W. Marston; Pinto, Peter A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Rogers, CG (reprint author), Henry Ford Hosp, Vattikuti Urol Inst, 2799 W Grand Blvd, Detroit, MI 48202 USA.
EM Crogers2@hfhs.org
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Center for Cancer Research.
NR 12
TC 84
Z9 88
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2008
VL 180
IS 6
BP 2353
EP 2356
DI 10.1016/j.juro.2008.08.022
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA 373OT
UT WOS:000260982200019
PM 18930263
ER
PT J
AU Simone, NL
Singh, AK
Cowan, JE
Soule, BP
Carroll, PR
Litwin, MS
AF Simone, Nicole L.
Singh, Anurag K.
Cowan, Janet E.
Soule, Benjamin P.
Carroll, Peter R.
Litwin, Mark S.
TI Pretreatment Predictors of Death From Other Causes in Men With Prostate
Cancer
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostatic neoplasms; mortality; therapeutics
ID BEAM RADIATION-THERAPY; RADICAL PROSTATECTOMY; SOCIOECONOMIC-STATUS;
CURATIVE INTENT; COMORBIDITY; SURVIVAL; NOMOGRAM; CARCINOMA
AB Purpose: Most men diagnosed with prostate cancer will die of other causes and pretreatment patient characteristics may identify those who are likely to die of other causes. Accurate stratification of patients by risk of other cause mortality may reduce needless treatment preventing morbidity and expense.
Materials and Methods: Using the CaPSURE(TM) database a cohort of men was identified with clinically localized prostate cancer who had definitive treatment with radical prostatectomy or radiation therapy between 1995 and 2004. Pretreatment patient characteristics were evaluated to determine if early other cause mortality could be predicted.
Results: Of 13,124 subjects enrolled in CaPSURE 5,070 had clinical T1c-T3a prostatic adenocarcinoma treated with radical prostatectomy (77%) or radiation therapy (23%) and posttreatment followup data. Median followup was 3.3 years. The cohort was divided into 3 groups. The prostate cancer specific mortality group included 55 men (1%) who died of prostate cancer. The 296 men (6%) who died of causes other than prostate cancer comprised the other cause mortality group. A third group contained the 4,719 (93%) men surviving at the end of the observation period. Factors that exclusively predicted death from nonprostate cancer causes included age at diagnosis, having a high school education or less, high clinical risk, smoking at time of diagnosis, concurrent nonprostate malignancy and worse scores on the Short Form-36 Health Survey physical function scale.
Conclusions: Several pretreatment patient characteristics may identify patients at high risk of nonprostate cancer mortality. Future studies should consider stratifying patients by or at least reporting these variables.
C1 [Simone, Nicole L.; Soule, Benjamin P.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Singh, Anurag K.] Roswell Pk Canc Inst, Dept Radiat Med, Buffalo, NY 14263 USA.
[Cowan, Janet E.; Carroll, Peter R.] Univ Calif San Francisco, Dept Urol, San Francisco, CA 94143 USA.
[Litwin, Mark S.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
RP Simone, NL (reprint author), NCI, Radiat Oncol Branch, NIH, Bldg 10-CRC,Rm B2-3500,10 Ctr Dr, Bethesda, MD 20892 USA.
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research; CaPSURE
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Center for Cancer Research and by
CaPSURE.
NR 20
TC 6
Z9 9
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2008
VL 180
IS 6
BP 2447
EP 2451
DI 10.1016/j.juro.2008.08.017
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 373OT
UT WOS:000260982200054
PM 18930498
ER
PT J
AU Grinev, A
Daniel, S
Laassri, M
Chumakov, K
Chizhikov, V
Rios, M
AF Grinev, Andriyan
Daniel, Sylvester
Laassri, Majid
Chumakov, Konstantin
Chizhikov, Vladimir
Rios, Maria
TI Microarray-based assay for the detection of genetic variations of
structural genes of West Nile virus
SO JOURNAL OF VIROLOGICAL METHODS
LA English
DT Article
DE Mosquito-borne virus; Flavivirus; Microarray technology; PCR; Mutations;
Genetic variability
ID OLIGONUCLEOTIDE MICROARRAY; UNITED-STATES; PHYLOGENETIC ANALYSIS; DNA
MICROARRAY; BLOOD-DONORS; NEW-YORK; HYBRIDIZATION; STRAINS;
DISCRIMINATION; IDENTIFICATION
AB Adaptation through fixation of spontaneous mutations in the viral genome is considered to be one of the important factors that enable recurrent West Nile virus (WNV) outbreaks in the U.S. Genetic variations can alter viral phenotype and virulence, and degrade the performance of diagnostic and screening assays, vaccines, and potential therapeutic agents. A microarray assay was developed and optimized for the simultaneous detection of any nucleotide mutations in the entire structural region of WNV in order to facilitate public health surveillance of genetic variation of WNV, The DNA microarray consists of 263 oligonucleotide probes overlapping at half of their lengths which have been immobilized on an amine-binding glass slide. The assay was validated using 23 WNV isolates from the 2002-2005 U.S. epidemics. Oligonucleotide-based WNV arrays detected unambiguously all mutations in the structural region of each one of the isolates identified previously by sequencing analysis, serving as a rapid and effective approach for the identification of mutations in the WNV genome. Published by Elsevier B.V.
C1 [Grinev, Andriyan; Daniel, Sylvester; Rios, Maria] Div Emerging & Transfus Transmitted Dis, Mol Virol Lab, Rockville, MD 20852 USA.
[Laassri, Majid; Chumakov, Konstantin; Chizhikov, Vladimir] US FDA, Lab Methods Dev, Div Viral Prod, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA.
RP Grinev, A (reprint author), 8800 Rockville Pike,NIH Bldg 29,Room B18, Bethesda, MD 20892 USA.
EM Andriyan.Grinev@fda.hhs.gov; Maria.Rios@fda.hhs.gov
FU National Institute of Allergy and Infectious Diseases Trans National
Institutes of Health/FDA Intramural Biodefense Program [FY06-08]
FX We thank Caren Chancey and Robert Duncan for helpful discussion and
review of the manuscript, and Dmitriy Volokhov for technical assistance.
The findings and conclusions in this article have not been formally
disseminated by the Food and Drug Administration and should not be
construed to represent any Agency determination or policy. This study
was supported by the FY06-08 National Institute of Allergy and
Infectious Diseases Trans National Institutes of Health/FDA Intramural
Biodefense Program.
NR 42
TC 7
Z9 8
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-0934
J9 J VIROL METHODS
JI J. Virol. Methods
PD DEC
PY 2008
VL 154
IS 1-2
BP 27
EP 40
DI 10.1016/j.jviromet.2008.09.015
PG 14
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Virology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Virology
GA 385UJ
UT WOS:000261838800005
PM 18930080
ER
PT J
AU Zahn, RC
Rett, MD
Korioth-Schmitz, B
Sun, Y
Buzby, AP
Goldstein, S
Brown, CR
Byrum, RA
Freeman, GJ
Letvin, NL
Hirsch, VM
Schmitz, JE
AF Zahn, Roland C.
Rett, Melisa D.
Korioth-Schmitz, Birgit
Sun, Yue
Buzby, Adam P.
Goldstein, Simoy
Brown, Charles R.
Byrum, Russell A.
Freeman, Gordon J.
Letvin, Norman L.
Hirsch, Vanessa M.
Schmitz, Joern E.
TI Simian Immunodeficiency Virus (SIV)-Specific CD8(+) T-Cell Responses in
Vervet African Green Monkeys Chronically Infected with SIVagm
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NEUTRALIZING ANTIBODY-RESPONSES; I-ASSOCIATED MYELOPATHY; HIV-1
INFECTION; NATURAL HOSTS; GRANZYME-B; VIRAL LOAD; PROLIFERATIVE
CAPACITY; PROGRAMMED DEATH-1; IMMUNE-RESPONSES; TYPE-1 INFECTION
AB African green monkeys (AGM) do not develop overt signs of disease following simian immunodeficiency virus (SIV) infection. While it is still unknown how natural hosts like AGM can cope with this lentivirus infection, a large number of investigations have shown that CD8(+) T-cell responses are critical for the containment of AIDS viruses in humans and Asian nonhuman primates. Here we have compared the phenotypes of T-cell subsets and magnitudes of SIV-specific CD8(+) T-cell responses in vervet AGM chronically infected with SIVagm and rhesus monkeys (RM) infected with SIVmac. In comparison to RM, vervet AGM exhibited weaker signs of immune activation and associated proliferation of CD8(+) T cells as detected by granzyme B, Ki-67, and programmed death 1 staining. By gamma interferon enzyme-linked immunospot assay and intracellular cytokine staining, SIV Gag- and Env-specific immune responses were detectable at variable but lower levels in vervet AGM than in RM. These observations demonstrate that natural hosts like SIV-infected vervet AGM develop SIV-specific T-cell responses, but the disease-free course of infection does not depend on the generation of robust CD8(+) T-cell responses.
C1 [Zahn, Roland C.; Rett, Melisa D.; Korioth-Schmitz, Birgit; Sun, Yue; Buzby, Adam P.; Letvin, Norman L.; Schmitz, Joern E.] Harvard Univ, Div Viral Pathogenesis, Beth Israel Deaconess Med Ctr, Sch Med,Ctr Life Sci, Boston, MA 02115 USA.
[Goldstein, Simoy; Brown, Charles R.; Hirsch, Vanessa M.] NIAID, Mol Microbiol Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Byrum, Russell A.] Bioqual Inc, Rockville, MD 20852 USA.
[Freeman, Gordon J.] Harvard Univ, Dept Med Oncol, Dana Farber Canc Inst, Dept Med,Sch Med, Boston, MA 02115 USA.
RP Schmitz, JE (reprint author), Harvard Univ, Div Viral Pathogenesis, Beth Israel Deaconess Med Ctr, Sch Med,Ctr Life Sci, ECLS 1037,3 Blackfan Circle, Boston, MA 02115 USA.
EM jschmitz@bidmc.harvard.edu
RI Korioth-Schmitz, Birgit/M-7816-2015
OI Korioth-Schmitz, Birgit/0000-0002-5271-9223
FU NIH [AI065335, AI56299]; NIAID Center for HIV/AIDS Vaccine Immunology
(CHAVI) [AI067854]; Harvard Medical School Center for AIDS Research
(CFAR) [AI060354]; Foundation for the NIH through the Grand Challenges
in Global Health initiative; Division of Intramural Research
FX This work was supported by the NIH grants AI065335 (to J.E.S.) and
AI56299 (to G.J.F.), NIAID Center for HIV/AIDS Vaccine Immunology
(CHAVI) grant AI067854 (to N.L.L.), Harvard Medical School Center for
AIDS Research (CFAR) grant AI060354, the Foundation for the NIH through
the Grand Challenges in Global Health initiative (G.J.F.), and the
Division of Intramural Research, NIAID, NIH (V. M. H., S. G., and C. R.
B.).
NR 76
TC 28
Z9 28
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2008
VL 82
IS 23
BP 11577
EP 11588
DI 10.1128/JVI.01779-08
PG 12
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700010
PM 18829748
ER
PT J
AU Petravic, J
Ribeiro, RM
Casimiro, DR
Mattapallil, JJ
Roederer, M
Shiver, JW
Davenport, MP
AF Petravic, Janka
Ribeiro, Ruy M.
Casimiro, Danilo R.
Mattapallil, Joseph J.
Roederer, Mario
Shiver, John W.
Davenport, Miles P.
TI Estimating the Impact of Vaccination on Acute Simian-Human
Immunodeficiency Virus/Simian Immunodeficiency Virus Infections
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-CELL DEPLETION; VIRAL DYNAMICS; IN-VIVO; ANTIRETROVIRAL THERAPY; HIV-1
INFECTION; TYPE-1 INFECTION; REPLICATION; LIMITATIONS; TISSUES; DECAY
AB The dynamics of HIV infection have been studied in humans and in a variety of animal models. The standard model of infection has been used to estimate the basic reproductive ratio of the virus, calculated from the growth rate of virus in acute infection. This method has not been useful in studying the effects of vaccination, since, for the vaccines developed so far, early growth rates of virus do not differ between control and vaccinated animals. Here, we use the standard model of viral dynamics to derive the reproductive ratio from the peak viral load and nadir of target cell numbers in acute infection. We apply this method to data from studies of vaccination in SHIV and SIV infection and demonstrate that vaccination can reduce the reproductive ratio by 2.3- and 2-fold, respectively. This method allows the comparison of vaccination efficacies among different viral strains and animal models in vivo.
C1 [Petravic, Janka; Davenport, Miles P.] Univ New S Wales, Complex Syst Biol Grp, Ctr Vasc Res, Sydney, NSW 2052, Australia.
[Ribeiro, Ruy M.] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
[Casimiro, Danilo R.; Shiver, John W.] Merck Res Labs, West Point, PA USA.
[Mattapallil, Joseph J.] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20824 USA.
[Roederer, Mario] NIAID, ImmunoTechnol Sect, NIH, Bethesda, MD 20892 USA.
RP Davenport, MP (reprint author), Univ New S Wales, Complex Syst Biol Grp, Ctr Vasc Res, Sydney, NSW 2052, Australia.
EM m.davenport@unsw.edu.au
OI Ribeiro, Ruy/0000-0002-3988-8241
FU James S. McDonnell Foundation; Australian National Health and Medical
Research Council; Charles Viertel Senior Medical Research; National
Institutes of Health [P20-RR18754]
FX This work was supported by the James S. McDonnell Foundation 21st
Century Research Award/Studying Complex Systems and the Australian
National Health and Medical Research Council. M. P. D. is a Sylvia and
Charles Viertel Senior Medical Research Fellow. R. M. R. was supported
by grant P20-RR18754 from the National Institutes of Health.
NR 32
TC 8
Z9 8
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2008
VL 82
IS 23
BP 11589
EP 11598
DI 10.1128/JVI.01596-08
PG 10
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700011
PM 18799584
ER
PT J
AU Binley, JM
Lybarger, EA
Crooks, ET
Seaman, MS
Gray, E
Davis, KL
Decker, JM
Wycuff, D
Harris, L
Hawkins, N
Wood, B
Nathe, C
Richman, D
Tomaras, GD
Bibollet-Ruche, F
Robinson, JE
Morris, L
Shaw, GM
Montefiori, DC
Mascola, JR
AF Binley, James M.
Lybarger, Elizabeth A.
Crooks, Emma T.
Seaman, Michael S.
Gray, Elin
Davis, Katie L.
Decker, Julie M.
Wycuff, Diane
Harris, Linda
Hawkins, Natalie
Wood, Blake
Nathe, Cory
Richman, Douglas
Tomaras, Georgia D.
Bibollet-Ruche, Frederic
Robinson, James E.
Morris, Lynn
Shaw, George M.
Montefiori, David C.
Mascola, John R.
TI Profiling the Specificity of Neutralizing Antibodies in a Large Panel of
Plasmas from Patients Chronically Infected with Human Immunodeficiency
Virus Type 1 Subtypes B and C
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN MONOCLONAL-ANTIBODIES; PROXIMAL EXTERNAL REGION; CONSENSUS
ENVELOPE GLYCOPROTEIN; HIV-1 ANTIBODIES; GP120 ENVELOPE; VIRAL ENVELOPE;
BINDING-SITE; ENV CLONES; CLADE-A; EPITOPE
AB Identifying the viral epitopes targeted by broad neutralizing antibodies (NAbs) that sometimes develop in human immunodeficiency virus type 1 (HIV-1)-infected subjects should assist in the design of vaccines to elicit similar responses. Here, we investigated the activities of a panel of 24 broadly neutralizing plasmas from subtype B- and C-infected donors using a series of complementary mapping methods, focusing mostly on JR-FL as a prototype subtype B primary isolate. Adsorption with gp120 immobilized on beads revealed that an often large but variable fraction of plasma neutralization was directed to gp120 and that in some cases, neutralization was largely mediated by CD4 binding site (CD4bs) Abs. The results of a native polyacrylamide gel electrophoresis assay using JR-FL trimers further suggested that half of the subtype B and a smaller fraction of subtype C plasmas contained a significant proportion of NAbs directed to the CD4bs. Anti-gp41 neutralizing activity was detected in several plasmas of both subtypes, but in all but one case, constituted only a minor fraction of the overall neutralization activity. Assessment of the activities of the subtype B plasmas against chimeric HIV-2 viruses bearing various fragments of the membrane proximal external region (MPER) of HIV-1 gp41 revealed mixed patterns, implying that MPER neutralization was not dominated by any single specificity akin to known MPER-specific monoclonal Abs. V3 and 2G12-like NAbs appeared to make little or no contribution to JR-FL neutralization titers. Overall, we observed significant titers of anti-CD4bs NAbs in several plasmas, but approximately two-thirds of the neutralizing activity remained undefined, suggesting the existence of NAbs with specificities unlike any characterized to date.
C1 [Lybarger, Elizabeth A.; Wycuff, Diane; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Binley, James M.; Crooks, Emma T.] Torrey Pines Inst Mol Studies, San Diego, CA 92121 USA.
[Seaman, Michael S.] Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02215 USA.
[Gray, Elin; Morris, Lynn] Natl Inst Communicable Dis, ZA-2131 Johannesburg, South Africa.
[Davis, Katie L.; Decker, Julie M.; Bibollet-Ruche, Frederic; Shaw, George M.] Univ Alabama, Div Hematol & Oncol, Birmingham, AL 35294 USA.
[Harris, Linda; Hawkins, Natalie; Wood, Blake; Nathe, Cory] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98109 USA.
[Richman, Douglas] Univ Calif San Diego, Dept Pathol, San Diego, CA 92093 USA.
[Tomaras, Georgia D.; Montefiori, David C.] Duke Univ, Med Ctr, Dept Surg, Dept Mol Genet & Microbiol, Durham, NC 27710 USA.
[Tomaras, Georgia D.; Montefiori, David C.] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC 27710 USA.
[Robinson, James E.] Tulane Univ, Med Ctr, Dept Pediat, New Orleans, LA 70112 USA.
RP Mascola, JR (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr, Bethesda, MD 20892 USA.
EM jmascola@mail.nih.gov
RI Tomaras, Georgia/J-5041-2016;
OI , Lynn/0000-0003-3961-7828; Gray, Elin/0000-0002-8613-3570
FU Bill and Melinda Gates Collaboration for AIDS Vaccine Discovery Vaccine
Immune Monitoring Consortium [38619]; NIH [RO1 AI58763]; California
HIV/AIDS Research Program [ID06-TPI-211]; AIDS and Infectious Disease
Science Center at the Torrey Pines Institute for Molecular Studies;
Grand Challenges [37874]; South African AIDS Vaccine Initiative (SAAVI);
intramural research program of the Vaccine Research Center, NIAID
FX This study was supported by Bill and Melinda Gates Collaboration for
AIDS Vaccine Discovery Vaccine Immune Monitoring Consortium grant number
38619. Additional support was provided by NIH RO1 AI58763 (J.M.B.),
California HIV/AIDS Research Program grant ID06-TPI-211 at the
University of California(J.M.B.), the AIDS and Infectious Disease
Science Center at the Torrey Pines Institute for Molecular Studies
(J.M.B.), Grand Challenges Grant number 37874 (G. M. S.), the South
African AIDS Vaccine Initiative (SAAVI), and the intramural research
program of the Vaccine Research Center, NIAID (E. A. L., D. W. and
J.R.M.).; We thank T. Wrin for providing assistance in selecting subtype
B plasmas; D. Burton for providing MAbs b12 and X5; H. Katinger for
providing MAbs 2G12, 2F5, and 4E10; Susan Zolla-Pazner for providing MAb
447-52D; B. F. Haynes and H. X. Liao for providing consensus gp140
proteins; M. Zwick for providing MAb Z13e1; L. Stamatatos, B. Hahn, R.
Desrosiers, and the NIH AIDS Repository for providing virus stocks and
Env plasmids; and G. Nabel for the guinea pig serum. We thank Judy T.
Lucas and Vicki C. Ashley for expert technical assistance and Brenda
Hartman for assistance with graphics.
NR 71
TC 245
Z9 247
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2008
VL 82
IS 23
BP 11651
EP 11668
DI 10.1128/JVI.01762-08
PG 18
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700017
PM 18815292
ER
PT J
AU Ostbye, T
Krause, KM
Brouwer, RJN
Lovelady, CA
Morey, MC
Bastian, LA
Peterson, BL
Swamy, GK
Chowdhary, J
McBride, CM
AF Ostbye, Truls
Krause, Katrina M.
Brouwer, Rebecca J. N.
Lovelady, Cheryl A.
Morey, Miriam C.
Bastian, Lori A.
Peterson, Bercedis L.
Swamy, Geeta K.
Chowdhary, Jaspreet
McBride, Colleen M.
TI Active Mothers Postpartum (AMP): Rationale, Design, and Baseline
Characteristics
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID GESTATIONAL WEIGHT-GAIN; PHYSICAL-ACTIVITY; LACTATING WOMEN; PREGNANCY;
RETENTION; PATTERNS; SMOKING; OBESITY; DIET; FOOD
AB Background: Pregnancy and the postpartum period have been suggested as important contributors to overweight and obesity among women. This paper presents the design, rationale, and baseline participant characteristics of a randomized controlled intervention trial to enhance weight loss in postpartum women who entered pregnancy overweight or obese.
Methods: Active Mothers Postpartum ( AMP) is based on the rationale that the birth of a child can be a teachable moment. AMP's primary objectives are to promote and sustain a reduction in body mass index (BMI) up to 2 years postpartum via changes in diet and exercise behavior, with a secondary aim to assess racial differences in these outcomes. Women in the intervention arm participate in ten physical activity group sessions, eight healthy eating classes, and six telephone counseling sessions over a 9-month period. They also receive motivational tools, including a workbook with recipes and exercises, a pedometer, and a sport stroller.
Results: Four hundred fifty women aged >= 18 ( mean 30.9), with a BMI >= 25 kg/m(2) ( mean 33.0) at baseline ( 6 weeks postpartum) were enrolled; 45% of the final sample are black and 53% are white. Baseline characteristics by study arm and by race are presented.
Conclusions: Our intervention is designed to be disseminated broadly to benefit the public health. Behavior change interventions based on principles of social cognitive theory, stage of readiness, and other models that coincide with a teachable moment, such as the birth of a child, could be important motivators for postpartum weight loss.
C1 [Ostbye, Truls; Krause, Katrina M.; Brouwer, Rebecca J. N.; Chowdhary, Jaspreet] Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA.
[Ostbye, Truls; Lovelady, Cheryl A.] Univ N Carolina, Dept Nutr, Greensboro, NC 27412 USA.
[Ostbye, Truls] Duke NUS Grad Med Sch, Singapore, Singapore.
[Morey, Miriam C.; Bastian, Lori A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Morey, Miriam C.; Bastian, Lori A.] Durham Vet Affairs Med Ctr, Durham, NC 27710 USA.
[Peterson, Bercedis L.] Duke Univ, Med Ctr, Dept Biostat & Bioinformat, Durham, NC 27710 USA.
[Swamy, Geeta K.] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
[McBride, Colleen M.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Ostbye, T (reprint author), Duke Univ, Med Ctr, Dept Community & Family Med, Box 104006, Durham, NC 27710 USA.
EM truls.ostbye@duke.edu
FU NIDDK NIH HHS [R01 DK064986]
NR 44
TC 29
Z9 29
U1 2
U2 10
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD DEC
PY 2008
VL 17
IS 10
BP 1567
EP 1575
DI 10.1089/jwh.2007.0674
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 378OG
UT WOS:000261331500006
PM 19049350
ER
PT J
AU Gomez, CR
Acuna-Castillo, C
Perez, C
Leiva-Salcedo, E
Riquelme, DM
Ordenes, G
Oshima, K
Aravena, M
Perez, VI
Nishimura, S
Sabaj, V
Walter, R
Sierra, F
AF Gomez, Christian R.
Acuna-Castillo, Claudio
Perez, Claudio
Leiva-Salcedo, Elias
Riquelme, Denise M.
Ordenes, Gamaliel
Oshima, Kiyoko
Aravena, Mauricio
Perez, Viviana I.
Nishimura, Sumiyo
Sabaj, Valeria
Walter, Robin
Sierra, Felipe
TI Diminished Acute Phase Response and Increased Hepatic Inflammation of
Aged Rats in Response to Intraperitoneal Injection of Lipopolysaccharide
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Liver; Inflammation; Injury; Acute phase response; Aging
ID GENE-EXPRESSION; IMMUNE-SYSTEM; MICE; INTERLEUKIN-6; PATHWAYS; INJURY;
LIVER; ENDOTOXEMIA; MODULATION; MECHANISMS
AB Aging is associated with a deterioration of the acute phase response to inflammatory challenges. However, the nature of these defects remains poorly defined. We analyzed the hepatic inflammatory response after intraperitoneal administration of lipopolysaccharide (LPS) given to Fisher 344 rats aged 6, 15, and 22-23 months. Induction of the acute phase proteins (APPs), haptoglobin, a-I-acid glycoprotein, and T-kininogen was reduced and/or retarded with aging. Initial induction of interleukin-6 in aged rats was normal, but the later response was increased relative to younger counterparts. An exacerbated hepatic injury was observed in aged rats receiving LPS, as evidenced by the presence of multiple microabscesses in portal tracts, confluent necrosis, higher nentrophil accumulation, and elevated serum levels of alanine aminotransferase, relative to younger animals. Our results suggest that aged rats displayed a reduced expression of APPS and increased hepatic injury in response to the inflammatory insult.
C1 [Gomez, Christian R.; Acuna-Castillo, Claudio; Perez, Claudio; Leiva-Salcedo, Elias; Riquelme, Denise M.; Aravena, Mauricio; Perez, Viviana I.; Nishimura, Sumiyo; Sabaj, Valeria; Walter, Robin; Sierra, Felipe] Univ Chile, Fac Med, Ctr FONDAP Estudios Mol Celula, Inst Ciencias Biomed, Santiago 7, Chile.
[Acuna-Castillo, Claudio] Univ Santiago Chile, Fac Quim & Biol, Dept Biol, USACH, Santiago, Chile.
[Gomez, Christian R.] Univ Diego Portales, Fac Ciencies Salud, Santiago, Chile.
[Ordenes, Gamaliel] Univ Chile, Fac Med, Escuela Tecnol Med, Santiago, Chile.
[Oshima, Kiyoko] Loyola Univ, Med Ctr, Dept Pathol, Maywood, IL 60153 USA.
[Walter, Robin; Sierra, Felipe] Lankenau Inst Med Res, Philadelphia, PA USA.
RP Sierra, F (reprint author), NIA, NIH, 7201 Wisconsin Ave,Suite 2C231, Bethesda, MD 20892 USA.
EM sierraf@nia.nih.gov
FU Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT)
[101061, 2000038, 2010071]; Fondo de Financiamiento de Centros de
Excelencia en Investigacion (FONDAP) [15010006]; National Institutes of
Health/National Institute on Aging [AG13902]
FX We thank Drs. Elizabeth J. Kovacs, Pamela Witte, and Patrick
Greiffenstein for thoughtful discussions and critical review of this
manuscript.
NR 41
TC 7
Z9 7
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2008
VL 63
IS 12
BP 1299
EP 1306
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 395PG
UT WOS:000262535400004
PM 19126842
ER
PT J
AU Kelly, VE
Schrager, MA
Price, R
Ferrucci, L
Shumway-Cook, A
AF Kelly, Valerie E.
Schrager, Matthew A.
Price, Robert
Ferrucci, Luigi
Shumway-Cook, Anne
TI Age-Associated Effects of a Concurrent Cognitive Task on Gait Speed and
Stability During Narrow-Base Walking
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Dual task; Gait; Frontal plane stability; Falls; Aging
ID DWELLING OLDER-ADULTS; CENTER-OF-MASS; POSTURAL STABILITY; FALL RISK;
BALANCE; TESTS; INDICATORS; MOBILITY; MOTION
AB Background. In older adults, changes in speed and stability during walking are associated with impaired balance and increased fall risk. Narrow-base walking requires increased frontal plane stability and can be used to assess postural control while walking. Performance of a concurrent cognitive task (dual task) may further increase the complexity of walking, potentially allowing identification of individuals with instability that is not detected under single-task conditions. The purpose of this study was to examine age-associated effects of a cognitive task on speed and frontal plane stability during narrow-base walking.
Methods. Thirty-four healthy adults participated, categorized by age: <65, 65-74, and >= 75 years. Participants walked at a comfortable pace within a narrow path tinder both single- and dual-task conditions. We examined spatiotemporal variables and frontal plane center of mass (CoM) parameters using a 13-segment biomechanical model.
Results. Increasing age (p < .001) and the performance of a concurrent cognitive task (p < .001) were both associated with decreased speed, with no interaction between these factors. Frontal plane CoM displacement and velocity increased with increasing age (both p < .001), but dual-task performance had no effect on these variables (both h > .450).
Conclusions. Age-associated changes in both speed and stability are observed during narrow-base walking. Among this sample of healthy older adults, the addition of a concurrent cognitive task resulted in reduced speed, with no effect on frontal plane stability. Further research is needed to determine if dual-task, narrow-base walking is a sensitive and specific approach to identifying older adults at risk for falls.
C1 [Kelly, Valerie E.; Price, Robert; Shumway-Cook, Anne] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
[Schrager, Matthew A.] Univ Kansas, Dept Hlth Sport & Exercise Sci, Lawrence, KS 66045 USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
RP Kelly, VE (reprint author), Univ Washington, Dept Rehabil Med, 1959 NE Pacific St,Box 356490, Seattle, WA 98195 USA.
EM vekelly@u.washington.edu
OI Kelly, Valerie E./0000-0002-0099-9219
FU National Institutes of Health; National Institute on Aging [Z01
AG000015]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging
contract number Z01 AG000015.
NR 22
TC 31
Z9 31
U1 3
U2 6
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2008
VL 63
IS 12
BP 1329
EP 1334
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 395PG
UT WOS:000262535400007
PM 19126845
ER
PT J
AU Volpato, S
Cavalieri, M
Guerra, G
Sioulis, F
Ranzini, M
Maraldi, C
Fellin, R
Guralnik, JM
AF Volpato, Stefano
Cavalieri, Margherita
Guerra, Gianklca
Sioulis, Fotini
Ranzini, Monica
Maraldi, Cinzia
Fellin, Renato
Guralnik, Jack M.
TI Performance-Based Functional Assessment in Older Hospitalized Patients:
Feasibility and Clinical Correlates
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Short Physical Performance Battery; Functional assessment; Hospital;
Feasibility; Prognosis; Aging
ID LOWER-EXTREMITY FUNCTION; ILLNESS RATING-SCALE; PHYSICAL PERFORMANCE;
SUBSEQUENT DISABILITY; MEDICAL ILLNESSES; BODY-COMPOSITION; WOMENS
HEALTH; GAIT SPEED; RELIABILITY; VALIDATION
AB Background. Functional evaluation is a cornerstone of multidimensional geriatric assessment; however, little is known of the clinical value of standardized performance-based assessment in the acute care setting. The aim of this study wits to evaluate the clinical correlates and short-teen predictive value of the Short Physical Performance Battery (SPPB) in older patients admitted to the hospital for an acute medical event.
Methods. We enrolled 92 women and men 65 years old or older who were able to walk, who had a Mini-Mental State Examination (MMSE) score >= 18, and who were admitted to the hospital with a clinical diagnosis of congestive heart failure, pneumonia, chronic obstructive pulmonary disease (COPD), or minor stroke. The SPPB was assessed at hospital admission and discharge. Self-report functional assessment included basic activities of daily living (ADL) and instrumental activities of daily living (IADL). Spearman's rank correlation coefficients and multivariable linear regression analyses were used to study the association of SPPB score and functional and clinical characteristics, including length of hospital stay.
Results. The mean age was 77.7 years (range 65-94 years), 49% were female, 64.1% had congestive heart failure, 16% COPD, 13.1% pneumonia, and 6.5% minor stroke. At hospital admission the mean SPPB score was 6.0 +/- 2.7. SPPB scores were inversely correlated with age, the severity of the index disease, and IADL and ADL difficulty 2 weeks before hospital admission (p < .01), and were directly correlated with MMSE score (p = .002). On average, SPPB score increased I point ((+0.97, standard error of the mean = 0.2; p for paired t test < .001) from baseline to hospital discharge assessment. After adjustment for potential confounders, baseline SPPB score wits significantly associated with the length of hospital stay) < .007).
Conclusion. In older acute care inpatients, SPPB is a valid indicator of functional and clinical status. SPPB score at hospital admission is an independent predictor of the length of hospital stay.
C1 [Volpato, Stefano; Cavalieri, Margherita; Guerra, Gianklca; Sioulis, Fotini; Ranzini, Monica; Maraldi, Cinzia; Fellin, Renato] Univ Ferrara, Dept Clin & Expt Med, Sect Internal Med Gerontol & Geriatr, I-44100 Ferrara, Italy.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
RP Volpato, S (reprint author), Univ Ferrara, Dept Clin & Expt Med, Sect Internal Med Gerontol & Geriatr, Via Savonarola 9, I-44100 Ferrara, Italy.
EM vlt@unife.it
RI Cavalieri, Margherita/G-8053-2012; VOLPATO, STEFANO/H-2977-2014
OI VOLPATO, STEFANO/0000-0003-4335-6034
FU National Institute on Aging; Intramural Research Program; National
Institutes of Health
FX This research was supported in pant by contracts from the National
Institute on Aging, Intramural Research Program, National Institutes of
Health.
NR 34
TC 47
Z9 47
U1 5
U2 15
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2008
VL 63
IS 12
BP 1393
EP 1398
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 395PG
UT WOS:000262535400016
PM 19126854
ER
PT J
AU Ferrucci, L
AF Ferrucci, Luigi
TI The Baltimore Longitudinal Study of Aging (BLSA): A 50-Year-Long Journey
and Plans for the Future
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Editorial Material
ID SUBCLINICAL CARDIOVASCULAR-DISEASE; BODY-MASS INDEX; OLDER-ADULTS; WAIST
CIRCUMFERENCE; FRAILTY; FAT; AGE; MORTALITY; WEIGHT; RISK
C1 NIA, Longitudinal Studies Sect, ASTRA Unit, Harbor Hosp,Clin Res Branch, Baltimore, MD 21225 USA.
RP Ferrucci, L (reprint author), NIA, Longitudinal Studies Sect, ASTRA Unit, Harbor Hosp,Clin Res Branch, 5th Floor,3001 S Hanover St, Baltimore, MD 21225 USA.
EM ferruccilu@grc.nia.nih.gov
FU Intramural NIH HHS [Z01 AG000015-49]
NR 25
TC 38
Z9 39
U1 0
U2 6
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2008
VL 63
IS 12
BP 1416
EP 1419
PG 4
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 395PG
UT WOS:000262535400020
PM 19126858
ER
PT J
AU Nash, TE
Pretell, EJ
Lescano, AG
Bustos, JA
Gilman, RH
Gonzalez, AE
Garcia, HH
AF Nash, Theodore E.
Pretell, E. Javier
Lescano, Andres G.
Bustos, Javier A.
Gilman, Robert H.
Gonzalez, Armando E.
Garcia, Hector H.
CA The Cysticerosis Working Grp Peru
TI Perilesional brain oedema and seizure activity in patients with
calcified neurocysticercosis: a prospective cohort and nested
case-control study
SO LANCET NEUROLOGY
LA English
DT Article
ID CEREBRAL CYSTICERCOSIS; EPILEPSY; LESIONS; CLASSIFICATION; PREVALENCE;
ETIOLOGY; PROPOSAL; GLIOSIS; DISEASE; CT
AB Background Cysticercosis due to Taenia solium is a cause of adult-acquired seizures and epilepsy even in patients with only calcified larval cysts. Transient perilesional brain oedema is seen around the calcified foci but its importance, association with seizures, incidence, and pathophysiology are unknown.
Methods 110 patients with only calcified lesions and a history of seizures or severe headaches were followed prospectively in a cohort design to assess the incidence of seizure relapse. In a nested case-control substudy, perilesional oedema was assessed by MRI at the time of seizure in symptomatic patients and in matched asymptomatic controls taken from the study population.
Findings Between November, 1999, and December, 2006, 29 patients had an incident seizure during a median follow up of 32.33 (SD 19.99) months, with an estimated 5-year seizure incidence of 36% (95% CI 25% to 49%). 24 of 29 (83%) patients with seizure relapse had an MRI evaluation within 5 days of the event; perilesional oedema was seen in 12 patients (50%) compared with two (9%) of 23 asymptomatic matched controls.
Interpretation Perilesional oedema is common and associated with episodic seizure activity in patients with calcified neurocysticercosis. Our findings are probably representative of symptomatic patients in regions where T solium neurocysticercosis is endemic and suggest a unique and possibly preventable cause of seizures in this population.
Funding US National Institute of Allergy and infectious Diseases; US National institutes of Health; Fogarty International Center.
C1 [Nash, Theodore E.] NIAID, NIH, Gastrointestinal Parasites Sect, Parasit Dis Lab, Bethesda, MD 20892 USA.
[Pretell, E. Javier] Inst Nacl Ciencias Neurol, Dept Transmissible Dis, Lima, Peru.
[Pretell, E. Javier] Hosp Alberto Sabogal, Dept Neurol, Callao, Peru.
[Lescano, Andres G.] Univ Peruana Cayetano Heredia, Fac Salud Publ & Adm, Lima, Peru.
[Bustos, Javier A.; Gilman, Robert H.; Garcia, Hector H.] Univ Peruana Cayetano Heredia, Dept Microbiol, Lima, Peru.
[Gilman, Robert H.; Gonzalez, Armando E.; Garcia, Hector H.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA.
[Gilman, Robert H.; Gonzalez, Armando E.] Inst Peruano Parasitol Clin & Expt INPPACE, Lima, Peru.
[Gonzalez, Armando E.] Univ Nacl Mayor San Marcos, Sch Vet Med, Dept Publ Hlth, Lima 14, Peru.
RP Nash, TE (reprint author), NIAID, NIH, Gastrointestinal Parasites Sect, Parasit Dis Lab, 9000 Rockville Pike,Bldg 4,Room 126, Bethesda, MD 20892 USA.
EM tnash@niaid.nih.gov
RI Lescano, Andres/B-8479-2008
OI Lescano, Andres/0000-0001-9779-633X
FU US National Institute of Allergy and infectious Diseases (NIAID); US
National institutes of Health (NIH); Fogarty International Center [R03
TW05562]
FX Funding for this study was provided by the US National Institute of
Allergy and infectious Diseases (NIAID), US National institutes of
Health (NIH), and Fogarty International Center (FIRCA grant R03
TW05562). We wish to thank the neurologists of the San Vicente
Infectious Disease Service who helped with patient care and management,
and the neurologists of other services at the Instituto de Ciencias
Neurologicas in Lima, Peru, for referral of patients.
NR 34
TC 64
Z9 65
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
J9 LANCET NEUROL
JI Lancet Neurol.
PD DEC
PY 2008
VL 7
IS 12
BP 1099
EP 1105
DI 10.1016/S1474-4422(08)70243-6
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 379KV
UT WOS:000261396000015
PM 18986841
ER
PT J
AU Al-Rahawan, MM
Alter, BP
Bryant, BJ
Elghetany, AT
AF Al-Rahawan, Mohamad M.
Alter, Blanche P.
Bryant, Barbara J.
Elghetany, A. Tarek
TI Bone marrow cell cycle markers in inherited bone marrow failure
syndromes
SO LEUKEMIA RESEARCH
LA English
DT Article
DE Inherited bone marrow failure syndromes; Myelodysplastic syndrome; Acute
myeloid leukemia; p53; Ki-67; Survivin
ID SHWACHMAN-DIAMOND-SYNDROME; MYELODYSPLASTIC SYNDROMES;
REFRACTORY-ANEMIA; EXPRESSION; P53; BIOPSIES; PROTEIN; OVEREXPRESSION;
SURVIVIN; LEUKEMIA
AB Patients with inherited bone marrow failure syndromes (IBMFS) are at increased risk of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), possibly related to cell cycle dysregulation. In a cross-sectional analysis of bone marrow from 77 IBMFS, 71 sporadic conditions (AML, MDS, acquired aplastic anemia) and 22 normal controls we found overexpression of p53 in IBMFS, AML, and MDS; of Ki-67 in IBMFS and AML; and of survivin in IBMFS compared with all other groups. The patterns of expression of cell cycle markers in IBMFS are thus distinct. Longitudinal studies will determine the diagnostic and prognostic significance of these findings. Published by Elsevier Ltd.
C1 [Al-Rahawan, Mohamad M.; Alter, Blanche P.] Natl Canc Inst, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Al-Rahawan, Mohamad M.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Bryant, Barbara J.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Elghetany, A. Tarek] Univ Texas Galveston, Med Branch, Dept Pathol, Galveston, TX 77550 USA.
RP Alter, BP (reprint author), 6120 Execut Blvd,Execut Plaza S,Room 7020, Rockville, MD 20852 USA.
EM alterb@mail.nih.gov
FU NIH; Shwachman-Diamond Syndrome Foundation
FX We thank Mark H. Greene, MD for a critical review of the manuscript and
Philip S. Rosenberg for providing statistical advice. We are grateful to
the many patients and physicians who submitted bone marrow samples. This
research was supported in part by the Intramural Research Program of the
NIH and the National Cancer Institute and by the Center for Cancer and
Blood Disorders at Children's National Medical Center, and by a grant
from the Shwachman-Diamond Syndrome Foundation.
NR 20
TC 8
Z9 8
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD DEC
PY 2008
VL 32
IS 12
BP 1793
EP 1799
DI 10.1016/j.leukres.2008.05.020
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 369UX
UT WOS:000260720500001
PM 18606449
ER
PT J
AU Ibrahim, JG
Chen, MH
Kim, S
AF Ibrahim, Joseph G.
Chen, Ming-Hui
Kim, Sungduk
TI Bayesian variable selection for the Cox regression model with missing
covariates
SO LIFETIME DATA ANALYSIS
LA English
DT Article
DE Conjugate prior; Deviance information criterion; Missing at random;
Proportional hazards models
ID GENERALIZED LINEAR-MODELS; PREDICTIVE APPROACH; PRIOR ELICITATION;
UNCERTAINTY; INFERENCE; CHOICE
AB In this paper, we develop Bayesian methodology and computational algorithms for variable subset selection in Cox proportional hazards models with missing covariate data. A new joint semi-conjugate prior for the piecewise exponential model is proposed in the presence of missing covariates and its properties are examined. The covariates are assumed to be missing at random (MAR). Under this new prior, a version of the Deviance Information Criterion (DIC) is proposed for Bayesian variable subset selection in the presence of missing covariates. Monte Carlo methods are developed for computing the DICs for all possible subset models in the model space. A Bone Marrow Transplant (BMT) dataset is used to illustrate the proposed methodology.
C1 [Ibrahim, Joseph G.] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
[Chen, Ming-Hui] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
[Kim, Sungduk] NICHHD, Div Epidemiol Stat & Prevent Res, NIH, Rockville, MD 20852 USA.
RP Ibrahim, JG (reprint author), Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
EM ibrahim@bios.unc.edu
FU NCI NIH HHS [CA 74015, R01 CA074015]; NIGMS NIH HHS [R01 GM070335-12,
GM70335, R01 GM070335]
NR 49
TC 7
Z9 7
U1 3
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1380-7870
EI 1572-9249
J9 LIFETIME DATA ANAL
JI Lifetime Data Anal.
PD DEC
PY 2008
VL 14
IS 4
BP 496
EP 520
DI 10.1007/s10985-008-9101-5
PG 25
WC Mathematics, Interdisciplinary Applications; Statistics & Probability
SC Mathematics
GA 367HB
UT WOS:000260542000009
PM 18836829
ER
PT J
AU Deoni, SCL
Rutt, BK
Arun, T
Pierpaoli, C
Jones, DK
AF Deoni, Sean C. L.
Rutt, Brian K.
Arun, Tarunya
Pierpaoli, Carlo
Jones, Derek K.
TI Gleaning Multicomponent T(1) and T(2) Information From Steady-State
Imaging Data
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE multicomponent relaxation; T(1); T(2); quantitative magnetic resonance
imaging; human brain imaging; steady-state imaging
ID LATTICE-RELAXATION-TIMES; NUCLEAR-MAGNETIC-RESONANCE; IN-VIVO;
WHITE-MATTER; MULTIPLE-SCLEROSIS; CHEMICAL-EXCHANGE; MYELIN WATER; HUMAN
BRAIN; CORRELATION RELAXOMETRY; PERIPHERAL-NERVE
AB The driven-equilibrium single-pulse observation of T(1) (DESPOT1) and T(2) (DESPOT2) are rapid, accurate, and precise methods for voxelwise determination of the longitudinal and transverse relaxation times. A limitation of the methods, however, is the inherent assumption of single-component relaxation. In a variety of biological tissues, in particular human white matter (WM) and gray matter (GM), the relaxation has been shown to be more completely characterized by a summation of two or more relaxation components, or species, each believed to be associated with unique microanatomical domains or water pools. Unfortunately, characterization of these components on a voxelwise, whole-brain basis has traditionally been hindered by impractical acquisition times. In this work we extend the conventional DESPOT(1) and DESPOT(2) approaches to include multicomponent relaxation analysis. Following numerical analysis of the new technique, renamed multicomponent driven equilibrium single pulse observation of T(1)/T(2) (mcDESPOT), wholebrain multicomponent T(1) and T(2) quantification is demonstrated in vivo with clinically realistic times of between 16 and 30 min. Results obtained from four healthy individuals and two primary progressive multiple sclerosis (MS) patients demonstrate the future potential of the approach for identifying and assessing tissue changes associated with several neurodegenerative conditions, in particular those associated with WM. Magn Reson Med 60:1372-1387, 2008. (C) 2008 Wiley-Liss, Inc.
C1 [Deoni, Sean C. L.] John Radcliffe Hosp, Oxford Ctr FMRIB, Oxford OX3 9DU, England.
[Deoni, Sean C. L.] Kings Coll London, Inst Psychiat, Ctr Neuroimaging Res, London WC2R 2LS, England.
[Rutt, Brian K.] Robarts Res Inst, Imaging Res Labs, London, ON N6A 5C1, Canada.
[Pierpaoli, Carlo] NICHHD, Sect Tissue Biophys & Biometr, LIMB, NIH, Bethesda, MD 20892 USA.
[Jones, Derek K.] Cardiff Univ, Sch Psychol, CUBRIC, Cardiff, S Glam, Wales.
RP Deoni, SCL (reprint author), John Radcliffe Hosp, Oxford Ctr FMRIB, Oxford OX3 9DU, England.
EM sdeoni@mac.com
RI Jones, Derek/D-1460-2009; Pierpaoli, Carlo/E-1672-2011;
OI Jones, Derek/0000-0003-4409-8049
FU Canadian Institutes of Health Research
FX Grant sponsor: Canadian Institutes of Health Research.
NR 56
TC 138
Z9 138
U1 3
U2 10
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD DEC
PY 2008
VL 60
IS 6
BP 1372
EP 1387
DI 10.1002/mrm.21704
PG 16
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 377AW
UT WOS:000261225100014
PM 19025904
ER
PT J
AU Sutter, NB
Mosher, DS
Gray, MM
Ostrander, EA
AF Sutter, Nathan B.
Mosher, Dana S.
Gray, Melissa M.
Ostrander, Elaine A.
TI Morphometrics within dog breeds are highly reproducible and dispute
Rensch's rule
SO MAMMALIAN GENOME
LA English
DT Article
ID MORPHOLOGICAL CHANGE; WILD CANIDS; SIZE; ASSOCIATION; DIMORPHISM;
TRAITS; GENOME
AB Using 27 body measurements, we have identified 13 breed-defining metrics for 109 of 159 domestic dog breeds, most of which are recognized by the American Kennel Club (AKC). The data set included 1,155 dogs at least 1 year old (average 5.4 years), and for 53 breed populations, complete measurement data were collected from at least three males and three females. We demonstrate, first, that AKC breed standards are rigorously adhered to for most domestic breeds with little variation observed within breeds. Second, Rensch's rule, which describes a scaling among taxa such that sexual dimorphism is greater among larger species if males are the larger sex, with less pronounced differences in male versus female body size in smaller species, is not maintained in domestic dog breeds because the proportional size difference between males and females of small and large breeds is essentially the same. Finally, principal components (PCs) analysis describes both the overall body size (PC1) and the shape (length versus width) of the skeleton (PC2). That the integrity of the data set is sufficiently rich to discern PCs has strong implications for mapping studies, suggesting that individual measurements may not be needed for genetic studies of morphologic traits, particularly in the case of breed-defining traits that are typically under strong selection. Rather, phenotypes derived from data sets such as these, collected at a fraction of the effort and cost, may be used to direct whole-genome association studies aimed at understanding the genetic basis of fixed morphologic phenotypes defining distinct dog breeds.
C1 [Sutter, Nathan B.; Mosher, Dana S.; Ostrander, Elaine A.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Gray, Melissa M.] Univ Calif Los Angeles, Dept Ecol & Evolutionary Biol, Los Angeles, CA 90095 USA.
RP Ostrander, EA (reprint author), NHGRI, Canc Genet Branch, NIH, Bldg 50,50 S Dr,Room 5351, Bethesda, MD 20892 USA.
EM eostrand@mail.nih.gov
RI Gray, Melissa/B-5025-2008;
OI Gray, Melissa/0000-0002-1756-5468; Ostrander, Elaine/0000-0001-6075-9738
FU Intramural NIH HHS [Z99 HG999999]
NR 18
TC 25
Z9 25
U1 5
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-8990
EI 1432-1777
J9 MAMM GENOME
JI Mamm. Genome
PD DEC
PY 2008
VL 19
IS 10-12
BP 713
EP 723
DI 10.1007/s00335-008-9153-6
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 383DX
UT WOS:000261655400007
PM 19020935
ER
PT J
AU Dube, L
Bechara, A
Bockenholt, U
Ansari, A
Dagher, A
Daniel, M
DeSarbo, WS
Fellows, LK
Hammond, RA
Huang, TTK
Huettel, S
Kestens, Y
Knauper, B
Kooreman, P
Moore, DS
Smidts, A
AF Dube, Laurette
Bechara, Antoine
Bockenholt, Ulf
Ansari, Asim
Dagher, Alain
Daniel, Mark
DeSarbo, Wayne S.
Fellows, Lesley K.
Hammond, Ross A.
Huang, Terry T-K
Huettel, Scott
Kestens, Yan
Knauper, Baerbel
Kooreman, Peter
Moore, Douglas Spencer
Smidts, Ale
TI Towards a brain-to-society systems model of individual choice
SO MARKETING LETTERS
LA English
DT Article
DE Choice models; Dual-process models; Agent systems; Sequential sampling
process models; Motivated adaptive behavior; Neuroscience;
Neuroeconomics
ID DECISION FIELD-THEORY; FOOD-INTAKE; ORBITOFRONTAL CORTEX; PARIETAL
CORTEX; DOPAMINE; REPRESENTATIONS; PLEASANTNESS; NEUROSCIENCE;
CONSUMPTION; CONSISTENCY
AB Canonical models of rational choice fail to account for many forms of motivated adaptive behaviors, specifically in domains such as food selections. To describe behavior in such emotion- and reward-laden scenarios, researchers have proposed dual-process models that posit competition between a slower, analytic faculty and a fast, impulsive, emotional faculty. In this paper, we examine the assumptions and limitations of these approaches to modeling motivated choice. We argue that models of this form, though intuitively attractive, are biologically implausible. We describe an approach to motivated choice based on sequential sampling process models that can form a solid theoretical bridge between what is known about brain function and environmental influences upon choice. We further suggest that the complex and dynamic relationships between biology, behavior, and environment affecting choice at the individual level must inform aggregate models of consumer choice. Models using agent-based complex systems may further provide a principled way to relate individual and aggregate consumer choices to the aggregate choices made by businesses and social institutions. We coin the term "brain-to-society systems" choice model for this broad integrative approach.
C1 [Dube, Laurette; Bockenholt, Ulf] McGill Univ, Desautels Fac Management, Montreal, PQ H3A 1G5, Canada.
[Bechara, Antoine] Univ So Calif, Brain & Creat Inst, Los Angeles, CA USA.
[Ansari, Asim] Columbia Business Sch, New York, NY USA.
[Dagher, Alain] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
[Daniel, Mark] CHUM Ctr Rech, Montreal, PQ, Canada.
[DeSarbo, Wayne S.] Penn State Univ, Smeal Coll Business, University Pk, PA 16802 USA.
[Fellows, Lesley K.] Montreal Neurol Hosp & Inst, Montreal, PQ H3A 2B4, Canada.
[Hammond, Ross A.] Brookings Inst, Econ Studies Program, Washington, DC 20036 USA.
[Huang, Terry T-K] NICHHD, Bethesda, MD 20892 USA.
[Huettel, Scott] Duke Univ, Dept Psychiat & Behav Sci, Durham, NC USA.
[Kestens, Yan] Univ Montreal, Dep Med Sociale & Prevent, Montreal, PQ, Canada.
[Knauper, Baerbel] McGill Univ, Dept Psychol, Montreal, PQ, Canada.
[Kooreman, Peter] Tilburg Univ, Dept Econ, NL-5000 LE Tilburg, Netherlands.
[Moore, Douglas Spencer] Queens Univ, Sch Kinesiol & Hlth Studies, Kingston, ON, Canada.
[Smidts, Ale] Erasmus Univ, Rotterdam Sch Management, Tilburg, Netherlands.
RP Dube, L (reprint author), McGill Univ, Desautels Fac Management, 1001 Sherbrooke St, Montreal, PQ H3A 1G5, Canada.
EM laurette.dube@mcgill.ca
RI Smidts, Ale/B-8701-2008; Daniel, Mark/A-1151-2009; Knauper,
Barbel/G-8405-2012;
OI Fellows, Lesley/0000-0002-9144-092X
NR 54
TC 6
Z9 6
U1 1
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0923-0645
J9 MARKET LETT
JI Mark. Lett.
PD DEC
PY 2008
VL 19
IS 3-4
BP 323
EP 336
DI 10.1007/s11002-008-9057-y
PG 14
WC Business
SC Business & Economics
GA 363EJ
UT WOS:000260250300010
ER
PT J
AU Liu, JM
Yao, JH
Summers, RM
AF Liu, Jiamin
Yao, Jianhua
Summers, Ronald M.
TI Scale-based scatter correction for computer-aided polyp detection in CT
colonography
SO MEDICAL PHYSICS
LA English
DT Article
DE biological organs; cancer; computerised tomography; image
classification; image enhancement; image segmentation; medical image
processing
ID IMAGE; SEGMENTATION; TOMOGRAPHY; POPULATION
AB CT colonography (CTC) is a feasible and minimally invasive method for the detection of colorectal polyps and cancer screening. Computer-aided detection (CAD) of polyps can improve consistency and sensitivity of virtual colonoscopy interpretation and reduce interpretation burden. However, high-density orally administered contrast agents have scatter effects on neighboring tissues. The scattering manifests itself as an artificial elevation in the observed CT attenuation values of the neighboring tissues. This pseudoenhancement phenomenon presents a problem for the application of computer-aided polyp detection, especially when polyps are submerged in the contrast agents. The authors have developed a scale-based correction method that minimizes scatter effects in CTC data by subtraction of the estimated scatter components from observed CT attenuations. By bringing a locally adaptive structure, object scale, into the correction framework, the region of neighboring tissues affected by contrast agents is automatically specified and adaptively changed in different parts of the image. The method was developed as one preprocessing step in the authors' CAD system and was tested by using leave-one-patient-out evaluation on 56 clinical CTC scans (supine or prone) from 28 patients. There were 50 colonoscopy-confirmed polyps measuring 6-9 mm. Visual evaluation indicated that the method reduced CT attenuation of pseudoenhanced polyps to the usual polyp Hounsfield unit range without affecting luminal air regions. For polyps submerged in contrast agents, the sensitivity of CAD with correction is increased 24% at a rate of ten false-positive detections per scan. For all polyps within 6-9 mm, the sensitivity of the authors' CAD with scatter correction is increased 8% at a rate of ten false-positive detections per scan. The authors' results indicated that CAD with this correction method as a preprocessing step can yield a high sensitivity and a relatively low FP rate in CTC.
C1 [Liu, Jiamin; Yao, Jianhua; Summers, Ronald M.] NIH, Dept Radiol, Bethesda, MD 20892 USA.
RP Summers, RM (reprint author), NIH, Dept Radiol, Bldg 10, Bethesda, MD 20892 USA.
EM rms@nih.gov
FU Intramural Research Program of the NIH Clinical Center
FX This research was supported by the Intramural Research Program of the
NIH Clinical Center. The authors thank Dr. Perry Pickhardt, Dr. J.
Richard Choi, and Dr. William Schindler for providing CT colonography
data.
NR 19
TC 16
Z9 17
U1 1
U2 4
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD DEC
PY 2008
VL 35
IS 12
BP 5664
EP 5671
DI 10.1118/1.3013552
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 376VB
UT WOS:000261210000045
PM 19175123
ER
PT J
AU Quarta, M
Stroka, D
Keogh, A
Sidler, D
Avital, I
Gloor, B
Muraca, M
Candinas, D
Inderbitzin, D
AF Quarta, Mattia
Stroka, Deborah
Keogh, Adrian
Sidler, Daniel
Avital, Itzhak
Gloor, Beat
Muraca, Maurizio
Candinas, Daniel
Inderbitzin, Daniel
TI Multiparameter flow cytometry characterization of MHC class I negative
mouse bone marrow cells
SO MEDICAL SCIENCE MONITOR
LA English
DT Article
DE stem cells; bone marrow; multiparameter flow cytometry; major
histocompatibility complex class I; rodent
ID HEMATOPOIETIC STEM-CELLS; MYOCARDIAL-INFARCTION; CELLULAR THERAPY;
PROGENITOR CELLS; MISSING SELF; PLASTICITY; LIVER; BETA-2-MICROGLOBULIN;
DIFFERENTIATE; EXPRESSION
AB Background: MHC-I down-regulation was described in foetal liver progenitors, and two different subsets of adult bone marrow derived stem cells. These cells, namely, MHC-I(-)/Thyl(+) bone marrow derived liver stem cells (BMDLSC) and the multipotent adult progenitors (MAPC) differentiated into functioning hepatocytes. The aim of this paper was to characterize the MHC-I negative bone marrow compartment as it pertains to BMDLSC and MAPC.
Material/Methods: We performed multiparameter flow-cytometry analyses of the MHC-I negative compartment using hematopoietic (CD45, Ter119), and stem cell markers (Thy 1.2, c-Kit, IL-3R, CD34) in adult mice.
Results: When analysing CD45 and Terl 19 expression, the MHC-I negative bone marrow compartment divides into four sub-populations: 1. CD45-/Ter119(+): 86.0 +/- 4.4%; 2. CD45(+)/Ter119(+): 0.2 +/- 0.1%; 3. CD45(+)/Ter119(-): 11.6 +/- 3.0%; 4. CD45(-)/Ter119(-): 2.0 +/- 2.1%. Stem cells markers were only expressed on MHC-I negative/ CD45(+)/Ter119(-) cells. In vivo, MAPC (Ter119(-)/CD45(-) cells) are composed of MHC-I negative (24%) and MHC-I positive cells and do not express any of the stem cell markers tested.
Conclusions: In conclusion, mouse BMDLSC and MAPC are two distinct stem cell populations. Down-regulation of MHC-I was the only common characteristic found between BMDLSC and MAPC suggesting that selection of MHC-I negative cells might represent an efficient strategy to enrich for bone marrow stem cells with liver developmental potential.
C1 [Quarta, Mattia; Stroka, Deborah; Keogh, Adrian; Sidler, Daniel; Gloor, Beat; Candinas, Daniel; Inderbitzin, Daniel] Univ Bern, Inselspital, Dept Visceral & Transplantat Surg, CH-3010 Bern, Switzerland.
[Quarta, Mattia; Stroka, Deborah; Keogh, Adrian; Sidler, Daniel; Gloor, Beat; Candinas, Daniel; Inderbitzin, Daniel] Univ Bern, Bern, Switzerland.
[Avital, Itzhak] NCI, Surg Branch, Bethesda, MD 20892 USA.
[Muraca, Maurizio] Bambino Gesu Pediat Hosp, Lab Med, Rome, Italy.
RP Inderbitzin, D (reprint author), Univ Hosp Bern, Dept Visceral & Transplantat Surg, CH-3010 Bern, Switzerland.
EM daniel.inderbitzin@insel.ch
RI Muraca, Maurizio /G-3063-2012; Stroka, Deborah/F-1806-2013
NR 35
TC 4
Z9 4
U1 0
U2 1
PU INT SCIENTIFIC LITERATURE, INC
PI ALBERTSON
PA 1125 WILLIS AVE, ALBERTSON, NY 11507 USA
SN 1234-1010
J9 MED SCI MONITOR
JI Med. Sci. Monitor
PD DEC
PY 2008
VL 14
IS 12
BP BR286
EP BR293
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 390CD
UT WOS:000262141000007
PM 19043363
ER
PT J
AU Mcclain, JJ
Abraham, TL
Brusseau, TA
Tudor-Locke, C
AF Mcclain, James J.
Abraham, Teresa L.
Brusseau, Timothy A., Jr.
Tudor-Locke, Catrine
TI Epoch Length and Accelerometer Outputs in Children: Comparison to Direct
Observation
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE PHYSICAL ACTIVITY; OBJECTIVE ASSESSMENT; RECORDING INTERVAL; DATA
COLLECTION
ID PHYSICAL-ACTIVITY ASSESSMENT; CALIBRATION; EDUCATION; VALIDATION;
STUDENTS; GRADE; FIELD
AB Purpose: To determine the effects of epoch length and activity count cutpoints oil ActiGraph (AG; ActiGraph Health Services, Pensacola, FL) accelerometer estimates of time in moderate-to-vigorous physical activity (MVPA) in fifth-grade children monitored during physical education (PE) compared with a direct observation (DO) criterion standard. Methods: A sample of 32 fifth-grade males and females (mean age = 10.3 +/- 0.5 yr) wore an AG attached at the waist for a 30-min PE class. Participants were concurrently videotaped, and the Computerized System for Observing Fitness Instruction Time (C-SOFIT) was used to create a DO measure of MVPA time (DO_MVPA). AG data were collected in 5-s epochs then integrated into 10-, 15- 20-, 30-, and 60-s epochs. AG activity counts were converted into time (in s) in MVPA using validated (and epoch-adjusted) children's activity count cutpoints established by Treuth et al. (AG_T), Mattocks et al. (AGM), and Freedson et al. (AG_F). Results: All AG_T and AGM epoch detected significantly lower time in MVPA than DO_MVPA. The percentage of DO_MVPA detected by AG_T and AG_M epochs ranged from 46% to 61% and from 26% to 47%, respectively. All AG_F epochs yielded similar (i.e., nonsignificant) mean estimates of MVPA versus DO_MVPA, with modest increases in root mean squared error (RMSE) with increasing epoch length. The percentage of DO_MVPA detected by AG_F epochs ranged front 93% to 100%. Conclusions: All AG_F epoch lengths provide comparable mean estimates to DO-detected MVPA time in fifth-grade children during PE. To minimize error among individual estimates. shorter epoch lengths should be used. with 5-s epochs yielding the lowest RMSE in the current study. Considerations of both epoch length and activity count cutpoint are important to improved detection of intermittent bouts of MVPA among fifth-grade children.
C1 [Mcclain, James J.] NCI, Off Prevent Oncol, Canc Prevent Fellowship Program, NIH, Bethesda, MD 20892 USA.
[Abraham, Teresa L.] SUNY Coll Brockport, Dept Exercise, Brockport, NY 14420 USA.
[Abraham, Teresa L.] SUNY Coll Brockport, Dept Wellness, Brockport, NY 14420 USA.
[Brusseau, Timothy A., Jr.] SUNY Coll Brockport, Dept Phys Educ & Sport, Brockport, NY 14420 USA.
[Tudor-Locke, Catrine] Pennington Biomed Res Ctr, Walking Behav Lab, Baton Rouge, LA USA.
RP Mcclain, JJ (reprint author), NCI, Off Prevent Oncol, Canc Prevent Fellowship Program, NIH, 6130 Execut Blvd,MSC 7344,Execut Plaza N, Bethesda, MD 20892 USA.
EM james.mcclain@nih.gov
NR 33
TC 81
Z9 82
U1 1
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0195-9131
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD DEC
PY 2008
VL 40
IS 12
BP 2080
EP 2087
DI 10.1249/MSS.0b013e3181824d98
PG 8
WC Sport Sciences
SC Sport Sciences
GA 376DY
UT WOS:000261164600010
PM 18981941
ER
PT J
AU Fozo, EM
Hemm, MR
Storz, G
AF Fozo, Elizabeth M.
Hemm, Matthew R.
Storz, Gisela
TI Small Toxic Proteins and the Antisense RNAs That Repress Them
SO MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS
LA English
DT Review
ID PROGRAMMED CELL-DEATH; PAD1-ENCODED STABILITY DETERMINANT; SEGREGATIONAL
KILLING SYSTEM; STABLE RIBONUCLEIC-ACID; HOK/SOK KILLER LOCUS;
PLASMID-FREE CELLS; SOS-INDUCED TOXIN; ESCHERICHIA-COLI;
ENTEROCOCCUS-FAECALIS; MEMBRANE-PERMEABILITY
AB There has been a great expansion in the number of small regulatory RNAs identified in bacteria. Some of these small RNAs repress the synthesis of potentially toxic proteins. Generally the toxin proteins are hydrophobic and less than 60 amino acids in length, and the corresponding antitoxin small RNA genes are antisense to the toxin genes or share long stretches of complementarity with the target mRNAs. Given their short length, only a limited number of these type I toxin-antitoxin loci have been identified, but it is predicted that many remain to be found. Already their characterization has given insights into regulation by small RNAs, has suggested functions for the small toxic proteins at the cell membrane, and has led to practical applications for some of the type I toxin-antitoxin loci.
C1 [Fozo, Elizabeth M.; Hemm, Matthew R.; Storz, Gisela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
RP Storz, G (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, 18 Lib Dr, Bethesda, MD 20892 USA.
EM storz@helix.nih.gov
OI Storz, Gisela/0000-0001-6698-1241
FU National Institute of Child Health and Human Development; National
Research Council; Life Sciences Foundation
FX This work was supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
as well as a Research Associateship from the National Research Council
(to E.M.F.) and a postdoctoral fellowship from the Life Sciences
Foundation (to M.R.H).
NR 57
TC 135
Z9 136
U1 3
U2 25
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1092-2172
J9 MICROBIOL MOL BIOL R
JI Microbiol. Mol. Biol. Rev.
PD DEC
PY 2008
VL 72
IS 4
BP 579
EP 589
DI 10.1128/MMBR.00025-08
PG 11
WC Microbiology
SC Microbiology
GA 379GO
UT WOS:000261384900002
PM 19052321
ER
PT J
AU Takatori, H
Kanno, Y
Chen, Z
O'Shea, JJ
AF Takatori, Hiroaki
Kanno, Yuka
Chen, Zhi
O'Shea, John J.
TI New complexities in helper T cell fate determination and the
implications for autoimmune diseases
SO MODERN RHEUMATOLOGY
LA English
DT Review
DE Th17 cells; Autoimmune diseases; Inflammation; IL-17; Rheumatoid
arthritis
ID GROWTH-FACTOR-BETA; ROR-GAMMA-T; COLLAGEN-INDUCED ARTHRITIS;
TRANSCRIPTION FACTOR FOXP3; RHEUMATOID-ARTHRITIS; TGF-BETA; TH17 CELLS;
INTESTINAL INFLAMMATION; CUTTING EDGE; AIRWAY NEUTROPHILIA
AB Recently, new complexities in cell fate decision for helper T cells have emerged. One new lineage, which has come to be called Th17 cells, selectively produces proinflammatory cytokines including interleukin-17 (IL-17, A and F), IL-21, and IL-22. In conjunction with transforming growth factor beta-1 (TGF beta-1), IL-6, IL-21, and IL-23, which activate the transcription factor, signal transducer, and activator of transcription 3 (Stat3), the expression of another transcription factor, retinoic acid-related orphan receptor-gamma t (ROR gamma t) leads to the differentiation of Th17 cells in mice. Other cytokines including IL-2, IL-4, interferon-gamma (IFN-gamma), and IL-27 inhibit Th17 differentiation. However, IL-2 acting with TGF beta-1 induces differentiation of naive CD4(+) T cells to become regulatory T cells (Tregs). Th17 cells are now known to play an important role not only in the pathogenesis of inflammation and autoimmune diseases, but also host defense against extracellular bacteria. Conversely, extensive data substantiate the role of Tregs as essential in maintenance of peripheral tolerance. Selectively targeting Tregs and Th17 cells are likely to be important strategies in the treatment of inflammatory and autoimmune diseases in humans.
C1 [Takatori, Hiroaki; Kanno, Yuka; Chen, Zhi; O'Shea, John J.] Natl Inst Arthrit & Musculoskeletal & Skin Dis, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
RP Takatori, H (reprint author), Natl Inst Arthrit & Musculoskeletal & Skin Dis, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bldg 10,Room 13C120,10 Ctr Dr,MSC-1930, Bethesda, MD 20892 USA.
EM takatorih@mail.nih.gov
RI Kanno, Yuka/B-5802-2013;
OI Kanno, Yuka/0000-0001-5668-9319
FU Intramural NIH HHS [NIH0012509554]; PHS HHS [NIH0012509554]
NR 92
TC 30
Z9 36
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1439-7595
J9 MOD RHEUMATOL
JI Mod. Rheumatol.
PD DEC
PY 2008
VL 18
IS 6
BP 533
EP 541
DI 10.1007/s10165-008-0099-z
PG 9
WC Rheumatology
SC Rheumatology
GA 418WC
UT WOS:000264179200001
PM 18679768
ER
PT J
AU Arora, PD
Conti, MA
Ravid, S
Sacks, DB
Kapus, A
Adelstein, RS
Bresnick, AR
McCulloch, CA
AF Arora, Pamela D.
Conti, Mary Anne
Ravid, Shoshana
Sacks, David B.
Kapus, Andras
Adelstein, Robert S.
Bresnick, Anne R.
McCulloch, Christopher A.
TI Rap1 Activation in Collagen Phagocytosis Is Dependent on Nonmuscle
Myosin II-A
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID RECEPTOR-MEDIATED PHAGOCYTOSIS; HAMSTER-KIDNEY CELLS; FC-GAMMA-R; GTPASE
RAP1; DICTYOSTELIUM-DISCOIDEUM; EXCHANGE FACTORS; MODEL SYSTEM;
LIGHT-CHAIN; LATEX BEADS; RHO GTPASES
AB Rap1 enhances integrin-mediated adhesion but the link between Rap1 activation and integrin function in collagen phagocytosis is not defined. Mass spectrometry of Rap1 immunoprecipitates showed that the association of Rap1 with nonmuscle myosin heavy-chain II-A (NMHC II-A) was enhanced by cell attachment to collagen beads. Rap1 colocalized with NM II-A at collagen bead-binding sites. There was a transient increase in myosin light-chain phosphorylation after collagen-bead binding that was dependent on myosin light-chain kinase but not Rho kinase. Inhibition of myosin light-chain phosphorylation, but not myosin II-A motor activity inhibited collagen-bead binding and Rap activation. In vitro binding assays demonstrated binding of Rap1A to filamentous myosin rods, and in situ staining of permeabilized cells showed that NM II-A filaments colocalized with F-actin at collagen bead sites. Knockdown of NM II-A did not affect talin, actin, or beta 1-integrin targeting to collagen beads but targeting of Rap1 and vinculin to collagen was inhibited. Conversely, knockdown of Rap1 did not affect localization of NM II-A to beads. We conclude that MLC phosphorylation in response to initial collagen-bead binding promotes NM II-A filament assembly; binding of Rap1 to myosin filaments enables Rap1-dependent integrin activation and enhanced collagen phagocytosis.
C1 [Arora, Pamela D.; McCulloch, Christopher A.] Univ Toronto, CIHR Grp Matrix Dynam, Toronto, ON M5S 3E2, Canada.
[Conti, Mary Anne; Adelstein, Robert S.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
[Ravid, Shoshana] Hebrew Univ Jerusalem, Hadassah Med Sch, IL-91120 Jerusalem, Israel.
[Sacks, David B.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kapus, Andras] St Michaels Hosp, Res Inst, Toronto, ON M5B 1W8, Canada.
[Bresnick, Anne R.] Albert Einstein Coll Med, Bronx, NY 10461 USA.
RP McCulloch, CA (reprint author), Univ Toronto, CIHR Grp Matrix Dynam, Toronto, ON M5S 3E2, Canada.
EM mccculloch@utoronto.ca
OI Adelstein, Robert/0000-0002-8683-2144; Sacks, David/0000-0003-3100-0735
FU Canadian Institutes of Health Research [416228, 450695]
FX We thank Tarek El Sayegh for reading the manuscript and for helpful
suggestions, Cheung Lo for cell culture, and Wilson Lee for flow
cytometry. This work was supported by Canadian Institutes of Health
Research operating (416228), group (450695), and major equipment grants
(C. A. M.).
NR 61
TC 17
Z9 17
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2008
VL 19
IS 12
BP 5032
EP 5046
DI 10.1091/mbc.E08-04-0430
PG 15
WC Cell Biology
SC Cell Biology
GA 377IK
UT WOS:000261244700001
PM 18799623
ER
PT J
AU McGough, JM
Yang, DF
Huang, S
Georgi, D
Hewitt, SM
Rocken, C
Tanzer, M
Ebert, MPA
Liu, KB
AF McGough, Jon M.
Yang, Dafeng
Huang, Shuang
Georgi, David
Hewitt, Stephen M.
Roecken, Christoph
Taenzer, Marc
Ebert, Matthias P. A.
Liu, Kebin
TI DNA Methylation Represses IFN-gamma-Induced and Signal Transducer and
Activator of Transcription 1-Mediated IFN Regulatory Factor 8 Activation
in Colon Carcinoma Cells
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID SEQUENCE-BINDING-PROTEIN; COLORECTAL-CANCER; GENE-EXPRESSION; PROFILING
REVEALS; FAS EXPRESSION; TUMOR-CELLS; ICSBP GENE; NUDE-MICE; RECEPTOR;
PROGRESSION
AB IFN regulatory factor 8 (IRF8) is both constitutively expressed and IFN-gamma inducible in hematopoietic and nonhematopoietic cells. We have shown that IRF8 expression is silenced by DNA methylation in human colon carcinoma cells, but the molecular mechanism underlying methylation-dependent IRF8 silencing remains elusive. In this study, we observed that IRF8 protein level is inversely correlated with the methylation status of the IRF8 promoter and the metastatic phenotype in human colorectal carcinoma specimens in vivo. Demethylation treatment or knocking down DNMT1 and DNMT3b expression rendered the tumor cells responsive to IFN-gamma to activate IRF8 transcription in vitro. Bisulfite genomic DNA sequencing revealed that the entire CpG island of the IRF8 promoter is methylated. Electrophoresis mobility shift assay revealed that DNA methylation does not directly inhibit IFN-gamma-activated phosphorylated signal transducer and activator of transcription 1 (pSTAT1) binding to the IFN-gamma activation site element in the IRF8 promoter in vitro. Chromatin immunoprecipitation assay revealed that pSTAT1 is associated with the IFN-gamma activation site element of the IRF8 promoter in vivo regardless of the methylation status of the IRF8 promoter. However, DNA methylation results in preferential association of PIAS1, a potent inhibitor of pSTAT1, with pSTAT1 in the methylated IRF8 promoter region. Silencing methyl-CpG binding domain protein 1 (MBD1) expression resulted in IRFS activation by IFN-gamma in human colon carcinoma cells with methylated IRF8 promoter. Our data thus suggest that human colon carcinoma cells silence IFN-gamma-activated IRF8 expression through MBD1-dependent and PIAS1-mediated inhibition of pSTAT1 function at the methylated IRF8 promoter. (Mol Cancer Res 2008;6(12):1841-51)
C1 [McGough, Jon M.; Yang, Dafeng; Huang, Shuang; Liu, Kebin] Med Coll Georgia, Dept Biochem & Mol Biol, Augusta, GA 30912 USA.
[Georgi, David] Med Coll Georgia, Dept Pathol, Augusta, GA 30912 USA.
[Hewitt, Stephen M.] NCI, Tissue Array Res Program, NIH, Bethesda, MD 20892 USA.
[Roecken, Christoph] Univ Med, Charite, Inst Pathol, Berlin, Germany.
[Taenzer, Marc; Ebert, Matthias P. A.] Tech Univ Munich, Klinikum Rechts Isar, Dept Med 2, D-8000 Munich, Germany.
RP Liu, KB (reprint author), Med Coll Georgia, Dept Biochem & Mol Biol, 1459 Laney Walker Blvd, Augusta, GA 30912 USA.
EM Kliu@mcg.edu
RI Rocken, Christoph/A-9239-2010;
OI Rocken, Christoph/0000-0002-6989-8002; Hewitt,
Stephen/0000-0001-8283-1788; Liu, Kebin/0000-0003-1965-7240
FU National Cancer Institute, NIH [CA133085]; Else
Kroner-Fresenius-Stiftung (Homburg, Germany)
FX Grant support: CA133085 (K. Liu) from the National Cancer Institute,
NIH. M.P.A. Ebert is supported by the Else Kroner-Fresenius-Stiftung
(Homburg, Germany).
NR 51
TC 25
Z9 25
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD DEC
PY 2008
VL 6
IS 12
BP 1841
EP 1851
DI 10.1158/1541-7786.MCR-08-0280
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 385OZ
UT WOS:000261824800005
PM 19074829
ER
PT J
AU Lam, ET
O'Bryant, CL
Basche, M
Gustafson, DL
Serkova, N
Baron, A
Holden, SN
Dancey, J
Eckhardt, SG
Gore, L
AF Lam, Elaine T.
O'Bryant, Cindy L.
Basche, Michele
Gustafson, Daniel L.
Serkova, Natalie
Baron, Anna
Holden, Scott N.
Dancey, Janet
Eckhardt, S. Gail
Gore, Lia
TI A phase I study of gefitinib, capecitabine, and celecoxib in patients
with advanced solid tumors
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID CELL LUNG-CANCER; ENDOTHELIAL GROWTH-FACTOR; BREAST-CANCER;
COLORECTAL-CANCER; TRIAL; THERAPY; EXPRESSION; IRESSA; PLUS;
ANGIOGENESIS
AB This phase I study was designed to determine the maximum tolerated dose (MTD) and toxicity profile of the combination of gefitinib, capecitabine, and celecoxib in patients with advanced solid tumors. Patients were treated with escalating doses of gefitinib once daily, capecitabine twice daily (14 of 28 days), and celecoxib twice daily. Plasma samples for biomarkers were obtained at baseline and weekly for the first 2 cycles. Pharmacokinetic variables were correlated with toxicity and presence of biological effect. Tumor biopsies from 5 patients were analyzed for changes in tumor metabolic activity by nuclear magnetic resonance spectroscopy. [(18)F]fluororodeoxyglucose positron emission tomography was done as a correlate in 6 patients at the MTD. Thirty-nine patients received 168 cycles of therapy. The dose-limiting toxicities observed included nausea, dehydration and nausea, diarrhea, and stomatitis. The MTD was 250 mg/d gefitinib (days 1-14) and 2,000 mg/m 2/d capecitabine divided twice daily (days 8-21) every 28 days. Celecoxib was eliminated clue to concerns of increased risk for cardiovascular toxicity, although no patients in this study had cardiac events. One patient with cholangiocarcinoma had a confirmed partial response. Fourteen of 39 (36%) patients maintained prolonged stable disease for a median of 4 months (range, 3-24 months). [(18)F]fluorodeoxyglulucose positron emission tomography scan and metabolomic analyses revealed differences in metabolic response to gefitinib versus capecitabine. The combination of gefitinib and capecitabine is well tolerated and appears to have activity against certain advanced solid tumors, providing a rationale for further evaluation in advanced solid malignancies. [Mol Cancer Ther 2008;7(12):3685-94]
C1 [Lam, Elaine T.; O'Bryant, Cindy L.; Basche, Michele; Serkova, Natalie; Holden, Scott N.; Eckhardt, S. Gail; Gore, Lia] Univ Colorado Denver, Dev Therapeut Program, Aurora, CO 80045 USA.
[O'Bryant, Cindy L.; Gustafson, Daniel L.] Univ Colorado Denver, Sch Pharm, Aurora, CO 80045 USA.
[Serkova, Natalie] Univ Colorado Denver, Dept Anesthesiol, Aurora, CO 80045 USA.
[Gore, Lia] Univ Colorado Denver, Dept Pediat, Aurora, CO 80045 USA.
[O'Bryant, Cindy L.; Basche, Michele; Gustafson, Daniel L.; Serkova, Natalie; Baron, Anna; Holden, Scott N.; Eckhardt, S. Gail; Gore, Lia] Univ Colorado, Ctr Canc, Aurora, CO USA.
[Dancey, Janet] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, Rockville, MD USA.
RP Gore, L (reprint author), Univ Colorado Denver, Dev Therapeut Program, Mail Stop 8302,POB 6511, Aurora, CO 80045 USA.
EM lia.gore@ucdenver.edu
FU National Cancer Institute; NIH [01 CA099176, R21 CA108624, P30 CA046934,
N01-C0-12400 (22XS047A-P3358)]
FX National Cancer Institute, NIH grants U01 CA099176, R21 CA108624, and
P30 CA046934 and contract N01-C0-12400 (22XS047A-P3358). Gefitinib was
provided by the Division of Cancer Treatment and Diagnosis at the
National Cancer Institute under a Cooperative Research and Development
Agreement between AstraZeneca and the Division of Cancer Treatment and
Diagnosis.
NR 48
TC 5
Z9 7
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD DEC
PY 2008
VL 7
IS 12
BP 3685
EP 3694
DI 10.1158/1535-7163.MCT-08-0436
PG 10
WC Oncology
SC Oncology
GA 385YC
UT WOS:000261848500004
PM 19074845
ER
PT J
AU Hu, JB
Xia, XM
Cheng, AW
Wang, GH
Luo, XL
Reed, MF
Fojo, T
Oetting, A
Gong, JP
Yen, PM
AF Hu, Junbo
Xia, Xianmin
Cheng, Aiwu
Wang, Guihua
Luo, Xuelai
Reed, Michael F.
Fojo, Tito
Oetting, Alexis
Gong, Jianping
Yen, Paul M.
TI A peptide inhibitor derived from p55PIK phosphatidylinositol 3-kinase
regulatory subunit: a novel cancer therapy
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID PHOSPHOINOSITIDE 3-KINASE; CELL-CYCLE; LOCATION; PATHWAY; MITOSIS;
PIK3CA; LINES; RB
AB p55PIK, a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), specifically interacts with retinoblastoma protein (Rb) through the unique NH(2) terminus of p55PIK, N24. This interaction is critical for cell proliferation and cell cycle progression. To examine p55PIK as a potential target for cancer therapy, we generated an adenovirus expressing N24 (Ad-N24-GFP) and studied its effects on the proliferation of cultured cancer cells, including human colon (HT29) and thyroid (FTC236) cancer cells. Ad-N24-GFP blocked cell proliferation and induced cell cycle arrest in all cancer cell lines tested. N24 induced cell cycle arrest at G(0)-G(1) phase in cell lines that expressed Rb. Interestingly, N24 inhibited cell proliferation by blocking cell cycle transition at both S and G(2)-M phases in FTC236 cells, which did not express Rb. When Rb was knocked down by short hairpin RNA in HT29 cells, N24 also inhibited cell cycle progression at S and G2-M phases, suggesting that p55PIK regulates cell cycle progression by Rb-dependent and Rb-independent mechanisms. Finally, Ad-N24-GFP markedly decreased the growth of xenograft tumors derived from HT29 and FTC236 cancer cells in athymic nude mice. Our data strongly suggest that N24 peptide is an effective anticancer therapy, which specifically inhibits PI3K signaling pathways mediated by p55PIK. Moreover, they show that the regulatory subunit of an enzyme, in addition to its catalytic subunit, can be an important target for drug development. [Mol Cancer Ther 2008;7(12):3719-28]
C1 [Hu, Junbo; Wang, Guihua; Luo, Xuelai; Gong, Jianping] Huazhong Univ Sci & Technol, Tongji Med Sch, Dept Surg, Wuhan 430074, Peoples R China.
[Cheng, Aiwu] NIA, Neurosci Lab, Ctr Gerontol Res, Bethesda, MD 20892 USA.
[Xia, Xianmin; Oetting, Alexis; Yen, Paul M.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Reed, Michael F.] Univ Cincinnati, Coll Med, Dept Surg, Cincinnati, OH 45267 USA.
[Fojo, Tito] NCI, Expt Therapeut Sect, Med Oncol Branch, Bethesda, MD 20892 USA.
RP Xia, XM (reprint author), Johns Hopkins Bayview Med Ctr, Dept Med, 5200 Eastern Ave, Baltimore, MD 21224 USA.
EM xxia2@jhmi.edu; jpgong@tjh.tjmu.edu.cn
FU American Thyroid Association ThyCa research; National Natural Science
Foundation of China [30300308]; Program for New Century Excellent
Talents in University [NCET-04-0699]; National Basic Research Program of
China [973-2002CB513100-2]
FX American Thyroid Association ThyCa research grant (X. Xia) and National
Natural Science Foundation of China grant 30300308, Program for New
Century Excellent Talents in University grant NCET-04-0699, and National
Basic Research Program of China 973-2002CB513100-2 (J. Hu).
NR 29
TC 19
Z9 31
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD DEC
PY 2008
VL 7
IS 12
BP 3719
EP 3728
DI 10.1158/1535-7163.MCT-08-0499
PG 10
WC Oncology
SC Oncology
GA 385YC
UT WOS:000261848500007
PM 19074847
ER
PT J
AU Park, JJ
Loh, YP
AF Park, Joshua J.
Loh, Y. Peng
TI How Peptide Hormone Vesicles Are Transported to the Secretion Site for
Exocytosis
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Review
ID TRANS-GOLGI NETWORK; ACTIVITY-DEPENDENT SECRETION; AMYLOID PRECURSOR
PROTEIN; PANCREATIC BETA-CELLS; PROHORMONE SORTING RECEPTOR;
MICROTUBULE-BASED TRANSPORT; GLOBULAR TAIL FRAGMENT; AP-1 ADAPTER
COMPLEX; CARBOXYPEPTIDASE-E; MYOSIN-VA
AB Post-Golgi transport of peptide hormone-containing vesicles from the site of genesis at the trans-Golgi network to the release site at the plasma membrane is essential for activity-dependent hormone secretion to mediate various endocrinological functions. It is known that these vesicles are transported on microtubules to the proximity of the release site, and they are then loaded onto an actin/myosin system for distal transport through the actin cortex to just below the plasma membrane. The vesicles are then tethered to the plasma membrane, and a subpopulation of them are docked and primed to become the readily releasable pool. Cytoplasmic tails of vesicular transmembrane proteins, as well as many cytosolic proteins including adaptor proteins, motor proteins, and guanosine triphosphatases, are involved in vesicle budding, the anchoring of the vesicles, and the facilitation of movement along the transport systems. In addition, a set of cytosolic proteins is also necessary for tethering/docking of the vesicles to the plasma membrane. Many of these proteins have been identified from different types of (neuro) endocrine cells. Here, we summarize the proteins known to be involved in the mechanisms of sorting various cargo proteins into regulated secretory pathway hormone-containing vesicles, movement of these vesicles along microtubules and actin filaments, and their eventual tethering/docking to the plasma membrane for hormone secretion. (Molecular Endocrinology 22: 2583-2595, 2008)
C1 [Park, Joshua J.; Loh, Y. Peng] NICHHD, Cellular Neurobiol Sect, NIH, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), NICHHD, Cellular Neurobiol Sect, NIH, Bldg 49,Room 5A22,49 Convent Dr, Bethesda, MD 20892 USA.
EM lohp@mail.nih.gov
FU Eunice Kennedy Shriver; NICHD; NIH
FX This work was supported by the Intramural Research Program of the Eunice
Kennedy Shriver, NICHD, NIH.
NR 148
TC 35
Z9 36
U1 1
U2 7
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD DEC
PY 2008
VL 22
IS 12
BP 2583
EP 2595
DI 10.1210/me.2008-0209
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 378EY
UT WOS:000261305200002
PM 18669645
ER
PT J
AU Chen, SY
Pan, CJ
Lee, S
Peng, WT
Chou, JY
AF Chen, Shih-Yin
Pan, Chi-Jiunn
Lee, Soojung
Peng, Wentao
Chou, Janice Y.
TI Functional analysis of mutations in the glucose-6-phosphate transporter
that cause glycogen storage disease type Ib
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Glycogen storage disease type Ib; Glucose-6-phosphate transport;
Phosphate transport; Proteoliposomes; Mutation analysis
ID PHOSPHOHISTIDINE-ENZYME INTERMEDIATE; ESCHERICHIA-COLI; NON-A; GENE;
TRANSLOCASE; DEFICIENT; CATALYSIS; SYSTEMS; 1B
AB The glucose-6-phosphate transporter (G6PT) deficient in glycogen storage disease type Ib is a phosphate (P(i))-linked antiporter capable of G6P: P(i) and P(i):P(i) exchanges. We previously characterized G6PT mutations by measuring G6P uptake activities in microsomes co-expressing G6PT and glucose-6-phosphatase-alpha. Here we report a new assay, based on reconstituted proteoliposomes carrying only G6PT, and characterize G6P and P(i) uptake activities of 23 G6PT mutations. We show that co-expression and G6PT-only assays are equivalent in measuring G6PT activity. However, the p.Q133P mutation exhibits differential G6P and P(i) transport activities, suggesting that characterizing G6P and P(i) transport activities of G6PT mutations may yield insights to this genetic disorder. Published by Elsevier Inc.
C1 [Chen, Shih-Yin; Pan, Chi-Jiunn; Lee, Soojung; Peng, Wentao; Chou, Janice Y.] NICHHD, Sect Cellular Differentiat, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Chou, JY (reprint author), NICHHD, Sect Cellular Differentiat, Program Dev Endocrinol & Genet, NIH, Bldg 10,Room 9D42,NIH 10 Ctr Dr, Bethesda, MD 20892 USA.
EM chouja@mail.nih.gov
FU Intramural Research Programs of the NICHD; NIH
FX This research was supported in part by the Intramural Research Programs
of the NICHD, NIH.
NR 25
TC 5
Z9 7
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 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2008
VL 95
IS 4
BP 220
EP 223
DI 10.1016/j.ymgme.2008.08.005
PG 4
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 381NH
UT WOS:000261542700005
PM 18835800
ER
PT J
AU Fozo, EM
Kawano, M
Fontaine, F
Kaya, Y
Mendieta, KS
Jones, KL
Ocampo, A
Rudd, KE
Storz, G
AF Fozo, Elizabeth M.
Kawano, Mitsuoki
Fontaine, Fanette
Kaya, Yusuf
Mendieta, Kathy S.
Jones, Kristi L.
Ocampo, Alejandro
Rudd, Kenneth E.
Storz, Gisela
TI Repression of small toxic protein synthesis by the Sib and OhsC small
RNAs
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI K-12; ANTISENSE RNA; COMPARATIVE GENOMICS;
STRESS-RESPONSE; NONCODING RNAS; ENCODING GENES; IDENTIFICATION;
CHROMOSOME; MEMBRANE; SYSTEM
AB The sequences encoding the QUAD1 RNAs were initially identified as four repeats in Escherichia coli. These repeats, herein renamed SIB, are conserved in closely related bacteria, although the number of repeats varies. All five Sib RNAs in E. coli MG1655 are expressed, and no phenotype was observed for a five-sib deletion strain. However, a phenotype reminiscent of plasmid addiction was observed for overexpression of the Sib RNAs, and further examination of the SIB repeat sequences revealed conserved open reading frames encoding highly hydrophobic 18- to 19-amino-acid proteins (Ibs) opposite each sib gene. The Ibs proteins were found to be toxic when overexpressed and this toxicity could be prevented by coexpression of the corresponding Sib RNA. Two other RNAs encoded divergently in the yfhL-acpS intergenic region were similarly found to encode a small hydrophobic protein (ShoB) and an antisense RNA regulator (OhsC). Overexpression of both IbsC and ShoB led to immediate changes in membrane potential suggesting both proteins affect the cell envelope. Whole genome expression analysis showed that overexpression of IbsC and ShoB, as well as the small hydrophobic LdrD and TisB proteins, has both overlapping and unique consequences for the cell.
C1 [Kaya, Yusuf; Jones, Kristi L.; Ocampo, Alejandro; Rudd, Kenneth E.] Univ Miami, Miller Sch Med, Dept Biochem & Mol Biol, Miami, FL 33136 USA.
[Fozo, Elizabeth M.; Kawano, Mitsuoki; Fontaine, Fanette; Mendieta, Kathy S.; Storz, Gisela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
RP Rudd, KE (reprint author), Univ Miami, Miller Sch Med, Dept Biochem & Mol Biol, Miami, FL 33136 USA.
EM krudd@miami.edu; storz@helix.nih.gov
OI Jones, Kristi/0000-0002-0242-7097; Storz, Gisela/0000-0001-6698-1241
FU NIH [R01-GM58560]; Japan Society for the Promotion of Science; National
Research Council
FX We thank V. Gallegos, A. Kimchi, Z. Li, J. Saud, G. Tolun and M.
Valledor for technical assistance and S. Gottesman and members of the
Storz lab for helpful discussions and comments. This research was
supported by NIH Grant No. R01-GM58560 (K. E. R.), the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development ( E. M. F., M. K., F. F., K. S. M.
and G. S.), a research fellowship from the Japan Society for the
Promotion of Science ( M. K.) and a Research Associateship from the
National Research Council ( E. M. F.).
NR 35
TC 78
Z9 86
U1 0
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD DEC
PY 2008
VL 70
IS 5
BP 1076
EP 1093
DI 10.1111/j.1365-2958.2008.06394.x
PG 18
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 374UX
UT WOS:000261070300004
PM 18710431
ER
PT J
AU Hemm, MR
Paul, BJ
Schneider, TD
Storz, G
Rudd, KE
AF Hemm, Matthew R.
Paul, Brian J.
Schneider, Thomas D.
Storz, Gisela
Rudd, Kenneth E.
TI Small membrane proteins found by comparative genomics and ribosome
binding site models
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI K-12; OPEN READING FRAMES; BACILLUS-SUBTILIS; BACTERIAL
GENES; ANTISENSE RNA; CELL-DEATH; IDENTIFICATION; SEQUENCE; PEPTIDE;
INITIATION
AB The correct annotation of genes encoding the smallest proteins is one of the biggest challenges of genome annotation, and perhaps more importantly, few annotated short open reading frames have been confirmed to correspond to synthesized proteins. We used sequence conservation and ribosome binding site models to predict genes encoding small proteins, defined as having 16-50 amino acids, in the intergenic regions of the Escherichia coli genome. We tested expression of these predicted as well as previously annotated genes by integrating the sequential peptide affinity tag directly upstream of the stop codon on the chromosome and assaying for synthesis using immunoblot assays. This approach confirmed that 20 previously annotated and 18 newly discovered proteins of 16-50 amino acids are synthesized. We summarize the properties of these small proteins; remarkably more than half of the proteins are predicted to be single-transmembrane proteins, nine of which we show co-fractionate with cell membranes.
C1 [Hemm, Matthew R.; Paul, Brian J.; Storz, Gisela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
[Schneider, Thomas D.] NCI, Ctr Canc Res, Nanobiol Program, NIH, Frederick, MD 21702 USA.
[Rudd, Kenneth E.] Univ Miami, Miller Sch Med, Dept Biochem & Mol Biol, Miami, FL 33101 USA.
RP Storz, G (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
EM storz@helix.nih.gov; krudd@miami.edu
OI Schneider, Thomas/0000-0002-9841-1531; Storz, Gisela/0000-0001-6698-1241
FU NIH [R01-GM58560]; Eunice Kennedy Shriver National Institute of Child
Health and Human Development; National Cancer Institute; Life Sciences
Foundation
FX We thank J. Miranda-Rios for pointing out the ORF in the ISO92/IsrB RNA,
R. Hegde for advice on cell fractionation, M. W. Stone and J. Zhou for
computational assistance, C. Raetz for communicating unpublished data
and S. Gottesman, E. Koonin and members of the Storz lab for helpful
discussions and comments. This research was supported by NIH grant
number R01-GM58560 (K.E.R.), the Intramural Research Programs of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (M.R.H., B.J.P. and G.S.) and the National Cancer Institute
(T.D.S.) and by a postdoctoral fellowship from the Life Sciences
Foundation ( M.R.H.).
NR 45
TC 79
Z9 118
U1 3
U2 11
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD DEC
PY 2008
VL 70
IS 6
BP 1487
EP 1501
DI 10.1111/j.1365-2958.2008.06495.x
PG 15
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 376TO
UT WOS:000261206100015
PM 19121005
ER
PT J
AU Dhasarathy, A
Wade, PA
AF Dhasarathy, Archana
Wade, Paul A.
TI The MBD protein family-Reading an epigenetic mark?
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Review
DE Epigenetics; DNA methylation; Methyl-CpG-binding protein;
Transcriptional repression; Histone deacetylase
ID CPG-BINDING DOMAIN; METHYL-CPG; DNA METHYLATION; RETT-SYNDROME;
CHROMOSOMAL-PROTEIN; HISTONE DEACETYLASE; MECP2; CHROMATIN; COMPLEX;
IDENTIFICATION
AB A family of proteins conserved throughout the eukaryotic lineage is characterized by the presence of a common sequence motif-the methyl-CpG-binding domain, or MBD. This sequence motif corresponds to a structural domain which, in some but not all cases, confers the ability to bind methylated cytosine residues in the context of the dinucleotide 5' CG 3'. Mammals have five well-characterized members of this family, each with unique biological characteristics. Recently, Much progress has been made in defining the biochemical properties of one member of this family, MeCP2. This protein has a very high affinity for chromatin and considerable insight has been gained into its interactions with naked DNA and with chromatin fibers. Previous models have proposed that several members of the MBD family contribute to establishment and/or maintenance of transcriptional repression by recruiting enzymes that locally modify histones. Surprisingly, recent data indicate that MeCP2 is likely to contribute to chromatin properties through an architectural role, participating in higher order chromatin structures that facilitate both gene repression as well as gene activation. These observations suggest that existing models probably do not explain the entire gamut of biological functions performed by this very interesting protein family. Published by Elsevier B.V.
C1 [Dhasarathy, Archana; Wade, Paul A.] Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27517 USA.
RP Wade, PA (reprint author), Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, 111 TW Alexander Dr,Bldg 101,Room D416, Res Triangle Pk, NC 27517 USA.
EM wadep2@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences [1Z01ES101965]
FX This research was supported (Project number 1Z01ES101965) by the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences. We thank the members of the Wade
laboratory for useful discussions throughout the Course of preparation
of this manuscript. We apologize to our colleagues whose work could not
be cited here due to space considerations.
NR 37
TC 64
Z9 67
U1 3
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD DEC 1
PY 2008
VL 647
IS 1-2
BP 39
EP 43
DI 10.1016/j.mrfmmm.2008.07.007
PG 5
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 383VZ
UT WOS:000261703600006
PM 18692077
ER
PT J
AU Kiefer, CM
Hou, CH
Little, JA
Dean, A
AF Kiefer, Christine M.
Hou, Chunhui
Little, Jane A.
Dean, Ann
TI Epigenetics of beta-globin gene regulation
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Review
DE beta-Globin; Chromatin; Epigenetics; Histone modifications; Locus
control regions; Insulators
ID LOCUS-CONTROL REGION; SICKLE-CELL-ANEMIA; HISTONE LYSINE METHYLATION;
CHROMATIN DOMAIN ACTIVATION; TRANSCRIPTION FACTOR GATA-1;
ENHANCER-BLOCKING ACTIVITY; PRIMARY ERYTHROID-CELLS; FETAL-HEMOGLOBIN
LEVELS; I-HYPERSENSITIVE SITES; HUMAN GAMMA-GLOBIN
AB It is widely recognized that the next great challenge in the post-genomic period is to understand how the genome establishes the cell and tissue specific patterns of gene expression that underlie development. The P-globin genes are among the most extensively studied tissue specific and developmentally regulated genes. The onset of erythropoiesis in precursor cells and the progressive expression of different members of the P-globin family during development are accompanied by dramatic epigenetic changes in the locus. In this review, we will consider the relationship between histone and DNA modifications and the transcriptional activity of the P-globin genes, the dynamic changes in epigenetic modifications observed during erythroid development, and the potential these changes hold as new targets for therapy in human disease. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Kiefer, Christine M.; Hou, Chunhui; Dean, Ann] NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Little, Jane A.] Albert Einstein Coll Med, Dept Med, Div Hematol, Bronx, NY 10461 USA.
RP Dean, A (reprint author), NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
EM anndean@helix.nih.gov
RI Hou, Chunhui/A-6596-2009
FU NIDDK, NIH; Albert Einstein College of Medicine
FX We would like to acknowledge support from the Intramural Program of the
NIDDK, NIH and the Albert Einstein College of Medicine.
NR 96
TC 35
Z9 38
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD DEC 1
PY 2008
VL 647
IS 1-2
BP 68
EP 76
DI 10.1016/j.mrfmmm.2008.07.014
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 383VZ
UT WOS:000261703600010
PM 18760288
ER
PT J
AU Pancrazio, JJ
AF Pancrazio, Joseph J.
TI Neural interfaces at the nanoscale
SO NANOMEDICINE
LA English
DT Review
DE charge density; deep-brain stimulation; iridium oxide; microelectrode
array; nanofiber; neuron; recording; stimulation
ID WALLED CARBON NANOTUBE; DEEP BRAIN-STIMULATION; SPINAL-CORD-INJURY;
ELECTRICAL-STIMULATION; NEURONAL NETWORKS; NANOFIBER ARRAYS; IN-VIVO;
ELECTRODES; TISSUE; CELLS
AB Bioelectrical neural interfaces provide a means of recording the activity from the nervous system and delivering therapeutic stimulation to restore neurological function lost during disease or injury. Although neural interfaces have reached clinical utility, reducing the size of the bioelectrical interface to minimize damage to neural tissue and maximize selectivity has proven problematic. Nanotechnology may offer a means of interfacing with the nervous system with unprecedented specificity. Emergent applications of nanotechnology to neuroscience include molecular imaging, drug delivery across the BBB, scaffolds for neural regeneration and bioelectrical interfaces. In particular, carbon nanotubes offer the promises of material stability and low electrical impedance at physical dimensions that could have a significant impact on the future on neural interfaces. The purpose of this review is to present recent advances in carbon nanotube-based bioelectrical interfaces for the nervous system and discuss research challenges and opportunities.
C1 NINDS, NIH, Bethesda, MD 20892 USA.
RP Pancrazio, JJ (reprint author), NINDS, NIH, 6001 Execut Blvd,NSC 2205, Bethesda, MD 20892 USA.
EM pancrazj@ninds.nih.gov
RI Pancrazio, Joseph/M-3206-2015
OI Pancrazio, Joseph/0000-0001-8276-3690
FU Intramural NIH HHS [NIH0011642045]; PHS HHS [NIH0011642045]
NR 70
TC 30
Z9 31
U1 6
U2 33
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD DEC
PY 2008
VL 3
IS 6
BP 823
EP 830
DI 10.2217/17435889.3.6.823
PG 8
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics
GA 381RA
UT WOS:000261552400010
PM 19025456
ER
PT J
AU Kastrup, CJ
Boedicker, JQ
Pomerantsev, AP
Moayeri, M
Bian, Y
Pompano, RR
Kline, TR
Sylvestre, P
Shen, F
Leppla, SH
Tang, WJ
Ismagilov, RF
AF Kastrup, Christian J.
Boedicker, James Q.
Pomerantsev, Andrei P.
Moayeri, Mahtab
Bian, Yao
Pompano, Rebecca R.
Kline, Timothy R.
Sylvestre, Patricia
Shen, Feng
Leppla, Stephen H.
Tang, Wei-Jen
Ismagilov, Rustem F.
TI Spatial localization of bacteria controls coagulation of human blood by
'quorum acting'
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID FACTOR PATHWAY INHIBITOR; BACILLUS-ANTHRACIS; TISSUE FACTOR; THRESHOLD
RESPONSE; IMMUNE-RESPONSE; PATCH SIZE; FACTOR-X; ACTIVATION;
FIBRINOLYSIS; INFECTION
AB Blood coagulation often accompanies bacterial infections and sepsis and is generally accepted as a consequence of immune responses. Though many bacterial species can directly activate individual coagulation factors, they have not been shown to directly initiate the coagulation cascade that precedes clot formation. Here we demonstrated, using microfluidics and surface patterning, that the spatial localization of bacteria substantially affects coagulation of human and mouse blood and plasma. Bacillus cereus and Bacillus anthracis, the anthrax-causing pathogen, directly initiated coagulation of blood in minutes when bacterial cells were clustered. Coagulation of human blood by B. anthracis required secreted zinc metalloprotease InhA1, which activated prothrombin and factor X directly (not via factor XII or tissue factor pathways). We refer to this mechanism as 'quorum acting' to distinguish it from quorum sensing-it does not require a change in gene expression, it can be rapid and it can be independent of bacterium-to-bacterium communication.
C1 [Kastrup, Christian J.; Boedicker, James Q.; Pompano, Rebecca R.; Kline, Timothy R.; Ismagilov, Rustem F.] Univ Chicago, Dept Chem, Chicago, IL 60637 USA.
[Kastrup, Christian J.; Boedicker, James Q.; Pompano, Rebecca R.; Kline, Timothy R.; Ismagilov, Rustem F.] Univ Chicago, Inst Biophys Dynam, Chicago, IL 60637 USA.
[Pomerantsev, Andrei P.; Moayeri, Mahtab; Leppla, Stephen H.] NIAID, Bacterial Toxins & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
[Bian, Yao; Tang, Wei-Jen] Univ Chicago, Ben May Inst Canc Res, Chicago, IL 60637 USA.
[Sylvestre, Patricia] Inst Pasteur, Unite Toxines & Pathogenie Bacteriennes, F-75724 Paris 15, France.
[Sylvestre, Patricia] CNRS, Unite Rech Associee 2172, F-75724 Paris 15, France.
RP Ismagilov, RF (reprint author), Univ Chicago, Dept Chem, 929 E 57th St, Chicago, IL 60637 USA.
EM r-ismagilov@uchicago.edu
OI Tang, Wei-Jen/0000-0002-8267-8995
FU US National Institutes of Health [DP1OD003584]; US National Science
Foundation [CHE-0349034]; US Office of Naval Research [N000140610630];
Camille Dreyfus Teacher-Scholar Awards Program; Cottrell Scholar of
Research Corporation; NIH [GM 62548, GM 81539]; NIAID; The University of
Chicago; University of Wisconsin; New York University
FX This work was supported in part by the US National Institutes of Health
(NIH) Director's Pioneer Award (grant number DP1OD003584), the US
National Science Foundation CAREER Award (grant number CHE-0349034), the
US Office of Naval Research (grant number N000140610630), the Camille
Dreyfus Teacher-Scholar Awards Program and the Cottrell Scholar of
Research Corporation Awards Program to R. F. I., by NIH grants (GM 62548
and GM 81539) to W.- J. T., and by the Intramural Research Program of
the NIAID. We thank J. Alverdy, B. Bishop, S. Crosson, C. Esmon, M.
Mock, M. Runyon, J. Shapiro, U. Spitz, T. Van Ha, D. Wiebel and O.
Zaborina for helpful discussions; O. Zaborina (The University of
Chicago) for the gift of the EGPF plasmid for E. coli and for assisting
in the transformation procedure; M. Mock (Institut Pasteur) for the gift
of the mouse anti- InhA1 serum; L. Cheng and D. Crown for assisting in
the animal studies; H. Herwald (Lund University) for the gift of the E.
coli Ymel-1 strain; J. Handelsman (University of Wisconsin) for the gift
of the B. cereus GFP strain; M. Blaser (New York University) for the
gift of the B. anthracis DluxS strain; and J. Price for contributions in
writing and editing this manuscript. We thank C. Tallant (Institut de
Biologia Molecular de Barcelona) for assistance in construction of the
protease gene knockout strains.
NR 50
TC 51
Z9 51
U1 1
U2 25
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD DEC
PY 2008
VL 4
IS 12
BP 742
EP 750
DI 10.1038/nchembio.124
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 373FH
UT WOS:000260955900010
PM 19031531
ER
PT J
AU Cravedi, P
Mannon, RB
Ruggenenti, P
Remuzzi, A
Remuzzi, G
AF Cravedi, Paolo
Mannon, Roslyn B.
Ruggenenti, Piero
Remuzzi, Andrea
Remuzzi, Giuseppe
TI Islet transplantation: need for a time-out?
SO NATURE CLINICAL PRACTICE NEPHROLOGY
LA English
DT Editorial Material
ID PANCREAS TRANSPLANTATION; NEPHROPATHY; SIROLIMUS; KIDNEY; MICE
C1 [Remuzzi, Giuseppe] Mario Negri Inst Pharmacol Res, Clin Res Ctr Rare Dis Aldo & Cele Dacco, I-24125 Bergamo, Italy.
[Cravedi, Paolo; Ruggenenti, Piero] Mario Negri Inst Pharmacol Res, Dept Renal Med, I-24125 Bergamo, Italy.
[Remuzzi, Andrea] Mario Negri Inst Pharmacol Res, Dept Biomed Engn, I-24125 Bergamo, Italy.
[Mannon, Roslyn B.] NIDDK, Transplantat Branch, NIH, Bethesda, MD USA.
RP Remuzzi, G (reprint author), Mario Negri Inst Pharmacol Res, Clin Res Ctr Rare Dis Aldo & Cele Dacco, 11 Gavazzeni St, I-24125 Bergamo, Italy.
EM gremuzzi@marionegri.it
OI Remuzzi, Andrea/0000-0002-4301-8927
NR 14
TC 4
Z9 4
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1745-8323
J9 NAT CLIN PRACT NEPHR
JI Nat. Clin. Pract. Nephrol.
PD DEC
PY 2008
VL 4
IS 12
BP 660
EP 661
DI 10.1038/ncpneph0961
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 375QB
UT WOS:000261127300008
PM 18813231
ER
PT J
AU Stadanlick, JE
Kaileh, M
Karnell, FG
Scholz, JL
Miller, JP
Quinn, WJ
Brezski, RJ
Treml, LS
Jordan, KA
Monroe, JG
Sen, R
Cancro, MP
AF Stadanlick, Jason E.
Kaileh, Mary
Karnell, Fredrick G.
Scholz, Jean L.
Miller, Juli P.
Quinn, William J., III
Brezski, Randall J.
Treml, Laura S.
Jordan, Kimberly A.
Monroe, John G.
Sen, Ranjan
Cancro, Michael P.
TI Tonic B cell antigen receptor signals supply an NF-kappa B substrate for
prosurvival BLyS signaling
SO NATURE IMMUNOLOGY
LA English
DT Article
ID TYROSINE KINASE INHIBITOR; NECROSIS-FACTOR FAMILY; MARGINAL ZONE;
LYMPHOCYTE STIMULATOR; MEMBRANE CHOLESTEROL; CUTTING EDGE; BAFF-R;
ACTIVATION; SURVIVAL; NF-KAPPA-B2
AB The survival of transitional and mature B cells requires both the B cell antigen receptor (BCR) and BLyS receptor 3 (BR3), which suggests that these receptors send signals that are nonredundant or that engage in crosstalk with each other. Here we show that BCR signaling induced production of the nonclassical transcription factor NF-kappa B pathway substrate p100, which is required for transmission of BR3 signals and thus B cell survival. The capacity for sustained p100 production emerged during transitional B cell differentiation, the stage at which BCR signals begin to mediate survival rather than negative selection. Our findings identify a molecular mechanism for the reliance of primary B cells on continuous BR3 and BCR signaling, as well as for the gradual resistance to negative selection that is acquired during B cell maturation.
C1 [Stadanlick, Jason E.; Karnell, Fredrick G.; Scholz, Jean L.; Miller, Juli P.; Quinn, William J., III; Brezski, Randall J.; Treml, Laura S.; Monroe, John G.; Cancro, Michael P.] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Kaileh, Mary; Sen, Ranjan] NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA.
[Jordan, Kimberly A.] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA.
RP Cancro, MP (reprint author), Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
EM cancro@mail.med.upenn.edu
OI Brezski, Randall/0000-0003-4028-4741
FU US Public Health Service [R01AI073939, R01AI0545488, T32HL07971,
T32AI055428, R01AI032592]; National Institute on Aging
FX We thank M. May, L. Solt and the University of Pennsylvania Flow
Cytometry Core for assistance and advice; C. A. Hunter (University of
Pennsylvania School of Veterinary Medicine) for NF-kappa B p50-deficient
mice; C. Thompson (University of Pennsylvania) for mice with B
cell-specific expression of the Bcl-xL transgene; V. Dixit (Genentech)
for pRK5B-hBR3; and J.M. Stadanlick for critical reading of this
manuscript. Supported by the US Public Health Service (R01AI073939 and
R01AI0545488 to M. P. C.; T32HL07971 to J.E. S.; T32AI055428 to F. G.
K.; and R01AI032592 to J.G.M.) and the Intramural Research Program of
the National Institute on Aging.
NR 50
TC 114
Z9 117
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD DEC
PY 2008
VL 9
IS 12
BP 1379
EP 1387
DI 10.1038/ni.1666
PG 9
WC Immunology
SC Immunology
GA 372FY
UT WOS:000260888700013
PM 18978795
ER
PT J
AU El Kasmi, KC
Qualls, JE
Pesce, JT
Smith, AM
Thompson, RW
Henao-Tamayo, M
Basaraba, RJ
Konig, T
Schleicher, U
Koo, MS
Kaplan, G
Fitzgerald, KA
Tuomanen, EI
Orme, IM
Kanneganti, TD
Bogdan, C
Wynn, TA
Murray, PJ
AF El Kasmi, Karim C.
Qualls, Joseph E.
Pesce, John T.
Smith, Amber M.
Thompson, Robert W.
Henao-Tamayo, Marcela
Basaraba, Randall J.
Koenig, Till
Schleicher, Ulrike
Koo, Mi-Sun
Kaplan, Gilla
Fitzgerald, Katherine A.
Tuomanen, Elaine I.
Orme, Ian M.
Kanneganti, Thirumala-Devi
Bogdan, Christian
Wynn, Thomas A.
Murray, Peter J.
TI Toll-like receptor-induced arginase 1 in macrophages thwarts effective
immunity against intracellular pathogens
SO NATURE IMMUNOLOGY
LA English
DT Article
ID NITRIC-OXIDE SYNTHASE; L-ARGININE METABOLISM;
MYCOBACTERIUM-TUBERCULOSIS; HELICOBACTER-PYLORI; MURINE MACROPHAGES;
PULMONARY TUBERCULOSIS; TOXOPLASMA-GONDII; CUTTING EDGE; INFECTION;
EXPRESSION
AB Toll-like receptor (TLR) signaling in macrophages is required for antipathogen responses, including the biosynthesis of nitric oxide from arginine, and is essential for immunity to Mycobacterium tuberculosis, Toxoplasma gondii and other intracellular pathogens. Here we report a 'loophole' in the TLR pathway that is advantageous to these pathogens. Intracellular pathogens induced expression of the arginine hydrolytic enzyme arginase 1 (Arg1) in mouse macrophages through the TLR pathway. In contrast to diseases dominated by T helper type 2 responses in which Arg1 expression is greatly increased by interleukin 4 and 13 signaling through the transcription factor STAT6, TLR-mediated Arg1 induction was independent of the STAT6 pathway. Specific elimination of Arg1 in macrophages favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection.
C1 [El Kasmi, Karim C.; Qualls, Joseph E.; Smith, Amber M.; Kanneganti, Thirumala-Devi; Murray, Peter J.] St Jude Childrens Hosp, Dept Immunol, Memphis, TN 38015 USA.
[Pesce, John T.; Thompson, Robert W.; Wynn, Thomas A.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Henao-Tamayo, Marcela; Basaraba, Randall J.; Orme, Ian M.] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA.
[Koenig, Till] Univ Clin Freiburg, Inst Med Microbiol & Hyg, Dept Microbiol & Hyg, D-79104 Freiburg, Germany.
[Koenig, Till] Univ Clin Erlangen, Inst Clin Microbiol Immunol & Hyg, D-91054 Erlangen, Germany.
[Koo, Mi-Sun; Kaplan, Gilla] Univ Med & Dent New Jersey, Publ Hlth Res Inst Ctr, Lab Mycobacterial Immun & Pathogenesis, Newark, NJ 07103 USA.
[Fitzgerald, Katherine A.] Univ Massachusetts, Sch Med, Dept Immunol & Infect Dis, Worcester, MA 01605 USA.
[El Kasmi, Karim C.; Qualls, Joseph E.; Smith, Amber M.; Murray, Peter J.] St Jude Childrens Hosp, Dept Infect Dis, Memphis, TN 38015 USA.
RP Murray, PJ (reprint author), Univ Colorado Denver, Dept Pediat, Div Gastroenterol & Hepatol, Anschutz Med Campus, Aurora, CO 80045 USA.
EM twynn@niaid.nih.gov; peter.murray@stjude.org
RI Wynn, Thomas/C-2797-2011; Henao-Tamayo, Marcela/D-8189-2017;
OI Henao-Tamayo, Marcela/0000-0002-4249-9650; Bogdan,
Christian/0000-0002-2300-0631; Kanneganti,
Thirumala-Devi/0000-0002-6395-6443; Tuomanen, Elaine/0000-0003-0349-8716
FU Sandler Program for Asthma Research; National Institutes of Health
[AI062921, AI27913, AI66046]; CORE [P30 CA21765]; NIAID; German Research
Foundation; American Lebanese Syrian Associated Charities
FX We thank I. Forster (Technical University of Munich) for the LysMcre
mice; M. Yanagisawa (University of Texas Southwestern) for the Tie2cre
mice; P. Ney (St. Jude Children's Research Hospital) for the CMV-cre
mice; D. Green (St. Jude Children's Research Hospital) and S. Akira
(Osaka University) for the MyD88-deficient mice; S. Morris (University
of Pittsburgh) for the antibodies to Arg1; C. Nathan (Weill Medical
School of Cornell University) for the antibody to iNOS; S. Smale
(University of California, Los Angeles) for the insulated reporter
constructs; D. Bush for nitrotyrosine staining of BCG-infected livers;
Xenogen for construction of luciferase-bearing pneumococci; Ozgene for
microinjection of the targeted Bruce4 cells into C57BL/6 blastocysts and
chimera generation; A. DeFreitas for technical assistance; B. Schulman
for discussions and generation of Supplementary Figure 6b; and M.
Koyanagi and M. Bix for discussion and preliminary infection
experiments. Supported by the Sandler Program for Asthma Research
(P.J.M.), the National Institutes of Health (AI062921 to P.J.M.; AI27913
to E. I. T.; AI66046 to G. K.; CORE grant P30 CA21765 and the NIAID
intramural research program to T. A. W.), the German Research Foundation
(SFB620 project A9 to C. B. and U. S.) and the American Lebanese Syrian
Associated Charities.
NR 50
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD DEC
PY 2008
VL 9
IS 12
BP 1399
EP 1406
DI 10.1038/ni.1671
PG 8
WC Immunology
SC Immunology
GA 372FY
UT WOS:000260888700015
PM 18978793
ER
PT J
AU Yu, PB
Deng, DY
Lai, CS
Hong, CC
Cuny, GD
Bouxsein, ML
Hong, DW
McManus, PM
Katagiri, T
Sachidanandan, C
Kamiya, N
Fukuda, T
Mishina, Y
Peterson, RT
Bloch, KD
AF Yu, Paul B.
Deng, Donna Y.
Lai, Carol S.
Hong, Charles C.
Cuny, Gregory D.
Bouxsein, Mary L.
Hong, Deborah W.
McManus, Patrick M.
Katagiri, Takenobu
Sachidanandan, Chetana
Kamiya, Nobuhiro
Fukuda, Tomokazu
Mishina, Yuji
Peterson, Randall T.
Bloch, Kenneth D.
TI BMP type I receptor inhibition reduces heterotopic ossification
SO NATURE MEDICINE
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; PROGRESSIVA FOP; BONE-FORMATION; SMAD PROTEINS;
DIFFERENTIATION; MOUSE; ACVR1; ALK2; MUTATION; ARREST
AB Fibrodysplasia ossificans progressiva (FOP) is a congenital disorder of progressive and widespread postnatal ossification of soft tissues(1-4) and is without known effective treatments. Affected individuals harbor conserved mutations in the ACVR1 gene that are thought to cause constitutive activation of the bone morphogenetic protein (BMP) type I receptor, activin receptor-like kinase-2 (ALK2)(5). Here we show that intramuscular expression in the mouse of an inducible transgene encoding constitutively active ALK2 (caALK2), resulting from a glutamine to aspartic acid change at amino acid position 207, leads to ectopic endochondral bone formation, joint fusion and functional impairment, thus phenocopying key aspects of human FOP. A selective inhibitor of BMP type I receptor kinases, LDN-193189 (ref. 6), inhibits activation of the BMP signaling effectors SMAD1, SMAD5 and SMAD8 in tissues expressing caALK2 induced by adenovirus specifying Cre (Ad. Cre). This treatment resulted in a reduction in ectopic ossification and functional impairment. In contrast to localized induction of caALK2 by Ad. Cre (which entails inflammation), global postnatal expression of caALK2 (induced without the use of Ad. Cre and thus without inflammation) does not lead to ectopic ossification. However, if in this context an inflammatory stimulus was provided with a control adenovirus, ectopic bone formation was induced. Like LDN-193189, corticosteroid treatment inhibits ossification in Ad.Cre-injected mutant mice, suggesting caALK2 expression and an inflammatory milieu are both required for the development of ectopic ossification in this model. These results support the role of dysregulated ALK2 kinase activity in the pathogenesis of FOP and suggest that small molecule inhibition of BMP type I receptor activity may be useful in treating FOP and heterotopic ossification syndromes associated with excessive BMP signaling.
C1 [Yu, Paul B.; Deng, Donna Y.; Lai, Carol S.; Hong, Deborah W.; McManus, Patrick M.; Sachidanandan, Chetana; Peterson, Randall T.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Div Cardiol, Dept Med, Boston, MA 02114 USA.
[Yu, Paul B.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Anesthesia Ctr Crit Care Res, Boston, MA 02114 USA.
[Yu, Paul B.; Bloch, Kenneth D.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Hong, Charles C.] Vanderbilt Univ, Sch Med, Div Cardiovasc Med, Nashville, TN 37232 USA.
[Hong, Charles C.] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37232 USA.
[Cuny, Gregory D.] Brigham & Womens Hosp, Lab Drug Discovery Neurodegenerat, Harvard NeuroDiscovery Ctr, Cambridge, MA 02139 USA.
[Cuny, Gregory D.] Harvard Univ, Sch Med, Cambridge, MA 02139 USA.
[Bouxsein, Mary L.] Beth Israel Deaconess Med Ctr, Orthopaed Biomech Lab, Boston, MA 02215 USA.
[Bouxsein, Mary L.] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Katagiri, Takenobu] Saitama Med Univ, Div Pathophysiol, Res Ctr Genom Med, Hidaka, Saitama 3501241, Japan.
[Kamiya, Nobuhiro; Fukuda, Tomokazu; Mishina, Yuji] NIEHS, Mol Dev Biol Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Yu, PB (reprint author), Massachusetts Gen Hosp, Div Cardiol, Dept Med, Thier 505,50 Blossom St, Boston, MA 02114 USA.
EM pbyu@partners.org
RI Hong, Charles/C-9989-2010
FU US National Institutes of Health [HL079943, HL074352]; US National
Institute of Environmental Health Sciences Intramural Research Program
[ES071003-10]; Howard Hughes Medical Institute Early Career Award;
GlaxoSmithKline Research & Education Foundation for Cardiovascular
Disease; Center for Research in Fibrodysplasia Ossificans Progressiva
and Related Disorders at the University of Pennsylvania
FX We thank P. ten Dijke (Leiden University Medical Center) for providing
BRE-Luc and CAGA-Luc and K. Miyazono (University of Tokyo) for providing
caALK2, caALK3, caALK4, caALK5, caALK6 and caALK7. We are grateful to H.
Beppu, E. Schipani, H. Kronenberg, A. Wagers, J. Groppe, W. Zapol and F.
Kaplan for insightful discussions and technical expertise, A. Graveline
and D. Panus for technical assistance and E. Buys for technical
expertise. This work was supported by US National Institutes of Health
grants HL079943 (P.B.Y.) and HL074352 (K. D. B.), the US National
Institute of Environmental Health Sciences Intramural Research Program
grant ES071003-10 (Y.M.) and Partners Healthcare. This work was also
supported by a Howard Hughes Medical Institute Early Career Award
(P.B.Y.), a Pulmonary Hypertension Association Mentored Clinical
Scientist Award (P.B.Y.), a grant from the GlaxoSmithKline Research &
Education Foundation for Cardiovascular Disease (P.B.Y.) and a
Developmental Grant from the Center for Research in Fibrodysplasia
Ossificans Progressiva and Related Disorders at the University of
Pennsylvania (C. C. H.).
NR 33
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2008
VL 14
IS 12
BP 1363
EP 1369
DI 10.1038/nm.1888
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 379JX
UT WOS:000261393600021
PM 19029982
ER
PT J
AU Hartley, JL
Salehi-Ashtiani, K
Hill, DE
AF Hartley, James L.
Salehi-Ashtiani, Kourosh
Hill, David E.
TI Proteome expression moves in vitro: resources and tools for harnessing
the human proteome
SO NATURE METHODS
LA English
DT Editorial Material
ID OPEN READING FRAMES; ORFEOME VERSION 1.1; COLLECTION; GENOME
AB Comprehensive sets of clones and improved high-throughput methods for production of functional proteins now allow proteome-scale in vitro experiments on nearly 15,000 human genes.
C1 [Hartley, James L.] NCI, SAIC Frederick, Frederick, MD 21702 USA.
[Salehi-Ashtiani, Kourosh; Hill, David E.] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
[Salehi-Ashtiani, Kourosh; Hill, David E.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Hartley, JL (reprint author), NCI, SAIC Frederick, Frederick, MD 21702 USA.
EM hartley@ncifcrf.gov; kourosh_salehi-ashtiani@dfci.harvard.edu;
david_hill@dfci.harvard.edu
RI Hill, David/B-6617-2011;
OI Salehi-Ashtiani, Kourosh/0000-0002-6521-5243
NR 12
TC 3
Z9 3
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD DEC
PY 2008
VL 5
IS 12
BP 1001
EP 1002
DI 10.1038/nmeth1208-1001
PG 2
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 376WC
UT WOS:000261212700009
PM 19034266
ER
PT J
AU Gould, TJ
Gunewardene, MS
Gudheti, MV
Verkhusha, VV
Yin, SR
Gosse, JA
Hess, ST
AF Gould, Travis J.
Gunewardene, Mudalige S.
Gudheti, Manasa V.
Verkhusha, Vladislav V.
Yin, Shu-Rong
Gosse, Julie A.
Hess, Samuel T.
TI Nanoscale imaging of molecular positions and anisotropies
SO NATURE METHODS
LA English
DT Article
ID OPTICAL RECONSTRUCTION MICROSCOPY; SINGLE MOLECULES; FLUORESCENCE
MICROSCOPY; LOCALIZATION MICROSCOPY; ORIENTATION; PROTEINS; CELLS;
LIMIT; NM
AB Knowledge of the orientation of molecules within biological structures is crucial to understanding the mechanisms of cell function. We present a method to image simultaneously the positions and fluorescence anisotropies of large numbers of single molecules with nanometer lateral resolution within a sample. Based on a simple modification of fluorescence photoactivation localization microscopy (FPALM), polarization (P)-FPALM does not compromise speed or sensitivity. We show results for mouse fibroblasts expressing Dendra2-actin or Dendra2-hemagglutinin.
C1 [Gould, Travis J.; Gunewardene, Mudalige S.; Gudheti, Manasa V.; Hess, Samuel T.] Univ Maine, Dept Phys & Astron, Orono, ME 04469 USA.
[Gould, Travis J.; Gunewardene, Mudalige S.; Gudheti, Manasa V.; Hess, Samuel T.] Univ Maine, Inst Mol Biophys, Orono, ME 04469 USA.
[Verkhusha, Vladislav V.] Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10461 USA.
[Yin, Shu-Rong] NICHHD, Lab Cellular & Mol Biophys, Program Phys Biol, Bethesda, MD 20892 USA.
[Gosse, Julie A.] Univ Maine, Dept Biochem Microbiol & Mol Biol, Orono, ME 04469 USA.
RP Hess, ST (reprint author), Univ Maine, Dept Phys & Astron, 5709 Bennett Hall, Orono, ME 04469 USA.
EM sam.hess@umit.maine.edu
FU US National Institute of Allergy and Infectious Diseases [K25-65459];
National Science Foundation [CHE-0722759]; University of Maine
[GM070358, GM073913]; National Institute of General Medical Sciences
FX We thank C. Fang-Yen, P. Blank, J. Bewersdorf, J. Zimmerberg and M.
Mason for useful discussions, G. Patterson (US National Institute of
Child Health and Human Development) for providing the construct encoding
the PA-GFP protein, J. Shim, J. Rochira and E. Allgeyer for laboratory
assistance, A. McGinn, T. Tripp and P. Byard for professional services.
This work was supported by grants K25-65459 from the US National
Institute of Allergy and Infectious Diseases, CHE-0722759 from the
National Science Foundation, start up funds from the University of Maine
(S. T. H.), and by grants GM070358 and GM073913 from the National
Institute of General Medical Sciences (V. V. V.).
NR 19
TC 75
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U1 3
U2 26
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD DEC
PY 2008
VL 5
IS 12
BP 1027
EP 1030
DI 10.1038/nmeth.1271
PG 4
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 376WC
UT WOS:000261212700016
PM 19011626
ER
PT J
AU Williams, MA
Baker, CI
Op de Beeck, HP
Shim, WM
Dang, S
Triantafyllou, C
Kanwisher, N
AF Williams, Mark A.
Baker, Chris I.
Op de Beeck, Hans P.
Shim, Won Mok
Dang, Sabin
Triantafyllou, Christina
Kanwisher, Nancy
TI Feedback of visual object information to foveal retinotopic cortex
SO NATURE NEUROSCIENCE
LA English
DT Article
ID FEATURE-BASED ATTENTION; CONTEXTUAL MODULATION; FMRI; REPRESENTATIONS;
PATTERNS; AREAS; V1; DISCRIMINATION; STIMULATION; SELECTIVITY
AB The mammalian visual system contains an extensive web of feedback connections projecting from higher cortical areas to lower areas, including primary visual cortex. Although multiple theories have been proposed, the role of these connections in perceptual processing is not understood. We found that the pattern of functional magnetic resonance imaging response in human foveal retinotopic cortex contained information about objects presented in the periphery, far away from the fovea, which has not been predicted by prior theories of feedback. This information was position invariant, correlated with perceptual discrimination accuracy and was found only in foveal, but not peripheral, retinotopic cortex. Our data cannot be explained by differential eye movements, activation from the fixation cross, or spillover activation from peripheral retinotopic cortex or from lateral occipital complex. Instead, our findings indicate that position-invariant object information from higher cortical areas is fed back to foveal retinotopic cortex, enhancing task performance.
C1 [Williams, Mark A.; Triantafyllou, Christina] MIT, McGovern Inst Brain Res, Athinoula A Martinos Imaging Ctr, Cambridge, MA 02139 USA.
[Williams, Mark A.] Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia.
[Baker, Chris I.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Op de Beeck, Hans P.] Katholieke Univ Leuven, Expt Psychol Lab, B-3000 Louvain, Belgium.
[Shim, Won Mok; Kanwisher, Nancy] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Williams, MA (reprint author), MIT, McGovern Inst Brain Res, Athinoula A Martinos Imaging Ctr, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM mark.williams@maccs.mq.edu.au
RI Triantafyllou, Christina/E-7724-2011;
OI Shim, Won Mok/0000-0002-9107-0471; Williams, Mark/0000-0002-3897-5167;
Baker, Chris/0000-0001-6861-8964
FU Australian National Health and Medical Research Council; US National
Institutes of Health [EY013455, EY016159]
FX We would like to thank the members and friends of the Kanwisher
laboratory for useful comments on the manuscript. M. A. W. was supported
by a grant from the Australian National Health and Medical Research
Council (C. J. Martin Fellowship) and H.P.O.d.B. was supported by the
Research Foundation Flanders. This work was supported by grants from the
US National Institutes of Health to N.K. (grants EY013455 and EY016159).
We would also like to thank the Athinoula A. Martinos Imaging Center at
the McGovern Institute for Brain Research for subsidizing the cost of
scanning.
NR 35
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD DEC
PY 2008
VL 11
IS 12
BP 1439
EP 1445
DI 10.1038/nn.2218
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 375JF
UT WOS:000261109300017
PM 18978780
ER
PT J
AU Bonner, WM
Redon, CE
Dickey, JS
Nakamura, AJ
Sedelnikova, OA
Solier, S
Pommier, Y
AF Bonner, William M.
Redon, Christophe E.
Dickey, Jennifer S.
Nakamura, Asako J.
Sedelnikova, Olga A.
Solier, Stephanie
Pommier, Yves
TI OPINION gamma H2AX and cancer
SO NATURE REVIEWS CANCER
LA English
DT Review
ID DOUBLE-STRAND BREAKS; DNA-DAMAGE-RESPONSE; HISTONE H2AX PHOSPHORYLATION;
NUCLEOTIDE EXCISION-REPAIR; TOPOISOMERASE-I INHIBITORS;
IONIZING-RADIATION; GENOMIC INSTABILITY; HUMAN-CELLS;
ATAXIA-TELANGIECTASIA; ATM ACTIVATION
AB Histone H2AX phosphorylation on a serine four residues from the carboxyl terminus (producing gamma H2AX) is a sensitive marker for DNA double-strand breaks (DSBs). DSBs may lead to cancer but, paradoxically, are also used to kill cancer cells. Using gamma H2AX detection to determine the extent of DSB induction may help to detect precancerous cells, to stage cancers, to monitor the effectiveness of cancer therapies and to develop novel anticancer drugs.
C1 [Bonner, William M.; Redon, Christophe E.; Dickey, Jennifer S.; Nakamura, Asako J.; Sedelnikova, Olga A.; Solier, Stephanie; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Bonner, WM (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM bonnerw@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute; Centre for
Cancer Research; National Institutes of Health
FX We thank K. W. Kohn for continuous insights during the course of our
H2AX studies. We thank B.J. Baird, National Cancer Institute, for
critical reading of the manuscript and J. Doroshow for his commitment to
the development of gamma H2AX as a clinical biomarker. The authors are
funded by the Intramural Research Program of the National Cancer
Institute, Centre for Cancer Research, National Institutes of Health.
NR 167
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD DEC
PY 2008
VL 8
IS 12
BP 957
EP 967
DI 10.1038/nrc2523
PG 11
WC Oncology
SC Oncology
GA 375QA
UT WOS:000261127200015
PM 19005492
ER
PT J
AU Caspi, RR
AF Caspi, Rachel R.
TI Immunotherapy of autoimmunity and cancer: the penalty for success
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Article
ID LYMPHOCYTE-ASSOCIATED ANTIGEN-4; REMITTING MULTIPLE-SCLEROSIS; STEM-CELL
TRANSPLANTATION; KOYANAGI-HARADA-DISEASE; ALTERED PEPTIDE LIGAND;
RHEUMATOID-ARTHRITIS; METASTATIC MELANOMA; ANTIBODY BLOCKADE;
TUMOR-REGRESSION; CLINICAL-TRIAL
C1 NEI, NIH, Bethesda, MD 20892 USA.
RP Caspi, RR (reprint author), NEI, NIH, Bethesda, MD 20892 USA.
EM rcaspi@helix.nih.gov
OI Caspi, Rachel/0000-0002-7140-7671
FU Intramural NIH HHS [Z01 EY000184-25]
NR 59
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U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD DEC
PY 2008
VL 8
IS 12
BP 970
EP 976
DI 10.1038/nri2438
PG 7
WC Immunology
SC Immunology
GA 376QD
UT WOS:000261197200016
PM 19008897
ER
PT J
AU Koonin, EV
Wolf, YI
Nagasaki, K
Dolja, VV
AF Koonin, Eugene V.
Wolf, Yuri I.
Nagasaki, Keizo
Dolja, Valerian V.
TI The Big Bang of picorna-like virus evolution antedates the radiation of
eukaryotic supergroups
SO NATURE REVIEWS MICROBIOLOGY
LA English
DT Review
ID DOUBLE-STRANDED-RNA; GROUP-II INTRON; NUCLEOTIDE-SEQUENCE; GENOME
ORGANIZATION; DNA VIRUSES; PLANT-VIRUSES; PHYLOGENETIC ANALYSIS;
CRYSTAL-STRUCTURE; COMMON ANCESTRY; CAPSID PROTEINS
AB The recent discovery of RNA viruses in diverse unicellular eukaryotes and developments in evolutionary genomics have provided the means for addressing the origin of eukaryotic RNA viruses. The phylogenetic analyses of RNA polymerases and helicases presented in this Analysis article reveal close evolutionary relationships between RNA viruses infecting hosts from the Chromalveolate and Excavate supergroups and distinct families of picorna-like viruses of plants and animals. Thus, diversification of picorna-like viruses probably occurred in a 'Big Bang' concomitant with key events of eukaryogenesis. The origins of the conserved genes of picorna-like viruses are traced to likely ancestors including bacterial group II retroelements, the family of HtrA proteases and DNA bacteriophages.
C1 [Dolja, Valerian V.] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA.
[Dolja, Valerian V.] Oregon State Univ, Ctr Genome Res & Biocomp, Corvallis, OR 97331 USA.
[Koonin, Eugene V.; Wolf, Yuri I.] Natl Lib Med, Natl Ctr Biotechnol Informat, Natl Inst Hlth, Bethesda, MD 20894 USA.
[Nagasaki, Keizo] Fisheries Res Agcy, Natl Res Inst Fisheries & Environm Inland Sea, Hiroshima 7390452, Japan.
RP Dolja, VV (reprint author), Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA.
EM koonin@ncbi.nlm.nih.gov; doljav@science.oregonstate.edu
FU Department of Health and Human Services; National Institutes for Health
[GM053190]; BARD [IS-3,784-05]
FX This paper is dedicated to Professor Vadim I. Agol. We thank V. Agol and
T. Senkevich for critical reading of the manuscript and useful comments.
E.V.K. and Y.I.W. are supported by the Department of Health and Human
Services (National Library of Medicine, National Institutes for Health)
intramural research funds. The research in V.V.D.'s laboratory is
partially supported by National Institutes for Health grant GM053190 and
BARD award no. IS-3,784-05.
NR 124
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1740-1526
J9 NAT REV MICROBIOL
JI Nat. Rev. Microbiol.
PD DEC
PY 2008
VL 6
IS 12
BP 925
EP 939
DI 10.1038/nrmicro2030
PG 15
WC Microbiology
SC Microbiology
GA 372LQ
UT WOS:000260903500014
PM 18997823
ER
PT J
AU Paus, T
Keshavan, M
Giedd, JN
AF Paus, Tomas
Keshavan, Matcheri
Giedd, Jay N.
TI OPINION Why do many psychiatric disorders emerge during adolescence?
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID MAGNETIC-RESONANCE-SPECTROSCOPY; HUMAN PREFRONTAL CORTEX; HUMAN
CEREBRAL-CORTEX; MEDIAL TEMPORAL-LOBE; BRAIN-DEVELOPMENT; WHITE-MATTER;
YOUNG-ADULTS; ALCOHOL-USE; DEVELOPMENTAL-CHANGES; COGNITIVE-DEVELOPMENT
AB The peak age of onset for many psychiatric disorders is adolescence, a time of remarkable physical and behavioural changes. The processes in the brain that underlie these behavioural changes have been the subject of recent investigations. What do we know about the maturation of the human brain during adolescence? Do structural changes in the cerebral cortex reflect synaptic pruning? Are increases in white-matter volume driven by myelination? Is the adolescent brain more or less sensitive to reward? Finding answers to these questions might enable us to further our understanding of mental health during adolescence.
C1 [Paus, Tomas] Univ Nottingham, Brain & Body Ctr, Nottingham NG7 2RD, England.
[Paus, Tomas] McGill Univ, Montreal Neurol Inst, Montreal, PQ H2A 3B4, Canada.
[Keshavan, Matcheri] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Keshavan, Matcheri] Harvard Univ, Boston, MA 02115 USA.
[Keshavan, Matcheri] Wayne State Univ, Detroit, MI 48201 USA.
[Giedd, Jay N.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
RP Paus, T (reprint author), Univ Nottingham, Brain & Body Ctr, Nottingham NG7 2RD, England.
EM tomas.paus@nottingham.ac.uk; jgiedd@mail.nih.gov
RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978
FU Canadian Institutes of Health Research; Royal Society, UK; US National
Institutes of Health
FX The authors' work is supported by the Canadian Institutes of Health
Research (T.P.), the Royal Society, UK (T.P.) and the US National
Institutes of Health (T.P., K.M. and J.N.G.).
NR 113
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U2 114
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD DEC
PY 2008
VL 9
IS 12
BP 947
EP 957
DI 10.1038/nrn2513
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 375IV
UT WOS:000261108300016
PM 19002191
ER
PT J
AU Yang, D
Rismanchi, N
Renvoise, B
Lippincott-Schwartz, J
Blackstone, C
Hurley, JH
AF Yang, Dong
Rismanchi, Neggy
Renvoise, Benoit
Lippincott-Schwartz, Jennifer
Blackstone, Craig
Hurley, James H.
TI Structural basis for midbody targeting of spastin by the ESCRT-III
protein CHMP1B
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID FACTOR RECEPTOR DEGRADATION; MIT DOMAIN; CYTOKINESIS; VPS4; RECOGNITION;
AUTOINHIBITION; REQUIREMENTS; COMPONENTS; COMPLEXES; INTERACTS
AB The endosomal sorting complex required for transport (ESCRT) machinery, including ESCRT-III, localizes to the midbody and participates in the membrane-abscission step of cytokinesis. The ESCRT-III protein charged multivesicular body protein 1B (CHMP1B) is required for recruitment of the MIT domain-containing protein spastin, a microtubule-severing enzyme, to the midbody. The 2.5-angstrom structure of the C-terminal tail of CHMP1B with the MIT domain of spastin reveals a specific, high-affinity complex involving a noncanonical binding site between the first and third helices of the MIT domain. The structural interface is twice as large as that of the MIT domain of the VPS4-CHMP complex, consistent with the high affinity of the interaction. A series of unique hydrogen-bonding interactions and close packing of small side chains discriminate against the other ten human ESCRT-III subunits. Point mutants in the CHMP1B binding site of spastin block recruitment of spastin to the midbody and impair cytokinesis.
C1 [Rismanchi, Neggy; Renvoise, Benoit; Blackstone, Craig] NINDS, Cellular Neurol Unit, Neurogenet Branch, Bethesda, MD 20892 USA.
[Yang, Dong; Hurley, James H.] NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA.
[Lippincott-Schwartz, Jennifer] NICHHD, Cell Biol & Metab Program, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Blackstone, C (reprint author), NINDS, Cellular Neurol Unit, Neurogenet Branch, Bethesda, MD 20892 USA.
EM blackstc@ninds.nih.gov; hurley@helix.nih.gov
FU US National Institute of Diabetes and Digestive and Kidney Diseases; US
National Institute of Neurological Disorders and Stroke; US National
Institute of Child Health and Human Development; US National Institutes
of Health (NIH)
FX We thank N. Elia for discussions, the staff of SER-CAT for user support
at the Advance Photon Source (APS), C.-R. Chang for technical
assistance, E. Tyler for generating Figure 6 and D. Davies for comments
on the manuscript. Use of the APS was supported by the US Department of
Energy, Basic Energy Sciences, Office of Science, under Contract No.
W-31-109-Eng-38. This project was funded by the Intramural Research
Programs of US National Institute of Diabetes and Digestive and Kidney
Diseases, US National Institute of Neurological Disorders and Stroke and
the US National Institute of Child Health and Human Development, and the
Bench-to-Bedside program of the US National Institutes of Health (NIH).
NR 39
TC 118
Z9 124
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2008
VL 15
IS 12
BP 1278
EP 1286
DI 10.1038/nsmb.1512
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 379GE
UT WOS:000261383900014
PM 18997780
ER
PT J
AU Lustig, R
Mikkelsen, T
Lesser, G
Grossman, S
Ye, X
Desideri, S
Fisher, J
Wright, J
AF Lustig, Robert
Mikkelsen, Tom
Lesser, Glenn
Grossman, Stuart
Ye, Xiaobu
Desideri, Serena
Fisher, Joy
Wright, John
CA New Approaches Brain Tumor Therapy
TI Phase II preradiation R115777 (tipifarnib) in newly diagnosed GBM with
residual enhancing disease
SO NEURO-ONCOLOGY
LA English
DT Article
DE glioblastoma; radiation; tipifarnib; Zarnestra
ID MALIGNANT GLIOMA; GLIOBLASTOMA-MULTIFORME; RAS PROTEIN; CHEMOTHERAPY;
FARNESYLTRANSFERASE; INHIBITOR; RADIATION; RADIOTHERAPY; TEMOZOLOMIDE;
IRINOTECAN
AB Glioblastoma multiforme (GBM) is a lethal primary malignant brain tumor in adults. R115777 (tipifarnib) is an oral agent with antiproliferative effects, being a potent and selective inhibitor of farnesyltransferase. This multicenter, open-label phase II study was designed to evaluate the efficacy and safety of R115777 given after surgery and prior to radiation in patients with newly diagnosed and residual enhancing GBM. Following surgery, an MRI confirmed the presence of residual enhancing tumor. Patients on enzyme-inducing antiseizure drugs (EIASDs) received 600 mg twice per day, and those not on EIASDs received 300 mg twice per day. One to three monthly cycles of R115777 were administered, and radiation was initiated with progression or after three cycles. A cycle consisted of 3 weeks of continuous R115777 followed by a 1-week rest. MRI was done monthly. The primary end point was overall survival; secondary end points were tumor response rate and toxicity. A total of 28 confirmed GBM patients entered the study; 15 patients (54%) were on EIASDs. The overall median time of survival was 7.7 months. There were no tumor responses. Eight patients (29%) had stable disease as the best response. The study was stopped early due to progression of the disease in 12 patients (48%). A total of 24 patients (85%) were off study before the planned treatment schedule for radiation therapy. R115777 administered prior to radiation therapy in patients with newly diagnosed GBM and residual enhancing disease did not result in any measurable responses or improvement in survival. R115777 administered prior to radiation therapy is not recommended for patients with newly diagnosed GBM. Neuro-Oncology 10, 1004-1009, 2008 (Posted to Neuro-Oncology [serial online], Doc. D07-00186, August 25, 2008. URL http://neuro-oncology.dukejournals.org; DOI: 10.1215/15228517-2008-070)
C1 [Lustig, Robert] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Mikkelsen, Tom] Henry Ford Hlth Syst, Detroit, MI USA.
[Lesser, Glenn] Wake Forest Univ, Ctr Comprehens Canc, Winston Salem, NC 27109 USA.
[Grossman, Stuart; Ye, Xiaobu; Desideri, Serena; Fisher, Joy] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Brain Canc Program, Baltimore, MD USA.
[Wright, John] NCI, Bethesda, MD 20892 USA.
RP Fisher, J (reprint author), NABTT CNS Consortium, David H Koch Canc Res Bldg,Suite IM-16,1550 Orlea, Baltimore, MD 21231 USA.
EM jfisher@jhmi.edu
FU National Cancer Institute, Bethesda [UO1-CA105689, P30-CA0516,
UO1-CA62475]
FX This study was supported by grants UO1-CA105689, P30-CA0516, and
UO1-CA62475 (Central Office Grant, NABTT, CNS Consortium) from the
National Cancer Institute, Bethesda, MD.
NR 27
TC 22
Z9 23
U1 0
U2 3
PU DUKE UNIV PRESS
PI DURHAM
PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2008
VL 10
IS 6
BP 1004
EP 1009
DI 10.1215/15228517-2008-070
PG 6
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 383TG
UT WOS:000261695800008
PM 18725460
ER
PT J
AU Wick, W
Puduvalli, VK
Chamberlain, M
Carpentier, A
Cher, L
Mason, W
Van den Bent, M
Hong, S
Thornton, D
Fine, H
AF Wick, W.
Puduvalli, V. K.
Chamberlain, M.
Carpentier, A.
Cher, L.
Mason, W.
Van den Bent, M.
Hong, S.
Thornton, D.
Fine, H.
TI ENZASTAURIN (ENZ) VERSUS LOMUSTINE (CCNU) IN THE TREATMENT OF RECURRENT,
INTRACRANIAL GLIOBLASTOMA (GBM): A PHASE III STUDY
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 8th Congress of the European-Association-for-Neuro-Oncology (EANO)
CY SEP 12-14, 2008
CL Barcelona, SPAIN
SP European Assoc Neuro Oncol
C1 [Wick, W.] Univ Heidelberg, Heidelberg, Germany.
[Puduvalli, V. K.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Chamberlain, M.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Carpentier, A.] Hop La Pitie Salpetriere, Paris, France.
[Cher, L.] Austin Hlth, Victoria, Australia.
[Mason, W.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Van den Bent, M.] Erasmus MC, Rotterdam, Netherlands.
[Hong, S.; Thornton, D.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
[Fine, H.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU DUKE UNIV PRESS
PI DURHAM
PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2008
VL 10
IS 6
BP 1068
EP 1068
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 383TG
UT WOS:000261695800036
ER
PT J
AU Finger, EC
Mitchell, DGV
Jones, M
Blair, RJR
AF Finger, Elizabeth C.
Mitchell, Derek G. V.
Jones, Matthew
Blair, R. J. R.
TI Dissociable roles of medial orbitofrontal cortex in human operant
extinction learning
SO NEUROIMAGE
LA English
DT Article
DE Frontopolar; Amygdala; Instrumental; Anterior cingulate cortex
ID VENTROMEDIAL PREFRONTAL CORTEX; BASOLATERAL AMYGDALA; FEAR EXTINCTION;
ANTERIOR CINGULATE; EXPECTED OUTCOMES; TASK-PERFORMANCE; RHESUS-MONKEY;
LESIONS; REVERSAL; ACQUISITION
AB Operant extinction, which features modi. cation of instrumental responses to stimuli following a change in associated reinforcement, is an important form of learning for organisms in dynamic environments. Animal studies have highlighted orbital and medial prefrontal cortex and amygdala as mediators of operant extinction. Yet little is known about the neural mediators of operant extinction learning in humans. Using a novel fMRI paradigm, we report dissociable functional responses in distinct regions of medial orbitofrontal cortex (mOFC) during successful appetitive and aversive based operant extinction. During successful operant extinction, increased activity was observed in frontopolar OFC, while decreased activity was observed in caudal mOFC and rostral anterior cingulate cortex (rACC) relative to both (i) successful control trials where the reinforcement associated with the stimulus does not change; and (ii) successful acquisition trials during initial learning of the stimulus-reinforcement associations. Functional connectivity analysis demonstrated inverse connectivity between frontopolar OFC and both rACC and the amygdala. These data support animal models suggesting the importance of mOFC-amygdala interaction during operant extinction and expand our knowledge of the neural systems in humans. These findings suggest that in humans, frontopolar OFC modulates activity in caudal mOFC, rACC and amygdala during successful operant extinction learning. Published by Elsevier Inc.
C1 [Finger, Elizabeth C.] Univ Western Ontario, Dept Clin Neurol Sci, London, ON N6A 5A5, Canada.
[Finger, Elizabeth C.; Mitchell, Derek G. V.; Jones, Matthew; Blair, R. J. R.] NIMH, Mood & Anxiety Disorders Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Mitchell, Derek G. V.] Univ Western Ontario, Dept Psychiat, London, ON N6A 5A5, Canada.
RP Finger, EC (reprint author), Univ Western Ontario, Dept Clin Neurol Sci, London, ON N6A 5A5, Canada.
EM Elizabeth.Finger@lhsc.on.ca
RI Finger, Elizabeth/B-6453-2015
FU National Institute of Mental Health Intramural Research Program
FX This research was funded by the National Institute of Mental Health
Intramural Research Program.
NR 56
TC 20
Z9 21
U1 2
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD DEC
PY 2008
VL 43
IS 4
BP 748
EP 755
DI 10.1016/j.neuroimage.2008.08.021
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 392KA
UT WOS:000262300400010
PM 18793731
ER
PT J
AU Fowler, JS
Volkow, ND
Logan, J
Alexoff, D
Telang, F
Wang, GJ
Wong, C
Ma, YM
Kriplani, A
Pradhan, K
Schlyer, D
Jayne, M
Hubbard, B
Carter, P
Warner, D
King, P
Shea, C
Xu, YW
Muench, L
Apelskog, K
AF Fowler, Joanna S.
Volkow, Nora D.
Logan, Jean
Alexoff, David
Telang, Frank
Wang, Gene-Jack
Wong, Christopher
Ma, Yeming
Kriplani, Aarti
Pradhan, Kith
Schlyer, David
Jayne, Millard
Hubbard, Barbara
Carter, Pauline
Warner, Donald
King, Payton
Shea, Colleen
Xu, Youwen
Muench, Lisa
Apelskog, Karen
TI Fast uptake and long-lasting binding of methamphetamine in the human
brain: Comparison with cocaine
SO NEUROIMAGE
LA English
DT Article
ID DOPAMINE TRANSPORTER; NEUROTOXICITY; ABUSERS; PHARMACOKINETICS; RATS;
MICE; PET; AMPHETAMINE; ADDICTION; EXPOSURE
AB Methamphetamine is one of the most addictive and neurotoxic drugs of abuse. It produces large elevations in extracellular dopamine in the striatum through vesicular release and inhibition of the dopamine transporter. In the U. S. abuse prevalence varies by ethnicity with very low abuse among African Americans relative to Caucasians, differentiating it from cocaine where abuse rates are similar for the two groups. Here we report the first comparison of methamphetamine and cocaine pharmacokinetics in brain between Caucasians and African Americans along with the measurement of dopamine transporter availability in striatum. Methamphetamine's uptake in brain was fast (peak uptake at 9 min) with accumulation in cortical and subcortical brain regions and in white matter. Its clearance from brain was slow (except for white matter which did not clear over the 90 min) and there was no difference in pharmacokinetics between Caucasians and African Americans. In contrast cocaine's brain uptake and clearance were both fast, distribution was predominantly in striatum and uptake was higher in African Americans. Among individuals, those with the highest striatal (but not cerebellar) methamphetamine accumulation also had the highest dopamine transporter availability suggesting a relationship between METH exposure and DAT availability. Methamphetamine's fast brain uptake is consistent with its highly reinforcing effects, its slow clearance with its long-lasting behavioral effects and its widespread distribution with its neurotoxic effects that affect not only striatal but also cortical and white matter regions. The absence of significant differences between Caucasians and African Americans suggests that variables other than methamphetamine pharmacokinetics and bioavailability account for the lower abuse prevalence in African Americans. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Fowler, Joanna S.; Logan, Jean; Alexoff, David; Wang, Gene-Jack; Wong, Christopher; Schlyer, David; Hubbard, Barbara; Carter, Pauline; Warner, Donald; King, Payton; Shea, Colleen; Xu, Youwen; Apelskog, Karen] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
[Fowler, Joanna S.; Wang, Gene-Jack] Mt Sinai Sch Med, New York, NY 10029 USA.
[Fowler, Joanna S.] SUNY Stony Brook, Dept Chem, Stony Brook, NY 11794 USA.
[Volkow, Nora D.] Natl Inst Drug Abuse, Bethesda, MD 20892 USA.
[Volkow, Nora D.; Telang, Frank; Ma, Yeming; Jayne, Millard; Muench, Lisa] NIAAA, Bethesda, MD 20892 USA.
[Kriplani, Aarti; Schlyer, David] SUNY Stony Brook, Dept Biomed Engn, Stony Brook, NY 11974 USA.
[Kriplani, Aarti; Schlyer, David] SUNY Stony Brook, Dept Appl Math & Stat, Stony Brook, NY 11974 USA.
RP Fowler, JS (reprint author), Brookhaven Natl Lab, Dept Med, Bldg 555, Upton, NY 11973 USA.
EM fowler@bnl.gov
OI Logan, Jean/0000-0002-6993-9994
FU Brookhaven National Laboratory [DE-AC02-98CH10886]; U.S. Department of
Energy; Office of Biological and Environmental Research; NIH
[K05DA020001]; NIAAA Intramural program; GCRC [MO1RR10710.]
FX This research was carried out at Brookhaven National Laboratory under
contract DE-AC02-98CH10886 with the U.S. Department of Energy and
supported by its Office of Biological and Environmental Research and by
NIH K05DA020001, the NIAAA Intramural program by GCRC grant #MO1RR10710.
We are grateful to Richard Ferrieri and Michael Schueller for cyclotron
and laboratory operations and to Anat Biegon for helpful discussions. We
also thank the individuals who volunteered for these studies.
NR 36
TC 43
Z9 44
U1 2
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD DEC
PY 2008
VL 43
IS 4
BP 756
EP 763
DI 10.1016/j.neuroimage.2008.07.020
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 392KA
UT WOS:000262300400011
PM 18708148
ER
PT J
AU Nugent, AC
Neumeister, A
Goldman, D
Herscovitch, P
Charney, DS
Drevets, WC
AF Nugent, Allison C.
Neumeister, Alexander
Goldman, David
Herscovitch, Peter
Charney, Dennis S.
Drevets, Wayne C.
TI Serotonin transporter genotype and depressive phenotype determination by
discriminant analysis of glucose metabolism under acute tryptophan
depletion
SO NEUROIMAGE
LA English
DT Article
DE Major depressive disorder; Positron emission tomography; FDG; 5-HTTLPR;
Tryptophan depletion
ID OBSESSIVE-COMPULSIVE DISORDER; POSITRON-EMISSION-TOMOGRAPHY; MEDIAL
PREFRONTAL CORTEX; ANTIDEPRESSANT RESPONSE; MAJOR DEPRESSION; PROMOTER
POLYMORPHISM; BIPOLAR DISORDER; 5-HTTLPR POLYMORPHISM;
BEHAVIORAL-RESPONSES; GENE POLYMORPHISM
AB Acute tryptophan depletion (ATD) putatively results in a transient reduction in central serotonin transmission, and induces depressed mood in some un-medicated subjects with remitted major depressive disorder (MDD). The 5-HT transporter promoter region length polymorphism (5-HTTLPR) has been shown to influence behavioral and metabolic responses to ATD, as well as the risk for developing MDD within the context of stress. The current study investigates the relationships between 5-HTTLPR genotype, neurophysiologic response to ATD, and diagnostic phenotype (healthy control subjects versus MDD subjects differentiated by their depressive response to ATD) using (18)FDG-PET. Un-medicated subjects with remitted MDD and healthy controls were genotyped for the long (l) and short (s) alleles of the 5-HTTLPR polymorphism and categorized into one of three genotypes. On two separate occasions, subjects received either a placebo or an amino acid mixture designed to deplete plasma tryptophan, followed by (18)FDG-PET scanning. Depressive symptoms were rated to determine the diagnostic phenotype. Descriptive and predictive discriminant analyses were performed using brain regional metabolic data to classify according to phenotype and genotype. Overall, 79% of the cases were classified correctly by genotype, and 85% were classified correctly by phenotype. In a leave-one-out cross-validation, 72% of the subjects were classified correctly as carrying an s-allele, and 79% of the subjects were classified correctly by primary diagnosis. The robust nature of the classification results indicates that much of the variance in metabolic response to ATD is accounted for by genotypic and phenotypic category. Published by Elsevier Inc.
C1 [Nugent, Allison C.; Drevets, Wayne C.] NIMH, Mood & Anxiety Disorders Program, Sect Neuroimaging Mood & Anxiety Disorders, NIH, Bethesda, MD 20892 USA.
[Neumeister, Alexander] Yale Univ, Sch Med, Mol Imaging Program Clin Neurosci Div, West Haven, CT 06516 USA.
[Goldman, David] NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA.
[Herscovitch, Peter] NIH, Positron Emiss Tomog Dept, CC, Bethesda, MD 20892 USA.
[Charney, Dennis S.] Mt Sinai Sch Med, New York, NY USA.
RP Nugent, AC (reprint author), NIMH, Mood & Anxiety Disorders Program, Sect Neuroimaging Mood & Anxiety Disorders, NIH, 9 Mem Dr,MSC 0940, Bethesda, MD 20892 USA.
EM nugenta@mail.nih.gov
RI Goldman, David/F-9772-2010;
OI Goldman, David/0000-0002-1724-5405; Nugent, Allison/0000-0003-2569-2480
FU Intramural NIH HHS [Z01 AA000301-09, Z01 AA000306-02, Z01 MH002817-05,
Z99 MH999999]
NR 71
TC 10
Z9 10
U1 4
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD DEC
PY 2008
VL 43
IS 4
BP 764
EP 774
DI 10.1016/j.neuroimage.2008.07.040
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 392KA
UT WOS:000262300400012
PM 18718871
ER
PT J
AU Olive, M
Shatunov, A
Gonzalez, L
Carmona, O
Moreno, D
Quereda, LG
Martinez-Matos, JA
Goldfarb, LG
Ferrer, I
AF Olive, Montse
Shatunov, Alexey
Gonzalez, Laura
Carmona, Olga
Moreno, Dolores
Quereda, Lidia Gonzalez
Martinez-Matos, J. A.
Goldfarb, Lev G.
Ferrer, Isidro
TI Transcription-terminating mutation in telethonin causing autosomal
recessive muscular dystrophy type 2G in a European patient
SO NEUROMUSCULAR DISORDERS
LA English
DT Article
DE LGMD 2G; Telethonin; TCAP mutation; Europe
ID SARCOMERIC PROTEIN TELETHONIN; HYPERTROPHIC CARDIOMYOPATHY; DILATED
CARDIOMYOPATHY; SKELETAL-MUSCLE; TITIN; PHENOTYPE
AB A 27-year-old woman of Moldavian origin presented at the age of 15 with progressive proximal limb weakness and painful cramps in her calf muscles. Clinical examination revealed prominent Muscle weakness in proximal muscles of the lower extremities and distal anterior compartment of legs, and mild weakness in shoulder girdle muscles. In addition, she had marked calf hypertrophy, Muscle atrophy involving the anterior and posterior compartments of the thighs, and the distal anterior compartment of legs, as well as mild scapular winging and hyperlordosis. A muscle biopsy taken from the biceps brachii showed mild dystrophic changes, absent vacuoles, and abundant lobulated fibers. Immunofluorescence and Western blot assays demonstrated complete telethonin deficiency. Molecular analysis revealed a homozygous Trp25X mutation in the telethonin (TCAP) gene resulting in termination of transcription at an early point. Four families from Brazil with telethonin deficiency have previously been reported and classified as LMD2G, but the actual frequency of this disease is unknown. With this current identification of a case outside the Brazilian Population, telethonin mutation-associated LGMD should be considered worldwide. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Olive, Montse; Gonzalez, Laura; Moreno, Dolores; Ferrer, Isidro] Bellvitge Hosp, IDIBELL, Inst Neuropatol, Barcelona 08907, Spain.
[Olive, Montse; Gonzalez, Laura; Moreno, Dolores; Ferrer, Isidro] Hosp Llobregat, CIBERNED, Barcelona 08907, Spain.
[Shatunov, Alexey; Goldfarb, Lev G.] NINDS, NIH, Bethesda, MD 20892 USA.
[Carmona, Olga] Hosp Figueres, Serv Neurol, Girona, Spain.
[Quereda, Lidia Gonzalez] Univ Autonoma Barcelona, CIBERER, Hosp St Pau, Serv Genet, E-08193 Barcelona, Spain.
[Martinez-Matos, J. A.] Hosp Llobregat, Bellvitge Hosp, Serv Neurol, Barcelona, Spain.
RP Olive, M (reprint author), Bellvitge Hosp, IDIBELL, Inst Neuropatol, Feixa Llargo S-N, Barcelona 08907, Spain.
EM 25169mop@comb.es
RI Shatunov, Aleksey/E-6946-2011;
OI Olive, Montse/0000-0001-5727-0165
FU F.I.S. [PI051213]; National Institute of Neurological Disorders and
Stroke; National Institutes of Health
FX The authors are grateful to the members of the affected family for
enthusiastic participation in the study. This research was supported by
F.I.S. Grant PI051213 (M.O.) and in part by the Intramural Research
Program of the National Institute of Neurological Disorders and Stroke,
National Institutes of Health (A.S. and L.C.C.). We thank Tom Yohanann
for editorial advice.
NR 18
TC 25
Z9 26
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD DEC
PY 2008
VL 18
IS 12
BP 929
EP 933
DI 10.1016/j.nmd.2008.07.009
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 388ZP
UT WOS:000262059600003
PM 18948002
ER
PT J
AU Hiranita, T
Nawata, Y
Sakimura, K
Yamamoto, T
AF Hiranita, Takato
Nawata, Yoko
Sakimura, Katsuya
Yamamoto, Tsuneyuki
TI Methamphetamine-seeking behavior is due to inhibition of nicotinic
cholinergic transmission by activation of cannabinoid CB1 receptors
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Cannabinoid CB1 receptors; Craving; Drug-seeking behavior;
Methamphetamine; Nicotinic ACh receptors; Relapse
ID MEDIAL-PREFRONTAL CORTEX; VENTRAL TEGMENTAL AREA;
ACETYLCHOLINE-RECEPTORS; COCAINE-SEEKING; NUCLEUS-ACCUMBENS; INDUCED
REINSTATEMENT; BASOLATERAL AMYGDALA; RATS; ANTAGONIST; REWARD
AB We previously reported the involvement of cannabinoid CB1 receptors (CB1Rs) and nicotinic acetylcholine receptors (nAChRs) in the reinstatement of methamphetamine (MAP)-seeking behavior (lever-pressing response for MAP reinforcement under saline infusion). The present study examined whether the reinstatement involves interactions between these receptors. Rats were trained to self-administer MAP with a light and tone (MAP-associated cues). Then, extinction sessions under saline infusion without cues were conducted. After that, a reinstatement tests were conducted by either presenting the Cues or a MAP-priming injection. Systemic and intracranial administration of HU210, a cannabinoid CB1R agonist, into the nucleus accumbens core (NAC) and prelimbic cortex (PrC) reinstated MAP-seeking behavior. The reinstatement caused by the systemic HU210 treatment was attenuated by intracranial administration of AM251, a cannabinoid CB1R antagonist, into each region mentioned above. Meanwhile, reinstatement induced by the MAP-associated cues and MAP-priming injection was also attenuated by intracranial administration of AM251 in each region. In these regions, the attenuating effects of AM251 on the reinstatement induced by each stimulus were blocked by the intracranial administration of mecamylamine, a non-selective nAChR antagonist, but not by scopolamine, a muscarinic ACh receptor (mAChR) antagonist. Furthermore. the intracranial administration of DH beta E, an alpha 4 beta 2 nAChR antagonist, but not MLA, an alpha 7 nAChR antagonist, into each region blocked the AM251-induced attenuation of the reinstatement. These findings suggest that relapses to MAP-seeking behavior may be due to two steps, first inhibition of ACh transmission by the activation of cannabinoid CB1Rs and then the inactivation of alpha 4 beta 2 nAChRs. (C) 2008 Elsevier Ltd. Ail rights reserved.
C1 [Hiranita, Takato; Nawata, Yoko; Yamamoto, Tsuneyuki] Nagasaki Int Univ, Fac Pharmaceut Sci, Dept Pharmacol, Nagasaki 8593298, Japan.
[Hiranita, Takato; Sakimura, Katsuya] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Pharmacol, Higashi Ku, Fukuoka 8128582, Japan.
[Hiranita, Takato] NIDA, NIH, Psychobiol Sect,Dept Hlth & Human Serv, Medicat Discovery Res Branch,Intramural Res Progr, Baltimore, MD 21224 USA.
RP Yamamoto, T (reprint author), Nagasaki Int Univ, Fac Pharmaceut Sci, Dept Pharmacol, 2825-7 Huis 10 Bosch, Nagasaki 8593298, Japan.
EM tyamamot@niu.ac.jp
RI Hiranita, Takato/G-6567-2011
FU Ministry of Education, Culture, Sports, Science and Technology; Ministry
of Health, Labor, and Welfare and Japan; Smoking Research Foundation,
Japan
FX We thank Dr. Paul L. Soto, National Institute on Drug Abuse, for
checking grammar and spelling of this manuscript. This study was
supported by Grants-in-Aid for scientific research from the Ministry of
Education, Culture, Sports, Science and Technology, the Ministry of
Health, Labor, and Welfare and Japan and Smoking Research Foundation,
Japan.
NR 36
TC 14
Z9 14
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD DEC
PY 2008
VL 55
IS 8
BP 1300
EP 1306
DI 10.1016/j.neuropharm.2008.08.012
PG 7
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 384LP
UT WOS:000261746600007
PM 18782581
ER
PT J
AU Kenworthy, L
Yerys, BE
Anthony, LG
Wallace, GL
AF Kenworthy, Lauren
Yerys, Benjamin E.
Anthony, Laura Gutermuth
Wallace, Gregory L.
TI Understanding Executive Control in Autism Spectrum Disorders in the Lab
and in the Real World
SO NEUROPSYCHOLOGY REVIEW
LA English
DT Review
DE Executive function; Autism; Ecological validity; Asperger's; Cognitive
control; Neuropsychology
ID HIGH-FUNCTIONING AUTISM; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; CARD
SORTING TEST; BEHAVIOR RATING INVENTORY; SPATIAL WORKING-MEMORY;
TRAUMATIC BRAIN-INJURY; FRONTAL-LOBE DAMAGE; ECOLOGICAL VALIDITY;
DYSEXECUTIVE SYNDROME; PREFRONTAL CORTEX
AB In this paper, we review the most recent and often conflicting findings on conventional measures of executive control in autism spectrum disorders. We discuss the obstacles to accurate measurement of executive control, such as: its prolonged developmental trajectory; lack of consensus on its definition and whether it is a unitary construct; the inherent complexity of executive control; and the difficulty measuring executive-control functions in laboratory or clinical settings. We review the potential of an ecological-validity framework to address some of these problems, and describe new tests claiming verisimilitude, or close resemblance to "real life" demands. We also review the concept of veridicality, which allows for the measurement of the ecological validity of any task, and discuss the few Studies addressing ecological validity in individuals with autism. Our review suggests that a multi-source approach emphasizing veridicality may provide the most comprehensive assessment of executive control in autism.
C1 [Kenworthy, Lauren] Childrens Natl Med Ctr, Ctr Autism Spectrum Disorders, Rockville, MD 20850 USA.
[Kenworthy, Lauren; Yerys, Benjamin E.; Anthony, Laura Gutermuth] Childrens Natl Med Ctr, Ctr Autism Spectrum Disorders, Childrens Res Inst Neurosci, Washington, DC 20010 USA.
[Kenworthy, Lauren; Anthony, Laura Gutermuth] George Washington Univ, Sch Med & Hlth Sci, Dept Psychiat & Behav Sci, Washington, DC 20052 USA.
[Kenworthy, Lauren; Wallace, Gregory L.] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
RP Kenworthy, L (reprint author), Childrens Natl Med Ctr, Ctr Autism Spectrum Disorders, 14801 Phys Lane,Suite 173, Rockville, MD 20850 USA.
EM lkenwort@cnmc.org
OI Wallace, Gregory/0000-0003-0329-5054
FU Organization for Autism Research; Isadore and Bertha Gudelsky Family
Foundation; Intramural Research Program of the NIMH; Intellectual and
Developmental Disabilities Research Center [P30HD40677]
FX We thank Alex Martin for his review and helpful comments on this
manuscript and Richard B. Roberson III and Kathryn F. Jankowski for
assistance with its preparation. We also thank the people with autism
and their families who have educated us over the years. The views
expressed in this article are those of the authors and do not
necessarily reflect the official position of the National Institute of
Mental Health (NIMH), the National Institutes of Health, or any part of
the U.S. Department of Health and Human Services. Mention of trade
names, commercial products, or organizations does not imply endorsement
by the U.S. government. LK is supported by all award from The Isadore
and Bertha Gudelsky Family Foundation and the Intramural Research
Program of the NIMH. LA is Supported by awards from the Organization for
Autism Research and The Isadore and Bertha Gudelsky Family Foundation.
GLW is supported by the Intramural Research Program of the NIMH. BEY is
supported by the Intellectual and Developmental Disabilities Research
Center (NIH IDDRC P30HD40677).
NR 140
TC 128
Z9 128
U1 10
U2 54
PU CONSULTANTS BUREAU/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1040-7308
J9 NEUROPSYCHOL REV
JI Neuropsychol. Rev.
PD DEC
PY 2008
VL 18
IS 4
BP 320
EP 338
DI 10.1007/s11065-008-9077-7
PG 19
WC Psychology, Clinical; Neurosciences
SC Psychology; Neurosciences & Neurology
GA 400HJ
UT WOS:000262858300006
PM 18956239
ER
PT J
AU Bigos, KL
Pollock, BG
Aizenstein, HJ
Fisher, PM
Bies, RR
Hariri, AR
AF Bigos, Kristin L.
Pollock, Bruce G.
Aizenstein, Howard J.
Fisher, Patrick M.
Bies, Robert R.
Hariri, Ahmad R.
TI Acute 5-HT Reuptake Blockade Potentiates Human Amygdala Reactivity
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE citalopram; SSRI; serotonin; amygdala; functional MRI; healthy subjects
ID SEROTONIN TRANSPORTER; GENETIC-VARIATION; FEAR; RESPONSES; ATLAS; RISK;
FMRI
AB Variability in serotonin (5-HT) function is associated with individual differences in normal mood and temperament, as well as psychiatric illnesses, all of which are influenced by amygdala function. This study evaluated the acute effects of 5-HT reuptake blockade on amygdala function using pharmacological functional MRI. Eight healthy men completed a double-blind balanced crossover study with the selective 5-HT reuptake inhibitor, citalopram (20 mg infused over 30 min), and normal saline. Amygdala reactivity in response to novel facial expressions was assessed on three successive scans, once before drug/placebo infusion, once early in the infusion, and once at the end of infusion. Acute citalopram administration resulted in concentration-dependent increases in human amygdala reactivity to salient stimuli. The current pattern of 5-HT-mediated amygdala reactivity may represent an important pathway through which SSRIs achieve an antidepressant effect. Intriguingly, our data may also reveal a mechanism contributing to clinical observations of extreme agitation, restlessness, and suicidal ideation in some individuals during acute SSRI treatment. Developing a comprehensive model of how 5-HT modulates human amygdala reactivity supporting behavioral and physiological arousal will be instrumental for our understanding of basic neurobehavioral processes, their dysfunction in psychiatric illnesses, and their contribution to mechanism of treatment response.
C1 [Bigos, Kristin L.; Bies, Robert R.] Univ Pittsburgh, Dept Pharmaceut Sci, Pittsburgh, PA 15260 USA.
[Pollock, Bruce G.] Univ Toronto, Rotman Res Inst, Ctr Addict & Mental Hlth, Toronto, ON M5S 1A1, Canada.
[Pollock, Bruce G.; Aizenstein, Howard J.; Bies, Robert R.; Hariri, Ahmad R.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Fisher, Patrick M.] Univ Pittsburgh, Ctr Neurosci, Pittsburgh, PA 15260 USA.
RP Bigos, KL (reprint author), NIMH, Clin Brain Disorders Branch, 10 Ctr Dr,Room 3C101, Bethesda, MD 20892 USA.
EM bigosk@mail.nih.gov
RI Bigos, Kristin/E-9768-2010; Hariri, Ahmad/D-5761-2011
OI Fisher, Patrick/0000-0002-8115-0611;
FU NIH [F31MH076420, K24MH065416, K23MH064678, K01MH072837, P41EB001975];
NARSAD; General Clinical Research Center of the University of Pittsburgh
Medical Center [MO1RR000056]; University of Pittsburgh Magnetic
Resonance Research Center
FX This research study was supported by NIH F31MH076420, K24MH065416,
K23MH064678, K01MH072837, P41EB001975, and NARSAD. Support was also
provided by the General Clinical Research Center of the University of
Pittsburgh Medical Center (MO1RR000056) and the University of Pittsburgh
Magnetic Resonance Research Center Pilot Imaging Program.
NR 22
TC 94
Z9 94
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2008
VL 33
IS 13
BP 3221
EP 3225
DI 10.1038/npp.2008.52
PG 5
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 370GP
UT WOS:000260751000023
PM 18463627
ER
PT J
AU Noronha, A
Harris, RA
AF Noronha, Antonio
Harris, R. Adron
TI Maharaj K Ticku, 1948-2007 Obituary
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Biographical-Item
C1 [Noronha, Antonio] NIAAA, Bethesda, MD USA.
[Harris, R. Adron] Univ Texas Austin, Austin, TX 78712 USA.
RP Noronha, A (reprint author), NIAAA, Bethesda, MD USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2008
VL 33
IS 13
BP 3247
EP 3247
DI 10.1038/npp.2008.25
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 370GP
UT WOS:000260751000027
ER
PT J
AU Fields, RD
AF Fields, R. Douglas
TI Oligodendrocytes Changing the Rules: Action Potentials in Glia and
Oligodendrocytes Controlling Action Potentials
SO NEUROSCIENTIST
LA English
DT Article
DE Myelin; Oligodendrocyte; Ischemia; Conduction velocity; Spike timing
plasticity; DTI; Hippocampus; OPC
ID CNS WHITE-MATTER; PROGENITOR CELLS; NMDA RECEPTORS; ION CHANNELS; AXONS;
MYELINATION; GLUTAMATE; IMPULSES; ISCHEMIA; RELEASE
AB Two long-standing rules in cellular neuroscience must now be amended with the publication of two studies on myelin-forming glia in the CNS: 1) Neurons can no longer be considered the only cells that fire electric impulses in the brain. 2) Synapses between neurons are not the only way electrical information is regulated as it propagates through neural circuits: oligodendrocytes can cause rapid activity-dependent changes in spike latency. A category of oligodendrocyte precursor cells (OPCs) has been identified that can fire action potentials, and their excitation is driven by synapses from axons. This finding has relevance to excitotoxicity in ischemia, but the normal function may be to regulate myelination according to functional activity in axons. A second study reveals that action potential propagation through CNS axons can be rapidly regulated by oligodendrocytes. Mature oligodendrocytes in the rat hippocampus are depolarized by theta burst stimulation of axons, and when the oligodendrocytes are depolarized by current injection in paired whole-cell recordings with CA1 pyramidal neurons, the latency of impulse conduction through the axons it ensheathes rapidly decreases. This unprecedented finding suggests a dynamic role for myelin in regulating impulse transmission through axons, promoting neural synchrony among the multiple axons under the domain of an individual oligodendrocyte. NEUROSCIENTIST 14(6):540-543, 2008. DOI: 10.1177/1073858408320294
C1 NICHD, Nervous Syst Dev & Plast Sect, NIH, Bethesda, MD 20892 USA.
RP Fields, RD (reprint author), NICHD, Nervous Syst Dev & Plast Sect, NIH, Bldg 35,Room 2A211,MSC 3713,35 Lincoln Dr, Bethesda, MD 20892 USA.
EM fieldsd@mail.nih.gov
FU NIH
FX Supported by the NIH intramural program.
NR 28
TC 42
Z9 44
U1 2
U2 10
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
J9 NEUROSCIENTIST
JI Neuroscientist
PD DEC
PY 2008
VL 14
IS 6
BP 540
EP 543
DI 10.1177/1073858408320294
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 375DY
UT WOS:000261095500009
PM 19029057
ER
PT J
AU Berezovskaya, FS
Novozhilov, AS
Karev, GP
AF Berezovskaya, Faina S.
Novozhilov, Artem S.
Karev, Georgy P.
TI Families of traveling impulses and fronts in some models with
cross-diffusion
SO NONLINEAR ANALYSIS-REAL WORLD APPLICATIONS
LA English
DT Article
DE Keller-Segel model; traveling wave solutions; cross-diffusion
ID REINFORCED RANDOM-WALKS; WAVES; CHEMOTAXIS; EQUATIONS; TAXIS; DYNAMICS;
SYSTEM; CELLS
AB Analysis of traveling wave solutions of partial differential equation (PDE) systems with cross-diffusion is presented. The systems under study fall in a general class of the classical Keller-Segel models to describe chemotaxis. The analysis is conducted using the theory of the phase plane analysis of the corresponding wave systems without a priory restrictions on the boundary conditions of the initial PDE. Special attention is paid to families of traveling wave solutions. Conditions for existence of front-impulse, impulse-front, and front-front traveling wave solutions are formulated. In particular, the simplest mathematical model is presented that has an impulse-impulse solution; we also show that a non-isolated singular point in the ordinary differential equation (ODE) wave system implies existence of free-boundary fronts. The results can be used for construction and analysis of different mathematical models describing systems with chemotaxis. Published by Elsevier Ltd.
C1 [Novozhilov, Artem S.; Karev, Georgy P.] NIH, Bethesda, MD 20894 USA.
[Berezovskaya, Faina S.] Howard Univ, Washington, DC 20059 USA.
RP Karev, GP (reprint author), NIH, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM karev@ncbi.nlm.nih.gov
RI Novozhilov, Artem/D-7544-2012; Novozhilov, Artem/C-9248-2013
OI Novozhilov, Artem/0000-0001-5469-2557
NR 26
TC 9
Z9 9
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1468-1218
J9 NONLINEAR ANAL-REAL
JI Nonlinear Anal.-Real World Appl.
PD DEC
PY 2008
VL 9
IS 5
BP 1866
EP 1881
DI 10.1016/j.nonrwa.2007.06.001
PG 16
WC Mathematics, Applied
SC Mathematics
GA 345UY
UT WOS:000259023900004
ER
PT J
AU Koonin, EV
Wolf, YI
AF Koonin, Eugene V.
Wolf, Yuri I.
TI Genomics of bacteria and archaea: the emerging dynamic view of the
prokaryotic world
SO NUCLEIC ACIDS RESEARCH
LA English
DT Review
ID HORIZONTAL GENE-TRANSFER; 2-COMPONENT SIGNAL-TRANSDUCTION; PROVIDES
ACQUIRED-RESISTANCE; UNIVERSAL COMMON ANCESTOR; ESCHERICHIA-COLI
O157-H7; DEINOCOCCUS-RADIODURANS; EVOLUTIONARY GENOMICS; PHYLOGENETIC
TREES; SELFISH OPERONS; PROTEIN-KINASES
AB The first bacterial genome was sequenced in 1995, and the first archaeal genome in 1996. Soon after these breakthroughs, an exponential rate of genome sequencing was established, with a doubling time of approximately 20 months for bacteria and approximately 34 months for archaea. Comparative analysis of the hundreds of sequenced bacterial and dozens of archaeal genomes leads to several generalizations on the principles of genome organization and evolution. A crucial finding that enables functional characterization of the sequenced genomes and evolutionary reconstruction is that the majority of archaeal and bacterial genes have conserved orthologs in other, often, distant organisms. However, comparative genomics also shows that horizontal gene transfer (HGT) is a dominant force of prokaryotic evolution, along with the loss of genetic material resulting in genome contraction. A crucial component of the prokaryotic world is the mobilome, the enormous collection of viruses, plasmids and other selfish elements, which are in constant exchange with more stable chromosomes and serve as HGT vehicles. Thus, the prokaryotic genome space is a tightly connected, although compartmentalized, network, a novel notion that undermines the Tree of Life model of evolution and requires a new conceptual framework and tools for the study of prokaryotic evolution.
C1 [Koonin, Eugene V.; Wolf, Yuri I.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM koonin@ncbi.nlm.nih.gov
RI asif, huma/C-1441-2012
FU DHHS (National Library of Medicine)
FX DHHS (National Library of Medicine) intramural funds. Funding for open
access charge: DHHS (National Library of Medicine) intramural funds.
NR 277
TC 326
Z9 339
U1 12
U2 87
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC
PY 2008
VL 36
IS 21
BP 6688
EP 6719
DI 10.1093/nar/gkn668
PG 32
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 378CW
UT WOS:000261299700005
PM 18948295
ER
PT J
AU Guillier, M
Gottesman, S
AF Guillier, Maude
Gottesman, Susan
TI The 5 end of two redundant sRNAs is involved in the regulation of
multiple targets, including their own regulator
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ESCHERICHIA-COLI K-12; SMALL NONCODING RNAS; MESSENGER-RNA;
OUTER-MEMBRANE; POSTTRANSCRIPTIONAL REGULATION; GLUCOSE-TRANSPORTER;
VIBRIO-CHOLERAE; TERMINAL HALF; IN-VIVO; HFQ
AB Small RNAs are widespread regulators of gene expression in numerous organisms. This study describes the mode of action of two redundant Escherichia coli sRNAs, OmrA and OmrB, that downregulate the expression of multiple targets, most of which encode outer membrane proteins. Our results show that both sRNAs directly interact with at least two of these target mRNAs, ompT and cirA, in the vicinity of the translation initiation region, consistent with control of these targets being dependent on both Hfq and RNase E. Interestingly, these interactions depend on short stretches of complementarity and involve the conserved 5 end of OmrA/B. A mutation in this region abolishes control of all OmrA/B targets tested thus far, thereby highlighting the crucial role of the OmrA/B 5 end. This allowed us, by looking for mRNA sequences complementary to the OmrA/B 5 end, to identify ompR as an additional direct target of these two sRNAs. Since the OmpR transcriptional regulator activates expression of both omrA and omrB genes, this newly identified control should result in an autoregulatory loop limiting the amount of OmrA/B sRNAs.
C1 [Guillier, Maude; Gottesman, Susan] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Gottesman, S (reprint author), NCI, Mol Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM susang@helix.nih.gov
FU The Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research
FX The Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. Funding for open access charge: Intramural
Research program of the NIH.
NR 51
TC 85
Z9 85
U1 0
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC
PY 2008
VL 36
IS 21
BP 6781
EP 6794
DI 10.1093/nar/gkn742
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 378CW
UT WOS:000261299700011
PM 18953042
ER
PT J
AU Christensen, LA
Wang, H
Van Houten, B
Vasquez, KM
AF Christensen, Laura A.
Wang, Hong
Van Houten, Bennett
Vasquez, Karen M.
TI Efficient processing of TFO-directed psoralen DNA interstrand crosslinks
by the UvrABC nuclease
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID NUCLEOTIDE EXCISION-REPAIR; TRIPLE-HELIX FORMATION; ACTION MECHANISM;
RECOGNITION; UVRB; INCISION; BINDING; DAMAGE; SITE; OLIGONUCLEOTIDE
AB Photoreactive psoralens can form interstrand crosslinks (ICLs) in double-stranded DNA. In eubacteria, the endonuclease UvrABC plays a key role in psoralen ICLs. Psoralen-modified triplex-forming oligonucleotides (TFOs) can be used to direct ICLs to specific genomic sites. Previous of pyrimidine-rich methoxypsoralen-modified TFOs indicated that the TFO inhibits cleavage by UvrABC. Because different chemistries may alter the processing of TFO-directed ICLs, we investigated the effect of another type of triplex formed by purine-rich TFOs on the processing of 4'-(hydroxymethyl)-4,5',8-trimethylpsoralen (HMT) ICLs by the UvrABC nuclease. Using an HMT-modified TFO to direct ICLs to a specific site, we found that UvrABC made incisions on the purine-rich strand of the duplex similar to 3 bases from the 3'-side and similar to 9 bases from the 5'-side of the ICL, within the region. In contrast to previous reports, the UvrABC nuclease cleaved the TFO-directed psoralen ICL with a greater efficiency than that of the psoralen ICL alone. Furthermore, the TFO was dissociated from its duplex binding site by UvrA and UvrB. As mutagenesis by TFO-directed ICLs requires nucleotide excision repair, the efficient of these lesions supports the use of triplex technology to direct DNA damage for genome modification.
C1 [Christensen, Laura A.; Vasquez, Karen M.] Univ Texas MD Anderson Canc Ctr, Div Sci Pk Res, Dept Carcinogenesis, Smithville, TX USA.
[Wang, Hong; Van Houten, Bennett] Natl Inst Environm Hlth Sci, Mol Genet Lab, Res Triangle Pk, NC USA.
RP Vasquez, KM (reprint author), Univ Texas MD Anderson Canc Ctr, Div Sci Pk Res, Dept Carcinogenesis, Smithville, TX USA.
EM kvasquez@mdanderson.org
RI Wang, Hong/F-3164-2014
OI Wang, Hong/0000-0003-0165-3559
FU National Institutes of Health/National Cancer Institute [CA097175,
CA093729]; National Institutes of Environmental Health Sciences Center
[ES007784]; [P01 CA097175]
FX National Institutes of Health/National Cancer Institute (CA097175 and
CA093729 to K. M. V.); National Institutes of Environmental Health
Sciences Center (ES007784). Funding for open access charge: P01
CA097175.
NR 39
TC 15
Z9 15
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC
PY 2008
VL 36
IS 22
BP 7136
EP 7145
DI 10.1093/nar/gkn880
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386SY
UT WOS:000261904100023
PM 18996898
ER
PT J
AU Rossi, M
Demidov, ON
Anderson, CW
Appella, E
Mazur, SJ
AF Rossi, Matteo
Demidov, Oleg N.
Anderson, Carl W.
Appella, Ettore
Mazur, Sharlyn J.
TI Induction of PPM1D following DNA-damaging treatments through a conserved
p53 response element coincides with a shift in the use of transcription
initiation sites
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID TARGET GENE ACTIVATION; GENOME-WIDE ANALYSIS; WILD-TYPE P53;
BINDING-PROTEIN; HISTONE ACETYLATION; IONIZING-RADIATION; SIGNALING
PATHWAYS; GENOTOXIC STRESS; HUMAN-CELLS; IN-VIVO
AB PPM1D (Wip1), a type PP2C phosphatase, is expressed at low levels in most normal tissues but is overexpressed in several types of cancers. In cells containing wild-type p53, the levels of PPM1D mRNA and protein increase following exposure to genotoxic stress, but the mechanism of regulation by p53 was unknown. PPM1D also has been identified as a CREB-regulated gene due to the presence of a cyclic AMP response element (CRE) in the promoter. Transient transfection and chromatin immunoprecipitation experiments in HCT116 cells were used to characterize a conserved p53 response element located in the 5' untranslated region (UTR) of the PPM1D gene that is required for the p53-dependent induction of transcription from the human PPM1D promoter. CREB binding to the CRE contributes to the regulation of basal expression of PPM1D and directs transcription initiation at upstream sites. Following exposure to ultraviolet (UV) or ionizing radiation, the abundance of transcripts with short 5' UTRs increased in cells containing wild-type p53, indicating increased utilization of downstream transcription initiation sites. In cells containing wild-type p53, exposure to UV resulted in increased PPM1D protein levels even when PPM1D mRNA levels remained constant, indicating post-transcriptional regulation of PPM1D protein levels.
C1 [Rossi, Matteo; Demidov, Oleg N.; Appella, Ettore; Mazur, Sharlyn J.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Anderson, Carl W.] Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA.
RP Mazur, SJ (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM mazurs@mail.nih.gov
OI Demidov, Oleg/0000-0003-4323-7174
FU Intramural Research Program of the National Institutes of Health; Center
for Cancer Research; National Cancer Institute; Brookhaven National
Laboratory; Office of Biological and Environmental Research of the US
Department of Energy
FX The Intramural Research Program of the National Institutes of Health,
Center for Cancer Research, National Cancer Institute; a Laboratory
Directed Research and Development Award at the Brookhaven National
Laboratory and the Low Dose Program of the Office of Biological and
Environmental Research of the US Department of Energy (to C. W. A.).
NR 82
TC 37
Z9 38
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC
PY 2008
VL 36
IS 22
BP 7168
EP 7180
DI 10.1093/nar/gkn888
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386SY
UT WOS:000261904100026
PM 19015127
ER
PT J
AU Agurs-Collins, T
Khoury, MJ
Simon-Morton, D
Olster, DH
Harris, JR
Milner, JA
AF Agurs-Collins, Tanya
Khoury, Muin J.
Simon-Morton, Denise
Olster, Deborah H.
Harris, Jennifer R.
Milner, John A.
TI Public Health Genomics: Translating Obesity Genomics Research Into
Population Health Benefits
SO OBESITY
LA English
DT Article; Proceedings Paper
CT Gene-Nutrition and Gene-Nutrition and Gene-Physical Activitity
Interactions in the Etiology of Obesity Workshop
CY SEP 24-26, 2007
CL Bethesda, MD
SP NIH, Natl Canc Inst, Div Canc Control & Populat Sci, NCI Div Nutr Sci, NIH Off Behav & Social Sci Res, Natl Heart, Lung & Blood Inst
ID GENE-ENVIRONMENT INTERACTION; BODY-MASS INDEX; VARIANCE-COMPONENTS
MODELS; FTO GENE; ADULT OBESITY; PHYSICAL-ACTIVITY; WIDE ASSOCIATION;
EATING BEHAVIOR; COMMON DISEASES; LIFE-STYLE
AB We examine how a public health genomics framework can be used to move genomic discoveries into clinical and public health practice for obesity prevention and treatment. There are four phases of translational research: T1: discovery to candidate health application; T2: health application to evidence-based practice guidelines; T3: practice guidelines to health practice; and T4: practice to population health impact. Types of multidisciplinary research and knowledge synthesis needed for each phase, as well as the importance of developing and disseminating evidence-based guidelines, are discussed. Because obesity genomics research is mostly in the discovery phase or in the very early phases of translation (T1), the authors present this framework to illustrate the range of translation activities needed to move genomic discoveries in obesity to actual applications that reduce the burden of obesity at the population level.
C1 [Agurs-Collins, Tanya] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Natl Off Publ Hlth Genom, Coordinating Ctr Hlth Promot, Atlanta, GA USA.
[Simon-Morton, Denise] NHLBI, Div Prevent & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Olster, Deborah H.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Harris, Jennifer R.] Norwegian Inst Publ Hlth, Oslo, Norway.
[Harris, Jennifer R.] NIA, NIH, Bethesda, MD 20892 USA.
[Milner, John A.] NCI, Nutr Sci Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
RP Agurs-Collins, T (reprint author), NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
EM collinsta@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 72
TC 13
Z9 14
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2008
VL 16
SU 3
BP S85
EP S94
DI 10.1038/oby.2008.517
PG 10
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 379ON
UT WOS:000261406200016
PM 19037221
ER
PT J
AU Agurs-Collins, T
Bouchard, C
AF Agurs-Collins, Tanya
Bouchard, Claude
TI Gene-Nutrition and Gene-Physical Activity Interactions in the Etiology
of Obesity INTRODUCTION
SO OBESITY
LA English
DT Editorial Material
C1 [Agurs-Collins, Tanya] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Bouchard, Claude] Pennington Biomed Res Ctr, Human Genome Lab, Baton Rouge, LA USA.
RP Agurs-Collins, T (reprint author), NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
EM collinsta@mail.nih.gov; BouchaC@pbrc.edu
RI Bouchard, Claude/A-7637-2009
FU Intramural NIH HHS [Z99 CA999999]
NR 22
TC 9
Z9 10
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2008
VL 16
SU 3
BP S2
EP S4
DI 10.1038/oby.2008.510
PG 3
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 379ON
UT WOS:000261406200001
PM 19037207
ER
PT J
AU Bouchard, C
Agurs-Collins, T
AF Bouchard, Claude
Agurs-Collins, Tanya
TI Studying Gene-Behavior Interactions: Summary of Recommendations
SO OBESITY
LA English
DT Editorial Material
ID OBESITY
C1 [Bouchard, Claude] Pennington Biomed Res Ctr, Human Genom Lab, Baton Rouge, LA USA.
[Agurs-Collins, Tanya] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Bouchard, C (reprint author), Pennington Biomed Res Ctr, Human Genom Lab, Baton Rouge, LA USA.
EM BouchaC@pbrc.edu
RI Bouchard, Claude/A-7637-2009
FU Intramural NIH HHS [Z99 CA999999]
NR 3
TC 4
Z9 4
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2008
VL 16
SU 3
BP S95
EP S96
DI 10.1038/oby.2008.525
PG 2
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 379ON
UT WOS:000261406200017
PM 19037222
ER
PT J
AU Ford, J
Grewal, J
Mikolajczyk, R
Meikle, S
Zhang, J
AF Ford, Jessie
Grewal, Jagteshwar
Mikolajczyk, Rafael
Meikle, Susan
Zhang, Jun
TI Primary Cesarean Delivery Among Parous Women in the United States,
1990-2003
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID SECTION RATES; BIRTH CERTIFICATES; TRENDS; MULTIPARA; PREGNANCY;
OBESITY; RISK; PREVALENCE; WEIGHT; PARITY
AB OBJECTIVE: To explore trends in primary cesarean delivery rates among parous women with singleton pregnancies in the United States between 1990 and 2003.
METHODS: The analysis used data from national birth files based on U.S. birth certificates between 1990 and 2003. The primary cesarean delivery rate was defined as the number of primary cesarean deliveries per 100 deliveries among parous women with singleton pregnancies who have not had a previous cesarean delivery. A stratified analysis was employed to investigate whether trends varied by maternal age, gestational age, race/ethnicity, or region.
RESULTS: In the United States, the primary cesarean delivery rate among parous women decreased modestly from 7.10% in 1990 to 6.6% in 1996 but increased progressively to 9.3% in 2003. The increase in cesarean rates from 1996 to 2003 varied substantially by race/ethnicity: Hispanic and non-Hispanic white women exhibited lower and similar rates, whereas rates for non-Hispanic black women were consistently higher and rose by a far greater extent across the years. There were substantial differences in cesarean delivery trends across geographic divisions, with greatest increases observed in the mid-Atlantic, South Central, and South Atlantic areas of the United States. Primary cesarean rates also declined considerably with increasing gestational age.
CONCLUSION: Similar to the overall cesarean delivery rate, primary cesarean rates among parous women with singleton pregnancies have increased substantially in the United States since 1996.
C1 [Grewal, Jagteshwar] Eunice Kennedy Shriver Natl Inst Chil Hlth & Huma, Epidemiol & Contracept & Reprod Hlth Branches, Div Epidemiol Stat & Prevent Res, NIH, Rockville, MD 20852 USA.
RP Grewal, J (reprint author), Eunice Kennedy Shriver Natl Inst Chil Hlth & Huma, Epidemiol & Contracept & Reprod Hlth Branches, Div Epidemiol Stat & Prevent Res, NIH, 6700 Execut Blvd,Room 7B03G, Rockville, MD 20852 USA.
EM grewalja@mail.nih.gov
OI Grewal, Jagteshwar/0000-0002-0141-4876
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX Supported by the Eunice Kennedy Shriver National Institute of Child
Health and Human Development.
NR 37
TC 17
Z9 18
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2008
VL 112
IS 6
BP 1235
EP 1241
DI 10.1097/AOG.0b013e31818ce092
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 378JE
UT WOS:000261316200008
PM 19037031
ER
PT J
AU Toso, L
Cameroni, I
Roberson, R
Abebe, D
Bissell, S
Spong, CY
AF Toso, Laura
Cameroni, Irene
Roberson, Robin
Abebe, Daniel
Bissell, Stephanie
Spong, Catherine Y.
TI Prevention of Developmental Delays in a Down Syndrome Mouse Model
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID VASOACTIVE-INTESTINAL-PEPTIDE; FETAL ALCOHOL SYNDROME; NEONATAL MICE;
TS65DN; GROWTH; ABNORMALITIES; NEUROPEPTIDES; CHILDREN; DEFICITS; VIP
AB OBJECTIVE: To estimate whether prenatal treatment with neuroprotective peptides prevents the developmental delay and the glial deficit in the Ts65Dn mouse model for Down syndrome and to explore the peptides' effects on achievement of normal development.
METHODS: Pregnant Ts65Dn females were randomly assigned to NAPVSIPQ+SALLRSIPA or control and were treated by investigators blinded to treatment and genotype on gestational days 8-12. Offspring were tested from postnatal day 5 to 21 for motor and sensory milestones with standardized tests by operators blinded to the pup's treatment and genotype. The pup's genotype was determined after completion of ail tests. Activity-dependent neurotrophic factor, glial fibrillary acidic protein, and vasoactive intestinal peptide expression were determined using real-time polymerase chain reaction.
RESULTS: Trisomic mice achieved milestones with a Significant delay in four of five motor and sensory milestones. Trisomic mice that were prenatally exposed to NAPVSIPQ+SALLRSIPA achieved developmental milestones at the same time as the controls in three of four motor and one of four sensory milestones (P <.01). Euploid pups prenatally treated with NAPVSIPQ+SALLRSIPA achieved developmental milestones significantly earlier than the euploid pups prenatally treated with placebo. Activity-dependent neurotrophic factor expression was significantly downregulated in the Ts65Dn brains compared with the controls, prenatal treatment with NAPVSIPQ+SALLRSIPA prevented the activity-dependent neurotrophic factor decrease in the Ts65Dn brains, and the expression was not different from the controls. The glial marker glial fibrillary acidic protein demonstrated the known glial deficit in the Ts65Dn mice, and treatment with NAPVSIPQ+SALLRSIPA prevented its downregulation. Lastly, vasoactive intestinal peptide levels were increased in the trisomic brains, whereas treatment with NAPVSIPQ+SALLRSIPA did not prevent its upregulation.
CONCLUSION: Prenatal treatment with NAPVSIPQ and SALLRSIPA prevented developmental delay and the glial deficit in Down syndrome. These findings highlight a possibility for the prevention of developmental sequelae in Down syndrome and suggest a potential intervention during pregnancy that may improve the outcome.
C1 [Toso, Laura] George Washington Univ, Dept Obstet & Gynecol, Washington, DC 20003 USA.
Eunice Kennedy Shriver Natl Inst Child & Human De, Unit Perinatal & Dev Neurobiol, NIH, Bethesda, MD USA.
Univ Milano Bicocca, Osped S Gerardo, Dept Obstet & Gynaecol, Monza, Italy.
RP Toso, L (reprint author), George Washington Univ, Dept Obstet & Gynecol, 2300 23rd St NW, Washington, DC 20003 USA.
EM laura_toso@hotmail.com
FU Division of Intramural Resarch Program; Institutes of Health; Eunice
Kennedy Shriver National Institute of Child and Human Development;
National Institute on Alcohol Abuse and Alcoholism
FX Supported by the Division of Intramural Resarch Program, National
Institutes of Health, Eunice Kennedy Shriver National Institute of Child
and Human Development, and National Institute on Alcohol Abuse and
Alcoholism. The authors thank Cecilia Schmidt, the Jackson Laboratory,
Bar Harbor, Maine, for animal genotyping.
NR 25
TC 27
Z9 27
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2008
VL 112
IS 6
BP 1242
EP 1251
DI 10.1097/AOG.0b013e31818c91dc
PG 10
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 378JE
UT WOS:000261316200009
PM 19037032
ER
PT J
AU Gunderson, EP
Chiang, V
Lewis, CE
Catov, J
Quesenberry, CP
Sidney, S
Wei, GS
Ness, R
AF Gunderson, Erica P.
Chiang, Vicky
Lewis, Cora E.
Catov, Janet
Quesenberry, Charles P., Jr.
Sidney, Stephen
Wei, Gina S.
Ness, Roberta
TI Long-Term Blood Pressure Changes Measured From Before to After Pregnancy
Relative to Nonparous Women
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID ARTERY RISK DEVELOPMENT; HEART-DISEASE RISK; YOUNG-ADULTS; REPRODUCTIVE
HISTORY; NITRIC-OXIDE; WEIGHT-GAIN; BODY-WEIGHT; CARDIA; HYPERTENSION;
TRENDS
AB OBJECTIVE: To prospectively examine whether blood pressure changes persist after pregnancy among women of reproductive age.
METHODS: This was a prospective, population-based, observational cohort of 2,304 (1,167 black, 1,137 white) women (aged 18-30 years) who were free of hypertension at baseline (1985-1986) and reexamined up to six times at 2, 5, 7, 10, or 20 years later (2005-2006). We obtained standardized blood pressure measurements before and after pregnancies and categorized women into time-dependent groups by the cumulative number of births since baseline within each time interval (zero births [referent]; one interim birth and two or more interim births; nonhypertensive pregnancies). The study assessed differences in systolic and diastolic blood pressures among interim birth groups using multivariable, repeated measures linear regression models stratified by baseline parity (nulliparous and parous), adjusted for time, age, race, baseline covariates (blood pressure, body mass index, education, and oral contraceptive use), and follow-up covariates (smoking, anti hypertensive medications, oral contraceptive use, and weight gain).
RESULTS: Among nulliparas at baseline, mean (95% confidence interval) fully adjusted systolic and diastolic blood pressures (mm Hg), respectively, were lower by -2.06 (-2.72 to -1.41) and -1.50 (-2.08 to -0.92) after one interim birth, and lower by -1.89 (-2.63 to -1.15) and -1.29 (-1.96 to -0.63) after two or more interim births compared with no births (all P <.001). Among women already parous at baseline, adjusted mean blood pressure changes did not differ by number of subsequent births.
CONCLUSION: A first birth is accompanied by persistent lowering of blood pressure from preconception to years after delivery. Although the biologic mechanism is unclear, pregnancy may create enduring alterations in vascular endothelial function.
C1 Kaiser Permanente, Div Res Epidemiol & Prevent, Oakland, CA USA.
Univ Alabama, Div Prevent Med, Birmingham, AL USA.
Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
Univ Pittsburgh, Magee Womens Hosp, Dept Obstet & Gynecol, Pittsburgh, PA 15213 USA.
NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
RP Gunderson, EP (reprint author), Kaiser Permanente, Div Res Epidemiol, Prevent Sect, 2000 Broadway, Oakland, CA 94612 USA.
EM epg@dor.kaiser.org
FU National Heart, Lung, and Blood Institute [N01-HC-48047, N01-HC-48048,
N01-HC-48049, N01-HC-48050, N01-HC-95095]; Career Development Award;
National Institute of Diabetes, Digestive, and Kidney Diseases [K01
DK059944]
FX Supported by contracts # N01-HC-48047, N01-HC-48048, N01-HC-48049,
N01-HC-48050, and N01-HC-95095, from the National Heart, Lung, and Blood
Institute and Career Development Award, Grant number K01 DK059944 from
the National Institute of Diabetes, Digestive, and Kidney Diseases.
NR 30
TC 19
Z9 20
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2008
VL 112
IS 6
BP 1294
EP 1302
DI 10.1097/AOG.0b013e31818da09b
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 378JE
UT WOS:000261316200016
PM 19037039
ER
PT J
AU Goldstein, DS
Holmes, C
Bentho, O
Sato, T
Moak, J
Sharabi, Y
Imrich, R
Conant, S
Eldadah, BA
AF Goldstein, David S.
Holmes, Courtney
Bentho, Oladi
Sato, Takuya
Moak, Jeffrey
Sharabi, Yehonatan
Imrich, Richard
Conant, Shielah
Eldadah, Basil A.
TI Biomarkers to detect central dopamine deficiency and distinguish
Parkinson disease from multiple system atrophy
SO PARKINSONISM & RELATED DISORDERS
LA English
DT Article
DE Parkinson; Multiple system atrophy; Fluorodopa; Fluorodopamine; DOPAC;
PET; Biomarker
ID CARDIAC SYMPATHETIC DENERVATION; PURE AUTONOMIC FAILURE; ORTHOSTATIC
HYPOTENSION; OLFACTORY DYSFUNCTION; ODOR IDENTIFICATION; HUMAN BRAIN;
METABOLISM; DIAGNOSIS; ACID; DIFFERENTIATION
AB Objective: Biomarkers are increasingly important to diagnose and test treatments of neurodegenerative diseases such as Parkinson disease (PD). This study compared neuroimaging, neurochemical, and olfactory potential biomarkers to detect central dopamine (DA) deficiency and distinguish PD from multiple system atrophy (MSA).
Methods: In 77 PD, 57 MSA, and 87 control subjects, radioactivity concentrations in the putamen (PUT), caudate (CAU), occipital cortex (OCC), and substantia nigra (SN) were measured 2 h after 6-[(18)F]fluorodopa injection, septal myocardial radioactivity measured 8 min after 6-[(18)F]fluorodopamine injection, CSF and plasma catechols assayed, or olfaction tested (University of Pennsylvania Smell Identification Test (UPSIT)). Receiver operating characteristic curves were constructed, showing test sensitivities at given specificities.
Results: PUT:OCC, CAU:OCC, and SN:OCC ratios of 6-[(18)F]fluorodopa-derived radioactivity were similarly low in PD and MSA (p < 0.0001, p < 0.0001, p = 0.003 compared to controls); as were CSF dihydroxyphenylacetic acid (DOPAC) and DOPA concentrations (p < 0.0001, each). PUT:SN and PUT:CAU ratios were lower in PD than in MSA (p=0.004; p=0.005). CSF DOPAC correlated positively with PUT:OCC ratios (r=0.61, p < 0.0001). Myocardial 6-[(18)F]fluorodopamine-derived radioactivity distinguished PD from MSA (83% sensitivity at 80% specificity, 100% sensitivity among patients with neurogenic orthostatic hypotension). Only PD patients were anosmic; only MSA patients had normal olfaction (61% sensitivity at 80% specificity).
Conclusions: PD and MSA feature low PUT:OCC ratios of 6-[(18)F]fluorodopa-derived radioactivity and low CSF DOPAC and DOPA concentrations, cross-validating the neuroimaging and neurochemical approaches but not distinguishing the diseases. PUT:SN and PUT:CAU ratios of 6-[(18)F]fluorodopa-derived radioactivity, cardiac 6-[(18)F]fluorodopamine-derived radioactivity, and olfactory testing separate PD from MSA. (c) Published by Elsevier Ltd.
C1 [Goldstein, David S.; Holmes, Courtney; Bentho, Oladi; Sato, Takuya; Sharabi, Yehonatan; Imrich, Richard; Eldadah, Basil A.] NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
[Moak, Jeffrey; Eldadah, Basil A.] NIH, PET Dept, Ctr Clin, Bethesda, MD 20892 USA.
[Conant, Shielah; Eldadah, Basil A.] NIA, Geriatr & Clin Gerontol Program, NIH, Bethesda, MD 20892 USA.
RP Goldstein, DS (reprint author), NINDS, Clin Neurocardiol Sect, NIH, 10 Ctr Dr MSC-1620,Bldg 10,Room 6N252, Bethesda, MD 20892 USA.
EM goldsteind@ninds.nih.gov
FU Intramural Research Program of the NIH; National Institute of
Neurological Disorders and Stroke
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Neurological Disorders and Stroke.
NR 41
TC 51
Z9 55
U1 1
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1353-8020
J9 PARKINSONISM RELAT D
JI Parkinsonism Relat. Disord.
PD DEC
PY 2008
VL 14
IS 8
BP 600
EP 607
DI 10.1016/j.parkreldis.2008.01.010
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 383GP
UT WOS:000261662400003
PM 18325818
ER
PT J
AU Kim, A
Ji, L
Balmaceda, C
Diez, B
Kellie, SJ
Dunkel, IJ
Gardner, SL
Sposto, R
Finlay, JL
AF Kim, AeRang
Ji, Lingyun
Balmaceda, Casilda
Diez, Blanca
Kellie, Stewart J.
Dunkel, Ira J.
Gardner, Sharon L.
Sposto, Richard
Finlay, Jonathan L.
TI The Prognostic Value of Tumor Markers in Newly Diagnosed Patients With
Primary Central Nervous System Germ Cell Tumors
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE germ cell tumors; pediatric neuro-oncology; survival; tumor markers
ID HUMAN CHORIONIC-GONADOTROPIN; INTRACRANIAL GERMINOMA; PRIMARY
CHEMOTHERAPY; COOPERATIVE TRIAL; RADIATION-THERAPY; SERUM; RADIOTHERAPY;
PATHOGENESIS; EXPERIENCE; CISPLATIN
AB Background. To determine the impact of diagnostic serum and/or cerebrospinal fluid (CSF) alpha-fetoprotein (AFP) and beta-human chorionic gonadotropin (b-HCG) elevations on survival in newly diagnosed patients with central nervous system germ cell tumors (CNS GCT) treated with chemotherapy with the intent to avoid irradiation. Procedure. Seventy-five patients with newly diagnosed CNS GCT enrolled in two sequential internationally conducted clinical trials with serum and CSF AFP and b-HCG levels available from initial diagnosis were retrospectively analyzed. Subjects received platinum based chemotherapy and were followed with serial imaging and tumor marker evaluations. Results. The 5-year overall survival (C)S) and event free survival (EFS) for patients with normal tumor markers compared with those with elevated markers at diagnosis was 78% (95% CI 51-91 %) versus 60% (95% CI 46-72%) (P = 0.08) and 22% (95% CI 7-43%) versus 28% (95% CI 16-40%) (P = 0.68). The hazard ratio of death for patients with elevated markers was 1.9 times as high as that for those with normal markers (95% CI 0.58-6.5) after adjusting for other baseline characteristics. There was no observed difference in survival among patients with histologically confirmed germinomas, irrespective of level of b-HCG. Conclusions. Patients with elevated tumor markers appear to have poorer OS independent of tumor histology, although these differences do not reach statistical significance (P <= 0.05). No differences were observed in EFS between groups likely due to the poor response of chemotherapy only approach to patients with normal markers. b-HCG elevations in biopsy proven germinomas do not seem to alter a patient's prognosis. Pediatr Blood Cancer 2008;51:768-773. (c) 2008 Wiley-Liss, Inc.
C1 [Kim, AeRang; Gardner, Sharon L.] NYU, Med Ctr, New York, NY 10016 USA.
[Ji, Lingyun; Sposto, Richard; Finlay, Jonathan L.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Ji, Lingyun; Sposto, Richard; Finlay, Jonathan L.] Childrens Ctr Canc & Blood Dis, Los Angeles, CA USA.
[Balmaceda, Casilda] Columbia Univ, Med Ctr, Columbia, NY USA.
[Diez, Blanca] Inst Neurol Res Dr Raul Carrea FLENI, Buenos Aires, DF, Argentina.
[Kellie, Stewart J.] Univ Sydney, Sydney, NSW 2006, Australia.
[Kellie, Stewart J.] Childrens Hosp Westmead, Sydney, NSW, Australia.
[Dunkel, Ira J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Kim, A (reprint author), NCI, Pediat Oncol Branch, 10 Ctr Dr,Bldg 10 CRC,Room 1-3872, Bethesda, MD 20892 USA.
EM kimaer@mail.nih.gov
OI Dunkel, Ira/0000-0001-8091-6067; gardner, sharon/0000-0002-8857-5487
NR 27
TC 21
Z9 21
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC
PY 2008
VL 51
IS 6
BP 768
EP 773
DI 10.1002/pbc.21741
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 363TI
UT WOS:000260289300011
PM 18802946
ER
PT J
AU Prasad, PA
Coffin, SE
Leckerman, KH
Walsh, TJ
Zaoutis, TE
AF Prasad, Priya A.
Coffin, Susan E.
Leckerman, Kateri H.
Walsh, Thomas J.
Zaoutis, Theoklis E.
TI Pediatric Antifungal Utilization New Drugs, New Trends
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article; Proceedings Paper
CT 44th Annual Meeting of the Infectious-Diseases-Society-of-America
CY OCT 12-15, 2006
CL Toronto, CANADA
SP Infect Dis Soc Amer
DE antifungal therapy; pediatric; drug utilization; fungal infections
ID INVASIVE FUNGAL-INFECTIONS; COMPLEX CHRONIC CONDITIONS; UNITED-STATES;
RISK-FACTORS; NEONATAL CANDIDIASIS; AMPHOTERICIN-B; CHILDREN; OUTCOMES;
CANDIDEMIA; ASPERGILLOSIS
AB Background: The frequency and severity of invasive fungal infections in immunocompromised patients has increased steadily over the last 2 decades. In response to the increased incidence and high mortality rates, novel antifungal agents have been developed to expand the breadth and effectiveness of treatment options available to clinicians. Despite these therapeutic advances, the impact of the availability of new antifungal agents on pediatric practice is unknown.
Methods: A retrospective cohort study was conducted using the Pediatric Health Information System database to describe the changes in pediatric antifungal therapy at 25 freestanding United States children's hospitals from 2000 to 2006. All pediatric inpatients who received a charge for one or more of the following agents were included in the analysis: conventional amphotericin B (AMB), lipid amphotericin B, fluconazole, itraconazole, voriconazole, flucytosine, caspofungin, and micafungin. Underlying conditions and fungal infection status were ascertained.
Results: A total of 62,842 patients received antifungal therapy, with prescriptions significantly increasing during the 7-year study period (P = 0.03). The most commonly prescribed antifungal agent was fluconazole (76%), followed by amphotericin preparations (26%). Prescription of AMB steadily decreased from 2000 to 2006 (P = 0.02). Prescription of voriconazole steadily increased during the Study period and replaced AMB for the treatment of aspergillosis. The echinocandins steadily increased in prescription for treatment of fungal infections, particularly in disseminated/systemic candidiasis.
Conclusions: We found that the number of pediatric inpatients requiring antifungal therapy has increased significantly and the choice of treatment has changed dramatically with the introduction of newer antifungal agents.
C1 [Prasad, Priya A.; Coffin, Susan E.; Leckerman, Kateri H.; Zaoutis, Theoklis E.] Childrens Hosp Philadelphia, Div Infect Dis, Dept Infect Prevent & Control, Philadelphia, PA 19104 USA.
[Coffin, Susan E.; Zaoutis, Theoklis E.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Coffin, Susan E.; Zaoutis, Theoklis E.] Ctr Pediat, Philadelphia, PA USA.
[Walsh, Thomas J.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
RP Zaoutis, TE (reprint author), Childrens Hosp Philadelphia, Div Infect Dis, Dept Infect Prevent & Control, 3535 Market St,Room 1527, Philadelphia, PA 19104 USA.
EM zaoutis@email.chop.edu
FU AHRQ HHS [U18 HS 103999]; NIAID NIH HHS [1K23 AI 0629753-01]
NR 25
TC 35
Z9 37
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD DEC
PY 2008
VL 27
IS 12
BP 1083
EP 1088
DI 10.1097/INF.0b013e31817eeee5
PG 6
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 377BD
UT WOS:000261225800008
PM 18989239
ER
PT J
AU Kim, W
Egan, JM
AF Kim, Wook
Egan, Josephine M.
TI The Role of Incretins in Glucose Homeostasis and Diabetes Treatment
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID GLUCAGON-LIKE PEPTIDE-1; DEPENDENT-INSULINOTROPIC POLYPEPTIDE;
GASTRIC-INHIBITORY-POLYPEPTIDE; PANCREATIC BETA-CELLS; DIPEPTIDYL
PEPTIDASE-4 INHIBITOR; PROTEIN-KINASE-A; PROGLUCAGON GENE-EXPRESSION;
ENDOCRINE-L-CELLS; CAMP RESPONSE ELEMENT; CYCLIC ADP-RIBOSE
AB Incretins are gut hormones that are secreted from enteroendocrine cells into the blood within minutes after eating. One of their many physiological roles is to regulate the amount of insulin that is secreted after eating. In this manner, as well as others to be described in this review, their final common raison d'(e) over cap tre is to aid in disposal of the products of digestion. There are two incretins, known as glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1), that share many common actions in the pancreas but have distinct actions outside of the pancreas. Both incretins are rapidly deactivated by an enzyme called dipeptidyl peptidase 4 (DPP4). A lack of secretion of incretins or an increase in their clearance are not pathogenic factors in diabetes. However, in type 2 diabetes (T2DM), GIP no longer modulates glucose-dependent insulin secretion, even at supra-physiological (pharmacological) plasma levels, and therefore GIP incompetence is detrimental to beta-cell function, especially after eating. GLP-1, on the other hand, is still insulinotropic in T2DM, and this has led to the development of compounds that activate the GLP-1 receptor with a view to improving insulin secretion. Since 2005, two new classes of drugs based on incretin action have been approved for lowering blood glucose levels in T2DM: an incretin mimetic (exenatide, which is a potent long-acting agonist of the GLP-1 receptor) and an incretin enhancer (sitagliptin, which is a DPP4 inhibitor). Exenatide is injected subcutaneously twice daily and its use leads to lower blood glucose and higher insulin levels, especially in the fed state. There is glucose-dependency to its insulin secretory capacity, making it unlikely to cause low blood sugars (hypoglycemia). DPP4 inhibitors are orally active and they increase endogenous blood levels of active incretins, thus leading to prolonged incretin action. The elevated levels of GLP-1 are thought to be the mechanism underlying their blood glucose-lowering effects.
C1 [Egan, Josephine M.] NIA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Egan, JM (reprint author), NIA, Intramural Res Program, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM eganj@grc.nia.nih.gov
FU Intramural Research program of the National Institutes of Health
National Institute on Aging
FX This work was supported by the Intramural Research program of the
National Institutes of Health National Institute on Aging. Data used to
construct Fig. 4 were collected from subjects in the Baltimore
Longitudinal Study of Aging, National Institutes of Health National
Institute on Aging.
NR 532
TC 291
Z9 308
U1 6
U2 53
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
EI 1521-0081
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD DEC
PY 2008
VL 60
IS 4
BP 470
EP 512
DI 10.1124/pr.108.000604
PG 43
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 388FL
UT WOS:000262005600003
PM 19074620
ER
PT J
AU Bell, RL
Rodd, ZA
Toalston, JE
McKinzie, DL
Lumeng, L
Li, TK
McBride, WJ
Murphy, JM
AF Bell, Richard L.
Rodd, Zachary A.
Toalston, Jamie E.
McKinzie, David L.
Lumeng, Lawrence
Li, Ting-Kai
McBride, William J.
Murphy, James M.
TI Autonomic activation associated with ethanol self-administration in
adult female P rats
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Alcohol; Stimulation; Activation; Autonomic; Cue-reactivity; Heart rate;
Alcohol-preferring rats; Contextual conditioning
ID ALCOHOL-RELATED CUES; ANTAGONISTIC PLACEBO-RESPONSE; BARORECEPTOR REFLEX
CONTROL; SYMPATHETIC-NERVE ACTIVITY; HEART-RATE REACTIVITY;
SEX-DIFFERENCES; ANIMAL-MODELS; DEPRESSOR RESPONSIVENESS; MULTIPLE
CONCENTRATIONS; REPEATED DEPRIVATIONS
AB The present study examined changes in heart rate (HR) prior to and during limited access ethanol drinking in adult female P rats. P rats were implanted with radio-telemetric transmitters to measure HR. Daily testing involved a 90-min pre-test period (water only available) and a subsequent 90-min test period [either water (W) or ethanol available]. After a week of habituation, one ethanol group had access to ethanol for 7 weeks (CE), and another ethanol group had access for 4 weeks, was deprived for 2 weeks and then had access for a final week (DEP). Analyses of HR revealed that CE and DEP rats had significantly higher HR than W rats during test periods that ethanol was present and that DEP rats displayed higher HR during the early test period of the ethanol deprivation interval, as well. These data indicate that ethanol drinking induces HR activation in adult female P rats, and that this activation can be conditioned to the test cage environment, paralleling reports on contextual conditioning and cue-reactivity in alcoholics exposed to alcohol-associated stimuli. Therefore, this behavioral test may prove advantageous in screening pharmacortherapies for reducing craving and relapse, which are associated with cue-reactivity in abstinent alcoholics. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Bell, Richard L.] Indiana Univ, Sch Med, Inst Psychiat Res, Dept Psychiat, Indianapolis, IN 46202 USA.
[Bell, Richard L.; Rodd, Zachary A.; Toalston, Jamie E.; Murphy, James M.] Indiana Univ Purdue Univ, Purdue Sch Sci, Dept Psychol, Indianapolis, IN 46202 USA.
[McKinzie, David L.] Lilly Corp Ctr, Lilly Res Labs, Neurosci Discovery Res, Indianapolis, IN 46285 USA.
[Lumeng, Lawrence; McBride, William J.] Indiana Univ, Sch Med, Dept Med, Indianapolis, IN 46202 USA.
[Lumeng, Lawrence] Indiana Univ, Sch Med, Dept Biochem, Indianapolis, IN 46202 USA.
[Li, Ting-Kai] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Bell, RL (reprint author), Indiana Univ, Sch Med, Inst Psychiat Res, Dept Psychiat, 791 Union Dr, Indianapolis, IN 46202 USA.
EM ribell@iupui.edu
RI Rodd, Zachary/L-1580-2015;
OI Rodd, Zachary/0000-0002-8105-1920; Toalston, Jamie/0000-0001-5115-6644
FU NIAAA [AA07462, AA07611, AA14346, AA13522]
FX This study was supported in part by NIAAA grants AA07462, AA07611,
AA14346, and AA13522 (an INIA project). We gratefully acknowledge the
expert technical assistance provided by Mrs. Caron Peper and Ms. Lindsay
Larson in conducting these experiments.
NR 88
TC 3
Z9 3
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD DEC
PY 2008
VL 91
IS 2
BP 223
EP 232
DI 10.1016/j.pbb.2008.07.016
PG 10
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 381QB
UT WOS:000261549900003
PM 18713644
ER
PT J
AU Kiyatkin, EA
AF Kiyatkin, Eugene A.
TI Brain temperature responses to salient stimuli persist during dopamine
receptor blockade despite a blockade of locomotor responses
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Brain metabolism; Brain and body temperature; Dopamine systems; Dopamine
antagonists; Natural arousing stimuli; Intravenous cocaine
ID CENTRAL-NERVOUS-SYSTEM; FREELY MOVING RATS; NUCLEUS-ACCUMBENS; SELECTIVE
BLOCKADE; UNRESTRAINED RATS; STRIATAL NEURONS; COCAINE; MECHANISMS;
VASOCONSTRICTION; TRANSMISSION
AB We examined how an acute dopamine (DA) receptor blockade affects locomotor and brain (nucleus accumbens or NAcc), muscle and skin temperature responses to three arousing stimuli (procedure of sc injection, tail-pinch and social interaction with another male rat) and intravenous cocaine (1 mg/kg). DA receptor blockade was induced by mixture of D1- (SCH23390) and D-2 selective (eticlopride) DA antagonists at 0.2 mg/kg doses. Each arousing stimulus and cocaine caused locomotor activation, prolonged increase in NAcc and muscle temperature (0.6-1.0 degrees C for 20-50 min) and transient skin hypothermia (-0.6 degrees C for 1-3 min) in drug-naive conditions. DA receptor blockade strongly decreased basal locomotor activity, but moderately increased brain, muscle and skin temperatures. Therefore, selective interruption of DA transmission does not inhibit the brain, making it more metabolically active and warmer despite skin vasodilatation and the enhanced heat loss to the body and the external environment. DA antagonists strongly decreased locomotor responses to all stimuli and cocaine, had no effects on acute skin vasoconstriction, but differentially affected stimuli- and drug-induced changes in NAcc and muscle temperatures. While brain and muscle temperatures induced by cocaine were fully blocked and both temperatures slightly decreased, temperature increases induced by tail-pinch and social interaction, despite a significant attenuation, persisted during DA receptor blockade. These data are discussed to define the role of the DA system in regulating the central activation processes and behavioral responsiveness to natural arousing and drug stimuli. Published by Elsevier Inc.
C1 Natl Inst Drug Abuse, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
RP Kiyatkin, EA (reprint author), Natl Inst Drug Abuse, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM ekiyatki@intra.nida.nih.gov
FU NIH; NIDA
FX This research was supported by the Intramural Research Program of the
NIH, NIDA. I wish to thank P. Leon Brown and David Bae for valuable
technical assistance in conducting the experiments described in this
paper and Michael Smirnov for editorial assistance.
NR 29
TC 7
Z9 7
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD DEC
PY 2008
VL 91
IS 2
BP 233
EP 242
DI 10.1016/j.pbb.2008.08.004
PG 10
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 381QB
UT WOS:000261549900004
PM 18727935
ER
PT J
AU Kanduc, M
Trulsson, M
Naji, A
Burak, Y
Forsman, J
Podgornik, R
AF Kanduc, M.
Trulsson, M.
Naji, A.
Burak, Y.
Forsman, J.
Podgornik, R.
TI Weak- and strong-coupling electrostatic interactions between
asymmetrically charged planar surfaces
SO PHYSICAL REVIEW E
LA English
DT Article
DE electric fields; electrochemistry; liquid theory; Monte Carlo methods
ID POISSON-BOLTZMANN EQUATION; DOUBLE-LAYER INTERACTIONS;
COUNTERION-RELEASE; COULOMB FLUID; SOFT MATTER; MONTE-CARLO; IONS;
ELECTROLYTES; FLUCTUATIONS; SIMULATIONS
AB We compare weak- and strong-coupling theory of counterion-mediated electrostatic interactions between two asymmetrically charged plates with extensive Monte Carlo simulations. Analytical results in both weak- and strong-coupling limits compare excellently with simulations in their respective regimes of validity. The system shows a surprisingly rich structure in terms of interactions between the surfaces as well as fundamental qualitative differences in behavior in the weak- and the strong-coupling limits.
C1 [Kanduc, M.; Podgornik, R.] Jozef Stefan Inst, Dept Theoret Phys, SI-1000 Ljubljana, Slovenia.
[Trulsson, M.; Forsman, J.] Lund Univ, Dept Theoret Chem, Ctr Chem, S-22100 Lund, Sweden.
[Naji, A.] Univ Calif Santa Barbara, Mat Res Lab, Santa Barbara, CA 93106 USA.
[Naji, A.] Univ Calif Santa Barbara, Kavli Inst Theoret Phys, Santa Barbara, CA 93106 USA.
[Burak, Y.] Harvard Univ, Ctr Brain Sci, Cambridge, MA 02138 USA.
[Podgornik, R.] Univ Ljubljana, Dept Phys, Fac Math & Phys, SI-1000 Ljubljana, Slovenia.
[Podgornik, R.] NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA.
[Naji, A.] Univ Calif Santa Barbara, Dept Chem & Biochem, Santa Barbara, CA 93106 USA.
RP Kanduc, M (reprint author), Jozef Stefan Inst, Dept Theoret Phys, SI-1000 Ljubljana, Slovenia.
RI Burak, Yoram/F-6885-2010; Naji, Ali/F-6352-2010; Podgornik,
Rudolf/C-6209-2008
OI Naji, Ali/0000-0003-3436-1499; Podgornik, Rudolf/0000-0002-3855-4637
FU DGAPA-UNAM PROFIP program
FX The author thanks P. Gaspard and R. MacKay for helpful comments and M.
Henk for useful correspondence and is grateful to the Erwin Schrodinger
Institute and the Universite Libre de Bruxelles for financial support,
which enabled discussions with N. Chernov, I. Melbourne, D. Szasz, I. P.
Toth, and T. Varju, and especially T. Gilbert, who also read the
manuscript critically. Supercomputing facilities were provided by
DGSCA-UNAM, and financial support from the DGAPA-UNAM PROFIP program is
also acknowledged. The author is grateful to the anonymous referees for
interesting comments.
NR 48
TC 27
Z9 27
U1 0
U2 10
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1539-3755
J9 PHYS REV E
JI Phys. Rev. E
PD DEC
PY 2008
VL 78
IS 6
AR 061105
DI 10.1103/PhysRevE.78.061105
PG 14
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 391NP
UT WOS:000262240300017
PM 19256800
ER
PT J
AU Fuxe, K
Marcellino, D
Guidolin, D
Woods, AS
Agnati, LF
AF Fuxe, Kjell
Marcellino, Daniel
Guidolin, Diego
Woods, Amina S.
Agnati, Luigi F.
TI Heterodimers and Receptor Mosaics of Different Types of
G-Protein-Coupled Receptors
SO PHYSIOLOGY
LA English
DT Review
ID ADENOSINE A(2A) RECEPTORS; NUCLEUS-TRACTUS-SOLITARII; CENTRAL
NERVOUS-SYSTEM; NEUROPEPTIDE-Y; DOPAMINE-D-2 RECEPTORS; GPCR
OLIGOMERIZATION; OPIOID RECEPTORS; HETEROMERIC ASSOCIATION; ALLOSTERIC
MODULATION; PARKINSONS-DISEASE
AB Through an assembly of interacting GPCRs, heterodimers and high-order heteromers (termed receptor mosaics) are formed and lead to changes in the agonist recognition, signaling, and trafficking of participating receptors via allosteric mechanisms, sometimes involving the appearance of cooperativity. This field has now become a major research area, and this review deals with their physiology being integrators of receptor signaling in the CNS and their use as targets for novel drug development based on their unique pharmacology.
C1 [Fuxe, Kjell; Marcellino, Daniel] Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
[Guidolin, Diego] Univ Padua, Dept Anat & Physiol, Padua, Italy.
[Woods, Amina S.] DHHS, Natl Inst Drug Abuse, NIH, Baltimore, MD USA.
[Agnati, Luigi F.] Univ Modena, Dept Biomed Sci, Venice, Italy.
[Agnati, Luigi F.] IRCCS Lido, Venice, Italy.
RP Fuxe, K (reprint author), Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
EM Kjell.Fuxe@ki.se
OI Marcellino, Daniel/0000-0002-4618-7267; Fuxe, Kjell/0000-0001-8491-4288;
Guidolin, Diego/0000-0003-2133-3552
NR 103
TC 34
Z9 34
U1 0
U2 5
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1548-9213
EI 1548-9221
J9 PHYSIOLOGY
JI Physiology
PD DEC
PY 2008
VL 23
IS 6
BP 322
EP 332
DI 10.1152/physiol.00028.2008
PG 11
WC Physiology
SC Physiology
GA 383TX
UT WOS:000261697600003
PM 19074740
ER
PT J
AU Pastorino, L
Bonelli, L
Ghiorzo, P
Queirolo, P
Battistuzzi, L
Balleari, E
Nasti, S
Gargiulo, S
Gliori, S
Savoia, P
Osella, SA
Bernengo, MG
Scarra, G
AF Pastorino, L.
Bonelli, L.
Ghiorzo, P.
Queirolo, P.
Battistuzzi, L.
Balleari, E.
Nasti, S.
Gargiulo, S.
Gliori, S.
Savoia, P.
Osella, S. Abate
Bernengo, M. G.
Scarra, G. Bianchi
TI CDKN2A mutations and MC1R variants in Italian patients with single or
multiple primary melanoma
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Article
DE multiple melanoma; familial melanoma; CDKN2A; MC1R; germline mutations
ID POPULATION-BASED PREVALENCE; GERM-LINE MUTATIONS; MELANOCORTIN-1
RECEPTOR; PRONE FAMILIES; MALIGNANT-MELANOMA; PANCREATIC-CANCER; CDK4
MUTATION; HUMAN PIGMENTATION; GENE; RISK
AB We evaluated the contribution of germline CDKN2A mutations and MC1R variants to the development of melanoma in a hospital-based study of single (SPM, n = 398) and multiple primary melanoma (MPM, n = 95). The overall frequency of CDKN2A mutations was 15.2%, and four-fold higher in MPM than in SPM cases (OR = 4.27; 95% CI 2.43-7.53). The likelihood of identifying a CDKN2A mutation increased with family history of melanoma and younger age at diagnosis in MPM cases. Compared to SPM patients, the risk of harboring a CDKN2A mutation rose as the number of primary melanomas increased and was not influenced by family history. The G101W and E27X founder mutations were the most common. Several other mutations (W15X, Q50X, R58X, A68L, A127P and H142R) were detected for the first time in Italian patients. One novel mutation, T77A, was identified. Several non-coding variants with unknown functional significance were also found (5'UTR -25C > T, -21C > T, -67G > C, IVS1 +37G > C); the novel 5'UTR -21C > T variant was not detected in controls. The CDKN2A A148T polymorphism was more frequent in MPM patients than in the control population (15.7% versus 6.6%). Compared to the SPM patients, MPM cases had a 2-fold increased probability of being MC1R variant carriers and a higher probability of carrying two or more variants. No specific association was observed between the type of variant and the number of melanomas, suggesting that the number rather than the type of MC1R variant increases the risk of MPM. We observed no interaction between CDKN2A status and the presence of MC1R variants. The high frequency of CDKN2A mutations in our MPM cases, independent of their family history, is of relevance to genetic counseling and testing in our population.
C1 [Pastorino, L.; Ghiorzo, P.; Battistuzzi, L.; Nasti, S.; Gargiulo, S.; Scarra, G. Bianchi] Univ Genoa, Dept Oncol Biol & Genet, Med Genet Serv, Genoa, Italy.
[Queirolo, P.; Gliori, S.] Natl Canc Inst, Dept Med Oncol A, Genoa, Italy.
[Balleari, E.] Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy.
[Savoia, P.; Osella, S. Abate; Bernengo, M. G.] Univ Turin, Dept Med Sci & Human Oncol, Dermatol Sect, Turin, Italy.
RP Pastorino, L (reprint author), Univ Genoa, Dept Oncol Biol & Genet, Med Genet Serv, Genoa, Italy.
EM l.pastorino@unige.it
RI Bianchi Scarra, Giovanna/G-8933-2014; Balleari, Enrico/R-3119-2016;
Queirolo, Paola/K-6778-2016
OI Bianchi Scarra, Giovanna/0000-0002-6127-1192; Balleari,
Enrico/0000-0003-2186-8012; Queirolo, Paola/0000-0002-9917-6633
FU EU FP6 GenoMEL Network of Excellence; Italian Ministry of Health
[88/2005]; ACC
FX We are grateful to all the participating patients, whose generous
cooperation made this study possible. This study was partially funded by
the EU FP6 GenoMEL Network of Excellence (2005-2010), the Italian
Ministry of Health 88/2005 grant to GBS and ACC funding 2007 to PQ.
NR 47
TC 28
Z9 28
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD DEC
PY 2008
VL 21
IS 6
BP 700
EP 709
DI 10.1111/j.1755-148X.2008.00512.x
PG 10
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 374YO
UT WOS:000261079800013
PM 18983535
ER
PT J
AU Follit, JA
Agustin, JTS
Xu, FH
Jonassen, JA
Samtani, R
Lo, CW
Pazour, GJ
AF Follit, John A.
Agustin, Jovenal T. San
Xu, Fenghui
Jonassen, Julie A.
Samtani, Rajeev
Lo, Cecilia W.
Pazour, Gregory J.
TI The Golgin GMAP210/TRIP11 Anchors IFT20 to the Golgi Complex
SO PLOS GENETICS
LA English
DT Article
ID POLYCYSTIC KIDNEY-DISEASE; INTRAFLAGELLAR TRANSPORT PROTEIN; OUTFLOW
TRACT DEVELOPMENT; PLANAR CELL POLARITY; PRIMARY CILIUM; CIS-GOLGI;
CILIARY MEMBRANE; CHLAMYDOMONAS-REINHARDTII; LUNG MORPHOGENESIS; SENSORY
NEURONS
AB Eukaryotic cells often use proteins localized to the ciliary membrane to monitor the extracellular environment. The mechanism by which proteins are sorted, specifically to this subdomain of the plasma membrane, is almost completely unknown. Previously, we showed that the IFT20 subunit of the intraflagellar transport particle is localized to the Golgi complex, in addition to the cilium and centrosome, and hypothesized that the Golgi pool of IFT20 plays a role in sorting proteins to the ciliary membrane. Here, we show that IFT20 is anchored to the Golgi complex by the golgin protein GMAP210/Trip11. Mice lacking GMAP210 die at birth with a pleiotropic phenotype that includes growth restriction, ventricular septal defects of the heart, omphalocele, and lung hypoplasia. Cells lacking GMAP210 have normal Golgi structure, but IFT20 is no longer localized to this organelle. GMAP210 is not absolutely required for ciliary assembly, but cilia on GMAP210 mutant cells are shorter than normal and have reduced amounts of the membrane protein polycystin-2 localized to them. This work suggests that GMAP210 and IFT20 function together at the Golgi in the sorting or transport of proteins destined for the ciliary membrane.
C1 [Follit, John A.; Agustin, Jovenal T. San; Xu, Fenghui; Pazour, Gregory J.] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
[Jonassen, Julie A.] Univ Massachusetts, Sch Med, Dept Physiol, Worcester, MA USA.
[Samtani, Rajeev; Lo, Cecilia W.] NHLBI, Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Pazour, GJ (reprint author), Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
EM gregory.pazour@umassmed.edu
OI Pazour, Gregory/0000-0002-6285-8796
FU NHLBI NIH HHS [Z01 HL005701]; NIDDK NIH HHS [DK32520, P30 DK032520];
NIGMS NIH HHS [GM060992, R01 GM060992]
NR 68
TC 71
Z9 73
U1 3
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2008
VL 4
IS 12
AR e1000315
DI 10.1371/journal.pgen.1000315
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 411RO
UT WOS:000263667900030
PM 19112494
ER
PT J
AU Sikdar, N
Banerjee, S
Zhang, H
Smith, S
Myung, K
AF Sikdar, Nilabja
Banerjee, Soma
Zhang, Han
Smith, Stephanie
Myung, Kyungjae
TI Spt2p Defines a New Transcription-Dependent Gross Chromosomal
Rearrangement Pathway
SO PLOS GENETICS
LA English
DT Article
ID CHROMATIN PROTEIN SIN1P/SPT2P; RNA-POLYMERASE-II; C-TERMINAL DOMAIN;
YEAST HO GENE; SACCHAROMYCES-CEREVISIAE; NEGATIVE REGULATOR; FORK
PROGRESSION; GENOME STABILITY; SIN1 INTERACTS; GASTRIC-CANCER
AB Large numbers of gross chromosomal rearrangements (GCRs) are frequently observed in many cancers. High mobility group 1 (HMG1) protein is a non-histone DNA-binding protein and is highly expressed in different types of tumors. The high expression of HMG1 could alter DNA structure resulting in GCRs. Spt2p is a non-histone DNA binding protein in Saccharomyces cerevisiae and shares homology with mammalian HMG1 protein. We found that Spt2p overexpression enhances GCRs dependent on proteins for transcription elongation and polyadenylation. Excess Spt2p increases the number of cells in S phase and the amount of single-stranded DNA (ssDNA) that might be susceptible to cause DNA damage and GCR. Consistently, RNase H expression, which reduces levels of ssDNA, decreased GCRs in cells expressing high level of Spt2p. Lastly, high transcription in the chromosome V, the location at which GCR is monitored, also enhanced GCR formation. We propose a new pathway for GCR where DNA intermediates formed during transcription can lead to genomic instability.
C1 [Sikdar, Nilabja; Banerjee, Soma; Zhang, Han; Smith, Stephanie; Myung, Kyungjae] NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
RP Sikdar, N (reprint author), NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
EM kmyung@mail.nih.gov
FU NHGRI; NIH [HG012003-06]
FX This research was supported by the intramural research program of the
NHGRI, NIH (HG012003-06 to KM).
NR 55
TC 18
Z9 18
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2008
VL 4
IS 12
AR e1000290
DI 10.1371/journal.pgen.1000290
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 411RO
UT WOS:000263667900005
PM 19057669
ER
PT J
AU Douoguih, M
AF Douoguih, Macaya
TI Accessing Maternal Health Services in Eastern Burma
SO PLOS MEDICINE
LA English
DT Editorial Material
ID HUMAN-RIGHTS VIOLATIONS; POPULATIONS; MORTALITY; OUTCOMES; KARENNI
C1 Eunice Kennedy Shriver NICHHD, Ctr Res Mothers & Children, NIH, Bethesda, MD 20892 USA.
RP Douoguih, M (reprint author), Eunice Kennedy Shriver NICHHD, Ctr Res Mothers & Children, NIH, Bethesda, MD 20892 USA.
EM macaya1@gmail.com
NR 12
TC 2
Z9 2
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD DEC
PY 2008
VL 5
IS 12
BP 1645
EP 1646
AR e250
DI 10.1371/journal.pmed.0050250
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 386WP
UT WOS:000261913600004
PM 19108602
ER
PT J
AU Race, B
Meade-White, K
Oldstone, MBA
Race, R
Chesebro, B
AF Race, Brent
Meade-White, Kimberly
Oldstone, Michael B. A.
Race, Richard
Chesebro, Bruce
TI Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice
SO PLOS PATHOGENS
LA English
DT Article
ID CREUTZFELDT-JAKOB-DISEASE; CHRONIC WASTING DISEASE; BLOOD-TRANSFUSION;
TRANSGENIC MICE; SKELETAL-MUSCLE; NERVOUS-SYSTEM; PROTEIN; SHEEP;
VARIANT; VIRUS
AB Distribution of prion infectivity in organs and tissues is important in understanding prion disease pathogenesis and designing strategies to prevent prion infection in animals and humans. Transmission of prion disease from cattle to humans resulted in banning human consumption of ruminant nervous system and certain other tissues. In the present study, we surveyed tissue distribution of prion infectivity in mice with prion disease. We show for the first time detection of infectivity in white and brown fat. Since high amounts of ruminant fat are consumed by humans and also incorporated into animal feed, fat-containing tissues may pose a previously unappreciated hazard for spread of prion infection.
C1 [Race, Brent; Meade-White, Kimberly; Race, Richard; Chesebro, Bruce] NIAID, Rocky Mt Labs, Lab Persistent Virus Dis, NIH, Hamilton, MT 59840 USA.
[Oldstone, Michael B. A.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
RP Race, B (reprint author), NIAID, Rocky Mt Labs, Lab Persistent Virus Dis, NIH, Hamilton, MT 59840 USA.
EM bchesebro@nih.gov
FU Intramural Research Program of the NIH; NIAID; NIA [AG04032]
FX This research was supported in part by the Intramural Research Program
of the NIH, NIAID. MBAO was funded through NIA grant AG04032.
NR 38
TC 15
Z9 15
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2008
VL 4
IS 12
AR e1000232
DI 10.1371/journal.ppat.1000232
PG 6
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 415IM
UT WOS:000263927500022
PM 19057664
ER
PT J
AU Simon, TR
Ikeda, RM
Smith, EP
Reese, LE
Rabiner, DL
Miller-Johnson, S
Winn, DM
Dodge, KA
Asher, SR
Horne, AM
Orpinas, P
Martin, R
Quinn, WH
Tolan, PH
Gorman-Smith, D
Henry, DB
Gay, FN
Schoeny, M
Farrell, AD
Meyer, AL
Sullivan, TN
Allison, KW
AF Simon, Thomas R.
Ikeda, Robin M.
Smith, Emilie Phillips
Reese, Le'Roy E.
Rabiner, David L.
Miller-Johnson, Shari
Winn, Donna-Marie
Dodge, Kenneth A.
Asher, Steven R.
Horne, Arthur M.
Orpinas, Pamela
Martin, Roy
Quinn, William H.
Tolan, Patrick H.
Gorman-Smith, Deborah
Henry, David B.
Gay, Franklin N.
Schoeny, Michael
Farrell, Albert D.
Meyer, Aleta L.
Sullivan, Terri N.
Allison, Kevin W.
TI The Multisite Violence Prevention Project: Impact of a Universal
School-Based Violence Prevention Program on Social-Cognitive Outcomes
SO PREVENTION SCIENCE
LA English
DT Article
DE Aggression; Violence prevention; Middle school; Adolescent problem
behavior; Social-cognitive
ID AMERICAN ADOLESCENT MALES; AGGRESSIVE-BEHAVIOR; ANTISOCIAL-BEHAVIOR;
REDUCING VIOLENCE; CHILDREN; INTERVENTION; RISK
AB This study evaluated the impact of a universal school-based violence prevention program on social-cognitive factors associated with aggression and nonviolent behavior in early adolescence. The effects of the universal intervention were evaluated within the context of a design in which two cohorts of students at 37 schools from four sites (N=5,581) were randomized to four conditions: (a) a universal intervention that involved implementing a student curriculum and teacher training with sixth grade students and teachers; (b) a selective intervention in which a family intervention was implemented with a subset of sixth grade students exhibiting high levels of aggression and social influence; (c) a combined intervention condition; and (d) a no-intervention control condition. Short-term and long-term (i.e., 2-year post-intervention) universal intervention effects on social-cognitive factors targeted by the intervention varied as a function of students' pre-intervention level of risk. High-risk students benefited from the intervention in terms of decreases in beliefs and attitudes supporting aggression, and increases in self-efficacy, beliefs and attitudes supporting nonviolent behavior. Effects on low-risk students were in the opposite direction. The differential pattern of intervention effects for low- and high-risk students may account for the absence of main effects in many previous evaluations of universal interventions for middle school youth. These findings have important research and policy implications for efforts to develop effective violence prevention programs.
C1 [Farrell, Albert D.; Meyer, Aleta L.; Sullivan, Terri N.; Allison, Kevin W.] Virginia Commonwealth Univ, Dept Psychol, Richmond, VA 23284 USA.
[Simon, Thomas R.; Ikeda, Robin M.; Smith, Emilie Phillips; Reese, Le'Roy E.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Smith, Emilie Phillips] Penn State Univ, University Pk, PA 16802 USA.
[Reese, Le'Roy E.] Morehouse Sch Med, Atlanta, GA USA.
[Rabiner, David L.; Miller-Johnson, Shari; Winn, Donna-Marie; Dodge, Kenneth A.; Asher, Steven R.] Duke Univ, Durham, NC USA.
[Winn, Donna-Marie] Univ N Carolina, Chapel Hill, NC 27515 USA.
[Horne, Arthur M.; Orpinas, Pamela; Martin, Roy; Quinn, William H.] Univ Georgia, Athens, GA 30602 USA.
[Quinn, William H.] Clemson Univ, Clemson, SC 29631 USA.
[Tolan, Patrick H.; Gorman-Smith, Deborah; Henry, David B.; Gay, Franklin N.; Schoeny, Michael] Univ Illinois, Chicago, IL USA.
[Meyer, Aleta L.] Natl Inst Drug Abuse, Lexington, KY USA.
RP Farrell, AD (reprint author), Virginia Commonwealth Univ, Dept Psychol, POB 842018, Richmond, VA 23284 USA.
EM afarrell@vcu.edu
OI Tolan, Patrick/0000-0001-5669-8442
NR 48
TC 38
Z9 39
U1 1
U2 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1389-4986
J9 PREV SCI
JI Prev. Sci.
PD DEC
PY 2008
VL 9
IS 4
BP 231
EP 244
DI 10.1007/s11121-008-0101-1
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 369AX
UT WOS:000260666100001
ER
PT J
AU Dunton, GF
Robertson, TP
AF Dunton, Genevieve Fridlund
Robertson, Trina P.
TI A tailored internet-plus-email intervention for increasing physical
activity among ethnically-diverse women
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Exercise; Walking; Intervention; Internet; Women; Compliance
ID PUBLIC-HEALTH; EXERCISE; PARTICIPATION; VALIDATION; PREVENTION;
NUTRITION; ALGORITHM; AMERICAN; BEHAVIOR; WEBSITE
AB Objective. To evaluate the feasibility and efficacy of an individually tailored, Internet-plus-email physical activity intervention designed for adult women.
Method. Healthy and ethnically-diverse adult females (N=156) (mean age = 42.8 years, 65% Caucasian) from California were randomly assigned to an intervention (access to a tailored website and weekly emails) or wait-list control group. Participants completed web-based assessments of physical activity, stage of behavior change, and psychosocial variables at baseline, one month, two months, and three months. Data were collected during 2006-2007. Multilevel random coefficient modeling examined group differences in rates of change.
Results. As compared to the control condition, the intervention group increased walking (+69 versus +32 min per week) and total moderate-to-vigorous physical activity (+23 versus -25 min per week) after three months. The intervention did not impact stage of behavior change or any of the other psychosocial variables.
Conclusion. A tailored, Internet-based intervention for adult women had a positive effect on walking and moderate-to-vigorous physical activity in an ethnically-diverse sample. However, given the lack of comparable research contact in the control group, these findings should be taken cautiously. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Robertson, Trina P.] Dairy Council Calif, Irvine, CA 92612 USA.
[Dunton, Genevieve Fridlund] NCI, Hlth Promot Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20852 USA.
RP Robertson, TP (reprint author), Dairy Council Calif, 2151 Michelson Dr,Ste 235, Irvine, CA 92612 USA.
EM trinar@dairycouncilofca.org
FU Cancer Prevention Fellowship Program
FX We would like to acknowledge Kathryn Juhl for proofreading the
manuscript. Genevieve F. Dunton was supported by the Cancer Prevention
Fellowship Program, National Cancer Institute during the preparation of
this paper.
NR 38
TC 23
Z9 23
U1 3
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD DEC
PY 2008
VL 47
IS 6
BP 605
EP 611
DI 10.1016/j.ypmed.2008.10.004
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 385MX
UT WOS:000261819400006
PM 18977243
ER
PT J
AU Swendsen, J
Anthony, JC
Conway, KP
Degenhardt, L
Dierker, L
Glantz, M
He, JP
Kalaydjian, A
Kessler, RC
Sampson, N
Merikangas, KR
AF Swendsen, Joel
Anthony, James C.
Conway, Kevin P.
Degenhardt, Louisa
Dierker, Lisa
Glantz, Meyer
He, Jianping
Kalaydjian, Amanda
Kessler, Ronald C.
Sampson, Nancy
Merikangas, Kathleen R.
TI Improving targets for the prevention of drug use disorders:
Sociodemographic predictors of transitions across drug use stages in the
national comorbidity survey replication
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Prevention; Substance-related disorders; Epidemiology; Demographic
factors
ID AGE-OF-ONSET; MALE-FEMALE DIFFERENCES; DSM-IV DISORDERS; UNITED-STATES;
EPIDEMIOLOGIC SURVEY; LIFETIME PREVALENCE; YOUNG-ADULTS; NCS-R;
DEPENDENCE; ALCOHOL
AB Objectives. Models of drug use etiology and prevention require precise information concerning the expression of population-based risk factors across the continuum of drug use. However, the majority of previous epidemiologic research on this topic has not addressed transitions between specific drug stages. The present investigation examined the sociodemographic predictors of progression across six stages of drug use in the National Comorbidity Survey Replication (NCS-R), a nationally representative household survey of the U.S. population conducted between February, 2001 and April, 2003.
Methods. Lifetime history of opportunity to use illicit substances, initial drug use, and DSM-IV drug use disorders were collected using in-person structured diagnostic interviews.
Results. The median age of first opportunity to use drugs as well as drug use, abuse and dependence each occurred prior to age 20, while the median remission from abuse and dependence occurred at 26 and 30 years, respectively. Most sociodemographic variables, in particular sex and ethnicity, demonstrated highly differential associations with transitions depending on the stage examined.
Conclusions. The findings may partially explain the effectiveness of strategies designed to reduce drug use, abuse and dependence, and indicate that increased correspondence is needed between available epidemiologic data and existing models of etiology or prevention. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Swendsen, Joel] Univ Bordeaux, CNRS 5231, Natl Ctr Sci Res, F-33076 Bordeaux, France.
[Anthony, James C.] Michigan State Univ, Dept Epidemiol, Lansing, MI USA.
[Conway, Kevin P.; Glantz, Meyer] Natl Inst Drug Abuse, Div Epidemiol Serv & Prevent Res, Bethesda, MD USA.
[Degenhardt, Louisa] Univ NSW, Natl Drug & Alcohol Res Ctr, Sydney, NSW, Australia.
[Dierker, Lisa] Wesleyan Univ, Dept Psychol, Middletown, CT USA.
[He, Jianping; Kalaydjian, Amanda; Merikangas, Kathleen R.] NIMH, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Kessler, Ronald C.; Sampson, Nancy] Harvard Univ, Dept Hlth Policy, Boston, MA 02115 USA.
RP Swendsen, J (reprint author), Univ Bordeaux, CNRS 5231, Natl Ctr Sci Res, 146 Rue Leo Saignat, F-33076 Bordeaux, France.
EM Joel.Swendsen@u-bordeaux2.fr
RI Degenhardt, Louisa/D-4515-2012;
OI Degenhardt, Louisa/0000-0002-8513-2218; Conway,
Kevin/0000-0002-7638-339X
FU National Institute of Mental Health (NIMH) [U01-MH60220]; National
Institute of Drug Abuse (NIDA) [K01 DA15454]; French National Center for
Scientific Research; Patrick and Catherine Weldon Donaghue Medical
Research Foundation
FX The National Comorbidity Survey Replication (NCS-R) was supported by
grant U01-MH60220 from the National Institute of Mental Health (NIMH)
with supplemental support from the National Institute of Drug Abuse
(NIDA), The Substance Abuse and Mental Health Services Administration;
grant 044708 from The Robert Wood Johnson Foundation and the John W.
Alden Trust. Manuscript preparation was also supported by an ATIP award
from the French National Center for Scientific Research (Dr. Swendsen),
the Intramural Research Program of the National Institutes of Health,
National Institute of Mental Health (Drs. Kalaydjian and Merikangas),
grant K01 DA15454 from the National Institute of Drug Abuse and an
Investigator Award from the Patrick and Catherine Weldon Donaghue
Medical Research Foundation (Dr. Dierker). The views and opinions
expressed in this report are those of the authors and should not be
construed to represent the views of any of the sponsoring organizations,
agencies, or U.S. Government.
NR 40
TC 15
Z9 16
U1 6
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD DEC
PY 2008
VL 47
IS 6
BP 629
EP 634
DI 10.1016/j.ypmed.2008.09.009
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 385MX
UT WOS:000261819400010
PM 18926848
ER
PT J
AU Chu, LW
Zhu, Y
Yu, K
Zheng, T
Yu, H
Zhang, Y
Sesterhenn, I
Chokkalingam, AP
Danforth, KN
Shen, MC
Stanczyk, FZ
Gao, YT
Hsing, AW
AF Chu, L. W.
Zhu, Y.
Yu, K.
Zheng, T.
Yu, H.
Zhang, Y.
Sesterhenn, I.
Chokkalingam, A. P.
Danforth, K. N.
Shen, M-C
Stanczyk, F. Z.
Gao, Y-T
Hsing, A. W.
TI Variants in circadian genes and prostate cancer risk: a population-based
study in China
SO PROSTATE CANCER AND PROSTATIC DISEASES
LA English
DT Article
DE circadian genes; genetic polymorphisms; China
ID EXTREME DIURNAL PREFERENCE; SLEEP PHASE SYNDROME; ANDROGEN RECEPTOR;
CLOCK; POLYMORPHISM; EPIDEMIOLOGY; ASSOCIATION; HOMEOSTASIS; SECRETION;
MORTALITY
AB Circadian genes influence a variety of biological processes that are important in prostate tumorigenesis including metabolism. To determine if variants in circadian genes alter prostate cancer risk, we genotyped five variants in five circadian genes in a population-based case-control study conducted in China ( 187 cases and 242 controls). These variants included CRY2 rs1401417:G > C, CSNK1E rs1005473:A > C, NPAS2 rs2305160:G > A, PER1 rs2585405:G > C and PER3 54-bp repeat length variant. Men with the cryptochrome 2 ( CRY2)-variant C allele had a significant 1.7-fold increased prostate cancer risk (95% confidence interval (CI), 1.1-2.7) relative to those with the GG genotype. This risk increased to 4.1-fold ( 95% CI, 2.2-8.0) in men who also had greater insulin resistance (IR) as compared to men with the GG genotype and less IR. In contrast, among men with less IR, the NPAS2-variant A allele was associated with decreased prostate cancer risk ( odds ratio 0.5, 95% CI, 0.3-1.0) as compared to the GG genotype. Our findings, although in need of confirmation, suggest that variations in circadian genes may alter prostate cancer risk and some biological processes may modify this effect.
C1 [Chu, L. W.] NCI, NIH, Canc Prevent Div, Off Prevent Oncol,Canc Prevent Fellowship Program, Bethesda, MD 20892 USA.
[Zhu, Y.; Zheng, T.; Yu, H.; Zhang, Y.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Yu, K.; Danforth, K. N.; Hsing, A. W.] NCI, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Sesterhenn, I.] Armed Forces Inst Pathol, Washington, DC 20306 USA.
[Chokkalingam, A. P.] Univ Calif Berkeley, Sch Publ Hlth, Dept Epidemiol, Berkeley, CA 94720 USA.
[Shen, M-C] Fudan Univ, Shanghai Tumor Hosp, Shanghai 200433, Peoples R China.
[Stanczyk, F. Z.] Univ So Calif, Keck Sch Med, Dept Obstet & Gynaecol, Los Angeles, CA 90033 USA.
[Gao, Y-T] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
RP Chu, LW (reprint author), NCI, NIH, Canc Prevent Div, Off Prevent Oncol,Canc Prevent Fellowship Program, 6130 Execut Blvd,EPN,Suite 321, Bethesda, MD 20892 USA.
EM chulisa@mail.nih.gov
NR 45
TC 40
Z9 42
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1365-7852
J9 PROSTATE CANCER P D
JI Prostate Cancer Prostatic Dis.
PD DEC
PY 2008
VL 11
IS 4
BP 342
EP 348
DI 10.1038/sj.pcan.4501024
PG 7
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA 370GQ
UT WOS:000260751100006
PM 17984998
ER
PT J
AU Davis, J
Wang, JW
Tropea, JE
Zhang, D
Dauter, Z
Waugh, DS
Wlodawer, A
AF Davis, Jamaine
Wang, Jiawei
Tropea, Joseph E.
Zhang, Di
Dauter, Zbigniew
Waugh, David S.
Wlodawer, Alexander
TI Novel fold of VirA, a type III secretion system effector protein from
Shigella flexneri
SO PROTEIN SCIENCE
LA English
DT Article
DE crystallography; protein crystallization; proteolysis; bacterial
virulence; novel fold
ID ENTEROPATHOGENIC ESCHERICHIA-COLI; SOFTWARE; ESPG; IDENTIFICATION;
MICROTUBULES; CELLS
AB VirA, a secreted effector protein from Shigella sp., has been shown to be necessary for its virulence. It was also reported that VirA might be related to papain-like cysteine proteases and cleave alpha-tubulin, thus facilitating intracellular spreading. We have now determined the crystal structure of VirA at 3.0 angstrom resolution. The shape of the molecule resembles the letter "V,'' with the residues in the N-terminal third of the 45-kDa molecule ( some of which are disordered) forming one clearly identifiable domain, and the remainder of the molecule completing the V-like structure. The fold of VirA is unique and does not resemble that of any known protein, including papain, although its N-terminal domain is topologically similar to cysteine protease inhibitors such as stefin B. Analysis of the sequence conservation between VirA and its Escherichia coli homologs EspG and EspG2 did not result in identification of any putative protease-like active site, leaving open a possibility that the biological function of VirA in Shigella virulence may not involve direct proteolytic activity.
C1 [Davis, Jamaine; Wlodawer, Alexander] NCI Frederick, Prot Struct Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
[Wang, Jiawei] SAIC Frederick Inc, Basic Res Program, Frederick, MD 21702 USA.
[Wang, Jiawei; Dauter, Zbigniew] NCI, Synchrotron Radiat Res Sect, Macromol Crystallog Lab, Argonne, IL 60439 USA.
[Zhang, Di; Waugh, David S.] NCI, Prot Engn Sect, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RP Wlodawer, A (reprint author), NCI Frederick, Prot Struct Sect, Macromol Crystallog Lab, POB B, Frederick, MD 21702 USA.
EM wlodawea@mail.nih.gov
FU U. S. Department of Energy, Office of Science, Office of Basic Energy
Sciences [W-31-109-Eng-38]; NIH, National Cancer Institute, Center for
Cancer Research; National Cancer Institute, NIH [NO1-CO-12400]
FX We thank Dr. Antonina Roll-Mecak for testing the microtubule-severing
activity of VirA. Diffraction data were collected at the Southeast
Regional Collaborative Access Team (SER-CAT) beamline 22-ID, located at
the Advanced Photon Source, Argonne National Laboratory. Use of the
Advanced Photon Source was supported by the U. S. Department of Energy,
Office of Science, Office of Basic Energy Sciences, under contract no.
W-31-109-Eng-38. This project was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research and in part with Federal funds from the National Cancer
Institute, NIH, under contract no. NO1-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does the mention of trade
names, commercial products, or organizations imply endorsement by the U.
S. Government.
NR 32
TC 13
Z9 14
U1 0
U2 4
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD DEC
PY 2008
VL 17
IS 12
BP 2167
EP 2173
DI 10.1110/ps.037978.108
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 375ZA
UT WOS:000261151100015
PM 18787201
ER
PT J
AU Lin, YJ
Umehara, T
Inoue, M
Saito, K
Kigawa, T
Jang, MK
Ozato, K
Yokoyama, S
Padmanabhan, B
Guntert, P
AF Lin, Yi-Jan
Umehara, Takashi
Inoue, Makoto
Saito, Kohei
Kigawa, Takanori
Jang, Moon-Kyoo
Ozato, Keiko
Yokoyama, Shigeyuki
Padmanabhan, Balasundaram
Guentert, Peter
TI Solution structure of the extraterminal domain of the
bromodomain-containing protein BRD4
SO PROTEIN SCIENCE
LA English
DT Article
DE BET protein family; bromodomain; chromatin; ET domain; histone; NMR
ID TORSION ANGLE DYNAMICS; NMR STRUCTURE; NUCLEAR ANTIGEN; INTERACTS;
PROGRAM; CHROMATIN; RECOGNITION; LANA-1; DYANA
AB BRD4, which is a member of the BET (bromodomains and extraterminal) protein family, interacts preferentially with acetylated chromatin and possesses multiple cellular functions in meiosis, embryonic development, the cell cycle, and transcription. BRD4 and its family members contain two bromodomains known to bind acetylated lysine, and a conserved ET domain whose function is unclear. Here we show the solution structure of the ET domain of mouse BRD4, which provides the first three-dimensional structure of an ET domain in the BET family. We determined the NMR structure of BRD4-ET with a root-mean-square deviation of 0.41 angstrom for the backbone atoms in the structured region of residues 608-676 on the basis of 1793 upper distance limits derived from NOE intensities measured in three-dimensional NOESY spectra. The structure of the BRD4-ET domain comprises three alpha-helices and a characteristic loop region of an irregular but well-defined structure. A DALI search revealed no close structural homologs in the current Protein Data Bank. The BRD4-ET structure has an acidic patch that forms a continuous ridge with a hydrophobic cleft, which may interact with other proteins and/or DNA.
C1 [Guentert, Peter] Univ Frankfurt, Inst Biophys Chem, D-60438 Frankfurt, Germany.
[Guentert, Peter] Univ Frankfurt, Frankfurt Inst Adv Studies, D-60438 Frankfurt, Germany.
[Lin, Yi-Jan; Guentert, Peter] RIKEN Genom Sci Ctr, Tatsuo Miyazawa Mem Program, Yokohama, Kanagawa 2300045, Japan.
[Lin, Yi-Jan] Kaohsiung Med Univ, Fac Biotechnol, Kaohsiung, Taiwan.
[Lin, Yi-Jan] Kaohsiung Med Univ, Ctr Excellence Environm Med, Kaohsiung, Taiwan.
[Jang, Moon-Kyoo; Ozato, Keiko] NICHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA.
[Yokoyama, Shigeyuki] Univ Tokyo, Grad Sch Sci, Dept Biophys & Biochem, Tokyo 1130033, Japan.
[Guentert, Peter] Tokyo Metropolitan Univ, Grad Sch Sci, Tokyo 1920397, Japan.
RP Guntert, P (reprint author), Univ Frankfurt, Inst Biophys Chem, Max von Lauestr 9, D-60438 Frankfurt, Germany.
EM paddy.b@AptuitLaurus.com; guentert@em.uni-frankfurt.de
RI Lin, Yi-Jan/C-9672-2009; Kigawa, Takanori/A-7679-2010; Guntert,
Peter/L-5577-2013; Fachbereich14, Dekanat/C-8553-2015; Umehara,
Takashi/N-5683-2015; Yokoyama, Shigeyuki/N-6911-2015
OI Kigawa, Takanori/0000-0003-0146-9719; Guntert,
Peter/0000-0002-2911-7574; Umehara, Takashi/0000-0003-3464-2960;
Yokoyama, Shigeyuki/0000-0003-3133-7338
FU National Project on Protein Structural; Ministry of Education, Culture,
Sports, Science and Technology of Japan (MEXT); Grant-in-Aid for
Scientific Research of the Japan Society for the Promotion of Science
(JSPS); Volkswagen Foundation
FX We thank Yasuko Tomo, Eiko Seki, Kazuharu Hanada, Yukiko Fujikura, and
Satoru Watanabe for sample preparation and Dr. Hua Li for help with the
programs KUJIRA and NMRView. This work was financed by the National
Project on Protein Structural and Functional Analyses of the Ministry of
Education, Culture, Sports, Science and Technology of Japan (MEXT). P.
G. is supported by a Grant-in-Aid for Scientific Research of the Japan
Society for the Promotion of Science (JSPS) and by a Lichtenberg
Professorship of the Volkswagen Foundation.
NR 26
TC 24
Z9 24
U1 0
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD DEC
PY 2008
VL 17
IS 12
BP 2174
EP 2179
DI 10.1110/ps.037580.108
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 375ZA
UT WOS:000261151100016
PM 18815416
ER
PT J
AU Rader, JS
Malone, JP
Gross, J
Gilmore, P
Brooks, RA
Nguyen, L
Crimmins, DL
Feng, S
Wright, JD
Taylor, N
Zighelboim, I
Funk, MC
Huettner, PC
Ladenson, JH
Gius, D
Townsend, RR
AF Rader, Janet S.
Malone, James P.
Gross, Julia
Gilmore, Petra
Brooks, Rebecca A.
Nguyen, Loan
Crimmins, Dan L.
Feng, Sheng
Wright, Jason D.
Taylor, Nicholas
Zighelboim, Israel
Funk, Margo C.
Huettner, Phyllis C.
Ladenson, Jack H.
Gius, David
Townsend, R. Reid
TI A unified sample preparation protocol for proteomic and genomic
profiling of cervical swabs to identify biomarkers for cervical cancer
screening
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Article
DE 2-D DIGE; Biomarkers; cDNA microarray; Cervical cancer; RNAlater
ID DIFFERENCE GEL-ELECTROPHORESIS; LUNG-CANCER; PROTEIN; RNA; PURIFICATION;
MICROARRAY; EXPRESSION; DISCOVERY; CARCINOMA; ANTIGEN
AB Cervical cancer screening is ideally suited for the development of biomarkers due to the ease of tissue acquisition and the well-established histological transitions. Furthermore, cell and biologic fluid obtained from cervix samples undergo specific molecular changes that can be profiled. However, the ideal manner and techniques for preparing cervical samples remains to be determined. To address this critical issue a patient screening protein and nucleic acid collection protocol was established. RNAlater was used to collect the samples followed by proteomic methods to identify proteins that were differentially expressed in normal cervical epithelial versus cervical cancer cells. Three hundred ninety spots were identified via 2-D DIGE that were expressed at either higher or lower levels (> three-fold) in cervical cancer samples. These proteomic results were compared to genes in a cDNA microarray analysis of microdissected neoplastic cervical specimens to identify overlapping patterns of expression. The most frequent pathways represented by the combined dataset were: cell cycle: G2/M DNA damage checkpoint regulation; aryl hydrocarbon receptor signaling; p53 signaling; cell cycle: G1/S checkpoint regulation; and the ER stress pathway. HNRPA2B1 was identified as a biomarker candidate with increased expression in cancer compared to normal cervix and validated by Western blot.
C1 [Rader, Janet S.; Brooks, Rebecca A.; Nguyen, Loan; Wright, Jason D.; Taylor, Nicholas; Zighelboim, Israel; Funk, Margo C.] Washington Univ, Sch Med, Div Gynecol Oncol, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
[Rader, Janet S.; Malone, James P.; Gross, Julia; Gilmore, Petra; Brooks, Rebecca A.; Nguyen, Loan; Crimmins, Dan L.; Feng, Sheng; Wright, Jason D.; Taylor, Nicholas; Zighelboim, Israel; Funk, Margo C.; Huettner, Phyllis C.; Ladenson, Jack H.; Townsend, R. Reid] Alvin J Siteman Canc Ctr, St Louis, MO USA.
[Rader, Janet S.] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA.
[Malone, James P.; Gross, Julia; Gilmore, Petra; Townsend, R. Reid] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
[Feng, Sheng] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA.
[Gius, David] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Townsend, R. Reid] Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA.
RP Rader, JS (reprint author), Washington Univ, Sch Med, Div Gynecol Oncol, Dept OB GYN, 660 S Euclid Ave,Campus Box 8064, St Louis, MO 63110 USA.
EM raderj@wustl.edu
FU Barnes-Jewish Hospital Foundation; NIH [CA094141, CA95713]; Alvin J.
Siteman Cancer Center at Barnes-Jewish Hospital and Washington
University School of Medicine; NCI Cancer Center [P30 CA91842]; National
Institutes of Health; National Cancer Institute; Center for Cancer
Research
FX The work was supported by grants from Barnes-Jewish Hospital Foundation
and NIH grants CA094141 and CA95713. This work was supported, in part,
by the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and
Washington University School of Medicine and by institutional resources
provided to the Proteomics Center at Washington University. The Siteman
Cancer Center is supported in part by a NCI Cancer Center Support Grant
P30 CA91842. This research was supported, in part, by the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, and the Center for Cancer Research.
NR 23
TC 5
Z9 5
U1 0
U2 1
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 1862-8346
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD DEC
PY 2008
VL 2
IS 12
BP 1658
EP 1669
DI 10.1002/prca.200780146
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 386WL
UT WOS:000261913200010
PM 21136816
ER
PT J
AU Liu, LX
Foroud, T
Xuei, XL
Berrettini, W
Byerley, W
Coryell, W
El-Mallakh, R
Gershon, ES
Kelsoe, JR
Lawson, WB
MacKinnon, DF
McInnis, M
McMahon, FJ
Murphy, DL
Rice, J
Scheftner, W
Zandi, PP
Lohoff, FW
Niculescu, AB
Meyer, ET
Edenberg, HJ
Nurnberger, JI
AF Liu, Lixiang
Foroud, Tatiana
Xuei, Xiaoling
Berrettini, Wade
Byerley, William
Coryell, William
El-Mallakh, Rif
Gershon, Elliot S.
Kelsoe, John R.
Lawson, William B.
MacKinnon, Dean F.
McInnis, Melvin
McMahon, Francis J.
Murphy, Dennis L.
Rice, John
Scheftner, William
Zandi, Peter P.
Lohoff, Falk W.
Niculescu, Alexander B.
Meyer, Eric T.
Edenberg, Howard J.
Nurnberger, John I., Jr.
TI Evidence of association between brain-derived neurotrophic factor gene
and bipolar disorder
SO PSYCHIATRIC GENETICS
LA English
DT Article
DE association study; bipolar disorder; brain-derived neurotrophic factor;
single nucleotide polymorphism
ID FACTOR BDNF GENE; FAMILY-BASED ASSOCIATION; GENOME-WIDE ASSOCIATION;
ONSET MOOD DISORDER; TRKB MESSENGER-RNA; VAL66MET POLYMORPHISM; CONFERS
SUSCEPTIBILITY; LINKAGE DISEQUILIBRIUM; INITIATIVE PEDIGREES;
DEPRESSED-PATIENTS
AB Objective Brain-derived neurotrophic factor (BDNF) plays an important role in the survival, differentiation, and outgrowth of select peripheral and central neurons throughout adulthood. Growing evidence suggests that BDNF is involved in the pathophysiology of mood disorders.
Methods Ten single nucleotide polymorphisms (SNPs) across the BDNF gene were genotyped in a sample of 1749 Caucasian Americans from 250 multiplex bipolar families. Family-based association analysis was used with three hierarchical bipolar disorder models to test for an association between SNPs in BDNF and the risk of bipolar disorder. In addition, an exploratory analysis was performed to test for an association of the SNPs in BDNF and the phenotypes of rapid cycling and episode frequency.
Results Evidence of association (P<0.05) was found with several of the SNPs using multiple models of bipolar disorder; one of these SNPs also showed evidence of association (P<0.05) with rapid cycling.
Conclusion These results provide further evidence that variation in BDNF affects the risk for bipolar disorder. Psychiatr Genet 18:267-274 (C) 2008 Wolters Kluwer Health / Lippincott Williams & Wilkins.
C1 [Foroud, Tatiana] Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Berrettini, Wade; Lohoff, Falk W.] Univ Penn, Philadelphia, PA 19104 USA.
[Byerley, William] Univ Calif Irvine, Irvine, CA USA.
[Kelsoe, John R.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Coryell, William] Univ Iowa, Iowa City, IA USA.
[El-Mallakh, Rif] Univ Louisville, Louisville, KY 40292 USA.
[Gershon, Elliot S.] Univ Chicago, Chicago, IL 60637 USA.
[Scheftner, William] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Lawson, William B.] Howard Univ, Washington, DC 20059 USA.
[MacKinnon, Dean F.; Zandi, Peter P.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[McMahon, Francis J.; Murphy, Dennis L.] NIMH, NIH, Bethesda, MD 20892 USA.
[McInnis, Melvin] Univ Michigan, Ann Arbor, MI 48109 USA.
[Rice, John] Washington Univ, St Louis, MO USA.
RP Foroud, T (reprint author), Indiana Univ, Sch Med, Dept Med & Mol Genet, Hlth Informat & Translat Sci HS 4000,410 W 10th S, Indianapolis, IN 46202 USA.
EM tforoud@iupui.edu
RI Niculescu, Alexander/A-3328-2012; Lohoff, Falk/M-7951-2016; Meyer,
Eric/C-1029-2011
OI Lawson, William/0000-0002-9324-7090; Nurnberger,
John/0000-0002-7674-1767; McMahon, Francis/0000-0002-9469-305X;
Edenberg, Howard/0000-0003-0344-9690; Meyer, Eric/0000-0002-1998-7162
FU Indiana Genomics Initiative (INGEN); Lilly Endowment, Inc
FX Data and biomaterials were collected as part of four projects that
participated in the National Institute of Mental Health (NIMH) Bipolar
Disorder Genetics Initiative. From 1991-98, the principal investigators
and co-investigators were Indiana University, Indianapolis, Indiana, U01
MH46282, John Nurnberger MD, PhD, Marvin Miller MD, and Elizabeth Bowman
MD; Washington University, St Louis, Missouri, U01 MH46280, Theodore
Reich MD, Allison Goate PhD, and John Rice PhD; Johns Hopkins
University, Baltimore, MD U01 MH46274, J. Raymond DePaulo Jr MD, Sylvia
Simpson MD, MPH, and Colin Stine PhD; NIMH Intramural Research Program,
Clinical Neurogenetics Branch, Bethesda, MD, Elliot Gershon MD, Diane
Kazuba BA, and Elizabeth Maxwell MSW.; Data and biomaterials were
collected as part of 10 projects that participated in the National
Institute of Mental Health (NIMH) Bipolar Disorder Genetics Initiative.
From 1999-03, the principal investigators and co-investigators were
Indiana University, Indianapolis, Indiana, R01 MH59545, John Nurnberger
MD, PhD, Marvin J. Miller MD, Elizabeth S. Bowman MD, N. Leela Rau MD,
P. Ryan Moe MD, Nalini Samavedy MD, Rif El-Mallakh MD (at University of
Louisville), Husseini Manji MD (at Wayne State University), Debra A.
Glitz MID (at Wayne State University), Eric T Meyer MS, Carrie Smiley
RN, Tatiana Foroud PhD, Leah Flury MS, Danielle M. Dick PhD, and Howard
Edenberg PhD; Washington University, St Louis, Missouri, R01 MH059534,
John Rice PhD, Theodore Reich MD, Allison Goate PhD, and Laura Bierut
MD; Johns Hopkins University, Baltimore, MD, R01 MH59533, Melvin McInnis
MD, J. Raymond DePaulo Jr MD, Dean F. MacKinnon MD, Francis M. Mondimore
MD, James B. Potash MD, Peter P. Zandi PhD, Dimitrios Avramopoulos, and
Jennifer Payne; University of Pennsylvania, Pennsylvania, R01 MH59553,
Wade Berrettini MD, PhD; University of California at Irvine, CA, R01
MH60068, William Byerley MD, and Mark Vawter MD; University of Iowa,
Iowa, R01 MH059548, William Coryell MD, and Raymond Crowe MD; University
of Chicago, Illinois, R01 MH59535, Elliot Gershon MD, Judith Badner PhD,
Francis McMahon MD, Chunyu Liu PhD, Alan Sanders MD, Maria Caserta,
Steven Dinwiddie MD, Tu Nguyen, and Donna Harakal; University of
California at San Diego, California, R01 MH59567, John Kelsoe MD, and
Rebecca McKinney BA; Rush University, Illinosis, R01 MH059556, William
Scheftner MD, Howard M. Kravitz DO, MPH, Diana Marta BS, Annette
Vaughn-Brown, MSN, RN, and Laurie Bederow, Massachusetts; NIMH
Intramural Research Program, Bethesda, MD, Z01MH002810-01, Francis J.
McMahon MD, Layla Kassem PsyD, Sevilla Detera-Wadleigh PhD, Lisa Austin
PhD, and Dennis L. Murphy MD. SNP genotyping by MALDI-TOF mass
spectrometry used the facilities of the Center for Medical Genomics at
Indiana University School of Medicine, which is supported in part by a
grant from the Indiana Genomics Initiative (INGEN). INGEN is Supported
in part by the Lilly Endowment, Inc.
NR 66
TC 35
Z9 35
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0955-8829
J9 PSYCHIAT GENET
JI Psychiatr. Genet.
PD DEC
PY 2008
VL 18
IS 6
BP 267
EP 274
DI 10.1097/YPG.0b013e3283060f59
PG 8
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 380OA
UT WOS:000261473800002
PM 19018231
ER
PT J
AU Feder, A
Southwick, SM
Goetz, RR
Wang, YP
Alonso, A
Smith, BW
Buchholz, KR
Waldeck, T
Ameli, R
Moore, J
Hain, R
Charney, DS
Vythilingam, M
AF Feder, Adriana
Southwick, Steven M.
Goetz, Raymond R.
Wang, Yanping
Alonso, Angelique
Smith, Bruce W.
Buchholz, Katherine R.
Waldeck, Tracy
Ameli, Rezvan
Moore, Jeffrey
Hain, Robert
Charney, Dennis S.
Vythilingam, Meena
TI Posttraumatic Growth in Former Vietnam Prisoners of War
SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES
LA English
DT Article
ID STRESS-DISORDER; POSITIVE AFFECT; LIFE; FOUNDATIONS; RESILIENCE;
INVENTORY; BENEFITS; ILLNESS; HEALTH
AB This study examined posttraumatic growth in 30 male veterans captured and held as prisoners of war during the Vietnam War. Participants were assessed with structured diagnostic interviews administered by trained clinicians as well as with the Posttraumatic Growth Inventory (PTGI) and other questionnaires measuring dispositional optimism, religious coping, social supports, and purpose in life, Mean age (standard deviation-SD) of participants was 66.7 (6.0) years. Mean total PTGI score (SD) was 66.3 (17.5), indicating a moderate degree of posttraumatic growth. The most strongly endorsed items corresponded to the Appreciation of Life and Personal Strength factors. The group as a whole was optimistic and reported moderate use of positive religious coping. Posttraumatic growth did not significantly differ in repatriates with and without psychopathology, but it was significantly positively correlated with dispositional optimism. In the final regression model, length of captivity and optimism were significant predictors of posttraumatic growth. Our findings confirm that it is possible to achieve long-lasting personal growth even in the face of prolonged extreme adversity. Prospective studies are needed to further evaluate whether pre-existing traits such as optimism can predict growth after trauma.
C1 [Feder, Adriana; Southwick, Steven M.; Wang, Yanping; Alonso, Angelique; Buchholz, Katherine R.; Charney, Dennis S.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10023 USA.
[Southwick, Steven M.] Yale Univ, Dept Psychiat, New Haven, CT 06520 USA.
[Goetz, Raymond R.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Smith, Bruce W.] Univ New Mexico, Dept Psychol, Albuquerque, NM 87131 USA.
[Waldeck, Tracy; Ameli, Rezvan; Vythilingam, Meena] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Moore, Jeffrey; Hain, Robert] Robert E Mitchell Ctr Prisoner War Studies, Pensacola, FL USA.
RP Feder, A (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1217, New York, NY 10023 USA.
EM adriana.feder@mssm.edu
FU NIMH Intramural Research Program
FX We gratefully acknowledge the support of the NIMH Intramural Research
Program and the work of Kayleen Hadd, R.N., Raini Agarwal, M.A., and the
staff at the NIMH Mood and Anxiety Disorders Program.
NR 42
TC 32
Z9 33
U1 1
U2 6
PU GUILFORD PUBLICATIONS INC
PI NEW YORK
PA 72 SPRING STREET, NEW YORK, NY 10012 USA
SN 0033-2747
J9 PSYCHIATRY
JI Psychiatry-Interpers. Biol. Process.
PD WIN
PY 2008
VL 71
IS 4
BP 359
EP 370
PG 12
WC Psychiatry
SC Psychiatry
GA 391PV
UT WOS:000262246100010
PM 19152285
ER
PT J
AU Fox, M
Jensen, C
French, H
Stein, A
Huang, SJ
Tolliver, T
Murphy, D
AF Fox, Meredith A.
Jensen, Catherine L.
French, Helen T.
Stein, Alison R.
Huang, Su-Jan
Tolliver, Teresa J.
Murphy, Dennis L.
TI Neurochemical, behavioral, and physiological effects of
pharmacologically enhanced serotonin levels in serotonin transporter
(SERT)-deficient mice
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE High-performance liquid chromatography (HPLC); Temperature; Serotonin
syndrome behaviors; Dopamine transporter (DAT); 5-hydroxy-L-tryptophan
(5-HTP); 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT);
N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanec
arboxamide maleate salt (WAY 100635); 5-carboxamidotryptamine maleate
(5-CT); SB 269970; GBR 12909
ID 5-HT7 RECEPTOR ANTAGONIST; KNOCK-OUT MICE; EARLY-LIFE BLOCKADE;
RAT-BRAIN; 8-HYDROXY-2-(DI-N-PROPYLAMINO)TETRALIN 8-OH-DPAT;
POSTNATAL-DEVELOPMENT; HYPOTHERMIC RESPONSE; TARGETED DISRUPTION;
REUPTAKE INHIBITOR; DEFICIENT MICE
AB Serotonin transporter (SERT) knockout (-/-) mice have an altered phenotype in adulthood, including high baseline anxiety and depressive-like behaviors, associated with increased baseline extracellular serotonin levels throughout life.
To examine the effects of increases in serotonin following the administration of the serotonin precursor 5-hydroxy- l-tryptophan (5-HTP) in SERT wild-type (+/+), heterozygous (+/-), and -/- mice.
5-HTP increased serotonin in all five brain areas examined with approximately 2- to 5-fold increases in SERT+/+ and +/- mice, and with greater 4.5- to 11.7-fold increases in SERT-/- mice. Behaviorally, 5-HTP induced exaggerated serotonin syndrome behaviors in SERT-/-, mice with similar effects in male and female mice. Studies suggest promiscuous serotonin uptake by the dopamine transporter (DAT) in SERT-/- mice, and here, the DAT blocker GBR 12909 enhanced 5-HTP-induced behaviors in SERT-/- mice. Physiologically, 5-HTP induced exaggerated temperature effects in SERT-deficient mice. The 5-HT1A antagonist WAY 100635 decreased 5-HTP-induced hypothermia in SERT+/+ and +/- mice with no effect in SERT-/- mice, whereas the 5-HT7 antagonist SB 269970 decreased this exaggerated response in SERT-/- mice only. WAY 100635 and SB 269970 together completely blocked 5-HTP-induced hypothermia in SERT+/- and -/- mice.
These studies demonstrate that SERT-/- mice have exaggerated neurochemical, behavioral, and physiological responses to further increases in serotonin, and provide the first evidence of intact 5-HT7 receptor function in SERT-/- mice, with interesting interactions between 5-HT1A and 5-HT7 receptors. As roles for 5-HT7 receptors in anxiety and depression were recently established, the current findings have implications for understanding the high anxiety and depressive-like phenotype of SERT-deficient mice.
C1 [Fox, Meredith A.; Jensen, Catherine L.; French, Helen T.; Stein, Alison R.; Huang, Su-Jan; Tolliver, Teresa J.; Murphy, Dennis L.] NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA.
RP Fox, M (reprint author), NIMH, Clin Sci Lab, NIH, 10 Ctr Dr,Bldg 10-3D41,MSC 1264, Bethesda, MD 20892 USA.
EM mfox@mail.nih.gov
FU NIMH
FX This research was supported by the NIMH Intramural Research program.
NR 83
TC 32
Z9 33
U1 3
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD DEC
PY 2008
VL 201
IS 2
BP 203
EP 218
DI 10.1007/s00213-008-1268-7
PG 16
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 373HO
UT WOS:000260961900005
PM 18712364
ER
PT J
AU Ohtani, M
Suzuki, J
Jacobson, KA
Oka, T
AF Ohtani, Masahiro
Suzuki, Jun-ichiro
Jacobson, Kenneth A.
Oka, Takami
TI Evidence for the possible involvement of the P2Y(6) receptor in Ca(2+)
mobilization and insulin secretion in mouse pancreatic islets
SO PURINERGIC SIGNALLING
LA English
DT Article
DE Pancreatic islets; P2Y(1) nucleotide receptor; Purines; Pyrimidines;
Insulin; Calcium
ID PERFUSED RAT PANCREAS; BETA-CELLS; P2 RECEPTORS; ADENINE-NUCLEOTIDES;
EXTRACELLULAR ATP; CYTOPLASMIC CA2+; DRUG TARGETS; RINM5F CELLS;
RELEASE; ACTIVATION
AB Subtypes of purinergic receptors involved in modulation of cytoplasmic calcium ion concentration ([Ca(2+)](i)) and insulin release in mouse pancreatic beta-cells were examined in two systems, pancreatic islets in primary culture and beta-TC6 insulinoma cells. Both systems exhibited some physiological responses such as acetylcholine-stimulated [Ca(2+)](i) rise via cytoplasmic Ca(2+) mobilization. Addition of ATP, ADP, and 2-MeSADP (each 100 mu M) transiently increased [Ca(2+)](i) in single islets cultured in the presence of 5.5 mM (normal) glucose. The potent P2Y(1) receptor agonist 2-MeSADP reduced insulin secretion significantly in islets cultured in the presence of high glucose (16.7 mM), whereas a slight stimulation occurred at 5.5 mM glucose. The selective P2Y(6) receptor agonist UDP (200 mu M) transiently increased [Ca(2+)](i) and reduced insulin secretion at high glucose, whereas the P2Y(2/4) receptor agonist UTP and adenosine receptor agonist NECA were inactive. [Ca(2+)](i) transients induced by 2-MeSADP and UDP were antagonized by suramin (100 mu M), U73122 (2 mu M, PLC inhibitor), and 2-APB (10 or 30 mu M, IP(3) receptor antagonist), but neither by staurosporine (1 mu M, PKC inhibitor) nor depletion of extracellular Ca(2+). The effect of 2-MeSADP on [Ca(2+)](i) was also significantly inhibited by MRS2500, a P2Y(1) receptor antagonist. These results suggested that P2Y(1) and P2Y(6) receptor subtypes are involved in Ca(2+) mobilization from intracellular stores and insulin release in mouse islets. In beta-TC6 cells, ATP, ADP, 2-MeSADP, and UDP transiently elevated [Ca(2+)](i) and slightly decreased insulin secretion at normal glucose, while UTP and NECA were inactive. RT-PCR analysis detected mRNAs of P2Y(1) and P2Y(6), but not P2Y(2) and P2Y(4) receptors.
C1 [Ohtani, Masahiro; Suzuki, Jun-ichiro; Oka, Takami] Musashino Univ, Pharmaceut Sci Res Inst, Tokyo 2028585, Japan.
[Jacobson, Kenneth A.] NIH, Natl Inst Diabet Digest & Kidney Dis, Bioorgan Chem Lab, Mol Recognit Sect, Bethesda, MD 20892 USA.
RP Oka, T (reprint author), Musashino Univ, Pharmaceut Sci Res Inst, 1-1-20 Shinmachi, Tokyo 2028585, Japan.
EM toka@musashino-u.ac.jp
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU MEXT; HAITEKU; Japan Society for the Promotion of Science; NIDDK
Intramural Program of NIH
FX This work was supported partly by MEXT. HAITEKU and a Grant-in-aid for
Scientific Research from the Japan Society for the Promotion of Science
and by the NIDDK Intramural Program of NIH.
NR 41
TC 13
Z9 14
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2008
VL 4
IS 4
BP 365
EP 375
DI 10.1007/s11302-008-9122-2
PG 11
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 373JC
UT WOS:000260966900009
PM 18784987
ER
PT J
AU Havekes, B
Lai, EW
Corssmit, PM
Romijn, JA
Timmers, HJLM
Pacak, K
AF Havekes, B.
Lai, E. W.
Corssmit, P. M.
Romijn, J. A.
Timmers, H. J. L. M.
Pacak, K.
TI Detection and treatment of pheochromocytomas and paragangliomas: current
standing of MIBG scintigraphy and future role of PET imaging
SO QUARTERLY JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Review
DE Pheochromocytomas; Paragangliomas; Radionuclide imaging; Tomography,
emission computed
ID POSITRON-EMISSION-TOMOGRAPHY; SOMATOSTATIN RECEPTOR SCINTIGRAPHY;
MALIGNANT PHEOCHROMOCYTOMA; I-123 METAIODOBENZYLGUANIDINE;
NEUROENDOCRINE TUMORS; I-131 METAIODOBENZYLGUANIDINE; ADRENAL-MEDULLA;
EXTRAADRENAL PHEOCHROMOCYTOMA; RADIOPHARMACEUTICAL TREATMENT; LOCALIZING
PHEOCHROMOCYTOMAS
AB Pheochromocytomas are rare tumors arising from chromaffin cells of adrenal medullary or extra-adrenal paraganglionic tissue. These tumors are characterized by synthesis, storage, metabolism and secretion of catecholamines. Similar to the sympathetic nervous system, pheochromocytomas express cellular norepinephrine transporters (NET) through which catecholamines can enter pheochromocytoma. cells to be stored in vesicles. Metaiodobenzylguanidine (MIBG) resemblance to norepinephrine and its good affinity and uptake by NET resulted in its use in pheochromocytoma. diagnosis from 1981. Both [I-123]MIBG and [I-131]MIBG (lower sensitivity) scintigraphy are used for localization of these tumors. Recent discoveries of different hereditary syndromes associated with pheochromocytomas led to the identification of several and new distinct genotype-phenotype associations. importantly, with this distinction of clinical phenotypes, MIBG was found to have a different performance in subsets of pheochromocytoma patients. Reduced sensitivity of MIBG scintigraphy in some familial paraganglioma syndromes, malignant disease and extra-adrenal paragangliomas has been found. Therefore, newer compounds, especially for positron emission tomography (PET), such as [C-11]hydroxyephedrine ([C-11]HED), [F-18]fluoro-2-deoxy-D-glucose ([F-18]FDG), [F-18]fluoro-dihydroxyphenylalanine ([F-18] FDOPA) and [F-18]fluorodopamine ([F-18]FDA) have emerged and were found to be superior to MIBG in the localization of certain types of pheochromocytoma and paragangliomas. Finally, using [I-131]MIBG represents an important treatment option in patients with malignant pheochromocytoma, but the development of newer treatment modalities is expected. in this review, we provide the reader with an overview of the current standing of [I-123]- and [I-131]MIBG in diagnosis and treatment of pheochromocytoma amongst the newer PET imaging agents.
C1 [Havekes, B.; Lai, E. W.; Pacak, K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Reprod Biol & Adult Endocrinol Program, NIH, Bethesda, MD 20892 USA.
[Havekes, B.; Corssmit, P. M.; Romijn, J. A.] Leiden Univ, Med Ctr, Dept Endocrinol & Metab, Leiden, Netherlands.
[Timmers, H. J. L. M.] Univ Med Ctr Nijmegan, Dept Endocrinol, Nijmegen, Netherlands.
RP Pacak, K (reprint author), NICHD, Sect Med Neuroendocrinol, Reprod Biol & Adult Endocrinol Program, NIH, Bldg 10,CRC,1 East,Room 1-3140,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
FU Intramural NIH HHS
NR 98
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Z9 43
U1 0
U2 3
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 1824-4785
J9 Q J NUCL MED MOL IM
JI Q. J. Nucl. Med. Mol. Imag.
PD DEC
PY 2008
VL 52
IS 4
BP 419
EP 429
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 415GU
UT WOS:000263923100010
PM 19088695
ER
PT J
AU Portier, C
AF Portier, Christopher
TI Discussion and summary
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Editorial Material
ID CHILDHOOD-CANCER INCIDENCE; LEUKEMIA; TRENDS
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Portier, C (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM portier@niehs.nih.gov
RI Portier, Christopher/A-3160-2010
OI Portier, Christopher/0000-0002-0954-0279
FU Intramural NIH HHS
NR 8
TC 5
Z9 6
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0144-8420
J9 RADIAT PROT DOSIM
JI Radiat. Prot. Dosim.
PD DEC
PY 2008
VL 132
IS 2
BP 273
EP 274
DI 10.1093/rpd/ncn282
PG 2
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 392XZ
UT WOS:000262336800024
PM 19066250
ER
PT J
AU Romanenko, A
Bebeshko, V
Hatch, M
Bazyka, D
Finch, S
Dyagil, I
Reiss, R
Churnak, V
Bouville, A
Gudzenko, N
Zablotska, L
Pilinskaya, M
Lyubarets, T
Bakhanova, E
Babkina, N
Trotsiuk, N
Ledoschuk, B
Belayev, Y
Dybsky, SS
Ron, E
Howe, G
AF Romanenko, A.
Bebeshko, V.
Hatch, M.
Bazyka, D.
Finch, S.
Dyagil, I.
Reiss, R.
Churnak, V.
Bouville, A.
Gudzenko, N.
Zablotska, L.
Pilinskaya, M.
Lyubarets, T.
Bakhanova, E.
Babkina, N.
Trotsiuk, N.
Ledoschuk, B.
Belayev, Y.
Dybsky, S. S.
Ron, E.
Howe, G.
TI The Ukrainian-American Study of Leukemia and Related Disorders among
Chornobyl Cleanup Workers from Ukraine: I. Study Methods
SO RADIATION RESEARCH
LA English
DT Article
ID MULTIPLE-MYELOMA; RADIATION; CANCER; MYELODYSPLASIA; ACCIDENT;
CLASSIFICATION
AB There are relatively few data on the risk of leukemia among those exposed to external radiation during cleanup operations after the Chornobyl nuclear accident, and results have not been consistent. To investigate this further, we assembled a cohort of 110,645 male cleanup workers from Ukraine and identified cases of leukemia occurring during the period 1986 to 2000. Detailed interviews were conducted and individual bone marrow doses estimated using a new time-and-motion method known as RAD-RUE described in companion paper II. For the initial analyses we used a nested case-control approach with a minimum of five controls per case, matched for year of birth, oblast (region) of registration, and residence. All identified cases were reviewed by an international panel of experts; 87 of III were confirmed. The dose-response analysis and results are given in companion paper III. As background, we describe herein the design, procedures, outcome of case finding and confirmation, control selection, dose estimation and interviewing of subjects. (C) 2008 by Radiation Research Society
C1 [Romanenko, A.; Bebeshko, V.; Bazyka, D.; Dyagil, I.; Churnak, V.; Gudzenko, N.; Pilinskaya, M.; Lyubarets, T.; Bakhanova, E.; Babkina, N.; Trotsiuk, N.; Ledoschuk, B.; Belayev, Y.; Dybsky, S. S.] AMS Ukraine, Res Ctr Radiat Med, Kiev, Ukraine.
[Hatch, M.; Bouville, A.; Ron, E.] NCI, DHHS, NIH, Div Cancer Epidemiol & Genet, Bethesda, MD 20892 USA.
[Finch, S.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Camden, NJ 08103 USA.
[Zablotska, L.; Howe, G.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
[Reiss, R.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
RP Hatch, M (reprint author), US Natl Canc Inst, 6120 Executive Blvd,Room 7098, Bethesda, MD 20892 USA.
EM hatchm@mail.nih.gov
RI Chumak, Vadim/N-6960-2015;
OI Chumak, Vadim/0000-0001-6045-9356; Bazyka, Dimitry/0000-0001-9982-5990
FU Intramural Research Program; U.S. National Cancer Institute; NIH; DHHS;
U.S. Nuclear Regulatory Commission; French Institute of Radioprotection
and Nuclear Safety; Ministry of Health Care; Academy of Medical Sciences
of Ukraine; Imperial College Faculty of Medicine; St. Mary's Hospital,
London; School of Medicine, Northwestern University, Illinois; Yale
University School of Medicine. Connecticut
FX This research was supported by the Intramural Research Program of the
U.S. National Cancer Institute. NIH, DHHS. and the Department of Energy.
The U.S. Nuclear Regulatory Commission and the French Institute of
Radioprotection and Nuclear Safety provided the initial funds for
purchase of equipment. The authors are grateful to the Ministry of
Health Care and the Academy of Medical Sciences of Ukraine for issuing
special orders supporting the project activities in the area of
interest. We are also grateful to the U.S. Working Group that helped to
develop the design for the study: among them the late Dr. G. Beebe, who
served as Chair of the Committee and was an inspiration throughout. The
late Dr. T Thomas and Dr. V. Klimenko, who also served as members,
contributed importantly in the areas of epidemiology and hematology,
respectively. All participated actively at the feasibility stage, as did
the other members of the Committee (L. Anspaugh, J. Boice. A. Bouville,
S. Davis. S. Finch, G. Howe, R. Jensen. L. G. Littlefield. I. Magrath,
L. Robison and B. Wachholz). The Ukrainian working group included Dr. A.
Romanenko. Chair. V. Bebeshko, O. Bobylova, V. Chumak, G. Kortushin, V.
Drozdova, Z. Federenko, A. Goritsky, V. Klimenko, B. Ledoschuk, M.
Pilinskaya, A. Prisyazhmuk. O. Pyatak, V. Torbin and N. Tretyak. Many of
the working group members have continued an active involvement with the
Study. Again we acknowledge the significant contribution of the
International Hematology Panel: Barbara J. Bain. Imperial College
Faculty of Medicine, St. Mary's Hospital, London; LoAnn Peterson,
Feinberg School of Medicine, Northwestern University, Illinois: Peter
McPhedran. Yale University School of Medicine. Connecticut: Svetlana N.
Gaidukova, National Academy for Postgraduate Medical Education. Kyiv:
Daniel F Gluzman, R. E. Kavetsky Institute of Experimental Pathology,
Kyiv. Finally, we would like to thank the member- of the Leukemia
Advisory Group for their wise counsel over the course of the study: Dr.
F L. Won-, chair. Dr. H. Checkoway. Dr. K. Eckernian, Dr. B. Chabner
and, most recently, Dr. B. Cheson.
NR 22
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U1 1
U2 1
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2008
VL 170
IS 6
BP 691
EP 697
DI 10.1667/RR1402.1
PG 7
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 377WH
UT WOS:000261282100002
PM 19138036
ER
PT J
AU Chumak, VV
Romanenko, AY
Voilleque, PG
Bakhanova, EV
Gudzenko, N
Hatch, M
Zablotska, LB
Golovanov, IA
Luckyanov, NK
Sholom, SV
Kryuchkov, VP
Bouville, A
AF Chumak, Vadim V.
Romanenko, Anatoly Ye.
Voilleque, Paul G.
Bakhanova, Elena V.
Gudzenko, Natalya
Hatch, Maureen
Zablotska, Lydia B.
Golovanov, Ivan A.
Luckyanov, Nickolas K.
Sholom, Sergey V.
Kryuchkov, Viktor P.
Bouville, Andre
TI The Ukrainian-American Study of Leukemia and Related Disorders among
Chornobyl Cleanup Workers from Ukraine: II. Estimation of Bone Marrow
Doses
SO RADIATION RESEARCH
LA English
DT Article
ID PRECISION EPR DOSIMETRY
AB After the accident that took place on 26 April 1986 at the Chornobyl nuclear power plant, hundreds of thousands of cleanup workers were involved in emergency measures and decontamination activities. In the framework of an epidemiological study of leukemia and other related blood diseases among Ukrainian cleanup workers, individual bone marrow doses have been estimated for 572 cases and controls. Because dose records were available for only about half of the study subjects, a time-and-motion method of dose reconstruction that would be applicable to all study subjects, whether dead or alive, was developed. The doses were calculated in a stochastic mode, thus providing estimates of uncertainties. The arithmetic mean individual bone marrow doses were found to range from 0.00004 to 3,300 mGy, with an average value of 87 mGy over the 572 study subjects. The uncertainties, characterized by the geometric standard deviation of the probability distribution of the individual dose, varied from subject to subject and had a median value of about 2. These results should be treated as preliminary; it is likely that the dose calculations and particularly the uncertainty estimates will be improved in the follow-up of this effort. (C) 2008 by Radiation Research Society
C1 [Chumak, Vadim V.; Romanenko, Anatoly Ye.; Bakhanova, Elena V.; Gudzenko, Natalya; Sholom, Sergey V.] Ukraine Acad Med Sci, Res Ctr Radiat Med, UA-04050 Kiev, Ukraine.
[Voilleque, Paul G.] MJP Risk Assessment Inc, Denver, CO USA.
[Hatch, Maureen; Bouville, Andre] NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Zablotska, Lydia B.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[Golovanov, Ivan A.; Kryuchkov, Viktor P.] Fed Res Ctr Inst Biophys, Moscow, Russia.
RP Chumak, VV (reprint author), Ukraine Acad Med Sci, Res Ctr Radiat Med, Melnikova 53, UA-04050 Kiev, Ukraine.
EM chumak@leed1.kiev.ua
RI Chumak, Vadim/N-6960-2015
OI Chumak, Vadim/0000-0001-6045-9356
FU Intramural Research Program of the U.S. National Cancer Institute; NIH;
DHHS; Department of Energy. The U.S. Nuclear Regulatory Commission;
French Institute of Protection and Nuclear Safety
FX Practical implementation of leukemia dosimetry relied greatly on the
dedicated work of expert dosimetrists-Mr. Alexander Tsykalo, Mr. Viktor
Glebov and Mr. Petro Bondarenko-as well as the team of interviewers-Mrs.
Nadezoda Gurova, Mr. Yuri Spichak and Mr. Vassily Kudreiko. The concept
of RADRUE was founded by Dr. Lynn Anspaugh, while the IARC team led by
Dr. Elisabeth Cardis contributed as motivated (and motivating) consumers
of dosimetric data and co-developers of interviewing and quality control
approaches. The success of this study is due to large extent to the
efforts and inspiration of the researchers of the Ukranian-American
team, including, but not limited to Academician Volodymir Bebeshko
(director of the Research Center for Radiation Medicine AMS Ukraine),
Prof. Dirnitry Bazyka, Prof. Maria Pilinskaya, Dr. Irina Dyagil, Mrs.
Natalia Babkina, Mr. Yuri Belyaev. the late Dr. Geoff Howe. Dr. Stuart
Finch and Dr. Robert Reiss. This research was supported by the
Intramural Research Program of the U.S. National Cancer Institute, NIH,
DHHS, and the Department of Energy. The U.S. Nuclear Regulatory
Commission and the French Institute of Protection and Nuclear Safety
provided the initial funds for purchase of equipment.
NR 10
TC 13
Z9 16
U1 0
U2 0
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2008
VL 170
IS 6
BP 698
EP 710
DI 10.1667/RR1403.1
PG 13
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 377WH
UT WOS:000261282100003
PM 19138037
ER
PT J
AU Romanenko, AY
Finch, SC
Hatch, M
Lubin, JH
Bebeshko, VG
Bazyka, DA
Gudzenko, N
Dyagil, IS
Reiss, RE
Bouville, A
Chumak, VV
Trotsiuk, NK
Babkina, NG
Belyayev, Y
Masnyk, I
Ron, E
Howe, GR
Zablotska, LB
AF Romanenko, Anatoly Ye.
Finch, Stuart C.
Hatch, Maureen
Lubin, Jay H.
Bebeshko, Volodymyr G.
Bazyka, Dimitry A.
Gudzenko, Nataliya
Dyagil, Irina S.
Reiss, Robert E.
Bouville, Andre
Chumak, Vadim V.
Trotsiuk, Nataliya K.
Babkina, Nataliya G.
Belyayev, Yuri
Masnyk, Ihor
Ron, Elaine
Howe, Geoffrey R.
Zablotska, Lydia B.
TI The Ukrainian-American Study of Leukemia and Related Disorders among
Chornobyl Cleanup Workers from Ukraine: III. Radiation Risks
SO RADIATION RESEARCH
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; CANCER-MORTALITY RISK; ATOMIC-BOMB
SURVIVORS; IONIZING-RADIATION; MULTIPLE-MYELOMA; EMERGENCY WORKERS;
THYROID-CANCER; ACCIDENT; COHORT; LYMPHOMA
AB Leukemia is one of the cancers most susceptible to induction by ionizing radiation, but the effects of lower doses delivered over time have not been quantified adequately. After the Chornobyl (Chernobyl) accident in Ukraine in April 1986, several hundred thousand workers who were involved in cleaning up the site and its surroundings received fractionated exposure, primarily from external gamma radiation. To increase our understanding of the role of protracted low-dose radiation exposure in the etiology of leukemia, we conducted a nested case-control study of leukemia in a cohort of cleanup workers identified from the Chornobyl State Registry of Ukraine. The analysis is based on 71 cases of histologically confirmed leukemia diagnosed in 1986-2000 and 501 age- and residence-matched controls selected from the same cohort. Study subjects or their proxies were interviewed about their cleanup activities and other relevant factors. Individual bone marrow radiation doses were estimated by the RADRUE dose reconstruction method (mean dose = 76.4 mGy, SD = 213.4). We used conditional logistic regression to estimate leukemia risks. The excess relative risk (ERR) of total leukemia was 3.44 per Gy [95% confidence interval (CI) 0.47-9.78, P < 0.01]. The dose response was linear and did not differ significantly by calendar period of first work in the 30-km Chornobyl zone, duration or type of work. We found a similar dose-response relationship for chronic and non-chronic lymphocytic leukemia [ERR = 4.09 per Gy (95% CI < 0-14.41) and 2.73 per Gy (95% CI < 0-13.50), respectively]. To further clarify these issues, we are extending the case-control study to ascertain cases for another 6 years (2001-2006). (C) 2008 by Radiation Research Society
C1 [Howe, Geoffrey R.; Zablotska, Lydia B.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA.
[Romanenko, Anatoly Ye.; Bebeshko, Volodymyr G.; Bazyka, Dimitry A.; Gudzenko, Nataliya; Dyagil, Irina S.; Chumak, Vadim V.; Trotsiuk, Nataliya K.; Babkina, Nataliya G.; Belyayev, Yuri] Res Ctr Radiat Med, Kiev, Ukraine.
[Finch, Stuart C.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Camden, NJ 08103 USA.
[Hatch, Maureen; Lubin, Jay H.; Bouville, Andre; Masnyk, Ihor; Ron, Elaine] NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Reiss, Robert E.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
RP Zablotska, LB (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, 722 W 168th St,Suite 1103, New York, NY 10032 USA.
EM LBZ7@columbia.edu
RI Chumak, Vadim/N-6960-2015;
OI Chumak, Vadim/0000-0001-6045-9356; Bazyka, Dimitry/0000-0001-9982-5990
FU Intramural Research Program of the U.S. National Cancer Institute; NIH;
DHHS; Department of Energy. The U.S. Nuclear Regulatory Commission;
French Institute of Radioprotection; Ministry of Health Care and the
Academy of Medical Sciences of Ukraine
FX This research was supported by the Intramural Research Program of the
U.S. National Cancer Institute, NIH, DHHS, and the Department of Energy.
The U.S. Nuclear Regulatory Commission and the French Institute of
Radioprotection and Nuclear Safety provided the initial funds for
purchase of equipment. The authors are grateful to the Ministry of
Health Care and the Academy of Medical Sciences of Ukraine for issuing
special orders supporting the project activities in the area of
interest. Practical implementation of leukemia dosimetry relied greatly
on the dedicated work of Victor Kryuchkov, Ivan Golovanov and Elena
Bakhanova.
NR 43
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U1 2
U2 3
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2008
VL 170
IS 6
BP 711
EP 720
DI 10.1667/RR1404.1
PG 10
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 377WH
UT WOS:000261282100004
PM 19138038
ER
PT J
AU Kesminiene, A
Evrard, AS
Ivanov, VK
Malakhova, IV
Kurtinaitis, J
Stengrevics, A
Tekkel, M
Anspaugh, LR
Bouville, A
Chekin, S
Chumak, VV
Drozdovitch, V
Gapanovichi, V
Golovanov, I
Hubert, P
Illichev, SV
Khait, SE
Kryuchkov, VP
Maceika, E
Maksyoutov, M
Mirkhaidarov, AK
Polyakov, S
Shchukina, N
Tenet, V
Tserakhovich, TI
Tsykalo, A
Tukov, AR
Cardis, E
AF Kesminiene, Ausrele
Evrard, Anne-Sophie
Ivanov, Viktor K.
Malakhova, Irina V.
Kurtinaitis, Juozas
Stengrevics, Aivars
Tekkel, Mare
Anspaugh, Lynn R.
Bouville, Andre
Chekin, Sergei
Chumak, Vadim V.
Drozdovitch, Vladimir
Gapanovichi, Vladimir
Golovanov, Ivan
Hubert, Phillipe
Illichev, Sergei V.
Khait, Svetlana E.
Kryuchkov, Viktor P.
Maceika, Evaldas
Maksyoutov, Marat
Mirkhaidarov, Anatoly K.
Polyakov, Semion
Shchukina, Natalia
Tenet, Vanessa
Tserakhovich, Tatyana I.
Tsykalo, Aleksandr
Tukov, Aleksandr R.
Cardis, Elisabeth
TI Risk of Hematological Malignancies among Chernobyl Liquidators
SO RADIATION RESEARCH
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; ATOMIC-BOMB SURVIVORS; CLEANUP WORKERS;
IONIZING-RADIATION; MULTIPLE-MYELOMA; CANCER-RISKS; TECHA RIVER;
MORTALITY; UNCERTAINTY; DOSIMETRY
AB A case-control study of hematological malignancies was conducted among Chernobyl liquidators (accident recovery workers) from Belarus, Russia and Baltic countries to assess the effect of low- to medium-dose protracted radiation exposures on the relative risk of these diseases. The study was nested within cohorts of liquidators who had worked around the Chernobyl plant in 1986-1987. A total of 117 cases [69 leukemia, 34 non-Hodgkin lymphoma (NHL) and 14 other malignancies of lymphoid and hematopoietic tissue] and 481 matched controls were included in the study. Individual dose to the bone marrow and uncertainties were estimated for each subject. The main analyses were restricted to 70 cases (40 leukemia, 20 NHL and 10 other) and their 287 matched controls with reliable information on work in the Chernobyl area. Most subjects received very low doses (median 13 mGy). For all diagnoses combined, a significantly elevated OR was seen at doses of 200 mGy and above. The excess relative risk (ERR) per 100 mGy was 0.60 [90% confidence interval (CI) -0.02, 2.35]. The corresponding estimate for leukemia excluding chronic lymphoid leukemia (CLL) was 0.50 (90% CI -0.38, 5.7). It is slightly higher than but statistically compatible with those estimated from A-bomb survivors and recent low-doserate studies. Although sensitivity analyses showed generally similar results, we cannot rule out the possibility that biases and uncertainties could have led to over- or underestimation of the risk in this study. (C) 2008 by Radiation Research Society
C1 [Kesminiene, Ausrele; Evrard, Anne-Sophie; Maceika, Evaldas; Tenet, Vanessa; Cardis, Elisabeth] Int Agcy Res Canc, F-69372 Lyon, France.
[Ivanov, Viktor K.; Chekin, Sergei; Khait, Svetlana E.; Maksyoutov, Marat; Shchukina, Natalia] Russian Acad Med Sci, MRRC, Obninsk, Russia.
[Malakhova, Irina V.; Polyakov, Semion; Tserakhovich, Tatyana I.] Med Technol Informat Adm & Management Hlth, RSPC, Minsk, Byelarus.
[Kurtinaitis, Juozas] Inst Oncol, Vilnius, Lithuania.
[Stengrevics, Aivars] Latvian Ctr Oncol, Riga, Latvia.
[Tekkel, Mare] Natl Inst Hlth Dev, Tallinn, Estonia.
[Anspaugh, Lynn R.] Univ Utah, Dept Radiol, Div Radiobiol, Salt Lake City, UT 84132 USA.
[Bouville, Andre; Drozdovitch, Vladimir] NCI, NIH, DCEG, Rockville, MD USA.
[Chumak, Vadim V.] Sci Ctr Radiat Med, Kiev, Ukraine.
[Gapanovichi, Vladimir] RIHBT, Minsk, Byelarus.
[Golovanov, Ivan; Kryuchkov, Viktor P.; Tukov, Aleksandr R.] Inst Biophys, Moscow, Russia.
[Hubert, Phillipe] Inst Natl Environ Ind & Risques INERIS, Direct Risques Chron, Verneuil En Halatte, France.
[Maceika, Evaldas] Lithuania Acad Sci, Inst Phys, LT-232600 Vilnius, Lithuania.
[Mirkhaidarov, Anatoly K.] Republican Sci Ctr Radiat Med & Human Ecol, Gomel, Byelarus.
[Tsykalo, Aleksandr] Chernobyl Nucl Power Plant, Dept Dose Reconstruct, Chernobyl, Ukraine.
RP Kesminiene, A (reprint author), Int Agcy Res Canc, 150 Cours A Thomas, F-69372 Lyon, France.
EM kesminiene@iarc.fr
RI Chumak, Vadim/N-6960-2015; Ivanov, Victor/R-9385-2016; Cardis,
Elisabeth/C-3904-2017;
OI Chumak, Vadim/0000-0001-6045-9356; Ivanov, Victor/0000-0003-1372-0018;
Maceika, Evaldas/0000-0002-9251-6789
FU ERBIC [F14C-CT96-0011]; European Union (Nuclear Fission Safety
[15-CT96-0317]; INCO-Copernicus Programmes; DHSS [IROI/CC/ ROI5763-01];
U.S. National Institute for Environmental Health Sciences
FX This Study was made possible by contracts F14C-CT96-0011 and ERBIC
15-CT96-0317 from the European Union (Nuclear Fission Safety and
INCO-Copernicus Programmes) and DHSS contract no. IROI/CC/ ROI5763-01
from the U.S. National Institute for Environmental Health Sciences.
NR 40
TC 41
Z9 48
U1 2
U2 16
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2008
VL 170
IS 6
BP 721
EP 735
DI 10.1667/RR1231.1
PG 15
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 377WH
UT WOS:000261282100005
PM 19138033
ER
PT J
AU DePaolo, LV
AF DePaolo, Louis V.
TI Stepping Back to Look Forward
SO REPRODUCTIVE SCIENCES
LA English
DT Editorial Material
C1 Eunice Kennedy Shriver NICHD, Peproduct Sci Branch, Populat Res Ctr, NIH, Bethesda, MD 20892 USA.
RP DePaolo, LV (reprint author), Eunice Kennedy Shriver NICHD, Peproduct Sci Branch, Populat Res Ctr, NIH, 6100 Execeut Blvd,Room 8B01A, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1933-7191
J9 REPROD SCI
JI Reprod. Sci.
PD DEC
PY 2008
VL 15
IS 10
BP 979
EP 983
DI 10.1177/1933719108327936
PG 5
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 381FA
UT WOS:000261519900003
PM 19088367
ER
PT J
AU Pratt, C
Webber, LS
Baggett, CD
Ward, D
Pate, RR
Murray, D
Lohman, T
Lytle, L
Elder, JP
AF Pratt, Charlotte
Webber, Larry S.
Baggett, Chris D.
Ward, Dianne
Pate, Russell R.
Murray, David
Lohman, Timothy
Lytle, Leslie
Elder, John P.
TI Sedentary Activity and Body Composition of Middle School Girls: The
Trial of Activity for Adolescent Girls
SO RESEARCH QUARTERLY FOR EXERCISE AND SPORT
LA English
DT Article
DE accelerometry; body fat; body mass index; sedentary behavior
ID PHYSICAL-ACTIVITY; UNITED-STATES; MASS INDEX; TELEVISION; OBESITY;
CHILDREN; OVERWEIGHT; BEHAVIOR; ADIPOSITY; WEIGHT
AB This study describes the relationships between sedentary activity and body composition in 1, 458 sixth-grade girls from 36 middle school, across the United States. Multivariate associations between sedentary activity and body composition were examined with regression analyses using general linear mixed, models. Mean age, body mass index, and percentage of body fat, were 12.0 +/- 0.51, 21.1 kg/m(2) +/- 4.8, 28.5 +/- 8.9, respectively. Girls averaged 7.7 +/- 1.2 sedentary hours per day and about 13 hr (similar to 97% of the day) of both sedentary and light activities. Overweight girls were significantly more (13 min; p < .003) sedentary, especially after school (> 2 p.m.; p < .01), and less physically active (p < .0001) than normal weight girls. The study documents small but significant associations between sedentary activity and adiposity.
C1 [Pratt, Charlotte] NHLBI, Bethesda, MD USA.
[Webber, Larry S.] Tulane Univ, Dept Biostat, New Orleans, LA 70118 USA.
[Baggett, Chris D.; Ward, Dianne] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA.
[Pate, Russell R.] Univ S Carolina, Dept Exercise Sci, Columbia, SC 29208 USA.
[Murray, David] Ohio State Univ, Coll Publ Hlth, Columbus, OH 43210 USA.
[Lohman, Timothy] Univ Arizona, Dept Physiol, Tucson, AZ 85721 USA.
[Lytle, Leslie] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN 55455 USA.
[Elder, John P.] San Diego State Univ, Sch Publ Hlth, San Diego, CA 92182 USA.
RP Pratt, C (reprint author), 6701 Rockledge Dr,MSC 7936,Room 10118, Bethesda, MD 20892 USA.
EM prattc@nhlbi.nih.gov
FU National Heart, Lung, and Blood [U01HL066858, U01HL066857, U01HL066845,
U01HL066856, U01HL066855, U01HL066853, U01HL066852]
FX This research was funded by grants from the National Heart, Lung, and
Blood Grant numbers: U01HL066858, U01HL066857, U01HL066845, U01HL066856,
U01HL066855, U01HL066853, and U01HL066852. The authors thank all the
study Staff, including project coordinators and measurement staff, the
schools,, parents, and sixth-grade girls. Please address all
correspondence concerning this article to Charlotte A. Pratt, 6701
Rockledge Drive, MSC 7936, Room 10118, Bethesda, MD 20892.
NR 34
TC 20
Z9 20
U1 0
U2 4
PU AMER ALLIANCE HEALTH PHYS EDUC REC & DANCE
PI RESTON
PA 1900 ASSOCIATION DRIVE, RESTON, VA 22091 USA
SN 0270-1367
J9 RES Q EXERCISE SPORT
JI Res. Q. Exerc. Sport
PD DEC
PY 2008
VL 79
IS 4
BP 458
EP 467
PG 10
WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology;
Sport Sciences
SC Social Sciences - Other Topics; Psychology; Sport Sciences
GA 391OM
UT WOS:000262242600003
PM 19177947
ER
PT J
AU Zitserman, VY
Makhnovskii, YA
Dagdug, L
Berezhkovskii, AM
AF Zitserman, V. Yu.
Makhnovskii, Yu. A.
Dagdug, L.
Berezhkovskii, A. M.
TI Diffusion in a Porous Medium with Dead Ends: An Analysis by Methods of
the Theory of Diffusion-Controlled Reactions
SO RUSSIAN JOURNAL OF PHYSICAL CHEMISTRY A
LA English
DT Article
ID KINETICS; TRANSPORT; CHANNEL
AB The problem of the diffusion of a particle in a porous medium with dead ends entering which is related to overcoming high entropy barriers is considered. Dead ends effectively decelerate migration, because, while residing in them, a particle does not participate in diffusion transfer. A new approach to the problem was suggested. The approach was based on the possibility of splitting the diffusion process into separate well-defined stages thanks to the presence of high entropy barriers. An analysis of these stages was performed using methods developed in the theory of diffusion-controlled reactions. The new approach was used to calculate the effective diffusion coefficient (characterizing the limiting particle migration deceleration caused by the presence of dead ends in a porous medium) and estimate the time of its establishment.
C1 [Zitserman, V. Yu.] Russian Acad Sci, Joint Inst High Temp OVIT, Moscow 125412, Russia.
[Makhnovskii, Yu. A.] Russian Acad Sci, AV Topchiev Petrochem Synth Inst, Moscow 117912, Russia.
[Dagdug, L.] Univ Autonoma Metropolitana Iztapalapa, Dept Fis, Mexico City 09340, DF, Mexico.
[Berezhkovskii, A. M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Zitserman, VY (reprint author), Russian Acad Sci, Joint Inst High Temp OVIT, Izhorskaya Ul 13-19, Moscow 125412, Russia.
EM vz1941@mail.ru
RI Makhnovskii, Yurii/B-1223-2014
OI Makhnovskii, Yurii/0000-0002-1517-536X
FU Russian Foundation for Basic Research [06-03-32373]
FX This work was financially supported by the Russian Foundation for Basic
Research, project no. 06-03-32373.
NR 22
TC 3
Z9 3
U1 0
U2 1
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 0036-0244
EI 1531-863X
J9 RUSS J PHYS CHEM A+
JI Russ. J. Phys. Chem. A
PD DEC
PY 2008
VL 82
IS 12
BP 2039
EP 2044
DI 10.1134/S0036024408120121
PG 6
WC Chemistry, Physical
SC Chemistry
GA 376KM
UT WOS:000261182500012
ER
PT J
AU Heilig, M
AF Heilig, Markus
TI TRIGGERING ADDICTION
SO SCIENTIST
LA English
DT Article
ID ALCOHOL DEPENDENCE; NALTREXONE; THERAPY
C1 [Heilig, Markus] NIAAA, Bethesda, MD 20892 USA.
[Heilig, Markus] Karolinska Inst, Stockholm, Sweden.
RP Heilig, M (reprint author), NIAAA, Bethesda, MD 20892 USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU SCIENTIST INC
PI PHILADELPHIA
PA 400 MARKET ST, STE 1250, PHILADELPHIA, PA 19106 USA
SN 0890-3670
J9 SCIENTIST
JI Scientist
PD DEC
PY 2008
VL 22
IS 12
BP 30
EP 35
PG 6
WC Information Science & Library Science; Multidisciplinary Sciences
SC Information Science & Library Science; Science & Technology - Other
Topics
GA 375KL
UT WOS:000261112500016
ER
PT J
AU Manor, U
Kachar, B
AF Manor, Uri
Kachar, Bechara
TI Dynamic length regulation of sensory stereocilia
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Length regulation; Stereocilia; Hair cells; Myosins; Actin protrusions;
Hearing; Actin treadmilling
ID HAIR-CELL STEREOCILIA; CLASS-III MYOSIN; NONSYNDROMIC HEARING-LOSS;
VASODILATOR-STIMULATED PHOSPHOPROTEIN; ACTIN CYTOSKELETAL ORGANIZATION;
PROTEIN-TYROSINE-PHOSPHATASE; PLASMA-MEMBRANE CA2+-ATPASE; INNER-EAR;
IN-VIVO; UNCONVENTIONAL MYOSIN
AB Stereocilia, the mechanosensory organelles of hair cells, are a distinctive class of actin-based cellular protrusions with an unparalleled ability to regulate their lengths over time. Studies on actin turnover in stereocilia, as well as the identification of several deafness-related proteins essential for proper stereocilia structure and function, provide new insights into the mechanisms and molecules involved in stereocilia length regulation and long-term maintenance. Comparisons of ongoing investigations on stereocilia with studies on other actin protrusions offer new opportunities to further understand common principles for length regulation, the diversity of its mechanisms, and how the specific needs of each cell are met. Published by Elsevier Ltd.
C1 [Manor, Uri; Kachar, Bechara] NIDCD, Sect Struct Cell Biol, NIH, Bethesda, MD 20892 USA.
RP Kachar, B (reprint author), NIDCD, Sect Struct Cell Biol, NIH, Building 50,Room 4249,50 South Dr, Bethesda, MD 20892 USA.
EM kacharb@nidcd.nih.gov
FU NIDCD/DIR; NIH
FX The authors would like to thank Ronald Petralia, Cole Graydon, and Aurea
De Sousa for their critical review of the manuscript and helpful
suggestions. This work was funded by NIDCD/DIR, NIH.
NR 122
TC 48
Z9 49
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD DEC
PY 2008
VL 19
IS 6
BP 502
EP 510
DI 10.1016/j.semcdb.2008.07.006
PG 9
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 397NZ
UT WOS:000262670700005
PM 18692583
ER
PT J
AU Brass, DM
Wise, AL
Schwartz, DA
AF Brass, David M.
Wise, Anastasia L.
Schwartz, David A.
TI Host-Environment Interactions in Exposure-Related Diffuse Lung Diseases
SO SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Review
DE Vulnerable epithelium; interstitial lung disease; fibrosis
ID IDIOPATHIC PULMONARY-FIBROSIS; SURFACTANT PROTEIN-C;
HERMANSKY-PUDLAK-SYNDROME; NIEMANN-PICK-DISEASE; USUAL INTERSTITIAL
PNEUMONIA; LAMELLAR BODY DEGENERATION; HYPERSENSITIVITY PNEUMONITIS;
HYPOCALCIURIC HYPERCALCEMIA; GENE-EXPRESSION; MOUSE MODEL
AB Diffuse lung disease (DLD), also known as interstitial lung disease (ILD), comprises a group of relatively rare but devastating lung diseases that involve varying degrees of acute and chronic inflammation, and which may present with end-stage fibroproliferation. There are currently no proven therapeutic strategies to halt progression of DLDs. Thinking about DLDs has evolved over time from hypotheses invoking inflammation as the prime mover in the etiology of disease, to the current hypothesis that interactions between a damaged and frustrated epithelium, and the response of underlying mesenchymal cells that takes place, contribute to the fibroproliferative milieu. The greatest challenge to understanding the role of environmental exposures in pathogenesis of DLDs is that there is no clear consensus on the etiology and pathogenesis of these diseases. Emerging data on the relationship between loss of epithelial integrity and mesenchymal fibroproliferation support the hypothesis that the damage to the epithelium is a critical component in the development of DLDs that progress to a fibroproliferative presentation. Thus it follows that environmental stress which impacts the well-being of the epithelium may play a critical role in shifting the balance of lung homeostasis through ongoing insult as a result of exposure to environmental agents. Animal models that recapitulate the vulnerable epithelium observed in patients who develop fibrotic lung disease associated with DLDs will provide the best Opportunity to understand mechanisms associated with the etiology of these diseases.
C1 [Brass, David M.; Wise, Anastasia L.; Schwartz, David A.] NHLBI, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Brass, DM (reprint author), DUMC Box 3373,Res Dr, Durham, NC 27710 USA.
EM David.brass@duke.edu
FU NHLBI; NIEHS
FX This work was funded by the NHLBI and NIEHS division of intramural
research.
NR 76
TC 2
Z9 4
U1 0
U2 1
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 1069-3424
J9 SEMIN RESP CRIT CARE
JI Semin. Respir. Crit. Care Med.
PD DEC
PY 2008
VL 29
IS 6
BP 603
EP 609
DI 10.1055/s-0028-1101270
PG 7
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 380EG
UT WOS:000261448400003
PM 19221958
ER
PT J
AU Nawa, NE
Nelson, EE
Pine, DS
Ernst, M
AF Nawa, Norberto Eiji
Nelson, Eric E.
Pine, Daniel S.
Ernst, Monique
TI Do you make a difference Social context in a betting task
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
ID TRANSCRANIAL MAGNETIC STIMULATION; MEDIAL PREFRONTAL CORTEX; RISK-TAKING
BEHAVIOR; DECISION-MAKING; NUCLEUS-ACCUMBENS; HUMAN AMYGDALA; LOSS
AVERSION; NEURAL BASES; BRAIN; REWARD
AB Social context strongly influences human motivated behavior. The triadic model implicates three major nodes in the regulation of motivated behavior, i.e. amygdala, medial prefrontal cortex (mPFC) and striatum. The present work examines how social context modulates this system. Nineteen healthy subjects completed an event-related functional magnetic resonance imaging study of a monetary betting task in the presence (social trials) and in the absence of a social peer (nonsocial trials). In the social trials, the scanned subject played along with another subject, although their performances were independent from one another. In the nonsocial trials the scanned subject played alone. Although behavioral performance did not differ between social and nonsocial trials, BOLD signal changes during betting were significantly greater in the amygdala bilaterally and the right dorsolateral prefrontal cortex (BA 9) in the social condition relative to the nonsocial condition. In contrast, activation was greater in ventral striatum in the nonsocial condition relative to the social condition. These findings suggest that social context modulates the triadic neural-systems ensemble to adjust motivated behavior to the unique demands associated with the presence of conspecifics.
C1 [Nawa, Norberto Eiji] Natl Inst Informat & Commun Technol, ATR Cognit Informat Sci Res Labs, Keihanna Sci City, Kyoto 6190288, Japan.
[Nawa, Norberto Eiji] Natl Inst Informat & Commun Technol, Multimodal Commun Grp, Keihanna Sci City, Kyoto 6190288, Japan.
[Nelson, Eric E.; Pine, Daniel S.; Ernst, Monique] NIMH, Mood & Anxiety Disorders Program, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Nawa, NE (reprint author), ATR Cognit Informat Sci Labs, 2-2-2 Hikari Dai, Keihanna Sci City, Kyoto 6190288, Japan.
EM eiji@atr.jp
RI Nelson, Eric/B-8980-2008
OI Nelson, Eric/0000-0002-3376-2453
FU Japan's Ministry of Education, Culture, Sports, Science and Technology
[17680023]
FX Functional imaging data were acquired at the ATR Brain Activity Imaging
Center, Kyoto, Japan. We thank their staff for the invaluable support.
We also thank Steven Fromm (NIMH/EDAN) for his critical help in data
analysis. This work was supported by a Grant-in-Aid for Encouragement of
Young Scientists (A) of Japan's Ministry of Education, Culture, Sports,
Science and Technology (17680023) to N.E.N.
NR 67
TC 10
Z9 10
U1 3
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD DEC
PY 2008
VL 3
IS 4
BP 367
EP 376
DI 10.1093/scan/nsn032
PG 10
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 386WO
UT WOS:000261913500008
PM 19015081
ER
PT J
AU Henning, EC
Latour, LL
Hallenbeck, JM
Warach, S
AF Henning, Erica C.
Latour, Lawrence L.
Hallenbeck, John M.
Warach, Steven
TI Reperfusion-Associated Hemorrhagic Transformation in SHR Rats Evidence
of Symptomatic Parenchymal Hematoma
SO STROKE
LA English
DT Article; Proceedings Paper
CT 15th Annual Meeting of the
International-Society-of-Magnetic-Resonance-in-Medicine/European-Society
-of-Magnetic-Resonance-in-Medicine-and-Biology
CY MAY 12-18, 2007
CL Berlin, GERMANY
SP Int Soc Magnet Resonance Med, European Soc Magnet Resonance Med & Biol
DE stroke; reperfusion; hemorrhagic transformation; parenchymal hematoma;
spontaneously hypertensive rats; middle cerebral artery occlusion
ID TISSUE-PLASMINOGEN ACTIVATOR; CEREBRAL-ARTERY OCCLUSION; SPONTANEOUSLY
HYPERTENSIVE-RATS; ACUTE ISCHEMIC-STROKE; COOPERATIVE ACUTE STROKE;
RT-PA TREATMENT; FOCAL ISCHEMIA; THROMBOLYTIC THERAPY; CONTROLLED-TRIAL;
EMBOLIC STROKE
AB Background and Purpose-Symptomatic hemorrhagic transformation (HT) is the most important complicating factor after treatment with intravenous tissue plasminogen activator. In this study, we used multimodal magnetic resonance imaging to investigate the incidence and severity of reperfusion-based HT in spontaneously hypertensive rats after ischemia/reperfusion.
Methods-Twenty male spontaneously hypertensive rats were subjected to 30 minutes of middle cerebral artery occlusion via the suture model. Diffusion-weighted, T2-weighted, and gradient-echo imaging were performed on days 1, 2, 3, 4, and 7 for longitudinal evaluation of lesion evolution, vasogenic edema, and HT, respectively. Findings on gradient-echo images were classified according to the severity of hemorrhage: no HT; punctate or small petechial hemorrhage (HI-1); confluent petechial hemorrhage (HI-2); hematoma with absent/mild space-occupying effect (PH-1, <= 30% lesion volume); and hematoma with significant space-occupying effect and potential perihematomal edema (PH-2, <= 30% lesion volume). Histopathologic evaluation of HT was performed after final imaging for comparison with magnetic resonance imaging results.
Results-Final hemorrhage scores based on severity were as follows: HI-1 23.1%, HI-2 30.8%, PH-1 30.8%, and PH-2 15.4%. Similar to clinical observations, only PH-2 was associated with neurologic deterioration and associated weight loss.
Conclusions-This model has a high incidence of parenchymal hematomas (46.2%) and therefore is appropriate for the evaluation of novel therapeutics targeting blood-brain barrier integrity and the reduction of symptomatic HT events (PH-2), as well as those potentially "at risk" for neurologic deterioration (PH-1). (Stroke. 2008; 39: 3405-3410.)
C1 [Henning, Erica C.; Latour, Lawrence L.; Warach, Steven] NINDS, Sect Stroke Diagnost & Therapeut, NIH, Bethesda, MD 20892 USA.
[Hallenbeck, John M.] NINDS, Sect Clin Invest, NIH, Bethesda, MD 20892 USA.
RP Henning, EC (reprint author), NINDS, Stroke Branch, Sect Stroke Diagnost & Therapeut, Bldg 10,Room B1D733,10 Ctr Dr,MSC 1063, Bethesda, MD 20892 USA.
EM henninge@ninds.nih.gov
RI Henning, Erica/E-8542-2010
FU Intramural NIH HHS [Z99 NS999999, , ZIA NS003120-03, ZIA NS003120-04,
ZIA NS003120-05, ZIA NS003120-06, ZIA NS003120-07, ZIC NS003044-09, ZIC
NS003044-10]
NR 34
TC 15
Z9 15
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD DEC
PY 2008
VL 39
IS 12
BP 3405
EP 3410
DI 10.1161/STROKEAHA.108.520304
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 377AT
UT WOS:000261224800040
PM 18757286
ER
PT J
AU Powell, AC
Alexander, HR
Pingpank, JF
Steinberg, SM
Skarutis, M
Bartlett, DL
Agarwal, S
Cochran, C
Seidel, G
Fraker, D
Hughes, MS
Jensen, RT
Marx, SJ
Libutti, SK
AF Powell, Anathea C.
Alexander, H. Richard
Pingpank, James F.
Steinberg, Seth M.
Skarutis, Monica
Bartlett, David L.
Agarwal, Sunita
Cochran, Craig
Seidel, Geoffrey
Fraker, Douglas
Hughes, Marybeth S.
Jensen, Robert T.
Marx, Stephen J.
Libutti, Steven K.
TI The utility of routine transcervical thymectomy for multiple endocrine
neoplasia 1-related hyperparathyroidism
SO SURGERY
LA English
DT Article
ID THYMIC CARCINOIDS; TYPE-1; PARATHYROIDECTOMY; SERIES
AB Background. Operation for multiple endocrine neoplasia (MEN) 1-related hyperparathyroidism (HPT) includes a neck exploration with resection of 3.5 or 4 parathyroid glands and transcervical thymectomy (TCT). We reviewed our experience with initial operation for primary HPT to determine the outcome and utility of routine TCT.
Methods. All patients with MEN1 who underwent initial neck exploration from 1993 to 2007 under an institutional review board-approved protocol were reviewed.
Results. We identified 66 patients with initial operation for HPT in MEN1. In 34 patients, 4 glands were found; in 32 patients, <4 glands were found. In 2 of the 34 (6%) and 17 of the 32 (53%), intrathymic parathyroid tissue was found on permanent pathology. No thymic carcinoid tissue was found in any specimen.
Conclusion. These data highlight the importance of performing TCT when <4 entopic parathyroid glands are found at first operation. (Surgery 2008; 144:878-84.)
C1 [Powell, Anathea C.; Alexander, H. Richard; Pingpank, James F.; Bartlett, David L.; Seidel, Geoffrey; Fraker, Douglas; Hughes, Marybeth S.; Libutti, Steven K.] NIDDKD, Tumor Angiogenesis Sect, Surg Branch, Ctr Canc Res,NCI,NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NIDDKD, Biostat & Data Management Sect, Off Clin Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Skarutis, Monica; Agarwal, Sunita; Cochran, Craig; Marx, Stephen J.] NIDDKD, NCI, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
[Jensen, Robert T.] NIDDKD, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Libutti, SK (reprint author), NIDDKD, Tumor Angiogenesis Sect, Surg Branch, Ctr Canc Res,NCI,NIH, 10 Ctr Dr,4W-5940, Bethesda, MD 20892 USA.
EM libuttis@mail.nih.gov
FU Intramural NIH HHS [NIH0010056261]; PHS HHS [NIH0010056261]
NR 19
TC 20
Z9 20
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6060
J9 SURGERY
JI Surgery
PD DEC
PY 2008
VL 144
IS 6
BP 878
EP 883
DI 10.1016/j.surg.2008.08.031
PG 6
WC Surgery
SC Surgery
GA 382CC
UT WOS:000261581600010
PM 19040992
ER
PT J
AU Liu, JJ
Alemozaffar, M
McHone, B
Dhanani, N
Gage, F
Pinto, PA
Gorbach, AM
Elster, E
AF Liu, Jack J.
Alemozaffar, Mehrdad
McHone, Benjamin
Dhanani, Nadeem
Gage, Fred
Pinto, Peter A.
Gorbach, Alexander M.
Elster, Eric
TI Evaluation of real-time infrared intraoperative cholangiography in a
porcine model
SO SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES
LA English
DT Article
DE Infrared imaging; Intraoperative cholangiogram; Laparoscopic
cholecystectomy
ID BILE-DUCT INJURIES; LAPAROSCOPIC CHOLECYSTECTOMY; CORONARY-ANGIOGRAPHY;
PATENCY CONTROL; ROUTINE; COMPLICATIONS; MULTICENTER
AB Background Intraoperative cholangiograms (IOCs) may increase cost, surgical time, and radiation exposure of staff and patients. The authors introduce the application of passive infrared imaging to intraoperative cholangiography as a feasible alternative to traditional fluoroscopic IOCs.
Methods A porcine model was used in which the gallbladder, cystic duct, common bile duct (CBD), and duodenum were exposed and an 18-gauge angiocatheter was inserted into the cystic duct. Infrared emission was detected using a digital infrared camera positioned 30 to 60 cm above the abdomen. Infrared images were taken in real time (similar to 1/s) during infusion of room-temperature saline. A thermoplastic polymer stone then was inserted into the CBD. Once the artificial stone was placed, room-temperature saline was again injected. A standard single-shot renograffin IOC was obtained to confirm the obstruction. The experiment was concluded by creation of a lateral 2-mm CBD injury immediately proximal to the duodenum followed by infusion of room-temperature saline.
Results Six pigs were used in this study. Baseline infrared imaging was able to capture a visible temperature decrease, outlining the lumen of the CBD. With injection of room-temperature saline, a decrease in temperature was visualized as a dark area representing flow from the CBD to the duodenum. After placement of the synthetic stone, real-time infrared images displayed slowing of the injected bolus by the obstruction. The obstruction was correlated with fluoroscopic IOCs. Finally, after partial transection of the CBD, the infrared camera visualized saline flowing from the site of injury out into the peritoneal cavity.
Conclusions The CBD anatomy, obstruction, and injury can be clearly visualized with an infrared camera. Intraoperative infrared imaging is an emerging method already being used in several surgical fields. Ultimately, the integration of infrared and laparoscopic technology will be necessary to make infrared technology important in laparoscopic cholecystectomy.
C1 [Gage, Fred; Elster, Eric] USN, Med Res Ctr, Silver Spring, MD 20910 USA.
[Liu, Jack J.; Alemozaffar, Mehrdad; McHone, Benjamin; Dhanani, Nadeem; Pinto, Peter A.] NCI, Urol Oncol Branch, Bethesda, MD 20892 USA.
[Gorbach, Alexander M.] Natl Inst Biomed Imaging & Bioengn, Div Bioengn & Phys Sci, Bethesda, MD USA.
[Elster, Eric] Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA.
RP Elster, E (reprint author), USN, Med Res Ctr, 503 Robert Grant Ave,Suite 2W123, Silver Spring, MD 20910 USA.
EM elstere@nmrc.navy.mil
FU Intramural NIH HHS [Z01 SC006659-25]
NR 19
TC 5
Z9 6
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0930-2794
J9 SURG ENDOSC
JI Surg. Endosc.
PD DEC
PY 2008
VL 22
IS 12
BP 2659
EP 2664
DI 10.1007/s00464-008-9792-4
PG 6
WC Surgery
SC Surgery
GA 389JR
UT WOS:000262089200022
PM 18347867
ER
PT J
AU Mankani, MH
Kuznetsov, SA
Marshall, GW
Robey, PG
AF Mankani, Mahesh H.
Kuznetsov, Sergei A.
Marshall, Grayson W.
Robey, Pamela Gehron
TI Creation of New Bone by the Percutaneous Injection of Human Bone Marrow
Stromal Cell and HA/TCP Suspensions
SO TISSUE ENGINEERING PART A
LA English
DT Article
ID TISSUE-ENGINEERED BONE; MESENCHYMAL STEM-CELLS; PLATELET-RICH PLASMA;
IN-VIVO; MECHANICAL-PROPERTIES; MOUSE; MICE; RECONSTRUCTION;
REGENERATION; OSTEOGENESIS
AB Background: The in vivo transplantation assay has become a valuable tool for assessing the osteogenic potential of diverse cell populations. It has required that cells are cotransplanted with a matrix into recipient animals using large incisions and extensive dissections. Here, we demonstrate that transplants of an osteogenic cell population, bone marrow stromal cells (BMSCs), are capable of assembling into mature bone organs when injected as suspensions of cells and a particulate matrix.
Methods: Human BMSCs, along with hydroxyapatite/tricalcium phosphate (HA/TCP) particles, were placed either into the dorsal subcutaneous space or onto the calvarium of immunodeficient mice, either via injection or via a wide operative exposure. Transplants were harvested from 7 to 110 weeks later; their histologic and mechanical properties and their cellular origin were analyzed.
Results: A total of 43 transplants were evaluated. The extent of new bone and hematopoiesis, the bone's adherence to the underlyingmouse calvarium, and the bone elasticmodulus and hardness were comparable between the two groups. In situ hybridization confirmed a human origin of the new bone.
Conclusions: Our data indicate that BMSCs and HA/TCP particles, when injected as a suspension, can assemble into mature bone organs, and that this bone has histologic and mechanical properties similar to bone formed in standard transplants delivered through a large incision. These results open the possibility for assessing the osteogenic capacities of cell populations, for modeling bone formation and repair and for treating bone deficits, all in the context of minimal surgical intervention or soft tissue disruption.
C1 [Mankani, Mahesh H.] Univ Calif San Francisco, Dept Surg, Div Plast Surg, San Francisco, CA 94143 USA.
[Kuznetsov, Sergei A.; Robey, Pamela Gehron] NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
RP Mankani, MH (reprint author), Univ Calif San Francisco, Dept Surg, Div Plast Surg, 1001 Potrero Ave,Box 0807, San Francisco, CA 94143 USA.
EM mahesh.mankani@ucsf.edu
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
FU University of California-San Francisco Research Evaluation and
Allocation Committee; National Institute of Dental and Craniofacial
Research, NIH, DHHS
FX The authors are indebted to Zimmer for its gift of HA/TCP particles.
Albert Kingman, Ph.D., provided invaluable statistical assistance; Vijay
Tiwari, M. B. B. S., assisted with the image analysis; and Ms. Katherine
Huang assisted with the in situ hybridization. This research was
supported in part by the University of California-San Francisco Research
Evaluation and Allocation Committee and in part by the Intramural
Research Program of the National Institute of Dental and Craniofacial
Research, NIH, DHHS.
NR 38
TC 27
Z9 29
U1 0
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1937-3341
J9 TISSUE ENG PT A
JI Tissue Eng. Part A
PD DEC
PY 2008
VL 14
IS 12
BP 1949
EP 1958
DI 10.1089/ten.tea.2007.0348
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 379NN
UT WOS:000261403500003
PM 18800877
ER
PT J
AU Butler, DL
Lewis, JL
Frank, CB
Banes, AJ
Caplan, AI
De Deyne, PG
Dowling, MA
Fleming, BC
Glowacki, J
Guldberg, RE
Johnstone, B
Kaplan, DL
Levenston, ME
Lotz, JC
Lu, EY
Lumelsky, N
Mao, JJ
Mauck, RL
McDevitt, CA
Mejia, LC
Murray, M
Ratcliffe, A
Spindler, KP
Tashman, S
Wagner, CT
Weisberg, EM
Williams, C
Zhang, RW
AF Butler, David L.
Lewis, Jack L.
Frank, Cyril B.
Banes, Albert J.
Caplan, Arnold I.
De Deyne, Patrick G.
Dowling, Mary-Ann
Fleming, Braden C.
Glowacki, Julie
Guldberg, Robert E.
Johnstone, Brian
Kaplan, David L.
Levenston, Marc E.
Lotz, Jeffrey C.
Lu, Ed Yiling
Lumelsky, Nadya
Mao, Jeremy J.
Mauck, Robert L.
McDevitt, Cahir A.
Mejia, Lito C.
Murray, Martha
Ratcliffe, Anthony
Spindler, Kurt P.
Tashman, Scott
Wagner, Christopher T.
Weisberg, Elijah M.
Williams, Chrysanthi (Sandy)
Zhang, Renwen
CA Functional Tissue Engn Conf Grp
TI Evaluation Criteria for Musculoskeletal and Craniofacial Tissue
Engineering Constructs: A Conference Report
SO TISSUE ENGINEERING PART A
LA English
DT Article
ID ANTERIOR CRUCIATE LIGAMENT; INTERVERTEBRAL DISC DEGENERATION; ROTATOR
CUFF; ARTICULAR-CARTILAGE; BIOCHEMICAL-PROPERTIES; KNEE-JOINT;
TEMPOROMANDIBULAR-JOINT; MECHANICAL-PROPERTIES; GAMMA-IRRADIATION;
MENISCAL REPAIR
AB Over the past 20 years, tissue engineering (TE) has evolved into a thriving research and commercial development field. However, applying TE strategies to musculoskeletal (MSK) and craniofacial tissues has been particularly challenging since these tissues must also transmit loads during activities of daily living. To address this need, organizers invited a small group of bioengineers, surgeons, biologists, and material scientists from academia, industry, and government to participate in a 2 1/2-day conference to develop general and tissue-specific criteria for evaluating new concepts and tissue-engineered constructs, including threshold values of success. Participants were assigned to four breakout groups representing commonly injured tissues, including tendon and ligament, articular cartilage, meniscus and temporomandibular joint, and bone and intervertebral disc. Working in multidisciplinary teams, participants first carefully defined one or two important unmet clinical needs for each tissue type, including current standards of care and the potential impact of TE solutions. The groups then sought to identify important parameters for evaluating repair outcomes in preclinical studies and to specify minimally acceptable values for these parameters. The importance of in vitro TE studies was then discussed in the context of these preclinical studies. Where data were not currently available from clinical, preclinical, or culture studies, the groups sought to identify important areas of preclinical research needed to speed the development process. This report summarizes the findings of the conference.
C1 [Butler, David L.] Univ Cincinnati, Dept Biomed Engn, Engn Res Ctr 840, Cincinnati, OH 45221 USA.
[Lewis, Jack L.] Univ Minnesota, Dept Orthopaed Surg, Minneapolis, MN 55455 USA.
[Frank, Cyril B.] Univ Calgary, Div Orthopaed Surg, Dept Surg, Calgary, AB, Canada.
[Banes, Albert J.] Univ N Carolina, Joint Dept Biomed Engn, Raleigh, NC USA.
[Caplan, Arnold I.] Case Western Reserve Univ, Dept Biol, Cleveland, OH 44106 USA.
[De Deyne, Patrick G.] Johnson & Johnson Regenerat Therapeut, Preclin Biol, Raynham, MA USA.
[Dowling, Mary-Ann] Smith & Nephew Res Ctr, York, N Yorkshire, England.
[Fleming, Braden C.] Brown Univ, Dept Orthopaed Surg, Providence, RI 02912 USA.
[Glowacki, Julie; Murray, Martha] Harvard Univ, Sch Med, Dept Orthoped Surg, Boston, MA 02115 USA.
[Glowacki, Julie] Harvard Univ, Sch Dent Med, Dept Oral & Maxillofacial Surg, Boston, MA 02115 USA.
[Guldberg, Robert E.] Georgia Inst Technol, George W Woodruff Sch Mech Engn, Atlanta, GA 30332 USA.
[Johnstone, Brian] Oregon Hlth & Sci Univ, Dept Orthopaed & Rehabil, Portland, OR 97201 USA.
[Kaplan, David L.] Tufts Univ, Dept Biomed Engn, Medford, MA 02155 USA.
[Levenston, Marc E.] Stanford Univ, Dept Mech Engn, Stanford, CA 94305 USA.
[Lumelsky, Nadya] Natl Inst Dent & Craniofacial Res, Tissue Engn & Dent & Craniofacial Regenerat Med R, Bethesda, MD USA.
[Mao, Jeremy J.] Columbia Univ, TERML, New York, NY USA.
[Mauck, Robert L.] Univ Penn, Dept Orthopaed Surg, Philadelphia, PA 19104 USA.
[McDevitt, Cahir A.] Cleveland Clin Fdn, Dept Biomed Engn, Cleveland, OH 44195 USA.
[Glowacki, Julie] Harvard Univ, Sch Dent Med, Dept Orthoped Surg, Boston, MA 02115 USA.
[Glowacki, Julie] Harvard Univ, Sch Med, Dept Oral & Maxillofacial Surg, Boston, MA USA.
[Ratcliffe, Anthony] Synthasome Inc, San Diego, CA USA.
[Spindler, Kurt P.] Vanderbilt Orthopaed Inst, Nashville, TN USA.
[Tashman, Scott] Univ Pittsburgh, Dept Orthopaed Surg, Pittsburgh, PA 15260 USA.
[Wagner, Christopher T.] LifeCell Corp, Branchburg, NJ USA.
[Weisberg, Elijah M.] Natl Inst Arthritis & Musculoskeletal Dis, Bethesda, MD USA.
[Williams, Chrysanthi (Sandy)] Bose Corp, Biomat & Tissue Engn, Prairie, MN USA.
[Zhang, Renwen] Orthobiol Grp, Mahwah, NJ USA.
RP Butler, DL (reprint author), Univ Cincinnati, Dept Biomed Engn, Engn Res Ctr 840, 2901 Woodside Dr, Cincinnati, OH 45221 USA.
EM david.butler@uc.edu; lewis001@umn.edu; cfrank@ucalgary.ca;
albert_banes@med.unc.edu; arnold.caplan@case.edu;
pdedeyne@rtxus.jnj.com; Mary-Ann.Dowling@Smith-Nephew.com;
Braden_Fleming@brown.edu; jglowacki@rics.bwh.harvard.edu;
robert.guldberg@me.gatech.edu; johnstob@ohsu.edu;
David.Kaplan@tufts.edu; levenston@stanford.edu;
lotzj@orthosurg.ucsf.edu; elu1@rtxus.jnj.com; nadyal@nidcr.nih.gov;
jmao@columbia.edu; lemauck@mail.med.upenn.edu; mcdevitt@bme.ri.ccf.org;
Lito_Mejia@bose.com; martha.murray@childrens.harvard.edu;
anthonyratcliffe@synthasome.com; kurt.spindler@vanderbilt.edu;
tashman@upmc.edu; cwagner@lifecell.com; weisberge@mail.nih.gov;
Sandy_Williams@bose.com; renwen.zhang@stryker.com
FU National Institutes of Health (National Institute of Arthritis and
Musculoskeletal and Skin Diseases [NIAMS], National Institute of
Biomedical Imaging and Bioengineering [NIBIB], and National Institute of
Dental and Craniofacial Research [NIDCR]) [R13AR54721-1]; Orthopaedic
Research and Education Foundation; Orthopaedic Research Society; Bose
Corporation; Flexcell International Corporation; LifeCell Corporation;
Johnson & Johnson Regenerative Therapeutics; Smith Nephew; Stryker
Orthopedics Corporation; Synthasome, Inc.
FX The organizers wish to thank the following organizations for support of
this conference: National Institutes of Health (R13AR54721-1; DB, PI)
(National Institute of Arthritis and Musculoskeletal and Skin Diseases
[NIAMS], National Institute of Biomedical Imaging and Bioengineering
[NIBIB], and National Institute of Dental and Craniofacial Research
[NIDCR]); the Orthopaedic Research and Education Foundation; the
Orthopaedic Research Society; Bose Corporation; Flexcell International
Corporation; LifeCell Corporation; Johnson & Johnson Regenerative
Therapeutics; Smith & Nephew; Stryker Orthopedics Corporation; and
Synthasome, Inc. We wish to also acknowledge Kathleen Derwin, Ph.D.,
Assistant Staff Scientist in the Department of Biomedical Engineering at
the Cleveland Clinic, who edited the rotator cuff portion of this paper
and provided relevant literature.
NR 76
TC 7
Z9 7
U1 0
U2 7
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1937-3341
J9 TISSUE ENG PT A
JI Tissue Eng. Part A
PD DEC
PY 2008
VL 14
IS 12
BP 2089
EP 2104
DI 10.1089/ten.tea.2007.0383
PG 16
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
Biology
SC Cell Biology; Biotechnology & Applied Microbiology
GA 379NN
UT WOS:000261403500016
ER
PT J
AU Wei, BR
Edwards, JB
Hoover, SB
Tillman, HS
Reed, LT
Sills, RC
Simpson, RM
AF Wei, Bih-Rong
Edwards, Jennifer B.
Hoover, Shelley B.
Tillman, Heather S.
Reed, L. Tiffany
Sills, Robert C.
Simpson, R. Mark
TI Altered beta-Catenin Accumulation in Hepatocellular Carcinomas of
Diethylnitrosamine-Exposed Rhesus Macaques
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE biological specimen banks; sequence analysis; DNA; carcinogens;
mutagens; signal transduction pathway
ID WNT SIGNALING PATHWAY; LIVER-CANCER; MOUSE-LIVER; ACTIVATION; MUTATIONS;
HEPATOCARCINOGENESIS; GENE; ADVANTAGES; ANTIBODY; FREQUENT
AB Chemical exposures are important risks for development of hepatocellular carcinoma (HCC). One such chemical, diethylnitrosamine (DENA), is present in food products as well as in industrial and research settings. Further examination of tumors induced by DENA may yield clues to human risk. HCC from seven rhesus macaques exposed to DENA was selected from a tissue archive to examine for evidence of Wnt/beta-catenin signaling events, which are frequently associated with HCC. DENA exposure durations ranged from 8 to 207 months, and total accumulated dose ranged from 0.7 to 4.08 mg. Unexposed colony breeder macaques served as controls. Previously unrecognized HCC metastases were discovered in lungs of three macaques. Overexpression of beta-catenin and glutamine synthetase was detected by immunohistochemistry in six confirmed primary HCC and all metastatic HCC, which implicated Wnt/beta-catenin activation. Concomitant beta-catenin gene mutation was detected in one primary HCC; similar findings have been reported in human and rodent HCC. Neither beta-catenin mutation nor beta-catenin overexpression appeared to influence metastatic potential. Accumulation of intracellular proteins involved in Wnt/beta-catenin signaling during HCC oncogenesis in rhesus macaques exposed to DENA appears to include other mechanisms, in addition to mutation of beta-catenin gene.
C1 [Wei, Bih-Rong; Edwards, Jennifer B.; Hoover, Shelley B.; Tillman, Heather S.; Reed, L. Tiffany; Simpson, R. Mark] NCI, Mol Pathol Unit, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
[Sills, Robert C.] NIEHS, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
RP Simpson, RM (reprint author), NCI, Mol Pathol Unit, Lab Canc Biol & Genet, Ctr Canc Res, 37 Convent Dr,2000, Bethesda, MD 20892 USA.
EM ms43b@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 31
TC 2
Z9 2
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2008
VL 36
IS 7
BP 972
EP 980
DI 10.1177/0192623308327120
PG 9
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 463WO
UT WOS:000267464300008
PM 18978308
ER
PT J
AU Huff, J
AF Huff, James
TI Long-term Cancer Bioassays of Ascorbic Acid
SO TOXICOLOGICAL SCIENCES
LA English
DT Letter
ID OXIDATIVE DNA-DAMAGE; SODIUM-NITRITE; FORESTOMACH CARCINOGENESIS; RATS;
INITIATION; PROMOTION
C1 Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
RP Huff, J (reprint author), Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
EM huff1@niehs.nih.gov
NR 11
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2008
VL 106
IS 2
BP 570
EP 571
DI 10.1093/toxsci/kfn185
PG 2
WC Toxicology
SC Toxicology
GA 373NX
UT WOS:000260979800027
PM 18755737
ER
PT J
AU Drecktrah, D
Levine-Wilkinson, S
Dam, T
Winfree, S
Knodler, LA
Schroer, TA
Steele-Mortimer, O
AF Drecktrah, Dan
Levine-Wilkinson, Seamus
Dam, Tapen
Winfree, Seth
Knodler, Leigh A.
Schroer, Trina A.
Steele-Mortimer, Olivia
TI Dynamic Behavior of Salmonella-Induced Membrane Tubules in Epithelial
Cells
SO TRAFFIC
LA English
DT Article
DE confocal; endosomes; lysosomes; microtubule; Salmonella-containing
vacuole; Sifs
ID ENTERICA SEROVAR TYPHIMURIUM; LATE ENDOCYTIC COMPARTMENTS; CONTAINING
VACUOLES; FILAMENTOUS STRUCTURES; FLUORESCENT PROTEIN; ENDOSOME
MOTILITY; LYSOSOMES; EFFECTOR; MICROTUBULES; SIFA
AB Salmonella Typhimurium is a facultative intracellular pathogen that causes acute gastroenteritis in man. Intracellular Salmonella survive and replicate within a modified phagosome known as the Salmonella-containing vacuole (SCV). The onset of intracellular replication is accompanied by the appearance of membrane tubules, called Salmonella-induced filaments (Sifs), extending from the SCV. Sifs are enriched in late endosomal/lysosomal membrane proteins such as lysosome-associated membrane protein 1, but their formation and ability to interact with endosomal compartments are not characterized. In this study, we use live cell imaging techniques to define the dynamics of Sif formation in infected epithelial cells. At early time-points, Sifs are simple tubules extending from the surface of SCVs. These tubules are highly dynamic and exhibit bidirectional, microtubule-dependent movement. At the distal ends of individual Sif tubules, furthest from the SCV, a distinct 'leader' domain was often observed. At later times, Sifs develop into highly complex tubular networks that extend throughout the cell and appear less dynamic than nascent Sifs; however, individual tubules continue to display bidirectional dynamics. Sifs can acquire endocytic content by fusion, indicating a sustained interaction with the endocytic pathway. Together, these results show that these Salmonella-induced tubules form a highly dynamic network that involves both microtubule-dependent motility and interactions with endosomal compartments.
C1 [Drecktrah, Dan; Winfree, Seth; Knodler, Leigh A.; Steele-Mortimer, Olivia] NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT 59840 USA.
[Levine-Wilkinson, Seamus; Dam, Tapen; Schroer, Trina A.] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
RP Steele-Mortimer, O (reprint author), NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT 59840 USA.
EM omortimer@niaid.nih.gov
OI Schroer, Trina/0000-0002-5065-1835
FU National Institutes of Health (NIH) [R21 AI69822]; National Institute of
Allergy and Infectious Diseases (NIAID)
FX This paper is dedicated to the memory of T. D. We are grateful to the
following for generously providing us with plasmids or constructs;
Esteban Dell'Angelica for the LAMP1-mGFP, Roger Tsein for mCherry, Matt
Scott and Dennis Ko for NPC1-eGFP and Nat Brown and B. Brett Finlay for
pBR-RFP. 1. Karen Guillemin and Michael Hensel generously provided S.
Typhimurium strains SL1344 and 12023 to T. A. S. Also we thank the
members of the Steele-Mortimer and Schroer laboratories for reading the
manuscript and constructive criticism. This study was funded by National
Institutes of Health (NIH) grant R21 AI69822 to T. A. S. and by the
Intramural Research Program of NIH, National Institute of Allergy and
Infectious Diseases (NIAID) for O. S-M.
NR 53
TC 54
Z9 54
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-9219
J9 TRAFFIC
JI Traffic
PD DEC
PY 2008
VL 9
IS 12
BP 2117
EP 2129
DI 10.1111/j.1600-0854.2008.00830.x
PG 13
WC Cell Biology
SC Cell Biology
GA 375AX
UT WOS:000261086000010
PM 18785994
ER
PT J
AU Moore, ER
Fischer, ER
Mead, DJ
Hackstadt, T
AF Moore, Elizabeth R.
Fischer, Elizabeth R.
Mead, David J.
Hackstadt, Ted
TI The Chlamydial Inclusion Preferentially Intercepts Basolaterally
Directed Sphingomyelin-Containing Exocytic Vacuoles
SO TRAFFIC
LA English
DT Article
DE Chlamydia; exocytosis; lipid trafficking; pathogenesis; polarized cell;
sphingomyelin
ID ENDOMETRIAL EPITHELIAL-CELLS; CANINE KIDNEY-CELLS; OBLIGATE
INTRACELLULAR PATHOGEN; OUTER-MEMBRANE PROTEIN; TRACHOMATIS SEROVAR-E;
IN-VITRO; HOST-CELL; PLASMA-MEMBRANE; ENDOCYTIC PATHWAY; GOLGI-APPARATUS
AB Chlamydiae replicate intracellularly within a unique vacuole termed the inclusion. The inclusion circumvents classical endosomal/lysosomal pathways but actively intercepts a subset of Golgi-derived exocytic vesicles containing sphingomyelin (SM) and cholesterol. To further examine this interaction, we developed a polarized epithelial cell model to study vectoral trafficking of lipids and proteins to the inclusion. We examined seven epithelial cell lines for their ability to form single monolayers of polarized cells and support chlamydial development. Of these cell lines, polarized colonic mucosal C2BBe1 cells were readily infected with Chlamydia trachomatis and remained polarized throughout infection. Trafficking of (6-((N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)hexanoyl)sphingosine) (NBD-C(6)-ceramide) and its metabolic derivatives, NBD-glucosylceramide (GlcCer) and NBD-SM, was analyzed. SM was retained within L2-infected cells relative to mock-infected cells, correlating with a disruption of basolateral SM trafficking. There was no net retention of GlcCer within L2-infected cells and purification of C. trachomatis elementary bodies from polarized C2BBe1 cells confirmed that bacteria retained only SM. The chlamydial inclusion thus appears to preferentially intercept basolaterally-directed SM-containing exocytic vesicles, suggesting a divergence in SM and GlcCer trafficking. The observed changes in lipid trafficking were a chlamydia-specific effect because Coxiella burnetii-infected cells revealed no changes in GlcCer or SM polarized trafficking.
C1 [Moore, Elizabeth R.; Mead, David J.; Hackstadt, Ted] NIAID, Host Parasite Interact Sect, Intracellular Parasites Lab, Rocky Mt Labs, Hamilton, MT 59840 USA.
[Fischer, Elizabeth R.] NIAID, Microscopy Unit, Rocky Mt Labs, Hamilton, MT 59840 USA.
RP Hackstadt, T (reprint author), NIAID, Host Parasite Interact Sect, Intracellular Parasites Lab, Rocky Mt Labs, 903 S 4th St, Hamilton, MT 59840 USA.
EM thackstadt@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases (NIAID) of the
National Institutes of Health
FX The authors would like to thank Travis Jewett, Jeff Mital, Olivia
Steele-Mortimer and Bob Heinzen for critical review of the manuscript,
Janet Sager for technical support and members of the Hackstadt
laboratory for helpful comments and suggestions. This study was
supported by the Intramural Research Program of the National Institute
of Allergy and Infectious Diseases (NIAID) of the National Institutes of
Health.
NR 90
TC 41
Z9 42
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-9219
J9 TRAFFIC
JI Traffic
PD DEC
PY 2008
VL 9
IS 12
BP 2130
EP 2140
DI 10.1111/j.1600-0854.2008.00828.x
PG 11
WC Cell Biology
SC Cell Biology
GA 375AX
UT WOS:000261086000011
PM 18778406
ER
PT J
AU Yoon, HY
Lee, JS
Randazzo, PA
AF Yoon, Hye-Young
Lee, Ju-Seog
Randazzo, Paul A.
TI ARAP1 Regulates Endocytosis of EGFR
SO TRAFFIC
LA English
DT Article
DE ADP ribosylation factor; ARAP1; GTPase-activating protein; EGF;
endocytosis; Rab5
ID GROWTH-FACTOR RECEPTOR; NUCLEOTIDE EXCHANGE FACTOR; CLATHRIN-COATED
PITS; GOLGI MATRIX PROTEIN; SMALL GTPASE RAB5; SIGNAL-TRANSDUCTION;
TYROSINE KINASES; ARF GAPS; MEDIATED ENDOCYTOSIS; FACTOR ARNO
AB Signaling through the EGF receptor is regulated by endocytosis. ARAP1 is a protein with Arf guanosine triphosphatase-activating protein (GAP) and Rho GAP domains. We investigated the role of ARAP1 in EGF receptor endocytic trafficking. Following EGF treatment of cells, ARAP1 rapidly and transiently associated with the edge of the cell and punctate structures containing Rab5, rabaptin 5 and EGFR but not early embryonic antigen 1 (EEA1). EGF associated with the ARAP1-positive punctate structures prior to EEA1-positive early endosomes. Recruitment of ARAP1 to the punctate structures required active Rab5 and an additional signal from EGFR. Decreasing ARAP1 levels with small interfering RNA accelerated association of EGF with EEA1 endosomes and degradation of EGFR. Phosphorylation of extracellular-signal-regulated kinase (ERK) and c-Jun-amino-terminal kinase (JNK) was diminished and more transient in cells with reduced levels of ARAP1 than in controls. Based on these findings, we propose that ARAP1 regulates the endocytic traffic of EGFR and, consequently, the rate of EGFR signal attenuation.
C1 [Yoon, Hye-Young; Randazzo, Paul A.] NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA.
[Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77054 USA.
RP Randazzo, PA (reprint author), NCI, Cellular & Mol Biol Lab, Bldg 37 Room 2042, Bethesda, MD 20892 USA.
EM randazzo@helix.nih.gov
FU National Cancer Institute, Department of Health and Human Services
FX We thank Drs Stanley Lipkowitz, Carole Parent and Lawrence Samelson and
the members of the Randazzo laboratory group for insightful discussions.
This study was supported by the Intramural Research Program of the
National Cancer Institute, Department of Health and Human Services.
NR 85
TC 24
Z9 24
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-9219
J9 TRAFFIC
JI Traffic
PD DEC
PY 2008
VL 9
IS 12
BP 2236
EP 2252
DI 10.1111/j.1600-0854.2008.00839.x
PG 17
WC Cell Biology
SC Cell Biology
GA 375AX
UT WOS:000261086000019
PM 18939958
ER
PT J
AU Shoham, S
Pic-Aluas, L
Taylor, J
Cortez, K
Rinaldi, MG
Shea, Y
Walsh, TJ
AF Shoham, S.
Pic-Aluas, L.
Taylor, J.
Cortez, K.
Rinaldi, M. G.
Shea, Y.
Walsh, T. J.
TI Transplant-associated Ochroconis gallopava infections
SO TRANSPLANT INFECTIOUS DISEASE
LA English
DT Article
DE Ochroconis gallopava; dematiaceous; transplant; brain abscess
ID DACTYLARIA-GALLOPAVA; CEREBRAL PHEOHYPHOMYCOSIS; DEMATIACEOUS FUNGI;
SUCCESSFUL THERAPY; CELL TYPE; ENCEPHALITIS; RECIPIENT; PATIENT;
CONSTRICTA; DISEASE
AB S. Shoham, L. Pic-Aluas, J. Taylor, K. Cortez, M.G. Rinaldi, Y. Shea, T.J. Walsh. Transplant-associated Ochroconis gallopava infections.Transpl Infect Dis 2008: 10: 442-448
Ochroconis gallopava is a neurotropic dematiaceous mold that causes respiratory and central nervous system (CNS) infection in domestic poultry and in immunocompromised patients. We recently treated 3 solid organ transplant (SOT) recipients for pulmonary Ochroconis infections with successful outcome, prompting us to review the literature on this unique pathogen.
We reviewed all published cases of O. gallopava infections in SOT recipients and analyzed the impact of CNS infection on the outcome.
In addition to the 3 new cases reported here, 9 published cases of Ochroconis infection were analyzed. The disease involved the lungs only in 5/12 (42%) of patients, brain in 6/12 (50%) patients, and lung and skin in 1 patient. Survival was significantly reduced with brain infection (33% vs. 100%; P < 0.03; Fisher's exact test).
O. gallopava may infect SOT recipients with a particular tropism for the CNS. Early recognition of O. gallopava pulmonary infection is important, as the prognosis is excellent before dissemination to the brain.
C1 [Shoham, S.; Pic-Aluas, L.] Washington Hosp Ctr, Infect Dis Sect, Washington, DC 20010 USA.
[Shoham, S.; Cortez, K.; Walsh, T. J.] NCI, Pediat Oncol Branch, Immunocompromised Host Sect, Bethesda, MD 20892 USA.
[Taylor, J.] NHLBI, Bethesda, MD 20892 USA.
[Rinaldi, M. G.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, Fungus Testing Lab, San Antonio, TX 78229 USA.
[Shea, Y.] NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA.
RP Shoham, S (reprint author), Washington Hosp Ctr, Infect Dis Sect, 110 Irving St NW, Washington, DC 20010 USA.
EM Shmuel.Shoham@medstar.net
OI Taylor, James/0000-0002-4421-1809
NR 33
TC 23
Z9 23
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-2273
J9 TRANSPL INFECT DIS
JI Transpl. Infect. Dis.
PD DEC
PY 2008
VL 10
IS 6
BP 442
EP 448
DI 10.1111/j.1399-3062.2008.00327.x
PG 7
WC Immunology; Infectious Diseases; Transplantation
SC Immunology; Infectious Diseases; Transplantation
GA 375AU
UT WOS:000261085700013
PM 18651872
ER
PT J
AU Bohr, VA
AF Bohr, Vilhelm A.
TI Rising from the RecQ-age: the role of human RecQ helicases in genome
maintenance
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
ID WERNER-SYNDROME PROTEIN; ROTHMUND-THOMSON-SYNDROME; BLOOMS-SYNDROME
HELICASE; BASE EXCISION-REPAIR; STRAND-ANNEALING ACTIVITIES; INTERSTRAND
CROSS-LINKS; SYNDROME GENE-PRODUCT; DNA-POLYMERASE-BETA; HOMOLOGOUS
RECOMBINATION; FUNCTIONAL INTERACTION
AB The RecQ helicases are guardians of the genome. Members of this conserved family of proteins have a key role in protecting and stabilizing the genome against deleterious changes. Deficiencies in RecQ helicases can lead to high levels of genomic instability and, in humans, to premature aging and increased susceptibility to cancer. Their diverse roles in DNA metabolism, which include a role in telomere maintenance, reflect interactions with multiple cellular proteins, some of which are multifunctional and also have very diverse functions. The results of in vitro cellular and biochemical studies have been complimented by recent in vivo studies using genetically modified mouse strains. Together, these approaches are helping to unravel the mechanism(s) of action and biological functions of the RecQ helicases.
C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
FU Intramural Research Program of the National Institute on Aging, National
Institutes of Health
FX I would like to thank M. Sander, D. Wilson and D. Croteau for
suggestions. I acknowledge support from the Intramural Research Program
of the National Institute on Aging, National Institutes of Health.
NR 99
TC 154
Z9 157
U1 2
U2 7
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD DEC
PY 2008
VL 33
IS 12
BP 609
EP 620
DI 10.1016/j.tibs.2008.09.003
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 385TO
UT WOS:000261836700007
PM 18926708
ER
PT J
AU Carrington, M
Martin, MP
van Bergen, J
AF Carrington, Mary
Martin, Maureen P.
van Bergen, Jeroen
TI KIR-HLA intercourse in HIV disease
SO TRENDS IN MICROBIOLOGY
LA English
DT Review
ID NATURAL-KILLER-CELLS; MHC CLASS-I; EXPOSED UNINFECTED INDIVIDUALS;
IMMUNOGLOBULIN-LIKE RECEPTORS; NK-CELLS; CUTTING EDGE; INHIBITORY
RECEPTORS; INNATE RESISTANCE; PERIPHERAL-BLOOD; MISSING-SELF
AB Human leukocyte antigen (HLA) class I loci are essential to an effective immune response against a wide variety of pathogenic microorganisms, and they represent the prototypes for genetic polymorphism that are sustained through balancing selection. The functional significance of HLA class I variation is better exemplified by studies involving HIV type 1 (HIV-1) than any other infectious organism. HLA class I molecules are essential to the acquired immune response, but they are also important in innate immunity as ligands for the killer cell immunoglobulin-like receptors (KIR), which modulate natural killer cell activity. Here we concentrate on the interaction between the HLA-B and KIR3DL1/KIR3DS1 genes, describe the effects of these loci on HIV disease, and discuss questions that remain unresolved.
C1 [Carrington, Mary; Martin, Maureen P.] NCI, SAIC Frederick Inc, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
[van Bergen, Jeroen] Leiden Univ, Med Ctr, Dept Immunohematol & Blood Transfus, Sect Immunochem, NL-2333 ZA Leiden, Netherlands.
RP Carrington, M (reprint author), NCI, SAIC Frederick Inc, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
EM carringt@ncifcrf.gov
FU National Cancer Institute, National Institute of Health [N01-CO-12400];
Landsteiner Foundation for Blood Transfusion Research [0515]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institute of Health, under
contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does, mention of trade names commercial products
or organizations imply endorsement by the U.S. Government. This research
Was Supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. JvB was supported
by grant 0515 from the Landsteiner Foundation for Blood Transfusion
Research.
NR 81
TC 91
Z9 94
U1 0
U2 5
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0966-842X
J9 TRENDS MICROBIOL
JI Trends Microbiol.
PD DEC
PY 2008
VL 16
IS 12
SI SI
BP 620
EP 627
DI 10.1016/j.tim.2008.09.002
PG 8
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 386RL
UT WOS:000261900200011
PM 18976921
ER
PT J
AU Seliger, B
Marincola, FM
Ferrone, S
Abken, H
AF Seliger, Barbara
Marincola, Francesco M.
Ferrone, Soldano
Abken, Hinrich
TI The complex role of B7 molecules in tumor immunology
SO TRENDS IN MOLECULAR MEDICINE
LA English
DT Review
ID RENAL-CELL-CARCINOMA; HUMAN OVARIAN-CARCINOMA; CROSS-LINKING ANTIBODY;
ACUTE MYELOID-LEUKEMIA; BREAST-CANCER PATIENTS; PHASE-I TRIAL; T-CELLS;
B7-H1 EXPRESSION; ANTITUMOR IMMUNITY; COSTIMULATORY MOLECULE
AB T-cell activation requires the interaction of the T-cell receptor with a cognate major histocompatibility complex (MHC)-peptide complex. Initiated by antigen engagement, the adaptive immune response is orchestrated by a complex balance between stimulatory and inhibitory signals that are predominantly controlled by members of the B7 family. Here, we review the current knowledge on B7 family members concerning their constitutive and regulated expression, modulation of the immune response and their role in the evasion of host immune surveillance. We also discuss recent therapeutic strategies that aim to improve immune-cell recognition of tumors and induce tolerance to autoreactive immune responses in normal tissues by manipulating B7 functions.
C1 [Seliger, Barbara] Univ Halle Wittenberg, Inst Med Immunol, D-06112 Halle, Germany.
[Marincola, Francesco M.] NIH, Dept Transfus Med & Immunogenet, Bethesda, MD 20862 USA.
[Ferrone, Soldano] Univ Pittsburgh, Inst Canc, Dept Surg, Pittsburgh, PA 15213 USA.
[Ferrone, Soldano] Univ Pittsburgh, Inst Canc, Dept Immunol, Pittsburgh, PA 15213 USA.
[Ferrone, Soldano] Univ Pittsburgh, Inst Canc, Dept Pathol, Pittsburgh, PA 15213 USA.
[Abken, Hinrich] Univ Cologne, Ctr Mol Med, D-50931 Cologne, Germany.
[Abken, Hinrich] Univ Cologne, Clin Internal Med 1, D-50931 Cologne, Germany.
RP Seliger, B (reprint author), Univ Halle Wittenberg, Inst Med Immunol, D-06112 Halle, Germany.
EM Barbara.Seligcr@medizin.uni-halle.de
RI Chen, Jin/B-3323-2012
FU Deutsche Krebshilfe; Mildred Scheel Cancer Foundation, Bonn, Germany
FX The study is supported by the Deutsche Krebshilfe, Mildred Scheel Cancer
Foundation, Bonn, Germany (B.S., H.A.). We thank A. Wasilewski for
excellent secretarial assistance.
NR 113
TC 45
Z9 52
U1 1
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4914
J9 TRENDS MOL MED
JI Trends Mol. Med
PD DEC
PY 2008
VL 14
IS 12
BP 550
EP 559
DI 10.1016/j.molmed.2008.09.010
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 384NK
UT WOS:000261751300005
PM 18986838
ER
PT J
AU Wise, SP
AF Wise, Steven P.
TI Forward frontal fields: phylogeny and fundamental function
SO TRENDS IN NEUROSCIENCES
LA English
DT Review
ID DORSOLATERAL PREFRONTAL CORTEX; VISUAL WORKING-MEMORY; ORBITOFRONTAL
CORTEX; ARCHITECTONIC SUBDIVISION; INFEROTEMPORAL CORTEX;
NEURONAL-ACTIVITY; DECISION-MAKING; MACAQUE MONKEYS; SELECTION; LESIONS
AB The largest part of the primate prefrontal cortex has no homolog in other mammals. Accordingly, it probably confers some advantage that other mammals either lack or attain through the function of other structures. Yet, this advantage remains enigmatic. This is not so for other parts of the cortex. For example, certain visual areas encode, represent and store knowledge about objects. By analogy, perhaps the primate prefrontal cortex encodes, represents and stores knowledge about behaviors, including the consequences of doing (or not doing) something in complex and challenging situations. The long list of functions often attributed to the prefrontal cortex could contribute to knowing what to do and what will happen when rare risks arise or outstanding opportunities knock.
C1 NIMH, Sect Neurophysiol, Lab Syst Neurosci, Bethesda, MD 20892 USA.
RP Wise, SP (reprint author), NIMH, Sect Neurophysiol, Lab Syst Neurosci, 49 Convent Dr,MSC 4401, Bethesda, MD 20892 USA.
EM stevenwise@mail.nih.gov
FU Intramural NIH HHS [Z01 MH001092-29]
NR 78
TC 141
Z9 142
U1 2
U2 7
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0166-2236
J9 TRENDS NEUROSCI
JI Trends Neurosci.
PD DEC
PY 2008
VL 31
IS 12
BP 599
EP 608
DI 10.1016/j.tins.2008.08.008
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 384AF
UT WOS:000261715000001
PM 18835649
ER
PT J
AU Wess, J
Han, SJ
Kim, SK
Jacobson, KA
Li, JH
AF Wess, Juergen
Han, Sung-Jun
Kim, Soo-Kyung
Jacobson, Kenneth A.
Li, Jian Hua
TI Conformational changes involved in G-protein-coupled-receptor activation
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; DISULFIDE CROSS-LINKING; BETA(2)
ADRENERGIC-RECEPTOR; TOGGLE SWITCH MODEL; AMINO-ACID-RESIDUES;
CRYSTAL-STRUCTURE; CYTOPLASMIC END; 7-TRANSMEMBRANE RECEPTORS;
SULFHYDRYL REACTIVITY; PALMITOYLATION SITES
AB Little is known about the nature of the conformational changes that convert G-protein-coupled receptors (GPCRs), which bind diffusible ligands, from their resting into their active states. To gain structural insight into this process, various laboratories have used disulfide cross-linking strategies involving cysteine-substituted mutant GPCRs. Several recent disulfide cross-linking studies using the M(3) muscarinic acetylcholine receptor as a model system have led to novel insights into the conformational changes associated with the activation of this prototypical class I GPCR. These structural changes are predicted to involve multiple receptor regions, primarily distinct segments of transmembrane helices III, VI and VII and helix 8. Given the high degree of structural homology found among most GPCRs, it is likely that these findings will be of considerable general relevance. A better understanding of the molecular mechanisms underlying GPCR activation might lead to novel strategies aimed at modulating GPCR function for therapeutic purposes.
C1 [Wess, Juergen; Han, Sung-Jun; Kim, Soo-Kyung; Jacobson, Kenneth A.; Li, Jian Hua] NIDDK, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Wess, Juergen; Han, Sung-Jun; Kim, Soo-Kyung; Jacobson, Kenneth A.; Li, Jian Hua] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Wess, J (reprint author), NIDDK, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bldg 8A,8 Ctr Dr MSC 0810, Bethesda, MD 20892 USA.
EM jwess@helix.nih.gov
RI Li, Jianhua/B-7671-2011; Han, Sung-Jun/B-9547-2012; Jacobson,
Kenneth/A-1530-2009
OI Li, Jianhua/0000-0002-5744-3182; Jacobson, Kenneth/0000-0001-8104-1493
FU National Institutes of Health (NIH); National Institute of Diabetes and
Digestive and Kidney Diseases
FX Our own research covered here was supported by the Intramural Research
Program of the National Institutes of Health (NIH), National Institute
of Diabetes and Digestive and Kidney Diseases (NIDDK;
www.niddk.nih.gov). We thank Stefano Costanzi and Joel D. Karpiak (NIH,
NIDDK) for preparing Figure 4.
NR 62
TC 55
Z9 55
U1 1
U2 4
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD DEC
PY 2008
VL 29
IS 12
BP 616
EP 625
DI 10.1016/j.tips.2008.08.006
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 384AD
UT WOS:000261714800004
PM 18838178
ER
PT J
AU Bellizzi, KM
Latini, DM
Cowan, JE
DuChane, J
Carroll, PR
AF Bellizzi, Keith M.
Latini, David M.
Cowan, Janet E.
DuChane, Janeen
Carroll, Peter R.
TI Fear of Recurrence, Symptom Burden, and Health-Related Quality of Life
in Men With Prostate Cancer
SO UROLOGY
LA English
DT Article
ID RADICAL PROSTATECTOMY; CARCINOMA; SURVIVORS; CAPSURE; PREDICTORS; ADULT;
ADJUSTMENT; DISTRESS
AB OBJECTIVES To examine the contributions of fear of recurrence and the more commonly examined treatment-related symptoms to the health-related quality of life (HRQOL) of men treated for localized prostate cancer.
METHODS A total of 730 men with localized disease were identified from the Cancer of the Prostate Strategic Urologic Research Endeavor, a national, prospective study of men with prostate cancer. Pre- to post-treatment changes in fear of recurrence, treatment-specific symptoms and burden, comorbidities at diagnosis, number of new symptoms, and post-treatment HRQOL data were analyzed.
RESULTS Linear regression, adjusted for clinical and demographic characteristics, showed that improved fear of recurrence (P <0.01), higher number of post-treatment symptoms (P <0.01), and improved bowel function (P <0.01) significantly predicted better mental health scores. For physical health, improved urinary bother (P <0.01) and lower number of post-treatment symptoms (P <0.01) were associated with better physical health.
CONCLUSION Understanding men's fears about cancer recurrence and how these fears influence physical and mental health are important components of providing care to this growing population. UROLOGY 72: 1269-1273, 2008. (C) 2008 Elsevier Inc.
C1 [Bellizzi, Keith M.] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
Baylor Coll Med, Scott Dept Urol, Houston, TX 77030 USA.
Baylor Coll Med, Dan L Duncan Canc Ctr, Houston, TX 77030 USA.
Univ Calif San Francisco, Dept Urol, San Francisco, CA 94143 USA.
TAP Pharmaceut Prod, Lake Forest, IL USA.
RP Bellizzi, KM (reprint author), NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, 6116 Execut Blvd,Suite 404,MSC 8336, Bethesda, MD 20892 USA.
EM bellizzk@mail.nih.gov
OI Latini, David/0000-0002-6161-4861
FU TAP Pharmaceutical Products, Lake Forest, Illinois; University of
California, San Francisco
FX CaPSURE is sponsored by TAP Pharmaceutical Products, Lake Forest,
Illinois, and is managed by the Urology Outcomes Research Group at the
University of California-San Francisco. Funding was provided by a
CaPSURE Scholars Grant from the University of California, San Francisco.
NR 30
TC 30
Z9 30
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
J9 UROLOGY
JI Urology
PD DEC
PY 2008
VL 72
IS 6
BP 1269
EP 1273
DI 10.1016/j.urology.2007.12.084
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 389VB
UT WOS:000262121500019
PM 18342930
ER
PT J
AU Lopez, JE
Schrumpf, ME
Raffel, SJ
Policastro, PF
Porcella, SF
Schwan, TG
AF Lopez, Job E.
Schrumpf, Merry E.
Raffel, Sandra J.
Policastro, Paul F.
Porcella, Stephen F.
Schwan, Tom G.
TI Relapsing Fever Spirochetes Retain Infectivity After Prolonged in vitro
Cultivation
SO VECTOR-BORNE AND ZOONOTIC DISEASES
LA English
DT Article
DE Borrelia; Genetics; Vector-borne
ID LYME-DISEASE SPIROCHETE; BACTERIUM BORRELIA-HERMSII; BURGDORFERI
SENSU-STRICTO; H-BINDING PROTEIN; ANTIGENIC VARIATION; CIRCULAR
PLASMIDS; MAJOR SEROTYPES; BLOOD; IDENTIFICATION; GENOME
AB Borrelia hermsii and Borrelin burgdorferi, two closely related spirochetes, are the etiological agents of tick-borne relapsing fever and Lyme disease, respectively. Previous studies have shown the loss of infectivity of B. burgdorferi is associated with in vitro cultivation. This diminished infectivity of B. burgdorferi has occurred as early as three in vitro passages, and the loss of plasmids have been observed with these less virulent to noninfective cultures. The effects of long-term in vitro cultivation on B. hermsii have not been investigated. However, understanding the degree of genomic degradation during in vitro cultivation is important for investigating pathogenic mechanisms of spirochetes. In this study, we analyzed the effects of continuous in vitro cultivation on the genomic composition and infectivity of B. hermsii and B. turicatae. We report that all seven isolates of B. hermsii and the one isolate Of B. turicatae examined retained infectivity in mice after 1 year of continuous in vitro cultivation. Furthermore, there were few apparent differences in the plasmid profiles after long-term cultivation. Two isolates of B. hermsii remained infective after high passage despite losing a portion of the 200-kb linear plasmid containing the fhbA gene encoding the factor H binding protein. Also, sequence analysis of multiple B. hermsii isolates demonstrated two types of fhbA with complete congruence with the two genomic groups of B. hermsii spirochetes. Therefore, these results suggest that relapsing fever spirochetes are genetically stable during in vitro cultivation, and the fhbA-containing segment of DNA that is lost during cultivation is not required for infection.
C1 [Lopez, Job E.; Schrumpf, Merry E.; Raffel, Sandra J.; Policastro, Paul F.; Schwan, Tom G.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Porcella, Stephen F.] NIAID, Res Technol Sect, Res Technol Branch, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA.
RP Lopez, JE (reprint author), NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM lopezjob@niaid.nih.gov
FU Division of Intramural Research; NIAID; NIH
FX We thank Mollie W. Jewett, Kit Tilly, and B. Joseph Hinnebusch for
reviewing this manuscript; Anita Mora and Gary Hettrick for photographic
assistance; and Bob Karstens for technical assistance. This work was
supported by the Division of Intramural Research, NIAID, NIH.
NR 52
TC 15
Z9 15
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1530-3667
EI 1557-7759
J9 VECTOR-BORNE ZOONOT
JI Vector-Borne Zoonotic Dis.
PD DEC
PY 2008
VL 8
IS 6
BP 813
EP 820
DI 10.1089/vbz.2008.0033
PG 8
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 388YK
UT WOS:000262056100013
PM 18637723
ER
PT J
AU Chung, HK
Pise-Masison, CA
Radonovich, MF
Brady, J
Lee, JK
Cheon, SY
Markham, P
Cristillo, A
Pal, R
AF Chung, Hye-Kyung
Pise-Masison, Cynthia A.
Radonovich, Michael F.
Brady, John
Lee, Jae K.
Cheon, Soo-Young
Markham, Phillip
Cristillo, Anthony
Pal, Ranajit
TI Cellular Gene Expression Profiles in Rhesus Macaques Challenged
Mucosally with a Pathogenic R5 Tropic Simian Human Immunodeficiency
Virus Isolate
SO VIRAL IMMUNOLOGY
LA English
DT Article
ID LONG-TERM NONPROGRESSORS; MEMORY T-CELLS; S100 FAMILY; VIRAL LOAD; RNA
LEVELS; INFECTION; AIDS; HIV-1; LYMPHOCYTES; SHIVSF162P3
AB Insights into the host factors that contribute to an effective antiviral immune response may be obtained by examining global gene expression in simian human immunodeficiency virus (SHIV)-infected nonhuman primates that exhibit different virological outcomes. Immune responses and gene expression profiles in peripheral blood mononuclear cells (PBMCs) were compared between animals that controlled or did not control viremia after infection. Rectal inoculation of eight rhesus macaques with R5-tropic SHIV(SF162P3) resulted in a high level of plasma viremia during the acute phase of infection. The viremia was controlled to below levels of detection in six of these animals at the set point (controllers), whereas two animals had persistent viremia throughout the 140 wk that the animals were monitored (non-controllers). CD4(+) T-cell counts declined slightly in both controllers and non-controllers in the acute phase of infection, but CD4(+) T-cell counts continued to decline only in the non-controllers. Neutralizing antibodies to the challenge virus were variable and could not account for the control of viremia. However, analysis of the cellular gene expression profiles in the PBMCs from both groups of animals revealed distinctive gene expression patterns between controllers and non-controllers. Using the paired LPE test, 59 genes with p values <0.01 were identified and specific differences in the gene expression profiles in PBMCs from controllers versus non-controllers were detected.
C1 [Chung, Hye-Kyung; Markham, Phillip; Cristillo, Anthony; Pal, Ranajit] Adv BioSci Labs Inc, Kensington, MD 20895 USA.
[Pise-Masison, Cynthia A.; Radonovich, Michael F.; Brady, John] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Lee, Jae K.; Cheon, Soo-Young] Univ Virginia, Sch Med, Dept Publ Hlth Sci, Charlottesville, VA 22908 USA.
RP Chung, HK (reprint author), Adv BioSci Labs Inc, 5510 Nicholson Lane, Kensington, MD 20895 USA.
EM hye.chung@ablinc.com
FU National Institute of Allergy and Infectious Diseases [N01-AI-15430]
FX We would like to thank Dr. Nancy Miller for many helpful discussions and
support of the study. We also would like to thank Dr. Deborah Weiss for
veterinary care and for performing the challenge studies, Ms. Lindsey
Galmin and Ms. Lauren Hudacik for technical assistance, and Ms. Sharon
Orndorff and Mr. Jim Treece for technical coordination. This study was
supported in part by National Institute of Allergy and Infectious
Diseases contract N01-AI-15430 to Advanced BioScience Laboratories.
NR 34
TC 6
Z9 6
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0882-8245
J9 VIRAL IMMUNOL
JI Viral Immunol.
PD DEC
PY 2008
VL 21
IS 4
BP 411
EP 423
DI 10.1089/vim.2008.0076
PG 13
WC Immunology; Virology
SC Immunology; Virology
GA 389IS
UT WOS:000262086700003
PM 19115930
ER
PT J
AU Hermon, TL
Moore, AB
Yu, LD
Kissling, GE
Castora, FJ
Dixon, D
AF Hermon, Tonia L.
Moore, Alicia B.
Yu, Linda
Kissling, Grace E.
Castora, Frank J.
Dixon, Darlene
TI Estrogen receptor alpha (ER alpha) phospho-serine-118 is highly
expressed in human uterine leiomyomas compared to matched myometrium
SO VIRCHOWS ARCHIV
LA English
DT Article
DE Uterine leiomyoma; Estrogen receptor alpha phosphorylated serine 118;
Phosphorylated mitogen-activated protein kinase
ID MITOGEN-ACTIVATED PROTEIN; MAP KINASE PATHWAY; MEDROXYPROGESTERONE
ACETATE; MODULATOR ASOPRISNIL; CELL-PROLIFERATION; MENSTRUAL-CYCLE;
CROSS-TALK; IN-VIVO; IGF-I; PROGESTERONE
AB It is thought that the growth of uterine leiomyomas may be mediated by the interaction of estrogen receptor alpha (ER alpha) and growth factor pathways and that phosphorylation of ER alpha at serine 118 (ER alpha-phospho-Ser118) is important in this interaction. In this study, immunoblotting and immunohistochemistry were used to investigate the expression of ER alpha-phospho-Ser118, phosphorylated p44/42 mitogen-activated protein kinase (phospho-p44/42 MAPK), and proliferating cell nuclear antigen (PCNA) in human leiomyoma and myometrial tissues during the proliferative and secretory phases of the menstrual cycle. We found that tumors taken from the proliferative phase expressed significantly higher levels of ER alpha-phospho-Ser118, phospho-p44/42 MAPK, and PCNA compared to patient-matched myometria and had significantly higher ER alpha-phospho-Ser118 and PCNA expression compared to secretory phase tumors. Also, enhanced colocalization and association of phospho-p44/42 MAPK and ER alpha-phospho-Ser118 were observed in proliferative phase tumors by confocal microscopy and immunoprecipitation, respectively. These data suggest that ER alpha-phospho-Ser118 may be important in leiomyoma growth and is possibly phosphorylated by phospho-p44/42 MAPK.
C1 [Hermon, Tonia L.; Moore, Alicia B.; Yu, Linda; Dixon, Darlene] NIEHS, Cellular & Mol Pathol Branch, NTP, NIH,DHHS, Res Triangle Pk, NC 27709 USA.
[Kissling, Grace E.] NIEHS, Biostat Branch, NTP, NIH,DHHS, Res Triangle Pk, NC 27709 USA.
[Hermon, Tonia L.; Castora, Frank J.] Eastern Virginia Med Sch, Dept Physiol Sci, Div Biochem, Norfolk, VA 23507 USA.
RP Dixon, D (reprint author), NIEHS, Cellular & Mol Pathol Branch, NTP, NIH,DHHS, POB 12233,MD C2-09, Res Triangle Pk, NC 27709 USA.
EM dixon@niehs.nih.gov
FU Intramural Research Program of the NIH; National Institute of
Environmental Health Sciences
FX The authors would like to thank Norris Flagler, Elizabeth Ney, Paul
Cacioppo, and C. Jeffrey Tucker for their technical assistance with
imaging. This research was supported, in part, by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences.
NR 43
TC 18
Z9 18
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD DEC
PY 2008
VL 453
IS 6
BP 557
EP 569
DI 10.1007/s00428-008-0679-5
PG 13
WC Pathology
SC Pathology
GA 370OJ
UT WOS:000260771200003
PM 18853184
ER
PT J
AU Alonzo, AA
Simon, AB
AF Alonzo, Angelo A.
Simon, Arthur B.
TI Have stethoscope, will travel: contingent employment among physician
health care providers in the United States
SO WORK EMPLOYMENT AND SOCIETY
LA English
DT Article
DE bad jobs; contingent professionals; gold collar; locum tenens;
non-standard employment; temporary physician employment
ID NONSTANDARD EMPLOYMENT; LOCUM DOCTORS; LABOR-MARKET; WORK; INDUSTRY;
LIFE; ARRANGEMENTS; SATISFACTION; EXPERIENCE; TRENDS
AB The goal of this study was to describe locum tenens physicians in the context of contingent, nonstandard employment in the US. The target population for this study was 1662 physicians who accepted at least one locum tenens assignment. Response rate for the 50-item questionnaire was 47 percentd One third of respondents considered a locum tenens practice pattern permanent. Female physicians were younger and disproportionately represented in primary care specialism: 64 percent used locum income as sole source of support and were motivated by a need for flexible scheduling. Male locum physicians were older, weighted toward the sub-specialisms and motivated to practice part-time. Overall, locum physicians were satisfied with contingent work. Shifts towards part-time employment among women and a desire for flexibility are changing the nature of physician employment. Locum physicians, as 'gold collar' contingent workers are very different from contingent workers in manufacturing and service sectors of the economy.
C1 [Alonzo, Angelo A.] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
[Simon, Arthur B.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Simon, Arthur B.] Univ Cincinnati, Coll Med, Cincinnati, OH USA.
[Alonzo, Angelo A.] Ohio State Univ, NIH, NHLBI, Columbus, OH 43210 USA.
RP Alonzo, AA (reprint author), Yale Univ, Sch Nursing, POB 9740,100 Church St S,Suite 200, New Haven, CT 06536 USA.
EM angelo.alonzov@yaled.edu; abs1300@sbcglobald.net
NR 61
TC 11
Z9 11
U1 2
U2 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0950-0170
J9 WORK EMPLOY SOC
JI Work Employ. Soc.
PD DEC
PY 2008
VL 22
IS 4
BP 635
EP 654
DI 10.1177/0950017008096740
PG 20
WC Economics; Industrial Relations & Labor; Sociology
SC Business & Economics; Sociology
GA 379UZ
UT WOS:000261423000004
ER
PT J
AU Hendrickson, SL
Hutcheson, HB
Ruiz-Pesini, E
Poole, JC
Lautenberger, J
Sezgin, E
Kingsley, L
Goedert, JJ
Vlahov, D
Donfield, S
Wallace, DC
O'Brien, SJ
AF Hendrickson, Sher L.
Hutcheson, Holli B.
Ruiz-Pesini, Eduardo
Poole, Jason C.
Lautenberger, James
Sezgin, Efe
Kingsley, Lawrence
Goedert, James J.
Vlahov, David
Donfield, Sharyne
Wallace, Douglas C.
O'Brien, Stephen J.
TI Mitochondrial DNA haplogroups influence AIDS progression
SO AIDS
LA English
DT Article
DE AIDS; apoptosis; disease; HIV-1; mitochondria
ID IMMUNODEFICIENCY-VIRUS TYPE-1; REVERSE-TRANSCRIPTASE INHIBITORS;
GENOME-WIDE ASSOCIATION; HIV-INFECTED PATIENTS; ANTIRETROVIRAL-THERAPY;
ADAPTIVE SELECTION; HUMAN MTDNA; CELL-DEATH; APOPTOSIS; DISEASE
AB Objective: Mitochondrial function plays a role in both AIDS progression and HAART toxicity; therefore, we sought to determine whether mitochondrial DNA variation revealed novel AIDS restriction genes, particularly as mitochondrial DNA single-nucleotide polymorphisms are known to influence regulation of oxidative phosphorylation, reactive oxygen species production, and apoptosis.
Design: This is a retrospective cohort study.
Methods: We performed an association study of mitochondrial DNA haplogroups among 1833 European American HIV-1 patients from five US cohorts: the Multicenter AIDS Cohort Study, the San Francisco City Clinic Study, Hemophilia Growth and Development Study, the Multicenter Hemophilia Cohort Study, and the AIDS Linked to Intravenous Experiences cohort to determine whether the mitochondrial DNA haplogroup correlated with AIDS progression rate.
Results: Mitochondrial DNA haplogroups J and U5a were elevated among HIV-1 infected people who display accelerated progression to AIDS and death. Haplogroups Uk, H3, and IWX appeared to be highly protective against AIDS progression.
Conclusion: The associations found in our study appear to support a functional explanation by which mitochondrial DNA variation among haplogroups, influencing ATP production, reactive oxygen species generation, and apoptosis, is correlated to AIDS disease progression; however, repeating these results in cohorts with different ethnic backgrounds would be informative. These data suggest that mitochondrial genes are important indicators of AIDS disease progression in HIV-1 infected persons. (C) 2008 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Hendrickson, Sher L.; Hutcheson, Holli B.; Lautenberger, James; Sezgin, Efe; O'Brien, Stephen J.] NCI, Lab Genom Divers, Frederick, MD 21702 USA.
[Ruiz-Pesini, Eduardo] Univ Zaragoza, CIBERER ISCIII, Dept Bioquim Biol Mol & Celular, Fdn ARAID, Zaragoza, Spain.
[Poole, Jason C.; Wallace, Douglas C.] Univ Calif Irvine, Ctr Mol & Mitochondrial Med & Genet, Dept Ecol & Evolutionary Biol, Irvine, CA USA.
[Poole, Jason C.; Wallace, Douglas C.] Univ Calif Irvine, Ctr Mol & Mitochondrial Med & Genet, Dept Biol Chem, Irvine, CA USA.
[Poole, Jason C.; Wallace, Douglas C.] Univ Calif Irvine, Ctr Mol & Mitochondrial Med & Genet, Dept Pediat, Irvine, CA USA.
[Kingsley, Lawrence] Univ Pittsburgh, Dept Infect Dis & Microbiol, Pittsburgh, PA USA.
[Goedert, James J.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Vlahov, David] New York Acad Med, Dept Biostat, Ctr Urban Epidemiol Studies, New York, NY USA.
[Donfield, Sharyne] Rho Inc, Dept Biostat, Chapel Hill, NC USA.
RP Hendrickson, SL (reprint author), NCI, Lab Genom Divers, Frederick, MD 21702 USA.
EM hendricksons@mail.nih.gov
RI Sezgin, Efe/B-8418-2012
OI Sezgin, Efe/0000-0002-8000-7485
FU National Cancer Institute (NCI) [N02-CP-55504, UO1-AI-35042,
5-MO1-RR-00722, UO1-AI-35043, UO1-AI-37984, UO1-AI-35039, UO1-AI-35040,
UO1-AI-37613, UO1-AI-35041]; National Institutes of Health (NIH)
[N01-CO-12400, AG25638, R01 AG24373, DK73691]; Center for Cancer
Research and Division of Cancer Epidemiology and Genetics, Spanish Fondo
de Investigacion Sanitaria [FIS-PI05-0647]; National Institute of
Allergy and Infectious Diseases
FX This project has been funded whole or in part with federal funds from
the National Cancer Institute (NCI), National Institutes of Health
(NIH), under contract N01-CO-12400, the Intramural Research of the NCI,
the Center for Cancer Research and Division of Cancer Epidemiology and
Genetics, Spanish Fondo de Investigacion Sanitaria grant #
FIS-PI05-0647, NIH postdoctoral fellowship AG25638 and NIH R01 AG24373
and DK73691. The MACS is funded by the National Institute of Allergy and
Infectious Diseases, with additional supplemental funding from the NCI.
The MHCS is supported by NCI contract N02-CP-55504 with RTI
International. The HGDS is funded by the NIH, National Institute of
Child Health and Human Development, 1 R01 HD41224. NCI contracts include
UO1-AI-35042, 5-MO1-RR-00722 (GCRC), UO1-AI-35043, UO1-AI-37984,
UO1-AI-35039, UO1-AI-35040, UO1-AI-37613, UO1-AI-35041.
NR 60
TC 53
Z9 53
U1 5
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 30
PY 2008
VL 22
IS 18
BP 2429
EP 2439
DI 10.1097/QAD.0b013e32831940bb
PG 11
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 384VM
UT WOS:000261772300003
PM 19005266
ER
PT J
AU Guvench, O
Greene, SN
Kamath, G
Brady, JW
Venable, RM
Pastor, RW
Mackerell, AD
AF Guvench, Olgun
Greene, Shannon N.
Kamath, Ganesh
Brady, John W.
Venable, Richard M.
Pastor, Richard W.
Mackerell, Alexander D., Jr.
TI Additive Empirical Force Field for Hexopyranose Monosaccharides
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE carbohydrate; glucose; galactose; pyranose; force field; molecular
dynamics; molecular mechanics; CHARMM
ID MOLECULAR-DYNAMICS SIMULATIONS; DENSITY-FUNCTIONAL THEORY; FREE-ENERGY
CALCULATIONS; NUCLEIC-ACIDS; AB-INITIO; CONFORMATIONAL ENERGETICS;
AQUEOUS-SOLUTIONS; LIPID-BILAYERS; WATER; CARBOHYDRATE
AB We present an all-atom additive empirical force field for the hexopyranose monosaccharide form of glucose and its diastereomers allose, altrose, galactose, gulose, idose, mannose, and talose. The model is developed to be consistent with the CHARMM all-atom biomolecular force fields, and the same parameters are used for all diastereomers, including both the alpha- and beta-anomers of each monosaccharide. The force field is developed in a hierarchical manner and reproduces the gas-phase and condensed-phase properties of small-molecule model compounds corresponding to fragments of pyranose monosaccharides. The resultant parameters are transferred to the full pyranose monosaccharides, and additional parameter development is done to achieve a complete hexopyranose monosaccharide force field. Parametrization target data include vibrational frequencies, crystal geometries, solute-water interaction energies, molecular volumes, heats of vaporization, and conformational energies, including those for over 1800 monosaccharide conformations at the MP2/cc-pVTZ//MP2/6-31G(d) level of theory. Although not targeted during parametrization, free energies of aqueous solvation for the model compounds compare favorably with experimental values. Also well-reproduced are monosaccharide crystal unit cell dimensions and ring pucker, densities of concentrated aqueous glucose systems, and the thermodynamic and dynamic properties of the exocyclic torsion in dilute aqueous systems. The new parameter set expands the CHARMM additive force field to allow for simulation of heterogeneous systems that include hexopyranose monosaccharides in addition to proteins, nucleic acids, and lipids. (C) 2008 Wiley Periodicals, Inc. J Comput Chem 29: 2543-2564, 2008
C1 [Guvench, Olgun; Greene, Shannon N.; Kamath, Ganesh; Mackerell, Alexander D., Jr.] Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore, MD 21201 USA.
[Brady, John W.] Cornell Univ, Dept Food Sci, Ithaca, NY 14853 USA.
[Venable, Richard M.; Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Mackerell, AD (reprint author), Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore,20 Penn St,HST II 629, Baltimore, MD 21201 USA.
EM alex@outerbanks.umaryland.edu
OI MacKerell, Alex/0000-0001-8287-6804
FU NIH [R01GM070855, F32CA1197712]; National Cancer Institute Advanced
Biomedical Computing Center
FX Contract/grant sponsor: NIH; contract/grant numbers: R01GM070855,
F32CA1197712; Contract/grant sponsor: National Cancer Institute Advanced
Biomedical Computing Center
NR 90
TC 233
Z9 233
U1 5
U2 47
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0192-8651
EI 1096-987X
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD NOV 30
PY 2008
VL 29
IS 15
BP 2543
EP 2564
DI 10.1002/jcc.21004
PG 22
WC Chemistry, Multidisciplinary
SC Chemistry
GA 369KM
UT WOS:000260693400006
PM 18470966
ER
PT J
AU Yoo, MH
Hatfield, DL
AF Yoo, Min-Hyuk
Hatfield, Dolph L.
TI The Cancer Stem Cell Theory: Is It Correct?
SO MOLECULES AND CELLS
LA English
DT Article
DE breast cancer cells; cancer stem cells; lung cancer cells; single cell
originated cells; tumor growth
ID ACUTE MYELOID-LEUKEMIA; LUNG-CARCINOMA CELLS; BREAST-CANCER; TUMOR;
IDENTIFICATION; HIERARCHY; PHENOTYPE; CULTURE
AB The cancer stem cell hypothesis posits that tumor growth is driven by a rare subpopulation of cells, designated cancer stem cells (CSC). Studies supporting this theory are based in large part on xenotransplantation experiments wherein human cancer cells are grown in immunocom-promised mice and only CSC, often constituting less than 1% of the malignancy, generate tumors. Herein, we show that all colonies derived from randomly chosen single cells in mouse lung and breast cancer cell lines form tumors following allografting histocompatible mice. Our study suggests that the majority of malignant cells rather than CSC can sustain tumors and that the cancer stem cell theory must be reevaluated.
C1 [Yoo, Min-Hyuk; Hatfield, Dolph L.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Hatfield, DL (reprint author), NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM hatfield@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute; Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 22
TC 22
Z9 24
U1 0
U2 5
PU KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
PI SEOUL
PA 635-4, YUCKSAM-DONG, GANGNAM-GU, SEOUL 135-703, SOUTH KOREA
SN 1016-8478
J9 MOL CELLS
JI Mol. Cells
PD NOV 30
PY 2008
VL 26
IS 5
BP 514
EP 516
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 384JR
UT WOS:000261741600015
PM 18711315
ER
PT J
AU Yan, J
Jetten, AM
AF Yan, Jun
Jetten, Anton M.
TI RAP80 and RNF8, key players in the recruitment of repair proteins to DNA
damage sites
SO CANCER LETTERS
LA English
DT Review
DE Double-strand breaks; RAP80; RNF8; Ubiquitination; CCDC98/Abraxas;
BRCA1; UIM; MDC1
ID DOUBLE-STRAND BREAKS; HISTONE H2AX PHOSPHORYLATION; UBIQUITIN-BINDING
DOMAINS; ESTROGEN-RECEPTOR-ALPHA; RING FINGER PROTEIN;
IONIZING-RADIATION; SIGNALING PATHWAYS; GENOMIC STABILITY; RESPONSE
PATHWAYS; MOLECULAR-BASIS
AB Chromosomal double-strand breaks (DSBs) in eukaryotes provoke a rapid, extensive modification in chromatin flanking the breaks. The DNA damage response (DDR) coordinates activation of cell cycle checkpoints, apoptosis, and DNA repair networks, to ensure accurate repair and genomic integrity. The checkpoint kinase ATM plays a critical role in the initiation of DDR in response to DSBs. The early ATM-mediated phosphorylation of the histone variant H2AX proteins near DSBs leads to the subsequent binding of MDC1, which functions as a scaffold for the recruitment and assembly of many DDR mediators and effectors, including BRCA1. Recent studies have provided new insights into the mechanism by which BRCA1 and associated proteins are recruited to DNA damage foci and revealed key roles for the receptor-associated protein 80 (RAP80) and the E3 ligase RNF8 in this process. RAP80 is an ubiquitin-interaction motif (UIM) containing protein that is associated with a BRCA1/BARD1 complex through its interaction with CCDC98 (Abraxas). The UIMs of RAP80 are critical for targeting this protein complex to DSB sites. Additional studies revealed that after binding gamma-H2AX, ATM-phosphorylated MDC1 is recognized by the FHA domain of RNF8, which subsequently binds the E2 conjugating enzyme UBC13. This complex catalyzes K63-linked polyubiquitination of histones H2A and gamma-H2AX, which are then recognized by the UIMs of RAP80, thereby facilitating the recruitment of the BRCA1/BARD1/CCDC98/RAP80 protein complex to DSB sites. Depletion of RAP80 or RNF8 impairs the translocation of BRCA1 to DNA damage sites and results in defective cell cycle checkpoint control and DSB repair. In this review, we discuss this cascade of protein phosphorylation and ubiquitination and the role it plays in the control of cellular responses to genotoxic stress by regulating the interactions, localization, and function of DDR proteins. Published by Elsevier Ltd.
C1 [Yan, Jun; Jetten, Anton M.] NIEHS, Cell Biol Sect, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
RP Jetten, AM (reprint author), NIEHS, Cell Biol Sect, Div Intramural Res, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM jetten@niehs.nih.gov
OI Jetten, Anton/0000-0003-0954-4445
FU NIH; National Institute of Environmental Health Sciences [Z01-ES-101586]
FX We thank Drs. Sonnet Arlander and Daniel Menendez for their valuable
comments on the manuscript. This research is supported by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences (Z01-ES-101586).
NR 101
TC 46
Z9 47
U1 1
U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD NOV 28
PY 2008
VL 271
IS 2
BP 179
EP 190
DI 10.1016/j.canlet.2008.04.046
PG 12
WC Oncology
SC Oncology
GA 373YV
UT WOS:000261010300001
PM 18550271
ER
PT J
AU Kang, SW
Hegde, RS
AF Kang, Sang-Wook
Hegde, Ramanujan S.
TI Lighting Up the Stressed ER
SO CELL
LA English
DT Editorial Material
ID UNFOLDED PROTEIN RESPONSE
AB Balancing the capacity for protein maturation with changes in protein flux through the endoplasmic reticulum (ER) is crucial for maintaining ER homeostasis. In this issue, Merksamer et al. (2008) exploit a redox-sensitive fluorescent protein to monitor the environment inside the ER of living yeast, illuminating how this organelle responds to different perturbations.
C1 [Kang, Sang-Wook; Hegde, Ramanujan S.] Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Hegde, RS (reprint author), Natl Inst Hlth, Bethesda, MD 20892 USA.
EM hegder@mail.nih.gov
RI Kang, Sang/F-3780-2014;
OI Hegde, Ramanujan/0000-0001-8338-852X
FU Intramural NIH HHS [ZIA HD008752-08]
NR 6
TC 6
Z9 6
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 28
PY 2008
VL 135
IS 5
BP 787
EP 789
DI 10.1016/j.cell.2008.11.004
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376LA
UT WOS:000261183900007
PM 19041740
ER
PT J
AU Kunos, G
Osei-Hyiaman, D
Liu, J
Godlewski, G
Batkai, S
AF Kunos, George
Osei-Hyiaman, Douglas
Liu, Jie
Godlewski, Gregorz
Batkai, Sandor
TI Endocannabinoids and the Control of Energy Homeostasis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Review
ID STEAROYL-COA DESATURASE-1; CANNABINOID-1 RECEPTOR BLOCKER; HEPATIC CB1
RECEPTORS; DIET-INDUCED OBESITY; ADIPOSE-TISSUE; ANTAGONIST SR141716;
METABOLIC SYNDROME; RISK-FACTORS; OVERWEIGHT PATIENTS;
INSULIN-RESISTANCE
AB Endocannabinoids (ECBs) are ubiquitous lipid mediators that act through the same G protein-coupled receptors (CB(1) and CB(2)) that recognize plant-derived cannabinoids. As regulators of metabolism, ECBs are anabolic: they increase the intake, promote the storage, and decrease the expenditure of energy. Recent work indicates that activation of peripheral CB(1) receptors by ECBs plays a key role in the hormonal/metabolic changes associated with obesity/metabolic syndrome and may be targeted for its pharmacotherapy.
C1 [Kunos, George; Osei-Hyiaman, Douglas; Liu, Jie; Godlewski, Gregorz; Batkai, Sandor] NIAAA, Lab Physiol Studies, Bethesda, MD 20892 USA.
RP Kunos, G (reprint author), NIAAA, Lab Physiol Studies, Bethesda, MD 20892 USA.
EM gkunos@mail.nih.gov
RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014
FU National Institutes of Health staff
FX This work was authored, in whole or in part, by National Institutes of
Health staff. This minireview will be reprinted in the 2008 Minireview
Compendium, which will be available in January, 2009.
NR 64
TC 55
Z9 59
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33021
EP 33025
DI 10.1074/jbc.R800012200
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700001
PM 18694938
ER
PT J
AU Inagaki, M
Omori, E
Kim, JY
Komatsu, Y
Scott, G
Ray, MK
Yamada, G
Matsumoto, K
Mishina, Y
Ninomiya-Tsuji, J
AF Inagaki, Maiko
Omori, Emily
Kim, Jae-Young
Komatsu, Yoshihiro
Scott, Greg
Ray, Manas K.
Yamada, Gen
Matsumoto, Kunihiro
Mishina, Yuji
Ninomiya-Tsuji, Jun
TI TAK1-binding Protein 1, TAB1, Mediates Osmotic Stress-induced TAK1
Activation but Is Dispensable for TAK1-mediated Cytokine Signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NF-KAPPA-B; KINASE TAK1; TRANSDUCTION PATHWAY; IN-VIVO; IL-1; COMPLEX;
MAPKKK; JNK; IKK; AUTOPHOSPHORYLATION
AB TAK1 kinase is an indispensable intermediate in several cytokine signaling pathways including tumor necrosis factor, interleukin-1, and transforming growth factor-beta signaling pathways. TAK1 also participates in stress-activated intracellular signaling pathways such as osmotic stress signaling pathway. TAK1-binding protein 1 (TAB1) is constitutively associated with TAK1 through its C-terminal region. Although TAB1 is known to augment TAK1 catalytic activity when it is overexpressed, the role of TAB1 under physiological conditions has not yet been identified. In this study, we determined the role of TAB1 in TAK1 signaling by analyzing TAB1-deficient mouse embryonic fibroblasts (MEFs). Tumor necrosis factor- and interleukin-1-induced activation of TAK1 was entirely normal in Tab1-deficient MEFs and could activate both mitogen-activated protein kinases and NF-kappa B. In contrast, we found that osmotic stress-induced activation of TAK1 was largely impaired in Tab1-deficient MEFs. Furthermore, we showed that the C-terminal 68 amino acids of TAB1 were sufficient to mediate osmotic stress-induced TAK1 activation. Finally, we attempted to determine the mechanism by which TAB1 activates TAK1. We found that TAK1 is spontaneously activated when the concentration is increased and that it is totally dependent on TAB1. Cell shrinkage under the osmotic stress condition increases the concentration of TAB1-TAK1 and may oligomerize and activate TAK1 in a TAB1-dependent manner. These results demonstrate that TAB1 mediates TAK1 activation only in a subset of TAK1 pathways that are mediated through spontaneous oligomerization of TAB1-TAK1.
C1 [Inagaki, Maiko; Omori, Emily; Kim, Jae-Young; Ninomiya-Tsuji, Jun] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA.
[Komatsu, Yoshihiro; Mishina, Yuji] NIEHS, Mol Dev Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Komatsu, Yoshihiro; Yamada, Gen] Kumamoto Univ, Grad Sch Mol & Genom Pharm, Ctr Anim Resources & Dev, Kumamoto 8600811, Japan.
[Matsumoto, Kunihiro] Nagoya Univ, Grad Sch Sci, Dept Mol Biol, Nagoya, Aichi 4648602, Japan.
[Matsumoto, Kunihiro] Japan Sci & Technol Agcy, Tokyo, Japan.
[Mishina, Yuji] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
RP Ninomiya-Tsuji, J (reprint author), N Carolina State Univ, Dept Environm & Mol Toxicol, Campus Box 7633, Raleigh, NC 27695 USA.
EM Jun_Tsuji@ncsu.edu
FU National Institutes of Health [ES071003-10, GM068812]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants ES071003-10 (Y.M.) and GM068812 (to J.N.-T.). The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 40
TC 37
Z9 37
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33080
EP 33086
DI 10.1074/jbc.M807574200
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700008
PM 18829460
ER
PT J
AU Yoshioka, H
Kamitani, H
Watanabe, T
Eling, TE
AF Yoshioka, Hiroki
Kamitani, Hideki
Watanabe, Takashi
Eling, Thomas E.
TI Nonsteroidal Anti-inflammatory Drug-activated Gene (NAG-1/GDF15)
Expression Is Increased by the Histone Deacetylase Inhibitor
Trichostatin A
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID COLORECTAL-CANCER CELLS; SP1 SITES; CYCLOOXYGENASE INHIBITORS; BETA
SUPERFAMILY; TUMOR-SUPPRESSOR; ASTROCYTE CELLS; NAG-1; TRANSCRIPTION;
APOPTOSIS; P53
AB Nonsteroidal anti-inflammatory drug-activated gene (NAG-1) is a putative tumor suppressor whose expression can be increased by drug treatment. Glioblastoma is the most common central nervous system tumor, is associated with high morbidity and mortality, and responds poorly to surgical, chemical, and radiation therapy. The histone deacetylase inhibitors are under current consideration as therapeutic agents in treating glioblastoma. We investigated whether trichostatin A(TSA) would alter the expression of NAG-1 in glioblastoma cells. The DNA demethylating agent 5-aza-dC did not increase NAG-1 expression, but TSA up-regulated NAG-1 expression and acted synergistically with 5-aza-dC to induce NAG-1 expression. TSA indirectly increases NAG-1 promoter activity and increases NAG-1mRNA and protein expression in the T98G human glioblastoma cell line. TSA also increases the expression of transcription factors Sp-1 and Egr-1. Small interfering RNA experiments link NAG-1 expression to apoptosis induced by TSA. Reporter gene assays, specific inhibition by small interfering RNA transfections, and chromatin immunoprecipitation assays indicate that Egr-1 and Sp-1 mediate TSA-induced NAG-1 expression. TSA also increases the stability of NAG-1 mRNA. TSA-induced NAG-1 expression involves multiple mechanisms at the transcriptional and post-transcriptional levels.
C1 [Yoshioka, Hiroki; Eling, Thomas E.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Yoshioka, Hiroki; Kamitani, Hideki; Watanabe, Takashi] Tottori Univ, Fac Med, Inst Neurol Sci, Div Neurosurg, Tottori 6838504, Japan.
RP Eling, TE (reprint author), 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM eling@niehs.nih.gov
FU National Institutes of Health Intramural Program from the NIEHS
FX This work was supported, in whole or in part, by the National Institutes
of Health Intramural Program from the NIEHS. The costs of publication of
this article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 47
TC 20
Z9 22
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33129
EP 33137
DI 10.1074/jbc.M805248200
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700014
PM 18801729
ER
PT J
AU Shi, CS
Kehrl, JH
AF Shi, Chong-Shan
Kehrl, John H.
TI MyD88 and Trif Target Beclin 1 to Trigger Autophagy in Macrophages
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID TOLL-LIKE RECEPTORS; ADAPTIVE IMMUNITY; SIGNALING PATHWAYS; DENDRITIC
CELLS; INNATE IMMUNITY; CUTTING EDGE; DOMAIN; PROTEINS; FAMILY;
TOLL-LIKE-RECEPTOR-4
AB The Toll-like receptors (TLR) play an instructive role in innate and adaptive immunity by recognizing specific molecular patterns from pathogens. Autophagy removes intracellular pathogens and participates in antigen presentation. Here, we demonstrate that not only TLR4, but also other TLR family members induce autophagy in macrophages, which is inhibited by MyD88, Trif, or Beclin 1 shRNA expression. MyD88 and Trif co-immunoprecipitate with Beclin 1, a key factor in autophagosome formation. TLR signaling enhances the interaction of MyD88 and Trif with Beclin 1, and reduces the binding of Beclin 1 to Bcl-2. These findings indicate TLR signaling via its adaptor proteins reduces the binding of Beclin 1 to Bcl-2 by recruiting Beclin 1 into the TLR-signaling complex leading to autophagy.
C1 [Shi, Chong-Shan; Kehrl, John H.] NIAID, B Cell Mol Immunol Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Shi, CS (reprint author), Bldg 10,Rm 11B08,10 Ctr Dr,MSC 1876, Bethesda, MD 20892 USA.
EM cshi@niaid.nih.gov; kehrl@niaid.nih.gov
OI Kehrl, John/0000-0002-6526-159X
NR 30
TC 182
Z9 193
U1 5
U2 23
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33175
EP 33182
DI 10.1074/jbc.M804478200
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700020
PM 18772134
ER
PT J
AU Becerra, SP
Perez-Mediavilla, LA
Weldon, JE
Locatelli-Hoops, S
Senanayake, P
Notari, L
Notario, V
Hollyfield, JG
AF Becerra, S. Patricia
Perez-Mediavilla, L. Alberto
Weldon, John E.
Locatelli-Hoops, Silvia
Senanayake, Preenie
Notari, Luigi
Notario, Vicente
Hollyfield, Joe G.
TI Pigment Epithelium-derived Factor Binds to Hyaluronan MAPPING OF A
HYALURONAN BINDING SITE
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID INTERPHOTORECEPTOR MATRIX; FACTOR PEDF; TUMOR-GROWTH; RETINOBLASTOMA
CELLS; EXTRACELLULAR-MATRIX; CHONDROITIN SULFATE; BOVINE EYES; GENE;
ANGIOGENESIS; EXPRESSION
AB Pigment epithelium-derived factor (PEDF) is a multifunctional serpin with antitumorigenic, antimetastatic, and differentiating activities. PEDF is found within tissues rich in the glycosaminoglycan hyaluronan (HA), and its amino acid sequence contains putative HA-binding motifs. We show that PEDF coprecipitation with glycosaminoglycans in media conditioned by human retinoblastoma Y-79 cells decreased after pretreatments with hyaluronidase, implying an association between HA and PEDF. Direct binding of human recombinant PEDF to highly purified HA was demonstrated by coprecipitation in the presence of cetylpyridinium chloride. Binding of PEDF to HA was concentration-dependent and saturable. The PEDF-HA interactions were sensitive to increasing NaCl concentrations, indicating an ionic nature of these interactions and having affinity higher than PEDF-heparin. Competition assays showed that PEDF can bind heparin and HA simultaneously. PEDF chemically modified with fluorescein retained the capacity for interacting with HA but lacked heparin affinity, suggesting one or more distinct HA-binding regions on PEDF. The HA-binding region was examined by site-directed mutagenesis. Single-point and cumulative alterations at basic residues within the putative HA-binding motif K189A/K191A/R194A/K197A drastically reduced the HA-binding activity without affecting heparin-or collagen I binding of PEDF. Cumulative alterations at sites critical for heparin binding (K146A/K147A/R149A) decreased HA affinity but not collagen I binding. Thus these clusters of basic residues (BXBXXBXXB and BX(3)AB(2)XB motifs) in PEDF are functional regions for binding HA. In the spatial PEDF structure they are located in distinct areas away from the collagen-binding site. The HA-binding activity of PEDF may contribute to deposition in the extracellular matrix and to its reported antitumor/antimetastatic effects.
C1 [Becerra, S. Patricia; Perez-Mediavilla, L. Alberto; Weldon, John E.; Locatelli-Hoops, Silvia; Notari, Luigi] NEI, NIH, Bethesda, MD 20892 USA.
[Perez-Mediavilla, L. Alberto] Univ Navarra, Ctr Appl Med Res, E-31080 Pamplona, Spain.
[Senanayake, Preenie; Hollyfield, Joe G.] Cleveland Clin, Lerner Coll Med, Dept Ophthalmol, Cleveland, OH 44195 USA.
[Notario, Vicente] Georgetown Univ, Med Ctr, Dept Radiat Med, Washington, DC 20007 USA.
RP Becerra, SP (reprint author), NEI, NIH, Bldg 7,Rm 304,7 Mem Dr, Bethesda, MD 20892 USA.
EM becerrap@nei.nih.gov
RI Perez-Mediavilla, Alberto/A-5246-2011;
OI Weldon, John/0000-0002-6516-9064
FU National Institutes of Health NEI Intramural Research Program;
Educational and Cultural Department of the "Gobierno de Navarra," Spain;
Foundation for Fighting Blindness; Research to Prevent Blindness to the
Department of Ophthalmology; Cleveland Clinic Lerner College of
Medicine; [EY14240-1]; [EY 15638]; [RO1 CA64472]
FX This work was supported, in whole or in part, by National Institutes of
Health NEI Intramural Research Program. This work was also supported by
the Educational and Cultural Department of the "Gobierno de Navarra,"
Spain (to A. P.-M.); by Grants EY14240-1 and EY 15638, Foundation for
Fighting Blindness, and a Challenge Grant from Research to Prevent
Blindness to the Department of Ophthalmology, Cleveland Clinic Lerner
College of Medicine (to J. G. H.); and by Grant RO1 CA64472 (to V. N.).
The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 U. S. C. Section 1734 solely to
indicate this fact.
NR 50
TC 26
Z9 26
U1 1
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33310
EP 33320
DI 10.1074/jbc.M801287200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700035
PM 18805795
ER
PT J
AU Feng, HZ
Chen, M
Weinstein, LS
Jin, JP
AF Feng, Han-Zhong
Chen, Min
Weinstein, Lee S.
Jin, Jian-Ping
TI Removal of the N-terminal Extension of Cardiac Troponin I as a
Functional Compensation for Impaired Myocardial beta-Adrenergic
Signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MYOSIN HEAVY-CHAIN; PROTEIN-KINASE-A; HEART-FAILURE; MOUSE HEART;
DILATED CARDIOMYOPATHY; RAT MYOCARDIUM; PHOSPHORYLATION; RECEPTOR;
MUSCLE; MICE
AB Although beta-adrenergic stimuli are essential for myocardial contractility, beta-blockers have a proven beneficial effect on the treatment of heart failure, but the mechanism is not fully understood. The stimulatory G protein alpha-subunit (G(s)alpha) couples the beta-adrenoreceptor to adenylyl cyclase and the intracellular cAMP response. In a mouse model of conditional G(s)alpha deficiency in the cardiac muscle (G(s)alpha-DF), we demonstrated heart failure phenotypes accompanied by increases in the level of a truncated cardiac troponin I (cTnI-ND) from restricted removal of the cTnI-specific N-terminal extension. To investigate the functional significance of the increase of cTnI-ND in G(s)alpha-DF cardiac muscle, we generated double transgenic mice to overexpress cTnI-ND in G(s)alpha-DF hearts. The overexpression of cTnI-ND in G(s)alpha-DF failing hearts increased relaxation velocity and left ventricular end diastolic volume to produce higher left ventricle maximum pressure and stroke volume. Supporting the hypothesis that up-regulation of cTnI-ND is a compensatory rather than a destructive myocardial response to impaired beta-adrenergic signaling, the aberrant expression of beta-myosin heavy chain in adult G(s)alpha-DF but not control mouse hearts was reversed by cTnI overexpression. These data indicate that the up-regulation of cTnI-ND may partially compensate for the cardiac inefficiency in impaired beta-adrenergic signaling.
C1 [Feng, Han-Zhong; Jin, Jian-Ping] Evanston NW Healthcare & NW Univ, Sect Mol Cardiol, Feinberg Sch Med, Evanston, IL 60201 USA.
[Chen, Min; Weinstein, Lee S.] NIDDK, Signal Transduct Sect, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Jin, JP (reprint author), Evanston NW Healthcare & NW Univ, Sect Mol Cardiol, Feinberg Sch Med, Evanston, IL 60201 USA.
EM jpjin@northwestern.edu
FU National Institutes of Health [HL-078773, AR-048816]; National
Institutes of Health, NIDDK
FX This work was supported, in whole or in part, by National Institutes of
Health Grants HL-078773 and AR-048816 (to J.-P.J.) and by the Intramural
Research Program of the National Institutes of Health, NIDDK. The costs
of publication of this article were defrayed in part by the payment of
page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 U. S. C. Section 1734 solely to
indicate this fact.
NR 51
TC 27
Z9 27
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 28
PY 2008
VL 283
IS 48
BP 33384
EP 33393
DI 10.1074/jbc.M803302200
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 376KY
UT WOS:000261183700043
PM 18815135
ER
PT J
AU Mattie, MD
McElwee, MK
Freedman, JH
AF Mattie, Michael D.
McElwee, Matthew K.
Freedman, Jonathan H.
TI Mechanism of Copper-Activated Transcription: Activation of AP-1, and the
JNK/SAPK and p38 Signal Transduction Pathways
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE copper; transcription; MAPK; signal transduction; reactive oxygen
species
ID MAP KINASE CASCADE; NF-KAPPA-B; ANTIOXIDANT RESPONSE ELEMENT;
LIPID-PEROXIDATION; GENE-EXPRESSION; OXIDATIVE STRESS; PROTEIN-KINASES;
C-JUN; EPITHELIAL-CELLS; END-PRODUCT
AB Copper is an essential metal that is able to produce reactive oxygen species and to induce intracellular oxidative stress. Several studies have examined the effects of excessive copper and oxidative stress on various organisms and tissues, but few have addressed the molecular mechanisms by which copper affects transcription. Our results demonstrated that, in COS-7 cells, copper treatment caused an increase in the binding of nuclear proteins to activating protein-1 and antioxidant response elements. The level of copper-inducible nuclear protein binding was modulated by increasing or decreasing the level of intracellular oxidative stress. Copper exposure also led to an increase in the steady-state levels of c-fos, c-jun, and c-myc mRNAs. Exposure to copper resulted in an increase in the levels of phosphorylation and activation of the c-jun N-terminal kinase/stress-activated protein kinase and p38 pathways. The activation of these pathways resulted in a concomitant increase in c-jun phosphorylation. We investigated the hypothesis that copper-induced oxidative stress leads to the formation of stable lipid peroxidation by-products that activate mitogen-activated protein kinase (MAPK) pathways, ultimately affecting transcription. While exposure did result in the production of 4-hydroxynonenal, the timing of the increased levels of proto-oncogene mRNA, phosphorylation of c-jun, and phosphorylation and activation of MAPKs, as well as the inability of the lipophilic antioxidant vitamin E to abrogate MAPK phosphorylation, suggest that the formation of stable lipid peroxidation by-products may not be the primary mechanism by which copper activates MAPKs. These results further elucidate the effects of copper on signal transduction pathways to alter gene expression. Published by Elsevier Ltd.
C1 [McElwee, Matthew K.; Freedman, Jonathan H.] NIEHS, Mol Toxicol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Mattie, Michael D.; McElwee, Matthew K.] Duke Univ, Nicholas Sch Environm & Earth Sci, Durham, NC 27708 USA.
RP Freedman, JH (reprint author), NIEHS, Mol Toxicol Lab, NIH, Dept Hlth & Human Serv, POB 12233,E1-05,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM freedma1@niehs.nih.gov
FU National Institute of Environmental Health Sciences [ES-10356,
5T32-ES-07031-22]; National Institutes of Health
FX This work was supported, in part, by National Institute of Environmental
Health Sciences grants ES-10356 and 5T32-ES-07031-22, and by the
Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences. We thank Dr. G.
Andrews (University of Kansas Medical Center) for the generous gift of
MT-1-based reporter genes.
NR 64
TC 27
Z9 29
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
EI 1089-8638
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 28
PY 2008
VL 383
IS 5
BP 1008
EP 1018
DI 10.1016/j.jmb.2008.08.080
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 374HD
UT WOS:000261033500007
PM 18793645
ER
PT J
AU Singh, R
Manjunatha, U
Boshoff, HIM
Ha, YH
Niyomrattanakit, P
Ledwidge, R
Dowd, CS
Lee, IY
Kim, P
Zhang, L
Kang, SH
Keller, TH
Jiricek, J
Barry, CE
AF Singh, Ramandeep
Manjunatha, Ujjini
Boshoff, Helena I. M.
Ha, Young Hwan
Niyomrattanakit, Pornwaratt
Ledwidge, Richard
Dowd, Cynthia S.
Lee, Ill Young
Kim, Pilho
Zhang, Liang
Kang, Sunhee
Keller, Thomas H.
Jiricek, Jan
Barry, Clifton E., III
TI PA-824 Kills Nonreplicating Mycobacterium tuberculosis by Intracellular
NO Release
SO SCIENCE
LA English
DT Article
ID NITRIC-OXIDE; COENZYME F-420; BOVIS BCG; METABOLISM; IDENTIFICATION;
BIOSYNTHESIS; RESISTANCE
AB Bicyclic nitroimidazoles, including PA- 824, are exciting candidates for the treatment of tuberculosis. These prodrugs require intracellular activation for their biological function. We found that Rv3547 is a deazaflavin- dependent nitroreductase ( Ddn) that converts PA- 824 into three primary metabolites; the major one is the corresponding des- nitroimidazole ( des- nitro). When derivatives of PA- 824 were used, the amount of des- nitro metabolite formed was highly correlated with anaerobic killing of Mycobacterium tuberculosis ( Mtb). Des- nitro metabolite formation generated reactive nitrogen species, including nitric oxide ( NO), which are the major effectors of the anaerobic activity of these compounds. Furthermore, NO scavengers protected the bacilli from the lethal effects of the drug. Thus, these compounds may act as intracellular NO donors and could augment a killing mechanism intrinsic to the innate immune system.
C1 [Singh, Ramandeep; Manjunatha, Ujjini; Boshoff, Helena I. M.; Ha, Young Hwan; Ledwidge, Richard; Dowd, Cynthia S.; Lee, Ill Young; Kim, Pilho; Zhang, Liang; Kang, Sunhee; Barry, Clifton E., III] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Manjunatha, Ujjini; Niyomrattanakit, Pornwaratt; Keller, Thomas H.; Jiricek, Jan] Novartis Inst Trop Dis, Singapore 138670, Singapore.
RP Barry, CE (reprint author), NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM cbarry@mail.nih.gov
RI Barry, III, Clifton/H-3839-2012;
OI Keller, Thomas/0000-0002-7553-6235
FU National Institute of Allergy and Infectious Diseases; NIH; Bill and
Melinda Gates Foundation; Wellcome Trust; Grand Challenges in Global
Health Initiative; Korea Foundation for International Cooperation of
Science and Technology; Korean Ministry of Education, Science and
Technology ( MEST) [No. K20501000001]
FX We thank C. Nathan ( Cornell University) and T. P. Begley ( Cornell
University) for insightful comments, S. Ehrt ( Cornell University) for
proteosome mutants, L. Daniels ( Texas A& M University) for F420 and M.
Goodwin ( Tuberculosis Research Section) for analytical support. This
work was funded ( in part) by the intramural research program of
National Institute of Allergy and Infectious Diseases, NIH, and ( in
part) by a grant from the Bill and Melinda Gates Foundation and the
Wellcome Trust through the Grand Challenges in Global Health Initiative.
This work was also supported by the Korea Foundation for International
Cooperation of Science and Technology ( KICOS) through a grant provided
by the Korean Ministry of Education, Science and Technology ( MEST) (
No. K20501000001).
NR 23
TC 240
Z9 251
U1 4
U2 37
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 28
PY 2008
VL 322
IS 5906
BP 1392
EP 1395
DI 10.1126/science.1164571
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 376FX
UT WOS:000261170600042
PM 19039139
ER
PT J
AU Zhou, QF
Shung, KK
Zhang, QQ
Djuth, FT
AF Zhou, Q. F.
Shung, K. K.
Zhang, Q. Q.
Djuth, F. T.
TI Temperature dependence of oriented growth of Pb[Yb1/2Nb1/2]O-3-PbTiO3
thin films deposited on LNO/Si substrates
SO THIN SOLID FILMS
LA English
DT Article
DE Piezoelectric films; Sol-gel deposition; Oriented growth; X-ray
diffraction
ID PIEZOELECTRIC PROPERTIES; SINGLE-CRYSTALS; SYSTEM;
PB(YB1/2NB1/2)O-3-PBTIO3; TRANSDUCERS; BEHAVIOR
AB (1-x)Pb[Yb1/2Nb1/2]O-3-xPbTiO(3) (PYbN-PT,x=0.5) (001)oriented thin films were deposited onto LaNiO3 (LNO)/Si (001) substrates by sol-gel processing. The crystallographic texture of the films was controlled by the annealing temperature and heating rate. Highly (001) oriented LNO thin films were prepared by a simple metal organic decomposition technique, and the samples were annealed at 700 degrees C and 750 degrees C using a rapid thermal annealing process and furnace, respectively. X-ray diffraction analysis revealed that the films of PYbN-PT were highly (001) oriented along LNO/Si substrates. The degree of PYbN-PT orientation is dependent on the heating rate and annealing temperature. Annealing heating rate of 10 degrees C/s and high annealing temperature near 750 degrees C produce the greatest degree of(001) orientation, which gives rise to improved dielectric properties. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Zhou, Q. F.; Shung, K. K.] Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
[Zhou, Q. F.; Shung, K. K.] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Zhang, Q. Q.; Djuth, F. T.] Geospace Res Inc, El Segundo, CA 90245 USA.
RP Zhou, QF (reprint author), Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
EM qifazhou@usc.edu
FU NSF [DMI-0339430]; NIH [P41-EB2182]
FX The authors acknowledge support from NSF Grant DMI-0339430 and NIH Grant
P41-EB2182.
NR 20
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0040-6090
J9 THIN SOLID FILMS
JI Thin Solid Films
PD NOV 28
PY 2008
VL 517
IS 2
BP 695
EP 698
DI 10.1016/j.tsf.2008.08.004
PG 4
WC Materials Science, Multidisciplinary; Materials Science, Coatings &
Films; Physics, Applied; Physics, Condensed Matter
SC Materials Science; Physics
GA 383SO
UT WOS:000261693900043
PM 20890456
ER
PT J
AU Pauly, GT
Loktionova, NA
Fang, QM
Vankayala, SL
Guida, WC
Pegg, AE
AF Pauly, Gary T.
Loktionova, Natalia A.
Fang, Qingming
Vankayala, Sai Lakshmana
Guida, Wayne C.
Pegg, Anthony E.
TI Substitution of Aminomethyl at the Meta-Position Enhances the
Inactivation of O-6-Alkylguanine-DNA Alkyltransferase by
O-6-Benzylguanine
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID MALIGNANT BRAIN-TUMORS; PHASE-II TRIAL; O(6)-ALKYLGUANINE-DNA
ALKYLTRANSFERASE; MOLECULAR DOCKING; ALKYLATING-AGENTS; ACCURATE
DOCKING; SOLID TUMORS; DNA-BINDING; IN-VITRO; TEMOZOLOMIDE
AB O-6-Benzylguanine is an irreversible inactivator of O-6-alkylguanine-DNA alkyltransferase currently in clinical trials to overcome alkyltransferase-mediated resistance to certain cancer chemotherapeutic alkylating agents. In order to produce more soluble alkyltransferase inhibitors, we have synthesized three aminomethyl-substituted O-6-benzylguanines and the three methyl analogs and found that the substitution of aminomethyl at the meta-position greatly enhances inactivation of alkyltransferase, whereas para-substitution has little effect and ortho-substitution virtually eliminates activity. Molecular modeling of their interactions with alkyltransferase provided a molecular explanation for these results. The square of the correlation coefficient (R-2) obtained between E-model scores (obtained from GLIDE XP/QPLD docking calculations) vs log(ED50) values via a linear regression analysis was 0.96. The models indicate that the ortho-substitution causes a steric clash interfering with binding, whereas the meta-aminomethyl substitution allows an interaction of the amino group to generate an additional hydrogen bond with the protein.
C1 [Loktionova, Natalia A.; Fang, Qingming; Pegg, Anthony E.] Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA.
[Pauly, Gary T.] NCI, Comparat Carcinogenesis Lab, Ft Detrick, MD 21702 USA.
[Loktionova, Natalia A.; Fang, Qingming; Pegg, Anthony E.] Penn State Univ, Coll Med, Dept Pharmacol, Hershey, PA 17033 USA.
[Vankayala, Sai Lakshmana; Guida, Wayne C.] Univ S Florida, Dept Chem, Tampa, FL 33620 USA.
[Vankayala, Sai Lakshmana; Guida, Wayne C.] Univ S Florida, Ctr Mol Divers Drug Design Discovery & Delivery, Tampa, FL 33620 USA.
[Guida, Wayne C.] H Lee Moffitt Canc Ctr & Res Inst, Drug Discovery Program, Tampa, FL 33612 USA.
RP Pegg, AE (reprint author), Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, POB 850, Hershey, PA 17033 USA.
EM aep1@psu.edu
RI Fang, Qingming/B-6839-2008
OI Fang, Qingming/0000-0002-4006-0636
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute [CA-018137, CA-097209, CA-071976]; Center for
Cancer Research; National Institutes of Health, U.S.A
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute, Center
for Cancer Research. Work in A.E.P.'s laboratory was supported by Grants
CA-018137, CA-097209, and CA-071976 from the National Cancer Institute,
National Institutes of Health, U.S.A.
NR 45
TC 13
Z9 14
U1 3
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 27
PY 2008
VL 51
IS 22
BP 7144
EP 7153
DI 10.1021/jm800675p
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 374PQ
UT WOS:000261056600015
PM 18973327
ER
PT J
AU Brosh, RM
AF Brosh, Robert M., Jr.
TI MOLECULAR BIOLOGY The Bloom's complex mousetrap
SO NATURE
LA English
DT Editorial Material
ID PROTEINS; BLM
C1 [Brosh, Robert M., Jr.] NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, Baltimore, MD 21224 USA.
EM broshr@mail.nih.gov
NR 7
TC 4
Z9 4
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 27
PY 2008
VL 456
IS 7221
BP 453
EP 454
DI 10.1038/456453a
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 376FW
UT WOS:000261170500024
PM 19037304
ER
PT J
AU Difilippantonio, S
Gapud, E
Wong, N
Huang, CY
Mahowald, G
Chen, HT
Kruhlak, MJ
Callen, E
Livak, F
Nussenzweig, MC
Sleckman, BP
Nussenzweig, A
AF Difilippantonio, Simone
Gapud, Eric
Wong, Nancy
Huang, Ching-Yu
Mahowald, Grace
Chen, Hua Tang
Kruhlak, Michael J.
Callen, Elsa
Livak, Ferenc
Nussenzweig, Michel C.
Sleckman, Barry P.
Nussenzweig, Andre
TI 53BP1 facilitates long-range DNA end-joining during V(D)J recombination
SO NATURE
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; REGION RECOMBINATION; GENOMIC INSTABILITY;
CHROMOSOME BREAKS; IN-VIVO; DAMAGE; ATM; MICE; H2AX; P53
AB Variable, diversity and joining (V(D)J) recombination and class-switch recombination use overlapping but distinct non- homologous end joining pathways to repair DNA double- strand- break intermediates. 53BP1 is a DNA- damage- response protein that is rapidly recruited to sites of chromosomal double- strand breaks, where it seems to function in a subset of ataxia telangiectasia mutated ( ATM) kinase-, H2A histone family member X ( H2AX, also known as H2AFX)- and mediator of DNA damage checkpoint 1 (MDC1)- dependent events(1,2). A 53BP1- dependent end- joining pathway has been described that is dispensable for V( D) J recombination but essential for class- switch recombination(3,4). Here we report a previously unrecognized defect in the joining phase of V( D) J recombination in 53BP1- deficient lymphocytes that is distinct from that found in classical non- homologous- end- joining-, H2ax-, Mdc1- and Atm- deficient mice. Absence of 53BP1 leads to impairment of distal V - DJ joining with extensive degradation of unrepaired coding ends and episomal signal joint reintegration at V( D) J junctions. This results in apoptosis, loss of T- cell receptor a locus integrity and lymphopenia. Further impairment of the apoptotic checkpoint causes propagation of lymphocytes that have antigen receptor breaks. These data suggest a more general role for 53BP1 in maintaining genomic stability during long- range joining of DNA breaks.
C1 [Difilippantonio, Simone; Wong, Nancy; Chen, Hua Tang; Kruhlak, Michael J.; Callen, Elsa; Nussenzweig, Andre] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Gapud, Eric; Huang, Ching-Yu; Mahowald, Grace; Sleckman, Barry P.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Livak, Ferenc] Univ Maryland, Sch Med, Dept Microbiol & Immunol, Baltimore, MD 21201 USA.
[Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA.
[Nussenzweig, Michel C.] Howard Hughes Med Inst, New York, NY 10021 USA.
RP Nussenzweig, A (reprint author), NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
EM andre_nussenzweig@nih.gov
RI Huang, Ching-Yu /E-3981-2010
FU NIH [R01AI074953]; Cancer Research Institute; Intramural Research
Program; National Cancer Institute; Center for Cancer Research
FX We are grateful to M. McAuliffe and co-workers for developing the three-
dimensional- FISH measurement algorithm; D.G. Schatz and J. Haber for
discussions; A. Wynshaw-Boris for Atm-/- mice and J. Chen for
53BP1-/- and Mdc1-/- mice; D. Venzon for help with
statistical analysis; and numbers of the A. Nussenzweig laboratory (J.
Daniel and A. Celeste) for comments on the manuscript. B.P.S. is
supported by NIH grant R01AI074953. E.G. is supported by pre-doctoral
fellowship from the Cancer Research Institute. M.C.N. is a HHMI
investigator. A.N. is supported by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research.
NR 30
TC 171
Z9 175
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 27
PY 2008
VL 456
IS 7221
BP 529
EP U57
DI 10.1038/nature07476
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 376FW
UT WOS:000261170500044
PM 18931658
ER
PT J
AU Lenz, G
Wright, G
Dave, SS
Xiao, W
Powell, J
Zhao, H
Xu, W
Tan, B
Goldschmidt, N
Iqbal, J
Vose, J
Bast, M
Fu, K
Weisenburger, DD
Greiner, TC
Armitage, JO
Kyle, A
May, L
Gascoyne, RD
Connors, JM
Troen, G
Holte, H
Kvaloy, S
Dierickx, D
Verhoef, G
Delabie, J
Smeland, EB
Jares, P
Martinez, A
Lopez-Guillermo, A
Montserrat, E
Campo, E
Braziel, RM
Miller, TP
Rimsza, LM
Cook, JR
Pohlman, B
Sweetenham, J
Tubbs, RR
Fisher, RI
Hartmann, E
Rosenwald, A
Ott, G
Muller-Hermelink, HK
Wrench, D
Lister, TA
Jaffe, ES
Wilson, WH
Chan, WC
Staudt, LM
AF Lenz, G.
Wright, G.
Dave, S. S.
Xiao, W.
Powell, J.
Zhao, H.
Xu, W.
Tan, B.
Goldschmidt, N.
Iqbal, J.
Vose, J.
Bast, M.
Fu, K.
Weisenburger, D. D.
Greiner, T. C.
Armitage, J. O.
Kyle, A.
May, L.
Gascoyne, R. D.
Connors, J. M.
Troen, G.
Holte, H.
Kvaloy, S.
Dierickx, D.
Verhoef, G.
Delabie, J.
Smeland, E. B.
Jares, P.
Martinez, A.
Lopez-Guillermo, A.
Montserrat, E.
Campo, E.
Braziel, R. M.
Miller, T. P.
Rimsza, L. M.
Cook, J. R.
Pohlman, B.
Sweetenham, J.
Tubbs, R. R.
Fisher, R. I.
Hartmann, E.
Rosenwald, A.
Ott, G.
Muller-Hermelink, H. -K
Wrench, D.
Lister, T. A.
Jaffe, E. S.
Wilson, W. H.
Chan, W. C.
Staudt, L. M.
CA Lymphoma Leukemia Mol Profiling Pr
TI Stromal Gene Signatures in Large-B-Cell Lymphomas
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID MESENCHYMAL STEM-CELLS; NON-HODGKINS-LYMPHOMA; TISSUE GROWTH-FACTOR;
ANGIOGENIC SWITCH; BREAST-CANCER; TUMOR-GROWTH; MOUSE MODEL; EXPRESSION;
SURVIVAL; CHEMOTHERAPY
AB Background: The addition of rituximab to combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), or R-CHOP, has significantly improved the survival of patients with diffuse large-B-cell lymphoma. Whether gene-expression signatures correlate with survival after treatment of diffuse large-B-cell lymphoma is unclear.
Methods: We profiled gene expression in pretreatment biopsy specimens from 181 patients with diffuse large-B-cell lymphoma who received CHOP and 233 patients with this disease who received R-CHOP. A multivariate gene-expression-based survival-predictor model derived from a training group was tested in a validation group.
Results: A multivariate model created from three gene-expression signatures - termed ``germinal-center B-cell,'' ``stromal-1,'' and ``stromal-2'' - predicted survival both in patients who received CHOP and patients who received R-CHOP. The prognostically favorable stromal-1 signature reflected extracellular-matrix deposition and histiocytic infiltration. By contrast, the prognostically unfavorable stromal-2 signature reflected tumor blood-vessel density.
Conclusions: Survival after treatment of diffuse large-B-cell lymphoma is influenced by differences in immune cells, fibrosis, and angiogenesis in the tumor microenvironment.
C1 [Lenz, G.; Dave, S. S.; Zhao, H.; Xu, W.; Tan, B.; Goldschmidt, N.; Wilson, W. H.; Staudt, L. M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Wright, G.] NCI, Biometr Res Branch, Div Canc Treatment & Diagnosis, NIH, Bethesda, MD 20892 USA.
[Xiao, W.; Powell, J.] NIH, Bioinformat & Mol Anal Sect, Bethesda, MD 20892 USA.
[Jaffe, E. S.] NIH, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
NIH, Computat Biosci & Engn Lab, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Iqbal, J.; Vose, J.; Bast, M.; Fu, K.; Weisenburger, D. D.; Greiner, T. C.; Armitage, J. O.; Chan, W. C.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Kyle, A.; May, L.; Gascoyne, R. D.; Connors, J. M.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Troen, G.; Delabie, J.] Univ Oslo, Rikshosp Univ Hosp, Pathol Clin, N-0027 Oslo, Norway.
[Holte, H.; Kvaloy, S.] Univ Oslo, Rikshosp Univ Hosp, Canc Clin, N-0027 Oslo, Norway.
[Smeland, E. B.] Univ Oslo, Rikshosp Univ Hosp, Canc Res Inst, N-0027 Oslo, Norway.
[Smeland, E. B.] Univ Oslo, Norwegian Radium Hosp, Ctr Canc Biomed, Fac Div, N-0027 Oslo, Norway.
[Dierickx, D.; Verhoef, G.] Katholieke Univ Leuven, Dept Hematol, Louvain, Belgium.
[Jares, P.; Martinez, A.; Lopez-Guillermo, A.; Montserrat, E.; Campo, E.] Univ Barcelona, Hosp Clin, Barcelona, Spain.
[Braziel, R. M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Braziel, R. M.; Miller, T. P.; Rimsza, L. M.; Cook, J. R.; Tubbs, R. R.; Fisher, R. I.] SW Oncol Grp, Tucson, AZ USA.
[Miller, T. P.; Rimsza, L. M.] Univ Arizona, Ctr Canc, Tucson, AZ USA.
[Pohlman, B.; Sweetenham, J.] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
[Cook, J. R.; Tubbs, R. R.] Cleveland Clin, Pathol & Lab Med Inst, Cleveland, OH 44106 USA.
[Fisher, R. I.] Univ Rochester, Sch Med, James P Wilmot Canc Ctr, Rochester, NY USA.
[Hartmann, E.; Rosenwald, A.; Ott, G.; Muller-Hermelink, H. -K] Univ Wurzburg, Dept Pathol, D-8700 Wurzburg, Germany.
[Ott, G.] Robert Bosch Krankenhaus, Dept Clin Pathol, Stuttgart, Germany.
[Wrench, D.; Lister, T. A.] St Bartholomews Hosp, Canc Res UK, London, England.
RP Staudt, LM (reprint author), NCI, Metab Branch, Ctr Canc Res, NIH, Bldg 10,Rm 4N114, Bethesda, MD 20892 USA.
EM lstaudt@mail.nih.gov
RI Martinez, Antonio/D-8188-2012; Lenz, Georg/I-6844-2012;
OI Martinez, Antonio/0000-0003-0790-9017; Delabie, Jan/0000-0001-5023-0689;
Campo, elias/0000-0001-9850-9793
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Center for Cancer Research; NCI Strategic
Partnering to Evaluate Cancer Signature [UO1-CA114778]; German Research
Foundation; Genentech; Imedex Future; Ziopharm; L'Oreal; Celgene;
Genitope; Biogen Idec; Roche Canada; Schering and Hoffmann-La Roche;
Ventana Medical Systems; Roche Molecular Systems; Genentech BioOncology;
Genentech BioOncology National Lymphocare Study; Allos Therapeutics;
Millennium; Amgen; Pharmion; Roche; Seattle Genetics; Imedex; Eleos;
Educational Concepts; Upside Endeavors
FX Supported by grants from the Intramural Research Program of the National
Institutes of Health, the National Cancer Institute ( NCI), and the
Center for Cancer Research; an NCI Strategic Partnering to Evaluate
Cancer Signature grant (UO1-CA114778); and a grant from the German
Research Foundation (to Dr. Lenz).; Dr. Vose reports receiving grant
support from Genentech; Dr. Greiner, lecture fees from Imedex Future;
Dr. Armitage, consulting fees from Ziopharm, L'Oreal, Celgene, Genitope,
and Biogen Idec and lecture fees from Genentech; Dr. Gascoyne,
consulting fees from Genentech and Roche Canada and lecture fees and
grant support from Roche Canada; Dr. Connors, grant support from Roche
Canada; Dr. Montserrat, consulting fees from Schering and Hoffmann-La
Roche; Dr. Miller, consulting fees and grant support from Genentech and
Biogen Idec; Dr. Rimsza, grant support from Ventana Medical Systems; Dr.
Cook, consulting fees from Roche Molecular Systems; Dr. Pohlman,
consulting fees from Genentech BioOncology and grant support from
Genentech BioOncology National Lymphocare Study; Dr. Fisher, consulting
fees from Allos Therapeutics, Millennium, Amgen, Pharmion, Celgene,
Roche, Genentech, and Seattle Genetics; Dr. Lister, consulting fees from
Imedex, Eleos, Educational Concepts, Genentech, and Upside Endeavors and
grant support from Millennium; and Dr. Chan, grant support from Roche
Molecular Systems. No other potential conflict of interest relevant to
this article was reported.; We thank Alexander Kohlmann, Mickey
Williams, and Lothar Wieczorek at Roche Molecular Systems for logistical
support.
NR 33
TC 687
Z9 702
U1 1
U2 24
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 27
PY 2008
VL 359
IS 22
BP 2313
EP 2323
DI 10.1056/NEJMoa0802885
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 377SG
UT WOS:000261270300003
PM 19038878
ER
PT J
AU Neff, RT
Hurst, FP
Falta, EM
Bohen, EM
Lentine, KL
Dharnidharka, VR
Agodoa, LY
Jindal, RM
Yuan, CM
Abbott, KC
AF Neff, Robert T.
Hurst, Frank P.
Falta, Edward M.
Bohen, Erin M.
Lentine, Krista L.
Dharnidharka, Vikas R.
Agodoa, Lawrence Y.
Jindal, Rahul M.
Yuan, Christina M.
Abbott, Kevin C.
TI Progressive Multifocal Leukoencephalopathy and Use of Mycophenolate
Mofetil After Kidney Transplantation
SO TRANSPLANTATION
LA English
DT Article
DE Kidney transplant; Mycophenolate mofetil; Progressive multifocal
leukoencephalopathy
ID VIRUS VP1 POLYPEPTIDES; RENAL-TRANSPLANTATION; BK VIRUS; RECIPIENT;
NEPHROPATHY; PATIENT; DISEASE; PML
AB Mycophenolate mofetil (MMF) use may be associated with progressive multifocal leukoencephalopathy (PML). We conducted a retrospective cohort study of 32,757 renal transplant recipients using the United States Renal Data System kidney transplant files for the incidence, prognosis, and clinical features associated with PML Occurring after kidney transplant. Subjects were transplanted from January 1, 2000 to July 31, 2004 and followed through December 31, 2004. The incidence density of PML in MMF users was 14.4 cases/100,000 person-years at risk versus 0 for non-MMF users (P=0.11) by log rank test. Factors significantly associated with PML were BK virus infection (22.2% vs. 1.1%), pretransplant transfusion (75% vs. 34%), panel reactive antibody more than 20% (56% vs. 14%), and use of antirejection medications in the first year (33% vs. 9.2%), all P less than 0.05. PML is rare in the renal transplant population. There was no significant association between PML and MMF, but MMF use in this cohort is too high to accurately assess an association.
C1 [Neff, Robert T.; Hurst, Frank P.; Bohen, Erin M.; Yuan, Christina M.; Abbott, Kevin C.] Walter Reed Army Med Ctr, Serv Nephrol, Washington, DC 20307 USA.
[Falta, Edward M.; Jindal, Rahul M.] Walter Reed Army Med Ctr, Organ Transplant Serv, Washington, DC 20307 USA.
[Lentine, Krista L.] St Louis Univ, Sch Med, Ctr Outcomes Res, Div Nephrol, St Louis, MO USA.
[Dharnidharka, Vikas R.] Univ Florida, Coll Med, Dept Pediat, Gainesville, FL USA.
[Agodoa, Lawrence Y.] NIDDKD, NIH, Bethesda, MD 20892 USA.
[Jindal, Rahul M.] Brookdale Univ Hosp, Dept Surg, Brooklyn, NY USA.
RP Neff, RT (reprint author), Walter Reed Army Med Ctr, Serv Nephrol, Washington, DC 20307 USA.
EM robert.neff@amedd.army.mil
OI Abbott, Kevin/0000-0003-2111-7112
NR 26
TC 77
Z9 77
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 27
PY 2008
VL 86
IS 10
BP 1474
EP 1478
DI 10.1097/TP.0b013e31818b62c8
PG 5
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 377XL
UT WOS:000261285600023
PM 19034021
ER
PT J
AU Unoki, M
Kumamoto, K
Robles, AI
Shen, JC
Zheng, ZM
Harris, CC
AF Unoki, Motoko
Kumamoto, Kensuke
Robles, Ana I.
Shen, Jiang Cheng
Zheng, Zhi-Ming
Harris, Curtis C.
TI A novel ING2 isoform, ING2b, synergizes with ING2a to prevent cell cycle
arrest and apoptosis
SO FEBS LETTERS
LA English
DT Article
DE ING2; ING2a; ING2b; p53; Isoform
ID CANCER; EXPRESSION; EXCISION; REPAIR; DOMAIN; P53
AB We identified a novel inhibitor of growth family member 2 (ING2) isoform, ING2b, which shares exon 2 with ING2a, but lacks the N-terminal p53 binding region. Contrary to ING2a, ING2b's promoter has no p53 binding sites. Consistently, activation of p53 led to suppression of ING2a, leaving ING2b unaffected. Through isoform-specific targeting, we showed that ING2a knockdown suppressed cell growth only in the presence of p53, ING2b knockdown had no effect on cell growth, and knockdown of both induced cell cycle arrest and apoptosis independently of p53. ING2a and ING2b have compensatory roles that protect cells from cell cycle arrest and apoptosis and may be involved in development of chemotherapeutic resistance. Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.
C1 [Unoki, Motoko; Kumamoto, Kensuke; Robles, Ana I.; Shen, Jiang Cheng; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zheng, Zhi-Ming] NCI, HIV & AIDS Malignancy Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Unoki, Motoko] RIKEN, Inst Phys & Chem Res, Lab Biomarker Dev, Tokyo 1088639, Japan.
[Kumamoto, Kensuke] Fukushima Med Univ, Sch Med, Dept Surg 2, Fukushima 9601295, Japan.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Rm 3068, Bethesda, MD 20892 USA.
EM Curtis_Harris@nih.gov
FU Intramural Research Program; CCR; NCI; NIH
FX We thank Dr. Kaori Fujita for helpful advice, and Dr. Tom Holroyd for
editorial help. This work was supported by the Intramural Research
Program of the CCR, NCI, NIH.
NR 11
TC 15
Z9 16
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD NOV 26
PY 2008
VL 582
IS 28
BP 3868
EP 3874
DI 10.1016/j.febslet.2008.10.024
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 377ER
UT WOS:000261235000005
PM 18951897
ER
PT J
AU Mccue, PP
Phang, JM
AF McCue, Patrick P.
Phang, James M.
TI Identification of Human Intracellular Targets of the Medicinal Herb St.
John's Wort by Chemical-Genetic Profiling in Yeast
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE St. John's wort; Hypericum perforatum; botanical; dietary supplement;
yeast; microarray; wound healing; depression; alternative medicine
ID PARKINSONS-DISEASE; SACCHAROMYCES-CEREVISIAE; HEAT-SHOCK-PROTEIN-70;
POLYMORPHISMS; DEPRESSION; HYPERICUM; DELETION; HSPA1B; GENOME; ALPHA
AB St. John's wort (SJW; Hypericum perforatum L.) is commonly known for its antidepressant properties and was traditionally used to promote wound healing, but its molecular mechanism of action is not known. Here, chemical-genetic profiling in yeast was used to predict the human intracellular targets of an aqueous extract of SJW. SJW source material was authenticated by TLC, digital microscopy, and HPLC and further characterized by colorimetric methods for antioxidant activity, protein content, and total soluble phenolic content. SJW extract contained 1.76 mu g/mL hyperforin, 10.14 mu g/mL hypericin, and 46.05 mu g/mL pseuclohypericin. The effect of SJW extract on similar to 5900 barcoded heterozygous diploid deletion strains of Saccharomyces cerevisiae was investigated using high-density oligonucleoticle microarrays. Seventy-eight yeast genes were identified as sensitive to SJW and were primarily associated with vesicle-mediated transport and signal transduction pathways. Potential human intracellular targets were identified using sequence-based comparisons and included proteins associated with neurological disease and angiogenesis-related pathways. Selected human targets were confirmed by cell-based immunocytochemical assays. The comprehensive and systematic nature of chemical-genetic profiling in yeast makes this technique attractive for elucidating the potential molecular mechanisms of action of botanical medicines and other bioactive dietary plants.
C1 [McCue, Patrick P.] Natl Ctr Complementary & Alternat Med, NIH, Bethesda, MD 20892 USA.
[McCue, Patrick P.; Phang, James M.] NCI, Metab & Canc Susceptibil Sect, Comparat Carcinogenesis Lab, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
RP Mccue, PP (reprint author), NCI, 6120 Execut Blvd,EPS Suite 450, Rockville, MD 20852 USA.
EM mccuepat@mail.nih.gov
FU Intramural NIH HHS [Z99 OD999999]
NR 25
TC 8
Z9 8
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD NOV 26
PY 2008
VL 56
IS 22
BP 11011
EP 11017
DI 10.1021/jf801593a
PG 7
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
Technology
SC Agriculture; Chemistry; Food Science & Technology
GA 374PR
UT WOS:000261056700086
PM 18975972
ER
PT J
AU Jung, SC
Kim, J
Hoffman, DA
AF Jung, Sung-Cherl
Kim, Jinhyun
Hoffman, Dax A.
TI Rapid, Bidirectional Remodeling of Synaptic NMDA Receptor Subunit
Composition by A-type K(+) Channel Activity in Hippocampal CA1 Pyramidal
Neurons
SO NEURON
LA English
DT Article
ID LONG-TERM POTENTIATION; D-ASPARTATE RECEPTOR; PROTEIN-KINASE-II;
DENDRITIC SPINES; HOMEOSTATIC PLASTICITY; POSTNATAL-DEVELOPMENT;
POTASSIUM CHANNELS; MOLECULAR-BASIS; AMPA RECEPTORS; RAT-BRAIN
AB The transient, A-type K(+) current (I(A)) controls the excitability of CA1 pyramidal neuron dendrites by regulating the back-propagation of action potentials and by shaping synaptic input. Dendritic A-type K(+) channels are targeted for modulation during long-term potentiation (LTP) and we have recently shown that activity-dependent internalization of the A-type channel subunit Kv4.2 enhances synaptic currents. However, the effect of changes in I(A) on the ability to induce subsequent synaptic plasticity (metaplasticity) has not been investigated. Here, we show that altering functional Kv4.2 expression level leads to a rapid, bidirectional remodeling of CA1 synapses. Neurons exhibiting enhanced I(A) showed a decrease in relative synaptic NR2B/NR2A subunit composition and did not exhibit LTP. Conversely, reducing I(A) by expression of a Kv4.2 dominant-negative or through genomic knockout of Kv4.2 led to an increased fraction of synaptic NR2B/NR2A and enhanced LTP. Bidirectional synaptic remodeling was mimicked in experiments manipulating intracellular Ca(2+) and dependent on spontaneous activation of NMDA receptors and CaMKII activity. Our data suggest that A-type K(+) channels are an integral part of a synaptic complex that regulates Ca(2+) signaling through spontaneous NIVIDAR activation to control synaptic NIVIDAR expression and plasticity.
C1 [Jung, Sung-Cherl; Kim, Jinhyun; Hoffman, Dax A.] NICHD, Mol Neurophysiol & Biophys Unit, LCSN, NIH, Bethesda, MD 20892 USA.
RP Hoffman, DA (reprint author), NICHD, Mol Neurophysiol & Biophys Unit, LCSN, NIH, Bethesda, MD 20892 USA.
EM hoffmand@mail.nih.gov
RI Hoffman, Dax/E-5155-2011
OI Hoffman, Dax/0000-0001-6999-2157
FU National Institute of Child Health and Human Development Intramural
Research Program
FX We thank Drs. Georg Koehr, Chris McBain and members of John Lisman's lab
for their critical review of earlier versions of this manuscript. We
thank Drs. Diana Medrano-Velasquez, Young Ho Suh, and Jeff Magee for
technical support. Dr. Thomas L. Schwarz for providing Kv4.2
/ mice, and Dr. Jose Esteban for providing the tCaMKII
construct. This work was supported by the National Institute of Child
Health and Human Development Intramural Research Program.
NR 64
TC 59
Z9 60
U1 1
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 26
PY 2008
VL 60
IS 4
BP 657
EP 671
DI 10.1016/j.neuron.2008.08.029
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 382JX
UT WOS:000261603200015
PM 19038222
ER
PT J
AU Hong, S
Hikosaka, O
AF Hong, Simon
Hikosaka, Okihide
TI The Globus Pallidus Sends Reward-Related Signals to the Lateral Habenula
SO NEURON
LA English
DT Article
ID BASAL GANGLIA; STRIATAL STIMULATION; DOPAMINE NEURONS; RAT; MONKEY;
MOVEMENT; BRAIN; NUCLEUS; LESIONS; CONNECTIONS
AB As a major output station of the basal ganglia, the globus pallidus internal segment (GPi) projects to the thalamus and brainstem nuclei thereby controlling motor behavior. A less well known fact is that the GPi also projects to the lateral habenula (LHb) which is often associated with the limbic system. Using the monkey performing a saccade task with positionally biased reward outcomes, we found that antidromically identified LHb-projecting neurons were distributed mainly in the dorsal and ventral borders of the GPi and that their activity was strongly modulated by expected reward outcomes. A majority of them were excited by the no-reward-predicting target and inhibited by the reward-predicting target. These reward-dependent modulations were similar to those in LHb neurons but started earlier than those in LHb neurons. These results suggest that GPi may initiate reward-related signals through its effects on the LHb, which then influences the dopaminergic and serotonergic systems.
C1 [Hong, Simon; Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Hikosaka, O (reprint author), NEI, Sensorimotor Res Lab, NIH, 49 Convent Dr, Bethesda, MD 20892 USA.
EM oh@lsr.nei.nih.gov
FU National Eye Institute
FX We are grateful to K.G. Thompson and B.G. Cumming for their help in
statistical analysis, M. Johnson, E. Bromberg-Martin, M. Yasuda for
helpful comments, and M. Matsumoto for providing the single unit LHb
data. We also thank M. Smith for his help in histology. This work was
supported by the intramural research program of the National Eye
Institute.
NR 37
TC 119
Z9 123
U1 2
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD NOV 26
PY 2008
VL 60
IS 4
BP 720
EP 729
DI 10.1016/j.neuron.2008.09.035
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 382JX
UT WOS:000261603200020
PM 19038227
ER
PT J
AU Ozhogina, OA
Grishaev, A
Bominaar, EL
Patthy, L
Trexler, M
Llinas, M
AF Ozhogina, Olga A.
Grishaev, Alexander
Bominaar, Emile L.
Patthy, Ldszlo
Trexler, Maria
Llinas, Miguel
TI NMR Solution Structure of the Neurotrypsin Kringle Domain
SO BIOCHEMISTRY
LA English
DT Article
ID SERINE-PROTEASE; PLASMINOGEN-ACTIVATOR; GLOBULAR-PROTEINS; BAYESIAN
PROTOCOL; NERVOUS-SYSTEM; BINDING-SITES; SPIN SYSTEMS; RICH MOTIFS;
AGRIN; SPECTROSCOPY
AB Neurotrypsin is a multidomain protein that serves as a brain-specific serine protease. Here we report the NMR structure of its kringle domain, NT/K. The data analysis was performed with the BACUS (Bayesian analysis of coupled unassigned spins) algorithm. This study presents the first application of BACUS to the structure determination of a (13)C unenriched protein for which no prior experimental 3D structure was available. NT/K adopts the kringle fold, consisting of an antiparallel beta-sheet bridged by an overlapping pair of disulfides. The structure reveals the presence of a surface-exposed left-handed polyproline H helix that is closely packed to the core beta-structure. This feature distinguishes NT/K from other members of the kringle fold and points toward a novel functional role for a kringle domain. Functional divergence among kringle domains is discussed on the basis of their surface and electrostatic characteristics.
C1 [Ozhogina, Olga A.; Bominaar, Emile L.; Llinas, Miguel] Carnegie Mellon Univ, Dept Chem, Pittsburgh, PA 15213 USA.
[Grishaev, Alexander] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Patthy, Ldszlo; Trexler, Maria] Hungarian Acad Sci, Biol Res Ctr, Inst Enzymol, Budapest, Hungary.
RP Ozhogina, OA (reprint author), Carnegie Mellon Univ, Dept Chem, 4400 5th Ave, Pittsburgh, PA 15213 USA.
EM oao.sputnik@gmail.com; llinas@andrew.cmu.edu
RI Patthy, Laszlo/A-2353-2013
FU NIH [HL-29409]; NSF [MCB-0424494]
FX This work was sponsored by NIH Grant HL-29409 to M.L., and E.L.B.
acknowledges financial support from NSF Grant MCB-0424494.
NR 47
TC 2
Z9 3
U1 1
U2 23
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 25
PY 2008
VL 47
IS 47
BP 12290
EP 12298
DI 10.1021/bi800555z
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 373UX
UT WOS:000261000100007
PM 18956887
ER
PT J
AU Barton, G
Abbott, J
Chiba, N
Huang, DW
Huang, Y
Krznaric, M
Mack-Smith, J
Saleem, A
Sherman, BT
Tiwari, B
Tomlinson, C
Aitman, T
Darlington, J
Game, L
Sternberg, MJE
Butcher, SA
AF Barton, G.
Abbott, J.
Chiba, N.
Huang, D. W.
Huang, Y.
Krznaric, M.
Mack-Smith, J.
Saleem, A.
Sherman, B. T.
Tiwari, B.
Tomlinson, C.
Aitman, T.
Darlington, J.
Game, L.
Sternberg, M. J. E.
Butcher, S. A.
TI EMAAS: An extensible grid-based Rich Internet Application for microarray
data analysis and management
SO BMC BIOINFORMATICS
LA English
DT Article
ID ARRAY DATA; BIOCONDUCTOR; EXPRESSION; ANNOTATION; DATABASES; PLATFORM;
MIMIR
AB Background: Microarray experimentation requires the application of complex analysis methods as well as the use of non-trivial computer technologies to manage the resultant large data sets. This, together with the proliferation of tools and techniques for microarray data analysis, makes it very challenging for a laboratory scientist to keep up-to-date with the latest developments in this field. Our aim was to develop a distributed e-support system for microarray data analysis and management.
Results: EMAAS (Extensible MicroArray Analysis System) is a multi-user rich internet application (RIA) providing simple, robust access to up-to-date resources for microarray data storage and analysis, combined with integrated tools to optimise real time user support and training. The system leverages the power of distributed computing to perform microarray analyses, and provides seamless access to resources located at various remote facilities. The EMAAS framework allows users to import microarray data from several sources to an underlying database, to pre-process, quality assess and analyse the data, to perform functional analyses, and to track data analysis steps, all through a single easy to use web portal. This interface offers distance support to users both in the form of video tutorials and via live screen feeds using the web conferencing tool EVO. A number of analysis packages, including R-Bioconductor and Affymetrix Power Tools have been integrated on the server side and are available programmatically through the Postgres-PLR library or on grid compute clusters. Integrated distributed resources include the functional annotation tool DAVID, GeneCards and the microarray data repositories GEO, CELSIUS and MiMiR. EMAAS currently supports analysis of Affymetrix 3' and Exon expression arrays, and the system is extensible to cater for other microarray and transcriptomic platforms.
Conclusion: EMAAS enables users to track and perform microarray data management and analysis tasks through a single easy-to-use web application. The system architecture is flexible and scalable to allow new array types, analysis algorithms and tools to be added with relative ease and to cope with large increases in data volume.
C1 [Barton, G.; Abbott, J.; Tomlinson, C.; Sternberg, M. J. E.; Butcher, S. A.] Univ London Imperial Coll Sci Technol & Med, Fac Nat Sci, Ctr Bioinformat, Div Mol Biosci, London SW7 2AZ, England.
[Huang, Y.; Krznaric, M.; Mack-Smith, J.; Saleem, A.; Darlington, J.] Univ London Imperial Coll Sci Technol & Med, London E Sci Ctr, Dept Comp, Fac Engn, London SW7 2AZ, England.
[Chiba, N.; Tiwari, B.; Tomlinson, C.; Aitman, T.; Game, L.] Univ London Imperial Coll Sci Technol & Med, MRC, Ctr Clin Sci, London W12 0NN, England.
[Huang, D. W.; Sherman, B. T.] NCI, Lab Immunopathogenesis & Bioinformat, Clin Serv Program, SAIC Frederick Inc, Ft Detrick, MD 21702 USA.
RP Butcher, SA (reprint author), Univ London Imperial Coll Sci Technol & Med, Fac Nat Sci, Ctr Bioinformat, Div Mol Biosci, Biochem Bldg,S Kensington Campus, London SW7 2AZ, England.
EM g.barton@imperial.ac.uk; j.abbott@imperial.ac.uk;
norie.chiba@imperial.ac.uk; huangdawei@mail.nih.gov;
y.huang@imperial.ac.uk; marko.krznaric@imperial.ac.uk;
jms3@doc.imperial.ac.uk; asif.saleem@moodys.com; bsherman@mail.nih.gov;
bhuwantiwari@yahoo.com; chris.tomlinson@imperial.ac.uk;
t.aitman@csc.mrc.ac.uk; j.darlington@imperial.ac.uk;
laurence.game@imperial.ac.uk; m.sternberg@imperial.ac.uk;
s.butcher@imperial.ac.uk
OI Sternberg, Michael/0000-0002-1884-5445; Abbott,
James/0000-0001-7701-4249; Tiwari, Brijesh/0000-0002-4834-6831
FU Biotechnology and Biological Sciences Research Council [BB/B/16488]
FX This work was supported by the Biotechnology and Biological Sciences
Research Council [BB/B/16488], as part of the Bioinformatics and
e-Science Programme II.
NR 25
TC 7
Z9 8
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 25
PY 2008
VL 9
AR 493
DI 10.1186/1471-2105-9-493
PG 11
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA 396NW
UT WOS:000262599400001
PM 19032776
ER
PT J
AU Brennan, P
van der Hel, O
Moore, LE
Zaridze, D
Matveev, V
Holcatova, I
Janout, V
Kollarova, H
Foretova, L
Szeszenia-Dabrowska, N
Mates, D
Rothman, N
Boffetta, P
Chow, WH
AF Brennan, P.
van der Hel, O.
Moore, L. E.
Zaridze, D.
Matveev, V.
Holcatova, I.
Janout, V.
Kollarova, H.
Foretova, L.
Szeszenia-Dabrowska, N.
Mates, D.
Rothman, N.
Boffetta, P.
Chow, W-H
TI Tobacco smoking, body mass index, hypertension, and kidney cancer risk
in central and eastern Europe
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE BMI; eastern Europe; hypertension; kidney cancer; smoking
ID RENAL-CELL CARCINOMA; ANTIHYPERTENSIVE MEDICATION; OBESITY; MEN; HEIGHT
AB In a case-control study of kidney cancer in four central European countries, with 1097 incident cases and 1476 controls, we found an increased risk for self-reported hypertension and for obesity. Additional unknown risk factors are likely to be responsible for the high rates of kidney cancer in this region.
C1 [Brennan, P.; van der Hel, O.; Boffetta, P.] IARC, Lyon, France.
[Moore, L. E.; Rothman, N.; Chow, W-H] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Zaridze, D.] Russian Acad Med Sci, Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia.
[Matveev, V.] NN Blokhin Canc Res Ctr, Dept Urol, Moscow, Russia.
[Holcatova, I.] Charles Univ Prague, Fac Med 1, Prague, Czech Republic.
[Janout, V.; Kollarova, H.] Palacky Univ, Fac Med, Dept Prevent Med, CR-77147 Olomouc, Czech Republic.
[Foretova, L.] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Szeszenia-Dabrowska, N.] Inst Occupat Med, Dept Epidemiol, Lodz, Poland.
[Mates, D.] Inst Publ Hlth, Bucharest, Romania.
RP Brennan, P (reprint author), IARC, Lyon, France.
EM brennan@iarc.fr
RI Zaridze, David/K-5605-2013; Janout, Vladimir/M-5133-2014;
Szeszenia-Dabrowska, Neonila/F-7190-2010;
OI mates, dana/0000-0002-6219-9807
FU Intramural Research Program of the NIH; National Cancer Institute;
Division of Cancer Epidemiology and Genetics
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Division of Cancer Epidemiology
and Genetics.
NR 16
TC 26
Z9 27
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 25
PY 2008
VL 99
IS 11
BP 1912
EP 1915
DI 10.1038/sj.bjc.6604761
PG 4
WC Oncology
SC Oncology
GA 376WP
UT WOS:000261214000021
PM 19034282
ER
PT J
AU Hosgood, HD
Chapman, R
Shen, M
Blair, A
Chen, E
Zheng, T
Lee, KM
He, X
Lan, Q
AF Hosgood, H. D., III
Chapman, R.
Shen, M.
Blair, A.
Chen, E.
Zheng, T.
Lee, K-M
He, X.
Lan, Q.
TI Portable stove use is associated with lower lung cancer mortality risk
in lifetime smoky coal users
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE lung cancer; stove; mortality; fuel; home
ID INDOOR AIR-POLLUTION; XUAN-WEI; CHINA; EXPOSURE; IMPROVEMENT
AB Domestic fuel combustion from cooking and heating, to which about 3 billion people worldwide are exposed, is associated with increased lung cancer risk. Lung cancer incidence in Xuanwei is the highest in China, and the attributable risk of lung cancer from unvented smoky coal burning is greater than 90%. To evaluate any lung cancer mortality reduction after changing from unvented stoves to portable stoves, we used lifetime smoky coal users in a retrospective cohort of all farmers born during 1917-1951 and residing in Xuanwei in 1976. Of the 42 422 enrolled farmers, 4054 lifetime smoky coal users changed to portable stoves, 4364 did not change, and 1074 died of lung cancer. Lung cancer morality associated with stove change was assessed by product-limit survival curves and multivariate Cox regression models. Both men (P < 0.0001) and women (P < 0.0001) who changed to portable stoves had a significantly increased probability of survival compared with those who did not change. Portable stoves were associated with decreased risk of lung cancer mortality in male participants (hazard ratio (HR) 0.62, 95% confidence interval (CI) 0.46-0.82) and female participants (HR 0.41, 95% CI 0.29-0.57). Portable stove use is associated with reduced lung cancer mortality risk, highlighting a cost-effective intervention that could substantially benefit health in developing countries.
C1 [Hosgood, H. D., III] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH,Occupat & Environm Epidemiol Branch, Bethesda, MD 20892 USA.
[Hosgood, H. D., III; Zheng, T.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Chapman, R.] Chulalongkorn Univ, Coll Publ Hlth Sci, Bangkok, Thailand.
[Chen, E.] Concordia Univ, Dept Math & Stat, Montreal, PQ, Canada.
[He, X.] Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China.
RP Hosgood, HD (reprint author), NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH,Occupat & Environm Epidemiol Branch, 6120 Execut Blvd,EPS 8118,MCS 7240, Bethesda, MD 20892 USA.
EM hosgoodd@mail.nih.gov
FU US National Cancer Institute (NCI); US Environmental Protection Agency
[5D2290NFFX]; Yale University - NCI Partnership Fellowship Training
Program [NCI TU2 CA105666]; Chinese Academy of Preventive Medicine
FX We had full access to all of the study data and have contributed to,
seen, and approved the final version of the manuscript. XH, QL, and RSC
designed this study, managed data collection, and participated in data
processing. HDH participated in data processing, conducted most of the
analyses, and was primarily responsible for writing the paper. The
analysis incorporated suggestions by RC, MS, KL, EC, TZ, AB, and QL.
This study was supported in part by the intramural research programme of
the US National Cancer Institute (NCI), the US Environmental Protection
Agency (5D2290NFFX), the Yale University - NCI Partnership Fellowship
Training Program (NCI TU2 CA105666), and the Chinese Academy of
Preventive Medicine.
NR 22
TC 27
Z9 27
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 25
PY 2008
VL 99
IS 11
BP 1934
EP 1939
DI 10.1038/sj.bjc.6604744
PG 6
WC Oncology
SC Oncology
GA 376WP
UT WOS:000261214000025
PM 19034286
ER
PT J
AU Ostroumova, E
Preston, DL
Ron, E
Krestinina, L
Davis, FG
Kossenko, M
Akleyev, A
AF Ostroumova, E.
Preston, D. L.
Ron, E.
Krestinina, L.
Davis, F. G.
Kossenko, M.
Akleyev, A.
TI Breast cancer incidence following low-dose rate environmental exposure:
Techa River Cohort, 1956-2004
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE breast cancer; incidence; ionising radiation; low-dose rate exposure;
Techa River
ID FEMALE FLIGHT ATTENDANTS; ATOMIC-BOMB SURVIVORS; RECONSTRUCTION SYSTEM;
RADIATION-EXPOSURE; DOSIMETRY SYSTEM; POOLED ANALYSIS; RISK; USSR;
MORTALITY; INFANCY
AB In the 1950s, the Mayak nuclear weapons facility in Russia discharged liquid radioactive wastes into the Techa River causing exposure of riverside residents to protracted low-to-moderate doses of radiation. Almost 10 000 women received estimated doses to the stomach of up to 0.47 Gray (Gy) (mean dose = 0.04 Gy) from external gamma-exposure and (137)Cs incorporation. We have been following this population for cancer incidence and mortality and as in the general Russian population, we found a significant temporal trend of breast cancer incidence. A significant linear radiation dose-response relationship was observed (P = 0.01) with an estimated excess relative risk per Gray (ERR/Gy) of 5.00 (95% confidence interval (CI), 0.80, 12.76). We estimated that approximately 12% of the 109 observed cases could be attributed to radiation.
C1 [Ostroumova, E.; Krestinina, L.; Kossenko, M.; Akleyev, A.] Urals Res Ctr Radiat Med, Lab Epidemiol, Chelyabinsk 454076, Russia.
[Ostroumova, E.; Ron, E.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Preston, D. L.] Hirosoft Int Corp, Eureka, CA 95501 USA.
[Davis, F. G.] Univ Illinois, Sch Publ Hlth, Div Epidemiol & Biostat, Chicago, IL 60612 USA.
RP Ostroumova, E (reprint author), Urals Res Ctr Radiat Med, Lab Epidemiol, 68-A Vorovsky St, Chelyabinsk 454076, Russia.
EM zhenia@urcrm.chel.su
RI Akleyev, Alexander/Q-1891-2015
OI Akleyev, Alexander/0000-0003-2583-5808
FU Chelyabinsk Oblast Oncology Dispensary; Russian Ministry of Health;
Russian Federal Medical-Biological Agency; United States Department of
Energy [DE-FC0204EH04014]
FX As with any long-term large-scale projects, many people have made
important contributions to this study. We are grateful for the support
of the Chelyabinsk Oblast Oncology Dispensary. We acknowledge the
contributions of Nickolai Startsev, Marina Degteva, Catherine Zhidkova,
Daniel Hoffman and the late Terry Thomas. Financial support has been
provided by the Russian Ministry of Health, the Russian Federal
Medical-Biological Agency and the United States Department of Energy
(Contract DE-FC0204EH04014).
NR 36
TC 11
Z9 11
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 25
PY 2008
VL 99
IS 11
BP 1940
EP 1945
DI 10.1038/sj.bjc.6604775
PG 6
WC Oncology
SC Oncology
GA 376WP
UT WOS:000261214000026
PM 19002173
ER
PT J
AU Velagaleti, RS
Gona, P
Levy, D
Aragam, J
Larson, MG
Tofler, GH
Lieb, W
Wang, TJ
Benjamin, EJ
Vasan, RS
AF Velagaleti, Raghava S.
Gona, Philimon
Levy, Daniel
Aragam, Jayashri
Larson, Martin G.
Tofler, Geoffrey H.
Lieb, Wolfgang
Wang, Thomas J.
Benjamin, Emelia J.
Vasan, Ramachandran S.
TI Relations of Biomarkers Representing Distinct Biological Pathways to
Left Ventricular Geometry
SO CIRCULATION
LA English
DT Article
DE aldosterone; biological markers; echocardiography; hypertrophy;
remodeling; renin
ID C-REACTIVE PROTEIN; ANGIOTENSIN-ALDOSTERONE SYSTEM; CONVERTING
ENZYME-INHIBITOR; CORONARY HEART-DISEASE; TARGET ORGAN DAMAGE;
ESSENTIAL-HYPERTENSION; BLOOD-PRESSURE; METABOLIC SYNDROME; SERUM
ALDOSTERONE; RISK-FACTORS
AB Background-Several biological pathways are activated concomitantly during left ventricular (LV) remodeling. However, the relative contribution of circulating biomarkers representing these distinct pathways to LV geometry is unclear.
Methods and Results-We evaluated 2119 Framingham Offspring Study participants (mean age, 57 years; 57% women) who underwent measurements of biomarkers of inflammation (C-reactive protein), hemostasis (fibrinogen and plasminogen activator inhibitor-1), neurohormonal activation (B-type natriuretic peptide), and renin-angiotensin-aldosterone system (aldosterone and renin modeled as a ratio [ARR]) and echocardiography at a routine examination. LV geometry was defined on the basis of sex-specific distributions of LV mass (LVM) and relative wall thickness (RWT): normal (LVM and RWT <80th percentile), concentric remodeling (LVM <80th percentile but RWT >= 80th percentile), eccentric hypertrophy (LVM >= 80th percentile but RWT <80th percentile), and concentric hypertrophy (LVM and RWT >80th percentile). We related the biomarker panel to LV geometry using polytomous logistic regression adjusting for clinical covariates and used backwards elimination to identify a parsimonious set of biomarkers associated with LV geometry. Modeled individually, C-reactive protein, fibrinogen, plasminogen activator inhibitor-1, and ARR were related to LV geometry (P<0.01). In multivariable analyses, the biomarker panel was significantly related to altered LV geometry (P<0.0001). On backwards elimination, logARR alone was significantly and positively associated with eccentric (odds ratio per SD increment, 1.20; 95% confidence interval, 1.05 to 1.37) and concentric LV hypertrophy (odds ratio per SD increment, 1.29; 95% confidence interval, 1.06 to 1.58).
Conclusions-Our cross-sectional observations on a large community-based sample identified ARR as a key correlate of concentric and eccentric LV hypertrophy, consistent with a major role for the renin-angiotensin-aldosterone system in LV remodeling. (Circulation. 2008; 118: 2252-2258.)
C1 [Velagaleti, Raghava S.; Gona, Philimon; Levy, Daniel; Larson, Martin G.; Lieb, Wolfgang; Wang, Thomas J.; Benjamin, Emelia J.; Vasan, Ramachandran S.] Framingham Heart Dis Epidemiol Study, Newark, NJ 07102 USA.
[Aragam, Jayashri] Vet Adm Hosp, W Roxbury, MA USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, W Roxbury, MA USA.
[Gona, Philimon; Larson, Martin G.] Dept Math & Stat, W Roxbury, MA USA.
[Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Tofler, Geoffrey H.] Royal N Shore Hosp, Dept Cardiol, Sydney, NSW, Australia.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Dept Sch Publ Hlth, Sch Med & Epidemiol, Prevent Med Sect, Boston, MA 02215 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Dept Sch Publ Hlth, Sch Med & Epidemiol, Cardiol Sect, Boston, MA 02215 USA.
RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave, Newark, NJ 07102 USA.
EM vasan@bu.edu
RI Lieb, Wolfgang/C-1990-2012;
OI Larson, Martin/0000-0002-9631-1254; Ramachandran,
Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336
FU National Heart, Lung, and Blood Institute [N01-HC-25195]; National
Institutes of Health [RO1-HL086875, RO1 HL67288, IIL080124, K24-HL04334]
FX This work was supported by the National Heart, Lung, and Blood Institute
(contract N01-HC-25195) and National Institutes of Health grants
RO1-HL086875 (Dr Wang), RO1 HL67288, IIL080124, and K24-HL04334 (Dr
Vasan).
NR 48
TC 14
Z9 14
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2252
EP U161
DI 10.1161/CIRCULATIONAHA.108.817411
PG 12
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300006
ER
PT J
AU Davis, BR
Kostis, JB
Simpson, LM
Black, HR
Cushman, WC
Einhorn, PT
Farber, MA
Ford, CE
Levy, D
Massie, BM
Nawaz, S
AF Davis, Barry R.
Kostis, John B.
Simpson, Lara M.
Black, Henry R.
Cushman, William C.
Einhorn, Paula T.
Farber, Michael A.
Ford, Charles E.
Levy, Daniel
Massie, Barry M.
Nawaz, Shah
CA ALLHAT Collaborative Res Grp
TI Heart Failure With Preserved and Reduced Left Ventricular Ejection
Fraction in the Antihypertensive and Lipid-Lowering Treatment to Prevent
Heart Attack Trial
SO CIRCULATION
LA English
DT Article
DE angiotensin-converting enzyme inhibitors; antihypertensive agents;
calcium channel blockers; diuretics; heart failure; hypertension;
ventricular ejection fraction
ID SYSTOLIC FUNCTION; DIASTOLIC DYSFUNCTION; CARDIOVASCULAR HEALTH; OLMSTED
COUNTY; PREVALENCE; COMMUNITY; POPULATION; PROGNOSIS; ALLHAT; MECHANISMS
AB Background-Heart failure (HF) developing in hypertensive patients may occur with preserved or reduced left ventricular ejection fraction (PEF [>= 50%] or REF [<50%]). In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 42 418 high-risk hypertensive patients were randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin, providing an opportunity to compare these treatments with regard to occurrence of hospitalized HFPEF or HFREF.
Methods and Results-HF diagnostic criteria were prespecified in the ALLHAT protocol. EF estimated by contrast ventriculography, echocardiography, or radionuclide study was available in 910 of 1367 patients (66.6%) with hospitalized events meeting ALLHAT criteria. Cox regression models adjusted for baseline characteristics were used to examine treatment differences for HF (overall and by PEF and REF). HF case fatality rates were examined. Of those with EF data, 44.4% had HFPEF and 55.6% had HFREF. Chlorthalidone reduced the risk of HFPEF compared with amlodipine, lisinopril, or doxazosin; the hazard ratios were 0.69 (95% confidence interval [CI], 0.53 to 0.91; P=0.009), 0.74 (95% CI, 0.56 to 0.97; P=0.032), and 0.53 (95% CI, 0.38 to 0.73; P<0.001), respectively. Chlorthalidone reduced the risk of HFREF compared with amlodipine or doxazosin; the hazard ratios were 0.74 (95% CI, 0.59 to 0.94; P=0.013) and 0.61 (95% CI, 0.47 to 0.79; P<0.001), respectively. Chlorthalidone was similar to lisinopril with regard to incidence of HFREF (hazard ratio, 1.07; 95% CI, 0.82 to 1.40; P=0.596). After HF onset, death occurred in 29.2% of participants (chlorthalidone/amlodipine/lisinopril) with new-onset HFPEF versus 41.9% in those with HFREF (P<0.001; median follow-up, 1.74 years); and in the chlorthalidone/doxazosin comparison that was terminated early, 20.0% of HFPEF and 26.0% of HFREF patients died (P=0.185; median follow-up, 1.55 years).
Conclusions-In ALLHAT, with adjudicated outcomes, chlorthalidone significantly reduced the occurrence of new-onset hospitalized HFPEF and HFREF compared with amlodipine and doxazosin. Chlorthalidone also reduced the incidence of new-onset HFPEF compared with lisinopril. Among high-risk hypertensive men and women, HFPEF has a better prognosis than HFREF. (Circulation. 2008; 118: 2259-2267.)
C1 [Davis, Barry R.; Simpson, Lara M.; Ford, Charles E.] Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, Houston, TX 77030 USA.
[Kostis, John B.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
[Black, Henry R.] NYU, Sch Med, New York, NY USA.
[Cushman, William C.] Memphis Vet Affairs Med Ctr, Memphis, TN USA.
[Einhorn, Paula T.] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Farber, Michael A.] Crozer Keystone Hlth Network, Upland, PA USA.
[Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Massie, Barry M.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Davis, BR (reprint author), Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, 1200 Herman Pressler,Suite E801, Houston, TX 77030 USA.
EM barry.r.davis@uth.tmc.edu
FU National Heart, Lung, and Blood Institute, National Institutes of
Health, US Department of Health and Human Services Bethesda, Md
[N01-HC-35130]
FX This research was supported by Health and Human Services contract
N01-HC-35130 from the National Heart, Lung, and Blood Institute,
National Institutes of Health, US Department of Health and Human
Services, Bethesda, Md. The ALLHAT investigators acknowledge
contributions of study medications supplied by Pfizer Inc (amlodipine
and doxazosin), AstraZeneca (atenolol and lisinopril), and Bristol-Myers
Squibb (pravastatin) and financial support provided by Pfizer Inc.
NR 45
TC 73
Z9 77
U1 2
U2 31
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2259
EP 2267
DI 10.1161/CIRCULATIONAHA.107.762229
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300007
PM 19001024
ER
PT J
AU Sun, YG
Tao, YG
Kagan, BL
He, YZ
Simons, SS
AF Sun, Yunguang
Tao, Yong-guang
Kagan, Benjamin L.
He, Yuangzheng
Simons, S. Stoney, Jr.
TI Modulation of transcription parameters in glucocorticoid
receptor-mediated repression
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Article
DE Glucocorticoid receptor; Gene repression; Coactivator and corepressor;
STAMP and Ubc9; Deacylcortivazol; Dose-response curve
ID LIGAND-BINDING DOMAIN; NUCLEAR HORMONE-RECEPTORS; DOSE-RESPONSE CURVE;
GENE-EXPRESSION; INDUCTION PROPERTIES; ESTROGEN-RECEPTOR; DEXAMETHASONE
21-MESYLATE; REGULATORY MECHANISMS; ANTAGONIST COMPLEXES; COREPRESSOR
BINDING
AB Glucocorticoid receptors (GRs) affect both gene induction and gene repression. The disparities of receptor binding to DNA and increased vs. decreased gene expression have suggested significant mechanistic differences between GR-mediated induction and repression. Numerous transcription factors are known to modulate three parameters of gene induction: the total activity (V(max)) and position of the dose-response curve with glucocorticoids (EC(50)) and the percent partial agonist activity with antiglucocorticoids. We have examined the effects on GR-mediated repression of five modulators (coactivators TIF2 [GRIP1, SRC-2] and SRC-1, corepressor SMRT, and comodulators STAMP and Ubc9), a glucocorticoid steroid (deacylcortivazol [DAC]) of very different structure, and an inhibitor of histone deacetylation (trichostatin A [TSA]). These factors interact with different domains of GR and thus are sensitive topological probes of GR action. These agents altered the V(max) EC(50), and percent partial agonist activity of endogenous and exogenous repressed genes similarly to that previously observed for GR-regulated gene induction. Collectively, these results suggest that GR-mediated induction and repression share many of the same molecular interactions and that the causes for different levels of gene transcription arise from more distal downstream steps. Published by Elsevier Ireland Ltd.
C1 [Sun, Yunguang; Tao, Yong-guang; Kagan, Benjamin L.; He, Yuangzheng; Simons, S. Stoney, Jr.] NIDDK, CEB, NIH, Steroid Hormones Sect, Bethesda, MD 20892 USA.
RP Simons, SS (reprint author), NIDDK, CEB, NIH, Steroid Hormones Sect, Bldg 10,Room 8N-307B, Bethesda, MD 20892 USA.
EM steroids@helix.nih.gov
FU Intramural Research Program of NIDDK; NIH
FX We thank Carson Chow (NIDDK, NIH) for assistance with the statistical
analysis, Ron Evans, Hinrich Gronerneyer, Sergio Onate, Inez Rogatsky,
Michael Rosenfeld, and Michael Stallcup for generously donating
reagents, and Jon Ashwell (NCI, NIH) and E. Brad Thompson for critical
review of the paper. This research was supported by the Intramural
Research Program of NIDDK, NIH.
NR 87
TC 19
Z9 19
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD NOV 25
PY 2008
VL 295
IS 1-2
BP 59
EP 69
DI 10.1016/j.mce.2008.05.008
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 377CM
UT WOS:000261229300008
PM 18583028
ER
PT J
AU Benjamin, LR
Chung, HJ
Sanford, S
Kouzine, F
Liu, JH
Levens, D
AF Benjamin, Lawrence R.
Chung, Hye-Jung
Sanford, Suzanne
Kouzine, Fedor
Liu, Juhong
Levens, David
TI Hierarchical mechanisms build the DNA-binding specificity of FUSE
binding protein
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE DNA conformation; KH-domain; ssDNA sequence specificity
ID STRANDED TELOMERIC DNA; C-MYC EXPRESSION; IN-VIVO; TORSIONAL STRESS;
GENE-EXPRESSION; UPSTREAM DNA; KH DOMAINS; SEQUENCE; FBP; RECOGNITION
AB The far upstream element (FUSE) binding protein (FBP), a single-stranded nucleic acid binding protein, is recruited to the c-myc promoter after melting of FUSE by transcriptionally generated dynamic supercoils. Via interactions with TFIIH and FBP-interacting repressor (FIR), FBP modulates c-myc transcription. Here, we investigate the contributions of FBP's 4 K Homology (KH) domains to sequence selectivity. EMSA and missing contact point analysis revealed that FBP contacts 4 separate patches spanning a large segment of FUSE. A SELEX procedure using paired KH-domains defined the preferred subsequences for each KH domain. Unexpectedly, there was also a strong selection for the noncontacted residues between these subsequences, showing that the contact points must be optimally presented in a backbone that minimizes secondary structure. Strategic mutation of contact points defined in this study disabled FUSE activity in vivo. Because the biological specificity of FBP is tuned at several layers: (i) accessibility of the site; (ii) supercoil-driven melting; (iii) presentation of unhindered bases for recognition; and (iv) modular interaction of KH-domains with cognate bases, the FBP-FIR system and sequence-specific, single-strand DNA binding proteins in general are likely to prove versatile tools for adjusting gene expression.
C1 [Benjamin, Lawrence R.; Chung, Hye-Jung; Sanford, Suzanne; Kouzine, Fedor; Liu, Juhong; Levens, David] NCI, Gene Regulat Sect, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Levens, D (reprint author), NCI, Gene Regulat Sect, Pathol Lab, Ctr Canc Res, Bldg 10,Room 2N106, Bethesda, MD 20892 USA.
EM levens@helix.nih.gov
RI Levens, David/C-9216-2009
OI Levens, David/0000-0002-7616-922X
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute, Center for Cancer Research
FX We thank the Levens Laboratory, in particular Z. Nie for assistance; G.
Stormo for discussions of secondary structure minimization in T-rich
DNA; M. Clore for helpful discussions of protein-DNA flexibility; and B.
Lewis, D. Singer and K. Zhao for critical comments. This work was
supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Center for Cancer Research.
NR 28
TC 20
Z9 22
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18296
EP 18301
DI 10.1073/pnas.0803279105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300048
PM 19015535
ER
PT J
AU Cellmer, T
Henry, ER
Hofrichter, J
Eaton, WA
AF Cellmer, Troy
Henry, Eric R.
Hofrichter, James
Eaton, William A.
TI Measuring internal friction of an ultrafast-folding protein
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE funneled energy landscape; Ising-like model; Kramers; polypeptide;
viscosity
ID BETA-HAIRPIN FORMATION; SOLVENT VISCOSITY; TRANSITION-STATE; DIFFUSIONAL
BARRIER; CHEMICAL-REACTIONS; ENERGY LANDSCAPE; COIL KINETICS; DYNAMICS;
MODEL; FUNNELS
AB Nanosecond laser T-jump was used to measure the viscosity dependence of the folding kinetics of the villin subdomain under conditions where the viscogen has no effect on its equilibrium properties. The dependence of the unfolding/refolding relaxation time on solvent viscosity indicates a major contribution to the dynamics from internal friction. The internal friction increases with increasing temperature, suggesting a shift in the transition state along the reaction coordinate toward the native state with more compact structures, and therefore, a smaller diffusion coefficient due to increased landscape roughness. Fitting the data with an Ising-like model yields a relatively small position dependence for the diffusion coefficient. This finding is consistent with the excellent correlation found between experimental and calculated folding rates based on free energy barrier heights using the same diffusion coefficient for every protein.
C1 [Cellmer, Troy; Henry, Eric R.; Hofrichter, James; Eaton, William A.] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Eaton, WA (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 2, Bethesda, MD 20892 USA.
EM eaton@helix.nih.gov
RI Henry, Eric/J-3414-2013
OI Henry, Eric/0000-0002-5648-8696
FU NIDDK, National Institutes of Health.
FX We thank Wai-Ming Yau for peptide synthesis and Robert Best, Gerhard
Hummer, and Attila Szabo for helpful discussion. This work was supported
by the intramural Research Program of NIDDK, National Institutes of
Health.
NR 49
TC 91
Z9 91
U1 1
U2 18
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18320
EP 18325
DI 10.1073/pnas.0806154105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300052
PM 19020085
ER
PT J
AU Paravastu, AK
Leapman, RD
Yau, WM
Tycko, R
AF Paravastu, Anant K.
Leapman, Richard D.
Yau, Wai-Ming
Tycko, Robert
TI Molecular structural basis for polymorphism in Alzheimer's beta-amyloid
fibrils
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Alzheimer's disease; electron microscopy; solid state NMR; amyloid
structure; protein misfolding
ID NUCLEAR-MAGNETIC-RESONANCE; SOLID-STATE NMR; PRION PROTEIN; DISTANCE
MEASUREMENTS; POLAR ZIPPERS; FULL-LENGTH; CONFORMATION; CONSTRAINTS;
RESIDUES; PEPTIDE
AB We describe a full structural model for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease (A beta(1-40)), based on numerous constraints from solid state NMR and electron microscopy. This model applies specifically to fibrils with a periodically twisted morphology, with twist period equal to 120 +/- 20 nm (defined as the distance between apparent minima in fibril width in negatively stained transmission electron microscope images). The structure has threefold symmetry about the fibril growth axis, implied by mass-per-length data and the observation of a single set of (13)C NMR signals. Comparison with a previously reported model for A beta(1-40) fibrils with a qualitatively different, striated ribbon morphology reveals the molecular basis for polymorphism. At the molecular level, the 2 A beta(1-40) fibril morphologies differ in overall symmetry (twofold vs. threefold), the conformation of non-beta-strand segments, and certain quaternary contacts. Both morphologies contain in-register parallel beta-sheets, constructed from nearly the same beta-strand segments. Because twisted and striated ribbon morphologies are also observed for amyloid fibrils formed by other polypeptides, such as the amylin peptide associated with type 2 diabetes, these structural variations may have general implications.
C1 [Paravastu, Anant K.; Yau, Wai-Ming; Tycko, Robert] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Leapman, Richard D.] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA.
RP Tycko, R (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 2, Bethesda, MD 20892 USA.
EM robertty@mail.nih.gov
FU Intramural Research Programs of the National Institute of Diabetes and
Digestive and Kidney Diseases; National Institute of Biomedical Imaging
and Bioengineering
FX We thank Dr. Sorin Luca for assistance with molecular modeling. This
work was supported by the Intramural Research Programs of the National
Institute of Diabetes and Digestive and Kidney Diseases and the National
Institute of Biomedical Imaging and Bioengineering.
NR 41
TC 495
Z9 502
U1 12
U2 137
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18349
EP 18354
DI 10.1073/pnas.0806270105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300057
PM 19015532
ER
PT J
AU Dabdoub, A
Puligilla, C
Jones, JM
Fritzsch, B
Cheah, KSE
Pevny, LH
Kelley, MW
AF Dabdoub, Alain
Puligilla, Chandrakala
Jones, Jennifer M.
Fritzsch, Bernd
Cheah, Kathryn S. E.
Pevny, Larysa H.
Kelley, Matthew W.
TI Sox2 signaling in prosensory domain specification and subsequent hair
cell differentiation in the developing cochlea
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE development; organ of Corti; inner ear; HMG box; bHLH
ID INNER-EAR DEVELOPMENT; MAMMALIAN COCHLEA; WNT; EXPRESSION; ROLES; ORGAN;
MATH1; MORPHOGENESIS; ACTIVATION; GENERATION
AB Sox2 is a high-mobility transcription factor that is one of the earliest markers of developing inner ear prosensory domains. In humans, mutations in SOX2 cause sensorineural hearing loss and a loss of function study in mice showed that Sox2 is required for prosensory formation in the cochlea. However, the specific roles of Sox2 have not been determined. Here we illustrate a dynamic role of Sox2 as an early permissive factor in prosensory domain formation followed by a mutually antagonistic relationship with Atoh1, a bHLH protein necessary for hair cell development. We demonstrate that decreased levels of Sox2 result in precocious hair cell differentiation and an over production of inner hair cells and that these effects are likely mediated through an antagonistic interaction between Sox2 and the bHLH molecule Atoh1. Using gain- and loss-of-function experiments we provide evidence for the molecular pathway responsible for the formation of the cochlear prosensory domain. Sox2 expression is promoted by Notch signaling and Prox1, a homeobox transcription factor, is a downstream target of Sox2. These results demonstrate crucial and diverse roles for Sox2 in the development, specification, and maintenance of sensory cells within the cochlea.
C1 [Dabdoub, Alain; Puligilla, Chandrakala; Jones, Jennifer M.; Kelley, Matthew W.] NIDCD, Sect Dev Neurosci, NIH, Bethesda, MD 20892 USA.
[Fritzsch, Bernd] Univ Iowa, Dept Biol Sci, Iowa City, IA 52242 USA.
[Cheah, Kathryn S. E.] Univ Hong Kong, Dept Biochem, Hong Kong, Hong Kong, Peoples R China.
[Cheah, Kathryn S. E.] Univ Hong Kong, Ctr Reprod Dev & Growth, Hong Kong, Hong Kong, Peoples R China.
[Pevny, Larysa H.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
RP Dabdoub, A (reprint author), NIDCD, Sect Dev Neurosci, NIH, Bethesda, MD 20892 USA.
EM adabdoub@ucsd.edu; puligillac@nidcd.nih.gov
OI Fritzsch, Bernd/0000-0002-4882-8398
FU Council of Hong Kong [HKU7385/02M]; National Institutes of Health [R01
DC005590, R01 EYO1861]; National Institute on Deafness and Other
Communication Disorders intramural program
FX We thank Drs. A. Kiernan, A. Felling, and T. Friedman for reading the
manuscript and C. Woods, CW. Kramer, T. Dennison, and Dr. EC Driver for
technical assistance. K.S.E.C. was supported by the Research Grants
Council of Hong Kong HKU7385/02M, B.F. by National Institutes of Health
Grant R01 DC005590, L.H.P. by National Institutes of Health Grant R01
EYO1861. This work was supported by the National Institute on Deafness
and Other Communication Disorders intramural program.
NR 26
TC 163
Z9 170
U1 1
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18396
EP 18401
DI 10.1073/pnas.0808175105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300065
PM 19011097
ER
PT J
AU Bonini, MG
Stadler, K
Fernandes, DC
Tanaka, LY
Laurindo, FRM
Mason, RP
AF Bonini, Marcelo G.
Stadler, Krisztian
Fernandes, Denise C.
Tanaka, Leonardo Y.
Laurindo, Francisco R. M.
Mason, Ronald P.
TI Reply to Daiber et al.: "Doubt about an essential role for constitutive
nitric oxide synthase in nitroglycerin-mediated vasodilation"
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Letter
ID HEART-FAILURE
C1 [Bonini, Marcelo G.; Stadler, Krisztian; Fernandes, Denise C.; Tanaka, Leonardo Y.; Laurindo, Francisco R. M.; Mason, Ronald P.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Bonini, MG (reprint author), NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM bonini@niehs.nih.gov
RI Laurindo, Francisco/J-6575-2015
NR 7
TC 0
Z9 0
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP E93
EP E93
DI 10.1073/pnas.0809563105
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300006
ER
PT J
AU Jeang, KT
AF Jeang, Kuan-Teh
TI H-index, mentoring-index, highly-cited and highly-accessed: how to
evaluate scientists?
SO RETROVIROLOGY
LA English
DT Editorial Material
ID IMPACT FACTOR; RETROVIRUSES
AB How best to evaluate scientists within a peer group is a difficult task. This editorial discusses the use of the H-index and total citations. It also raises the consideration of a mentoring-index and the value of understanding the frequency that a published paper is accessed by readers.
C1 NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM kjeang@niaid.nih.gov
RI Jeang, Kuan-Teh/A-2424-2008
FU Intramural NIH HHS
NR 12
TC 20
Z9 21
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 25
PY 2008
VL 5
AR 106
DI 10.1186/1742-4690-5-106
PG 5
WC Virology
SC Virology
GA 389SX
UT WOS:000262115900001
PM 19032780
ER
PT J
AU Martin, JE
Louder, MK
Holman, LA
Gordon, IJ
Enama, ME
Larkin, BD
Andrews, CA
Vogel, L
Koup, RA
Roederer, M
Bailer, RT
Gomez, PL
Nason, M
Mascola, JR
Nabel, GJ
Graham, BS
AF Martin, Julie E.
Louder, Mark K.
Holman, LaSonji A.
Gordon, Ingelise J.
Enama, Mary E.
Larkin, Brenda D.
Andrews, Charla A.
Vogel, Leatrice
Koup, Richard A.
Roederer, Mario
Bailer, Robert T.
Gomez, Phillip L.
Nason, Martha
Mascola, John R.
Nabel, Gary J.
Graham, Barney S.
CA VRC Study Team
TI A SARS DNA vaccine induces neutralizing antibody and cellular immune
responses in healthy adults in a Phase I clinical trial
SO VACCINE
LA English
DT Article
DE T-cell vaccine; Emerging infectious disease; Vaccine clinical trial
ID ACUTE RESPIRATORY SYNDROME; SYNDROME CORONAVIRUS; PROTECTIVE IMMUNITY;
SPIKE GLYCOPROTEIN; CANDIDATE VACCINE; PROTEIN; IMMUNOGENICITY; VIRUS;
MICE; REPLICATION
AB Background: The severe acute respiratory syndrome (SARS) virus is a member of the Coronaviridae (CoV) family that first appeared in the Guangdong Province of China in 2002 and was recognized as an emerging infectious disease in March 2003. Over 8000 cases and 900 deaths occurred during the epidemic. We report the safety and immunogenicity of a SARS DNA vaccine in a Phase I human study.
Methods: A single-plasmid DNA vaccine encoding the Spike (S) glycoprotein was evaluated in 10 healthy adults. Nine subjects completed the 3 dose vaccination schedule and were evaluated for vaccine safety and immune responses. Immune response was assessed by intracellular cytokine staining (ICS), ELIspot, ELISA, and neutralization assays.
Results: The vaccine was well tolerated. SARS-CoV-specific antibody was detected by ELISA in 8 of 10 subjects and neutralizing antibody way detected in all subjects who received 3 doses of vaccine. SARS-CoV-specific CD4+ T-cell responses were detected in all vaccinees, and CD8+ T-cell responses in similar to 20% of individuals.
Conclusions: The VRC SARS DNA vaccine was well tolerated and produced cellular immune responses and neutralizing antibody in healthy adults. (c) Published by Elsevier Ltd.
C1 [Martin, Julie E.; Louder, Mark K.; Holman, LaSonji A.; Gordon, Ingelise J.; Enama, Mary E.; Larkin, Brenda D.; Andrews, Charla A.; Koup, Richard A.; Roederer, Mario; Bailer, Robert T.; Gomez, Phillip L.; Nason, Martha; Mascola, John R.; Nabel, Gary J.; Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Vogel, Leatrice] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Graham, BS (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr,MSC-2610, Bethesda, MD 20892 USA.
EM bgraham@mail.nih.gov
FU National Institute of Allergy and Infectious Diseases Intramural
Research Program
FX The work was funded by the National Institute of Allergy and Infectious
Diseases Intramural Research Program.
NR 28
TC 43
Z9 44
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 25
PY 2008
VL 26
IS 50
BP 6338
EP 6343
DI 10.1016/j.vaccine.2008.09.026
PG 6
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 385OE
UT WOS:000261822700008
PM 18824060
ER
PT J
AU Mitzel, DN
Best, SM
Masnick, MF
Porcella, SF
Wolfinbarger, JB
Bloom, ME
AF Mitzel, Dana N.
Best, Sonja M.
Masnick, Max F.
Porcella, Stephen F.
Wolfinbarger, James B.
Bloom, Marshall E.
TI Identification of genetic determinants of a tick-borne flavivirus
associated with host-specific adaptation and pathogenicity
SO VIROLOGY
LA English
DT Article
DE Tick-borne flavivirus; Langat virus; Genetic correlates; Replication;
Neuroinvasiveness; Attenuation
ID WEST-NILE-VIRUS; AMINO-ACID SUBSTITUTION; HUMAN LIVER-CELLS;
ENCEPHALITIS-VIRUS; DENGUE VIRUS; JAPANESE ENCEPHALITIS;
IXODES-SCAPULARIS; NONSTRUCTURAL PROTEINS; IMMUNODEFICIENT MICE;
ENVELOPE PROTEIN
AB Tick-borne flaviviruses are maintained in nature in an enzootic cycle involving a tick vector and a vertebrate host. Thus, the virus replicates in two disparate hosts, each providing selective pressures that can influence virus replication and pathogenicity. To identify Viral determinants associated with replication in the individual hosts, plaque purified Langat virus (TP21pp) was adapted to growth in mouse or tick cell lines to generate two virus variants, MNBp20 and ISEp20, respectively. Virus adaptation to mouse cells resulted in four amino acid changes in MNBp20 relative to TP21pp, occurring in E, NS4A and NS4B. A comparison between TP21pp and ISEp20 revealed three amino acid modifications in M, NS3 and NS4A of ISEp20. ISEp20, but not MNBp20, was attenuated following intraperitoneal inoculation of mice. Following isolation from mice brains, additional mutations reproducibly emerged in E and NS3 of ISEp20 that were possibly compensatory for the initial adaptation to tick cells. Thus, our data implicate a role for E, M, NS3, NS4A and NS4B in host adaptation and pathogenicity of tick-borne flaviviruses. Published by Elsevier Inc.
C1 [Mitzel, Dana N.; Best, Sonja M.; Masnick, Max F.; Wolfinbarger, James B.; Bloom, Marshall E.] NIAID, Virol Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Porcella, Stephen F.] NIAID, Genom Unit, Res Technol Sect, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA.
RP Bloom, ME (reprint author), NIAID, Virol Lab, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM dmitzel@niaid.nih.gov; mbloom@niaid.nih.gov
OI Masnick, Max/0000-0001-6299-6251
FU National Institutes of Health; National Institute of Allergy and
Infectious Diseases
FX The authors thank Kent Barbian, Stacy Ricklefs, Julia Marie and Kimmo
Virtaneva from the Genomics Unit Research Technologies Section for their
technical support and advice, Drs. John Portis, Shelly Robertson,
Kristin McNally, and Travis Taylor for the critical review of the
manuscript, and Gary Hettrick and Anita Mora for their graphical
expertise. This research was supported by the intramural research
program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases.
NR 46
TC 20
Z9 20
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 25
PY 2008
VL 381
IS 2
BP 268
EP 276
DI 10.1016/j.virol.2008.08.030
PG 9
WC Virology
SC Virology
GA 371OU
UT WOS:000260841500014
PM 18823640
ER
PT J
AU Yu, YY
Pinsky, PF
Caporaso, NE
Chatterjee, N
Baumgarten, M
Langenberg, P
Furuno, JP
Lan, Q
Engels, EA
AF Yu, Ying-Ying
Pinsky, Paul F.
Caporaso, Neil E.
Chatterjee, Nilanjan
Baumgarten, Mona
Langenberg, Patricia
Furuno, Jon P.
Lan, Qing
Engels, Eric A.
TI Lung Cancer Risk Following Detection of Pulmonary Scarring by Chest
Radiography in the Prostate, Lung, Colorectal, and Ovarian Cancer
Screening Trial
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID EPIDEMIOLOGIC EVIDENCE; UNITED-STATES; INFLAMMATION; SMOKING; DISEASE;
WOMEN
AB Background: Fibrotic scars are frequently found in proximity to lung cancer at the time of cancer diagnosis. However, the nature of the relationship between pulmonary scarring and lung cancer remains uncertain. Our objective was to test whether localized pulmonary scarring is associated with increased lung cancer risk.
Methods: Cohort analysis of data from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. We included 66 863 cancer-free trial participants aged 55 to 74 years, who received a baseline chest radiographic examination and were followed up subsequently for up to 12 years. We used proportional hazards models to estimate hazard ratios ( HRs) for lung cancer associated with scarring, adjusting for age, sex, race, and cigarette smoking, and in relation to laterality of scarring. The main outcome measure was incident lung cancer.
Results: Scarring was present on the baseline chest radiograph for 5041 subjects ( 7.5%). Scarring was associated with elevated lung cancer risk ( 809 lung cancer cases [ HR, 1.5; 95% confidence interval {CI}, 1.2-1.8]). This association was specific for cancer in the lung ipsilateral to the scar ( HR, 1.8; 95% CI, 1.4-2.4) and absent for contralateral cancer ( HR, 0.9; 95% CI, 0.7-1.2). Ipsilateral lung cancer risk was elevated throughout the follow-up period ( interval-specific HRs, 1.6, 2.0, 2.1, and 1.7 during 0.01-2.00, 2.01-4.00, 4.01-6.00, and 6.01-12.00 years after baseline chest radiography, respectively).
Conclusions: The relationship between pulmonary scarring and lung cancer was specific to the same lung and extended over time. These findings are consistent with the hypothesis that localized inflammatory processes associated with scarring promote the subsequent development of lung cancer.
C1 [Yu, Ying-Ying; Caporaso, Neil E.; Chatterjee, Nilanjan; Lan, Qing; Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20892 USA.
[Yu, Ying-Ying; Caporaso, Neil E.; Chatterjee, Nilanjan; Lan, Qing; Engels, Eric A.] NCI, Canc Prevent Div, NIH, Rockville, MD 20892 USA.
[Yu, Ying-Ying; Baumgarten, Mona; Langenberg, Patricia; Furuno, Jon P.] Univ Maryland, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
RP Engels, EA (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 7076, Rockville, MD 20892 USA.
EM engelse@exchange.nih.gov
FU National Cancer Institute Intramural Research Program
FX Funding/Support: This work was supported by the National Cancer
Institute Intramural Research Program.
NR 25
TC 28
Z9 29
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD NOV 24
PY 2008
VL 168
IS 21
BP 2326
EP 2332
DI 10.1001/archinte.168.21.2326
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 375ZG
UT WOS:000261151700006
PM 19029496
ER
PT J
AU Liu, AZ
Wang, JF
Lu, ZW
Yao, LS
Li, Y
Yan, HG
AF Liu, Aizhuo
Wang, Jifeng
Lu, Zhenwei
Yao, Lishan
Li, Yue
Yan, Honggao
TI Hydrogen-Bond Detection, Configuration Assignment and Rotamer Correction
of Side-Chain Amides in Large Proteins by NMR Spectroscopy through
Protium/Deuterium Isotope Effects
SO CHEMBIOCHEM
LA English
DT Article
DE configuration determination; hydrogen bonds; isotope effects; NMR
spectroscopy; rotamer assignment
ID YEAST CYTOSINE DEAMINASE; L-ASPARAGINE MONOHYDRATE; C-13
CHEMICAL-SHIFTS; MOLECULAR-DYNAMICS; NEUTRON-DIFFRACTION; DIPOLAR
COUPLINGS; CRYSTAL-STRUCTURE; ATOM CONTACTS; NQ-FLIPPER; GLUTAMINE
AB The configuration and hydrogen-bonding network of side-chain amides in a 35 kDa protein were determined by measuring differential and trans-hydrogen-bond HID isotope effects by using the isotopomer-selective (IS)-TROSY technique, which leads to a reliable recognition and correction of erroneous rotamers that are frequently found in protein structures. First, the differential two-bond isotope effects on carbonyl (13)C' shifts, which are defined as Delta(2)Delta(13)C'(ND) = (2)Delta(13)C'(ND(E))-(2)Delta(13)C'(ND(Z)), provide a reliable means for the configuration assignment for side-chain amides, because environmental effects (hydrogen bonds and charges, etc.) are greatly attenuated over the two bonds that separate the carbon and hydrogen atoms, and the isotope effects fall into a narrow range of positive values. Second and more importantly, the significant variations in the differential one-bond isotope effects on (15)N chemical shifts, which are defined as Delta(1)Delta(15)N(D) = (1)Delta(15)N(D(E))-(1)Delta(15)N(D(Z)) can be correlated with hydrogen-bonding interactions, particularly those involving charged acceptors. The differential one-bond isotope effects are additive, with major contributions from intrinsic differential conjugative interactions between the E and Z configurations, H-bonding interactions, and charge effects. Furthermore, the pattern of trans-H-bond HID isotope effects con be mapped onto more complicated hydrogen-bonding networks that involve bifurcated hydrogen-bonds. Third, the correlations between Delta(1)Delta(15)N(D) and hydrogen-bonding interactions afford an effective means for the correction of erroneous rotamer assignments of side-chain amides. Rotamer correction by differential isotope effects is not only robust, but also simple and can be applied to large proteins.
C1 [Liu, Aizhuo; Wang, Jifeng; Lu, Zhenwei; Yao, Lishan; Li, Yue; Yan, Honggao] Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA.
[Yao, Lishan] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Liu, AZ (reprint author), Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA.
EM liua@msu.edu; yanh@msu.edu
RI Yao, Lishan /C-6961-2009; yao, lishan/H-3662-2012; lu,
zhenwei/L-6630-2014
OI yao, lishan/0000-0003-1797-922X; lu, zhenwei/0000-0001-9614-3038
FU NIGMS NIH HHS [GM58221, R01 GM058221, R01 GM058221-05A1]
NR 48
TC 9
Z9 9
U1 0
U2 10
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 1439-4227
J9 CHEMBIOCHEM
JI ChemBioChem
PD NOV 24
PY 2008
VL 9
IS 17
BP 2860
EP 2871
DI 10.1002/cbic.200800467
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 380RP
UT WOS:000261483200018
PM 18973166
ER
PT J
AU Jones, RB
Ndhlovu, LC
Barbour, JD
Sheth, PM
Jha, AR
Long, BR
Wong, JC
Satkunarajah, M
Schweneker, M
Chapman, JM
Gyenes, G
Vali, B
Hyrcza, MD
Yue, FY
Kovacs, C
Sassi, A
Loutfy, M
Halpenny, R
Persad, D
Spotts, G
Hecht, FM
Chun, TW
McCune, JM
Kaul, R
Rini, JM
Nixon, DF
Ostrowski, MA
AF Jones, R. Brad
Ndhlovu, Lishomwa C.
Barbour, Jason D.
Sheth, Prameet M.
Jha, Aashish R.
Long, Brian R.
Wong, Jessica C.
Satkunarajah, Malathy
Schweneker, Marc
Chapman, Joan M.
Gyenes, Gabor
Vali, Bahareh
Hyrcza, Martin D.
Yue, Feng Yun
Kovacs, Colin
Sassi, Aref
Loutfy, Mona
Halpenny, Roberta
Persad, Desmond
Spotts, Gerald
Hecht, Frederick M.
Chun, Tae-Wook
McCune, Joseph M.
Kaul, Rupert
Rini, James M.
Nixon, Douglas F.
Ostrowski, Mario A.
TI Tim-3 expression defines a novel population of dysfunctional T cells
with highly elevated frequencies in progressive HIV-1 infection
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS-INFECTION; CHRONIC VIRAL-INFECTION; DISEASE
PROGRESSION; MULTIPLE-SCLEROSIS; SKEWED MATURATION; IMPAIRED FUNCTION;
LYMPHOCYTES; CD4(+); ACTIVATION; ANTIGEN
AB Progressive loss of T cell functionality is a hallmark of chronic infection with human immunodeficiency virus 1 (HIV-1). We have identified a novel population of dysfunctional T cells marked by surface expression of the glycoprotein Tim-3. The frequency of this population was increased in HIV-1-infected individuals to a mean of 49.4 +/- SD 12.9% of CD8(+) T cells expressing Tim-3 in HIV-1-infected chronic progressors versus 28.5 +/- 6.8% in HIV-1-uninfected individuals. Levels of Tim-3 expression on T cells from HIV-1-infected inviduals correlated positively with HIV-1 viral load and CD38 expression and inversely with CD4(+) T cell count. In progressive HIV-1 infection, Tim-3 expression was up-regulated on HIV-1 specific CD8(+) T cells. Tim-3-expressing T cells failed to produce cytokine or proliferate in response to antigen and exhibited impaired Stat5, Erk1/2, and p38 signaling. Blocking the Tim-3 signaling pathway restored proliferation and enhanced cytokine production in HIV-1-specifi c T cells. Thus, Tim-3 represents a novel target for the therapeutic reversal of HIV-1-associated T cell dysfunction.
C1 [Jones, R. Brad; Wong, Jessica C.; Gyenes, Gabor; Yue, Feng Yun; Ostrowski, Mario A.] Univ Toronto, Dept Immunol, Toronto, ON M5S 1A8, Canada.
[Sheth, Prameet M.; Vali, Bahareh; Hyrcza, Martin D.; Kaul, Rupert; Ostrowski, Mario A.] Univ Toronto, Div Clin Sci, Toronto, ON M5S 1A8, Canada.
[Satkunarajah, Malathy; Rini, James M.] Univ Toronto, Dept Biochem, Toronto, ON M5S 1A8, Canada.
[Kovacs, Colin] Univ Toronto, Dept Med, Toronto, ON M5S 1A8, Canada.
[Ndhlovu, Lishomwa C.; Jha, Aashish R.; Long, Brian R.; Schweneker, Marc; Chapman, Joan M.; McCune, Joseph M.; Nixon, Douglas F.] Univ Calif San Francisco, Div Expt Med, San Francisco, CA 94110 USA.
[Barbour, Jason D.; Spotts, Gerald; Hecht, Frederick M.] Univ Calif San Francisco, Div HIV AIDS, Dept Med, San Francisco Gen Hosp, San Francisco, CA 94110 USA.
[Loutfy, Mona; Halpenny, Roberta] Canadian Immunodeficiency Res Collaborat, Toronto, ON M5B 1L6, Canada.
[Sassi, Aref; Persad, Desmond] Maple Leaf Med Clin, Toronto, ON M5B 1L6, Canada.
[Chun, Tae-Wook] NIAID, NIH, Bethesda, MD 20892 USA.
[Ostrowski, Mario A.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
RP Jones, RB (reprint author), Univ Toronto, Dept Immunol, 100 Coll St, Toronto, ON M5S 1A8, Canada.
EM brad.jones@utoronto.ca; mario.ostrowski@gmail.com
OI Nixon, Douglas/0000-0002-2801-1786
FU Canadian Institutes for Health Research (CIHR); UCSF Gladstone Institute
of Virology & Immunology Center for AIDS Research [P30 AI027763]; UCSF
AIDS Biology Program of the AIDS Research Institute (ARI); National
Institutes of Health [AI60379, AI68498, AI64520, AI066917, U01 AI43641];
Irvington Institute/Dana Foundation; University- wide AIDS Research
Program [F05-GI-219]; Burroughs Wellcome Fund Clinical Scientist Award
in Translational Research; National Institutes of Health Roadmap for
Medical Research [DPI OD00329]; Canada Research Chair Program; CIHR
Operating [HOP-81735]
FX This research was supported by funds from the Canadian Institutes for
Health Research (CIHR), UCSF Gladstone Institute of Virology &
Immunology Center for AIDS Research (P30 AI027763), the UCSF AIDS
Biology Program of the AIDS Research Institute (ARI), and the National
Institutes of Health (AI60379, AI68498, AI64520, and AI066917). L. C.
Ndhlovu was supported by the Irvington Institute/Dana Foundation
Fellowship from the Cancer Research Institute. M. A. Ostrowski received
salary support from the Ontario HIV Treatment Network (OHTN) and the
CIHR. R. B. Jones receives a studentship from the OHTN. M. P. Sheth was
supported by a grant from the University- wide AIDS Research Program
(F05-GI-219). J. M. McCune was supported in part by National Institutes
of Health grant U01 AI43641, by the Burroughs Wellcome Fund Clinical
Scientist Award in Translational Research, and by the National
Institutes of Health Director's Pioneer Award Program, which is part of
the National Institutes of Health Roadmap for Medical Research (DPI
OD00329). R. Kaul receives salary support from the Canada Research Chair
Program and grant support from a CIHR Operating Grant (HOP-81735) and an
OHTN Operating Grant. Biosafety level 3 laboratory space and equipment
was provided by the Canadian Foundation for HIV Research (CANFAR) in
partnership with the Canadian Foundation for Innovation and the Ontario
Innovation Trust.
NR 52
TC 326
Z9 348
U1 1
U2 11
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD NOV 24
PY 2008
VL 205
IS 12
BP 2763
EP 2779
DI 10.1084/jem.20081398
PG 17
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 378BE
UT WOS:000261295300011
PM 19001139
ER
PT J
AU Watford, WT
Hissong, BD
Durant, LR
Yamane, H
Muul, LM
Kanno, Y
Tato, CM
Ramos, HL
Berger, AE
Mielke, L
Pesu, M
Solomon, B
Frucht, DM
Paul, WE
Sher, A
Jankovic, D
Tsichlis, PN
O'Shea, JJ
AF Watford, Wendy T.
Hissong, Bruce D.
Durant, Lydia R.
Yamane, Hidehiro
Muul, Linda M.
Kanno, Yuka
Tato, Cristina M.
Ramos, Haydee L.
Berger, Alan E.
Mielke, Lisa
Pesu, Marko
Solomon, Benjamin
Frucht, David M.
Paul, William E.
Sher, Alan
Jankovic, Dragana
Tsichlis, Philip N.
O'Shea, John J.
TI Tpl2 kinase regulates T cell interferon-gamma production and host
resistance to Toxoplasma gondii
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; NF-KAPPA-B; TNF-ALPHA PRODUCTION; SIGNALING
PATHWAYS; IFN-GAMMA; EXPRESSION; STAT4; IL-12; CYTOKINE; MICE
AB Tpl2 (Tumor progression locus 2), also known as Cot/MAP3K8, is a hematopoietically expressed serine-threonine kinase. Tpl2 is known to have critical functions in innate immunity in regulating tumor necrosis factor-alpha, Toll-like receptor, and G protein-coupled receptor signaling; however, our understanding of its physiological role in T cells is limited. We investigated the potential roles of Tpl2 in T cells and found that it was induced by interleukin-12 in human and mouse T cells in a Stat4-dependent manner. Deficiency of Tpl2 was associated with impaired interferon (IFN)-gamma production. Accordingly, Tpl2(-/-) mice had impaired host defense against Toxoplasma gondii with reduced parasite clearance and decreased IFN-gamma production. Furthermore, reconstitution of Rag2(-/-) mice with Tpl2-deficient T cells followed by T. gondii infection recapitulated the IFN-gamma defect seen in the Tpl2-deficient mice, confirming a T cell-intrinsic defect. CD4(+) T cells isolated from Tpl2(-/-) mice showed poor induction of T-bet and failure to up-regulate Stat4 protein, which is associated with impaired TCR-dependent extracellular signal-regulated kinase activation. These data underscore the role of Tpl2 as a regulator of T helper cell lineage decisions and demonstrate that Tpl2 has an important functional role in the regulation of Th1 responses.
C1 [Watford, Wendy T.; Hissong, Bruce D.; Durant, Lydia R.; Muul, Linda M.; Kanno, Yuka; Tato, Cristina M.; Ramos, Haydee L.; Berger, Alan E.; Mielke, Lisa; Pesu, Marko; Solomon, Benjamin; O'Shea, John J.] NIAMSD, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
[Yamane, Hidehiro; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Sher, Alan; Jankovic, Dragana] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Frucht, David M.] US FDA, Cell Biol Lab, Div Monoclonal Antibodies, Ctr Drug Evaluat & Res, Bethesda, MD 20892 USA.
[Tsichlis, Philip N.] Tufts Med Ctr, Mol Oncol Res Inst, Boston, MA 02111 USA.
RP Watford, WT (reprint author), NIAMSD, Lymphocyte Cell Biol Sect, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
EM watfordw@mail.nih.gov
RI Kanno, Yuka/B-5802-2013; Pesu, marko/L-6344-2013;
OI Kanno, Yuka/0000-0001-5668-9319
FU National Institute of Arthritis; National Institutes of Health [1 K22
AR53953-01, R01 CA095431]
FX This research was supported, in part, by the Intramural Research Program
of the National Institute of Arthritis and Musculoskeletal and Skin
Diseases of the National Institutes of Health. W. T. Watford is
supported by National Institutes of Health grant # 1 K22 AR53953-01. P.
Tsichlis is supported by National Institutes of Health grant # R01
CA095431.
NR 44
TC 48
Z9 51
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD NOV 24
PY 2008
VL 205
IS 12
BP 2803
EP 2812
DI 10.1084/jem.20081461
PG 10
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 378BE
UT WOS:000261295300014
PM 19001140
ER
PT J
AU Jani, A
Wan, MM
Zhang, JM
Cui, KR
Wu, J
Preston-Hurlburt, P
Khatri, R
Zhao, KJ
Chi, T
AF Jani, Anant
Wan, Mimi
Zhang, Jianmin
Cui, Kairong
Wu, Jie
Preston-Hurlburt, Paula
Khatri, Rohini
Zhao, Keji
Chi, Tian
TI A novel genetic strategy reveals unexpected roles of the Swi-Snf-like
chromatin-remodeling BAF complex in thymocyte development
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID T-CELL DEVELOPMENT; MAMMALIAN SWI/SNF COMPLEXES; CD4 GENE; EXPRESSION;
TRANSCRIPTION; SELECTION; BRG1; MECHANISMS; PROMOTER; LINEAGE
AB We have developed a general strategy for creating littermates bearing either a tissue-specific point mutation or deletion in any target gene, and used the method to dissect the roles of Brg, the ATPase subunit of the chromatin-remodeling Brg-associated factor (BAF) complex, in early thymocyte development. We found that a point mutation that inactivates the Brg ATPase recapitulates multiple defects previously described for Brg deletion (Chi, T. H., M. Wan, P. P. Lee, K. Akashi, D. Metzger, P. Chambon, C. B. Wilson, and G. R. Crabtree. 2003. Immunity. 19: 169-182). However, the point mutant helps reveal unexpected roles of Brg in CD25 repression and CD4 activation. Surprisingly, CD4 activation occurs independently of the Brg ATPase and is perhaps mediated by physical interactions between Brg and the CD4 locus. Our study thus suggests that the BAF complex harbors novel activities that can be necessary and even sufficient for stimulating transcription from an endogenous chromatin template in the absence of Brg-dependent remodeling of that template. We conclude that conditional point mutants, rarely used in mammalian genetics, can help uncover important gene functions undetectable or overlooked in deletion mutants.
C1 [Jani, Anant; Wan, Mimi; Zhang, Jianmin; Wu, Jie; Preston-Hurlburt, Paula; Khatri, Rohini; Chi, Tian] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA.
[Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Chi, T (reprint author), Yale Univ, Sch Med, Dept Immunobiol, 333 Cedar St, New Haven, CT 06520 USA.
EM Tian.Chi@yale.edu
FU National Institutes of Health [R01AI063554-02]; Anna Fuller Foundation;
Intramural Research Program of the National Heart, Lung, and Blood
Institute/National Institutes of Health
FX This work is funded by the National Institutes of Health (grant
R01AI063554-02 to T. Chi), the Anna Fuller Foundation (to A. Jani), and
the Intramural Research Program of the National Heart, Lung, and Blood
Institute/National Institutes of Health (K. Zhao).
NR 37
TC 19
Z9 19
U1 1
U2 3
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD NOV 24
PY 2008
VL 205
IS 12
BP 2813
EP 2825
DI 10.1084/jem.20080938
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 378BE
UT WOS:000261295300015
PM 18955569
ER
PT J
AU Coleman, HR
Chan, CC
Ferris, FL
Chew, EY
AF Coleman, Hanna R.
Chan, Chi-Chao
Ferris, Frederick L., III
Chew, Emily Y.
TI Age-related macular degeneration
SO LANCET
LA English
DT Review
ID COMPLEMENT FACTOR-H; BLUE-MOUNTAINS EYE; BEAVER DAM EYE; NUTRITION
EXAMINATION SURVEY; VISUAL IMPAIRMENT PROJECT; RANDOMIZED
CLINICAL-TRIALS; VITAMIN-E SUPPLEMENTATION; 3RD NATIONAL-HEALTH;
BODY-MASS INDEX; RISK-FACTORS
AB Age-related macular degeneration is the leading cause of blindness in elderly populations of European descent. The most consistent risk factors associated with this ocular condition are increasing age and cigarette smoking. Genetic investigations have shown that complement factor H, a regulator of the alternative complement pathway, and LOC387715/HtrA1 are the most consistent genetic risk factors for age-related macular degeneration. Although the pathogenesis of this disease is unknown, oxidative stress might have an important role. Treatment with antioxidant vitamins and zinc can reduce the risk of developing advanced age-related macular degeneration by about a quarter in those at least at moderate risk. Intravitreal injections of ranibizumab, a monoclonal antibody that inhibits all forms of vascular endothelial growth factor, have been shown to stabilise loss of vision and, in some cases, improve vision in individuals with neovascular age-related macular degeneration. These findings, combined with assessments of possible environmental and genetic interactions and new approaches to modulate inflammatory pathways, will hopefully further expand our ability to understand and treat age-related macular degeneration.
C1 [Coleman, Hanna R.; Ferris, Frederick L., III; Chew, Emily Y.] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA.
[Chan, Chi-Chao] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Chew, EY (reprint author), NEI, Div Epidemiol & Clin Res, NIH, Bldg 10,CRC,Room 3-2531,10 Ctr Dr,MSC-1204, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
FU Intramural NIH HHS [Z01 EY000222-22, Z01 EY000418-04, Z99 EY999999]
NR 163
TC 234
Z9 245
U1 7
U2 34
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 22
PY 2008
VL 372
IS 9652
BP 1835
EP 1845
DI 10.1016/S0140-6736(08)61759-6
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 375KG
UT WOS:000261112000026
PM 19027484
ER
PT J
AU Ferre, S
AF Ferre, Sergi
TI Caffeine in Parkinson's disease
SO MEDICINA CLINICA
LA Spanish
DT Editorial Material
ID A(2A) RECEPTOR ANTAGONIST; ADENOSINE A(1); 6-HYDROXYDOPAMINE-LESIONED
RATS; DOPAMINE RELEASE; MONOAMINE TRANSPORTERS; DEFICIENT MICE; BASAL
GANGLIA; DOUBLE-BLIND; MOTOR; INVOLVEMENT
C1 NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Ferre, S (reprint author), NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM sferre@intra.nida.nih.gov
RI Ferre, Sergi/K-6115-2014
OI Ferre, Sergi/0000-0002-1747-1779
NR 75
TC 0
Z9 0
U1 0
U2 4
PU EDICIONES DOYMA S A
PI BARCELONA
PA TRAV DE GRACIA 17-21, 08021 BARCELONA, SPAIN
SN 0025-7753
J9 MED CLIN-BARCELONA
JI Med. Clin.
PD NOV 22
PY 2008
VL 131
IS 18
BP 710
EP 715
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 377ZA
UT WOS:000261289700007
PM 19087830
ER
PT J
AU Mueller, SC
Jackson, CPT
Skelton, RW
AF Mueller, Sven C.
Jackson, Carl P. T.
Skelton, Ron W.
TI Sex differences in a virtual water maze: An eye tracking and
pupillometry study
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE spatial navigation; eye tracking; pupillometry; sex differences;
strategy; allocentric; egocentric; water maze
ID GENDER-RELATED DIFFERENCES; HUMAN SPATIAL NAVIGATION; TRAUMATIC
BRAIN-INJURY; VISUAL-SEARCH; AGE-DIFFERENCES; WORKING-MEMORY; MOVEMENTS;
ABILITY; TASK; ENVIRONMENT
AB Sex differences in human spatial navigation are well known. However, the exact strategies that males and females employ in order to navigate successfully around the environment are unclear. While some researchers propose that males prefer environment-centred (allocentric) and females prefer self-centred (egocentric) navigation, these findings have proved difficult to replicate. In the present study we examined eye movements and physiological measures of memory (pupillometry) in order to compare visual scanning of spatial orientation using a human virtual analogue of the Morris Water Maze task. Twelve women and twelve men (average age= 24 years) were trained on a visible platform and had to locate an invisible platform over a series of trials. On all but the first trial, participants' eye movements were recorded for 3 s and they were asked to orient themselves in the environment. While the behavioural data replicated previous findings of improved spatial performance for males relative to females, distinct sex differences in eye movements were found. Males tended to explore consistently more space early on while females demonstrated initially longer fixation durations and increases in pupil diameter usually associated with memory processing. The eye movement data provides novel insight into differences in navigational strategies between the sexes. Published by Elsevier B.V.
C1 [Mueller, Sven C.; Jackson, Carl P. T.] Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England.
[Jackson, Carl P. T.] Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England.
[Skelton, Ron W.] Univ Victoria, Dept Psychol, Victoria, BC V8W 2Y2, Canada.
RP Mueller, SC (reprint author), NIMH, MAP, NIH, Bethesda, MD 20892 USA.
EM msven@mail.nih.gov
RI Skelton, Ronald/E-5605-2012
NR 48
TC 35
Z9 38
U1 3
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 21
PY 2008
VL 193
IS 2
BP 209
EP 215
DI 10.1016/j.bbr.2008.05.017
PG 7
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 350NP
UT WOS:000259359700008
PM 18602173
ER
PT J
AU Ryan, BC
Young, NB
Moy, SS
Crawley, JN
AF Ryan, Bryce C.
Young, Nancy B.
Moy, Sheryl S.
Crawley, Jacqueline N.
TI Olfactory cues are sufficient to elicit social approach behaviors but
not social transmission of food preference in C57BL/6J mice
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE mouse; autism; social behavior; three-chambered social approach task;
social transmission of food preference
ID AUTISM SPECTRUM DISORDERS; BTBR-T+TF/J MICE; LONG-TERM-MEMORY; INBRED
STRAINS; TASKS RELEVANT; KNOCKOUT MICE; MOUSE MODELS; MUS-MUSCULUS; BODY
ODORS; RATS
AB Mouse models for the study of autistic-like behaviors are increasingly needed to test hypotheses about the causes of autism, and to evaluate potential treatments. Both the automated three-chambered social approach test and social transmission of food preference have been proposed as mouse behavioral assays with face validity to diagnostic symptoms of autism, including aberrant reciprocal social interactions and impaired communication. Both assays measure aspects of normal social behavior in the mouse. However, little is known regarding the salient cues present in each assay that elicit normal social approach and communication. To deconstruct the critical components, we focused on delivering discrete social and non-social olfactory and visual cues within the context of each assay. Results indicate that social olfactory cues were sufficient to elicit normal sociability in the three-chambered social approach test. On social transmission of food preference, isolated social olfactory cues were sufficient to induce social investigation, but not sufficient to induce food preference. These findings indicate that olfactory cues are important in mouse social interaction, but that additional sensory cues are necessary in certain situations. The present evidence that both the three-chambered social approach assay and the social transmission of food preference assay require socially relevant cues to elicit normal behavior supports the use of these two assays to investigate autism-related behavioral phenotypes in mice. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Ryan, Bryce C.; Young, Nancy B.; Moy, Sheryl S.; Crawley, Jacqueline N.] Univ N Carolina, Sch Med, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA.
[Moy, Sheryl S.; Crawley, Jacqueline N.] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Intramural Res Program, Bethesda, MD 20892 USA.
RP Ryan, BC (reprint author), Univ N Carolina, Sch Med, Neurodev Disorders Res Ctr, 130 Mason Farm Rd,4161W Bioinformat,Campus Box 33, Chapel Hill, NC 27599 USA.
EM bcryan@email.unc.edu
FU the Neurodevelopmental Disorders Research Center at University of North
Carolina at Chapel Hill NICHD [T32-HD40127]; NICHD [P30-HD03110]; the
National Institute of Mental Health Intramural Research Program
FX Support for this project was provided by the Neurodevelopmental
Disorders Research Center at University of North Carolina at Chapel Hill
NICHD training grant #T32-HD40127 (BCR), NICHD grant P30-HD03110 (SSM),
and the National Institute of Mental Health Intramural Research Program
(JNC). The authors would also like to thank Randy Nonneman for
assistance with animal care and Joe Piven for advice on autism
phenotypes and assay design.
NR 66
TC 40
Z9 40
U1 1
U2 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 21
PY 2008
VL 193
IS 2
BP 235
EP 242
DI 10.1016/j.bbr.2008.06.002
PG 8
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 350NP
UT WOS:000259359700012
PM 18586054
ER
PT J
AU Sethi, AA
Stonik, JA
Thomas, F
Demosky, SJ
Amar, M
Neufeld, E
Brewer, HB
Davidson, WS
D'Souza, W
Sviridov, D
Remaley, AT
AF Sethi, Amar A.
Stonik, John A.
Thomas, Fairwell
Demosky, Steve J.
Amar, Marcelo
Neufeld, Edward
Brewer, H. Bryan
Davidson, W. Sean
D'Souza, Wilissa
Sviridov, Dmitri
Remaley, Alan T.
TI Asymmetry in the Lipid Affinity of Bihelical Amphipathic Peptides A
STRUCTURAL DETERMINANT FOR THE SPECIFICITY OF ABCA1-DEPENDENT
CHOLESTEROL EFFLUX BY PEPTIDES
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID APOLIPOPROTEIN-A-I; CASSETTE TRANSPORTER A1; CELLULAR CHOLESTEROL;
HELICAL PEPTIDES; APOA-I; MIMETIC PEPTIDES; ALPHA-HELICES;
DOMAIN-STRUCTURE; TANGIER DISEASE; BINDING
AB ApoA-I contains a tandem array of amphipathic helices with varying lipid affinity, which are critical in its ability to bind and remove lipids from cells by the ABCA1 transporter. In this study, the effect of asymmetry in the lipid affinity of amphipathic helices in a bihelical apoA-I mimetic peptide, 37pA, on lipid efflux by the ABCA1 transporter was examined. Seven peptide variants of 37pA were produced by substituting a varying number of hydrophobic amino acids for alanine on either one or both helices. The 5A peptide with five alanine substitutions in the second helix had decreased helical content compared with 37pA (5A, 12 +/- 1% helicity; 37pA, 28 +/- 2% helicity) and showed less self-association but, similar to the parent peptide, was able to readily solubilize phospholipid vesicles. Furthermore, 5A, unlike the parent peptide 37pA, was not hemolytic (37pA, 27 +/- 2% RBC lysis, 2 h, 18 mu M). Finally, the 5A peptide stimulated cholesterol and phospholipid efflux by the ABCA1 transporter with higher specificity (ABCA1-transfected versus untransfected cells) than 37pA(5A, 9.7 +/- 0.77%, 18 h, 18 mu M versus 1.5 +/- 0.27%, 18 h, 18 mu M (p < 0.0001); 37pA, 7.4 +/- 0.85%, 18h, 18 mu M versus 5.8 +/- 0.20%, 18h, 18 mu M(p = 0.03)). In summary, we describe a novel bihelical peptide with asymmetry in the lipid affinity of its helices and properties similar to apoA-I in terms of specificity for cholesterol efflux by the ABCA1 transporter and low cytotoxicity.
C1 [Neufeld, Edward] NHLBI, NIH, Bethesda, MD 20892 USA.
[Sethi, Amar A.; Stonik, John A.; Thomas, Fairwell; Demosky, Steve J.; Amar, Marcelo; Remaley, Alan T.] NHLBI, Lipoprot Metab Sect, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Brewer, H. Bryan] Washington Hosp Ctr, Cardiovasc Res Inst, MedStar Res Inst, Washington, DC 20010 USA.
[Davidson, W. Sean] Univ Cincinnati, Ctr Lipid & Arteriosclerosis Studies, Cincinnati, OH 45221 USA.
[D'Souza, Wilissa; Sviridov, Dmitri] Baker Heart Res Inst, Melbourne, Vic, Australia.
RP Remaley, AT (reprint author), NHLBI, NIH, Bldg 10,Rm 7N-115,10 Ctr Dr, Bethesda, MD 20892 USA.
EM aremaley@cc.nih.gov
RI Sviridov, Dmitri/E-7943-2010
FU National Institutes of Health; NHLBI
FX This work was supported, in whole or in part, by intramural funds from
the National Institutes of Health, NHLBI. The costs of publication of
this article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 49
TC 58
Z9 59
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32273
EP 32282
DI 10.1074/jbc.M804461200
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700014
PM 18805791
ER
PT J
AU Sobhany, M
Kakuta, Y
Sugiura, N
Kimata, K
Negishi, M
AF Sobhany, Mack
Kakuta, Yoshimitsu
Sugiura, Nobuo
Kimata, Koji
Negishi, Masahiko
TI The Chondroitin Polymerase K4CP and the Molecular Mechanism of Selective
Bindings of Donor Substrates to Two Active Sites
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PASTEURELLA-MULTOCIDA; HYALURONAN SYNTHASE; ENZYME-ACTIVITY; SULFATE;
GLYCOSYLTRANSFERASES; BIOSYNTHESIS; PROTEOGLYCAN; EXPRESSION; CARTILAGE;
CLONING
AB Bacterial chondroitin polymerase K4CP is a multifunctional enzyme with two active sites. K4CP catalyzes alternative transfers of glucoronic acid (GlcA) and N-acetylgalactosamine (GalNAc) to elongate a chain consisting of the repeated disaccharide sequence GlcA beta 1-3GalNAc beta 1-4. Unlike the polymerization reactions of DNA and RNA and polypeptide synthesis, which depend upon templates, the monosaccharide polymerization by K4CP does not. To investigate the catalytic mechanism of this reaction, we have used isothermal titration calorimetry to determine the binding of the donor substrates UDP-GlcA and UDP-GalNAc to purified K4CP protein and its mutants. Only one donor molecule bound to one molecule of K4CP at a time. UDP-GlcA bound only to the C-terminal active site at a high affinity (K-d = 6.81 mu M), thus initiating the polymerization reaction. UDP-GalNAc could bind to either the N-terminal or C-terminal active sites at a low affinity (K-d = 266-283 mu M) but not to both sites at the same time. The binding affinity of UDP-GalNAc to a K4CP N-terminal fragment (residues 58-357) was profoundly decreased, yielding the average K-d value of 23.77 mu M, closer to the previously reported K-m value for the UDP-GalNAc transfer reaction that takes place at the N-terminal active site. Thus, the first step of the reaction appears to be the binding of UDP-GlcA to the C-terminal active site, whereas the second step involves the C-terminal region of the K4CP molecule regulating the binding of UDP-GalNAc to only the N-terminal active site. Alternation of these two specific bindings advances the polymerization reaction by K4CP.
C1 [Sobhany, Mack; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Kakuta, Yoshimitsu] Kyushu Univ, Fac Agr, Dept Biochem, Fukuoka 8128581, Japan.
[Sugiura, Nobuo; Kimata, Koji] Aichi Med Univ, Inst Mol Sci Med, Aichi 4801195, Japan.
RP Negishi, M (reprint author), NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM negishi@niehs.nih.gov
FU National Institutes of Health
FX This work was supported, in whole or in part, by the National Institutes
of Health Grant Intramural Research Program. The costs of publication of
this article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 26
TC 19
Z9 19
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32328
EP 32333
DI 10.1074/jbc.M804332200
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700019
PM 18806260
ER
PT J
AU Guyot, N
Butler, MW
Mcnally, P
Weldon, S
Greene, CM
Levine, RL
O'Neill, SJ
Taggart, CC
McElvaney, NG
AF Guyot, Nicolas
Butler, Marcus W.
McNally, Paul
Weldon, Sinead
Greene, Catherine M.
Levine, Rodney L.
O'Neill, Shane J.
Taggart, Clifford C.
McElvaney, Noel G.
TI Elafin, an Elastase-specific Inhibitor, Is Cleaved by Its Cognate Enzyme
Neutrophil Elastase in Sputum from Individuals with Cystic Fibrosis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LEUKOCYTE PROTEINASE-INHIBITOR; HUMAN KERATINOCYTES; PROTEASE INHIBITOR;
EPITHELIAL-CELLS; PRE-ELAFIN; KAPPA-B; GENE-EXPRESSION;
LIPOPOLYSACCHARIDE; TRANSGLUTAMINASE; SKALP/ELAFIN
AB Elafin is a neutrophil serine protease inhibitor expressed in lung and displaying anti-inflammatory and anti-bacterial properties. Previous studies demonstrated that some innate host defense molecules of the cystic fibrosis (CF) and chronic obstructive pulmonary disease airways are impaired due to increased proteolytic degradation observed during lung inflammation. In light of these findings, we thus focused on the status of elafin in CF lung. We showed in the present study that elafin is cleaved in sputum from individuals with CF. Pseudomonas aeruginosa-positive CF sputum, which was found to contain lower elafin levels and higher neutrophil elastase (NE) activity compared with P. aeruginosa-negative samples, was particularly effective in cleaving recombinant elafin. NE plays a pivotal role in the process as only NE inhibitors are able to inhibit elafin degradation. Further in vitro studies demonstrated that incubation of recombinant elafin with excess of NE leads to the rapid cleavage of the inhibitor. Two cleavage sites were identified at the N-terminal extremity of elafin (Val-5-Lys-6 and Val-9-Ser-10). Interestingly, purified fragments of the inhibitor (Lys-6-Gln-57 and Ser-10-Gln-57) were shown to still be active for inhibiting NE. However, NE in excess was shown to strongly diminish the ability of elafin to bind lipopolysaccharide(LPS) and its capacity to be immobilized by transglutamination. In conclusion, this study provides evidence that elafin is cleaved by its cognate enzyme NE present at excessive concentration in CF sputum and that P. aeruginosa infection promotes this effect. Such cleavage may have repercussions on the innate immune function of elafin.
C1 [Guyot, Nicolas; Butler, Marcus W.; McNally, Paul; Weldon, Sinead; Greene, Catherine M.; O'Neill, Shane J.; Taggart, Clifford C.; McElvaney, Noel G.] Beaumont Hosp, Royal Coll Surg Ireland, Pulm Res Div, Dept Med, Dublin 9, Ireland.
[Levine, Rodney L.] NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
RP Taggart, CC (reprint author), Beaumont Hosp, Royal Coll Surg Ireland, Pulm Res Div, Dept Med, Dublin 9, Ireland.
EM c.taggart@qub.ac.uk
RI McElvaney, Noel/A-6809-2010; Greene, Catherine/D-3513-2012; Taggart,
Clifford/G-4492-2014; Weldon, Sinead/J-5451-2014; Levine,
Rodney/D-9885-2011;
OI Greene, Catherine/0000-0003-2549-2569; Weldon,
Sinead/0000-0001-5628-6624; McNally, Paul/0000-0001-7102-1712
FU Health Research Board; Alpha One Foundation; rogram for Research in
Third Levels Institutes administered by Higher Education Authority,
Science Foundation Ireland; Cystic Fibrosis Hope Source; Cystic Fibrosis
Research Trust; Cystic Fibrosis Association of Ireland; Royal College of
Surgeons in Ireland
FX This work was authored, in whole or in part, by National Institutes of
Health staff. This work was also supported by the Health Research Board,
The Alpha One Foundation, The Program for Research in Third Levels
Institutes administered by Higher Education Authority, Science
Foundation Ireland, Cystic Fibrosis Hope Source, Cystic Fibrosis
Research Trust, Cystic Fibrosis Association of Ireland (to C. T.), and
the Royal College of Surgeons in Ireland. The costs of publication of
this article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 49
TC 39
Z9 40
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32377
EP 32385
DI 10.1074/jbc.M803707200
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700025
PM 18799464
ER
PT J
AU von Marschall, Z
Fisher, LW
AF von Marschall, Zofia
Fisher, Larry W.
TI Dentin Matrix Protein-1 Isoforms Promote Differential Cell Attachment
and Migration
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID COMPLEMENT-MEDIATED ATTACK; INTEGRIN-BINDING LIGAND; BONE SIALOPROTEIN;
SIBLING PROTEINS; IN-VITRO; ALPHA-V-BETA-5 INTEGRINS; PHOSPHATE
HOMEOSTASIS; SUBSTRATUM ADHESION; OSTEOPONTIN; EXPRESSION
AB Dentin matrix protein-1 (DMP1), bone sialoprotein (BSP), and osteopontin (OPN) are three SIBLINGs (small integrin-binding ligand, N-linked glycoproteins) co-expressed/secreted by skeletal and active ductal epithelial cells. Although etiological mechanisms remain unclear, DMP1 is the only one of these three genes currently known to have mutations resulting in human disease, and yet it remains the least studied. All three contain the highly conserved integrin-binding tripeptide, RGD, and experiments comparing the cell attachment and haptotactic migration-enhancing properties of DMP1 to BSP and OPN were performed using human skeletal (MG63 and primary dental pulp cells) and salivary gland (HSG) cells. Mutation of any SIBLING's RGD destroyed all attachment and migration activity. Using its alpha V beta 5 integrin, HSG cells attached to BSP but not to DMP1 or OPN. However, HSG cells could not migrate onto BSP in a modified Boyden chamber assay. Expression of alpha V beta 3 integrin enhanced HSG attachment to DMP1 and OPN and promoted haptotactic migration onto all three proteins. Interchanging the first four coding exons or the conserved amino acids adjacent to the RGD of DMP1 with corresponding sequences of BSP did not enhance the ability of DMP1 to bind alpha V beta 5. For alpha V beta 3 expressing cells, intact DMP1, its BMP1-cleaved C-terminal fragment, and exon six lacking all post-translational modifications worked equally well but the proteoglycan isoform of DMP1 had greatly reduced ability for cell attachment and migration. The sequence specificity of the proposed BMP1-cleavage site of DMP1 was verified by mutation analysis. Direct comparison of the three proteins showed that cells discriminate among these SIBLINGs and among DMP1 isoforms.
C1 [von Marschall, Zofia; Fisher, Larry W.] NIDCR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Fisher, LW (reprint author), Bldg 30,Room 228,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM lfisher@dir.nidcr.nih.gov
FU National Institutes of Health Division of Intramural Research, NIDCR;
Intramural Research Program
FX This work was supported, in whole or in part, by National Institutes of
Health Division of Intramural Research, NIDCR, and the Intramural
Research Program.
NR 41
TC 33
Z9 33
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32730
EP 32740
DI 10.1074/jbc.M804283200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700062
PM 18819913
ER
PT J
AU Bandyopadhyay, BC
Ong, HL
Lockwich, TP
Liu, XB
Paria, BC
Singh, BB
Ambudkar, IS
AF Bandyopadhyay, Bidhan C.
Ong, Hwei L.
Lockwich, Timothy P.
Liu, Xibao
Paria, Biman C.
Singh, Brij B.
Ambudkar, Indu S.
TI TRPC3 Controls Agonist-stimulated Intracellular Ca2+ Release by
Mediating the Interaction between Inositol 1,4,5-Trisphosphate Receptor
and RACK1
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-KINASE-C; PLASMA-MEMBRANE; INOSITOL-1,4,5-TRISPHOSPHATE
RECEPTOR; CATION CHANNELS; CELL-MIGRATION; BINDING; ACTIVATION; COMPLEX;
INFLUX; DOMAIN
AB Activation of TRPC3 channels is concurrent with inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-mediated intracellular Ca2+ release and associated with phosphatidylinositol 4,5-bisphosphate hydrolysis and recruitment to the plasma membrane. Here we report that interaction of TRPC3 with receptor for activated C-kinase-1 (RACK1) not only determines plasma membrane localization of the channel but also the interaction of IP3R with RACK1 and IP3-dependent intracellular Ca2+ release. We show that TRPC3 interacts with RACK1 via N-terminal residues Glu-232, Asp-233, Glu-240, and Glu-244. Carbachol (CCh) stimulation of HEK293 cells expressing wild type TRPC3 induced recruitment of a ternary TRPC3-RACK1-IP3R complex and increased surface expression of TRPC3 and Ca2+ entry. Mutation of the putative RACK1 binding sequence in TRPC3 disrupted plasma membrane localization of the channel. CCh-stimulated recruitment of TRPC3-RACK1-IP3R complex as well as increased surface expression of TRPC3 and receptor-operated Ca2+ entry were also attenuated. Importantly, CCh-induced intracellular Ca2+ release was significantly reduced as was RACK1-IP3R association without any change in thapsigargin-stimulated Ca2+ release and entry. Knockdown of endogenous TRPC3 also decreased RACK1-IP3R association and decreased CCh-stimulated Ca2+ entry. Furthermore, an oscillatory pattern of CCh-stimulated intracellular Ca2+ release was seen in these cells compared with the more sustained pattern seen in control cells. Similar oscillatory pattern of Ca2+ release was seen after CCh stimulation of cells expressing the TRPC3 mutant. Together these data demonstrate a novel role for TRPC3 in regulation of IP3R function. We suggest TRPC3 controls agonist-stimulated intracellular Ca2+ release by mediating interaction between IP3R and RACK1.
C1 [Bandyopadhyay, Bidhan C.; Ong, Hwei L.; Lockwich, Timothy P.; Paria, Biman C.; Ambudkar, Indu S.] NIDCR, Secretory Physiol Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Singh, Brij B.] Univ N Dakota, Dept Biochem & Mol Biol, Sch Med & Hlth Sci, Grand Forks, ND 58203 USA.
RP Ambudkar, IS (reprint author), NIDCR, Secretory Physiol Sect, Mol Physiol & Therapeut Branch, NIH, Bldg 10,Rm 1N-113, Bethesda, MD 20892 USA.
EM indu.ambudkar@nih.gov
FU National Institutes of Health [R01 DE 017102]
FX This work was supported in part by National Institutes of Health Grant
R01 DE 017102 ( to B. B. S.).
NR 41
TC 30
Z9 31
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32821
EP 32830
DI 10.1074/jbc.M805382200
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700071
PM 18755685
ER
PT J
AU Copeland, WC
Longley, MJ
AF Copeland, William C.
Longley, Matthew J.
TI DNA2 Resolves Expanding Flap in Mitochondrial Base Excision Repair
SO MOLECULAR CELL
LA English
DT Editorial Material
ID REPLICATION; HELICASE
C1 [Copeland, William C.; Longley, Matthew J.] Natl Inst Environm Hlth Sci, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
RP Copeland, WC (reprint author), Natl Inst Environm Hlth Sci, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
EM copelan1@niehs.nih.gov
FU Intramural NIH HHS [Z01 ES065078-14]
NR 10
TC 29
Z9 29
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 21
PY 2008
VL 32
IS 4
BP 457
EP 458
DI 10.1016/j.molcel.2008.11.007
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 377ZD
UT WOS:000261290000001
PM 19026774
ER
PT J
AU Anderson, JM
Sonenshine, DE
Valenzuela, JG
AF Anderson, Jennifer M.
Sonenshine, Daniel E.
Valenzuela, Jesus G.
TI Exploring the mialome of ticks: an annotated catalogue of midgut
transcripts from the hard tick, Dermacentor variabilis (Acari: Ixodidae)
SO BMC GENOMICS
LA English
DT Review
ID SERINE PROTEINASE-INHIBITORS; ORNITHODOROS-MOUBATA ACARI; CU,ZN
SUPEROXIDE-DISMUTASE; AMERICAN DOG TICK; BOOPHILUS-MICROPLUS;
HAEMAPHYSALIS-LONGICORNIS; SOFT TICK; IXODES-RICINUS; CDNA CLONING;
RHIPICEPHALUS-APPENDICULATUS
AB Background: Ticks are obligate blood feeders. The midgut is the first major region of the body where blood and microbes ingested with the blood meal come in contact with the tick's internal tissues. Little is known about protein expression in the digestive tract of ticks. In this study, for analysis of global gene expression during tick attachment and feeding, we generated and sequenced 1,679 random transcripts (ESTs) from cDNA libraries from the midguts of female ticks at varying stages of feeding.
Results: Sequence analysis of the 1,679 ESTs resulted in the identification of 835 distinct transcripts, from these, a total of 82 transcripts were identified as proteins putatively directly involved in blood meal digestion, including enzymes involved in oxidative stress reduction/antimicrobial activity/detoxification, peptidase inhibitors, protein digestion (cysteine-, aspartic-, serine-, and metallo-peptidases), cell, protein and lipid binding including mucins and iron/heme metabolism and transport. A lectin-like protein with a high match to lectins in other tick species, allergen-like proteins and surface antigens important in pathogen recognition and/or antimicrobial activity were also found. Furthermore, midguts collected from the 6-day-fed ticks expressed twice as many transcripts involved in bloodmeal processing as midguts from unfed/2-day-fed ticks.
Conclusion: This tissue-specific transcriptome analysis provides an opportunity to examine the global expression of transcripts in the tick midgut and to compare the gut response to host attachment versus blood feeding and digestion. In contrast to those in salivary glands of other Ixodid ticks, most proteins in the D. variabilis midgut cDNA library were intracellular. Of the total ESTs associated with a function, an unusually large number of transcripts were associated with peptidases, cell, lipid and protein binding, and oxidative stress or detoxification. Presumably, this is consistent with their role in intracellular processing of the blood meal and response to microbial infections. The presence of many proteins with similar functions is consistent with the hypothesis that gene duplication contributed to the successful adaptation of ticks to hematophagy. Furthermore, these transcripts may be useful to scientists investigating the role of the tick midgut in blood-meal digestion, antimicrobial activity or the transmission of tick-borne pathogens.
C1 [Anderson, Jennifer M.; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Unit, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Sonenshine, Daniel E.] Old Dominion Univ, Dept Biol Sci, Norfolk, VA 23529 USA.
RP Anderson, JM (reprint author), NIAID, Vector Mol Biol Unit, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
EM jenanderson@niaid.nih.gov; dsonensh@odu.edu; jvalenzuela@niaid.nih.gov
FU The Division of Intramural Research; National Institutes of Allergy and
Infectious Diseases; National Institutes of Health; National Science
Foundation [IBN 0212901]
FX The authors express their sincere appreciation to Dr. Jose Ribeiro,
NIAID/NIH, for assembling the data into clusters and tentative
identifications using the different databases identified in this
manuscript, and for review of the manuscript, Dr. Robert Gwadz for his
continuous support, Dr. Fabiano Oliveira for assistance in carrying out
the procedures involved in constructing the cDNA library, Ryan Jochim
for critical review of the manuscript and Nancy Shulman for editorial
assistance. This research was supported in part by The Division of
Intramural Research, National Institutes of Allergy and Infectious
Diseases, National Institutes of Health. Support to DES, in part, is
gratefully acknowledged by a grant from the National Science Foundation,
IBN 0212901.
NR 103
TC 64
Z9 64
U1 1
U2 14
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD NOV 20
PY 2008
VL 9
AR 552
DI 10.1186/1471-2164-9-552
PG 37
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 417VK
UT WOS:000264106400001
PM 19021911
ER
PT J
AU Booth, CM
Cescon, DW
Wang, L
Tannock, IF
Krzyzanowska, MK
AF Booth, Christopher M.
Cescon, David W.
Wang, Lisa
Tannock, Ian F.
Krzyzanowska, Monika K.
TI Evolution of the Randomized Controlled Trial in Oncology Over Three
Decades
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 43rd Annual Meeting of the American-Society-of-Clinical-Oncology
CY JUN 01-05, 2007
CL Chicago, IL
SP Amer Soc Clin Oncol
ID CELL LUNG-CANCER; CLINICAL-TRIALS; BREAST-CANCER; DRUG TRIALS;
OF-INTEREST; QUALITY; ASSOCIATION; INDUSTRY; ORGANIZATIONS; CONCLUSIONS
AB Purpose
The randomized controlled trial (RCT) is the gold standard for establishing new therapies in clinical oncology. Here we document changes with time in design, sponsorship, and outcomes of oncology RCTs.
Methods
Reports of RCTs evaluating systemic therapy for breast, colorectal (CRC), and non-small-cell lung cancer (NSCLC) published 1975 to 2004 in six major journals were reviewed. Two authors abstracted data regarding trial design, results, and conclusions. Conclusions of authors were graded using a 7-point Likert scale. For each study the effect size for the primary end point was converted to a summary measure.
Results
A total of 321 eligible RCTs were included (48% breast, 24% CRC, 28% NSCLC). Over time, the number and size of RCTs increased considerably. For-profit/mixed sponsorship increased substantially during the study period (4% to 57%; P < .001). There was increasing use of time-to-event measures (39% to 78%) and decreasing use of response rate (54% to 14%) as primary end point (P < .001). Effect size remained stable over the study period. Authors have become more likely to strongly endorse the experimental arm (P = .017). A significant P value for the primary end point and industry sponsorship were each independently associated with endorsement of the experimental agent (odds ratio [OR] = 19.6, 95% CI, 8.9 to 43.1, and OR = 3.5, 95% CI, 1.6 to 7.5, respectively).
Conclusion
RCTs in oncology have become larger and are more likely to be sponsored by industry. Authors of modern RCTs are more likely to strongly endorse novel therapies. For-profit sponsorship and statistically significant results are independently associated with endorsement of the experimental arm.
C1 [Krzyzanowska, Monika K.] Univ Toronto, Dept Med Oncol & Hematol, Princess Margaret Hosp, Toronto, ON M5G 2M9, Canada.
Queens Univ, NCI, Canada Clin Trials Grp, Kingston, ON K7L 3N6, Canada.
RP Krzyzanowska, MK (reprint author), Univ Toronto, Dept Med Oncol & Hematol, Princess Margaret Hosp, 610 Univ Ave, Toronto, ON M5G 2M9, Canada.
EM monika.krzyzanowska@uhn.on.ca
NR 28
TC 55
Z9 57
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2008
VL 26
IS 33
BP 5458
EP 5464
DI 10.1200/JCO.2008.16.5456
PG 7
WC Oncology
SC Oncology
GA 376RA
UT WOS:000261199500024
PM 18955452
ER
PT J
AU Misteli, T
AF Misteli, Tom
TI CELL BIOLOGY Nuclear order out of chaos
SO NATURE
LA English
DT Editorial Material
ID ORGANIZATION; ASSOCIATION
C1 [Misteli, Tom] NCI, NIH, Bethesda, MD 20892 USA.
RP Misteli, T (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM mistelit@mail.nih.gov
NR 7
TC 27
Z9 28
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 20
PY 2008
VL 456
IS 7220
BP 333
EP 334
DI 10.1038/456333a
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374JM
UT WOS:000261039600028
PM 19020607
ER
PT J
AU Knepper, MA
AF Knepper, Mark A.
TI PHYSIOLOGY Courier service for ammonia
SO NATURE
LA English
DT Editorial Material
ID TRANSPORTERS; RH
C1 [Knepper, Mark A.] NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
RP Knepper, MA (reprint author), NHLBI, Div Intramural Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM knep@helix.nih.gov
FU Intramural NIH HHS [Z01 HL001285-21, Z99 HL999999]
NR 10
TC 4
Z9 4
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 20
PY 2008
VL 456
IS 7220
BP 336
EP 337
DI 10.1038/456336a
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374JM
UT WOS:000261039600031
PM 19020610
ER
PT J
AU McAlonan, K
Cavanaugh, J
Wurtz, RH
AF McAlonan, Kerry
Cavanaugh, James
Wurtz, Robert H.
TI Guarding the gateway to cortex with attention in visual thalamus
SO NATURE
LA English
DT Article
ID LATERAL GENICULATE-NUCLEUS; RETICULAR NUCLEUS; MACAQUE MONKEY;
ORGANIZATION; NEURONS; GALAGO; SECTOR; MODULATION; PROJECTION; RESPONSES
AB The massive visual input from the eye to the brain requires selective processing of some visual information at the expense of other information, a process referred to as visual attention. Increases in the responses of visual neurons with attention have been extensively studied along the visual processing streams in monkey cerebral cortex, from primary visual areas to parietal and frontal cortex(1-4). Here we show, by recording neurons in attending macaque monkeys ( Macaca mulatta), that attention modulates visual signals before they even reach cortex by increasing responses of both magnocellular and parvocellular neurons in the first relay between retina and cortex, the lateral geniculate nucleus ( LGN). At the same time, attention decreases neuronal responses in the adjacent thalamic reticular nucleus ( TRN). Crick(5) argued for such modulation of the LGN by observing that it is inhibited by the TRN, and suggested that " the thalamus is the gateway to the cortex, the reticular complex might be described as the guardian of the gateway'', a reciprocal relationship we now show to be more than just hypothesis. The reciprocal modulation in LGN and TRN appears only during the initial visual response, but the modulation of LGN reappears later in the response, suggesting separate early and late sources of attentional modulation in LGN.
C1 [McAlonan, Kerry; Cavanaugh, James; Wurtz, Robert H.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP McAlonan, K (reprint author), NEI, Sensorimotor Res Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM km@nei.nih.gov
FU National Eye Institute
FX This work was supported by the intramural research program of the
National Eye Institute. We are grateful for the assistance of J.
McClurkin, A. Nichols, M. Smith, T. Ruffner and G. Tansey.
NR 30
TC 199
Z9 200
U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 20
PY 2008
VL 456
IS 7220
BP 391
EP U56
DI 10.1038/nature07382
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374JM
UT WOS:000261039600044
PM 18849967
ER
PT J
AU Meigs, JB
Shrader, P
Sullivan, LM
McAteer, JB
Fox, CS
Dupuis, J
Manning, AK
Florez, JC
Wilson, PWF
D'Agostino, RB
Cupples, LA
AF Meigs, James B.
Shrader, Peter
Sullivan, Lisa M.
McAteer, Jarred B.
Fox, Caroline S.
Dupuis, Josee
Manning, Alisa K.
Florez, Jose C.
Wilson, Peter W. F.
D'Agostino, Ralph B., Sr.
Cupples, L. Adrienne
TI Genotype Score in Addition to Common Risk Factors for Prediction of Type
2 Diabetes
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GLUCOSE-TOLERANCE; LIFE-STYLE; LOCI;
POLYMORPHISMS; MELLITUS; DISEASE; METAANALYSIS; REPLICATION; POPULATION
AB Background: Multiple genetic loci have been convincingly associated with the risk of type 2 diabetes mellitus. We tested the hypothesis that knowledge of these loci allows better prediction of risk than knowledge of common phenotypic risk factors alone.
Methods: We genotyped single-nucleotide polymorphisms (SNPs) at 18 loci associated with diabetes in 2377 participants of the Framingham Offspring Study. We created a genotype score from the number of risk alleles and used logistic regression to generate C statistics indicating the extent to which the genotype score can discriminate the risk of diabetes when used alone and in addition to clinical risk factors.
Results: There were 255 new cases of diabetes during 28 years of follow-up. The mean (+/-SD) genotype score was 17.7+/-2.7 among subjects in whom diabetes developed and 17.1+/-2.6 among those in whom diabetes did not develop (P<0.001). The sex-adjusted odds ratio for diabetes was 1.12 per risk allele (95% confidence interval, 1.07 to 1.17). The C statistic was 0.534 without the genotype score and 0.581 with the score (P=>0.01). In a model adjusted for sex and self-reported family history of diabetes, the C statistic was 0.595 without the genotype score and 0.615 with the score (P=0.11). In a model adjusted for age, sex, family history, body-mass index, fasting glucose level, systolic blood pressure, high-density lipoprotein cholesterol level, and triglyceride level, the C statistic was 0.900 without the genotype score and 0.901 with the score (P=0.49). The genotype score resulted in the appropriate risk reclassification of, at most, 4% of the subjects.
Conclusions: A genotype score based on 18 risk alleles predicted new cases of diabetes in the community but provided only a slightly better prediction of risk than knowledge of common risk factors alone.
C1 [Meigs, James B.; Shrader, Peter] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.; Shrader, Peter; Florez, Jose C.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[McAteer, Jarred B.; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[McAteer, Jarred B.; Florez, Jose C.] Massachusetts Gen Hosp, Diabet Unit, Dept Med, Boston, MA 02114 USA.
[Sullivan, Lisa M.; Dupuis, Josee; Manning, Alisa K.; Cupples, L. Adrienne] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[McAteer, Jarred B.; Florez, Jose C.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Wilson, Peter W. F.] Emory Univ, Sch Med, Emory Program Cardiovasc Outcomes Res & Epidemiol, Atlanta, GA USA.
[D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
RP Meigs, JB (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Fl, Boston, MA 02114 USA.
EM jmeigs@partners.org
OI Cupples, L. Adrienne/0000-0003-0273-7965; Dupuis,
Josee/0000-0003-2871-3603; Sullivan, Lisa/0000-0003-0726-7149
FU National Heart, Lung, and Blood Institute's Framingham Heart Study
[N01-HC-25195]; National Institute for Diabetes and Digestive and Kidney
Diseases [R01 DK078616, K24 DK080140, K23 DK65978]; Boston University
Linux Cluster for Genetic Analysis; National Institutes of Health
National Center for Research Resources Shared Instrumentation
[1S10RR163736-01A1]; Sanofi-Aventis; GlaxoSmithKline; Merck; Publicis
Healthcare Communications Group
FX Supported by a contract from the National Heart, Lung, and Blood
Institute's Framingham Heart Study (N01-HC-25195), grants from the
National Institute for Diabetes and Digestive and Kidney Diseases
(NIDDK) (R01 DK078616 and K24 DK080140, to Dr. Meigs), an NIDDK Research
Career Award (K23 DK65978, to Dr. Florez), and the Boston University
Linux Cluster for Genetic Analysis, funded by a grant from the National
Institutes of Health National Center for Research Resources Shared
Instrumentation (1S10RR163736-01A1). Dr. Meigs reports serving on a
consultancy board for Interleukin Genetics and receiving grants from
Sanofi-Aventis and GlaxoSmithKline; and Dr. Florez, receiving consulting
fees from Merck and Publicis Healthcare Communications Group, a global
advertising agency engaged by Amylin Pharmaceuticals. No other potential
conflict of interest relevant to this article was reported.
NR 40
TC 392
Z9 405
U1 1
U2 14
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 20
PY 2008
VL 359
IS 21
BP 2208
EP 2219
DI 10.1056/NEJMoa0804742
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373SW
UT WOS:000260994000004
PM 19020323
ER
PT J
AU Violari, A
Cotton, MF
Gibb, DM
Babiker, AG
Steyn, J
Madhi, SA
Jean-Philippe, P
McIntyre, JA
AF Violari, Avy
Cotton, Mark F.
Gibb, Diana M.
Babiker, Abdel G.
Steyn, Jan
Madhi, Shabir A.
Jean-Philippe, Patrick
McIntyre, James A.
CA CHER Study Team
TI Early Antiretroviral Therapy and Mortality among HIV-Infected Infants.
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID DISEASE PROGRESSION; HIV-1-INFECTED CHILDREN; METAANALYSIS; ZIDOVUDINE;
SURVIVAL; REGIMENS; COHORT; TRIAL
AB Background: In countries with a high seroprevalence of human immunodeficiency virus type 1 (HIV-1), HIV infection contributes significantly to infant mortality. We investigated antiretroviral-treatment strategies in the Children with HIV Early Antiretroviral Therapy (CHER) trial.
Methods: HIV-infected infants 6 to 12 weeks of age with a CD4 lymphocyte percentage (the CD4 percentage) of 25% or more were randomly assigned to receive antiretroviral therapy (lopinavir-ritonavir, zidovudine, and lamivudine) when the CD4 percentage decreased to less than 20% (or 25% if the child was younger than 1 year) or clinical criteria were met (the deferred antiretroviral-therapy group) or to immediate initiation of limited antiretroviral therapy until 1 year of age or 2 years of age (the early antiretroviral-therapy groups). We report the early outcomes for infants who received deferred antiretroviral therapy as compared with early antiretroviral therapy.
Results: At a median age of 7.4 weeks (interquartile range, 6.6 to 8.9) and a CD4 percentage of 35.2% (interquartile range, 29.1 to 41.2), 125 infants were randomly assigned to receive deferred therapy, and 252 infants were randomly assigned to receive early therapy. After a median follow-up of 40 weeks (interquartile range, 24 to 58), antiretroviral therapy was initiated in 66% of infants in the deferred-therapy group. Twenty infants in the deferred-therapy group (16%) died versus 10 infants in the early-therapy groups (4%) (hazard ratio for death, 0.24; 95% confidence interval [CI], 0.11 to 0.51; P<0.001). In 32 infants in the deferred-therapy group (26%) versus 16 infants in the early-therapy groups (6%), disease progressed to Centers for Disease Control and Prevention stage C or severe stage B (hazard ratio for disease progression, 0.25; 95% CI, 0.15 to 0.41; P<0.001). Stavudine was substituted for zidovudine in four infants in the early-therapy groups because of neutropenia in three infants and anemia in one infant; no drugs were permanently discontinued. After a review by the data and safety monitoring board, the deferred-therapy group was modified, and infants in this group were all reassessed for initiation of antiretroviral therapy.
Conclusions: Early HIV diagnosis and early antiretroviral therapy reduced early infant mortality by 76% and HIV progression by 75%. (ClinicalTrials.gov number, NCT00102960.).
C1 [Violari, Avy; Steyn, Jan; McIntyre, James A.] Univ Witwatersrand, Perinatal HIV Res Unit, ZA-1864 Johannesburg, South Africa.
[Madhi, Shabir A.] Univ Witwatersrand, Dept Sci & Technol, Natl Res Fdn Vaccine Preventable Dis, ZA-1864 Johannesburg, South Africa.
[Cotton, Mark F.] Univ Stellenbosch, Fac Hlth Sci, Childrens Infect Dis Clin Res Unit, ZA-7505 Tygerberg, South Africa.
[Gibb, Diana M.; Babiker, Abdel G.] MRC, Clin Trials Unit, London, England.
[Jean-Philippe, Patrick] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
RP Violari, A (reprint author), Univ Witwatersrand, Perinatal HIV Res Unit, POB 114, ZA-1864 Johannesburg, South Africa.
EM violari@mweb.co.za
FU National Institute of Allergy and Infectious Diseases; National
Institutes for Health; Comprehensive International Program of Research
on AIDS network [U19 AI53217]; Departments of Health of the Western Cape
and Gauteng, South Africa; GlaxoSmithKline; Abbott Laboratories;
Meningitis Research Foundation; Gilead
FX Supported by a grant from the National Institute of Allergy and
Infectious Diseases of the National Institutes for Health through the
Comprehensive International Program of Research on AIDS network (U19
AI53217); the Departments of Health of the Western Cape and Gauteng,
South Africa; and GlaxoSmithKline. Drs. Violari and Cotton report
receiving lecture fees from Abbott Laboratories; Dr. Babiker, research
support from Abbott Laboratories; and Dr. Gibb, research support from
the Meningitis Research Foundation, GlaxoSmithKline, and Gilead. No
other potential conflict of interest relevant to this article was
reported. The views expressed in this report do not necessarily reflect
the views or policies of the National Institute of Allergy and
Infectious Diseases, nor does mention of trade names, commercial
projects, or organizations imply endorsement by the U. S. government. We
thank the families and children who participated in the trial.
NR 28
TC 628
Z9 655
U1 4
U2 14
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 20
PY 2008
VL 359
IS 21
BP 2233
EP 2244
DI 10.1056/NEJMoa0800971
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373SW
UT WOS:000260994000006
PM 19020325
ER
PT J
AU Ghosh, AK
Chapsal, BD
Baldridge, A
Ide, K
Koh, Y
Mitsuya, H
AF Ghosh, Arun K.
Chapsal, Bruno D.
Baldridge, Abigail
Ide, Kazuhiko
Koh, Yashiro
Mitsuya, Hiroaki
TI Design and Synthesis of Stereochemically Defined Novel Spirocyclic
P2-Ligands for HIV-1 Protease Inhibitors
SO ORGANIC LETTERS
LA English
DT Article
ID DRUG-RESISTANCE
AB The synthesis of a series of stereochemically defined spirocyclic compounds and their use as novel P2-ligands for HIV-1 protease inhibitors are described. The bicyclic core of the ligands was synthesized by an efficient nBu(3)SnH-promoted radical cyclization of a 1,6-enyne followed by oxidative cleavage. Structure-based design, synthesis of ligands, and biological evaluations of the resulting inhibitors are reported.
C1 [Ghosh, Arun K.; Chapsal, Bruno D.; Baldridge, Abigail] Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
[Ghosh, Arun K.; Chapsal, Bruno D.; Baldridge, Abigail] Purdue Univ, Dept Med Chem, W Lafayette, IN 47907 USA.
[Ide, Kazuhiko; Koh, Yashiro; Mitsuya, Hiroaki] Kumamoto Univ, Sch Med, Dept Hematol & Infect Dis, Kumamoto 8608556, Japan.
[Mitsuya, Hiroaki] NCI, Expt Retrovirol Sect, HIV & AIDS Malignancy Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Ghosh, AK (reprint author), Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
EM akghosh@purdue.edu
FU National Institutes of Health [53386]; Intramural Research Program of
the Center for Cancer Research; National Cancer Institute; National
Institutes of Health; Ministry of Education, Culture, Sports, Science,
and Technology of Japan (Monbu Kagakusho); Ministry of Health; Welfare,
and Labor of Japan
FX Financial support by the National Institutes of Health (GM 53386,
A.K.G.) is gratefully acknowledged. This work was also supported in part
by the Intramural Research Program of the Center for Cancer Research,
National Cancer Institute, National Institutes of Health, and in part by
a Grant-in-aid for Scientific Research (Priority Areas) from the
Ministry of Education, Culture, Sports, Science, and Technology of Japan
(Monbu Kagakusho) and a Grant for Promotion of AIDS Research from the
Ministry of Health, Welfare, and Labor of Japan. We thank Mr. David D.
Anderson (Purdue University) for his help with the HPLC and NOESY
analysis.
NR 14
TC 11
Z9 12
U1 1
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1523-7060
J9 ORG LETT
JI Org. Lett.
PD NOV 20
PY 2008
VL 10
IS 22
BP 5135
EP 5138
DI 10.1021/ol8020308
PG 4
WC Chemistry, Organic
SC Chemistry
GA 372SP
UT WOS:000260922500010
PM 18928291
ER
PT J
AU Chakrapani, H
Maciag, AE
Citro, ML
Keefer, LK
Saavedra, JE
AF Chakrapani, Harinath
Maciag, Anna E.
Citro, Michael L.
Keefer, Larry K.
Saavedra, Joseph E.
TI Cell-Permeable Esters of Diazeniumdiolate-Based Nitric Oxide Prodrugs
SO ORGANIC LETTERS
LA English
DT Article
ID VITRO ANTILEUKEMIC ACTIVITY; IN-VITRO; ANTICANCER LEAD; DONOR PRODRUG;
JS-K; RATS; CARCINOGENICITY; NITROSOPROLINE; PROLI/NO; COMPOUND
AB Although O(2)-(2,4-dinitrophenyl) derivatives of diazeniumdiolate-based nitric oxide (NO) prodrugs bearing a free carboxylic acid group were activated by glutathione to release NO, these compounds were poor sources of intracellular NO and showed diminished anti pro I iterative activity against human leukemia HL-60 cells. The carboxylic acid esters of these prodrugs, however, were found to be superior sources of intracellular NO and potent inhibitors of HL-60 cell proliferation.
C1 [Chakrapani, Harinath; Keefer, Larry K.] NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
[Maciag, Anna E.; Citro, Michael L.; Saavedra, Joseph E.] NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA.
RP Chakrapani, H (reprint author), NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
EM chakrah@ncifcrf.gov; saavj@ncifcrf.gov
RI Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU Intramural Research Program of the NIH; National Cancer Institute;
National Cancer Institute [N01-CO-12400]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, as
well as by National Cancer Institute contract N01-CO-12400 to
SAIC-Frederick.
NR 37
TC 16
Z9 16
U1 0
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1523-7060
J9 ORG LETT
JI Org. Lett.
PD NOV 20
PY 2008
VL 10
IS 22
BP 5155
EP 5158
DI 10.1021/ol8020989
PG 4
WC Chemistry, Organic
SC Chemistry
GA 372SP
UT WOS:000260922500015
PM 18956868
ER
PT J
AU Auerbach, SS
Mahler, J
Travlos, GS
Irwin, RD
AF Auerbach, Scott S.
Mahler, Joel
Travlos, Gregory S.
Irwin, Richard D.
TI A comparative 90-day toxicity study of allyl acetate, allyl alcohol and
acrolein
SO TOXICOLOGY
LA English
DT Article
DE Allyl acetate; Allyl alcohol; Acrolein; Prechronic; Gavage
ID CYSTEINE LIGASE MODIFIER; ZERO DOSE CONTROL; ALDEHYDE DEHYDROGENASE;
DNA-REPAIR; RAT-LIVER; CARCINOGENESIS; HEPATOTOXICITY; SUSCEPTIBILITY;
SCHIZOPHRENIA; GENOTOXICITY
AB Allyl acetate (AAC), allyl alcohol (AAL). and acrolein (ACR) are used in the Manufacture of detergents, plastics, pharmaceuticals, and chemicals and as agricultural agents. A metabolic relationship exists between these chemicals in which allyl acetate is metabolized to allyl alcohol and Subsequently to the highly reactive, alpha,beta-unsaturated aldehyde, acrolein. Due to the weaker reactivity or the protoxicants, allyl acetate and allyl alcohol, relative to acrolien we hypothesized the protoxicants would attain greater systemic exposure and therefore deliver higher doses of acrolein to the internal organs. By extension, the higher systemic exposure to acrolein we hypothesized should lead to more internal organ toxicity in the allyl acetate and allyl alcohol treated animals relative to those treated with acrolein. To address our hypothesis we compared the range of toxicities produced by all three chemicals in male and female Fischer 344/N rats and B6C3F1 mice exposed 5 days a week for 3 months by gavage in 0.5% methylcellulose. Rats (10/group) were dosed with 0-100 mg/kg allyl acetate, 0-25 mg/kg allyl alcohol, or 0-10 mg/kg acrolein. Mice (10/group) were dosed with 0-125mg/kg allyl acetate, 0-50mg/kg allyl alcohol, or 0-20mg/kg acrolein. The highest dose of allyl acetate and acrolein decreased survival in both mice and rats. The primary target organ for the toxicity of all three chemicals in both species and sexes was the forestomach: squamous epithelial hyperplasia was observed following exposure to each chemical. In both species the highest allyl acetate dose group exhibited forestomach epithelium necrosis and hemorrhage and the highest dose of acrolein led to glandular stomach hemorrhage. Liver histopathology was the most apparent with allyl acetate, was also observed with allyl alcohol, but was not observed with acrolein. All chemicals had effects on the hematopoietic system with allyl acetate having the most pronounced effect. When dosed at quantities limited by toxicity, allyl acetate and allyl alcohol produce higher levels of urinary mercapturic acids than the minimally toxic dose of acrolein.This observation is likely due to biotransformation of allyl acetate and ally alcohol to acrolein that occurs after absorption and Suggests that these chemicals are protoxicants that increase systemic exposure of acrolein. Increased systemic exposure to acrolein is likely responsible for the differences in hepatic toxicological profile observed with these chemicals. Published by Elsevier Ireland Ltd.
C1 [Auerbach, Scott S.; Mahler, Joel; Travlos, Gregory S.; Irwin, Richard D.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Auerbach, SS (reprint author), NIEHS, Natl Toxicol Program, Res Triangle Pk, Res Triangle Pk, NC 27709 USA.
EM auerbachs@niehs.nih.gov; travlos@niehs.nih.gov; irwin@niehs.nih.gov
FU Intramural NIH HHS [Z99 ES999999]
NR 43
TC 18
Z9 19
U1 0
U2 10
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD NOV 20
PY 2008
VL 253
IS 1-3
BP 79
EP 88
DI 10.1016/j.tox.2008.08.014
PG 10
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 381JI
UT WOS:000261531800049
PM 18817840
ER
PT J
AU Boger, HA
Middaugh, LD
Zaman, V
Hoffer, B
Granholm, AC
AF Boger, Heather A.
Middaugh, Lawrence D.
Zaman, Vandana
Hoffer, Barry
Granholm, Ann-Charlotte
TI Differential effects of the dopamine neurotoxin MPTP in animals with a
partial deletion of the GDNF receptor, GFR alpha 1, gene
SO BRAIN RESEARCH
LA English
DT Article
DE Growth factor receptor; Aging; Neurodegeneration; Neuroinflammation;
Dopamine neurotoxin
ID PARKINSONIAN TOXIN MPTP; NEUROTROPHIC FACTOR; SUBSTANTIA-NIGRA;
NERVOUS-SYSTEM; IN-VIVO; NEUROPROTECTIVE STRATEGIES; MICROGLIAL
ACTIVATION; BETA SUPERFAMILY; MICE LACKING; MOUSE MODEL
AB Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming factor beta (TGF) superfamily, is a potent neurotrophic protein promoting the maintenance of dopaminergic (DA) neurons in the substantia nigra during adulthood. DA neurons that project to the striatum in the nigrostriatal pathway GDNF receptors, GFR alpha 1. The purpose of this study was to determine whether these are especially sensitive to neurotoxic insults. Therefore, we examined effects dopaminergic toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on and DA neurons in 26-month-old male GFR alpha 1 heterozygous (GFR alpha 1(+/-)) mice aged-matched wild-type (WT) littermates. MPTP gave rise to increased locomotion, of genotype, while GFR alpha 1(+/-) mice treated with saline exhibited lower spontaneous compared to WT mice. Moreover, GFR alpha 1(+/-) saline mice had fewer TH-positive greater expression of inflammatory markers (CD45 immunostaining and phosphorylated p38 MAPK) in the nigra, and reduced striatal TH staining. MPTP exacerbated these with the lowest density of striatal TH and highest density of nigral CD45 and MAPK immunoreactivity observed in GFR alpha 1(+/-) mice. The findings point to sensitivity of the DAergic system with age and neurotoxic exposure as a result of a reduction of GFR alpha 1. Published by Elsevier B.V.
C1 [Boger, Heather A.; Middaugh, Lawrence D.; Zaman, Vandana; Granholm, Ann-Charlotte] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
[Middaugh, Lawrence D.] Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA.
[Hoffer, Barry] Natl Inst Drug Abuse, Intramural Res Program, Baltimore, MD USA.
RP Boger, HA (reprint author), Med Univ S Carolina, Dept Neurosci, 173 Ashley Ave,BSB Suite 403, Charleston, SC 29425 USA.
EM boger@musc.edu
FU DAMD [17-99-1-9480, AG023630, AG15239]
FX Supported by DAMD 17-99-1-9480, AG023630, and AG15239. The authors are
thankful to Ms. Claudia Umphlet, Mr. Joe Vallone, and Mr. Alfred Moore
for their expert technical assistance.
NR 73
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U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 19
PY 2008
VL 1241
BP 18
EP 28
DI 10.1016/j.brainres.2008.09.011
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 383LC
UT WOS:000261674100003
PM 18822276
ER
PT J
AU MacBeth, AH
Gautreaux, C
Luine, VN
AF Macbeth, A. H.
Gautreaux, C.
Luine, V. N.
TI Pregnant rats show enhanced spatial memory, decreased anxiety, and
altered levels of monoaminergic neurotransmitters
SO BRAIN RESEARCH
LA English
DT Article
DE Pregnancy; Spatial memory; Anxiety; Monoamines
ID MEDIAL PREFRONTAL CORTEX; ESTROGEN-RECEPTOR-BETA; REPRODUCTIVE
EXPERIENCE; WORKING-MEMORY; MATERNAL-BEHAVIOR; FEMALE RAT;
PARAVENTRICULAR NUCLEUS; OVARIECTOMIZED RATS; NEUROTROPHIC FACTOR;
OBJECT RECOGNITION
AB Spatial memory, anxiety and central monoaminergic activities were measured in nonpregnant (NP) and pregnant females during two time periods of pregnancy: gestational days 7-9 (GD7, GD9) and gestation days 16-18 (GD16, GD18). Pregnant females discriminated between object locations on both test days on an object placement task, whereas NP females were unable to discriminate between locations. Pregnant females displayed decreased anxiety on the elevated plus maze on GD9 compared to NP females, followed by increased anxiety-like behavior on the elevated plus maze on GD18. Monoamine levels and activity (as indexed by turnover ratio) were measured in prefrontal cortex (PFC), CA1 and CA3 regions of the hippocampus (areas important for memory), and medial preoptic area (mPOA, an area important in display of maternal behaviors). In the PFC, NP females generally had higher monoamine levels and turnover ratios; however, norepinephrine (NE) turnover was higher in pregnant females at GD18. In the CA1 and CA3 regions of the hippocampus, monoamine levels and turnover ratios were generally higher during pregnancy, particularly on GD9. In the mPOA, pregnancy was associated with increases in NE activity, a previously unreported finding. The present study expands upon existing research indicating that pregnancy is beneficial to spatial memory and may decrease anxiety. Changes in monoamine levels and activity in specific brain regions indicate that the dopamine, norepinephrine and serotonin systems may contribute to the observed behavioral differences. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Macbeth, A. H.; Gautreaux, C.; Luine, V. N.] CUNY Hunter Coll, Dept Psychol, New York, NY 10021 USA.
[Macbeth, A. H.; Luine, V. N.] CUNY, Grad Ctr, New York, NY 10016 USA.
RP MacBeth, AH (reprint author), NIMH, Sect Neural Gene Express, NIH, DHHS, Bethesda, MD 20892 USA.
EM macbetha@mail.nih.gov; vluine@hunter.cuny.edu
FU Division of Research Infrastructure of the National Center for Research
Resources of NIH [G12 RR-03037]; [S06-CM-60654]
FX The authors thank G. Mohan for assistance in behavior testing. This
research is supported by S06-CM-60654 and a Research Centers in Minority
Institutions award (G12 RR-03037) from the Division of Research
Infrastructure of the National Center for Research Resources of NIH,
which supports the infrastructure of the Biopsychology program at Hunter
College. The contents are solely the responsibility of the authors and
do not necessarily represent the official views of the NCRR/NIH.
NR 63
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U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 19
PY 2008
VL 1241
BP 136
EP 147
DI 10.1016/j.brainres.2008.09.006
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 383LC
UT WOS:000261674100015
PM 18823955
ER
PT J
AU Emanuel, EJ
Fuchs, VR
AF Emanuel, Ezekiel J.
Fuchs, Victor R.
TI Health Care Overutilization in the United States Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID TRUST
C1 [Emanuel, Ezekiel J.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Fuchs, Victor R.] Stanford Univ, Dept Econ, Stanford, CA 94305 USA.
RP Emanuel, EJ (reprint author), NIH, Dept Bioeth, Bldg 10, Bethesda, MD 20892 USA.
EM eemanuel@nih.gov
NR 3
TC 0
Z9 0
U1 1
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 19
PY 2008
VL 300
IS 19
BP 2251
EP 2251
DI 10.1001/jama.2008.605
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373IO
UT WOS:000260965500021
ER
PT J
AU Zarin, DA
Tse, T
AF Zarin, Deborah A.
Tse, Tony
TI Tracking Health Services Research Studies
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Zarin, Deborah A.; Tse, Tony] NIH, Natl Lib Med, Bethesda, MD 20892 USA.
RP Zarin, DA (reprint author), NIH, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM dzarin@mail.nih.gov
NR 2
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 19
PY 2008
VL 300
IS 19
BP 2252
EP 2252
DI 10.1001/jama.2008.612
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373IO
UT WOS:000260965500022
PM 19017910
ER
PT J
AU DeKosky, ST
Williamson, JD
Fitzpatrick, AL
Kronmal, RA
Ives, DG
Saxton, JA
Lopez, OL
Burke, G
Carlson, MC
Fried, LP
Kuller, LH
Robbins, JA
Tracy, RP
Woolard, NF
Dunn, L
Snitz, BE
Nahin, RL
Furberg, CD
AF DeKosky, Steven T.
Williamson, Jeff D.
Fitzpatrick, Annette L.
Kronmal, Richard A.
Ives, Diane G.
Saxton, Judith A.
Lopez, Oscar L.
Burke, Gregory
Carlson, Michelle C.
Fried, Linda P.
Kuller, Lewis H.
Robbins, John A.
Tracy, Russell P.
Woolard, Nancy F.
Dunn, Leslie
Snitz, Beth E.
Nahin, Richard L.
Furberg, Curt D.
CA GEM Study Investigators
TI Ginkgo biloba for Prevention of Dementia A Randomized Controlled Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID EXTRACT EGB 761; MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; VASCULAR
DEMENTIA; CLINICAL-CRITERIA; DOUBLE-BLIND; EFFICACY; DIAGNOSIS; MEMORY;
CONSENSUS
AB Context Ginkgo biloba is widely used for its potential effects on memory and cognition. To date, adequately powered clinical trials testing the effect of G biloba on dementia incidence are lacking.
Objective To determine effectiveness of G biloba vs placebo in reducing the incidence of all- cause dementia and Alzheimer disease ( AD) in elderly individuals with normal cognition and those with mild cognitive impairment ( MCI).
Design, Setting, and Participants Randomized, double- blind, placebo-controlled clinical trial conducted in 5 academic medical centers in the United States between 2000 and 2008 with a median follow- up of 6.1 years. Three thousand sixty- nine community volunteers aged 75 years or older with normal cognition ( n= 2587) or MCI ( n= 482) at study entry were assessed every 6 months for incident dementia.
Intervention Twice- daily dose of 120- mg extract of G biloba ( n= 1545) or placebo ( n= 1524).
Main Outcome Measures Incident dementia and AD determined by expert panel consensus.
Results Five hundred twenty- three individuals developed dementia ( 246 receiving placebo and 277 receiving G biloba) with 92% of the dementia cases classified as possible or probable AD, or AD with evidence of vascular disease of the brain. Rates of dropout and loss to follow- up were low ( 6.3%), and the adverse effect profiles were similar for both groups. The overall dementia rate was 3.3 per 100 person-years in participants assigned to G biloba and 2.9 per 100 person- years in the placebo group. The hazard ratio ( HR) for G biloba compared with placebo for all cause dementia was 1.12 ( 95% confidence interval [ CI], 0.94- 1.33; P=. 21) and for AD, 1.16 ( 95% CI, 0.97- 1.39; P=. 11). G biloba also had no effect on the rate of progression to dementia in participants with MCI ( HR, 1.13; 95% CI, 0.85- 1.50; P=. 39).
Conclusions In this study, G biloba at 120 mg twice a day was not effective in reducing either the overall incidence rate of dementia or AD incidence in elderly individuals with normal cognition or those with MCI.
Trial Registration clinicaltrials. gov Identifier: NCT00010803.
C1 [DeKosky, Steven T.] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[DeKosky, Steven T.; Ives, Diane G.; Saxton, Judith A.; Lopez, Oscar L.; Kuller, Lewis H.; Dunn, Leslie; Snitz, Beth E.] Univ Pittsburgh, Pittsburgh, PA USA.
[Williamson, Jeff D.; Burke, Gregory; Woolard, Nancy F.; Furberg, Curt D.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Fitzpatrick, Annette L.; Kronmal, Richard A.] Univ Washington, Seattle, WA 98195 USA.
[Carlson, Michelle C.; Fried, Linda P.] Johns Hopkins Univ, Baltimore, MD USA.
[Robbins, John A.] Univ Calif Davis, Sacramento, CA 95817 USA.
[Tracy, Russell P.] Univ Vermont, Burlington, VT USA.
[Nahin, Richard L.] Natl Ctr Complementary & Alternat Med, Bethesda, MD USA.
RP DeKosky, ST (reprint author), Univ Virginia, Sch Med, POB 800793, Charlottesville, VA 22908 USA.
EM dekosky@virginia.edu
FU National Center for Complementary and Alternative Medicine [U01
AT000162]; Office of Dietary Supplements; National Institute on Aging;
National Heart, Lung, and Blood Institute; University of Pittsburgh
Alzheimer's Disease Research Center [P50AG05133]; Roena Kulynych Center
for Memory and Cognition Research; Wake Forest University School of
Medicine; National Institute of Neurological Disorders and Stroke
FX This study was supported by grant U01 AT000162 from the National Center
for Complementary and Alternative Medicine (NCCAM) and the Office of
Dietary Supplements and National Institute on Aging; National Heart,
Lung, and Blood Institute; University of Pittsburgh Alzheimer's Disease
Research Center (P50AG05133); Roena Kulynych Center for Memory and
Cognition Research; Wake Forest University School of Medicine; and
National Institute of Neurological Disorders and Stroke. Schwabe
Pharmaceuticals, Karlsruhe, Germany, donated the G biloba tablets and
identical placebos in blister packs for the study.
NR 49
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U1 3
U2 41
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 19
PY 2008
VL 300
IS 19
BP 2253
EP 2262
DI 10.1001/jama.2008.683
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373IO
UT WOS:000260965500025
PM 19017911
ER
PT J
AU Li, WX
Huang, Y
Reid, R
Steiner, J
Malpica-Llanos, T
Darden, TA
Shankar, SK
Mahadevan, A
Satishchandra, P
Nath, A
AF Li, Wenxue
Huang, Yan
Reid, Rollie
Steiner, Joseph
Malpica-Llanos, Tanya
Darden, Thomas A.
Shankar, Susarla K.
Mahadevan, Anita
Satishchandra, Parthasarthy
Nath, Avindra
TI NMDA Receptor Activation by HIV-Tat Protein Is Clade Dependent
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE injury; NMDA receptor; neuron; neuronal death; nitric oxide;
neurotoxicity
ID IMMUNODEFICIENCY-VIRUS TYPE-1; S-NITROSYLATION; AIDS DEMENTIA;
NEUROTOXICITY; ASTROCYTES; SURVIVAL; NEURONS; COMPLEX; MOTIF
AB In countries infected with HIV clade B, some patients develop a rapidly progressive dementia that if untreated results in death. In regions of the world infected with HIV clade C, only milder forms of cognitive impairment have been recognized. HIV-infected macrophages are the principal mediators of dementia. HIV clade C, however, efficiently infects macrophages and HIV-infected macrophages are found in the brains of clade C-infected patients. HIV-infected macrophages release Tat protein, which may act directly on neurons to cause toxicity. We found that Tat released from Tat-expressing cells was at least 1000-fold more toxic than recombinant Tat protein. We determined whether Tat could interact with NMDA receptors and whether these interactions are clade dependent. It is demonstrated that Tat binds directly to the NMDA receptor leading to excitotoxicity. The Cys 30-Cys 31 motif in Tat is critical for exciting the NMDA receptor and the Cys31Ser mutation found in clade C Tat has a significantly attenuated neurotoxic response. Through molecular modeling and site-directed mutagenesis, we predict that Cys 31 disrupts the disulfide bond between Cys 744 and Cys 798 on the NR1 subunit of the NMDA receptor by directly interacting with Cys 744 leading to a free thiol group on Cys 798 and subsequent persistent activation of the NMDA receptor.
C1 [Li, Wenxue; Huang, Yan; Reid, Rollie; Steiner, Joseph; Malpica-Llanos, Tanya; Nath, Avindra] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21287 USA.
[Nath, Avindra] Johns Hopkins Univ, Dept Neurosci, Baltimore, MD 21287 USA.
[Darden, Thomas A.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Shankar, Susarla K.; Mahadevan, Anita] Natl Inst Mental Hlth & Neurosci, Dept Neuropathol, Bangalore 560029, Karnataka, India.
[Satishchandra, Parthasarthy] Natl Inst Mental Hlth & Neurosci, Dept Neurol, Bangalore 560029, Karnataka, India.
RP Nath, A (reprint author), Johns Hopkins Univ, Dept Neurol, 509 Pathol,600 N Wolfe St, Baltimore, MD 21287 USA.
EM anath1@jhmi.edu
FU National Institutes of Health (NIH) [P01MH070306, R01NS039253,
R01NS056884]; Intramural Research Program of the NIH; National Institute
of Environmental Health Sciences
FX This work was supported by National Institutes of Health (NIH) Grants
P01MH070306, R01NS039253, and R01NS056884 and by the Intramural Research
Program of the NIH, National Institute of Environmental Health Sciences.
We are grateful to Dr. Joan Berman for critically reading this
manuscript, Dr. Richard Huganir for helpful comments, and Dr. Solomon
Snyder's laboratory for assistance with the biotin switch assay.
NR 24
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U1 0
U2 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 19
PY 2008
VL 28
IS 47
BP 12190
EP 12198
DI 10.1523/JNEUROSCI.3019-08.2008
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 376NT
UT WOS:000261191000006
PM 19020013
ER
PT J
AU Koenigs, M
Huey, ED
Calamia, M
Raymont, V
Tranel, D
Grafman, J
AF Koenigs, Michael
Huey, Edward D.
Calamia, Matthew
Raymont, Vanessa
Tranel, Daniel
Grafman, Jordan
TI Distinct Regions of Prefrontal Cortex Mediate Resistance and
Vulnerability to Depression
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE depression; emotion; prefrontal cortex; ventromedial; dorsolateral;
neuropathology
ID TRANSCRANIAL MAGNETIC STIMULATION; ORBITOFRONTAL CORTEX; MAJOR
DEPRESSION; UNIPOLAR DEPRESSION; GLUCOSE-METABOLISM; ANXIETY DISORDERS;
LESION LOCATION; MOOD DISORDERS; INVENTORY-II; BDI-II
AB The neuroanatomical correlates of depression remain unclear. Functional imaging data have associated depression with abnormal patterns of activity in prefrontal cortex (PFC), including the ventromedial (vmPFC) and dorsolateral (dlPFC) sectors. If vmPFC and dlPFC are critical neural substrates for the pathogenesis of depression, then damage to either area should affect the expression of depressive symptoms. Using patients with brain lesions we show that, relative to nonfrontal lesions, bilateral vmPFC lesions are associated with markedly low levels of depression, whereas bilateral dorsal PFC lesions (involving dorsomedial and dorsolateral areas in both hemispheres) are associated with substantially higher levels of depression. These findings demonstrate that vmPFC and dorsal PFC are critically and causally involved in depression, although with very different roles: vmPFC damage confers resistance to depression, whereas dorsal PFC damage confers vulnerability.
C1 [Huey, Edward D.; Raymont, Vanessa; Grafman, Jordan] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
[Koenigs, Michael] Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA.
[Calamia, Matthew; Tranel, Daniel] Univ Iowa Hosp & Clin, Dept Neurol, Iowa City, IA 52242 USA.
[Raymont, Vanessa] Natl Naval Med Ctr, Henry M Jackson Fdn, Vietnam Head Injury Study, Bethesda, MD 20889 USA.
RP Grafman, J (reprint author), NINDS, Cognit Neurosci Sect, NIH, 10 Ctr Dr,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
OI Grafman, Jordan H./0000-0001-8645-4457; Koenigs,
Michael/0000-0002-5799-4881; Calamia, Matthew/0000-0002-7252-7181
FU National Institute of Neurological Disorders and Stroke (NINDS)
[DAMD17-01-1-0675, P01 NS19632]; National Institute on Drug Abuse [R01
DA022549]
FX This work was supported in part by the National Institute of
Neurological Disorders and Stroke (NINDS) intramural research program,
DAMD17-01-1-0675 (J. G.), National Institute on Drug Abuse Grant R01
DA022549 (D. T.), and NINDS Grant P01 NS19632 (D. T.).
NR 58
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U1 6
U2 16
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 19
PY 2008
VL 28
IS 47
BP 12341
EP 12348
DI 10.1523/JNEUROSCI.2324-08.2008
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 376NT
UT WOS:000261191000020
PM 19020027
ER
PT J
AU Aschrafi, A
Schwechter, AD
Mameza, MG
Natera-Naranjo, O
Gioio, AE
Kaplan, BB
AF Aschrafi, Armaz
Schwechter, Azik D.
Mameza, Marie G.
Natera-Naranjo, Orlangie
Gioio, Anthony E.
Kaplan, Barry B.
TI MicroRNA-338 Regulates Local Cytochrome c Oxidase IV mRNA Levels and
Oxidative Phosphorylation in the Axons of Sympathetic Neurons
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE mitochondria; ATP synthesis; RNA localization; inhibitory RNA; oxidative
phosphorylation; local translation; norepinephrine uptake
ID NEURODEGENERATIVE DISEASES; ALZHEIMERS-DISEASE; PROTEIN-SYNTHESIS;
ANIMAL MICRORNAS; GROWTH CONES; IN-VITRO; MITOCHONDRIA; TRANSLATION;
DROSOPHILA; TRANSPORT
AB MicroRNAs (miRs) are evolutionarily conserved, noncoding RNA molecules of similar to 21 nt that regulate the expression of genes that are involved in various biological processes, such as cell proliferation and differentiation. Previously, we reported the presence of a heterogeneous population of mRNAs present in the axons and nerve terminals of primary sympathetic neurons to include the nuclear-encoded mitochondrial mRNA coding for COXIV. Sequence analysis of the 3'UTRof this mRNA revealed the presence of a putative binding site for miR-338, a brain-specific microRNA. Transfection of precursor miR-338 into the axons of primary sympathetic neurons decreases COXIV mRNA and protein levels and results in a decrease in mitochondrial activity, as measured by the reduction of ATP levels. Conversely, the transfection of synthetic anti-miR oligonucleotides that inhibit miR-338 increases COXIV levels, and results in a significant increase in oxidative phosphorylation and also norepinephrine uptake in the axons. Our results point to a molecular mechanism by which this microRNA participates in the regulation of axonal respiration and function by modulating the levels of COXIV, a protein which plays a key role in the assembly of the mitochondrial cytochrome c oxidase complex IV.
C1 [Aschrafi, Armaz; Schwechter, Azik D.; Mameza, Marie G.; Natera-Naranjo, Orlangie; Gioio, Anthony E.; Kaplan, Barry B.] NIMH, Mol Neurobiol Sect, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Kaplan, BB (reprint author), NIMH, Mol Neurobiol Sect, Mol Biol Lab, NIH, Bldg 10,Room 4A15,10 Ctr Dr, Bethesda, MD 20892 USA.
EM kaplanb@mail.nih.gov
RI Aschrafi, Armaz/E-2202-2012
FU National Institute of Mental Health
FX This work was supported by the Division of Intramural Research Programs
of the National Institute of Mental Health. We thank Dr. Neil Smalheiser
(University of Illinois) for the kind gift of the DICER and eIF2c
antibodies. We thank Elena Perry for assistance with the miR maturation
studies. We express our gratitude to Dr. Howard Nash (National Institute
of Mental Health) for a critical evaluation of this manuscript.
NR 49
TC 113
Z9 117
U1 1
U2 20
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 19
PY 2008
VL 28
IS 47
BP 12581
EP 12590
DI 10.1523/JNEUROSCI.3338-08.2008
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 376NT
UT WOS:000261191000043
PM 19020050
ER
PT J
AU Kaye, FJ
AF Kaye, Frederic J.
TI Defining a Candidate Lung Cancer Gene
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID SQUAMOUS-CELL CARCINOMA; DIFFERENTIALLY EXPRESSED GENES;
SACCHAROMYCES-CEREVISIAE; IDENTIFICATION; DNA
C1 [Kaye, Frederic J.] NCI, NIH, Bethesda, MD 20889 USA.
[Kaye, Frederic J.] Natl Naval Med Ctr, NCI Navy Oncol, Bethesda, MD USA.
RP Kaye, FJ (reprint author), NCI, NIH, NCI Navy Oncol Bldg 8,Rm 5101,8901 Wisconsin Ave, Bethesda, MD 20889 USA.
EM kayef@mail.nih.gov
RI kaye, frederic/E-2437-2011
NR 20
TC 3
Z9 3
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 19
PY 2008
VL 100
IS 22
BP 1564
EP 1565
DI 10.1093/jnci/djn381
PG 2
WC Oncology
SC Oncology
GA 376FR
UT WOS:000261170000002
PM 19001597
ER
PT J
AU Chlebowski, RT
Johnson, KC
Kooperberg, C
Pettinger, M
Wactawski-Wende, J
Rohan, T
Rossouw, J
Lane, D
O'Sullivan, MJ
Yasmeen, S
Hiatt, RA
Shikany, JM
Vitolins, M
Khandekar, J
Hubbell, FA
AF Chlebowski, Rowan T.
Johnson, Karen C.
Kooperberg, Charles
Pettinger, Mary
Wactawski-Wende, Jean
Rohan, Tom
Rossouw, Jacques
Lane, Dorothy
O'Sullivan, Mary Jo
Yasmeen, Shagufta
Hiatt, Robert A.
Shikany, James M.
Vitolins, Mara
Khandekar, Janu
Hubbell, F. Allan
CA Women's Health Initiative Investig
TI Calcium Plus Vitamin D Supplementation and the Risk of Breast Cancer
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; WOMENS HEALTH; POSTMENOPAUSAL WOMEN;
COLORECTAL-CANCER; DAIRY-PRODUCTS; PREVENTION; TAMOXIFEN;
MICRONUTRIENTS; INTERVENTIONS; MEDICATION
AB Although some observational studies have associated higher calcium intake and especially higher vitamin D intake and 25-hydroxyvitamin D levels with lower breast cancer risk, no randomized trial has evaluated these relationships.
Postmenopausal women (N = 36 282) who were enrolled in a Women's Health Initiative clinical trial were randomly assigned to 1000 mg of elemental calcium with 400 IU of vitamin D(3) daily or placebo for a mean of 7.0 years to determine the effects of supplement use on incidence of hip fracture. Mammograms and breast exams were serially conducted. Invasive breast cancer was a secondary outcome. Baseline serum 25-hydroxyvitamin D levels were assessed in a nested case-control study of 1067 case patients and 1067 control subjects. A Cox proportional hazards model was used to estimate the risk of breast cancer associated with random assignment to calcium with vitamin D(3). Associations between 25-hydroxyvitamin D serum levels and total vitamin D intake, body mass index (BMI), recreational physical activity, and breast cancer risks were evaluated using logistic regression models. Statistical tests were two-sided.
Invasive breast cancer incidence was similar in the two groups (528 supplement vs 546 placebo; hazard ratio = 0.96; 95% confidence interval = 0.85 to 1.09). In the nested case-control study, no effect of supplement group assignment on breast cancer risk was seen. Baseline 25-hydroxyvitamin D levels were modestly correlated with total vitamin D intake (diet and supplements) (r = 0.19, P < .001) and were higher among women with lower BMI and higher recreational physical activity (both P < .001). Baseline 25-hydroxyvitamin D levels were not associated with breast cancer risk in analyses that were adjusted for BMI and physical activity (P(trend) = .20).
Calcium and vitamin D supplementation did not reduce invasive breast cancer incidence in postmenopausal women. In addition, 25-hydroxyvitamin D levels were not associated with subsequent breast cancer risk. These findings do not support a relationship between total vitamin D intake and 25-hydroxyvitamin D levels with breast cancer risk.
C1 [Chlebowski, Rowan T.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90502 USA.
[Johnson, Karen C.] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN USA.
[Kooperberg, Charles; Pettinger, Mary] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Rohan, Tom] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Rossouw, Jacques] NHLBI, Bethesda, MD 20892 USA.
[Lane, Dorothy] SUNY Stony Brook, Dept Prevent Med, Stony Brook, NY 11794 USA.
[O'Sullivan, Mary Jo] Univ Miami, Dept Obstet & Gynecol, Miami, FL USA.
[Yasmeen, Shagufta] Univ Calif Davis, Dept Med, Sacramento, CA 95817 USA.
[Hiatt, Robert A.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Shikany, James M.] Univ Alabama, Dept Prevent Med, Birmingham, AL USA.
[Vitolins, Mara] Wake Forest Univ, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA.
[Khandekar, Janu] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Hubbell, F. Allan] Univ Calif Irvine, Dept Med, Irvine, CA 92717 USA.
RP Chlebowski, RT (reprint author), Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, 1124 W Carson St, Torrance, CA 90502 USA.
EM rchlebowski@gmail.com
RI Cauley, Jane/N-4836-2015
OI Cauley, Jane/0000-0003-0752-4408
FU National Heart, Lung and Blood Institute of the National Institutes of
Health, Department of Health and Human Services
FX The Women's Health Initiative program was funded by the National Heart,
Lung and Blood Institute of the National Institutes of Health,
Department of Health and Human Services.
NR 40
TC 206
Z9 208
U1 1
U2 24
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 19
PY 2008
VL 100
IS 22
BP 1581
EP 1591
DI 10.1093/jnci/djn360
PG 11
WC Oncology
SC Oncology
GA 376FR
UT WOS:000261170000007
PM 19001601
ER
PT J
AU Brinton, LA
Sherman, ME
Carreon, JD
Anderson, WF
AF Brinton, Louise A.
Sherman, Mark E.
Carreon, J. Daniel
Anderson, William F.
TI Recent Trends in Breast Cancer Among Younger Women in the United States
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID AFRICAN-AMERICAN WOMEN; REPRODUCTIVE FACTORS; BRCA2 MUTATIONS;
RISK-FACTORS; WHITE WOMEN; AGE; PHENOTYPE; RATES; MAMMOGRAPHY; CARCINOMA
AB Increases in the incidence of postmenopausal breast cancers have been linked to screening and menopausal hormone use, but younger women have received less attention. Thus, we analyzed trends in breast cancer incidence (N = 387 231) using the National Cancer Institute's Surveillance, Epidemiology, and End Results Program 13-Registry database (1992-2004). Whites had higher incidence rates than blacks after age 40 years, but the reverse was true among younger women (black-white crossover). Among younger women, the rate per 100 000 woman-years was 16.8 for black vs 15.1 for white women; the highest black-white incidence rate ratio (IRR) was seen among women younger than 30 years (IRR = 1.52, 95% confidence interval = 1.34 to 1.73). This risk pattern was not observed in other ethnic groups. The black-white crossover among younger women was largely restricted to breast cancers with favorable tumor characteristics. The annual percentage change in the incidence of invasive breast cancers decreased modestly among older women but increased among younger (< 40 years) white women. Continued surveillance of trends is needed, particularly for molecular subtypes that preferentially occur among young women.
C1 [Brinton, Louise A.; Sherman, Mark E.; Carreon, J. Daniel] NCI, Div Canc Epidemiol & Genet, Hormonal & Reprod Epidemiol Branch, Bethesda, MD 20852 USA.
[Anderson, William F.] NCI, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD 20852 USA.
RP Brinton, LA (reprint author), NCI, Div Canc Epidemiol & Genet, Hormonal & Reprod Epidemiol Branch, 6120 Execut Blvd,Suite 550,Room 5018, Bethesda, MD 20852 USA.
EM brinton@nih.gov
RI Brinton, Louise/G-7486-2015
OI Brinton, Louise/0000-0003-3853-8562
FU National Institutes of Health; National Cancer Institute
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute.
NR 31
TC 101
Z9 113
U1 1
U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 19
PY 2008
VL 100
IS 22
BP 1643
EP 1648
DI 10.1093/jnci/djn344
PG 6
WC Oncology
SC Oncology
GA 376FR
UT WOS:000261170000011
PM 19001605
ER
PT J
AU Prosser, JM
Eisenberg, D
Davey, EE
Steinfeld, M
Cohen, LJ
London, ED
Galynker, II
AF Prosser, James M.
Eisenberg, Daniel
Davey, Emily E.
Steinfeld, Matthew
Cohen, Lisa J.
London, Edythe D.
Galynker, Igor I.
TI Character pathology and neuropsychological test performance in remitted
opiate dependence
SO SUBSTANCE ABUSE TREATMENT PREVENTION AND POLICY
LA English
DT Article
ID METHADONE-MAINTENANCE PATIENTS; SCHIZOTYPAL PERSONALITY-DISORDER;
WORD-ASSOCIATION TEST; COGNITIVE IMPAIRMENT; TREATMENT OUTCOMES;
ADDICTION; ABUSE; RETENTION; NORMS; DETOXIFICATION
AB Background: Cognitive deficits and personality pathology are prevalent in opiate dependence, even during periods of remission, and likely contribute to relapse. Understanding the relationship between the two in vulnerable, opiate-addicted patients may contribute to the design of better treatment and relapse prevention strategies.
Methods: The Millon Multiaxial Clinical Inventory (MCMI) and a series of neuropsychological tests were administered to three subject groups: 29 subjects receiving methadone maintenance treatment (MM), 27 subjects in protracted abstinence from methadone maintenance treatment (PA), and 29 healthy non-dependent comparison subjects. Relationships between MCMI scores, neuropsychological test results, and measures of substance use and treatment were examined using bivariate correlation and regression analysis.
Results: MCMI scores were greater in subjects with a history of opiate dependence than in comparison subjects. A significant negative correlation between MCMI scores and neuropsychological test performance was identified in all subjects. MCMI scores were stronger predictors of neuropsychological test performance than measures of drug use.
Conclusion: Formerly methadone-treated opiate dependent individuals in protracted opiate abstinence demonstrate a strong relationship between personality pathology and cognitive deficits. The cause of these deficits is unclear and most likely multi-factorial. This finding may be important in understanding and interpreting neuropsychological testing deficiencies in opiate-dependent subjects.
C1 [Prosser, James M.; Cohen, Lisa J.; Galynker, Igor I.] Beth Israel Deaconess Med Ctr, Dept Psychiat & Behav Sci, New York, NY 10003 USA.
[Eisenberg, Daniel] NIMH, Div Clin Res, Bethesda, MD 20892 USA.
[Davey, Emily E.; Steinfeld, Matthew] New Sch Social Res, Dept Psychol, New York, NY 10011 USA.
[London, Edythe D.] Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst, Dept Med & Mol Pharmacol, Los Angeles, CA 90095 USA.
[Prosser, James M.] Beth Israel Deaconess Med Ctr, Dept Psychiat, New York, NY 10003 USA.
RP Prosser, JM (reprint author), Beth Israel Deaconess Med Ctr, Dept Psychiat & Behav Sci, 1st Ave,16th St, New York, NY 10003 USA.
EM jprosser@chpnet.org; eisenbegd@mail.nih.gov; davee299@newschool.edu;
steim075@newschool.edu; lcohen@chpnet.org; elondon@mednet.ucla.edu;
igalyner@chpnet.org
RI Eisenberg, Daniel/C-7432-2014
FU Intramural NIH HHS; NIDA NIH HHS [R01 DA 12273]
NR 59
TC 4
Z9 4
U1 1
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1747-597X
J9 SUBST ABUSE TREAT PR
JI Subst/ Abus. Treatment Prev. Pol.
PD NOV 19
PY 2008
VL 3
AR 23
DI 10.1186/1747-597X-3-23
PG 11
WC Substance Abuse
SC Substance Abuse
GA 432EY
UT WOS:000265117500001
PM 19019247
ER
PT J
AU Levy, MM
Rapoport, J
Lemeshow, S
Phillips, G
Chalfin, DB
Danis, M
AF Levy, Mitchell M.
Rapoport, John
Lemeshow, Stan
Phillips, Gary
Chalfin, Donald B.
Danis, Marion
TI What Conclusions Should Be Drawn between Critical Care Physician
Management and Patient Mortality in the Intensive Care Unit? Reply
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Levy, Mitchell M.] Rhode Isl Hosp, Providence, RI 02903 USA.
[Rapoport, John] Mt Holyoke Coll, S Hadley, MA 01077 USA.
[Lemeshow, Stan; Phillips, Gary] Ohio State Univ, Coll Hlth, Columbus, OH 43210 USA.
[Chalfin, Donald B.] Abbott Point Care, E Windsor, NJ 08520 USA.
[Danis, Marion] NIH, Bethesda, MD 20892 USA.
RP Levy, MM (reprint author), Rhode Isl Hosp, Providence, RI 02903 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 18
PY 2008
VL 149
IS 10
BP 772
EP 772
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373FL
UT WOS:000260956300018
ER
PT J
AU Braun, R
Cope, L
Parmigiani, G
AF Braun, Rosemary
Cope, Leslie
Parmigiani, Giovanni
TI Identifying differential correlation in gene/pathway combinations
SO BMC BIOINFORMATICS
LA English
DT Article
ID EXPRESSED GENE COMBINATIONS; WIDE COEXPRESSION DYNAMICS; MICROARRAY
DATA; STATISTICAL-METHODS; SET ENRICHMENT; CANCER; TUMOR
AB Background: An important emerging trend in the analysis of microarray data is to incorporate known pathway information a priori. Expression level "summaries" for pathways, obtained from the expression data for the genes constituting the pathway, permit the inclusion of pathway information, reduce the high dimensionality of microarray data, and have the power to elucidate gene-interaction dependencies which are not already accounted for through known pathway identification.
Results: We present a novel method for the analysis of microarray data that identifies joint differential expression in gene-pathway pairs. This method takes advantage of known gene pathway memberships to compute a summary expression level for each pathway as a whole. Correlations between the pathway expression summary and the expression levels of genes not already known to be associated with the pathway provide clues to gene interaction dependencies that are not already accounted for through known pathway identification, and statistically significant differences between gene-pathway correlations in phenotypically different cells (e. g., where the expression level of a single gene and a given pathway summary correlate strongly in normal cells but weakly in tumor cells) may indicate biologically relevant gene-pathway interactions. Here, we detail the methodology and present the results of this method applied to two gene-expression datasets, identifying gene-pathway pairs which exhibit differential joint expression by phenotype.
Conclusion: The method described herein provides a means by which interactions between large numbers of genes may be identified by incorporating known pathway information to reduce the dimensionality of gene interactions. The method is efficient and easily applied to data sets of similar to 10(2) arrays. Application of this method to two publicly-available cancer data sets yields suggestive and promising results. This method has the potential to complement gene-at-a-time analysis techniques for microarray analysis by indicating relationships between pathways and genes that have not previously been identified and which may play a role in disease.
C1 [Braun, Rosemary] NCI, NIH, Bethesda, MD 20892 USA.
[Cope, Leslie; Parmigiani, Giovanni] Johns Hopkins Univ, Sydney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA.
RP Braun, R (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM braunr@mail.nih.gov; lcope1@jhmi.edu; gp@jhu.edu
OI Braun, Rosemary/0000-0001-9668-9866
FU Cancer Prevention Fellowship Program; Division of Cancer Prevention;
National Cancer Institute; National Institutes of Health; National
Science Foundation [DMS034211]
FX RB was supported by the Cancer Prevention Fellowship Program, Division
of Cancer Prevention, National Cancer Institute, National Institutes of
Health. LC and GP were supported by National Science Foundation grant
DMS034211.
NR 31
TC 7
Z9 7
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 18
PY 2008
VL 9
AR 488
DI 10.1186/1471-2105-9-488
PG 17
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA 396NV
UT WOS:000262599300001
PM 19017408
ER
PT J
AU Stevenson, LW
Hellkamp, AS
Leier, CV
Sopko, G
Koelling, T
Warnica, JW
Abraham, WT
Kasper, EK
Rogers, JG
Califf, RM
Schramm, EE
O'Connor, CM
AF Stevenson, Lynne W.
Hellkamp, Anne S.
Leier, Carl V.
Sopko, George
Koelling, Todd
Warnica, J. Wayne
Abraham, William T.
Kasper, Edward K.
Rogers, Joseph G.
Califf, Robert M.
Schramm, Elizabeth E.
O'Connor, Christopher M.
TI Changing Preferences for Survival After Hospitalization With Advanced
Heart Failure
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE heart failure; quality of life; health utilities; hospitalization;
cardiomyopathy
ID QUALITY-OF-LIFE; PATIENT PREFERENCES; BREAST-CANCER; TRADE-OFF; TRIAL;
OUTCOMES; THERAPY; UTILITY
AB Objectives This study was designed to analyze how patient preferences for survival versus quality-of-life change after hospitalization with advanced heart failure (HF).
Background Although patient-centered care is a priority, little is known about preferences to trade length of life for quality among hospitalized patients with advanced HF, and it is not known how those preferences change after hospitalization.
Methods The time trade-off utility, symptom scores, and 6-min walk distance were measured in 287 patients in the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness) trial at hospitalization and again during 6 months after therapy to relieve congestion.
Results Willingness to trade was bimodal. At baseline, the median trade for better quality was 3 months' survival time, with a modest relation to symptom severity. Preference for survival time was stable for most patients, but increase after discharge occurred in 98 of 145 (68%) patients initially willing to trade survival time, and was more common with symptom improvement and after therapy guided by pulmonary artery catheters (p = 0.034). Adjusting days alive after hospital discharge for patients' survival preference reduced overall days by 24%, with the largest reduction among patients dying early after discharge (p = 0.0015).
Conclusions Preferences remain in favor of survival for many patients despite advanced HF symptoms, but increase further after hospitalization. The bimodal distribution and the stability of patient preference limit utility as a trial end point, but support its relevance in design of care for an individual patient. (J Am Coll Cardiol 2008; 52: 1702-8) (C) 2008 by the American College of Cardiology Foundation
C1 [Stevenson, Lynne W.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Hellkamp, Anne S.; Califf, Robert M.; Schramm, Elizabeth E.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Rogers, Joseph G.; O'Connor, Christopher M.] Duke Univ, Med Ctr, Div Cardiol, Durham, NC USA.
[Leier, Carl V.; Abraham, William T.] Ohio State Univ, Med Ctr, Div Cardiol, Columbus, OH 43210 USA.
[Sopko, George] NHLBI, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Koelling, Todd] Univ Michigan, Ctr Cardiovasc, Div Cardiol, Ann Arbor, MI 48109 USA.
[Warnica, J. Wayne] Univ Calgary, Div Cardiol, Calgary, AB T2N 1N4, Canada.
[Kasper, Edward K.] Div Cardiol, Baltimore, MD USA.
RP Stevenson, LW (reprint author), Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA.
EM LStevenson@partners.org
FU National Heart, Lung, and Blood Institute [N01-HV-98177]
FX This study was supported by contract N01-HV-98177 from the National
Heart, Lung, and Blood Institute.
NR 15
TC 69
Z9 69
U1 2
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 18
PY 2008
VL 52
IS 21
BP 1702
EP 1708
DI 10.1016/j.jacc.2008.08.028
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 374GD
UT WOS:000261030900003
PM 19007689
ER
PT J
AU Houlden, H
Laura, M
Wavrant-De Vrieze, F
Blake, J
Wood, N
Reilly, MM
AF Houlden, H.
Laura, M.
Wavrant-De Vrieze, F.
Blake, J.
Wood, N.
Reilly, M. M.
TI Mutations in the HSP27 (HSPB1) gene cause dominant, recessive, and
sporadic distal HMN/CMT type 2
SO NEUROLOGY
LA English
DT Article
ID MARIE-TOOTH-DISEASE; DIFFERENTIATION-ASSOCIATED PROTEIN-1;
AMYOTROPHIC-LATERAL-SCLEROSIS; HEREDITARY MOTOR NEUROPATHY;
ALPHA-B-CRYSTALLIN; HEAT-SHOCK; MISSENSE MUTATION; FOUNDER; MUTANT;
GDAP1
AB Background: Charcot-Marie-Tooth disease (CMT) is the most common inherited neuromuscular disorder and is characterized by significant clinical and genetic heterogeneity. Recently, mutations in both the small heat shock protein 27 ( HSP27 or HSPB1) and 22 ( HSP22 or HSPB8) genes have been reported to cause autosomal dominant CMT with minimal sensory involvement ( CMT 2F/CMT2L) and autosomal dominant distal hereditary motor neuropathy type II ( dHMN II).
Methods: We analyzed the HSPB1 and HSPB8 genes in a large clinically well-characterized series of dHMN and CMT type 2 ( CMT2) cases and families using linkage analysis and direct sequencing of these genes.
Results: We identified a novel homozygous mutation in the alpha-crystallin domain of HSPB1 segregating in an autosomal recessive fashion in a family with distal HMN/CMT2. A further four heterozygous HSPB1 mutations were identified in four autosomal dominant families dHMN/CMT2, and two sporadic cases were identified with probable de novo mutations. In the autosomal dominant and autosomal recessive families, there were no clinical sensory findings, but reduced sural nerve action potential amplitudes were found in some affected individuals, indicating that long sensory axons are mildly affected in this predominantly motor disorder.
Conclusions: This extends the clinical and electrophysiologic spectrum of HSPB1 mutations and identifies four unreported dominant HSPB1 mutations and the first family where the HSPB1 mutation acts in a recessive way to cause distal HMN. Neurology (R) 2008;71:1660-1668
C1 [Houlden, H.; Laura, M.; Wood, N.; Reilly, M. M.] Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
[Houlden, H.; Laura, M.; Blake, J.; Wood, N.; Reilly, M. M.] Inst Neurol, Ctr Neuromuscular Dis, London WC1N 3BG, England.
Natl Hosp Neurol & Neurosurg, London WC1N 3BG, England.
[Wavrant-De Vrieze, F.] NIA, NIH, Neurogenet Lab, Bethesda, MD 20892 USA.
[Blake, J.] Norfolk & Norwich Univ Hosp, Dept Clin Neurophysiol, Norwich, Norfolk, England.
RP Houlden, H (reprint author), Inst Neurol, Dept Mol Neurosci, Queen Sq, London WC1N 3BG, England.
EM h.houlden@ion.ucl.ac.uk
RI Houlden, Henry/C-1532-2008; Reilly, Mary/C-8482-2013; Wood,
Nicholas/C-2505-2009
OI Houlden, Henry/0000-0002-2866-7777; Wood, Nicholas/0000-0002-9500-3348
FU Medical Research Council (MRC); Muscular Dystrophy Campaign and Brain
Research Trust (BRT); Department of Health's National Institute for
Health Research Biomedical Research Centers
FX The authors acknowledge the Medical Research Council (MRC) for the
clinician scientist fellowship to H. H. and the Muscular Dystrophy
Campaign and Brain Research Trust (BRT) for funding support. This work
was undertaken at University College London Hospitals/University College
London, which received a proportion of funding from the Department of
Health's National Institute for Health Research Biomedical Research
Centers funding scheme.
NR 27
TC 100
Z9 100
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV 18
PY 2008
VL 71
IS 21
BP 1660
EP 1668
DI 10.1212/01.wnl.0000319696.14225.67
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 373EK
UT WOS:000260953600003
PM 18832141
ER
PT J
AU Zhang, CL
Qiu, CF
Hu, FB
David, RM
van Dam, RM
Bralley, A
Williams, MA
AF Zhang, Cuilin
Qiu, Chunfang
Hu, Frank B.
David, Robert M.
van Dam, Rob M.
Bralley, Alexander
Williams, Michelle A.
TI Maternal Plasma 25-Hydroxyvitamin D Concentrations and the Risk for
Gestational Diabetes Mellitus
SO PLOS ONE
LA English
DT Article
AB Background: Evidence is accumulating for a role of vitamin D in maintaining normal glucose homeostasis. However, studies that prospectively examined circulating concentrations of 25-hydroxyvitamin D ( 25-[OH] D) in relation to diabetes risk are limited. Our objective is to determine the association between maternal plasma 25-[OH] D concentrations in early pregnancy and the risk for gestational diabetes mellitus (GDM).
Methods: A nested case-control study was conducted among a prospective cohort of 953 pregnant women. Among them, 57 incident GDM cases were ascertained and 114 women who were not diagnosed with GDM were selected as controls. Controls were frequency matched to cases for the estimated season of conception of the index pregnancy. Results: Among women who developed GDM, maternal plasma 25-[OH] D concentrations at an average of 16 weeks of gestation were significantly lower than controls (24.2 vs. 30.1 ng/ml, P < 0.001). This difference remained significant (3.62 ng/ml lower on average in GDM cases than controls (P value = 0.018)) after the adjustment for maternal age, race, family history of diabetes, and pre-pregnancy BMI. Approximately 33% of GDM cases, compared with 14% of controls (P < 0.001), had maternal plasma 25-[OH] D concentrations consistent with a pre-specified diagnosis of vitamin D deficiency (<20 ng/ml). After adjustment for the aforementioned covariates including BMI, vitamin D deficiency was associated with a 2.66-fold (OR (95% CI): 2.66 (1.01-7.02)) increased GDM risk. Moreover, each 5 ng/ml decrease in 25-[OH] D concentrations was related to a 1.29-fold increase in GDM risk (OR (95% CI): 1.29 (1.05-1.60)). Additional adjustment for season and physical activity did not change findings substantially.
Conclusions: Findings from the present study suggest that maternal vitamin D deficiency in early pregnancy is significantly associated with an elevated risk for GDM.
C1 [Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD USA.
[Qiu, Chunfang; Williams, Michelle A.] Swedish Med Ctr, Ctr Perinatal Studies, Seattle, WA USA.
[Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Hu, Frank B.; van Dam, Rob M.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Hu, Frank B.; van Dam, Rob M.] Harvard Univ, Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[David, Robert M.; Bralley, Alexander] Metametrix Clin Lab, Norcross, GA USA.
[Williams, Michelle A.] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA.
RP Zhang, CL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD USA.
EM zhangcu@mail.nih.gov
RI van Dam, Rob/F-9674-2010
OI van Dam, Rob/0000-0002-7354-8734
FU National Institutes of Health [HD/HL 32562]; Intramural Research Program
of the Eunice Kennedy Shriver National Institute of Child Health & Human
Development, National Institutes of Health
FX This research was supported by award (HD/HL 32562) from the National
Institutes of Health. Dr. Cuilin Zhang was supported by the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health & Human Development, National Institutes of Health.
NR 40
TC 142
Z9 161
U1 2
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 18
PY 2008
VL 3
IS 11
AR e3753
DI 10.1371/journal.pone.0003753
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436XC
UT WOS:000265448400010
PM 19015731
ER
PT J
AU Conroy, RS
Zabow, G
Moreland, J
Koretsky, AP
AF Conroy, Richard S.
Zabow, Gary
Moreland, John
Koretsky, Alan P.
TI Controlled transport of magnetic particles using soft magnetic patterns
SO APPLIED PHYSICS LETTERS
LA English
DT Article
DE galvanomagnetic effects; magnetic domains; magnetic particles; magnetic
structure; microfluidics; permanent magnets; soft magnetic materials;
superparamagnetism
ID SEPARATION; GUIDES
AB Inspired by magnetic bubble memory technology, we demonstrate the temporal and spatial manipulation of superparamagnetic beads guided by soft magnetic patterns in a rotating magnetic field. Soft magnetic structures allow complex and repetitive tasks to be performed. As a demonstration, we show cyclic capture and release of antibodies from different microfluidic streams.
C1 [Conroy, Richard S.; Zabow, Gary; Koretsky, Alan P.] Natl Inst Neurol Disorders & Stroke, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
[Conroy, Richard S.; Zabow, Gary; Moreland, John] Natl Inst Stand & Technol, Boulder, CO 80305 USA.
RP Conroy, RS (reprint author), Natl Inst Neurol Disorders & Stroke, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA.
EM conroyri@mail.nih.gov
RI Conroy, Richard/D-1979-2009; Koretsky, Alan/C-7940-2015
OI Conroy, Richard/0000-0002-8896-6090; Koretsky, Alan/0000-0002-8085-4756
NR 16
TC 26
Z9 26
U1 0
U2 16
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0003-6951
J9 APPL PHYS LETT
JI Appl. Phys. Lett.
PD NOV 17
PY 2008
VL 93
IS 20
AR 203901
DI 10.1063/1.3009197
PG 3
WC Physics, Applied
SC Physics
GA 375VH
UT WOS:000261141400083
ER
PT J
AU Kochan, KJ
Amaral, MEJ
Agarwala, R
Schaffer, AA
Riggs, PK
AF Kochan, Kelli J.
Amaral, M. Elisabete J.
Agarwala, Richa
Schaeffer, Alejandro A.
Riggs, Penny K.
TI Application of dissociation curve analysis to radiation hybrid panel
marker scoring: generation of a map of river buffalo (B-bubalis)
chromosome 20
SO BMC GENOMICS
LA English
DT Article
ID MICROSATELLITE MARKERS; QUANTITATIVE PCR; HUMAN GENOME; LINKAGE MAP;
BOVINE; CATTLE; GENE; CONSTRUCTION; OVINE; STRATEGY
AB Background: Fluorescence of dyes bound to double-stranded PCR products has been utilized extensively in various real-time quantitative PCR applications, including post-amplification dissociation curve analysis, or differentiation of amplicon length or sequence composition. Despite the current era of whole-genome sequencing, mapping tools such as radiation hybrid DNA panels remain useful aids for sequence assembly, focused resequencing efforts, and for building physical maps of species that have not yet been sequenced. For placement of specific, individual genes or markers on a map, low-throughput methods remain commonplace. Typically, PCR amplification of DNA from each panel cell line is followed by gel electrophoresis and scoring of each clone for the presence or absence of PCR product. To improve sensitivity and efficiency of radiation hybrid panel analysis in comparison to gel-based methods, we adapted fluorescence-based real-time PCR and dissociation curve analysis for use as a novel scoring method.
Results: As proof of principle for this dissociation curve method, we generated new maps of river buffalo (Bubalus bubalis) chromosome 20 by both dissociation curve analysis and conventional marker scoring. We also obtained sequence data to augment dissociation curve results. Few genes have been previously mapped to buffalo chromosome 20, and sequence detail is limited, so 65 markers were screened from the orthologous chromosome of domestic cattle. Thirty bovine markers (46%) were suitable as cross-species markers for dissociation curve analysis in the buffalo radiation hybrid panel under a standard protocol, compared to 25 markers suitable for conventional typing. Computational analysis placed 27 markers on a chromosome map generated by the new method, while the gel-based approach produced only 20 mapped markers. Among 19 markers common to both maps, the marker order on the map was maintained perfectly.
Conclusion: Dissociation curve analysis is reliable and efficient for radiation hybrid panel scoring, and is more sensitive and robust than conventional gel-based typing methods. Several markers could be scored only by the new method, and ambiguous scores were reduced. PCR-based dissociation curve analysis decreases both time and resources needed for construction of radiation hybrid panel marker maps and represents a significant improvement over gel-based methods in any species.
C1 [Kochan, Kelli J.; Riggs, Penny K.] Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA.
[Amaral, M. Elisabete J.] Univ Estadual Paulista, IBILCE, Dept Biol, Sao Paulo, Brazil.
[Agarwala, Richa; Schaeffer, Alejandro A.] NIH, Natl Ctr Biotechnol Informat, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Riggs, PK (reprint author), Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA.
EM kkochan@tamu.edu; eamaral@ibilce.unesp.br; richa@helix.nih.gov;
schaffer@helix.nih.gov; riggs@tamu.edu
RI Schaffer, Alejandro/F-2902-2012; Amaral, Elisabete/K-9246-2013; Riggs,
Penny/A-8192-2008
OI Riggs, Penny/0000-0003-3296-320X
FU Texas A&M AgriLife Research; National Institutes of Health, NLM (R.A.,
A.A.S); M.E.J.A.; FAPESP-Brazil [02/10150-5]; NSF-USA [OISE-0405743]
FX We thank Jooha Jeong, A.J. Greco, Colette Abbey, Ashley
Gustafson-Seabury, and Robert E. King for technical assistance, and Alan
R. Silverman for use of an ABI 7500 Sequence Detection System. This work
was supported in part by Texas A&M AgriLife Research project RI-9192
(P.K.R.), and in part by the Intramural Research Program of the National
Institutes of Health, NLM (R.A., A.A.S). The BBURH5000 panel
DNA was provided by M.E.J.A. and James E.Womack. Original construction
of the BBURH5000 panel was supported by grants from FAPESP-Brazil
(02/10150-5) to M.E.J.A. and NSF-USA (OISE-0405743) to J.E.W.
NR 48
TC 2
Z9 3
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD NOV 17
PY 2008
VL 9
AR 544
DI 10.1186/1471-2164-9-544
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 403UM
UT WOS:000263107500002
PM 19014630
ER
PT J
AU Yun, CW
Wang, YG
Mukhopadhyay, D
Backlund, P
Kolli, N
Yergey, A
Wilkinson, KD
Dasso, M
AF Yun, Chawon
Wang, Yonggang
Mukhopadhyay, Debaditya
Backlund, Peter
Kolli, Nagamalleswari
Yergey, Alfred
Wilkinson, Keith D.
Dasso, Mary
TI Nucleolar protein B23/nucleophosmin regulates the vertebrate SUMO
pathway through SENP3 and SENP5 proteases
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID PRE-RIBOSOMAL-RNA; SACCHAROMYCES-CEREVISIAE; CELL-PROLIFERATION; YEAST;
SUMOYLATION; B23; NUCLEOPHOSMIN; ARF; P53
AB Ubiquitin-like protein/sentrin-specific proteases (Ulp/SENPs) mediate both processing and deconjugation of small ubiquitin-like modifier proteins (SUMOs). Here, we show that Ulp/SENP family members SENP3 and SENP5 localize within the granular component of the nucleolus, a subnucleolar compartment that contains B23/nucleophosmin. B23/nucleophosmin is an abundant shuttling phosphoprotein, which plays important roles in ribosome biogenesis and which has been strongly implicated in hematopoietic malignancies. Moreover, we found that B23/nucleophosmin binds SENP3 and SENP5 in Xenopus laevis egg extracts and that it is essential for stable accumulation of SENP3 and SENP5 in mammalian tissue culture cells. After either codepletion of SENP3 and SENP5 or depletion of B23/nucleophosmin, we observed accumulation of SUMO proteins within nucleoli. Finally, depletion of these Ulp/SENPs causes defects in ribosome biogenesis reminiscent of phenotypes observed in the absence of B23/nucleophosmin. Together, these results suggest that regulation of SUMO deconjugation may be a major facet of B23/nucleophosmin function in vivo.
C1 [Yun, Chawon; Wang, Yonggang; Mukhopadhyay, Debaditya; Dasso, Mary] NICHHD, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA.
[Backlund, Peter; Yergey, Alfred] NICHHD, Sect Mass Spectrometry & Metab, Off Sci Director, Bethesda, MD 20892 USA.
[Kolli, Nagamalleswari; Wilkinson, Keith D.] Emory Univ, Dept Biochem, Atlanta, GA 30322 USA.
RP Dasso, M (reprint author), NICHHD, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA.
EM mdasso@helix.nih.gov
OI Dasso, Mary/0000-0002-5410-1371
FU National Institute of Child Health and Human Development; National
Institutes of Health [5R01GM066355]
FX This work was supported by National Institute of Child Health and Human
Development intramural funds (to C. Yun, Y. Wang, D. Mukhopadhyay, P.
Backlund, A. Yergey, and M. Dasso) and by National Institutes of Health
grant # 5R01GM066355 (to N. Kolli and K. D. Wilkinson).
NR 29
TC 50
Z9 53
U1 0
U2 5
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 17
PY 2008
VL 183
IS 4
BP 589
EP 595
DI 10.1083/jcb.200807185
PG 7
WC Cell Biology
SC Cell Biology
GA 377DM
UT WOS:000261231900006
PM 19015314
ER
PT J
AU Hong, SK
Dawid, IB
AF Hong, Sung-Kook
Dawid, Igor B.
TI Alpha2 Macroglobulin-Like Is Essential for Liver Development in
Zebrafish
SO PLOS ONE
LA English
DT Article
AB Background: Alpha 2 Macroglobulin family members have been studied extensively with respect to their roles in physiology and human disease including innate immunity and Alzheimer's disease, but little is known about a possible role in liver development loss-of-function in model systems.
Principal Findings: We report the isolation of the zebrafish alpha 2 macroglobulin-like (A2ML) gene and its specific expression in the liver during differentiation. Morpholino-based knock-down of A2ML did not block the initial formation of the liver primordium, but inhibited liver growth and differentiation.
Significance: This report on A2ML function in zebrafish development provides the first evidence for a specific role of an A2M family gene in liver formation during early embryogenesis in a vertebrate.
C1 [Hong, Sung-Kook; Dawid, Igor B.] Eunice Kennedy Shriver NICHHD, Mol Genet Lab, NIH, Bethesda, MD USA.
RP Hong, SK (reprint author), Eunice Kennedy Shriver NICHHD, Mol Genet Lab, NIH, Bethesda, MD USA.
EM idawid@nih.gov
FU NICHD, NIH
FX This work was supported by the Intramural Research Program of the NICHD,
NIH.
NR 33
TC 6
Z9 6
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 17
PY 2008
VL 3
IS 11
AR e3736
DI 10.1371/journal.pone.0003736
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436XB
UT WOS:000265448300004
PM 19011686
ER
PT J
AU Stern, ST
Johnson, DN
AF Stern, Stephan T.
Johnson, Denise N.
TI Role for nanomaterial-autophagy interaction in neurodegenerative disease
SO AUTOPHAGY
LA English
DT Article
DE autophagy; nanomaterial; pollution; Alzheimers disease; Parkinsons
disease; neurodegeneration; nanotechnology
ID ALPHA-SYNUCLEIN; QUANTUM DOTS; ULTRAFINE PARTICLES; ALZHEIMERS-DISEASE;
CELL-DEATH; NANOPARTICLES; DEGRADATION; TOXICITY; NEURONS; MICE
AB Nanotechnology is the control and manipulation of materials in the size range of 1-100 nm. Due to increasing research into the potential beneficial applications of nano technology, there is an urgent need for the study of possible health risks. Several researchers, including those in our laboratory, have demonstrated elevated levels of autophagic vacuoles upon exposure of cells to certain nanomaterials, including carbon- and metal-based nanoparticles. While this apparent increase in autophagic activity may be an appropriate cellular response toward nanomaterial clearance, often the interaction between nanomaterials and the autophagy pathway is disruptive, resulting in severe morphological changes and coincident cell death. Interestingly, epidemiological studies have identified an association between exposure to combustion -derived ambient particles (which are predominantly nanoscale) and neurological conditions with Alzheimer's and Parkinson's disease-like pathologies. Becuse impaired autophagy may play an important role in the pathogenesis of these and other diseases, it is intriguing to speculate about the plausible involvement of nanoscale particulates in this process. The interaction of nanomaterials with the autophagy pathway, and the potential negative consequences of resulting autophagy dysfunction, should be explored further.
C1 [Stern, Stephan T.; Johnson, Denise N.] SAIC Frederick Inc, Adv Technol Program, Nanotechnol Characterizat Lab, NCI Frederick, Frederick, MD 21702 USA.
RP Stern, ST (reprint author), SAIC Frederick Inc, Adv Technol Program, Nanotechnol Characterizat Lab, NCI Frederick, Frederick, MD 21702 USA.
EM sternstephan@mail.nih.gov
RI Nanotechnology Characterization Lab, NCL/K-8454-2012
FU National Cancer Institute; National Institutes of Health [NO1-CO-12400]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract NO1-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. government.
NR 48
TC 33
Z9 36
U1 6
U2 42
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
SN 1554-8627
J9 AUTOPHAGY
JI Autophagy
PD NOV 16
PY 2008
VL 4
IS 8
BP 1097
EP 1100
PG 4
WC Cell Biology
SC Cell Biology
GA 382ZL
UT WOS:000261643800024
PM 18927490
ER
PT J
AU Boztug, K
Appaswamy, G
Ashikov, A
Schaffer, AA
Salzer, U
Diestelhorst, J
Germeshausen, M
Brandes, G
Lee-Gossler, J
Noyan, F
Gatzke, AK
Minkov, M
Greil, J
Kratz, C
Petropoulou, T
Pellier, I
Bellanne-Chantelot, C
Rezaei, N
Monkemoller, K
Irani-Hakimeh, N
Bakker, H
Gerardy-Schahn, R
Zeidler, C
Grimbacher, B
Welte, K
Klein, C
AF Boztug, Kaan
Appaswamy, Giridharan
Ashikov, Angel
Schaeffer, Alejandro A.
Salzer, Ulrich
Diestelhorst, Jana
Germeshausen, Manuela
Brandes, Gudrun
Lee-Gossler, Jacqueline
Noyan, Fatih
Gatzke, Anna-Katherina
Minkov, Milen
Greil, Johann
Kratz, Christian
Petropoulou, Theoni
Pellier, Isabelle
Bellanne-Chantelot, Christine
Rezaei, Nima
Moenkemoeller, Kirsten
Irani-Hakimeh, Noha
Bakker, Hans
Gerardy-Schahn, Rita
Zeidler, Cornelia
Grimbacher, Bodo
Welte, Karl
Klein, Christoph
TI A Novel Clinical Syndrome Associating Severe Congenital Neutropenia and
Complex Developmental Aberrations Caused by Deficiency of G6PC3
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Boztug, Kaan; Appaswamy, Giridharan; Diestelhorst, Jana; Germeshausen, Manuela; Noyan, Fatih; Gatzke, Anna-Katherina; Zeidler, Cornelia; Welte, Karl; Klein, Christoph] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Ashikov, Angel; Bakker, Hans] Hannover Med Sch, Dept Cellular Chem, D-3000 Hannover, Germany.
[Schaeffer, Alejandro A.] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Salzer, Ulrich] Univ Med Ctr Freiburg, Dept Rheumat & Clin Immunol, Freiburg, Germany.
[Brandes, Gudrun; Lee-Gossler, Jacqueline; Gerardy-Schahn, Rita] Hannover Med Sch, Dept Cell Biol, D-3000 Hannover, Germany.
[Minkov, Milen] St Anna Childrens Hosp, Dept Pediat Hematol Oncol, A-1090 Vienna, Austria.
[Greil, Johann] Univ Heidelberg, Childrens Hosp, Dept Pediat Oncol Hematol & Immunol, D-6900 Heidelberg, Germany.
[Kratz, Christian] Univ Freiburg, Dept Pediat Hematol Oncol, Freiburg, Germany.
[Petropoulou, Theoni] Aghia Sophia Childrens Hosp, Athens, Greece.
[Pellier, Isabelle] CHU Angers, Unite Immunohematooncol Pediat, Angers, France.
[Bellanne-Chantelot, Christine] AP HP PitiA SalpA Triere, Dept Genet, Paris, France.
[Rezaei, Nima] Univ Tehran Med Sci, Immunol Asthma & Allergy Res Inst, Tehran, Iran.
[Moenkemoeller, Kirsten] Childrens Hosp, Dept Gen Pediat, Cologne, Germany.
[Irani-Hakimeh, Noha] St George Univ Hosp, Dept Lab Med, Beirut, Lebanon.
[Irani-Hakimeh, Noha] St George Univ Hosp, Blood Bank, Beirut, Lebanon.
[Grimbacher, Bodo] Royal Free Hosp, Dept Immunol, London NW3 2QG, England.
[Grimbacher, Bodo] UCL, London, England.
RI Rezaei, Nima/B-4245-2008; Schaffer, Alejandro/F-2902-2012; isabelle,
pellier/L-5683-2015; Ashikov, Angel/N-7714-2015
OI Rezaei, Nima/0000-0002-3836-1827; Ashikov, Angel/0000-0001-9679-7955
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 4
EP 4
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700006
ER
PT J
AU Devlin, EE
DaCosta, L
Narla, M
Elliott, G
Bodine, DM
AF Devlin, Emily E.
DaCosta, Lydie
Narla, Mohandas
Elliott, Gene
Bodine, David M.
TI A Mouse Model for Diamond-Blackfan Anemia Demonstrates a Dominant
Negative Effect of a Point Mutation in the RPS19 Gene
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Devlin, Emily E.; Bodine, David M.] GMBB, Hematopoiesis Sect, Nhgri, Bethesda, MD USA.
[DaCosta, Lydie] Inst Gustave Roussy, Paris, France.
[Narla, Mohandas] New York Blood Ctr, New York, NY 10021 USA.
[Elliott, Gene] Transgen Mouse Core Facil, Nhgri, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 20
EP 21
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700039
ER
PT J
AU Rosenberg, PS
Giri, N
Savage, SA
Alter, BP
AF Rosenberg, Philip S.
Giri, Neelam
Savage, Sharon A.
Alter, Blanche P.
TI Cancer Epidemiology in the National Cancer Institute Inherited Bone
Marrow Failure Syndromes Cohort: First Report
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Savage, Sharon A.] NCI, Div Canc Epidemiol & Gene, Rockville, MD USA.
[Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 21
EP 21
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700041
ER
PT J
AU Krauss, AC
Guimond, M
Dobre, S
Mackall, CL
AF Krauss, Aviva C.
Guimond, Martin
Dobre, Stefania
Mackall, Crystal L.
TI Tyrosine Kinase Inhibition with Sunitinib Facilitates Thymic Engraftment
by Modulating Thymic Niche Accessibility
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Krauss, Aviva C.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Krauss, Aviva C.; Guimond, Martin; Dobre, Stefania; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 34
EP 34
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700073
ER
PT J
AU Hsu, LL
Shiva, S
Mendelsohn, C
Hsu, MR
Noguchi, AC
Mendelsohn, L
Gladwin, M
AF Hsu, Lewis L.
Shiva, Sruti
Mendelsohn, Caroline
Hsu, Michael R.
Noguchi, Audrey C.
Mendelsohn, Laurel
Gladwin, Mark
TI Sickle Cell Mice with Hypoxia-Reoxygenation Have Oxidative and
Inflammatory Liver Injury - toward a New Experimental Model for
Vaso-Occlusive Injury
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hsu, Lewis L.] Drexel Univ, Coll Med, Marian Anderson Comprehens Sickle Cell Ctr, Philadelphia, PA 19104 USA.
[Shiva, Sruti; Hsu, Michael R.; Noguchi, Audrey C.; Mendelsohn, Laurel; Gladwin, Mark] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Mendelsohn, Caroline] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 51
EP 51
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700122
ER
PT J
AU Zorca, SM
Freeman, LA
Littel, PL
Kato, GJ
AF Zorca, Suzana M.
Freeman, Lita A.
Littel, Patricia L.
Kato, Gregory J.
TI Hypocholesterolemia in a Large Sickle Cell Cohort: Correlations of Serum
Lipids to Markers of Intravascular Hemolysis and Vascular Dysfunction
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zorca, Suzana M.; Freeman, Lita A.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Littel, Patricia L.; Kato, Gregory J.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 51
EP 52
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700124
ER
PT J
AU Nagamachi, A
Asou, H
Matsui, H
Ozaki, Y
Aki, D
Miyazaki, K
Yamasaki, N
Miyazaki, M
Wolff, L
Koller, R
Oda, H
Inaba, T
Honda, H
AF Nagamachi, Akiko
Asou, Hiroya
Matsui, Hirotaka
Ozaki, Yuko
Aki, Daisuke
Miyazaki, Kazuko
Yamasaki, Norimasa
Miyazaki, Masaki
Wolff, Linda
Koller, Richard
Oda, Hideaki
Inaba, Toshiya
Honda, Hiroaki
TI Haploinsufficiency and Deficiency of a 7q Gene Titan (Samd9L) Predispose
Leukemia Development in Cooperation with Deregulated Expression of a
Transcription Factor, Evil, or a Histone Demethylase, Fbxl10
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Nagamachi, Akiko; Asou, Hiroya; Matsui, Hirotaka; Ozaki, Yuko; Aki, Daisuke; Inaba, Toshiya] Hiroshima Univ, Dept Mol Oncol, Res Inst Radiat Biol & Med, Hiroshima, Japan.
[Miyazaki, Kazuko; Yamasaki, Norimasa; Honda, Hiroaki] Hiroshima Univ, Dept Dev Biol, Res Inst Radiat Biol & Med, Hiroshima, Japan.
[Miyazaki, Masaki] Hiroshima Univ, Dept Immunol, Grad Sch Biomed Sci, Hiroshima, Japan.
[Wolff, Linda; Koller, Richard] NCI, NIH, Bethesda, MD 20892 USA.
[Oda, Hideaki] Tokyo Womens Med Univ, Dept Pathol, Tokyo, Japan.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 80
EP 80
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700198
ER
PT J
AU O'Mahony, D
Janik, JE
Carrasquillo, JA
Seam, P
Fiorillo, JA
Stewart, D
Paik, CH
Fioravanti, S
Whatley, M
Pittaluga, S
Brechbiel, MW
Morris, JC
Waldmann, TA
AF O'Mahony, Deirdre
Janik, John E.
Carrasquillo, Jorge A.
Seam, Pamela
Fiorillo, Joseph A.
Stewart, Donn
Paik, Chang H.
Fioravanti, Suzanne
Whatley, Millie
Pittaluga, Stefania
Brechbiel, Martin W.
Morris, John C.
Waldmann, Thomas A.
TI Yttrium-90 Radiolabeled Humanized Monoclonal Antibody to CD25 in
Refractory and Relapsed Hodgkin's Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [O'Mahony, Deirdre; Janik, John E.; Seam, Pamela; Fiorillo, Joseph A.; Stewart, Donn; Fioravanti, Suzanne; Morris, John C.; Waldmann, Thomas A.] NCI, Metab Branch, Bethesda, MD 20892 USA.
[Carrasquillo, Jorge A.; Paik, Chang H.; Whatley, Millie] NCI, Dept Nucl Med, Ctr Canc Res, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Brechbiel, Martin W.] NCI, Radiat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Carrasquillo, Jorge/E-7120-2010
NR 0
TC 1
Z9 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 92
EP 92
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700232
ER
PT J
AU Miller, CB
Mullighan, CG
Su, XP
Ma, J
Wang, M
Zhang, JH
Williams, RT
Downing, JR
AF Miller, Christopher B.
Mullighan, Charles G.
Su, Xiaoping
Ma, Jing
Wang, Michael
Zhang, Jinghui
Williams, Richard T.
Downing, James R.
TI Pax5 Haploinsufficiency Cooperates with BCR-ABL1 to Induce Acute
Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ma, Jing; Wang, Michael] St Jude Childrens Hosp, Hartwell Ctr, Memphis, TN 38105 USA.
[Zhang, Jinghui] NCI, Rockville, MD USA.
[Williams, Richard T.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
NR 0
TC 3
Z9 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 114
EP 114
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700294
ER
PT J
AU Gavathiotis, E
Suzuki, M
Davis, ML
Pitter, K
Bird, GH
Katz, SG
Tu, HC
Kim, H
Cheng, E
Tjandra, N
Walensky, LD
AF Gavathiotis, Evripidis
Suzuki, Motoshi
Davis, Marguerite L.
Pitter, Kenneth
Bird, Gregory H.
Katz, Samuel G.
Tu, Ho-Chou
Kim, Hyungjin
Cheng, Emily
Tjandra, Nico
Walensky, Loren D.
TI Structural Analysis of a BAX-BIM SAHB Complex Reveals a Novel BH3
Interaction Site on BAX for Therapeutic Activation of Apoptosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gavathiotis, Evripidis; Davis, Marguerite L.; Pitter, Kenneth; Bird, Gregory H.; Katz, Samuel G.; Walensky, Loren D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Suzuki, Motoshi; Tjandra, Nico] NHLBI, Lab Mol Biophys, Bethesda, MD 20892 USA.
[Tu, Ho-Chou; Kim, Hyungjin; Cheng, Emily] Washington Univ, St Louis Sch Med, Div Mol Oncol, St Louis, MO USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 117
EP 117
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700301
ER
PT J
AU Montuori, N
Ricci, P
Serio, B
Visconte, V
La Penna, C
Pesapane, A
Risitano, AM
Rotoli, B
Rossi, G
Ragno, P
Selleri, C
AF Montuori, Nunzia
Ricci, Patrizia
Serio, Bianca
Visconte, Valeria
La Penna, Claudio
Pesapane, Ada
Risitano, Antonio M.
Rotoli, Bruno
Rossi, Guido
Ragno, Pia
Selleri, Carmine
TI Role of the Urokinase Receptor (uPAR) in the Cross-Talk of Hematopoietic
Stem Cells with the Bone Marrow Microenvironment
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Montuori, Nunzia; La Penna, Claudio; Pesapane, Ada; Rossi, Guido; Ragno, Pia] Univ Naples Federico 2, Naples, Italy.
[Visconte, Valeria] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Montuori, Nunzia/J-8542-2013
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 124
EP 125
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700325
ER
PT J
AU Herishanu, Y
Vire, B
Liu, DL
Gibellini, F
Marti, GE
White, T
Njuguna, N
Raghavachari, N
Liu, PC
Pittaluga, S
Munson, PJ
Wilson, WH
Wiestner, A
AF Herishanu, Yair
Vire, Berengere
Liu, Delong
Gibellini, Federica
Marti, Gerald E.
White, Therese
Njuguna, Ndegwa
Raghavachari, Nalini
Liu, Poching
Pittaluga, Stefania
Munson, Peter J.
Wilson, Wyndham H.
Wiestner, Adrian
TI The Role of the Microenvironment for CLL Proliferation and Survival:
Gene Expression Profiling of Leukemic Cells Derived from Blood, Bone
Marrow and Lymph Nodes Reveals the B-Cell Receptor and NF-kappa B as
Dominant Signaling Pathways
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Herishanu, Yair; Vire, Berengere; Gibellini, Federica; Njuguna, Ndegwa; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Liu, Delong; Munson, Peter J.] NIH, Stat Comp Lab, DCB, CIT, Bethesda, MD 20892 USA.
[Marti, Gerald E.] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
[Raghavachari, Nalini; Liu, Poching] NHLBI, Genom Core Facil, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 139
EP 139
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700357
ER
PT J
AU Amarnath, S
Chen, H
Costanzo, CM
Swerczek, JM
Solomon, MA
Fowler, DH
AF Amarnath, Shoba
Chen, Hao
Costanzo, Carliann M.
Swerczek, Joanna M.
Solomon, Michael A.
Fowler, Daniel H.
TI Prevention of Rat Cardiac Allograft Rejection by Host Th2 Cell Adoptive
Transfer
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Amarnath, Shoba; Costanzo, Carliann M.; Fowler, Daniel H.] NCI, Expt Transplantat Immunol Branch, Bethesda, MD 20892 USA.
[Chen, Hao; Swerczek, Joanna M.; Solomon, Michael A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 142
EP 142
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700366
ER
PT J
AU Rao, E
McKeithan, T
Jiang, CS
Ji, M
Iqbal, J
Wright, G
Staudt, LM
Zhao, Y
Chan, WC
Fu, K
AF Rao, Enyu
McKeithan, Timothy
Jiang, Chunsun
Ji, Ming
Iqbal, Javeed
Wright, George
Staudt, Louis M.
Zhao, Yong
Chan, Wing C.
Fu, Kai
TI The Mir-17 similar to 92 Cluster Enhances Cell Growth and Resistance to
Chemotherapy in Mantle Cell Lymphoma by Down-Regulating PTEN, PHLPP2 and
BIM
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rao, Enyu; McKeithan, Timothy; Jiang, Chunsun; Ji, Ming; Iqbal, Javeed; Fu, Kai] Univ Nebraska Med Ctr, Omaha, NE USA.
[Wright, George; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zhao, Yong] Chinese Acad Sci, Inst Zool, Beijing, Peoples R China.
[Chan, Wing C.] Univ Nebraska Med Ctr, Coll Nursing, Omaha, NE 68198 USA.
NR 0
TC 1
Z9 2
U1 2
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 145
EP 145
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700374
ER
PT J
AU Tanno, T
Noh, SJ
Byrnes, C
Bhupatiraju, A
Meier, ER
Rabel, A
Lee, YT
Leitman, S
Miller, JL
AF Tanno, Toshihko
Noh, Seung-Jae
Byrnes, Colleen
Bhupatiraju, Ajoy
Meier, Emily Riehrn
Rabel, Antoinette
Lee, Y. Terry
Leitman, Susan
Miller, Jeffery L.
TI Iron Depleted Erythropoiesis: Slow but Effective
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Tanno, Toshihko; Noh, Seung-Jae; Byrnes, Colleen; Bhupatiraju, Ajoy; Meier, Emily Riehrn; Rabel, Antoinette; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Leitman, Susan] NIH, Blood Serv Sect, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 159
EP 160
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700419
ER
PT J
AU Mullighan, CG
Su, XP
Zhang, JH
Radtke, I
Phillips, LA
Miller, CB
Ma, J
Liu, W
Cheng, C
Harvey, RC
Chen, IM
Clifford, R
Carroll, WL
Reaman, G
Devidas, M
Gerhard, DS
Yang, WJ
Bowman, WP
Shurtleff, SA
Relling, MV
Smith, M
Hunger, SP
Willman, CL
Downing, JR
AF Mullighan, Charles G.
Su, Xiaoping
Zhang, Jinghui
Radtke, Ina
Phillips, Letha A.
Miller, Christopher B.
Ma, Jing
Liu, Wei
Cheng, Cheng
Harvey, Richard C.
Chen, I-Ming
Clifford, Robert
Carroll, William L.
Reaman, Gregory
Devidas, Meenakshi
Gerhard, Daniela S.
Yang, Wenjian
Bowman, W. Paul
Shurtleff, Sheila A.
Relling, Mary V.
Smith, Malcolm
Hunger, Stephen P.
Willman, Cheryl L.
Downing, James R.
TI Deletion of IKZF1 (Ikaros) Predicts Poor Outcome and Impaired Maturation
in B-Progenitor Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ma, Jing] St Jude Childrens Hosp, Hartwell Ctr, Memphis, TN 38105 USA.
[Zhang, Jinghui] NCI, Ctr Biomed Informat & Informat Technol, NIH, Rockville, MD USA.
[Harvey, Richard C.; Chen, I-Ming; Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Clifford, Robert] NCI, Lab Populat Genet, NIH, Rockville, MD USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Reaman, Gregory] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Devidas, Meenakshi] Childrens Oncol Grp, Gainesville, FL USA.
[Devidas, Meenakshi] Univ Florida, Gainesville, FL USA.
[Smith, Malcolm] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Bowman, W. Paul] Cook Childrens Med Ctr, Ft Worth, TX USA.
[Hunger, Stephen P.] Univ Colorado Denver, Sch Med, Aurora, CO USA.
[Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 163
EP 163
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700428
ER
PT J
AU Cooper, JN
Calado, R
Wu, C
Scheinberg, P
Young, N
AF Cooper, James N.
Calado, Rodrigo
Wu, Colin
Scheinberg, Phillip
Young, Neal
TI Telomere Length of Peripheral Blood Leukocytes Predicts Relapse and
Clonal Evolution after Immunosuppressive Therapy in Severe Aplastic
Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cooper, James N.] NIH, Clin Res Training Program, Bethesda, MD 20892 USA.
[Calado, Rodrigo; Wu, Colin; Scheinberg, Phillip; Young, Neal] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 168
EP 169
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700443
ER
PT J
AU Hakim, FT
Rehman, N
Dickinson, J
Baskar, S
Rader, CM
Cowen, EW
Pavletic, SZ
Gress, RE
AF Hakim, Frances T.
Rehman, Najibah
Dickinson, John
Baskar, Sivasubramanian
Rader, Christoph M.
Cowen, Edward W.
Pavletic, Steven Z.
Gress, Ronald E.
TI Elevated BAFF Is Correlated with Inflammatory Processes in Chronic Graft
Versus Host Disease and Supports Increases in Transitional B Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hakim, Frances T.; Rehman, Najibah; Dickinson, John; Baskar, Sivasubramanian; Rader, Christoph M.; Pavletic, Steven Z.; Gress, Ronald E.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 177
EP 178
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700466
ER
PT J
AU Lenz, G
Wright, G
Dave, S
Xiao, WM
Powell, J
Zhao, H
Xu, WH
Tan, B
Goldschmidt, N
Iqbal, J
Vose, J
Bast, MA
Fu, K
Weisenburger, DD
Greiner, TC
Armitage, JO
Kyle, A
May, L
Gascoyne, RD
Connors, JM
Troen, G
Holte, H
Kvaloy, S
Dierickx, D
Verhoef, G
Delabie, J
Smeland, EB
Jares, P
Martinez, A
Lopez-Guillermo, A
Montserrat, E
Campo, E
Braziel, RM
Miller, TP
Rimsza, LM
Cook, JR
Pohlman, B
Sweetenham, JW
Tubbs, RR
Fisher, RI
Hartmann, E
Rosenwald, A
Ott, G
Muller-Hermelink, HK
Wrench, D
Lister, TA
Jaffe, ES
Wilson, W
Chan, WC
Staudt, LM
AF Lenz, Georg
Wright, George
Dave, Sandeep
Xiao, Wenming
Powell, John
Zhao, Hong
Xu, Weihong
Tan, Bruce
Goldschmidt, Neta
Iqbal, Javeed
Vose, Julie
Bast, Martin A.
Fu, Kai
Weisenburger, Dennis D.
Greiner, Timothy C.
Armitage, James O.
Kyle, Alastair
May, Lorraine
Gascoyne, Randy D.
Connors, Joseph M.
Troen, Gunhild
Holte, Harald
Kvaloy, Stein
Dierickx, Daan
Verhoef, Gregor
Delabie, Jan
Smeland, Erlend B.
Jares, Pedro
Martinez, Antonio
Lopez-Guillermo, Armando
Montserrat, Emili
Campo, Elias
Braziel, Rita M.
Miller, Thomas P.
Rimsza, Lisa M.
Cook, James R.
Pohlman, Brad
Sweetenham, John William
Tubbs, Raymond R.
Fisher, Richard I.
Hartmann, Elena
Rosenwald, Andreas
Ott, German
Muller-Hermelink, Hans-Konrad
Wrench, David
Lister, T. Andrew
Jaffe, Elaine S.
Wilson, Wyndham
Chan, Wing C.
Staudt, Louis M.
TI Molecular Signatures Implicate Innate Immune Cells, Fibrosis, and
Angiogenesis in Survival Following R-CHOP Treatment of Diffuse Large B
Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Lenz, Georg; Xiao, Wenming; Powell, John; Zhao, Hong; Xu, Weihong; Tan, Bruce; Goldschmidt, Neta; Vose, Julie; Fu, Kai; Weisenburger, Dennis D.; Greiner, Timothy C.; Armitage, James O.; Kyle, Alastair; May, Lorraine; Gascoyne, Randy D.; Connors, Joseph M.; Troen, Gunhild; Holte, Harald; Kvaloy, Stein; Dierickx, Daan; Verhoef, Gregor; Smeland, Erlend B.; Jares, Pedro; Lopez-Guillermo, Armando; Montserrat, Emili; Campo, Elias; Braziel, Rita M.; Miller, Thomas P.; Rimsza, Lisa M.; Cook, James R.; Pohlman, Brad; Sweetenham, John William; Tubbs, Raymond R.; Fisher, Richard I.; Hartmann, Elena; Rosenwald, Andreas; Ott, German; Muller-Hermelink, Hans-Konrad; Wrench, David; Jaffe, Elaine S.; Wilson, Wyndham] LLMPP, Bethesda, MD USA.
[Wright, George; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Dave, Sandeep] Duke Univ, Durham, NC USA.
[Iqbal, Javeed; Chan, Wing C.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Delabie, Jan] Norwegian Radium Hosp, Oslo, Norway.
[Martinez, Antonio] Hosp Clin Barcelona, Barcelona, Spain.
[Lister, T. Andrew] Barts & London Queen Marys Sch Med & Dent, Ctr Med Oncol, London, England.
NR 0
TC 0
Z9 0
U1 1
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 181
EP 181
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700476
ER
PT J
AU Hill, A
Rother, RP
Wang, XD
Sapsford, RJ
Collinson, PO
Gaze, DC
Morris, SM
Scally, A
Quinn-Senger, K
Richards, SJ
Bessler, M
Kelly, R
Hillmen, P
Gladwin, M
AF Hill, Anita
Rother, Russell P.
Wang, Xunde
Sapsford, Robert J.
Collinson, Paul O.
Gaze, David C.
Morris, Sidney M., Jr.
Scally, Andrew
Quinn-Senger, Kerry
Richards, Stephen J.
Bessler, Monica
Kelly, Richard
Hillmen, Peter
Gladwin, Mark
TI Eculizumab Reduces Pulmonary Hypertension through Inhibition of
Hemolysis-Associated Nitric Oxide Consumption in Patients with
Paroxysmal Nocturnal Hemoglobinuria
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hill, Anita] Bradford Royal Infirm, Dept Haematol, Bradford BD9 6RJ, W Yorkshire, England.
[Rother, Russell P.; Quinn-Senger, Kerry] Alex Pharmaceut, Cheshire, CT USA.
[Wang, Xunde; Gladwin, Mark] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
[Sapsford, Robert J.] Leeds Gen Infirm, Dept Echocardiog, Leeds, W Yorkshire, England.
[Collinson, Paul O.; Gaze, David C.] St George Hosp, Dept Chem Pathol, London, England.
[Morris, Sidney M., Jr.] Univ Pittsburgh, Pittsburgh, PA USA.
[Scally, Andrew] Univ Bradford, Bradford BD7 1DP, W Yorkshire, England.
[Richards, Stephen J.; Kelly, Richard; Hillmen, Peter] St James Inst Oncol, Dept Haematol, Leeds, W Yorkshire, England.
[Bessler, Monica] Washington Univ, Sch Med, St Louis, MO USA.
[Gladwin, Mark] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 185
EP 185
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700487
ER
PT J
AU Steidl, C
Lee, T
Shah, SP
Han, GM
Nayar, T
Delaney, A
Jones, S
Chan, WC
Rosenwald, A
Rimsza, LM
Campo, E
Jaffe, ES
Staudt, LM
Lenz, G
Connors, JM
Gascoyne, RD
AF Steidl, Christian
Lee, Tang
Shah, Sohrab P.
Han, Guangming
Nayar, Tarun
Delaney, Allen
Jones, Steven
Chan, Wing C.
Rosenwald, Andreas
Rimsza, Lisa M.
Campo, Elias
Jaffe, Elaine S.
Staudt, Louis M.
Lenz, Georg
Connors, Joseph M.
Gascoyne, Randy D.
TI Genome-Wide Expression Profiling Predicts Treatment Outcome in Classical
Hodgkin Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Nayar, Tarun; Delaney, Allen; Jones, Steven] British Columbia Canc Agcy, Michael Smith Genome Sci Ctr, Vancouver, BC V5Z 4E6, Canada.
[Chan, Wing C.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Rosenwald, Andreas] Univ Wurzburg, Wurzburg, Germany.
[Rimsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Campo, Elias] Hosp Clin Barcelona, Barcelona, Spain.
[Staudt, Louis M.; Lenz, Georg] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 196
EP 196
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700521
ER
PT J
AU Herishanu, Y
Gibellini, F
Njuguna, N
Keyvanfar, K
Wiestner, A
AF Herishanu, Yair
Gibellini, Federica
Njuguna, Ndegwa
Keyvanfar, Keyvan
Wiestner, Adrian
TI CD44 Signaling Via PI3K/AKT and MAPK/FRK Pathways Protects CLL Cells
from Spontaneous and Drug Induced Apoptosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Herishanu, Yair] Tel Aviv Sourasky Med Ctr, Bethesda, MD USA.
[Herishanu, Yair; Gibellini, Federica; Njuguna, Ndegwa; Keyvanfar, Keyvan; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 203
EP 203
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700542
ER
PT J
AU Klemm, L
Duy, C
Feldhahn, N
Groffen, J
Kim, YM
Hofmann, WK
Jumaa, H
Lieber, MR
Casellas, R
Muschen, M
AF Klemm, Lars
Duy, Cihangir
Feldhahn, Niklas
Groffen, John
Kim, Yong-mi
Hofmann, Wolf-Karsten
Jumaa, Hassan
Lieber, Michael R.
Casellas, Rafael
Muschen, Markus
TI Lymphoid Blast Crisis Transformation and Development of Drug-Resistance
in Chronic Myeloid Leukemia Are Driven by Aberrant Somatic Hypermutation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Klemm, Lars; Duy, Cihangir; Groffen, John; Kim, Yong-mi; Muschen, Markus] Childrens Hosp Los Angeles, Leukemia Res Program, Los Angeles, CA 90027 USA.
[Feldhahn, Niklas] Rockefeller Univ, New York, NY 10021 USA.
[Hofmann, Wolf-Karsten] European LeukemiaNet ELN WP13, MILE Study Grp, Munich, Germany.
[Jumaa, Hassan] Max Planck Inst Immunol, Freiburg, Germany.
[Lieber, Michael R.] Univ So Calif, Los Angeles, CA USA.
[Casellas, Rafael] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 214
EP 214
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700572
ER
PT J
AU Roccaro, AM
Sacco, A
Chen, CZ
Leleu, X
Runnels, J
Azab, F
Azab, AK
Jia, XY
Ngo, HT
Melhem, MR
Burwick, N
Quang, P
Varticovski, L
Novina, CD
Rollins, BJ
Anderson, KC
Ghobrial, IM
AF Roccaro, Aldo M.
Sacco, Antonio
Chen, Changzhong
Leleu, Xavier
Runnels, Judith
Azab, Feda
Azab, Abdel Kareem
Jia, Xiaoying
Ngo, Hai T.
Melhem, Molly R.
Burwick, Nicholas
Quang, Phong
Varticovski, Lyuba
Novina, Carl D.
Rollins, Barrett J.
Anderson, Kenneth C.
Ghobrial, Irene M.
TI MicroRNA Signature in Waldenstrom Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Roccaro, Aldo M.; Sacco, Antonio; Chen, Changzhong; Leleu, Xavier; Runnels, Judith; Azab, Feda; Azab, Abdel Kareem; Jia, Xiaoying; Ngo, Hai T.; Melhem, Molly R.; Burwick, Nicholas; Quang, Phong; Novina, Carl D.; Rollins, Barrett J.; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Varticovski, Lyuba] Natl Canc Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 235
EP 235
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700631
ER
PT J
AU Matloub, Y
Gaynon, PS
Jayabose, S
Bostrom, BC
Hunger, SP
Angiolillo, AL
Devidas, M
Linda, S
Carroll, WL
Winick, N
Sather, H
Pine, SR
AF Matloub, Yousif
Gaynon, Paul S.
Jayabose, Somasundaram
Bostrom, Bruce C.
Hunger, Stephen P.
Angiolillo, Anne L.
Devidas, Meenakshi
Linda, Stephen
Carroll, William L.
Winick, Naomi
Sather, Harland
Pine, Sharon R.
TI Bone Marrow (BM) Minimal Residual Disease (MRD) at End of Induction and
Interim Maintenance Is Highly Predictive of Outcome in Children with
Standard Risk (SR) Acute Lymphoblastic Leukemia (ALL) Treated on the
Children's Oncology Group Study 1991
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Matloub, Yousif] Univ Wisconsin, Madison, WI USA.
[Gaynon, Paul S.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Jayabose, Somasundaram] New York Med Coll, Valhalla, NY 10595 USA.
[Bostrom, Bruce C.] Childrens Hosp & Clin Minnesota, Minneapolis, MN USA.
[Hunger, Stephen P.] Univ Colorado Denver, Sch Med, Aurora, CO USA.
[Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
[Angiolillo, Anne L.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Devidas, Meenakshi] Univ Florida, Coll Med, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
[Linda, Stephen] Childrens Oncol Grp, Gainesville, FL USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
[Winick, Naomi] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Sather, Harland] Childrens Oncol Grp, Arcadia, CA USA.
[Pine, Sharon R.] NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 261
EP 261
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700702
ER
PT J
AU Zhang, J
Jima, DD
Jacobs, CL
Gottwein, E
Huang, G
Lugar, PL
Lagoo, AS
Rizzieri, DA
Lipsky, PE
Dave, SS
AF Zhang, Jenny
Jima, Dereje D.
Jacobs, Cassandra L.
Gottwein, Eva
Huang, Grace
Lugar, Patricia L.
Lagoo, Anand S.
Rizzieri, David A.
Lipsky, Peter E.
Dave, Sandeep S.
TI MicroRNAs Regulate Mature B Cell Differentiation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhang, Jenny; Jima, Dereje D.; Jacobs, Cassandra L.; Gottwein, Eva; Huang, Grace; Lugar, Patricia L.; Lagoo, Anand S.; Rizzieri, David A.; Dave, Sandeep S.] Duke Univ, Durham, NC USA.
[Lipsky, Peter E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 262
EP 262
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700706
ER
PT J
AU Hyde, RK
Kamikubo, Y
Alemu, L
Zhao, L
Wang, CW
Liu, PP
AF Hyde, R. Katherine
Kamikubo, Yasuhiko
Alemu, Lemlem
Zhao, Ling
Wang, Chenwei
Liu, Pu Paul
TI Cbfb-MYH11 Can Block Hematopoiesis and Alter Gene Expression through
Mechanisms Independent of Cbfb and Runx1 Repression
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hyde, R. Katherine; Kamikubo, Yasuhiko; Alemu, Lemlem; Zhao, Ling; Liu, Pu Paul] NHGRI, Gmbb Ods, NIH, Bethesda, MD 20892 USA.
[Wang, Chenwei] NHGRI, Gtb, NIH, Bethesda, MD 20892 USA.
RI Liu, Paul/A-7976-2012
OI Liu, Paul/0000-0002-6779-025X
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 277
EP 277
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700748
ER
PT J
AU Colvin, GA
Berz, D
Ramanathan, M
Winer, E
Fast, LD
Elfenbein, GJ
Quesenberry, PJ
AF Colvin, Gerald A.
Berz, David
Ramanathan, Muthalagu
Winer, Eric
Fast, Loren D.
Elfenbein, Gerald Jay
Quesenberry, Peter J.
TI Non-Engraftment Haploidentical Cellular Immunotherapy for Refractory
Malignancies: Tumor Responses without Chimerism
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Berz, David; Winer, Eric] Rhode Isl Hosp, Dept Med, Div Hematol Oncol, Providence, RI 02903 USA.
[Ramanathan, Muthalagu] NHLBI, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Fast, Loren D.] Brown Univ, Rhode Isl Hosp, Div Hem Onc, Providence, RI 02912 USA.
[Elfenbein, Gerald Jay] Boston Univ, Franklin, MA USA.
[Quesenberry, Peter J.] Rhode Isl Hosp, Ctr Stem Cell Biol Res, Providence, RI USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 308
EP 308
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701055
ER
PT J
AU Freyer, DR
Seibel, NL
La, MK
Devidas, M
Carroll, WL
Hunger, SP
Gaynon, PS
AF Freyer, David Robert
Seibel, Nita L.
La, Mei K.
Devidas, Meenakshi
Carroll, William L.
Hunger, Stephen P.
Gaynon, Paul S.
TI Survival after Relapse in Higher Risk Acute Lymphoblastic Leukemia (ALL)
in Children and Adolescents Is Independent of Prior Treatment Intensity:
A Report from the Children's Oncology Group (COG)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Freyer, David Robert; La, Mei K.; Devidas, Meenakshi; Carroll, William L.; Hunger, Stephen P.; Gaynon, Paul S.] COG, Arcadia, CA USA.
[Seibel, Nita L.] NCI, Canc Therapy Evaluat Program, NIH, 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 NOV 16
PY 2008
VL 112
IS 11
BP 340
EP 340
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701141
ER
PT J
AU Rizzatti, FG
Qazi, MA
Stroncek, D
Sibmooh, N
Piknova, B
Schechter, AN
AF Rizzatti, Fabiola G.
Qazi, Melissa A.
Stroncek, David
Sibmooh, Nathawut
Piknova, Barbora
Schechter, Alan N.
TI Effect of Storage on Levels of Nitric Oxide Derivatives in Blood
Components.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rizzatti, Fabiola G.; Qazi, Melissa A.; Sibmooh, Nathawut; Piknova, Barbora; Schechter, Alan N.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 368
EP 368
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701223
ER
PT J
AU Feng, XM
Scheinberg, P
Wu, CO
Samsel, L
Nunez, O
Prince, C
Weinstein, B
Ganetzky, RD
McCoy, JP
Maciejewski, JP
Young, NS
AF Feng, Xingmin
Scheinberg, Phillip
Wu, Colin O.
Samsel, Leigh
Nunez, Olga
Prince, Courtney
Weinstein, Barbara
Ganetzky, Rebecca D.
McCoy, J. Philip
Maciejewski, Jaroslaw P.
Young, Neal S.
TI Circulating Cytokine Profiles of Patients with Acquired Aplastic Anemia
and Myelodysplastic Syndrome.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Feng, Xingmin; Nunez, Olga; Weinstein, Barbara; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[Prince, Courtney; Maciejewski, Jaroslaw P.] Cleveland Clin, Taussig Canc Ctr, Expt Hematol & Hematopoiesis Sect, Cleveland, OH 44106 USA.
[Ganetzky, Rebecca D.] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
NR 0
TC 1
Z9 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 380
EP 381
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701262
ER
PT J
AU Tang, Y
Chen, J
Young, N
AF Tang, Yong
Chen, Jichun
Young, Neal
TI Critical Role of the Th1 Transcription Factor T-Bet in An Animal Model
of Immune-Mediated Bone Marrow Failure.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chen, Jichun] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 380
EP 380
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701261
ER
PT J
AU Chen, JC
Omokaro, SO
Sarcon, AK
Young, N
AF Chen, Jichun
Omokaro, Stephanie O.
Sarcon, Annahita K.
Young, Neal
TI Fas- and Fas Ligand Rather Than Perforin-Mediated Apoptosis Has a
Dominant Role in Target Cell Death in Murine Models of Immune-Mediated
Bone Marrow Failure.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chen, Jichun; Omokaro, Stephanie O.; Sarcon, Annahita K.; Young, Neal] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 381
EP 381
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701263
ER
PT J
AU Alter, BP
Baerlocher, G
Giri, N
Lansdorp, PM
Savage, SA
AF Alter, Blanche P.
Baerlocher, Gabriela
Giri, Neelam
Lansdorp, Peter M.
Savage, Sharon A.
TI Very Short Telomeres Are Characteristic of Dyskeratosis Congenita and
Not Other Inherited Bone Marrow Failure Syndromes.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
[Baerlocher, Gabriela] Univ Hosp Bern, Dept Hematol, CH-3010 Bern, Switzerland.
[Lansdorp, Peter M.] British Columbia Canc Res Ctr, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada.
[Savage, Sharon A.] NCI, Div Canc Epidemiol & Gene, Bethesda, MD 20892 USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
U1 0
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 382
EP 382
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701268
ER
PT J
AU Tamary, H
Nishri, D
Yacobovich, J
Zilber, R
Aviner, S
Stepensky, P
Vilk-Ravel, SS
Bitan, M
Kaplinsky, C
Barak, AB
Kapelusnik, J
Koren, A
Levin, C
Yaniv, I
Rosenberg, PS
Alter, BP
AF Tamary, Hannah
Nishri, Daniella
Yacobovich, Joanne
Zilber, Rama
Aviner, Shraga
Stepensky, Polina
Vilk-Ravel, Shoshana S.
Bitan, Menachem
Kaplinsky, Chaim
Barak, Ayelet Ben
Kapelusnik, Joseph
Koren, Ariel
Levin, Carina
Yaniv, Isaac
Rosenberg, Philip S.
Alter, Blanche P.
TI Frequency and Natural History of Inherited Bone Marrow Failure
Syndromes: The Israeli Inherited Bone Marrow Failure Registry.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Tamary, Hannah; Nishri, Daniella; Yacobovich, Joanne; Zilber, Rama; Levin, Carina; Yaniv, Isaac] Schneider Childrens Med Ctr, Petah Tiqwa, Israel.
[Aviner, Shraga] Barzilai Govt Hosp, Ashqelon, Israel.
[Stepensky, Polina; Vilk-Ravel, Shoshana S.; Bitan, Menachem] Hadassah Med Ctr, Jerusalem, Israel.
[Kaplinsky, Chaim] Chaim Sheba Med Ctr, Tel Hashomer, Israel.
[Kapelusnik, Joseph] Soroka Med Ctr, Beer Sheva, Israel.
[Rosenberg, Philip S.] NCI, Biostat Branch, Rockville, MD USA.
NR 0
TC 2
Z9 2
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 NOV 16
PY 2008
VL 112
IS 11
BP 382
EP 383
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701269
ER
PT J
AU Arons, E
Suntum, T
Sunshine, J
Orthwein, A
Margulies, I
Stetler-Stevenson, M
Kreitman, R
AF Arons, Evgeny
Suntum, Tara
Sunshine, Joel
Orthwein, Anna
Margulies, Inger
Stetler-Stevenson, Maryalice
Kreitman, Robert
TI Molecular Characteristic of Variant and Classic Hairy Cell Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Arons, Evgeny; Suntum, Tara; Sunshine, Joel; Orthwein, Anna; Margulies, Inger] Natl Canc Inst, NIH, Mol Biol Lab, Bethesda, MD USA.
[Stetler-Stevenson, Maryalice] Natl Canc Inst, NIH, Ctr Canc Res, Pathol Lab, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 389
EP 389
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701287
ER
PT J
AU Mullighan, CG
Radtke, I
Zhang, JH
Phillips, LA
Su, XP
Ma, J
Cai, ZL
Hughes, TP
White, DL
Roberts, AW
Campbell, LJ
Shurtleff, SA
Downing, JR
AF Mullighan, Charles G.
Radtke, Ina
Zhang, Jinghui
Phillips, Letha A.
Su, Xiaoping
Ma, Jing
Cai, Zhongling
Hughes, Timothy P.
White, Deborah L.
Roberts, Andrew W.
Campbell, Lynda J.
Shurtleff, Sheila A.
Downing, James R.
TI Genome-Wide Analysis of Genetic Alterations in Chronic Myelogenous
Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ma, Jing] St Jude Childrens Hosp, Hartwell Ctr, Memphis, TN 38105 USA.
[Zhang, Jinghui] Natl Canc Inst, Rockville, MD USA.
[Campbell, Lynda J.] St Vincents Hosp, Melbourne, Vic, Australia.
[Roberts, Andrew W.] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Div Canc & Haem, Parkville, Vic 3050, Australia.
[Hughes, Timothy P.; White, Deborah L.] Inst Med & Vet Sci, Adelaide, SA 5000, Australia.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 397
EP 398
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701313
ER
PT J
AU Yong, ASM
Keyvanfar, K
Eniafe, R
Savani, BN
Rezvani, K
Shenoy, A
Koklanaris, EK
Musse, L
Donohue, T
Le, Q
Goldman, JM
Barrett, AJ
AF Yong, Agnes S. M.
Keyvanfar, Keyvan
Eniafe, Rhoda
Savani, Bipin N.
Rezvani, Katayoun
Shenoy, Aarthi
Koklanaris, Eleftheria K.
Musse, Laura
Donohue, Theresa
Le, Quan
Goldman, John M.
Barrett, A. John
TI The Level of Minimal Residual Disease in Primitive Progenitor Cells from
CM L Patients after Allogeneic Stem Cell Transplantation Is Higher Than
after Treatment with Tyrosine Kinase Inhibitors
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Yong, Agnes S. M.; Keyvanfar, Keyvan; Eniafe, Rhoda; Savani, Bipin N.; Rezvani, Katayoun; Shenoy, Aarthi; Koklanaris, Eleftheria K.; Musse, Laura; Donohue, Theresa; Le, Quan; Goldman, John M.; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 404
EP 404
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701331
ER
PT J
AU Mielke, S
Shenoy, A
Fellowes, VS
Rezvani, K
Savani, BN
Musse, L
Wisch, L
Kurlander, R
Khuu, H
Boss, C
Barrett, AJ
AF Mielke, Stephan
Shenoy, Aarthi
Fellowes, Vicki S.
Rezvani, Katayoun
Savani, Bipin N.
Musse, Laura
Wisch, Laura
Kurlander, Roger
Khuu, Hanh
Boss, Carol
Barrett, A. John
TI Selective Allodepletion by TH9402-Mediated Photosensitization Results in
Early Full Donor T Cell Reconstitution in the Absence of High-Grade,
Acute GvHD and Is Associated with Favorable Outcome after HLA Matched
Sibling SCT for Hematologic Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mielke, Stephan; Shenoy, Aarthi; Rezvani, Katayoun; Savani, Bipin N.; Musse, Laura; Wisch, Laura; Boss, Carol; Barrett, A. John] NHLBI, Allotransplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Fellowes, Vicki S.; Khuu, Hanh] NIH, Cell Proc Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Kurlander, Roger] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 426
EP 427
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701390
ER
PT J
AU Le, Q
Melenhorst, JJ
Savani, BN
Hill, B
Memon, S
Shenoy, A
Hensel, NF
Koklanaris, EK
Keyvanfar, K
Hakim, F
Douek, D
Barrett, AJ
AF Le, Quan
Melenhorst, J. Joseph
Savani, Bipin N.
Hill, Brenna
Memon, Sarfraz
Shenoy, Aarthi
Hensel, Nancy F.
Koklanaris, Elefteria K.
Keyvanfar, Keyvan
Hakim, Fran
Douek, Daniel
Barrett, A. John
TI Long-Term T Cell Immune Reconstitution in Patients Surviving 10 or More
Years after Allogeneic Stem Cell Transplantation for Hematologic
Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Le, Quan; Melenhorst, J. Joseph; Savani, Bipin N.; Shenoy, Aarthi; Hensel, Nancy F.; Koklanaris, Elefteria K.; Keyvanfar, Keyvan; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Hill, Brenna; Douek, Daniel] NIAID, Human Immunol Sect, VRC, NIH, Bethesda, MD 20892 USA.
[Memon, Sarfraz; Hakim, Fran] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RI Memon, Sarfraz/E-1198-2013
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 428
EP 429
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701395
ER
PT J
AU McHale, C
Zhang, LP
Lan, Q
Li, QL
Hubbard, A
Porter, K
Vermeulen, R
Shen, M
Rappaport, S
Yin, SN
Smith, MT
Rothman, N
AF McHale, Cliona
Zhang, Luoping
Lan, Qing
Li, Quilan
Hubbard, Alan
Porter, Kristin
Vermeulen, Roel
Shen, Min
Rappaport, Stephen
Yin, Songnian
Smith, Marlyn T.
Rothman, Nathaniel
TI Low-Dose, Occupational Exposure to the Leukemogen Benzene Induces Robust
Changes in the Blood Transcriptome Associated with Altered Immune System
Biology.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [McHale, Cliona; Zhang, Luoping; Hubbard, Alan; Porter, Kristin; Rappaport, Stephen; Smith, Marlyn T.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Lan, Qing; Shen, Min; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Li, Quilan; Yin, Songnian] Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China.
[Vermeulen, Roel] Inst Risk Assessment Sci, Utrecht, Netherlands.
RI Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 440
EP 440
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701429
ER
PT J
AU Meguro, A
Ozaki, K
Oh, I
Matsu, H
Hatanaka, K
Tatara, R
Leonard, WJ
Sato, K
Ozawa, K
AF Meguro, Akiko
Ozaki, Katsutoshi
Oh, Iekuni
Matsu, Haruko
Hatanaka, Keiko
Tatara, Raine
Leonard, Warren J.
Sato, Kazuya
Ozawa, Keiya
TI Blocking of IL-21 Signal Attenuates Graft-Versus-Host Disease but Not
Graft-Versus-Leukemia Effect in a Mouse Model.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Meguro, Akiko; Ozaki, Katsutoshi; Oh, Iekuni; Matsu, Haruko; Hatanaka, Keiko; Tatara, Raine; Sato, Kazuya; Ozawa, Keiya] Jichi Med Univ, Dept Med, Div Hematol, Shimotsukeshi, Japan.
[Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 453
EP 453
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701470
ER
PT J
AU Aerbajinai, W
Chin, K
Zhu, JQ
Li, HZ
Rodgers, GP
AF Aerbajinai, Wulin
Chin, Kyung
Zhu, Jianqiong
Li, Hongzhen
Rodgers, Griffin P.
TI Glia Maturation Factor-Gamma Mediates Neutrophil Chemotaxis Via p38 MAPK
and PTEN
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Aerbajinai, Wulin; Chin, Kyung; Zhu, Jianqiong; Li, Hongzhen; Rodgers, Griffin P.] NIDDK, Mol & Clin Hematol Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 459
EP 460
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701491
ER
PT J
AU Kimura, A
Rieger, MA
Chen, W
Simmon, JM
Robinson, G
Zhu, B
O'Shea, J
Schroeder, T
Hennighausen, L
AF Kimura, Akiko
Rieger, Michael A.
Chen, WeiPing
Simmon, James M.
Robinson, Gertraud
Zhu, BingMei
O'Shea, John
Schroeder, Timm
Hennighausen, Lothar
TI GM-CSF Controls Proliferation and Survival of the Granulocyte Lineage
through the Transcription Factors STAT5A/B
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kimura, Akiko; Robinson, Gertraud; Zhu, BingMei; Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
[Rieger, Michael A.; Schroeder, Timm] German Res Ctr Environm Hlth, Hematopoiesis Grp, Inst Stem Cell Res, Helmholtz Zentrum Munchen, Neuherberg, 20892, Germany.
[Chen, WeiPing] NIDDK, Microarray Core Facil, NIH, Bethesda, MD USA.
[Simmon, James M.] NIAMSD, Flow Cytometry Sect, Off Sci & Technol, NIH, Bethesda, MD USA.
[O'Shea, John] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 460
EP 460
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701494
ER
PT J
AU Merrill, CT
Miller, JL
Steiner, C
AF Merrill, Chaya T.
Miller, Jeffery L.
Steiner, Claudia
TI Analysis of Increased Blood Transfusions in US Hospitals, 1997-2006.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Merrill, Chaya T.] Thomson Reuters Agcy Healthcare Res & Qual, Hlth Serv Res, Washington, DC USA.
[Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Steiner, Claudia] Agcy Healthcare Res & Qual, Rockville, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 471
EP 471
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701524
ER
PT J
AU Morisot, S
Wayne, AS
Bohana-Kashtan, O
Kaplan, IM
Hildreth, R
Brown, P
Stetler-Stevenson, M
Civin, CI
AF Morisot, Sebastien
Wayne, Alan S.
Bohana-Kashtan, Osnat
Kaplan, Ian M.
Hildreth, Richard
Brown, Patrick
Stetler-Stevenson, Maryalice
Civin, Curt I.
TI Leukemia Stem Cells, (LSCs) Are Frequent in Childhood Precursor B Acute
Lymphoblastic Leukemia (ALL)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Morisot, Sebastien; Bohana-Kashtan, Osnat; Kaplan, Ian M.; Hildreth, Richard; Civin, Curt I.] Johns Hopkins Univ, Sch Med, Div Immunol & Hematopoiesis, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Brown, Patrick] Johns Hopkins Univ, Div Pediat Oncol, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, 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 NOV 16
PY 2008
VL 112
IS 11
BP 487
EP 488
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701576
ER
PT J
AU Donahue, RE
Jin, P
Bonifacino, AC
Metzger, ME
Stroncek, D
AF Donahue, Robert E.
Jin, Ping
Bonifacino, Aylin C.
Metzger, Mark E.
Stroncek, David
TI AMD3100 and Granulocyte Colony Stimulating Factor (G-CSF) Mobilize
Different CD34(+) Cell Populations Based on Global Gene and MicroRNA
Expression
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Donahue, Robert E.; Bonifacino, Aylin C.; Metzger, Mark E.] NHLBI, Hematol Branch, NIH, Rockville, MD USA.
[Jin, Ping; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 496
EP 496
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701607
ER
PT J
AU Bartelmez, S
Ruscetti, FW
Iversen, P
Bhatwadekar, A
Grant, M
AF Bartelmez, Stephen
Ruscetti, Francis W.
Iversen, Patrick
Bhatwadekar, Ashay
Grant, Maria
TI Accelerated Repair of Vascular Injury in Diabetes by TGF-beta 1 Modified
Hematopoietic Stem Cells (HSC).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bartelmez, Stephen] BetaStem Therapeut, Stem Cells, San Francisco, CA USA.
[Ruscetti, Francis W.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21701 USA.
[Iversen, Patrick] AVI BioPharma, Biol, Corvallis, OR USA.
[Bhatwadekar, Ashay; Grant, Maria] Univ Florida, Gainesville, FL USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 500
EP 500
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701620
ER
PT J
AU Stumpo, DJ
Broxmeyer, HE
Cooper, S
Hangoc, G
Aplan, PD
Chung, YJ
Yoder, MC
Shelley, WC
Blackshear, PJ
AF Stumpo, Deborah J.
Broxmeyer, Hal E.
Cooper, Scott
Hangoc, Giao
Aplan, Peter D.
Chung, Yang Jo
Yoder, Mervin C.
Shelley, William C.
Blackshear, Perry J.
TI Targeted Disruption of Zfp36l2, Encoding a CCCH Tandem Zinc Finger
RNA-Binding Protein, Results in Defective Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Stumpo, Deborah J.; Blackshear, Perry J.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
[Broxmeyer, Hal E.; Cooper, Scott; Hangoc, Giao] Indiana Univ, Sch Med, Walther Oncol Ctr, Indianapolis, IN 46202 USA.
[Aplan, Peter D.; Chung, Yang Jo] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
[Yoder, Mervin C.; Shelley, William C.] Wells Ctr Pediat Rsch, Canc Res Inst, Indianapolis, IN USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 500
EP 501
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701623
ER
PT J
AU Campbell, AD
Minniti, C
Rana, SR
Onyekwere, OC
Nouraie, M
Arteta, M
Sable, C
Ensing, G
Dham, N
Darbari, DS
Luchtman-Jones, L
Kato, GJ
Gladwin, M
Castro, O
Gordeuk, VR
AF Campbell, Andrew D.
Minniti, Caterina
Rana, Sohail R.
Onyekwere, Onyinye C.
Nouraie, Mehdi
Arteta, Manuel
Sable, Craig
Ensing, Gregory
Dham, Niti
Darbari, Deepika S.
Luchtman-Jones, Lori
Kato, Gregory J.
Gladwin, Mark
Castro, Oswaldo
Gordeuk, Victor R.
TI Oxygen Desaturation at Rest and after Exercise in Pediatric Sickle Cell
Disease Patients: Correlations with Hemolysis and Elevated Tricuspid
Regurgitant Jet Velocity.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Campbell, Andrew D.; Arteta, Manuel; Ensing, Gregory] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
[Minniti, Caterina; Kato, Gregory J.; Gladwin, Mark] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Rana, Sohail R.] Howard Univ, Dept Pediat & Child Hlth, Washington, DC 20059 USA.
[Onyekwere, Onyinye C.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Nouraie, Mehdi; Castro, Oswaldo; Gordeuk, Victor R.] Howard Univ Hosp, Ctr Sickle Cell Dis, Washington, DC USA.
[Sable, Craig; Dham, Niti; Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Darbari, Deepika S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 507
EP 508
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701645
ER
PT J
AU Presley, T
Bain, L
Ballas, S
Nichols, J
Sabio, H
Gladwin, M
Kato, GJ
Kim-Shapiro, D
AF Presley, Tennille
Bain, Lauren
Ballas, Samir
Nichols, James
Sabio, Hernan
Gladwin, Mark
Kato, Gregory J.
Kim-Shapiro, Daniel
TI The Mechanism of Hemolysis in Sickle Cell Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kim-Shapiro, Daniel] Wake Forest Univ, Olin Phys Lab, Winston Salem, NC 27109 USA.
[Ballas, Samir] Thomas Jefferson Univ, Cardeza Fdn Hematol Res, Philadelphia, PA 19107 USA.
[Nichols, James; Gladwin, Mark] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Kato, Gregory J.] NHLBI, NIH, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 513
EP 513
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701661
ER
PT J
AU Franchini, G
Fukumoto, R
Andresen, V
Bialuk, I
Cecchinato, V
Walser, JC
Valeri, VW
Nauroth, JM
Gessain, A
Nicot, C
AF Franchini, Genoveffa
Fukumoto, Risaku
Andresen, Vibeke
Bialuk, Izabela
Cecchinato, Valentina
Walser, Jean Claude
Valeri, Valerio William
Nauroth, Julie M.
Gessain, Antoine
Nicot, Christophe
TI In Vivo Genetic Mutations Define Predominant Functions of the Human
T-Cell Leukemia/Lymphoma Virus p12(1) Protein
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Franchini, Genoveffa; Fukumoto, Risaku; Andresen, Vibeke; Bialuk, Izabela; Cecchinato, Valentina; Valeri, Valerio William; Nicot, Christophe] NIH, Bethesda, MD 20892 USA.
[Walser, Jean Claude] NIDDKD, Mol & Cellular Biol Lab, Sect Genom Struct & Funct, Bethesda, MD 20892 USA.
[Nauroth, Julie M.] Martek Biosci Corp, Columbia, MD USA.
[Gessain, Antoine] Unite Epidemiol & Physiopathol Virus Oncogenes, Paris, France.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 524
EP 524
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701696
ER
PT J
AU Wang, HS
Beaty, N
Shin, DM
Feng, JX
Chen, S
Morse, H
AF Wang, Hongsheng
Beaty, Natalie
Shin, Dong-Mi
Feng, Jianxun
Chen, Sophia
Morse, Herbert, III
TI Identification of Plasma Cell Antigen PC-1 as a Novel Cell Surface
Marker of Germinal Center, Memory and Plasmacytoma B Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wang, Hongsheng; Beaty, Natalie; Shin, Dong-Mi; Feng, Jianxun; Chen, Sophia] NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 543
EP 543
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701749
ER
PT J
AU Melenhorst, JJ
Biancotto, A
Schemberg, P
Wu, CO
Mccoy, JP
Schemberg, P
Hensel, NF
Barrett, AJ
AF Melenhorst, J. Joseph
Biancotto, Angelique
Schemberg, Phillip
Wu, Colin O.
McCoy, J. Philip
Schemberg, Priscila
Hensel, Nancy F.
Barrett, A. John
TI Inflammatory Cytokine Levels in the Peri-Stem Cell Transplantation
Period Correlate with Fluctuations in Peripheral Blood Counts but Not
with Inflammation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Melenhorst, J. Joseph; Biancotto, Angelique; Schemberg, Phillip; Wu, Colin O.; McCoy, J. Philip; Schemberg, Priscila; Hensel, Nancy F.; Barrett, A. John] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 547
EP 548
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701762
ER
PT J
AU Kirschbaum, M
Popplewell, L
Nademanee, AP
Pullarkat, V
Delioukina, M
Zain, JM
Matsuoka, D
Pulone, B
Frankel, P
Espinoza-Delgado, I
Forman, SJ
Gandara, D
Newman, E
AF Kirschbaum, Mark
Popplewell, Leslie
Nademanee, Auayporn P.
Pullarkat, Vinod
Delioukina, Maria
Zain, Jasmine M.
Matsuoka, Deron
Pulone, Bernadette
Frankel, Paul
Espinoza-Delgado, Igor
Forman, Stephen J.
Gandara, David
Newman, Edward
TI A Phase 2 Study of Vorinostat (Suberoylanilide Hydroxamic Acid, SAHA) in
Relapsed or Refractory Indolent Non-Hodgkin's Lymphoma. A California
Cancer Consortium Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kirschbaum, Mark] City Hope Natl Med Ctr, Div Hematol, Duarte, CA 91010 USA.
[Pullarkat, Vinod] City Hope Natl Med Ctr, Div Hematol HCT, Duarte, CA 91010 USA.
[Zain, Jasmine M.] Columbia Univ, Coll Phys & Surg, Div Med Oncol, New York, NY USA.
[Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Forman, Stephen J.] Hematol HCT, Duarte, CA USA.
[Gandara, David] Univ Calif Davis, Sacramento, CA 95817 USA.
NR 0
TC 1
Z9 2
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 NOV 16
PY 2008
VL 112
IS 11
BP 554
EP 555
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701785
ER
PT J
AU Piekarz, R
Wright, J
Frye, R
Allen, SL
Craig, M
Geskin, L
Hutchins, L
Joske, D
Kirschbaum, M
Leonard, JP
Prince, M
Reeder, CB
Jaffe, E
Bates, S
AF Piekarz, Richard
Wright, John
Frye, Robin
Allen, Steven L.
Craig, Michael
Geskin, Larisa
Hutchins, Laura
Joske, David
Kirschbaum, Mark
Leonard, John P.
Prince, Miles
Reeder, Craig B.
Jaffe, Elaine
Bates, Susan
TI Results of a Phase 2 NCI Multicenter Study of Romidepsin in Patients
with Relapsed Peripheral T-Cell Lymphoma (PTCL)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Piekarz, Richard; Frye, Robin; Jaffe, Elaine] NCI, Bethesda, MD 20892 USA.
[Wright, John] IDB CTEP NCI, Rockville, MD USA.
[Allen, Steven L.] N Shore Univ, Hosp LIJ, Lake Success, NY USA.
[Craig, Michael] Mary Babb Randolph Canc Ctr, Morgantown, WV USA.
[Geskin, Larisa] Univ Pittsburgh, Pittsburgh, PA USA.
[Hutchins, Laura] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Joske, David] Sir Charles Gairdner Hosp, Haematol Care Ctr, Perth, WA, Australia.
[Kirschbaum, Mark] City Hope Natl Med Ctr, Div Hematol, Duarte, CA 91010 USA.
[Leonard, John P.] Weill Cornell Med Coll, New York, NY USA.
[Prince, Miles] Peter MacCallum Canc Inst, Melbourne, Australia.
[Reeder, Craig B.] Mayo Clin Arizona, Scottsdale, AZ USA.
[Bates, Susan] NCI, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
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 NOV 16
PY 2008
VL 112
IS 11
BP 555
EP 556
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701788
ER
PT J
AU Bates, S
Piekarz, R
Wright, J
Frye, R
Figg, WD
Allen, SL
Craig, M
Geskin, L
Hutchins, L
Joske, D
Kirschbaum, M
Leonard, JP
Prince, M
Reeder, CB
Stetler-Stevenson, M
Ling, A
Nichols, J
AF Bates, Susan
Piekarz, Richard
Wright, John
Frye, Robin
Figg, William Douglas, Sr.
Allen, Steven L.
Craig, Michael
Geskin, Larisa
Hutchins, Laura
Joske, David
Kirschbaum, Mark
Leonard, John P.
Prince, Miles
Reeder, Craig B.
Stetler-Stevenson, Maryalice
Ling, Alex
Nichols, Jean
TI Final Clinical Results of a Phase 2 NCI Multicenter Study of Romidepsin
in Recurrent Cutaneous T-Cell Lymphoma (Molecular Analyses Included)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bates, Susan; Piekarz, Richard; Frye, Robin; Figg, William Douglas, Sr.; Stetler-Stevenson, Maryalice; Ling, Alex] NCI, Bethesda, MD 20892 USA.
[Wright, John] IDB CTEP NCI, Rockville, MD USA.
[Allen, Steven L.] N Shore Univ Hosp LIJ, Lake Success, NY USA.
[Craig, Michael] W Virginia Univ Hosp, Morgantown, WV USA.
[Geskin, Larisa] Univ Pittsburgh, Pittsburgh, PA USA.
[Hutchins, Laura] Univ Arkansas Med Sci, Arkansas Canc Res Ctr, Little Rock, AR 72205 USA.
[Joske, David] Sir Charles Gairdner Hosp, Nedlands, WA 6009, Australia.
[Kirschbaum, Mark] City Hope Natl Med Ctr, Div Hematol, Duarte, CA 91010 USA.
[Leonard, John P.] Weill Cornell Med Coll, Div Hem & Onc, New York, NY USA.
[Prince, Miles] Peter MacCallum Canc Inst, Melbourne, Australia.
[Reeder, Craig B.] Mayo Clin, Scottsdale, AZ USA.
[Nichols, Jean] Gloucester Pharmaceut, Cambridge, MA USA.
RI Figg Sr, William/M-2411-2016
NR 0
TC 3
Z9 3
U1 0
U2 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 556
EP 556
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701789
ER
PT J
AU Sehn, LH
Macdonald, DA
Rubin, SH
Rubinger, M
Imrie, KR
Chapman, JAW
Djurfeldt, M
Shepherd, L
Couban, S
Crump, M
AF Sehn, Laurie H.
Macdonald, David A.
Rubin, Sheldon H.
Rubinger, More
Imrie, Kevin R.
Chapman, Judy-Anne W.
Djurfeldt, Marina
Shepherd, Lois
Couban, Stephen
Crump, Michael
TI Tolerability and Efficacy of Bortezomib Added to CVP-R for Previously
Untreated Advanced Stage Follicular Lymphoma: Interim Analysis of a
Phase II Study by the NCIC Clinical Trials Group
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sehn, Laurie H.] British Columbia Canc Agcy, Vancouver, BC, Canada.
[Macdonald, David A.] QEII Hlth Sci Ctr, Halifax, NS, Canada.
[Rubin, Sheldon H.] Moncton Hosp, Moncton, NB, Canada.
[Rubinger, More] Canc Care Manitoba, Winnipeg, MB, Canada.
[Imrie, Kevin R.] Sunnybrook Med Ctr, Toronto, ON, Canada.
[Chapman, Judy-Anne W.; Shepherd, Lois] Queens Univ, Kingston, ON, Canada.
[Djurfeldt, Marina] NCI, Canada Clin Trials Grp, Kingston, ON, Canada.
[Couban, Stephen] Queen Elizabeth II Hlth, Ctr Sci, Halifax, NS, Canada.
[Crump, Michael] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 559
EP 559
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701797
ER
PT J
AU Lin, YW
Song, JH
Zhang, ZH
Aplan, PD
Smith, CD
Kraft, A
Beharry, ZM
AF Lin, Yingwei
Song, Jin H.
Zhang, Zhenhua
Aplan, Peter D.
Smith, Charles D.
Kraft, Andrew
Beharry, Zanna M.
TI Novel Small Molecule Pim Protein Kinase Inhibitors Induce Cell Cycle
Arrest and Apoptosis in Human Leukemias: A Potential Therapeutic
Approach
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Song, Jin H.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
[Zhang, Zhenhua; Aplan, Peter D.] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
[Smith, Charles D.] Med Univ S Carolina, Hollings Canc Ctr, Dept Pharmaceut & Biomed Sci, Charleston, SC 29425 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 576
EP 577
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701853
ER
PT J
AU Shenoy, A
Pfannes, L
Wilhelm, F
Maniar, M
Young, N
Sloand, EM
AF Shenoy, Aarthi
Pfannes, Loretta
Wilhelm, Francois
Maniar, Manoj
Young, Neal
Sloand, Elaine M.
TI Suppression of Cyclin D 1 (CD1) by on 01910.Na Is Associated with
Decreased Survival or Trisomy 8 Myelodysplastic Bone Marrow: A Potential
Targetted Therapy for Trisomy 8 MDS
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Shenoy, Aarthi; Pfannes, Loretta; Young, Neal; Sloand, Elaine M.] NhIbi, NIH, Bethesda, MD USA.
[Wilhelm, Francois; Maniar, Manoj] Onconova Therapeut, Newtown, PA USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 583
EP 583
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701872
ER
PT J
AU Molnar, S
Zepeda, VJJ
Van Wier, S
Braggio, E
Keats, J
Kuehl, M
Price-Troska, T
Ahmann, G
Rempel, R
Henderson, K
Rajkumar, SV
Greipp, PR
Auclair, D
Carpten, J
Baker, A
Stewart, K
Bergsagel, PL
Chng, WJ
Fonseca, R
AF Molnar, Soledad
Zepeda, Victor J. Jimenez
Van Wier, Scott
Braggio, Esteban
Keats, Jonathan
Kuehl, Michael
Price-Troska, Tammy
Ahmann, Greg
Rempel, Rachel
Henderson, Kim
Rajkumar, S. Vincent
Greipp, Philip. R.
Auclair, Daniel
Carpten, John
Baker, Angela
Stewart, Keith
Bergsagel, P. Leif
Chng, Wee Joo
Fonseca, Rafael
TI Loss of p53 Is a Marker of Progression in Plasma Cell Neoplasias and Is
a Negative Prognostic Factor in Relapsed Disease.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Molnar, Soledad; Zepeda, Victor J. Jimenez; Van Wier, Scott; Braggio, Esteban; Keats, Jonathan; Ahmann, Greg; Rempel, Rachel; Stewart, Keith; Bergsagel, P. Leif; Fonseca, Rafael] Mayo Clin Arizona, Scottsdale, AZ USA.
[Kuehl, Michael; Henderson, Kim] NCI, Bethesda, MD 20892 USA.
[Price-Troska, Tammy; Greipp, Philip. R.] Mayo Clin Rochester, Rochester, MN USA.
[Rajkumar, S. Vincent] Mayo Clin, Coll Med, Rochester, MN USA.
[Auclair, Daniel] Multiple Myeloma Res Ctr, Phoenix, AZ USA.
[Carpten, John; Baker, Angela] Translat Genom Res Inst, Phoenix, AZ USA.
[Chng, Wee Joo] Natl Univ Singapore Hosp, Singapore, Singapore.
RI Keats, Jonathan/B-2047-2009
NR 0
TC 0
Z9 0
U1 0
U2 4
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 NOV 16
PY 2008
VL 112
IS 11
BP 587
EP 587
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701884
ER
PT J
AU Berndt, SI
Johnson, DC
Crowley, J
Durie, BG
Hoover, R
Katz, M
Rothman, N
Van Ness, BG
Baris, D
Morgan, GJ
AF Berndt, Sonja I.
Johnson, David C.
Crowley, John
Durie, Brian G.
Hoover, Robert
Katz, Michael
Rothman, Nathaniel
Van Ness, Brian G.
Baris, Dalsu
Morgan, Gareth J.
TI Large Scale Evaluation of Genetic Variation and the Risk of Multiple
Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Berndt, Sonja I.; Hoover, Robert; Rothman, Nathaniel; Baris, Dalsu] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Johnson, David C.] Inst Canc Res, Sect Hematooncol, London SW3 6JB, England.
[Crowley, John] SWOG Stat Ctr, Seattle, WA USA.
[Durie, Brian G.] Samuel Oschin Comprehens Canc Inst, Hematol Oncol Cedars Sinai Outpatient Canc Ctr, Los Angeles, CA USA.
[Katz, Michael] Int Myeloma Fdn, N Hollywood, CA USA.
[Van Ness, Brian G.] Univ Minnesota, Minneapolis, MN USA.
[Morgan, Gareth J.] Inst Canc Res, Sect Hematooncol, London SW3 6JB, England.
RI Johnson, David/A-3907-2011
OI Johnson, David/0000-0003-0887-3343
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 NOV 16
PY 2008
VL 112
IS 11
BP 593
EP 593
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702013
ER
PT J
AU Kristinsson, SY
Bjorkholm, M
Goldin, LR
Blimark, C
Mellqvist, UH
Wahlin, A
Turesson, I
Landgren, O
AF Kristinsson, Sigurdur Y.
Bjorkholm, Magnus
Goldin, Lynn R.
Blimark, Cecilie
Mellqvist, Ulf-Henrik
Wahlin, Anders
Turesson, Ingemar
Landgren, Ola
TI Familial Aggregation of Multiple Myeloma and Its Precursor Monoclonal
Gammopathy of Undetermined Significance (MGUS): A Population-Based Study
in Sweden
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
[Goldin, Lynn R.; Landgren, Ola] NCI, NIH, Bethesda, MD 20892 USA.
[Blimark, Cecilie; Mellqvist, Ulf-Henrik] Sahlgrens Univ Hosp, Dept Med, Sect Hematol & Coagulat, Gothenburg, Sweden.
[Wahlin, Anders] Umea Univ Hosp, S-90185 Umea, Sweden.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Malmo, Sweden.
RI Wahlin, Anders/F-6043-2013; Kristinsson, Sigurdur /M-2910-2015
OI Wahlin, Anders/0000-0001-6402-0463; Kristinsson, Sigurdur
/0000-0002-4964-7476
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 593
EP 593
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702012
ER
PT J
AU Weiss, BM
Verma, P
Abadie, J
Howard, R
Kuehl, M
AF Weiss, Brendan M.
Verma, Pramvir
Abadie, Jude
Howard, Robin
Kuehl, Michael
TI A Pre-Existing Plasma Cell Disorder Occurs in Most Patients with
Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Weiss, Brendan M.] Walter Reed Army Med Ctr, Hematol Oncol Serv, Washington, DC 20307 USA.
[Verma, Pramvir] Womack Army Med Ctr, Hematol Oncol Serv, Ft Bragg, NC USA.
[Abadie, Jude] Walter Reed Army Med Ctr, Pathol & Area Lab Serv, Washington, DC 20307 USA.
[Howard, Robin] Walter Reed Army Med Ctr, Dept Clin Invest, Washington, DC 20307 USA.
[Kuehl, Michael] Natl Canc Inst, Genet Branch, Ctr Canc Res, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 598
EP 598
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702027
ER
PT J
AU Klier, M
Bonzheim, I
Anastasov, N
Angermeier, D
Raffeld, M
Fend, F
Quintanilla-Martinez, L
AF Klier, Margit
Bonzheim, Irina
Anastasov, Natasa
Angermeier, Daniela
Raffeld, Mark
Fend, Falko
Quintanilla-Martinez, Leticia
TI Targeting CDK4 in Mantle Cell Lymphoma (MCL) Cell Lines by Specific
Lentiviral shRNA Mediated Knockdown Has Profound Effects on Cell Growth
and Cell Cycle but Minimal Effects on Apoptosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Klier, Margit; Bonzheim, Irina; Fend, Falko; Quintanilla-Martinez, Leticia] Univ Tubingen, Univ Tubingen Hosp, D-72074 Tubingen, Germany.
[Bonzheim, Irina] Helmholtz Ctr Munich German Res Ctr Environm, Neuherberg, Germany.
[Angermeier, Daniela] Tech Univ Munich, Munich, Germany.
[Raffeld, Mark] NCI, NIH, Bethesda, MD 20892 USA.
RI Anastasov, Natasa/M-9848-2014
OI Anastasov, Natasa/0000-0002-4088-1119
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 624
EP 624
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702101
ER
PT J
AU Domingo-Domenech, E
Benavente, Y
Montalban, C
Bosch, R
Guma, J
Wang, S
Rothman, N
Gonzalez-Barca, E
de Sanjose, S
AF Domingo-Domenech, Eva
Benavente, Yolanda
Montalban, Carlos
Bosch, Ramon
Guma, Josep
Wang, Sophia
Rothman, Nathaniel
Gonzalez-Barca, Eva
de Sanjose, Silvia
TI Family History of Cancer and Risk of Lymphoma: Influence of IL8RB, GGH
IVS7 and IL10 Polymorphisms
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Montalban, Carlos] Hosp Ramon & Cajal, Madrid, Spain.
[Guma, Josep] Hosp Sant Joan Reus, Barcelona, Spain.
[Wang, Sophia; Rothman, Nathaniel] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA.
RI de Sanjose Llongueras, Silvia/H-6339-2014; Bosch Princep,
Ramon/F-4229-2016; Benavente, Yolanda/H-9810-2014
OI Bosch Princep, Ramon/0000-0003-4104-5515;
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 628
EP 628
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702111
ER
PT J
AU Wilkinson, ST
Fernandez, DR
Murphy, SP
Chan, WC
Gascoyne, RD
Campo, E
Jaffe, ES
Staudt, LM
Delabie, J
Rosenwald, A
Riinsza, LM
AF Wilkinson, Sarah T.
Fernandez, Diane R.
Murphy, Shawn P.
Chan, Wing C.
Gascoyne, Randy D.
Campo, Elias
Jaffe, Elaine S.
Staudt, Louis M.
Delabie, Jan
Rosenwald, Andreas
Riinsza, Lisa M.
TI Loss of CIITA and MHC Class II Expression in Diffuse Large B-Cell
Lymphoma Is Not Explained by Methylation of CIITA Promoters III and IV
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wilkinson, Sarah T.; Fernandez, Diane R.; Riinsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Murphy, Shawn P.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Chan, Wing C.] Univ Nebraska, Med Ctr, Omaha, NE USA.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Campo, Elias] Univ Barcelona, Barcelona, Spain.
[Jaffe, Elaine S.; Staudt, Louis M.] Natl Canc Inst, Bethesda, MD USA.
[Delabie, Jan] Radium Hosp, Oslo, Norway.
[Rosenwald, Andreas] Univ Wurzburg, Wurzburg, Germany.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 631
EP 631
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702120
ER
PT J
AU Washington, AV
Gibot, S
Acevedo, I
De La Mota, A
Gattis, J
Rivera, L
Quigley, L
Gomez-Rodriguez, J
Cheng, J
Dutra, A
Lubkowski, J
Pak, E
Hunter, R
Schwartzberg, PL
McVicar, DW
AF Washington, A. Valance
Gibot, Sebastien
Acevedo, Ismael
De La Mota, Alina
Gattis, James
Rivera, Linette
Quigley, Laura
Gomez-Rodriguez, Julio
Cheng, Jun
Dutra, Amalia
Lubkowski, Jacek
Pak, Evgenia
Hunter, Robert
Schwartzberg, Pamela L.
McVicar, Daniel W.
TI TLT-1 (TREM-Like transcript-1) Protects against Hemorrhage Associated
with Inflammation by Facilitating Platelet Aggregation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Washington, A. Valance; Acevedo, Ismael; De La Mota, Alina; Rivera, Linette; Hunter, Robert] Univ Cent Caribe, Bayamon, PR USA.
[Gibot, Sebastien] Nancy Univ, Fac Med, Contrat Avenir Inserm, Grp Choc,Hop Cent, F-54034 Nancy, France.
[Gattis, James; Lubkowski, Jacek] NCI, Macromol Crystallog Lab, Frederick, MD USA.
[McVicar, Daniel W.] NCI, Canc & Inflammat Program, Frederick, MD USA.
[Gomez-Rodriguez, Julio; Cheng, Jun; Pak, Evgenia; Schwartzberg, Pamela L.] NHGRI, NIH, Bethesda, MD 20892 USA.
RI McVicar, Daniel/G-1970-2015
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 646
EP 647
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702170
ER
PT J
AU Li, XG
Hu, X
Zhou, Z
Qiu, Y
Felsenfeld, G
Bungert, J
Huang, SM
AF Li, Xingguo
Hu, Xin
Zhou, Zhuo
Qiu, Yi
Felsenfeld, Gary
Bungert, Jorg
Huang, Suming
TI Regulation of Chromatin Looping and Transcription by PRMT1 Mediated H4R3
Methylation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Li, Xingguo; Hu, Xin; Zhou, Zhuo; Qiu, Yi; Bungert, Jorg; Huang, Suming] Univ Florida, Coll Med, Gainesville, FL USA.
[Felsenfeld, Gary] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 654
EP 654
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702197
ER
PT J
AU Noh, SJ
Miller, S
Lee, YT
Marincola, FM
Stroncek, D
Reed, C
Wang, E
Miller, JL
AF Noh, Seung-Jae
Miller, Samuel
Lee, Y. Terry
Marincola, Francesco M.
Stroncek, David
Reed, Christopher
Wang, Ena
Miller, Jeffery L.
TI Fetal-to-Adult Hemoglobin Switching Is Associated with up-Regulation of
Specific MicroRNA Species in Circulating Human Erythroid Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Noh, Seung-Jae; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Reed, Christopher] Natl Naval Med Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 654
EP 654
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702198
ER
PT J
AU Sripichal, O
Lee, YT
Tanno, T
Noh, SJ
Byrnes, C
Meier, ER
Miller, JL
AF Sripichal, Orapan
Lee, Y. Terry
Tanno, Toshihiko
Noh, Seung-Jae
Byrnes, Colleen
Meier, Emily Riehm
Miller, Jeffery L.
TI Gamma-Globin Gene Expression in Adult Human Erythroblasts Is Associated
with Concurrent Changes in the Nuclear Protein Levels of at Least Seven
Transcription Factors
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sripichal, Orapan; Lee, Y. Terry; Tanno, Toshihiko; Noh, Seung-Jae; Byrnes, Colleen; Meier, Emily Riehm; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 655
EP 655
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702199
ER
PT J
AU Galanello, R
Sanna, S
Perseu, L
Sollaino, MC
Satta, S
Uda, M
Usala, G
Abecasis, G
Schlessinger, D
Cao, A
AF Galanello, Renzo
Sanna, Serena
Perseu, Lucia
Sollaino, Maria Carla
Satta, Stefania
Uda, Manuela
Usala, Gianluca
Abecasis, Goncalo
Schlessinger, David
Cao, Antonio
TI Genetic Modifiers of Homozygous Beta Zero Thalassemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Galanello, Renzo; Sollaino, Maria Carla; Satta, Stefania] Osped Reg Microcitemici ASL, Dip Sci Biomed E Biotec, Cagliari, Italy.
[Sanna, Serena; Perseu, Lucia; Uda, Manuela; Usala, Gianluca] CNR, Ist Genet & Neurofarmacol, Calgary, AB, Canada.
[Abecasis, Goncalo] Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Schlessinger, David] NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Cao, Antonio] Inst Clin Bio Eta Evolut, Cagliari, Italy.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 657
EP 657
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702207
ER
PT J
AU Bhatia, H
Hallock, JL
Sterner, LE
Karkashon, S
Dutta, A
Miyazaki, T
Dean, A
Little, J
AF Bhatia, Himanshu
Hallock, Jennifer L.
Sterner, Lauren E.
Karkashon, Shay
Dutta, Armita
Miyazaki, Toru
Dean, Ann
Little, Jane
TI A Novel Model of Short Chain Fatty Acid (SCFA)- Mediated up-Regulation
of Embryonic/Fetal Globin Genes during Definitive Erythropoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bhatia, Himanshu; Karkashon, Shay; Dutta, Armita; Little, Jane] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Hallock, Jennifer L.; Sterner, Lauren E.; Dean, Ann] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD USA.
[Miyazaki, Toru] Univ Tokyo, Fac Med, Ctr Dis Biol & Integrat Med, Div Mol Biomed Pathogenesis, Tokyo 1130033, Japan.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 658
EP 658
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702211
ER
PT J
AU Singer, T
Kim, HY
Olivieri, NF
Kwiatkowski, J
Lal, A
Coates, TD
Carson, S
Cunningham, MJ
Giardina, PJ
Mueller, BU
Quinn, C
Vichinsky, E
AF Singer, Titi
Kim, Hae-Young
Olivieri, Nancy F.
Kwiatkowski, Janet
Lal, Ashutosh
Coates, Thomas D.
Carson, Susan
Cunningham, Melody J.
Giardina, Patricia J.
Mueller, Brigitta U.
Quinn, Charles
Vichinsky, Elliott
CA Thalassemia Clinical Res Network
TI Hemoglobin H-Constant Spring in North America: A Common Alpha
Thalassemia with Frequent Complications
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Singer, Titi; Lal, Ashutosh; Vichinsky, Elliott] Childrens Hosp, Oakland, CA 94609 USA.
[Singer, Titi; Lal, Ashutosh; Vichinsky, Elliott] Res Ctr Oakland, Oakland, CA USA.
[Kim, Hae-Young] New England Res Inst, Watertown, MA 02172 USA.
[Olivieri, Nancy F.] Toronto Gen Hosp, Univ Hlth Network, Toronto, ON, Canada.
[Kwiatkowski, Janet] Childrens Hosp Philadelphia, Div Hematol, Philadelphia, PA 19104 USA.
[Coates, Thomas D.; Carson, Susan] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
[Cunningham, Melody J.] Childrens Hosp Boston, Boston, MA USA.
[Giardina, Patricia J.] Weill Cornell Med Coll, New York, NY USA.
[Mueller, Brigitta U.] Texas Childrens Hosp, Baylor Coll Med, Houston, TX 77030 USA.
[Quinn, Charles] Univ Texas SW Med Ctr Dallas, Div Pediat Hematol Oncol, Dallas, TX 75390 USA.
[Thalassemia Clinical Res Network] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 658
EP 659
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702213
ER
PT J
AU Jankowitz, RC
Foon, KA
Luong, M
Land, SR
DeMonaco, NA
Swerdlow, SH
Joyce, J
Osborn, J
Evans, T
Jacobs, SA
AF Jankowitz, Rachel C.
Foon, Kenneth A.
Luong, Minh
Land, Stephanie R.
DeMonaco, Nicholas A.
Swerdlow, Steven H.
Joyce, Judith
Osborn, Jennifer
Evans, Terry
Jacobs, Samuel A.
TI Phase II Study of Short Course CHOP-Rituximab Followed by 90-Y
Ibritumomab Tiuxetan as First-Line Treatment for Follicular Lymphoma: An
Update and Extension of Preliminary Findings on Predictors of Relapse
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Jankowitz, Rachel C.; Jacobs, Samuel A.] Univ Pittsburgh, Dept Med, Div Hematol Oncol, Pittsburgh, PA USA.
[Foon, Kenneth A.] Nevada Canc Inst, Las Vegas, NV USA.
[Luong, Minh] Univ Pittsburgh, Inst Canc, Biostat Facil, Pittsburgh, PA USA.
[Land, Stephanie R.] NSABP, Dept Publ Hlth, Pittsburgh, PA USA.
[DeMonaco, Nicholas A.] Oncol Hematol Associates, Clinton, MD USA.
[Swerdlow, Steven H.] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA.
[Joyce, Judith] Univ Pittsburgh, Sch Med, Dept Radiol, Pittsburgh, PA USA.
[Osborn, Jennifer] UPMC Canc Ctr, UPMC Passavant, Pittsburgh, PA USA.
[Evans, Terry] Univ Pittsburgh, Med Ctr, UPMC Canc Ctr Arnold Palmer Pavil, Greensburg, PA USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 698
EP 698
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702334
ER
PT J
AU Sharma, K
Janik, JE
O'Mahony, D
Stewart, D
Pittaluga, S
Stetler-Stevenson, M
Jaffe, ES
Raffeld, M
Fleisher, TA
Lee, CC
Urquhart, N
Steinberg, S
Waldmann, TA
Morris, JC
AF Sharma, Kamal
Janik, John E.
O'Mahony, Deirdre
Stewart, Donn
Pittaluga, Stefania
Stetler-Stevenson, Maryalice
Jaffe, Elaine S.
Raffeld, Mark
Fleisher, Thomas A.
Lee, Cathryn C.
Urquhart, Nicole
Steinberg, Seth
Waldmann, Thomas A.
Morris, John C.
TI Alemtuzumab (Campath 1-H) in Patients with HTLV-1 Associated Adult
T-Cell Leukemia/Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sharma, Kamal; Janik, John E.; O'Mahony, Deirdre; Stewart, Donn; Lee, Cathryn C.; Waldmann, Thomas A.; Morris, John C.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania; Stetler-Stevenson, Maryalice; Jaffe, Elaine S.; Raffeld, Mark] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Fleisher, Thomas A.] NIH, Dept Lab Med, Ctr Canc Res, Bethesda, MD 20892 USA.
[Urquhart, Nicole] Univ W Indies, ATL Treatment Project, Dept Pathol, Jamaica, NY USA.
[Steinberg, Seth] NCI, Biostat & Data Management Sect, Office Clin Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 701
EP 701
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702343
ER
PT J
AU Visconte, V
Raghavachari, N
Keyvanfar, K
Liu, DL
Desierto, M
Chen, JC
Young, NS
AF Visconte, Valeria
Raghavachari, Nalini
Keyvanfar, Keyvan
Liu, Delong
Desierto, Marie
Chen, Jichun
Young, Neal S.
TI Clonally-Restricted T-Lymphocytes in PigA Mutant Mice.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Visconte, Valeria; Keyvanfar, Keyvan; Desierto, Marie; Chen, Jichun; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Raghavachari, Nalini] NIH, Pulm & Vasc Branch, Bethesda, MD USA.
[Liu, Delong] NIH, Math & Stat Comp Lab, DCB, CIT, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 711
EP 711
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702373
ER
PT J
AU Giri, N
Mueller, C
Weinstein, S
Hill, S
Butman, J
Tsilou, E
Hung, JK
Savage, SA
Alter, BP
AF Giri, Neelam
Mueller, Christine
Weinstein, Sarah
Hill, Suvimol
Butman, John
Tsilou, Ekaterini
Hung, Jeffrey Kim
Savage, Sharon A.
Alter, Blanche P.
TI The First Single Center Phenotypic Comparison of Fanconi Anemia,
Dyskeratosis Congenita, Diamond-Blackfan Anemia, and Shwachman-Diamond
Syndrome: The NCI IBMFS Cohort.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Giri, Neelam; Mueller, Christine; Weinstein, Sarah; Savage, Sharon A.; Alter, Blanche P.] NCI, Clin Genet Branch, DCEG, Bethesda, MD 20892 USA.
[Hill, Suvimol; Butman, John] NIH, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
[Tsilou, Ekaterini] NEI, Bethesda, MD 20892 USA.
[Hung, Jeffrey Kim] Natl Inst Deafness & Other Commun Disorders, Bethesda, MD USA.
RI Butman, John/A-2694-2008; Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 712
EP 712
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702376
ER
PT J
AU Deffenbacher, KE
Wright, G
Iqbal, J
Geng, HM
O'Shea, D
Lister, TA
Fitzgibbon, J
Fu, K
Liu, ZF
Weisenburger, D
Greiner, TC
Gascoyne, RD
Rosenwald, A
Campo, E
Rimsza, LM
Delabie, J
Jaffe, ES
Staudt, LM
Chan, WC
AF Deffenbacher, Karen E.
Wright, George
Iqbal, Javeed
Geng, Huimin
O'Shea, Derville
Lister, T. Andrew
Fitzgibbon, Jude
Fu, Kai
Liu, Zhongfeng
Weisenburger, Dennis
Greiner, Timothy C.
Gascoyne, Randy D.
Rosenwald, Andreas
Campo, Elias
Rimsza, Lisa M.
Delabie, Jan
Jaffe, Elaine S.
Staudt, Louis M.
Chan, Wing C.
TI Genetic Abnormalities Involved in the Development and Progression of
Follicular Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wright, George; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[O'Shea, Derville; Lister, T. Andrew; Fitzgibbon, Jude] Barts & London Queen Marys Sch Med & Dent, Ctr Med Oncol, London, England.
[Fu, Kai] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Campo, Elias] Hosp Clin Barcelona, Barcelona, Spain.
[Delabie, Jan] Norwegian Radium Hosp, Oslo, Norway.
[Jaffe, Elaine S.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 714
EP 714
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702382
ER
PT J
AU Kovalchuk, AL
Casellas, R
Dubois, W
Tolarova, H
Hausner, PF
Mushinski, E
Nelson, PJ
Morse, H
Potter, M
AF Kovalchuk, Alexander L.
Casellas, Rafael
duBois, Wendy
Tolarova, Helena
Hausner, Petr F.
Mushinski, Elizabeth
Nelson, Patrick J.
Morse, Herbert, III
Potter, Michael
TI Tissue Origin of Igh/Myc Chromosomal Translocations in An Accelerated
Pristane-Induced Plasma Cell Tumor Model using BALB/C-Bcl-Xl Transgenic
Mice and the Inhibitory Effects of Defective Genes Governing Class
Switch recombination in Ung and Aicda Knockout Mice
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kovalchuk, Alexander L.; Morse, Herbert, III] NIAID, Immunopathol Lab, NIH, Rockville, MD USA.
[Casellas, Rafael; Tolarova, Helena] NIAMS, NIH, Bethesda, MD USA.
[duBois, Wendy; Mushinski, Elizabeth; Nelson, Patrick J.; Potter, Michael] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD USA.
[Hausner, Petr F.] Univ Maryland, Greenebaum Canc Cente, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 714
EP 715
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702384
ER
PT J
AU Aue, G
Njuguna, N
Tian, X
Valdez, J
Soto, S
Mccoy, JP
Samsel, L
Vire, B
Keyvanfar, K
Pittaluga, S
Wiestner, A
AF Aue, Georg
Njuguna, Ndegwa
Tian, Xin
Valdez, Janet
Soto, Susan
McCoy, J. Philip, Jr.
Samsel, Leigh
Vire, Berengere
Keyvanfar, Keyvan
Pittaluga, Stefania
Wiestner, Adrian
TI Lenalidomide Induced Cytokine Release Syndrome in Chronic Lymphocytic
Leukemia (CLL): Clinical and Laboratory Correlates of Immune Activation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Aue, Georg; Njuguna, Ndegwa; Valdez, Janet; Soto, Susan; Vire, Berengere; Keyvanfar, Keyvan; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Tian, Xin] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[McCoy, J. Philip, Jr.; Samsel, Leigh] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
[Pittaluga, Stefania] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 730
EP 730
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702432
ER
PT J
AU Wilson, WH
O'Connor, O
Czuczman, MS
LaCasce, A
Gerecitano, J
Leonard, JP
Tulpule, A
Xiong, H
Chiu, YL
Busman, T
Knight, RA
Enschede, S
Krivoshik, A
Humerickhouse, R
AF Wilson, Wyndham H.
O'Connor, O.
Czuczman, Myron S.
LaCasce, Ann
Gerecitano, J.
Leonard, John P.
Tulpule, Anil
Xiong, Hao
Chiu, Yi-Lin
Busman, Todd
Knight, Raymond A.
Enschede, Sari
Krivoshik, Andrew
Humerickhouse, Rod
TI Phase 1 Study of ABT-263, a Bcl-2 Family Inhibitor, in Relapsed or
Refractory Lymphoid Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[O'Connor, O.] Columbia Univ, Med Ctr, New York, NY USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[LaCasce, Ann] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gerecitano, J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Leonard, John P.] Weill Cornell Med Coll, Div Hem Onc, New York, NY USA.
[Tulpule, Anil] USC, Norris Canc Ctr, Sch Med, Los Angeles, CA USA.
[Xiong, Hao; Chiu, Yi-Lin; Busman, Todd; Knight, Raymond A.; Enschede, Sari; Krivoshik, Andrew; Humerickhouse, Rod] Abbott Labs, Abbott Pk, IL 60064 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 NOV 16
PY 2008
VL 112
IS 11
BP 734
EP 734
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702441
ER
PT J
AU Drew, DZ
Melenhorst, J
Hensel, NF
Barrett, AJ
AF Drew, David Z.
Melenhorst, Jan
Hensel, Nancy F.
Barrett, A. John
TI Higher Absolute NK Count on Day30 after HLA Identical Sibling Allogeneic
Stem Cell Transplantation and a "Favorable KIR" Genotype Are Associated
with Faster NK Maturation and Other Functional Differences
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Drew, David Z.] NCI, BMT, NIH, Bethesda, MD 20892 USA.
[Hensel, Nancy F.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 755
EP 756
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702500
ER
PT J
AU Arantes, AM
Sanson, G
Primo, AG
Oliveira, JSR
DeLima, MG
Shulzhenko, N
Morgun, A
AF Arantes, Adriano Moraes
Sanson, Gerdine
Primo, Amador Goncalves
Rodrigues Oliveira, Jose Salvador
DeLima, Maria Gerbase
Shulzhenko, Natalia
Morgun, Andrey
TI Early Prediction of Acute Gvhd Based on Molecular Profiling at the Time
of Engraftment after Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Arantes, Adriano Moraes; Rodrigues Oliveira, Jose Salvador] Univ Fed Sao Paulo, Div Hematol, Sao Paulo, Brazil.
[Sanson, Gerdine; Primo, Amador Goncalves; DeLima, Maria Gerbase] Univ Fed Sao Paulo, Div Immunogenet, Sao Paulo, Brazil.
[Shulzhenko, Natalia; Morgun, Andrey] NIAID, Ghost Lab, LCMI, NIH, Bethesda, MD 20892 USA.
RI de Oliveira, Jose Salvador/M-9322-2015
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 778
EP 779
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702566
ER
PT J
AU Imanguli, MM
Swaim, WD
League, S
Gress, RE
Pavletic, SZ
Hakim, FT
AF Imanguli, Matrin M.
Swaim, William D.
League, Stacy
Gress, Ronald E.
Pavletic, Steven Z.
Hakim, Frances T.
TI Increased Type I Interferon Signaling and Inflammatory Factors
Associated with T-Bet plus Cytotoxic Effectors in Chronic Graft Versus
Host Disease of Oral Mucosa
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Imanguli, Matrin M.; League, Stacy; Gress, Ronald E.; Pavletic, Steven Z.; Hakim, Frances T.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Swaim, William D.] NIDCR, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 778
EP 778
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702564
ER
PT J
AU Harvey, RC
Chen, IM
Ar, K
Hunger, SP
Loh, M
Larsen, EC
Devidas, M
Raetz, E
Reaman, G
Carroll, WL
Winick, N
Smith, M
Dobbin, KK
Willman, CL
AF Harvey, Richard C.
Chen, I-Ming
Ar, Kerem
Hunger, Stephen P.
Loh, Mignon
Larsen, Eric C.
Devidas, Meenakshi
Raetz, Elizabeth
Reaman, Gregory
Carroll, William L.
Winick, Naomi
Smith, Malcolm
Dobbin, Kevin K.
Willman, Cheryl L.
TI Identification of Novel Cluster Groups in High-Risk Pediatric
B-Precursor Acute Lymphoblastic Leukemia (HR-ALL) by Gene Expression
Profiling: Correlation with Clinical and Outcome Variables. a Children's
Oncology Group (COG) Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Harvey, Richard C.; Ar, Kerem; Willman, Cheryl L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
[Chen, I-Ming] Univ New Mexico, Dept Pathol, Canc Res & Treatment Ctr, Albuquerque, NM 87131 USA.
[Hunger, Stephen P.; Loh, Mignon; Larsen, Eric C.; Devidas, Meenakshi; Raetz, Elizabeth; Reaman, Gregory; Carroll, William L.; Winick, Naomi] Childrens Oncol Grp, Arcadia, CA USA.
[Smith, Malcolm; Dobbin, Kevin K.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 787
EP 787
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702589
ER
PT J
AU Kim, I
Larochelle, A
Kim, YJ
Dunbar, CE
AF Kim, Inho
Larochelle, Andre
Kim, Yoo-Jin
Dunbar, Cynthia E.
TI siRNA-Induced Transient Silencing of PTEN Expression Enhances Human
Hematopoietic Cell Engraftment in NOD/SCID/gamma(null)(c) Mice and
Increases Gene Transduction Efficiency.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Kim, Inho; Larochelle, Andre; Kim, Yoo-Jin; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 812
EP 812
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702662
ER
PT J
AU Barao-Silvestre, I
Redelman, D
Ames, E
Weiss, J
Sun, K
Welniak, L
Ortaldo, J
Wiltrout, R
Murphy, W
AF Barao-Silvestre, Isabel
Redelman, Doug
Ames, Erik
Weiss, Jonathan
Sun, Kai
Welniak, Lisbeth
Ortaldo, John
Wiltrout, Robert
Murphy, William
TI In Vivo Development of Murine NK Cells Early after Congeneic BMT:
Effects of MHC Molecules, and the Administration of hIL-15.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Barao-Silvestre, Isabel; Redelman, Doug; Ames, Erik; Murphy, William] UNR, Reno, NV USA.
[Weiss, Jonathan; Ortaldo, John; Wiltrout, Robert] NCI, Frederick, MD 21701 USA.
[Sun, Kai] UNR Sch Med, Reno, NV USA.
[Welniak, Lisbeth] Univ Nevada, Reno, NV 89557 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 813
EP 813
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702667
ER
PT J
AU Hayakawa, J
Hsieh, M
Uchida, N
Washington, K
Phang, O
Kang, E
Tisdale, JF
AF Hayakawa, Jun
Hsieh, Matthew
Uchida, Naoya
Washington, Kareem
Phang, Oswald
Kang, Elizabeth
Tisdale, John F.
TI Long-Term Vector Integration Site Analysis Following Retroviral Mediated
Gene Transfer to Hematopoietic Stem Cells for the Treatment of HIV
Infection
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hayakawa, Jun; Hsieh, Matthew; Uchida, Naoya; Washington, Kareem; Phang, Oswald; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Kang, Elizabeth] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 818
EP 819
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702683
ER
PT J
AU Uchida, N
Washington, K
Hayakawa, J
Hsieh, M
Bonifacino, AC
Krouse, AE
Metzger, ME
Donahue, RE
Tisdale, JF
AF Uchida, Naoya
Washington, Kareem
Hayakawa, Jun
Hsieh, Matthew
Bonifacino, Aylin C.
Krouse, Allen E.
Metzger, Mark E.
Donahue, Robert E.
Tisdale, John F.
TI Development of An HIV1-Based Lentiviral Vector Able to Transduce Both
Human and Rhesus Blood Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Uchida, Naoya; Washington, Kareem; Hayakawa, Jun; Hsieh, Matthew; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Bonifacino, Aylin C.; Krouse, Allen E.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, HB, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 819
EP 820
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702686
ER
PT J
AU Sirohi, B
Powles, R
Niederweiser, D
Coleman, N
Chao, NJ
Bader, J
Case, C
Chute, J
Confer, DL
Gourmelon, P
Gorin, NC
Ganser, A
Port, M
Meineke, V
Krawisz, R
Weinstock, DM
Wiley, A
Fliedner, T
AF Sirohi, Bhawna
Powles, Raymond
Niederweiser, Dietger
Coleman, Norm
Chao, Nelson J.
Bader, Judith
Case, Cullen, Jr.
Chute, John
Confer, Dennis L.
Gourmelon, Patrick
Gorin, Norbert C.
Ganser, Arnold
Port, Matthias
Meineke, Viktor
Krawisz, Robert
Weinstock, David M.
Wiley, Albert
Fliedner, Ted
TI Trans-Atlantic Consensus on the Medical Management of Radiation Accident
Victims
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sirohi, Bhawna] Addenbrookes Hosp, Cambridge, England.
[Powles, Raymond] Parkside Oncol Clin, Wimbledon, England.
[Niederweiser, Dietger] Univ Leipzig, Leipzig, Germany.
[Coleman, Norm; Bader, Judith] NCI, NIH, Bethesda, MD 20892 USA.
[Chao, Nelson J.] Duke Univ, Med Ctr, Med Div Cellular Therapy, Durham, NC USA.
[Case, Cullen, Jr.; Confer, Dennis L.] Natl Marrow Donor Program, Minneapolis, MN USA.
[Chute, John] Duke Univ, Div Cellular Therapy, Durham, NC USA.
[Gorin, Norbert C.] Hop St Antoine, F-75571 Paris, France.
[Gorin, Norbert C.] Univ Paris 06, Paris, France.
[Ganser, Arnold] Hannover Med Sch, Dept Hematol Hemostaseol Oncol & Stem Cell Transp, D-3000 Hannover, Germany.
[Weinstock, David M.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Wiley, Albert] REAC TS, Oak Ridge, TN USA.
[Fliedner, Ted] Univ Ulm, D-89069 Ulm, Germany.
RI Port, Matthias/D-5230-2011
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 822
EP 822
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702694
ER
PT J
AU Richey, EA
Shankaran, V
Hirschfeld, S
Trifilio, SM
McKoy, J
Carson, KR
Edwards, BJ
Luu, TH
Nonzee, N
Sartor, AO
Bennett, CL
AF Richey, Elizabeth A.
Shankaran, Veena
Hirschfeld, Steven
Trifilio, Steven M.
McKoy, June
Carson, Kenneth R.
Edwards, Beatrice J.
Luu, Thanh Ha
Nonzee, Narissa
Sartor, A. Oliver
Bennett, Charles L.
TI "Getting to go" for FDA Approvals for the Treatment of Hematologic
Versus Solid Tumor Malignancies: A Report from the Research on Adverse
Drug Events and Reports (RADAR) Project
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Edwards, Beatrice J.] Northwestern Univ, Feinberg Sch Med, Bone Hlth & Osteoporosis Ctr, Chicago, IL 60611 USA.
[Hirschfeld, Steven] NICHD, NIH, Bethesda, MD USA.
[Trifilio, Steven M.] NW Mem Hosp, Chicago, IL 60611 USA.
[Carson, Kenneth R.] Washington Univ, Sch Med, Siteman Comprehens Canc Ctr, St Louis, MO USA.
[Sartor, A. Oliver] Tulane Univ, Tulane Canc Ctr, New Orleans, LA 70118 USA.
RI Hirschfeld, Steven/E-2987-2016
OI Hirschfeld, Steven/0000-0003-0627-7249
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 837
EP 837
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702735
ER
PT J
AU Suh, HC
Ji, M
Gooya, J
Lee, M
Klarmann, K
Keller, JR
AF Suh, Hyung Chan
Ji, Ming
Gooya, John
Lee, Michael
Klarmann, Kimberly
Keller, Jonathan R.
TI Id1 Provides a Proper Hematopoietic Progenitor Niche Function.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Suh, Hyung Chan; Ji, Ming; Gooya, John; Lee, Michael; Klarmann, Kimberly; Keller, Jonathan R.] Natl Canc Inst, Lab Canc Prevent, Frederick, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 845
EP 845
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702760
ER
PT J
AU Owen, AN
Laflamme, K
Pilon, AM
Garrett, LJ
Gallagher, PG
Bodine, DM
AF Owen, Ashley N.
Laflamme, Karina
Pilon, Andre M.
Garrett, Lisa J.
Gallagher, Patrick G.
Bodine, David M.
TI Local and Distant Elements Regulate Tissue-Specific Expression of ANK-1
Gene Transcripts
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Owen, Ashley N.; Laflamme, Karina; Pilon, Andre M.; Bodine, David M.] GMBB, Hematopoiesis Sect, Nhgri, Bethesda, MD USA.
[Garrett, Lisa J.] Transgen Mouse Core Facil, Nhgri, Bethesda, MD USA.
[Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 846
EP 847
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702765
ER
PT J
AU Hayakawa, J
Hsieh, M
Uchida, N
Washington, K
Phang, O
Anderson, DE
Tisdale, J
AF Hayakawa, Jun
Hsieh, Matthew
Uchida, Naoya
Washington, Kareem
Phang, Oswald
Anderson, David Eric
Tisdale, John
TI A Practical Erythroid Assay in Humanized Xenograft Mouse Model
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hayakawa, Jun; Hsieh, Matthew; Uchida, Naoya; Washington, Kareem; Phang, Oswald; Tisdale, John] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Anderson, David Eric] NIDDK, Prote & Mass Spectrometry Facili, OD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 851
EP 851
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702779
ER
PT J
AU Nouraie, M
Minniti, C
Sable, C
Campbell, AD
Rana, SR
Ensing, G
Dham, N
Onyekwere, OC
Darbari, DS
Kato, GJ
Gladwin, M
Castro, O
Gordeuk, VR
AF Nouraie, Mem
Minniti, Caterina
Sable, Craig
Campbell, Andrew D.
Rana, Sohail R.
Ensing, Gregory
Dham, Niti
Onyekwere, Onyinye C.
Darbari, Deepika S.
Kato, Gregory J.
Gladwin, Mark
Castro, Oswaldo
Gordeuk, Victor R.
TI Association of Hemolysis with Clinical Manifestations of Sickle Cell
Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol (ASH), Sanofi Aventis U.S.
C1 [Nouraie, Mem; Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Minniti, Caterina; Gladwin, Mark] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Sable, Craig] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Campbell, Andrew D.] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
[Rana, Sohail R.] Howard Univ Hosp, Dept Pediat & Child Hlth, Washington, DC USA.
[Dham, Niti] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Darbari, Deepika S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 862
EP 863
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702814
ER
PT J
AU Niu, XM
Nouraie, M
Minniti, C
Sable, C
Campbell, A
Rana, SR
Kato, GJ
Gladwin, M
Castro, O
Ammosova, T
Nekhai, S
Gordeuk, VR
AF Niu, Xiaomei
Nouraie, Mehdi
Minniti, Caterina
Sable, Craig
Campbell, Andrew
Rana, Sohail R.
Kato, Gregory J.
Gladwin, Mark
Castro, Oswaldo
Ammosova, Tatiana
Nekhai, Sergei
Gordeuk, Victor R.
TI Correlations Between Cytokines and Elevated Tricuspid Regurgitant Jet
Velocity in Children and Adolescents with Sickle Cell Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Minniti, Caterina; Gladwin, Mark] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Sable, Craig] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Campbell, Andrew] Univ Michigan, Med Ctr, Dept Pediat & Communicable Dis, Ann Arbor, MI USA.
[Rana, Sohail R.] Howard Univ Hosp, Dept Pediat & Child Hlth, Washington, DC USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Ammosova, Tatiana] Howard Univ, Ctr Sickle Cell Dis, HU, Washington, DC 20059 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 863
EP 863
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702816
ER
PT J
AU Krajewski, ML
Kim, JA
Mendelsohn, LG
Williams, CB
Gladwin, MT
Kato, GJ
AF Krajewski, Megan L.
Kim, James A.
Mendelsohn, Laurel G.
Williams, Candice B.
Gladwin, Mark T.
Kato, Gregory J.
TI Nitric Oxide-Dependent Blood Flow in Patients with Sickle Cell Disease
Is Reflected by the Reactive Hyperemia-Peripheral Arterial Tonometry
Index
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Krajewski, Megan L.; Kim, James A.; Mendelsohn, Laurel G.; Williams, Candice B.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Bethesda, MD USA.
[Kato, Gregory J.] NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 864
EP 864
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702818
ER
PT J
AU Minniti, CP
AF Minniti, Caterina P.
TI Elevated Tricuspid Regurgitant Jet Velocity in Children and Adolescents
with Sickle Cell Disease: Association with Hemolysis and Hemoglobin
Oxygen Desaturation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
DE Sickle cell disease; Pulmonary hypertension; Hemolysis; Oxygen
desaturation; Anemia
C1 [Minniti, Caterina P.] NIH, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 866
EP 866
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702824
ER
PT J
AU Hsu, LL
El-Haddad, H
Amar, M
Kato, GJ
Remaley, AT
Champion, HC
AF Hsu, Lems L.
El-Haddad, Hazinn
Amar, Marcelo
Kato, Gregory J.
Remaley, Alan T.
Champion, Hunter C.
TI Sickle Cell Pulmonary Hypertension and Dysregulated NO Axis in a Mouse
Model Are Modulated by Apolipoprotein a-1 Availability
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hsu, Lems L.] Drexel Univ, Coll Med, Marian Anderson Comprehens Sickle Cell Ctr, Philadelphia, PA 19104 USA.
[El-Haddad, Hazinn; Champion, Hunter C.] Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA.
[Amar, Marcelo; Remaley, Alan T.] NIH, Lab Med, Bethesda, MD 20892 USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 868
EP 868
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702831
ER
PT J
AU Chuk, M
McIntyre, E
Small, D
Brown, P
AF Chuk, Meredith
McIntyre, Emily
Small, Donald
Brown, Patrick
TI Discordance of MLL-Rearranged (MLL-R) Infant ALL in Monozygotic Twins
with Spontaneous Clearance of Preleukemic Clone in Unaffected Twin.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chuk, Meredith] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[McIntyre, Emily; Small, Donald; Brown, Patrick] Johns Hopkins Univ, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 883
EP 883
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702875
ER
PT J
AU Yokoyama, H
Lundqvist, A
Berg, M
Ramanathan, M
Lopez, R
Smith, A
Gormley, N
Su, S
McCcoy, JP
Childs, RW
AF Yokoyama, Hisayuki
Lundqvist, Andreas
Berg, Maria
Ramanathan, Muthalagu
Lopez, Rebecca
Smith, Aleah
Gormley, Nicole
Su, Su
McCcoy, J. Phillip
Childs, Richard W.
TI Adoptively-In fused NK Cells Maintain Their Antitumor Effects in Vivo in
the Presence of CyclosporineA (CSA).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Yokoyama, Hisayuki; Lundqvist, Andreas; Berg, Maria; Ramanathan, Muthalagu; Lopez, Rebecca; Smith, Aleah; Gormley, Nicole; Su, Su; Childs, Richard W.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 890
EP 890
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703005
ER
PT J
AU Walsh, M
Krauss, AC
Davis, JPE
Kim, SY
Guimond, M
Mackall, CL
Fry, TJ
AF Walsh, Meghaan
Krauss, Aviva C.
Davis, Jessica P. E.
Kim, Su Young
Guimond, Martin
Mackall, Crystal L.
Fry, Terry J.
TI Dipeptidyl Peptidase Inhibition Accelerates Dendritic Cell Cross Priming
of Tumor-Reactive T Cells Resulting in Regression of Established Tumors.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Walsh, Meghaan; Krauss, Aviva C.; Davis, Jessica P. E.; Kim, Su Young; Guimond, Martin; Mackall, Crystal L.; Fry, Terry J.] NCI, Pediat Oncol Branch, CCR, NIH, Bethesda, MD 20892 USA.
[Fry, Terry J.] Childrens Natl Med Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 894
EP 895
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703021
ER
PT J
AU Vatsveen, TK
Tian, E
Kresse, SH
Meza-Zepeda, LA
Gabrea, A
Dai, HY
Kuehl, M
Sundan, A
Borset, M
AF Vatsveen, Thea Kristin
Tian, Erming
Kresse, Stine H.
Meza-zepeda, Leonardo A.
Gabrea, Ana
Dai, Hong Yan
Kuehl, Michael
Sundan, Anders
Borset, Magne
TI OH-2, a Hyperdiploid Myeloma Cell Line without An IGH Translocation, Has
a Complex Translocation Juxtaposing MYC near MAFB and the IGK Locus.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Vatsveen, Thea Kristin; Sundan, Anders] NTNU, Trondheim, Norway.
[Tian, Erming] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
[Kresse, Stine H.; Meza-zepeda, Leonardo A.] RR, Oslo, Norway.
[Gabrea, Ana; Kuehl, Michael] NCI, Canc Res Ctr, Genet Branch, Bethesda, MD 20892 USA.
[Dai, Hong Yan] St Olavs Hosp, Trondheim, Norway.
[Borset, Magne] Norwegian Univ Sci & Technol, N-7034 Trondheim, Norway.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 945
EP 945
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703176
ER
PT J
AU Samuelson, SJ
Sanddmaier, BM
Heslop, HE
Popat, U
Boyer, M
Hickman, K
Prchal, JT
Deeg, HJ
AF Samuelson, Scott James
Sanddmaier, Brenda M.
Heslop, Helen E.
Popat, U.
Boyer, Michael
Hickman, Kimberly
Prchal, Josef T.
Deeg, H. Joachim
TI Allogeneic Hematopoietic Cell Transplants in Patients with Myelofibrosis
Age 60 and Older
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Samuelson, Scott James; Boyer, Michael; Hickman, Kimberly; Prchal, Josef T.] Univ Utah, Salt Lake City, UT USA.
[Samuelson, Scott James; Boyer, Michael; Hickman, Kimberly; Prchal, Josef T.] NCI Myeloproliferat Disorders Consortium, Salt Lake City, UT USA.
[Sanddmaier, Brenda M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Heslop, Helen E.] Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Popat, U.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 966
EP 966
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703237
ER
PT J
AU McDevitt, MA
Karp, JE
Yen, Y
Maciejewski, J
Espinoza-Delgado, I
AF McDevitt, Michael A.
Karp, Judith E.
Yen, Yun
Maciejewski, Jaroslaw
Espinoza-Delgado, Igor
TI Preliminary Results from a Phase II Trial of Triapine Plus Fludarabine
for Adults with Aggressive Myeloproliferative Disorders
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [McDevitt, Michael A.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Karp, Judith E.] JHUSOM, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Yen, Yun] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Maciejewski, Jaroslaw] Taussig Canc Ctr, Expt Hematol & Hematopoiesis Sect, Cleveland, OH USA.
[Espinoza-Delgado, Igor] NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 971
EP 971
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703250
ER
PT J
AU Bonzheim, I
Irmler, M
Anastasov, N
Klier, M
Beckers, J
Pittaluga, S
Fend, F
Raffeld, M
Quintanilla-Martinez, L
AF Bonzheim, Irina
Irmler, Martin
Anastasov, Natasa
Klier, Margit
Beckers, Johannes
Pittaluga, Stefania
Fend, Falko
Raffeld, Mark
Quintanilla-Martinez, Leticia
TI Gene Expression Profiling Reveals a Crucial Role for C/EBPbeta in
Proliferation Pathways of ALK(+) ALCL Cell Lines
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Bonzheim, Irina; Klier, Margit; Fend, Falko; Quintanilla-Martinez, Leticia] Univ Tubingen, Univ Tubingen Hosp, Inst Pathol, D-7400 Tubingen, Germany.
[Irmler, Martin; Beckers, Johannes] German Res Ctr Environm Hlth, Helmholtz Ctr Munich, Inst Expt Genet, Neuherberg, Germany.
[Pittaluga, Stefania] NCI, NIH, Bethesda, MD 20892 USA.
RI Irmler, Martin/B-3317-2013; Anastasov, Natasa/M-9848-2014
OI Irmler, Martin/0000-0003-3169-479X; Anastasov,
Natasa/0000-0002-4088-1119
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 973
EP 974
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703257
ER
PT J
AU Rezvani, K
Yong, ASM
Tawab, A
Jafarpour, B
Eniafe, R
Mielke, S
Savani, BN
Keyvanfar, K
Li, YX
Kurlander, R
Barrett, AJ
AF Rezvani, Katayoun
Yong, Agnes S. M.
Tawab, Abdul
Jafarpour, Behnam
Eniafe, Rhoda
Mielke, Stephan
Savani, Bipin N.
Keyvanfar, Keyvan
Li Yixin
Kurlander, Roger
Barrett, A. John
TI Ex-Vivo Characterization of Polyclonal Memory CD8+T-Cell Responses to
PRAME-Specific Peptides in Patients with Acute Leukemia and Chronic
Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rezvani, Katayoun; Yong, Agnes S. M.; Jafarpour, Behnam; Eniafe, Rhoda; Mielke, Stephan; Savani, Bipin N.; Keyvanfar, Keyvan; Kurlander, Roger; Barrett, A. John] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1001
EP 1001
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703347
ER
PT J
AU Chaubey, A
Hormon, S
Velu, CS
Bourdeau, T
Zhu, JF
Paul, W
Jegga, A
Gebelein, B
Grimes, L
AF Chaubey, Aditya
Hormon, Shane
Velu, Chinavenmeni S.
Bourdeau, Tristan
Zhu, Jinfang
Paul, William
Jegga, Anil
Gebelein, Brian
Grimes, Leighton
TI GFI1 Is a Tumor Suppressor in Myeloid Progenitors
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chaubey, Aditya; Hormon, Shane; Velu, Chinavenmeni S.; Bourdeau, Tristan; Jegga, Anil; Gebelein, Brian; Grimes, Leighton] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Zhu, Jinfang; Paul, William] NIAID, NIH, Bethesda, MD 20892 USA.
RI Nakafuku, Masato/J-3068-2013
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1011
EP 1011
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703379
ER
PT J
AU Grant, S
Kolla, S
Sirulnik, LA
Shapiro, G
Supko, J
Cooper, B
Perkins, E
Ramakrishnan, V
Espinoza-Delgado, I
Tombes, MB
Roberts, JD
AF Grant, Steven
Kolla, Sarah
Sirulnik, Leonardo Andres
Shapiro, Geoffrey
Supko, Jeffrey
Cooper, Brenda
Perkins, Edward
Ramakrishnan, Viswanathan
Espinoza-Delgado, Igor
Tombes, M. B.
Roberts, John D.
TI Phase I Trial of Vorinostat (SAHA) in Combination with Alvocidib
(Flavopiridol) in Patients with Relapsed, Refractory or (Selected) Poor
Prognosis Acute Leukemia or Refractor), Anemia with Excess Blasts-2
(RAEB-2)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Grant, Steven; Kolla, Sarah; Perkins, Edward; Ramakrishnan, Viswanathan; Tombes, M. B.; Roberts, John D.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 02115 USA.
[Sirulnik, Leonardo Andres; Shapiro, Geoffrey; Supko, Jeffrey] Dana Farber Canc Inst, Boston, MA 44106 USA.
[Cooper, Brenda] Case Western Reserve Univ, Univ Hosp Cleveland, Ireland Canc Ctr, Cleveland, OH 20892 USA.
[Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1026
EP 1026
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703423
ER
PT J
AU Fasano, R
Monaco, A
Meier, ER
Otridge, J
Lee-Stroka, H
Pary, P
Klein, HG
Marincola, FM
Luban, NLC
Stroncek, D
AF Fasano, Ross
Monaco, Alessandro
Meier, Emily Riehm
Otridge, John
Lee-Stroka, Hallie
Pary, Philippe
Klein, Harvey G.
Marincola, Francesco M.
Luban, Naomi L. C.
Stroncek, David
TI The Emerging Role of RH Genotyping in Chronically Transfused Sickle Cell
Disease Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Fasano, Ross; Meier, Emily Riehm; Pary, Philippe; Luban, Naomi L. C.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Monaco, Alessandro; Lee-Stroka, Hallie; Klein, Harvey G.; Marincola, Francesco M.; Stroncek, David] NIH, Bethesda, MD 20892 USA.
[Otridge, John] Progenika Inc, Cambridge, MA USA.
RI Monaco, Alessandro/O-5338-2015
OI Monaco, Alessandro/0000-0002-9941-7003
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1043
EP 1044
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703472
ER
PT J
AU Xin, ZT
Calado, R
Savage, SA
Lansdorp, PM
Young, NS
Ly, H
AF Xin, Zhong-Tao
Calado, Rodrigo
Savage, Sharon A.
Lansdorp, Peter M.
Young, Neal S.
Ly, Hinh
TI Characterization of Novel Natural Mutations in Telomere Binding Protein
Factor(TIN2) Identified in Patients with Bone-Marrow Failure Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Xin, Zhong-Tao; Ly, Hinh] Emory Univ, Dept Pathol, Atlanta, GA 30322 USA.
[Calado, Rodrigo; Young, Neal S.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Savage, Sharon A.] NCI, Div Canc Epidemiol & Gene, Bethesda, MD 20892 USA.
[Lansdorp, Peter M.] British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 4E6, Canada.
RI Calado, Rodrigo/G-2619-2011; Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1064
EP 1064
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703538
ER
PT J
AU Stone, S
Sobeck, A
Landais, I
Wang, WD
Hoatlin, M
AF Stone, Stacie
Sobeck, Alexandra
Landais, Igor
Wang, Weidong
Hoatlin, Maureen
TI Identification and Partial Characterization of a Novel Partner Protein
for Fanconi Anemia Protein FANCM
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Stone, Stacie; Sobeck, Alexandra; Landais, Igor; Hoatlin, Maureen] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Wang, Weidong] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1065
EP 1065
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703541
ER
PT J
AU Sloand, EM
Padilla-Nash, H
Furnari, M
Calado, R
Casey, L
Reid, T
Young, NS
AF Sloand, Elaine M.
Padilla-Nash, Hesed
Furnari, Megan
Calado, Rodrigo
Casey, Ling
Reid, Thomas
Young, Neal S.
TI Inflammation Caused by Allogeneic Lymphocytes Results in Aneuploidy in
Bone Marrow Mononuclear Cells (BMMNC)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sloand, Elaine M.; Furnari, Megan; Calado, Rodrigo; Casey, Ling; Young, Neal S.] NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Padilla-Nash, Hesed] NCI, Canc Genom Branch, Bethesda, MD 20892 USA.
[Reid, Thomas] NIAID, NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1067
EP 1067
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703549
ER
PT J
AU Landgren, O
Kristinsson, SY
Liang, XS
Turesson, I
Bjorkholm, M
Caporaso, NE
McMaster, ML
Chanock, S
Goldin, LR
AF Landgren, Ola
Kristinsson, Sigurdur Y.
Liang, Xueying Sharon
Turesson, Ingemar
Bjorkholm, Magnus
Caporaso, Neil E.
McMaster, Mary L.
Chanock, Stephen
Goldin, Lynn R.
TI Germline Genes Specific to Chronic Lymphocytic Leukemia (CLL) and Genes
Common to CLL, Lymphoplasmacytic Lymphoma/Waldenstrom's
Macroglobulinemia, and Other Non-Hodgkin Lymphomas Are Important in
Susceptibility
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Landgren, Ola; Liang, Xueying Sharon; Caporaso, Neil E.; McMaster, Mary L.; Chanock, Stephen; Goldin, Lynn R.] NCI, NIH, Bethesda, MD 20892 USA.
[Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Malmo, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1072
EP 1072
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703564
ER
PT J
AU Lanasa, MC
Allgood, SD
Slager, SL
Camp, N
Spector, L
Rassenti, L
Kay, NE
Gockerman, JP
Volkheimer, A
Goodman, BK
Strom, S
Call, T
Cerhan, J
Leis, JF
Goldin, L
Marti, G
Weinberg, JB
Caporaso, N
Levesque, MC
AF Lanasa, Mark C.
Allgood, Sallie D.
Slager, Susan L.
Camp, Nicola
Spector, Logan
Rassenti, Laura
Kay, Neil E.
Gockerman, Jon P.
Volkheimer, Alicia
Goodman, Barbara K.
Strom, Sara
Call, Timothy
Cerhan, James
Leis, Jose F.
Goldin, Lynn
Marti, Gerald
Weinberg, J. Brice
Caporaso, Neil
Levesque, Marc C.
TI Family-Associated Monoclonal B Lymphocytosis Is Commonly Oligoclonal and
Expresses Markers Associated with Adverse Risk in CLL
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Lanasa, Mark C.; Allgood, Sallie D.; Gockerman, Jon P.; Volkheimer, Alicia; Goodman, Barbara K.; Weinberg, J. Brice; Levesque, Marc C.] Duke Univ, Med Ctr, Durham, NC USA.
[Slager, Susan L.; Call, Timothy; Cerhan, James] Mayo Clin, Rochester, MN USA.
[Camp, Nicola] Univ Utah, La Jolla, CA USA.
[Spector, Logan] Univ Minnesota, La Jolla, CA USA.
[Rassenti, Laura] Moores Canc Ctr, UCSD, La Jolla, CA USA.
[Kay, Neil E.] Mayo Clin, Coll Med, Rochester, MN USA.
[Strom, Sara] MD Anderson Canc Ctr, Phoenix, AZ USA.
[Leis, Jose F.] Mayo Clin Arizona, Phoenix, AZ USA.
[Goldin, Lynn; Marti, Gerald; Caporaso, Neil] Natl Canc Inst, Bethesda, MD USA.
RI Slager, Susan/B-6756-2009
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 NOV 16
PY 2008
VL 112
IS 11
BP 1078
EP 1078
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703581
ER
PT J
AU Kreitman, RJ
Wilson, WH
Stetler-Stevenson, M
Noel, P
FitzGerald, DJ
Pastan, I
AF Kreitman, Robert J.
Wilson, Wyndham H.
Stetler-Stevenson, Maryalice
Noel, Pierre
FitzGerald, David J.
Pastan, Ira
TI Interim Phase I Results of Recombinant Immunotoxin HA22 in Patients with
Hairy Cell and Chronic Lymphocytic Leukemias
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kreitman, Robert J.; Wilson, Wyndham H.; Stetler-Stevenson, Maryalice; Noel, Pierre; FitzGerald, David J.; Pastan, Ira] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1084
EP 1084
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703597
ER
PT J
AU Zhang, J
Jima, DD
Gao, Y
Wu, H
Zhu, J
deLong, M
Lipsky, PE
Dave, SS
AF Zhang, Jenny
Jima, Dereje D.
Gao, Yuan
Wu, Han
Zhu, Jun
deLong, Mark
Lipsky, Peter E.
Dave, Sandeep S.
TI Massively Parallel High Throughput Sequencing Identifies Novel Micrornas
in Normal and Malignant B Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhang, Jenny; Jima, Dereje D.; Wu, Han; Zhu, Jun; deLong, Mark; Dave, Sandeep S.] Duke Univ, Durham, NC USA.
[Gao, Yuan] Virginia Commonwealth Univ, Richmond, VA 23284 USA.
[Lipsky, Peter E.] NIH, Bethesda, MD 20892 USA.
RI Gao, Yuan/E-1706-2011
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1150
EP 1150
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703786
ER
PT J
AU Paul, TA
Muresan, H
Prentice, E
Wolff, L
AF Paul, Thomas A.
Muresan, Horatiu
Prentice, Emily
Wolff, Linda
TI Historic Modifications Associated with DNA Methylation and
Transcriptional Repression of p151NK4b in Acute Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Paul, Thomas A.; Muresan, Horatiu; Prentice, Emily; Wolff, Linda] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1151
EP 1152
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703790
ER
PT J
AU Fiskus, W
Wang, YC
Jillella, A
Ustun, C
Johnston, P
Joshi, R
Rao, R
Ataja, P
Marquez, V
Bhalla, KN
AF Fiskus, Warren
Wang, Yongchao
Jillella, Anand
Ustun, Celalettin
Johnston, Pace
Joshi, Rajeshree
Rao, Rekha
Ataja, Peter
Marquez, Victor
Bhalla, Kapil N.
TI Synergistic Pre-Clinical Activity of Combined Epigenetic Therapy with
the Novel Histone Methyltransferase EZH2 Inhibitor 3-Deazaneplanocin and
Histone Deacetylase Inhibitor Panobinostat against Human AML Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Fiskus, Warren; Wang, Yongchao; Jillella, Anand; Ustun, Celalettin; Johnston, Pace; Joshi, Rajeshree; Rao, Rekha; Bhalla, Kapil N.] Med Coll Georgia, MCG Canc Ctr, Augusta, GA 30912 USA.
[Ataja, Peter] Novartis Inst Biomed Res, Cambridge, MA USA.
[Marquez, Victor] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1152
EP 1152
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703792
ER
PT J
AU Gellen, T
Kuo, PY
Shaknovich, R
Figueroa, ME
Melnick, A
Wiestner, A
Parekh, S
AF Gellen, Tobias
Kuo, Pei-Yu
Shaknovich, Rita
Figueroa, Maria E.
Melnick, Ari
Wiestner, Adrian
Parekh, Samir
TI Epigenetic Determinants of Pathogenesis and Resistance to Proteosome
Inhibition in Mantle Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gellen, Tobias; Kuo, Pei-Yu; Parekh, Samir] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Shaknovich, Rita] Cornell Med Ctr, Dept Med, New York, NY USA.
[Shaknovich, Rita] Cornell Med Ctr, Dept Pathol, New York, NY USA.
[Figueroa, Maria E.; Melnick, Ari] Weill Cornell Med Coll, Med Div Hematol Oncol, New York, NY USA.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1158
EP 1158
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703809
ER
PT J
AU Tamary, H
Shalev, H
Avraham, G
Zoldan, M
Levi, I
Swinkels, DW
Tanno, T
Miller, JL
AF Tamary, Hannah
Shalev, Hanna
Avraham, Galit
Zoldan, Meira
Levi, Itai
Swinkels, Dorine W.
Tanno, Toshihiko
Miller, Jeffery L.
TI High Levels of Growth Differentiation Factor 15 in Patients with
Congenital Dyserythtopoietic Anemia Type I
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Tamary, Hannah; Zoldan, Meira] Schneider Childrens Med Ctr, Petah Tiqwa, Israel.
[Swinkels, Dorine W.] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Tanno, Toshihiko; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
RI Swinkels, D.W./H-8098-2014
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1186
EP 1186
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704074
ER
PT J
AU Li, M
Sun, K
Hubbard, M
Redelman, D
Panoskaltsis-Mortari, A
Nedospasov, S
Taub, D
Blazar, B
Welniak, LA
Murphy, WJ
AF Li, Minghui
Sun, Kai
Hubbard, Mark
Redelman, Doug
Panoskaltsis-Mortari, Angela
Nedospasov, Sergei
Taub, Dennis
Blazar, Bruce
Welniak, Lisbeth A.
Murphy, William J.
TI Critical and Opposing Effects of T Cell-Derived TNF alpha and
Interferon-gamma on IL-17 Induction Assessed in Vitro and in Vivo
Following Allogeneic Bone Marrow Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Li, Minghui; Sun, Kai; Hubbard, Mark; Welniak, Lisbeth A.; Murphy, William J.] Univ Nevada, Dept Microbiol & Immunol, Sch Med, Reno, NV 89557 USA.
[Redelman, Doug] Univ Nevada, Sch Med, Dept Physiol & Cell Biol, Reno, NV 89557 USA.
[Panoskaltsis-Mortari, Angela; Blazar, Bruce] Univ Minnesota, Ctr Canc, Minneapolis, MN USA.
[Panoskaltsis-Mortari, Angela; Blazar, Bruce] Univ Minnesota, Dept Pediat, Div Bone Marrow Transplantat, Minneapolis, MN 55455 USA.
[Nedospasov, Sergei] Russian Acad Sci, VA Engelhardt Mol Biol Inst, Moscow, Russia.
[Taub, Dennis] NIA, Immunol Lab, NIH, Baltimore, MD 21224 USA.
RI Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015;
Nedospasov, Sergei/Q-7319-2016
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1194
EP 1194
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704100
ER
PT J
AU Mariot, J
Foley, J
Ryan, K
Buxhoeveden, N
Fowler, D
AF Mariot, Jacopo
Foley, Jason
Ryan, Kaitlyn
Buxhoeveden, Nicole
Fowler, Daniel
TI Pentostatin Is Advantageous Relative to Fludarabine for in Vivo Murine T
Cell Depletion, Suppression of T Cell Cytokine Secretion, and Inhibition
of HVGR.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mariot, Jacopo; Ryan, Kaitlyn; Buxhoeveden, Nicole] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1194
EP 1194
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704101
ER
PT J
AU Capitini, CM
Larabee, SM
Mackall, CL
Fry, TJ
AF Capitini, Christian M.
Larabee, Shannon M.
Mackall, Crystal L.
Fry, Terry J.
TI Disruption of Gamma Interferon Signaling through the STAT1 Pathway
Enhances Alloreactivity While Abrogating GvHD
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Capitini, Christian M.; Larabee, Shannon M.; Mackall, Crystal L.; Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1204
EP 1204
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704130
ER
PT J
AU Xie, JJ
Larochelle, A
Faulhaber, M
Donahue, RE
Dunbar, CE
AF Xie, Jianjun
Larochelle, Andre
Faulhaber, Marion
Donahue, Robert E.
Dunbar, Cynthia E.
TI Repetitive Busulfan Administration Induces Emergence of Dominant and
Expanding Hematopoietic Clones with Retroviral Vector Insertion in
Rhesus Macaques
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Xie, Jianjun; Larochelle, Andre; Faulhaber, Marion; Donahue, Robert E.; Dunbar, Cynthia E.] NIH, Hematol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1208
EP 1208
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704142
ER
PT J
AU Ramanathan, M
Su, S
Lundqvist, A
Berg, M
Smith, A
Lopez, R
Williams, A
Bahceci, E
McCoy, JP
Boissel, L
Klingemann, HG
Childs, R
AF Ramanathan, Muthalagu
Su, Su
Lundqvist, Andreas
Berg, Maria
Smith, Aleah
Lopez, Rebecca
Williams, Ann
Bahceci, Erkut
McCoy, J. Philip
Boissel, Laurent
Klingemann, Hans-Georg
Childs, Richard
TI Lentiviral Transduction of Ex Vivo Expanded Natural Killer Cells with a
CD19 Chimeric Antigen Receptor Induces Cytotoxicity against Resistant B
Cell Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ramanathan, Muthalagu; Su, Su; Lundqvist, Andreas; Berg, Maria; Smith, Aleah; Lopez, Rebecca; Williams, Ann; McCoy, J. Philip; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bahceci, Erkut] Bayer HealthCare Pharmaceut, West Haven, CT USA.
[Boissel, Laurent; Klingemann, Hans-Georg] Tufts Univ New England Med Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1213
EP 1213
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704158
ER
PT J
AU Larochelle, A
Gan, HZ
Clevenger, JR
Dunbar, CE
AF Larochelle, Andre
Gan, Hezhi
Clevenger, Joshua R.
Dunbar, Cynthia E.
TI Culture of Mobilized Human CD34+Cells in Hypoxic Conditions Improves
Lentiviral Transduction Efficiency in SCID-Repopulating Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Larochelle, Andre; Gan, Hezhi; Clevenger, Joshua R.; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1214
EP 1214
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704163
ER
PT J
AU Boxer, LA
Bolyard, AA
Newburger, PE
Bonilla, MA
Kannourakis, G
Dror, Y
Link, DC
Alter, BP
Rosenberg, PS
Dale, DC
AF Boxer, Laurence A.
Bolyard, Audrey Anna
Newburger, Peter E.
Bonilla, Mary Ann
Kannourakis, George
Dror, Yigal
Link, Daniel C.
Alter, Blanche P.
Rosenberg, Philip S.
Dale, David C.
TI Risk for Septic Death in Severe Congenital Neutropenia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Boxer, Laurence A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Bolyard, Audrey Anna] Univ Washington, Severe Chron Neutropenia Int Registry, Seattle, WA 98195 USA.
[Newburger, Peter E.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Bonilla, Mary Ann] St Josephs Childrens Hosp, Paterson, NJ USA.
[Kannourakis, George] Univ Ballarat, Ballarat Onc & Hem Serv, Ballarat, Vic 3350, Australia.
[Dror, Yigal] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Link, Daniel C.] Washington Univ, Sch Med, St Louis, MO USA.
[Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1215
EP 1215
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704166
ER
PT J
AU Rogers, HM
Wang, L
Yu, XB
Noguchi, CT
AF Rogers, Heather Marie
Wang, Li
Yu, Xiaobing
Noguchi, Constance Tom
TI Erythropoietin Receptor Expression: A Role for the Tal1/SCL and GATA-1
Complex.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rogers, Heather Marie; Wang, Li; Noguchi, Constance Tom] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Yu, Xiaobing] Harbor Hosp, Dept Med, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1225
EP 1226
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704201
ER
PT J
AU Steiner, LA
Maksimova, Y
Lin, J
Owen, AN
Schulz, V
Bodine, DM
Gallagher, PG
AF Steiner, Laurie A.
Maksimova, Yelena
Lin, Jolinta
Owen, Ashley Nicole
Schulz, Vincent
Bodine, David M.
Gallagher, Patrick G.
TI Insulator Elements in Erythrocyte Membrane Genes.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Steiner, Laurie A.; Maksimova, Yelena; Schulz, Vincent; Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
[Owen, Ashley Nicole] NHGRI, Hematopoiesis Sect, NIH, Bethesda, MD 20892 USA.
[Bodine, David M.] GMBB, Hematopoiesis Sect, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1226
EP 1226
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704202
ER
PT J
AU Dunleavy, K
Pittaluga, S
Grant, N
Steinberg, S
Shovlin, M
Tay, K
Janik, JE
Jaffe, ES
Wilson, WH
AF Dunleavy, Kieron
Pittaluga, Stefania
Grant, Nicole
Steinberg, Seth
Shovlin, Margaret
Tay, Kevin
Janik, John E.
Jaffe, Elaine S.
Wilson, Wyndham H.
TI Gray Zone Lymphomas: Clinical and Histological Characteristics and
Treatment with Dose-Adjusted-EPOCH-R.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Dunleavy, Kieron; Pittaluga, Stefania; Grant, Nicole; Steinberg, Seth; Shovlin, Margaret; Tay, Kevin; Janik, John E.; Jaffe, Elaine S.; Wilson, Wyndham H.] Natl Canc Inst, Ctr Canc Res, Bethesda, MD USA.
NR 0
TC 2
Z9 2
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 NOV 16
PY 2008
VL 112
IS 11
BP 1228
EP 1228
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704208
ER
PT J
AU Dunleavy, K
Little, R
Wayne, AS
Grant, N
Pittaluga, S
Jaffe, ES
Steinberg, S
Yarchoan, R
Carrasquillo, JA
Janik, JE
Wilson, WH
AF Dunleavy, Kieron
Little, Richard
Wayne, Alan S.
Grant, Nicole
Pittaluga, Stefania
Jaffe, Elaine S.
Steinberg, Seth
Yarchoan, Robert
Carrasquillo, Jorge A.
Janik, John E.
Wilson, Wyndham H.
TI Long-Term Outcome of AIDS-Related Lymphoma Treated with Abbreviated
Cycles of EPOCH-RR: A Prospective Study of 40 Patients.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Dunleavy, Kieron; Little, Richard; Wayne, Alan S.; Grant, Nicole; Pittaluga, Stefania; Jaffe, Elaine S.; Steinberg, Seth; Yarchoan, Robert; Carrasquillo, Jorge A.; Janik, John E.; Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Carrasquillo, Jorge/E-7120-2010
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1233
EP 1234
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704224
ER
PT J
AU Fiskus, W
Wang, YC
Jillella, A
Johnston, P
Joshi, R
Rao, R
Sotomayor, E
Tao, JG
Atadja, P
Marqez, V
Bhalla, KN
AF Fiskus, Warren
Wang, Yongchao
Jillella, Anand
Johnston, Pace
Joshi, Rajeshree
Rao, Rekha
Sotomayor, Eduardo
Tao, Jianguo
Atadja, Peter
Marqez, Victor
Bhalla, Kapil N.
TI Combined Epigenetic Therapy with the Novel Histone Methyl Transferase
EZH2 Inhibitor 3-Deazaneplanocin and -Histone Deacetylase Inhibitor
Panobinostat Exerts Synergistic Activity against Human Mantle Cell
Lymphoma Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Fiskus, Warren; Wang, Yongchao; Jillella, Anand; Johnston, Pace; Joshi, Rajeshree; Rao, Rekha; Bhalla, Kapil N.] Med Coll Georgia, Ctr Canc, Augusta, GA 30912 USA.
[Sotomayor, Eduardo; Tao, Jianguo] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Atadja, Peter] Novartis Inst Biomed Res, Cambridge, MA USA.
[Marqez, Victor] NIH, 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 NOV 16
PY 2008
VL 112
IS 11
BP 1239
EP 1239
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704240
ER
PT J
AU Chung, YJ
Aplan, PD
AF Chung, Yang Jo
Aplan, Peter D.
TI Increased Reactive oxygen Species Induced by NUP98-HOXD13 Fusion Gene in
MDS Mouse Model
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chung, Yang Jo; Aplan, Peter D.] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1242
EP 1242
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704249
ER
PT J
AU Zou, JX
Rollison, DE
Boulware, D
Sloand, EM
Pfannes, L
Bai, FQ
Painter, JS
Wei, S
Cosgrove, D
List, AF
Epling-Bumette, PK
AF Zou, JianXiang
Rollison, Dana E.
Boulware, David
Sloand, Elaine M.
Pfannes, Loretta
Bai, Fanqi
Painter, Jeffrey S.
Wei, Sheng
Cosgrove, Denise
List, Alan F.
Epling-Bumette, P. K.
TI Altered Naive and Memory T Cell Homeostasis and Immunosenescence
Characterize Younger Patients with Immunosuppressive-Responsive
Myelodysplastic Syndrome
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zou, JianXiang; Bai, Fanqi; Painter, Jeffrey S.; Wei, Sheng; Epling-Bumette, P. K.] Univ S Florida, H Lee Moffitt Canc Ctr, Program Immunol, Tampa, FL 33682 USA.
[Rollison, Dana E.] Univ S Florida, H Lee Moffitt Canc Ctr, Risk Assessment Detectio & Intervent Program, Tampa, FL 33682 USA.
[Boulware, David] Univ S Florida, H Lee Moffitt Canc Ctr, Biostat Program, Tampa, FL 33682 USA.
[Sloand, Elaine M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Pfannes, Loretta] NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Cosgrove, Denise] Univ S Florida, H Lee Moffitt Canc Ctr, Malignant Hematol Div, Tampa, FL 33682 USA.
[List, Alan F.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1248
EP 1248
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704265
ER
PT J
AU Silverman, LR
Verma, A
Odchimar-Reissig, R
LeBlanc, A
Najfeld, V
Gabrilove, J
Isola, L
Espinoza-Delgado, I
Zwiebel, J
AF Silverman, Lewis R.
Verma, Amit
Odchimar-Reissig, Rosalie
LeBlanc, Amanda
Najfeld, Vesna
Gabrilove, Janice
Isola, Luis
Espinoza-Delgado, Igor
Zwiebel, James
TI A Phase I Trial of the Epigenetic Modulators Vorinostat, in Combination
with Azacitidine (azaC) in Patients with the Myelodysplastic Syndrome
(MDS) and Acute Myeloid Leukemia (AML): A Study of the New York Cancer
Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Silverman, Lewis R.; Odchimar-Reissig, Rosalie; LeBlanc, Amanda; Najfeld, Vesna; Gabrilove, Janice; Isola, Luis] Mt Sinai Sch Med, Div Hematol, New York, NY USA.
[Verma, Amit] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Espinoza-Delgado, Igor; Zwiebel, James] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
NR 0
TC 5
Z9 5
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 NOV 16
PY 2008
VL 112
IS 11
BP 1252
EP 1252
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704274
ER
PT J
AU Gibellini, F
Chapman, CM
Herishanu, Y
Vire, B
Keyvanfar, K
Njuguna, N
Wiestner, A
AF Gibellini, Federica
Chapman, Colby M.
Herishanu, Yair
Vire, Berengere
Keyvanfar, Keyvan
Njuguna, Ndegwa
Wiestner, Adrian
TI Receptor Tyrosine Kinase-Like Orphan Receptor 1 (ROR-1) Is Expressed in
Low Grade NHL and B-CLL and Activates the Non Canonical Wnt Pathway
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gibellini, Federica; Chapman, Colby M.; Herishanu, Yair; Vire, Berengere; Keyvanfar, Keyvan; Njuguna, Ndegwa; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1284
EP 1284
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704366
ER
PT J
AU Kristinsson, SY
Bjorkhohn, M
Koshiol, J
Goldin, LR
McMaster, ML
Turesson, I
Landgren, O
AF Kristinsson, Sigurdur Y.
Bjorkhohn, Magnus
Koshiol, Jill
Goldin, Lynn R.
McMaster, Mary L.
Turesson, Ingemar
Landgren, Ola
TI Immune-Related and Inflammatory Conditions Likely Play a Role in the
Development of Lymphoplasmacytic Lymphoma/Waidenstrom's
Macroglobulinemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kristinsson, Sigurdur Y.; Bjorkhohn, Magnus] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Bjorkhohn, Magnus] Karolinska Inst, Stockholm, Sweden.
[Koshiol, Jill; Goldin, Lynn R.; McMaster, Mary L.; Landgren, Ola] NCI, NIH, Bethesda, MD 20892 USA.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Malmo, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1287
EP 1287
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704376
ER
PT J
AU Caudell, D
Pierce, RM
Harper, DP
Novak, RL
Slape, C
Wolff, L
Aplan, PD
AF Caudell, David
Pierce, Rachel M.
Harper, David P.
Novak, Rachel L.
Slape, Christopher
Wolff, Linda
Aplan, Peter D.
TI Identification of Genes That Collaborate with CALM-AF10 to Induce
Leukemia by Retroviral Insertional Mutagenesis and Candidate Gene
Sequencing.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Caudell, David; Novak, Rachel L.; Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD USA.
[Harper, David P.] Uniformed Serv Univ Hlth Sci, Dept Pediat, Bethesda, MD 20814 USA.
[Slape, Christopher] Royal Melbourne Hosp, Bone Marrow Res Lab, Parkville, Vic 3050, Australia.
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1296
EP 1296
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704405
ER
PT J
AU Kamikubo, Y
Garrett-Beal, L
Kirby, M
Liu, PP
AF Kamikubo, Yasuhiko
Garrett-Beal, Lisa
Kirby, Martha
Liu, Pu Paul
TI The C-Terminus of the CBF beta-SMMHC Fusion Protein Is Required for the
Myeloblastic Transformation of inv16 Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kamikubo, Yasuhiko; Liu, Pu Paul] NHGRI, Gmbb Ods, NIH, Bethesda, MD USA.
RI Liu, Paul/A-7976-2012
OI Liu, Paul/0000-0002-6779-025X
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1300
EP 1300
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704417
ER
PT J
AU Yang, J
Liu, X
Nyland, S
Zhang, R
Thomas, K
Jarbadan, RN
Loughran, TP
AF Yang, Jun
Liu, Xin
Nyland, Susan
Zhang, Ranran
Thomas, Kendall
Jarbadan, Ruth Nancy
Loughran, Thomas P., Jr.
TI Platelet-Derived Growth Factor (PDGF)-BB Mediates Survival of Leukemic
Large Granular Lymphocyte Via An Autocrine Regulatory Pathway
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Yang, Jun; Liu, Xin; Zhang, Ranran; Thomas, Kendall; Jarbadan, Ruth Nancy; Loughran, Thomas P., Jr.] Penn State Hershey Canc Inst, Hershey, PA USA.
[Nyland, Susan] NIH, Rare Dis Clin Res Network, Bone Marrow Failure Dis Consortium, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1301
EP 1301
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704421
ER
PT J
AU Resar, L
Hillion, J
Dhara, S
Sumter, TF
Mukherjee, M
Di Cello, F
Belton, A
Turkson, J
Jaganathan, S
Cheng, LZ
Ye, ZH
Lin, YW
Aplan, PD
Jove, R
Kowalski, J
Wertzler, K
Reeves, R
Elbahlouh, O
Bhattacharya, R
AF Resar, Linda
Hillion, Joelle
Dhara, Surajit
Sumter, Takita Felder
Mukherjee, Mita
Di Cello, Francescopaolo
Belton, Amy
Turkson, James
Jaganathan, Souyma
Cheng, Linzhao
Ye, Zhaohui
Lin, Yingwei
Aplan, Peter D.
Jove, Richard
Kowalski, Jeanne
Wertzler, Kelsey
Reeves, Ray
Elbahlouh, Ossama
Bhattacharya, Raka
TI The HMGA1a-STAT3 axis: an "Achitles Heel" for Hematopoietic Malignancies
Overexpressing HMGA1a?
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Resar, Linda; Hillion, Joelle; Dhara, Surajit; Sumter, Takita Felder; Mukherjee, Mita; Di Cello, Francescopaolo; Belton, Amy; Elbahlouh, Ossama; Bhattacharya, Raka] Johns Hopkins Univ SOM, Div Hematol, Baltimore, MD USA.
[Turkson, James; Jaganathan, Souyma] Univ Cent Florida, Orlando, FL 32816 USA.
[Ye, Zhaohui] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Lin, Yingwei] Med Univ S Carolina, Coll Med, Hollings Canc Ctr, Charleston, SC 29425 USA.
[Aplan, Peter D.] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
[Jove, Richard] City Hope Natl Canc Ctr, Duarte, CA USA.
[Wertzler, Kelsey; Reeves, Ray] Washington State Univ, Sch Mol Biosci, Pullman, WA 99164 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1302
EP 1302
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704427
ER
PT J
AU Vasu, S
Berg, M
Lundqvist, A
Ramanathan, M
Lopez, R
Mccoy, P
Zhang, H
Mackall, C
Childs, R
AF Vasu, Sumithira
Berg, Maria
Lundqvist, Andreas
Ramanathan, Muthalagu
Lopez, Rebecca
McCoy, Phil, Jr.
Zhang, Hua
Mackall, Crystal
Childs, Richard
TI A Highly Efficient Method to Expand CD3-CD56(+) NK Cells from Cord Blood
Segments
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Vasu, Sumithira; Berg, Maria; Lundqvist, Andreas; Ramanathan, Muthalagu; Lopez, Rebecca; McCoy, Phil, Jr.; Zhang, Hua; Mackall, Crystal; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1330
EP 1330
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704508
ER
PT J
AU Lopez, R
Lundqvist, A
Sellers, S
Berg, M
Ramanathan, M
Vasu, S
Smith, A
Dunbar, CE
Childs, RW
AF Lopez, Rebecca
Lundqvist, Andreas
Sellers, Stephanie
Berg, Maria
Ramanathan, Muthalagu
Vasu, Sumithiru
Smith, Aleah
Dunbar, Cynthia E.
Childs, Richard W.
TI A Rhesus Macaque Model to Optimize Adoptive NK Cell Therapy
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Lopez, Rebecca; Lundqvist, Andreas; Sellers, Stephanie; Berg, Maria; Ramanathan, Muthalagu; Vasu, Sumithiru; Smith, Aleah; Dunbar, Cynthia E.; Childs, Richard W.] Nhlbi, NIH, Hematol Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1331
EP 1331
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704511
ER
PT J
AU Muranski, P
Hinrichs, CS
Sanchez-Perez, L
Boni, A
Kerkar, S
Gattinoni, L
Yu, Z
Restifo, NP
AF Muranski, Pawel
Hinrichs, Christian S.
Sanchez-Perez, Luis
Boni, Andrea
Kerkar, Sid
Gattinoni, Luca
Yu, Zhia
Restifo, Nicholas P.
TI Treatment of Large Established Murine Melanoma with Th17 Polarized CD4+T
Helper Cells Genetically Engineered to Express MHC Class II-Restricted T
Cell Receptor
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Muranski, Pawel; Hinrichs, Christian S.; Sanchez-Perez, Luis; Boni, Andrea; Kerkar, Sid; Gattinoni, Luca; Yu, Zhia; Restifo, Nicholas P.] NCI, NIH, Bethesda, MD 20892 USA.
RI Restifo, Nicholas/A-5713-2008; Muranski, Pawel/E-5572-2010
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1333
EP 1333
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704517
ER
PT J
AU Chesi, M
Bergsagel, PL
Kuehl, M
AF Chesi, Marta
Bergsagel, Peter Leif
Kuehl, Michael
TI Genetic Origin of Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chesi, Marta; Bergsagel, Peter Leif] Mayo Clin, Scottsdale, AZ USA.
[Kuehl, Michael] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1343
EP 1344
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704547
ER
PT J
AU Longo, DL
Ferrucci, L
Ershler, W
AF Longo, Dan L.
Ferrucci, Lumi
Ershler, William
TI Mild Pro-inflammatory State and Anemia in Older Persons
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Longo, Dan L.; Ferrucci, Lumi] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1343
EP 1343
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704546
ER
PT J
AU Longo, DL
AF Longo, Dan L.
TI Bone Marrow in Aging: Changes? Yes; Clinical Malfunction? Not So Clear
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Longo, Dan L.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1343
EP 1343
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704543
ER
PT J
AU Willman, CL
Kang, HN
Harvey, RC
Chen, IM
Mullighan, C
Downing, JR
Relling, MV
Zhang, JH
Gerhard, D
Smith, M
Dobbin, KK
Reaman, G
Hunger, S
AF Willman, Cheryl L.
Kang, Huining
Harvey, Richard C.
Chen, I-Ming
Mullighan, Charles
Downing, James R.
Relling, Mary V.
Zhang, Jinghui
Gerhard, Daniela
Smith, Malcolm
Dobbin, Kevin K.
Reaman, Gregory
Hunger, Stephen
TI Use of Genomic Technologies to Identify Novel Genetic Abnormalities and
Therapeutic Targets In Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Willman, Cheryl L.; Kang, Huining] Univ New Mexico, Canc Res & Treatment Ctr, UNM Canc Res Facil, Albuquerque, NM 87131 USA.
[Harvey, Richard C.] Univ New Mexico, Sch Med, Albuquerque, NM 87131 USA.
[Mullighan, Charles; Downing, James R.; Relling, Mary V.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Zhang, Jinghui] NCI, NIH, Rockville, MD USA.
[Smith, Malcolm] NIA, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
[Dobbin, Kevin K.] NIA, Biometr Res Branch, NIH, Bethesda, MD 20892 USA.
[Dobbin, Kevin K.] NIA, Canc Diag Program, NIH, Bethesda, MD 20892 USA.
[Reaman, Gregory] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Hunger, Stephen] Univ Colorado, Coll Med, Pediat Heme Onc BMT, Aurora, CO 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 NOV 16
PY 2008
VL 112
IS 11
BP 1344
EP 1345
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704550
ER
PT J
AU Grimes, HL
Velu, CS
Horman, S
Chaubey, A
Bourdeau, T
Xu, HM
Zhu, JF
Paul, W
Colmenares, C
Williams, DA
Gebelein, B
AF Grimes, H. Leighton
Velu, Chinavenmeni S.
Horman, Shane
Chaubey, Aditya
Bourdeau, Tristan
Xu, Haiming
Zhu, Jinfang
Paul, William
Colmenares, Clemencia
Williams, David A.
Gebelein, Brian
TI Gfi1 as a Regulator of Hematopoietic Differentiation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Grimes, H. Leighton; Velu, Chinavenmeni S.; Horman, Shane; Chaubey, Aditya; Bourdeau, Tristan; Xu, Haiming; Gebelein, Brian] Cincinnati Children Hosp, Med Ctr, Cincinnati, OH USA.
[Zhu, Jinfang; Paul, William] NIAID, NIH, Bethesda, MD 20892 USA.
[Colmenares, Clemencia] Cleveland Clin, Cleveland, OH 44106 USA.
[Williams, David A.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
RI Nakafuku, Masato/J-3068-2013
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1347
EP 1347
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704558
ER
PT J
AU Saczynski, JS
Jonsdottir, MK
Garcia, ME
Jonsson, PV
Peila, R
Eiriksdottir, G
Olafsdottir, E
Harris, TB
Gudnason, V
Launer, LJ
AF Saczynski, Jane S.
Jonsdottir, Maria K.
Garcia, Melissa E.
Jonsson, Palmi V.
Peila, Rita
Eiriksdottir, Gudny
Olafsdottir, Elin
Harris, Tamara B.
Gudnason, Vilmundur
Launer, Lenore J.
TI Cognitive Impairment: An Increasingly Important Complication of Type 2
Diabetes
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
ID CORONARY-HEART-DISEASE; WHITE-MATTER LESIONS; FASTING GLUCOSE; OLDER
WOMEN; RISK; DEMENTIA; DYSFUNCTION; MELLITUS; BRAIN; MEN
AB Persons with type 2 diabetes are at increased risk of cognitive dysfunction. Less is known about which cognitive abilities are affected and how undiagnosed diabetes and impaired fasting glucose relate to cognitive performance. The authors explored this question using data from 1,917 nondemented men and women (average age = 76 years) in the population-based Age, Gene/Environment Susceptibility-Reykjavik Study (2002-2006). Glycemic status groups included diagnosed diabetes (self-reported diabetes or diabetic medication use; n = 163 (8.5%)), undiagnosed diabetes (fasting blood glucose >= 7.0 mmol/L without diagnosed diabetes; n = 55 (2.9%)), and impaired fasting glucose (fasting blood glucose 5.6-6.9 mmol/L; n = 744 (38.8%)). Composites of memory, processing speed (PS), and executive function were constructed from a neuropsychological battery. Linear regression was used to investigate cross-sectional differences in cognitive performance between glycemic groups, adjusted for demographic and health factors. Persons with diagnosed diabetes had slower PS than normoglycemics (beta = -0.12; P < 0.05); diabetes duration of >= 15 years was associated with significantly poorer PS and executive function. Undiagnosed diabetics had slower PS (beta = -0.22; P < 0.01) and poorer memory performance (beta = -0.22; P < 0.05). Persons with type 2 diabetes have poorer cognitive performance than normoglycemics, particularly in PS. Those with undiagnosed diabetes have the lowest cognitive performance.
C1 [Saczynski, Jane S.] Univ Massachusetts, Sch Med, Div Geriatr Med, Worcester, MA 01605 USA.
[Saczynski, Jane S.] Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Worcester, MA 01605 USA.
[Saczynski, Jane S.; Garcia, Melissa E.; Peila, Rita; Harris, Tamara B.; Launer, Lenore J.] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Jonsdottir, Maria K.; Jonsson, Palmi V.; Eiriksdottir, Gudny; Olafsdottir, Elin; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
RP Saczynski, JS (reprint author), Univ Massachusetts, Sch Med, Div Geriatr Med, Biotech 4,Suite 315,377 Plantat St, Worcester, MA 01605 USA.
EM jane.saczynski@umassmed.edu
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
FU National Institutes of Health [N01-AG-12100]; National Institute on
Aging Intramural Research Program, Hjartavernd; Althingi
FX This study was funded by National Institutes of Health contract
N01-AG-12100, the National Institute on Aging Intramural Research
Program, Hjartavernd (the Icelandic Heart Association), and the Althingi
(the Icelandic Parliament).
NR 51
TC 59
Z9 62
U1 2
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2008
VL 168
IS 10
BP 1132
EP 1139
DI 10.1093/aje/kwn228
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 373JY
UT WOS:000260969100006
PM 18836152
ER
PT J
AU Beydoun, MA
Lhotsky, A
Wang, YF
Dal Forno, G
An, Y
Metter, EJ
Ferrucci, L
O'Brien, R
Zonderman, AB
AF Beydoun, May A.
Lhotsky, April
Wang, Youfa
Dal Forno, Gloria
An, Yang
Metter, E. Jeffrey
Ferrucci, Luigi
O'Brien, Richard
Zonderman, Alan B.
TI Association of Adiposity Status and Changes in Early to Mid-Adulthood
With Incidence of Alzheimer's Disease
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
ID BODY-MASS INDEX; VASCULAR RISK-FACTORS; WEIGHT-LOSS; METABOLIC SYNDROME;
COGNITIVE IMPAIRMENT; DIABETES-MELLITUS; OBESITY EPIDEMIC;
APOLIPOPROTEIN-E; DEMENTIA RISK; POPULATION
AB Adiposity status and change are potential risk factors for Alzheimer's disease (AD). The authors used data on 2,322 participants in the Baltimore Longitudinal Study of Aging to analyze the relation between AD incidence and adiposity in Cox proportional hazards models, with adjustment for sociodemographic factors and smoking status. Body mass index (BMI; weight (kg)/height (m)(2)) and waist circumference at specific ages were predicted by empirical Bayes estimators from mixed-effects regression models. After a median of 23.4 years of follow-up between 1958 and 2006, 187 participants developed AD. Among men, being underweight (BMI <= 18.5) at age 30, 40, or 45 years increased the likelihood of AD (hazard ratio (HR) = 5.76, 95% confidence interval (CI): 2.07, 16.00); among women, being obese (BMI >= 30) at age 30, 40, or 45 years and jointly centrally obese (waist circumference >= 80th percentile) at age 30, 35, or 50 years increased AD risk (HR = 6.57, 95% CI: 1.96, 22.02). Women who lost weight (BMI change < 10th percentile) between ages 30 and 45 years were also at increased risk (HR = 2.02, 95% CI: 1.06, 3.85). Weight gain among men (BMI change > 90th percentile) between ages 30 and 50 years increased AD risk (HR = 3.70, 95% CI: 1.43, 9.56). Future studies should identify age- and gender-specific optimal weights and weight-loss strategies for preventing AD and investigate potential mechanisms.
C1 [Zonderman, Alan B.] NIA, NIH, Biomed Res Ctr, Intramural Res Program, Baltimore, MD 21224 USA.
[Wang, Youfa] Johns Hopkins Univ, Sch Publ Hlth, Dept Int Hlth, Ctr Human Nutr, Baltimore, MD USA.
[Dal Forno, Gloria] Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA.
[O'Brien, Richard] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
RP Zonderman, AB (reprint author), NIA, NIH, Biomed Res Ctr, Intramural Res Program, 251 Bayview Blvd,Suite 100,Room 04B136, Baltimore, MD 21224 USA.
EM zondermana@mail.nih.gov
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural Research Program of the National Institutes of Health,
National Institute on Aging
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging.
NR 67
TC 46
Z9 47
U1 1
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2008
VL 168
IS 10
BP 1179
EP 1189
DI 10.1093/aje/kwn229
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 373JY
UT WOS:000260969100012
PM 18835864
ER
PT J
AU Harper, S
Lynch, J
Meersman, SC
Breen, N
Davis, WW
Reichman, ME
AF Harper, Sam
Lynch, John
Meersman, Stephen C.
Breen, Nancy
Davis, William W.
Reichman, Marsha E.
TI THE AUTHORS REPLY
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
C1 [Harper, Sam; Lynch, John] McGill Univ, Fac Med, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3G 1Y6, Canada.
[Meersman, Stephen C.; Breen, Nancy; Davis, William W.; Reichman, Marsha E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Harper, S (reprint author), McGill Univ, Fac Med, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3G 1Y6, Canada.
RI Lynch, John/A-4797-2008; Harper, Sam/A-3406-2008
OI Lynch, John/0000-0003-2781-7902; Harper, Sam/0000-0002-2767-1053
NR 2
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2008
VL 168
IS 10
DI 10.1093/aje/kwn314
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 373JY
UT WOS:000260969100019
ER
PT J
AU Prentice, RL
Chlebowski, RT
Rossouw, JE
Anderson, GL
AF Prentice, Ross L.
Chlebowski, Rowan T.
Rossouw, Jacques E.
Anderson, Garnet L.
TI FOUR AUTHORS REPLY
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
ID HORMONE-REPLACEMENT THERAPY; BREAST-CANCER; WOMEN
C1 [Prentice, Ross L.; Anderson, Garnet L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Chlebowski, Rowan T.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90502 USA.
[Rossouw, Jacques E.] NHLBI, Bethesda, MD 20824 USA.
RP Prentice, RL (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
EM rprentic@fhcrc.org
NR 5
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2008
VL 168
IS 10
DI 10.1093/aje/kwn313
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 373JY
UT WOS:000260969100016
ER
PT J
AU Vergara, C
Tsai, YJ
Grant, AV
Rafaels, N
Gao, L
Hand, T
Stockton, M
Campbell, M
Mercado, D
Faruque, M
Dunston, G
Beaty, TH
Oliveira, RR
Ponte, EV
Cruz, AA
Carvalho, E
Araujo, ML
Watson, H
Schleimer, RP
Caraballo, L
Nickel, RG
Mathias, RA
Barnes, KC
AF Vergara, Candelaria
Tsai, Yuhjung J.
Grant, Audrey V.
Rafaels, Nicholas
Gao, Li
Hand, Tracey
Stockton, Maria
Campbell, Monica
Mercado, Dilia
Faruque, Mezbah
Dunston, Georgia
Beaty, Terri H.
Oliveira, Ricardo Riccio
Ponte, Eduardo V.
Cruz, Alvaro A.
Carvalho, Edgar
Araujo, Maria Llma
Watson, Harold
Schleimer, Robert P.
Caraballo, Luis
Nickel, Renate G.
Mathias, Rasika A.
Barnes, Kathleen C.
TI Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with
Asthma and IgE in Three Populations
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE Duffy antigen/receptor for chemokines; continental population groups;
lung diseases; hypersensitivity
ID BONE-MINERAL DENSITY; BLOOD-GROUP ANTIGEN; GENOME-WIDE SEARCH;
BLACK-AND-WHITE; AFRICAN-AMERICAN; CAUCASIAN POPULATIONS; NEGATIVE
INDIVIDUALS; SUSCEPTIBILITY LOCI; ETHNIC-DIFFERENCES; ENDOTHELIAL-CELLS
AB Rationale: Asthma prevalence and severity are high among under-served minorities, including those of African descent. The Duffy antigen/receptor for chemokines is the receptor for Plasmodium vivax on erythrocytes and functions as a chemokine-clearing receptor. Unlike European populations, decreased expression of the receptor on erythrocytes is common among populations of African descent, and results from a functional T-46C polymorphism (rs2814778) in the promoter. This variant provides an evolutionary advantage in malaria-endemic regions, because Duffy antigen/receptor for chemokines-negative erythrocytes are more resistant to infection by P. vivax.
Objectives: To determine the role of the rs2814778 polymorphism in asthma and atopy as measured by total serum IgE levels among four populations of African descent (African Caribbean, African American, Brazilian, and Colombian) and a European American population. Methods: Family-based association tests were performed in each of the five populations to test for association between the rs2814778 polymorphism and asthma or total IgE concentration.
Measurements and Main Results: Asthma was significantly associated with the rs2814778 polymorphism in the African Caribbean, Colombian, and Brazilian families (P < 0.05). High total IgE levels were associated with this variant in African Caribbean and Colombian families (P < 0.05). The variant allele was not polymorphic among European Americans.
Conclusions: Susceptibility to asthma and atopy among certain populations of African descent is influenced by a functional polymorphism in the gene encoding Duffy antigen/receptor for chemokines. This genetic variant, which confers resistance to malarial parasitic infection, may also partially explain ethnic differences in morbidity of asthma.
C1 [Vergara, Candelaria; Tsai, Yuhjung J.; Grant, Audrey V.; Rafaels, Nicholas; Gao, Li; Hand, Tracey; Stockton, Maria; Campbell, Monica; Barnes, Kathleen C.] Johns Hopkins Univ, Johns Hopkins Asthma & Allergy Ctr, Div Clin Immunol & Allergy, Dept Med, Baltimore, MD 21224 USA.
[Vergara, Candelaria; Mercado, Dilia; Caraballo, Luis] Univ Cartagena, Immunol Res Inst, Cartagena, Colombia.
[Faruque, Mezbah; Dunston, Georgia] Howard Univ, Natl Genome Ctr, Washington, DC 20059 USA.
[Beaty, Terri H.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Oliveira, Ricardo Riccio; Carvalho, Edgar; Araujo, Maria Llma] Hosp Univ Prof Edgard Santos, Serv Imunol, Salvador, BA, Brazil.
[Ponte, Eduardo V.; Cruz, Alvaro A.] Univ Fed Bahia, ProAR, Fac Med, Salvador, BA, Brazil.
[Watson, Harold] Univ W Indies, Fac Med, Cave Hill, Barbados.
[Schleimer, Robert P.] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA.
[Nickel, Renate G.] Dept Pediat Pneumonol & Immunol, Charite, Berlin, Germany.
[Mathias, Rasika A.] NHGRI, Genometr Sect, Inherited Dis Res Branch, Natl Inst Hlth, Baltimore, MD USA.
RP Barnes, KC (reprint author), Johns Hopkins Univ, Johns Hopkins Asthma & Allergy Ctr, Div Clin Immunol & Allergy, Dept Med, 5501 Hopkins Bayview Circle,Room 3A-62, Baltimore, MD 21224 USA.
EM kbarnes@jhmi.edu
RI Cruz, Alvaro/I-1676-2012; Oliveira, Ricardo/E-7707-2017
OI Cruz, Alvaro/0000-0002-7403-3871; Oliveira, Ricardo/0000-0001-9586-2313
FU National Institutes of Health [HL087699, A1050024]; COLCIENCIAS
[331-2004]; Mary Beryl Patch Turnbull Scholar Program; National Human
Genome Research Institute
FX Supported by National Institutes of Health grants HL087699 and A1050024;
and by a grant from COLCIENCIAS, Colombia no. 331-2004. A.V.G.'s
fieldwork was supported in part by GlaxoSmithKIine project VVE445.
K.C.B. was supported in part by the Mary Beryl Patch Turnbull Scholar
Program. R.A.M. was supported in part by the Intramural Research Program
of the National Human Genome Research Institute, National Institutes of
Health.
NR 51
TC 33
Z9 34
U1 1
U2 4
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD NOV 15
PY 2008
VL 178
IS 10
BP 1017
EP 1022
DI 10.1164/rccm.200801-182OC
PG 6
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 371VF
UT WOS:000260859200005
PM 18827265
ER
PT J
AU Kim, RD
Greenberg, DE
Ehrmantraut, ME
Guide, SV
Ding, L
Shea, Y
Brown, MR
Chernick, M
Steagall, WK
Glasgow, CG
Lin, J
Jolley, C
Sorbara, L
Raffeld, M
Hii, S
Avila, N
Sachdev, V
Barnhart, LA
Anderson, VL
Claypool, R
Hilligoss, DM
Garofalo, M
Fitzgerald, A
Anaya-O'Brien, S
Darnell, D
DeCastrol, R
Menning, HM
Ricklefs, SM
Porcella, SF
Olivier, KN
Moss, J
Holland, SM
AF Kim, Richard D.
Greenberg, David E.
Ehrmantraut, Mary E.
Guide, Shireen V.
Ding, Li
Shea, Yvonne
Brown, Margaret R.
Chernick, Milica
Steagall, Wendy K.
Glasgow, Connie G.
Lin, JingPing
Jolley, Clara
Sorbara, Lynn
Raffeld, Mark
Hii, Suvimol
Avila, Nilo
Sachdev, Vandana
Barnhart, Lisa A.
Anderson, Victoria L.
Claypool, Reginald
Hilligoss, Dianne M.
Garofalo'O, Mary
Fitzgerald, Alan
Anaya-O'Brien'O, Sandra
Darnell, Dirk
DeCastrol, Rosamma
Menning, Heather M.
Ricklefs, Stacy M.
Porcella, Stephen F.
Olivier, Kenneth N.
Moss, Joel
Holland, Steven M.
TI Pulmonary Nontuberculous Mycobacterial Disease Prospective Study of a
Distinct Preexisting Syndrome
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE immunodeficiency; IFN-gamma/IL-12; bronchiectasis; leanness; cystic
fibrosis
ID AVIUM COMPLEX INFECTION; MITRAL-VALVE-PROLAPSE; CYSTIC-FIBROSIS;
LUNG-DISEASE; PECTUS EXCAVATUM; INTERFERON-GAMMA; WINDERMERE-SYNDROME;
MARFAN-SYNDROME; CT; BRONCHIECTASIS
AB Rationale: Pulmonary nontuberculous mycobacterial (PNTM) disease is increasing, but predisposing features have been elusive.
Objectives: To prospectively determine the morphotype, immuno-phenotype, and cystic fibrosis transmembrane conductance regulator genotype in a large cohort with PNTM.
Methods: We prospectively enrolled 63 patients with PNTM infection, each of whom had computerized tomography, echocardiogram, pulmonary function, and flow cytometry of peripheral blood. In vitro cytokine production in response to mitogen, LPS, and cytokines was performed. Anthropometric measurements were compared with National Health and Nutrition Examination Survey (NHANES) age- and ethnicity-matched female control subjects extracted from the NHANES 2001-2002 dataset.
Measurements and Main Results: Patients were 59.9 (+/-9.8yr [SD]) old, and 5.4 (+/-7.9 yr) from diagnosis to enrollment. Patients were 95% female, 91% white, and 68% lifetime nonsmokers. A total of 46 were infected with Mycobacterium avium complex, M. xenopi, or M. kansasii; 17 were infected with rapidly growing mycobacteria. Female patients were significantly taller (164.7 vs. 161.0 cm; P < 0.001) and thinner (body mass index, 21.1 vs. 28.2; P < 0.001) than matched NHANES control subjects, and thinner (body mass index, 21.1 vs. 26.8; P = 0.002) than patients with disseminated nontuberculous mycobacterial infection. A total of 51% of patients had scoliosis, 11% pectus excavatum, and 9% mitral valve prolapse, all significantly more than reference populations. Stimulated cytokine production was similar to that of healthy control subjects, including the IFN-gamma/IL-12 pathway. CD4(+), CD8(+), B, and natural killer cell numbers were normal. A total of 36% of patients had mutations in the cystic fibrosis transmembrane conductance regulator gene.
Conclusions: Patients with PNTM infection are taller and leaner than control subjects, with high rates of scoliosis, pectus excavatum, mitral valve prolapse, and cystic fibrosis transmembrane conductance regulator mutations, but without recognized immune defects.
C1 [Kim, Richard D.; Greenberg, David E.; Guide, Shireen V.; Ding, Li; Barnhart, Lisa A.; Anderson, Victoria L.; Claypool, Reginald; Fitzgerald, Alan; Darnell, Dirk; DeCastrol, Rosamma; Olivier, Kenneth N.; Holland, Steven M.] NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Ehrmantraut, Mary E.; Steagall, Wendy K.; Glasgow, Connie G.; Moss, Joel] NHLBI, Translat Med Branch, Bethesda, MD 20892 USA.
[Shea, Yvonne; Brown, Margaret R.] Ctr Clin, Dept Lab Med, Bethesda, MD USA.
[Chernick, Milica] NIDDK, Kidney Dis Sect, Bethesda, MD USA.
[Lin, JingPing] NHLBI, Off Biostatist Res, Bethesda, MD 20892 USA.
[Jolley, Clara] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
[Sorbara, Lynn; Raffeld, Mark] Natl Canc Inst, Mol Pathol Serv, Bethesda, MD USA.
[Hii, Suvimol; Avila, Nilo] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
[Sachdev, Vandana] NHLBI, Cardiol Branch, Bethesda, MD 20892 USA.
[Hilligoss, Dianne M.; Garofalo'O, Mary; Anaya-O'Brien'O, Sandra] NIAID, Host Def Lab, Bethesda, MD 20892 USA.
NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Menning, Heather M.; Ricklefs, Stacy M.; Porcella, Stephen F.] NIAID, Res Technol Sect, Genom Unit, Rocky Mt Labs,NIH,US Dept HHS, Hamilton, MT USA.
RP Holland, SM (reprint author), NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike,CRC B3-4141,MSC 1684, Bethesda, MD 20892 USA.
EM smh@nih.gov
NR 49
TC 139
Z9 141
U1 0
U2 5
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD NOV 15
PY 2008
VL 178
IS 10
BP 1066
EP 1074
DI 10.1164/rccm.200805-686OC
PG 9
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 371VF
UT WOS:000260859200012
PM 18703788
ER
PT J
AU Shan, L
Zhang, RS
Zhang, WH
Lee, E
Sridhar, R
Snyderwine, EG
Wang, PC
AF Shan, Liang
Zhang, Renshu
Zhang, Wanghai
Lee, Edward
Sridhar, Rajagopalan
Snyderwine, Elizabeth G.
Wang, Paul C.
TI Image-based evaluation of the molecular events underlying HC11 mammary
epithelial cell differentiation
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE mammary epithelial cells; differentiation; signal pathways; optical
imaging
ID GLAND DEVELOPMENT; GENE-EXPRESSION; HIGH-THROUGHPUT; BREAST-CANCER;
PROLACTIN; HORMONE; GROWTH; CARCINOGENESIS; ACTIVATION; ESTROGEN
AB We have developed an image-based technique for signal pathway analysis, target validation, and compound screening related to mammary epithelial cell differentiation. This technique used the advantages of optical imaging and the HC11-Lux model system. The HC11-Lux cell line is a subclone of HC11 mammary epithelial cells transfected stably with a luciferase construct of the beta-casein gene promoter (p-344/-1 beta c-Lux). The promoter activity was imaged optically in real time following lactogenic induction. The imaging signal intensity was closely correlated with that measured using a luminometer following protein extraction (R = 0.99, P < 0.0001) and consistent with the messenger RNA (mRNA) level of the endogenous beta-casein gene. Using this technique, we examined the roles of JAK2/Stat5A, Raf-1/MEK/MAKP, and PI3K/Akt signal pathways with respect to differentiation. The imaging studies showed that treatment of the cells with epidermal growth factor (EGF), AG490 (JAK2-specific inhibitor), and LY294002 (PI3K-specific inhibitor) blocked lactogenic differentiation in a dose-dependent manner. PD98059 (MEK-specific inhibitor) could reverse EGF-mediated differentiation arrest. These results indicate that these pathways are essential in cell differentiation. This simple, sensitive, and reproducible technique permits visualization and real-time evaluation of the molecular events related to milk protein production. It can be adopted for high-through put screening of small molecules for their effects on mammary epithelial cell growth, differentiation, and carcinogenesis. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Shan, Liang; Wang, Paul C.] Howard Univ, Dept Radiol, Washington, DC 20060 USA.
[Zhang, Renshu; Sridhar, Rajagopalan] Howard Univ, Dept Radiat Oncol, Washington, DC 20060 USA.
[Zhang, Wanghai; Lee, Edward] Howard Univ, Dept Pathol, Washington, DC 20060 USA.
[Snyderwine, Elizabeth G.] NCI, NIH, Bethesda, MD 20892 USA.
RP Wang, PC (reprint author), Howard Univ, Dept Radiol, Washington, DC 20060 USA.
EM pwang@howard.edu
FU USAMRMC [W81XWH-05-1-0291]; Charles and Mary Latham Fund [7023185]; NIH
[5P20 CA118770]; RCMI Program Division of Research Infrastructure,
National Center for Research Resources, NIH [2 G12 RR003048]
FX We thank Drs. David S. Salomon and Nancy E. Hynes for providing HC11-Lux
cell line. This work was supported in part by USAMRMC W81XWH-05-1-0291,
Charles and Mary Latham Fund (#7023185), NIH 5P20 CA118770. This work
was also supported in part by grant 2 G12 RR003048 from the RCMI Program
Division of Research Infrastructure, National Center for Research
Resources, NIH.
NR 28
TC 4
Z9 4
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD NOV 15
PY 2008
VL 382
IS 2
BP 122
EP 128
DI 10.1016/j.ab.2008.08.004
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 356OP
UT WOS:000259787800007
PM 18722992
ER
PT J
AU Yang, MH
Kostov, Y
Bruck, HA
Rasooly, A
AF Yang, Minghui
Kostov, Yordan
Bruck, Hugh A.
Rasooly, Avraharn
TI Carbon Nanotubes with Enhanced Chemiluminescence Immunoassay for
CCD-Based Detection of Staphylococcal Enterotoxin B in Food
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID LINKED-IMMUNOSORBENT-ASSAY; FIELD-EFFECT TRANSISTORS; SIZED CANTILEVER
SENSORS; REAL-TIME; ELECTROCHEMICAL IMMUNOSENSOR; KIT TECRA; ENZYME;
BIOSENSOR; AUREUS; AGENTS
AB Enhanced chemiluminescence (ECL) detection can significantly enhance the sensitivity of immunoassays but often requires expensive and complex detectors. The need for these detectors limits broader use of ECL in immunoassay applications. To make ECL more practical for immunoassays, we utilize a simple cooled charge-coupled device (CCD) detector combined with carbon nanotubes (CNTs) for primary antibody immobilization to develop a simple and portable point-of-care immunosensor. This combination of ECL, CNT, and CCD detector technologies is used to improve the detection of Staphylococcal enterotoxin B (SEB) in food. Anti-SEB primary antibodies were immobilized onto the CNT surface, and the antibody-nanotube mixture was immobilized onto a polycarbonate surface. SEB was then detected by an ELISA assay on the CNT-polycarbonate surface with an ECL assay. SEB in buffer, soy milk, apple juice, and meat baby food was assayed with a LOD of 0.01 ng/mL using our CCD detector, a level similar to the detection limit obtained with a fluorometric detector when using the CNTs. This level is far more sensitive than the conventional ELISA, which has a LOD of similar to 1 ng/mL. Our simple, versatile, and inexpensive point-of-care immunosensor combined with the CNT-ECL immunoassay method described in this work can also be used to simplify and increase sensitivity for many other types of diagnostics and detection assays.
C1 [Yang, Minghui; Kostov, Yordan] Univ Maryland Baltimore Cty, Ctr Adv Sensor Technol, Baltimore, MD 21250 USA.
[Rasooly, Avraharn] US FDA, Div Biol, Off Sci & Engn, Silver Spring, MD 20993 USA.
[Bruck, Hugh A.] UMCP, College Pk, MD 20742 USA.
[Rasooly, Avraharn] NCI, Bethesda, MD 20892 USA.
RP Rasooly, A (reprint author), NCI, NIH, 6130 Execut Blvd EPN,Room 6035A, Rockville, MD 20852 USA.
EM rasoolya@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 60
TC 57
Z9 63
U1 7
U2 44
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD NOV 15
PY 2008
VL 80
IS 22
BP 8532
EP 8537
DI 10.1021/ac801418n
PG 6
WC Chemistry, Analytical
SC Chemistry
GA 372OM
UT WOS:000260910900023
PM 18855418
ER
PT J
AU Kitabatake, T
Moaddel, R
Cole, R
Gandhari, M
Frazier, C
Hartenstein, J
Rosenberg, A
Bernier, M
Wainer, IW
AF Kitabatake, T.
Moaddel, R.
Cole, R.
Gandhari, M.
Frazier, C.
Hartenstein, J.
Rosenberg, A.
Bernier, M.
Wainer, I. W.
TI Characterization of a Multiple Ligand-Gated Ion Channel Cellular
Membrane Affinity Chromatography Column and Identification of
Endogenously Expressed Receptors in Astrocytoma Cell Lines
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTOR; D-ASPARTATE RECEPTORS;
ALZHEIMERS-DISEASE; LUNG-CARCINOMA; BINDING-SITES; RAT-BRAIN;
BUNGAROTOXIN; SUBUNIT; ANTAGONIST; INCREASE
AB Cellular membranes obtained from the 1321N1 and A172 astrocytoma cell lines were immobilized on a chromatographic phase to create cellular membrane affinity chromatography (CMAC) columns, CMAC(1321N1) and CMAC(A172). The columns were characterized using frontal affinity chromatography with [H-3]-epibatidine as the marker ligand and epibatidine, nicotine, and methyllycaconitine as the displacers. The results indicated that the columns contained homomeric alpha(7) nicotinic acetylcholine receptors (alpha(7) nAChR) and heteromeric nicotinic acetylcholine receptors (alpha(x)beta(y) nAChRs), which was confirmed by the addition of subtype-specific inhibitors, alpha-bungarotoxin (alpha(7) nAChR) and K-bungarotoxin (alpha(x)beta(y) nAChR) to the mobile phase. The presence of two additional ligand-gated ion channels (LGICs), gamma-aminobutyric acid (GABA(A)) and N-methyl-D-aspartic acid (NMDA), was established using frontal affinity chromatography with flunitrazepam and diazepam (GABAA receptor) and MK-801 and NMDA (NMDA receptor). The presence of the four LGICs was confirmed using confocal microscopy and flowcytometry.The results indicate that the CMAC(1321N1) and CMAC(A172) columns contain four independently functioning LGICs, that the columns can be used to characterize binding affinities of small molecules to each of the receptors, and that the CMAC approach can be used to probe the expression of endogenous membrane receptors.
C1 [Kitabatake, T.; Moaddel, R.; Cole, R.; Gandhari, M.; Frazier, C.; Hartenstein, J.; Rosenberg, A.; Bernier, M.; Wainer, I. W.] NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Wainer, IW (reprint author), NIA, Gerontol Res Ctr, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM Wainerir@grc.nia.nih.gov
OI Bernier, Michel/0000-0002-5948-368X
FU National Institute on Aging; NIH; Research Resources Branch, National
Institute on Aging/NIH
FX Ibis work was supported by funds from the Intramural Research Program of
the National Institute on Aging, NIH. The authors would like to thank
Magdalena Juhaszova from the Laboratory of Cardiovascular Sciences,
National Institute on Aging/NIH and Christa M. Morris, Francis J.
Chrest, Robert Wersto, and Brittany Frank from the Research Resources
Branch, National Institute on Aging/NIH for their assistance in this
project.
NR 28
TC 8
Z9 10
U1 0
U2 13
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD NOV 15
PY 2008
VL 80
IS 22
BP 8673
EP 8680
DI 10.1021/ac8016407
PG 8
WC Chemistry, Analytical
SC Chemistry
GA 372OM
UT WOS:000260910900043
PM 18847217
ER
PT J
AU Blonder, J
Johann, DJ
Veenstra, TD
Xiao, Z
Emmert-Buck, MR
Ziegler, RG
Rodriguez-Canales, J
Hanson, JA
Xu, X
AF Blonder, Josip
Johann, Donald J.
Veenstra, Timothy D.
Xiao, Zhen
Emmert-Buck, Michael R.
Ziegler, Regina G.
Rodriguez-Canales, Jaime
Hanson, Jeffrey A.
Xu, Xia
TI Quantitation of Steroid Hormones in Thin Fresh Frozen Tissue Sections
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID TANDEM MASS-SPECTROMETRY; PROTEOMIC ANALYSIS; ENDOGENOUS ESTROGENS;
BREAST-CANCER; PROGESTERONE; SERUM
AB As analytical technologies in proteomics and metabolomics continue to mature, there is an increasing need to apply these to clinically relevant biologic samples. In this study, a liquid chromatography-tandem mass spectrometry method that utilizes selected reaction monitoring was used to measure the absolute quantity of estrogens and estrogen metabolites and testosterone in 8-mu m tissue sections obtained from a fresh frozen lymph node tumor infiltrated by metastatic breast carcinoma. Total (conjugated plus unconjugated) and unconjugated levels of these steroid hormones were measured using two cohorts, each containing five adjacent serial sections cut from this tumor. The results were highly reproducible across replicate samples, showing that typical histological tissue sections represent an important sample type for the measurement of these specific metabolites.
C1 [Blonder, Josip; Veenstra, Timothy D.; Xiao, Zhen; Xu, Xia] SAIC Frederick Inc, Natl Canc Inst Frederick, Lab Prote & Analyt Technol, Frederick, MD 21702 USA.
[Emmert-Buck, Michael R.; Rodriguez-Canales, Jaime; Hanson, Jeffrey A.] NCI, Ctr Canc Res, Pathol Lab, Laser Capture Microdissect Core Lab, Bethesda, MD 20877 USA.
[Ziegler, Regina G.] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Veenstra, TD (reprint author), SAIC Frederick Inc, Natl Canc Inst Frederick, Lab Prote & Analyt Technol, Frederick, MD 21702 USA.
EM veenstra@ncifcrf.gov
OI Rodriguez-Canales, Jaime/0000-0002-0885-2377
FU National Cancer Institute, National Institutes of Health [N01-CO-12400];
Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research and Division of Cancer Epidemiology and
Genetics
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract N01-CO-12400 and by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research and Division of
Cancer Epidemiology and Genetics. The content of this publication does
not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 21
TC 12
Z9 12
U1 2
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD NOV 15
PY 2008
VL 80
IS 22
BP 8845
EP 8852
DI 10.1021/ac801402a
PG 8
WC Chemistry, Analytical
SC Chemistry
GA 372OM
UT WOS:000260910900065
PM 18937426
ER
PT J
AU Stern, AJ
Savostyanova, AA
Goldman, A
Barnett, AS
van der Veen, JWC
Callicott, JH
Mattay, VS
Weinberger, DR
Marenco, S
AF Stern, Alexa J.
Savostyanova, Antonina A.
Goldman, Aaron
Barnett, Alan S.
van der Veen, Jan Willem C.
Callicott, Joseph H.
Mattay, Venkata S.
Weinberger, Daniel R.
Marenco, Stefano
TI Impact of the Brain-Derived Neurotrophic Factor Val66Met Polymorphism on
Levels of Hippocampal N-Acetyl-Aspartate Assessed by Magnetic Resonance
Spectroscopic Imaging at 3 Tesla
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Aging; choline; gray matter; healthy; hippocampal volume; IQ
ID BDNF GENE VARIANTS; POSTTRAUMATIC-STRESS-DISORDER; ACTIVITY-DEPENDENT
SECRETION; PROTON MR SPECTROSCOPY; AGE-OF-ONSET; RAT HIPPOCAMPUS;
IN-VIVO; ELECTROCONVULSIVE-THERAPY; ANTIDEPRESSANT TREATMENT; CEREBRAL
METABOLITES
AB Background: This study was conducted to corroborate prior evidence of an effect of the brain-derived neurotrophic factor (BDNF) valine (val) to methionine (met) amino acid substitution at codon 66 (val66met) polymorphism on measures of N-acetyl-aspartate (NAA) containing compounds in healthy subjects.
Methods: The NAA to creatine (Cre) ratio (NAA/Cre), NAA to choline (Cho) ratio (NAA/Cho), and Cho to Cre ratio (Cho/Cre) were measured in the left and right hippocampi, left and right dorsolateral prefrontal cortices, occipital lobe, anterior cingulate, and white matter of the centrum semiovale of 69 carefully screened healthy volunteers utilizing proton magnetic resonance spectroscopic imaging (MRSI) at 3 Tesla (T).
Results: Val/met subjects exhibited significantly reduced levels of left hippocampal NAA/Cre and NAA/Cho compared with val/val subjects. This effect was independent of age, IQ, number of voxels, hippocampal volume, or gray matter content in the voxels of interest. Analysis of other brain regions showed no effect of BDNF genotype on NAA measures.
Conclusions: We confirmed the association between the met-BDNF variant and reduced levels of hippocampal NAA found with a similar technique at 1.5T. The consonance of our results with prior findings adds to the evidence that the BDNF val/met genotype affects hippocampal biology with implications for a variety of neuropsychiatric disorders.
C1 [Stern, Alexa J.; Savostyanova, Antonina A.; Goldman, Aaron; Barnett, Alan S.; van der Veen, Jan Willem C.; Callicott, Joseph H.; Mattay, Venkata S.; Weinberger, Daniel R.; Marenco, Stefano] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, NIH,Intramural Res Program, Bethesda, MD 20892 USA.
RP Marenco, S (reprint author), NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, NIH,Intramural Res Program, Bldg 10-Room 4S235,10 Ctr Dr, Bethesda, MD 20892 USA.
EM marencos@mail.nih.gov
RI Marenco, Stefano/A-2409-2008; Farmer, Antonina/M-8914-2013; Callicott,
Joseph/C-9102-2009
OI Marenco, Stefano/0000-0002-2488-2365; Farmer,
Antonina/0000-0002-3305-8300; Callicott, Joseph/0000-0003-1298-3334
FU National Institute of Mental Health (NIMH)
FX The funding for this work was provided entirely by the National
Institute of Mental Health (NIMH) Intramural Research Program (IRP).;
This work was presented in part at the Annual Meeting of the Society of
Biological Pshychiatry, May 18, 2007. Sam Diego, California.; The
authors reported no biomedical financial interests or potential
conflicts of interest.; Supplementary material cited in this article is
available online.
NR 69
TC 24
Z9 24
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 15
PY 2008
VL 64
IS 10
BP 856
EP 862
DI 10.1016/j.biopsych.2008.07.009
PG 7
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 372OW
UT WOS:000260911900005
PM 18707679
ER
PT J
AU Cizza, G
Marques, AH
Eskandari, F
Christie, IC
Torvik, S
Silverman, MN
Phillips, TM
Sternberg, EM
AF Cizza, Giovanni
Marques, Andrea H.
Eskandari, Farideh
Christie, Israel C.
Torvik, Sara
Silverman, Marni N.
Phillips, Terry M.
Sternberg, Esther M.
CA POWER Study Grp
TI Elevated Neuroimmune Biomarkers in Sweat Patches and Plasma of
Premenopausal Women with Major Depressive Disorder in Remission: The
POWER Study
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Autonomic nervous system; calcitonin-gene-related peptide; depression;
interleukins; neuropeptide Y; pain; substance P; vasoactive intestinal
peptide
ID RECYCLING IMMUNOAFFINITY CHROMATOGRAPHY; DISEASE; CYTOKINES; LIFE; CSF
AB Background: Major depressive disorder (MDD) is inconsistently associated with elevations in proinflammatory cytokines and neuropeptides. We used a skin sweat patch, recently validated in healthy control subjects, and recycling immunoaffinity chromatography to measure neuroimmune biomarkers in patients with MDD mostly in remission.
Methods: We collected blood at 8:00 Am and applied skin sweat patches for 24 hours in 21 - to 45-year-old premenopausal women (n = 19) with MDD (17/19 in remission) and age-matched healthy controls (n = 17) participating in the POWER (Premenopausal, Osteopenia/Osteoporosis, Women, Alendronate, Depression) Study.
Results: Proinflammatory cytokines, neuropeptide Y, substance P, and calcitonin-gene-related peptide were significantly higher and vasoactive intestinal peptide,a marker of parasympathetic activity, was significantly lower in patients compared to controls, and depressive symptomatology strongly correlated with biomarker levels. All analytes were strongly correlated in the skin sweat patch and plasma in patients (r = .73 to .99; p < .0004).
Conclusions: The skin sweat patch allows detection of disrupted patterns of proinflammatory cytokines and neuropeptides in women with MDD in clinical remission, which could predispose to medical consequences such as cardiovascular disease, osteoporosis, and diabetes. This method permits measurement of cytokines in ambulatory settings where blood collection is not feasible.
C1 [Marques, Andrea H.; Eskandari, Farideh; Silverman, Marni N.; Sternberg, Esther M.] NIMH, Integrat Neural Immune Program, Sect Neuroendocrine Immunol & Behav, NIH, Rockville, MD 20852 USA.
[Cizza, Giovanni; Torvik, Sara] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD USA.
[Eskandari, Farideh] NIMH, Sect Neuroendocrine Immunol & Behav, Integrat Neural Immune Program, NIH, Seattle, WA USA.
Virginia Mason Med Ctr, Seattle, WA 98101 USA.
[Christie, Israel C.] Univ Pittsburgh, Med Ctr, Cardiovasc Behav Med Program, Dept Psychiat, Pittsburgh, PA USA.
[Phillips, Terry M.] NIBIB, Nanoscale Immunodiagnost Sect, Lab Bioengn & Phys Sci, NIH, Bethesda, MD USA.
RP Sternberg, EM (reprint author), NIMH, Integrat Neural Immune Program, Sect Neuroendocrine Immunol & Behav, NIH, 5625 Fishers Lane,MSC-9401,Room 4N13, Rockville, MD 20852 USA.
EM sternbee@mail.nih.gov
FU National Institutes of Health (NIH) Intramural Research Program;
National Institute of Mental Health (NIMH), Section on Neuroendocrine
Immunology and Behavior, Integrative Neural Immune Program; National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK),
Clinical Endocrinology Branch; National Institute of Biomedical Imaging
and Bioengineering (NIBIB), Nanoscale Immunodiagnosis, Laboratory of
Bioengineering & Physical Science
FX The study was fully supported by the National Institutes of Health (NIH)
Intramural Research Program; National Institute of Mental Health (NIMH),
Section on Neuroendocrine Immunology and Behavior, Integrative Neural
Immune Program; National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK), Clinical Endocrinology Branch; and National Institute
of Biomedical Imaging and Bioengineering (NIBIB), Nanoscale
Immunodiagnosis, Laboratory of Bioengineering & Physical Science. The
following individuals were investigators of the POWER Protocol
(Premenopausal Osteoporosis Women Alendronate Depression): Giovanni
Cizza (Principal Investigator), Ann Berger, Marc R. Blackman, Karim A.
Calis, George Csako, Bart Drinkard, Farideh Eskandari, Philip W. Gold,
McDonald Horne, Christine Kotila, Pedro Martinez, Kate Musallam, Terry
M. Phillips, James, C. Reynolds, Nancy G. Sehring, Esther Sternherg, and
Sara Torvik.; All authors reported no biomedical financial interests or
potential conflicts of interest.; Supplementary material cited in this
article is available online.
NR 20
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U1 0
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 15
PY 2008
VL 64
IS 10
BP 907
EP 911
DI 10.1016/j.biopsych.2008.05.035
PG 5
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 372OW
UT WOS:000260911900014
PM 18657799
ER
PT J
AU Chakrapani, H
Kalathur, RC
Maciag, AE
Citro, ML
Ji, XH
Keefer, LK
Saavedra, JE
AF Chakrapani, Harinath
Kalathur, Ravi C.
Maciag, Anna E.
Citro, Michael L.
Ji, Xinhua
Keefer, Larry K.
Saavedra, Joseph E.
TI Synthesis, mechanistic studies, and anti-proliferative activity of
glutathione/glutathione S-transferase-activated nitric oxide prodrugs
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Nitric oxide; Prodrug; JS-K; Diazeniumdiolate; Cancer; GST
ID VITRO ANTILEUKEMIC ACTIVITY; JS-K; IN-VITRO; ANTICANCER LEAD;
LEUKEMIA-CELLS; BIOLOGICAL APPLICATIONS; NOBEL LECTURE; DONOR DRUGS;
GLUTATHIONE; DIAZENIUMDIOLATE
AB Nitric oxide (NO) prodrugs such as O-2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate (JS-K) are a growing class of promising NO-based therapeutics. Nitric oxide release from the anti-cancer lead compound, JS-K, is proposed to occur through a nucleophilic aromatic substitution by glutathione (GSH) catalyzed by glutathione S-transferase (GST) to form a diazeniumdiolate anion that spontaneously releases NO. In this study, a number of structural analogues of JS-K were synthesized and their chemical and biological properties were compared with those of JS-K. The homopiperazine analogue of JS-K showed anti-cancer activity that is comparable with that of JS-K but with a diminished reactivity towards both GSH and GSH/GST; both the aforementioned compounds displayed no cytotoxic activity towards normal renal epithelial cell line at concentrations where they significantly diminished the proliferation of a panel of renal cancer cell lines. These properties may prove advantageous in the further development of this class of nitric oxide prodrugs as cancer therapeutic agents. Published by Elsevier Ltd.
C1 [Chakrapani, Harinath; Keefer, Larry K.] NCI, Comparat Carcinogenesis Lab, Chem Sect, Frederick, MD 21702 USA.
[Kalathur, Ravi C.; Ji, Xinhua] NCI, Macromol Crystallog Sect, Biomol Struct Sect, Frederick, MD 21702 USA.
[Maciag, Anna E.; Citro, Michael L.; Saavedra, Joseph E.] NCI, SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA.
RP Chakrapani, H (reprint author), NCI, Comparat Carcinogenesis Lab, Chem Sect, Frederick, MD 21702 USA.
EM chakrah@ncifcrf.gov; saavj@ncifcrf.gov
RI Ji, Xinhua/C-9664-2012; Keefer, Larry/N-3247-2014; Kalathur,
Ravi/L-7696-2016
OI Ji, Xinhua/0000-0001-6942-1514; Keefer, Larry/0000-0001-7489-9555;
Kalathur, Ravi/0000-0003-1669-9277
FU NIH, National Cancer Institute, Center for Cancer Research
[N01-CO-12400]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, as
well as by National Cancer Institute contract N01-CO-12400 to
SAIC-Frederick. We are grateful to Dr. James Phang, Metabolism and
Cancer Susceptibility Section, NCI and Ms. Susan Kenney, NCI-Frederick
Screening Technology Branch for providing us cell lines.
NR 46
TC 27
Z9 28
U1 0
U2 13
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 NOV 15
PY 2008
VL 16
IS 22
BP 9764
EP 9771
DI 10.1016/j.bmc.2008.09.063
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 370JJ
UT WOS:000260758200015
PM 18930407
ER
PT J
AU Jang, H
Ma, B
Lal, R
Nussinov, R
AF Jang, Hyunbum
Ma, Buyong
Lal, Ratnesh
Nussinov, Ruth
TI Models of Toxic beta-Sheet Channels of Protegrin-1 Suggest a Common
Subunit Organization Motif Shared with Toxic Alzheimer beta-Amyloid Ion
Channels
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID SOLID-STATE NMR; HAIRPIN ANTIMICROBIAL PEPTIDE; LIPID-BILAYERS; PORE
FORMATION; MOLECULAR-DYNAMICS; CATIONIC PEPTIDES; MEMBRANES; MECHANISM;
PROTEIN; DISEASE
AB Antimicrobial peptides (AMPs) induce cytotoxicity by altering membrane permeability. The electrical properties of membrane-associated AMPs as well as their cellular effects have been extensively documented; however their three-dimensional structure is poorly understood. Gaining insight into channel structures is important to the understanding of the protegrin-1 (PG-1) and other AMP cytolytic mechanisms, and to antibiotics design. We studied the beta-sheet channels morphology using molecular dynamics simulations. We modeled PG-1 channels as intrinsic barrel-stave and toroidal membrane pores, and simulated them in zwitterionic and anionic lipid bilayers. PG-1 channels consist of eight beta-hairpins in a consecutive NCCN (N and C represent the beta-hairpin's N-and C-termini) packing organization yielding antiparallel and parallel b-sheet channels. Both channels preserve the toroidal, but not the barrel-stave pores. The two lipid leaflets of the bilayer bend toward each other at the channels' edges, producing a semitoroidal pore with the outward-pointing hydrophobic residues preventing the polar lipid headgroups from moving to the bilayer center. In all simulated lipid environments, PG-1 channels divide into four or five beta-sheet subunits consisting of single or dimeric b-hairpins. The channel morphology with subunit organization is consistent with the four to five subunits observed by NMR in the POPE/POPG bilayer. Remarkably, a b-sheet subunit channel motif is in agreement with Alzheimer ion channels modeled using the universal U-shape beta-strand-turn-beta-strand structure, as well as with high resolution atomic force microscopy images of beta-amyloid channels with four to six subunits. Consistent with the toxic b-amyloid channels that are ion-conducting, the PG-1 channels permeate anions.
C1 [Jang, Hyunbum; Ma, Buyong; Nussinov, Ruth] NCI, Canc Res Ctr, Nanobiol Program, SAIC Frederick, Frederick, MD 21702 USA.
[Lal, Ratnesh] Univ Chicago, Ctr Nanomed, Chicago, IL 60637 USA.
[Lal, Ratnesh] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Inst Mol Med, Sackler Sch Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Jang, H (reprint author), NCI, Canc Res Ctr, Nanobiol Program, SAIC Frederick, Frederick, MD 21702 USA.
EM jangh@ncifcrf.gov
RI Ma, Buyong/F-9491-2011
OI Ma, Buyong/0000-0002-7383-719X
FU National Cancer Institute, National Institutes of Health [N01-CO-12400];
National Institutes of Health, National Cancer Institute, Center for
Cancer Research; National Institutes of Health; US Army Medical Research
Acquisition Activity [W81XWH-05-1-0002]
FX This project has been funded in whole or in part with funds from the
National Cancer Institute, National Institutes of Health (contract
number N01-CO-12400). This research was supported (in part) by the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research. It was also
supported by the Extramural Research Program of the National Institutes
of Health (R.L.). This research was funded in part by the US Army
Medical Research Acquisition Activity (grant W81XWH-05-1-0002) (B.M.).
This study used the high-performance computational capabilities of the
Biowulf PC/Linux cluster at the National Institutes of Health, Bethesda,
MD (http://biowulf. nih.gov).
NR 48
TC 57
Z9 57
U1 1
U2 6
PU BIOPHYSICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 15
PY 2008
VL 95
IS 10
BP 4631
EP 4642
DI 10.1529/biophysj.108.134551
PG 12
WC Biophysics
SC Biophysics
GA 366YK
UT WOS:000260519300016
PM 18708452
ER
PT J
AU Osteen, JD
Mindell, JA
AF Osteen, Jeremiah D.
Mindell, Joseph A.
TI Insights into the ClC-4 Transport Mechanism from Studies of Zn2+
Inhibition
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID CHLORIDE CHANNEL; MAMMALIAN-CELLS; MOLECULAR-BASIS; DENTS-DISEASE; ZINC;
PROTEINS; CONSERVATION; TRAFFICKING; SELECTIVITY; NEURONS
AB The CLC family of chloride channels and transporters is a functionally diverse group of proteins important in a wide range of physiological processes. ClC-4 and ClC-5 are localized to endosomes and seem to play roles in the acidification of these compartments. These proteins were recently shown to function as Cl-/H+ antiporters. However, relatively little is known about the detailed mechanism of CLC-mediated Cl-/H+ antiport, especially for mammalian isoforms. We attempted to identify molecular tools that might be useful in probing structure-function relationships in these proteins. Here, we record currents from human ClC-4 (hClC-4) expressed in Xenopus oocytes, and find that Zn2+ inhibits these currents, with an apparent affinity of similar to 50 mu M. Although Cd2+ has a similar effect, Co2+ and Mn2+ do not inhibit hClC-4 currents. In contrast, the effect of Zn2+ on the ClC-0 channel, Zn2+-mediated inhibition of hClC-4 is minimally voltage-dependent, suggesting an extracellular binding site for the ion. Nine candidate external residues were tested; only mutations of three consecutive histidine residues, located in a single extracellular loop, significantly reduced the effect of Zn2+, with one of these making a larger contribution than the other two. An analogous tri-His sequence is absent from ClC-0, suggesting a fundamentally different inhibitory mechanism for the ion on hClC-4. Manipulations that alter transport properties of hClC-4, varying permeant ions as well as mutating the "gating glutamate", dramatically affect Zn2+ inhibition, suggesting the involvement of a heretofore unexplored part of the protein in the transport process.
C1 [Osteen, Jeremiah D.; Mindell, Joseph A.] NINDS, Membrane Transport Biophys Unit, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Mindell, JA (reprint author), NINDS, Membrane Transport Biophys Unit, Porter Neurosci Res Ctr, NIH, 35 Convent Dr,Bldg 35,MSC 3701, Bethesda, MD 20892 USA.
EM mindellj@ninds.nih.gov
OI Mindell, Joseph/0000-0002-6952-8247
FU National Institute of Neurological Disorders and Stroke Intramural
Program
FX This work was funded by the National Institute of Neurological Disorders
and Stroke Intramural Program.
NR 29
TC 11
Z9 13
U1 1
U2 2
PU BIOPHYSICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 15
PY 2008
VL 95
IS 10
BP 4668
EP 4675
DI 10.1529/biophysj.108.137158
PG 8
WC Biophysics
SC Biophysics
GA 366YK
UT WOS:000260519300019
PM 18658230
ER
PT J
AU Zhang, M
Fendler, B
Peercy, B
Goel, P
Bertram, R
Sherman, A
Satin, L
AF Zhang, Min
Fendler, Bernard
Peercy, Bradford
Goel, Pranay
Bertram, Richard
Sherman, Arthur
Satin, Leslie
TI Long Lasting Synchronization of Calcium Oscillations by Cholinergic
Stimulation in Isolated Pancreatic Islets
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID PULSATILE INSULIN-SECRETION; CYTOPLASMIC CA2+ OSCILLATIONS; BURSTING
ELECTRICAL-ACTIVITY; BETA-CELLS; ENDOCRINE PANCREAS; NEURAL CONTROL;
IN-VIVO; B-CELL; INOSITOL 1,4,5-TRISPHOSPHATE; SUSTAINED OSCILLATIONS
AB Individual mouse pancreatic islets exhibit oscillations in [Ca2+](i) and insulin secretion in response to glucose in vitro, but how the oscillations of a million islets are coordinated within the human pancreas in vivo is unclear. Islet to islet synchronization is necessary, however, for the pancreas to produce regular pulses of insulin. To determine whether neurohormone release within the pancreas might play a role in coordinating islet activity, [Ca2+](i) changes in 4 - 6 isolated mouse islets were simultaneously monitored before and after a transient pulse of a putative synchronizing agent. The degree of synchronicity was quantified using a novel analytical approach that yields a parameter that we call the "Synchronization Index''. Individual islets exhibited [Ca2+](i) oscillations with periods of 3 - 6 min, but were not synchronized under control conditions. However, raising islet [Ca2+](i) with a brief application of the cholinergic agonist carbachol (25 mu M) or elevated KCl in glucose- containing saline rapidly synchronized islet [Ca2+](i) oscillations for >= 30 min, long after the synchronizing agent was removed. In contrast, the adrenergic agonists clonidine or norepinephrine, and the K-ATP channel inhibitor tolbutamide, failed to synchronize islets. Partial synchronization was observed, however, with the KATP channel opener diazoxide. The synchronizing action of carbachol depended on the glucose concentration used, suggesting that glucose metabolism was necessary for synchronization to occur. To understand how transiently perturbing islet [Ca2+](i) produced sustained synchronization, we used a mathematical model of islet oscillations in which complex oscillatory behavior results from the interaction between a fast electrical subsystem and a slower metabolic oscillator. Transient synchronization simulated by the model was mediated by resetting of the islet oscillators to a similar initial phase followed by transient "ringing'' behavior, during which the model islets oscillated with a similar frequency. These results suggest that neurohormone release from intrapancreatic neurons could help synchronize islets in situ. Defects in this coordinating mechanism could contribute to the disrupted insulin secretion observed in Type 2 diabetes.
C1 [Zhang, Min; Satin, Leslie] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
[Fendler, Bernard] Florida State Univ, Dept Phys, Tallahassee, FL 32306 USA.
[Bertram, Richard] Florida State Univ, Dept Math, Tallahassee, FL 32306 USA.
[Bertram, Richard] Florida State Univ, Programs Neurosci & Mol Biophys, Tallahassee, FL 32306 USA.
[Peercy, Bradford; Goel, Pranay; Sherman, Arthur] NIDDKD, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
RP Satin, L (reprint author), Univ Michigan, Sch Med, Dept Pharmacol, BSRB,Rm 2037,109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
EM lsatin@umich.edu
RI Goel, Pranay/D-1081-2013;
OI Goel, Pranay/0000-0002-2249-0288
FU National Institutes of Health [RO1-DK-46409B]; American Heart
Association predoctoral fellowship [AHA-0715126B]; National Science
Foundation [DMS-0613179]; National Institutes of Health, National
Institute of Diabetes and Digestive and Kidney Diseases, Intramural
Research Program
FX Work in the Satin lab is supported by National Institutes of Health
grant RO1-DK-46409B. B.F. is supported by American Heart Association
predoctoral fellowship AHA-0715126B. R.B. is supported by National
Science Foundation grant DMS-0613179. A.S., B.P., and P.G. are supported
by the National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases, Intramural Research Program.
NR 92
TC 20
Z9 20
U1 0
U2 4
PU BIOPHYSICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 15
PY 2008
VL 95
IS 10
BP 4676
EP 4688
DI 10.1529/biophysj.107.125088
PG 13
WC Biophysics
SC Biophysics
GA 366YK
UT WOS:000260519300020
PM 18708464
ER
PT J
AU Schechter, AN
AF Schechter, Alan N.
TI Hemoglobin research and the origins of molecular medicine
SO BLOOD
LA English
DT Review
ID SICKLE-CELL-DISEASE; GLOBIN GENE-EXPRESSION; HUMAN FETAL-HEMOGLOBIN;
BETA-THALASSEMIA; NITRIC-OXIDE; ERYTHROID-DIFFERENTIATION;
ALPHA-THALASSEMIA; PHARMACOLOGICAL INDUCTION; CHROMATIN DOMAINS; ANEMIA
AB Much of our understanding of human physiology, and of many aspects of pathology, has its antecedents in laboratory and clinical studies of hemoglobin. Over the last century, knowledge of the genetics, functions, and diseases of the hemoglobin proteins has been refined to the molecular level by analyses of their crystallographic structures and by cloning and sequencing of their genes and surrounding DNA. In the last few decades, research has opened up new paradigms for hemoglobin related to processes such as its role in the transport of nitric oxide and the complex developmental control of the alpha-like and beta-like globin gene clusters. It is noteworthy that this recent work has had implications for understanding and treating the prevalent diseases of hemoglobin, especially the use of hydroxyurea to elevate fetal hemoglobin in sickle cell disease. It is likely that current research will also have significant clinical implications, as well as lessons for other aspects of molecular medicine, the origin of which can be largely traced to this research tradition. (Blood. 2008; 112: 3927-3938)
C1 NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
RP Schechter, AN (reprint author), NIDDK, Mol Med Branch, NIH, Bldg 10,9N-314, Bethesda, MD 20892 USA.
EM aschecht@helix.nih.gov
OI Schechter, Alan N/0000-0002-5235-9408
NR 110
TC 110
Z9 123
U1 9
U2 41
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 NOV 15
PY 2008
VL 112
IS 10
BP 3927
EP 3938
DI 10.1182/blood-2008-04-078188
PG 12
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300009
PM 18988877
ER
PT J
AU Wang, HS
Lee, CH
Qi, CF
Tailor, P
Feng, JX
Abbasi, S
Atsumi, T
Morse, HC
AF Wang, Hongsheng
Lee, Chang Hoon
Qi, Chenfeng
Tailor, Prafullakumar
Feng, Jianxun
Abbasi, Sadia
Atsumi, Toru
Morse, Herbert C., III
TI IRF8 regulates B-cell lineage specification, commitment, and
differentiation
SO BLOOD
LA English
DT Article
ID SEQUENCE-BINDING-PROTEIN; TRANSCRIPTION FACTOR PU.1; MYELOID PROGENITOR
CELLS; MOUSE BONE-MARROW; HEMATOPOIETIC PROGENITORS; GENE-EXPRESSION;
DENDRITIC CELLS; FACTOR FAMILY; FACTOR EBF; PRO-B
AB PU.1, IKAROS, E2A, EBF, and PAX5 comprise a transcriptional network that orchestrates B-cell lineage specification, commitment, and differentiation. Here we identify interferon regulatory factor 8 (IRF8) as another component of this complex, and show that it also modulates lineage choice by hematopoietic stem cells (HSCs). IRF8 binds directly to an IRF8/Ets consensus sequence located in promoter regions of Sfpi1 and Ebf1, which encode PU.1 and EBF, respectively, and is associated with transcriptional repression of Sfpi1 and transcriptional activation of Ebf1. Bone marrows of IRF8 knockout mice (IRF8(-/-)) had significantly reduced numbers of pre-pro-B cells and increased numbers of myeloid cells. Although HSCs of IRF8(-/-) mice failed to differentiate to B220(+) B-lineage cells in vitro, the defect could be rescued by transfecting HSCs with wild-type but not with a signaling-deficient IRF8 mutant. In contrast, overexpression of IRF8 in HSC-differentiated progenitor cells resulted in growth inhibition and apoptosis. We also found that IRF8 was expressed at higher levels in pre-pro-B cells than more mature B cells in wild-type mice. Together, these results indicate that IRF8 modulates lineage choice by HSCs and is part of the transcriptional network governing B-cell lineage specification, commitment, and differentiation. (Blood. 2008; 112: 4028-4038)
C1 [Wang, Hongsheng; Lee, Chang Hoon; Qi, Chenfeng; Feng, Jianxun; Abbasi, Sadia; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
[Tailor, Prafullakumar; Atsumi, Toru] NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA.
RP Morse, HC (reprint author), NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
EM wanghongs@niaid.nih.gov; hmorse@niaid.nih.gov
RI Fuller, Stephen/C-1200-2009;
OI Morse, Herbert/0000-0002-9331-3705
FU National Institute of Allergy and Infectious Diseases (NIAID); National
Institute of Child Health and Human Development (NICHD); National
Institutes of Health
FX This work was supported by the Intramural Research Program of National
Institute of Allergy and Infectious Diseases (NIAID) and National
Institute of Child Health and Human Development (NICHD), National
Institutes of Health.
NR 59
TC 65
Z9 67
U1 0
U2 3
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 NOV 15
PY 2008
VL 112
IS 10
BP 4028
EP 4038
DI 10.1182/blood-2008-01-129049
PG 11
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300022
PM 18799728
ER
PT J
AU Lan, Q
Lim, U
Liu, CS
Weinstein, SJ
Chanock, S
Bonner, MR
Virtamo, J
Albanes, D
Rothman, N
AF Lan, Qing
Lim, Unhee
Liu, Chin-San
Weinstein, Stephanie J.
Chanock, Stephen
Bonner, Matthew R.
Virtamo, Jarmo
Albanes, Demetrius
Rothman, Nathaniel
TI Aprospective study of mitochondrial DNA copy number and risk of
non-Hodgkin lymphoma
SO BLOOD
LA English
DT Article
ID OXIDATIVE STRESS; CANCER; CELLS; BIOGENESIS; LEUKOCYTES; INCREASE;
GENOME; ADULT; MTDNA; TRIAL
AB Mitochondrial DNA( mtDNA) copy number is increased in patients with chronic lymphocytic leukemia (CLL), in Burkitt lymphoma and Epstein-Barrvirus-transformed lymphoblastoid cell lines, and in T cells activated via the T-cell receptor. We hypothesized that having a higher mtDNA copy number in peripheral white blood cell DNA from healthy subjects would be associated with future risk of non-Hodgkin lymphoma (NHL). We analyzed mtDNA copy number in 104 incident male NHL cases and 104 matched controls within the prospective Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention cohort. There was a dose-response relationship between tertiles of mtDNA copy number and risk of NHL (odds ratio [OR], 95% confidence interval [CI]: 1.0; 1.4 [0.7-2.8]; and 2.4 [1.0-5.5], respectively; P(trend) = .046). The effect was most pronounced for the CLL/small lymphocytic lymphoma (SLL) subtype (OR: 1.0; 3.2 [0.7-15.7]; 14.1 [1.9-103.2]; P(trend) = .009). These results suggest that mtDNA copy number could be associated with the risk of NHL, particularly CLL/SLL. (Blood. 2008; 112: 4247-4249)
C1 [Lan, Qing] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Lim, Unhee] Canc Res Ctr Hawaii, Program Epidemiol, Honolulu, HI 96813 USA.
[Liu, Chin-San] Changhua Christian Hosp, Dept Neurol, Changhua, Taiwan.
[Liu, Chin-San] Changhua Christian Hosp, Vasc & Genom Res Ctr, Changhua, Taiwan.
[Bonner, Matthew R.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland.
RP Lan, Q (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, MSC 7240,6120 Execut Blvd,EPS 8109, Bethesda, MD 20892 USA.
EM qingl@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU National Cancer Institute (Bethesda, MD); Wen Ling of the Department of
Neurology and Vascular and Genomic Research Center; Changhua Christian
Hospital (Changhua, Taiwan)
FX This work was supported by intramural funds from the National Cancer
Institute (Bethesda, MD). We would like to acknowledge the invaluable
laboratory work carried out by Wen Ling of the Department of Neurology
and Vascular and Genomic Research Center, Changhua Christian Hospital
(Changhua, Taiwan).
NR 23
TC 58
Z9 59
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 NOV 15
PY 2008
VL 112
IS 10
BP 4247
EP 4249
DI 10.1182/blood-2008-05-157974
PG 3
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300046
PM 18711000
ER
PT J
AU Kurtzberg, J
Prasad, VK
Carter, SL
Wagner, JE
Baxter-Lowe, LA
Wall, D
Kapoor, N
Guinan, EC
Feig, SA
Wagner, EL
Kernan, NA
AF Kurtzberg, Joanne
Prasad, Vinod K.
Carter, Shelly L.
Wagner, John E.
Baxter-Lowe, Lee Ann
Wall, Donna
Kapoor, Neena
Guinan, Eva C.
Feig, Stephen A.
Wagner, Elizabeth L.
Kernan, Nancy A.
CA COBLT Steering Comm
TI Results of the Cord Blood Transplantation Study (COBLT): clinical
outcomes of unrelated donor umbilical cord blood transplantation in
pediatric patients with hematologic malignancies
SO BLOOD
LA English
DT Article
ID STEM-CELL TRANSPLANTATION; BONE-MARROW; ACUTE-LEUKEMIA; CHILDREN;
RECONSTITUTION; RECIPIENTS; ADULTS
AB Outcomes of unrelated donor cord blood transplantation in 191 hematologic malignancy children (median age, 7.7 years; median weight, 25.9 kg) enrolled between 1999 and 2003 were studied (median follow-up, 27.4 months) in a prospective phase 2 multicenter trial. Human leukocyte antigen (HLA) matching at enrollment was 6/6 (n = 17), 5/6 (n = 58), 4/6 (n = 111), or 3/6 (n = 5) by low-resolution HLA-A, -B, and high-resolution (HR) DRB1. Retrospectively, 179 pairs were HLA typed by HR. The median precryopreservation total nucleated cell (TNC) dose was 5.1 x 107 TNC/kg (range, 1.5-23.7) with 3.9 x 107 TNC/kg (range, 0.8-22.8) infused. The median time to engraftment (absolute neutrophil count > 500/mm(3) and platelets 50 000/mu L) was 27 and 174 days. The cumulative incidence of neutrophil engraftment by day 42 was 79.9% (95% confidence interval [CI], 75.1%-85.2%); acute grades III/IV GVHD by day 100 was 19.5% ( 95% CI, 13.9%-25.5%); and chronic GVHD at 2 years was 20.8% (95% CI, 14.8%-27.7%). HR matching decreased the probability of severe acute GVHD. The cumulative incidence of relapse at 2 years was 19.9% (95% CI, 14.8%-25.7%). The probabilities of 6-month and 2-year survivals were 67.4% and 49.5%. Unrelated donor cord blood transplantation from partially HLA-mismatched units can cure many children with leukemias. The study was registered at www. clinicaltrials. gov as #NCT00000603. (Blood. 2008; 112: 4318-4327)
C1 [Kurtzberg, Joanne; Prasad, Vinod K.] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Carter, Shelly L.] EMMES Corp, Rockville, MD USA.
[Wagner, John E.] Univ Minnesota, Minneapolis, MN USA.
[Baxter-Lowe, Lee Ann] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wall, Donna] Texas Transplant Inst, San Antonio, TX USA.
[Kapoor, Neena] Childrens Hosp, Los Angeles, CA 90027 USA.
[Guinan, Eva C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Feig, Stephen A.] Mattel Childrens Hosp, Los Angeles, CA USA.
[Wagner, Elizabeth L.] NHLBI, Bethesda, MD 20892 USA.
[Kernan, Nancy A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Kurtzberg, J (reprint author), Duke Univ, Med Ctr, Box 3350, Durham, NC 27710 USA.
EM kurtz001@mc.duke.edu
OI Kernan, Nancy/0000-0003-1417-1823
FU NHLBI NIH HHS [N01-HB 67135, N01-HB 67139, N01-HB-67132, N01HB67132,
N01HB67135, N01HB67138, N01HB67139]
NR 25
TC 178
Z9 188
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 NOV 15
PY 2008
VL 112
IS 10
BP 4318
EP 4327
DI 10.1182/blood-2007-06-098020
PG 10
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300056
PM 18723429
ER
PT J
AU Chu, KC
Chen, MS
Dignan, MB
Taylor, E
Partridge, E
AF Chu, Kenneth C.
Chen, Moon S., Jr.
Dignan, Mark B.
Taylor, Emmanuel
Partridge, Edward
CA Community Network Program Principa
TI Parallels Between the Development of Therapeutic Drugs and Cancer Health
Disparity Programs Implications for Disparities Reduction
SO CANCER
LA English
DT Article
DE therapeutic drugs; cancer health disparity; disparities-reducing
intervention; information dissemination; community-based participatory
research
ID SPECIAL POPULATIONS NETWORKS; TRENDS
AB BACKGROUND. There are analogies between the development of therapeutic drugs for cancer and the development of interventions for reducing cancer health disparities. In both cases, it can take between 12 and 15 years for the benefits to become apparent.
METHODS. The initial preclinical phase of drug development is analogous to the development Of Community partnerships and helping the community learn about cancer. The preclinical phase of in vitro and in vivo testing is analogous to identifying the disparities in the community Then clinical testing begins with phase 1, toxicity, and dose-establishing studies. Analogously, community-based participatory research is used to develop disparities-reducing interventions (DRIs) within the community
RESULTS. The phase 2 clinical Studies to determine whether the drug has activity are analogous to the DRI being implemented in the community to determine whether it can cause behavioral changes that will reduce cancer health disparities. If a drug passes phase 1 and 2 studies, phase 3 clinical trials are initiated. These are controlled studies to examine the efficacy of the drug. The similar activity for disparities research is to determine whether the DRI is better than the current standard/usual practice in controlled trials. If the drug is beneficial, the final phase is the dissemination and adoption of the drug. Analogously in disparities, if the DRI is beneficial, it is disseminated and is culturally adapted to other racial/ethnic groups and finally adopted as standard practice.
CONCLUSIONS. The process of creating an effective DRI can be envisioned to have 4 stages, which can be used to aid in measuring the progress being made in reducing cancer health disparities. Cancer 2008;113:2790-6. Published 2008 by the American Cancer Society.
C1 [Chu, Kenneth C.; Taylor, Emmanuel] NCI, Ctr Reduce Canc Hlth Dispar, Dispar Res Branch, Bethesda, MD 20892 USA.
[Chen, Moon S., Jr.] Univ Calif Davis, Davis Canc Ctr, Dept Internal Med Populat Res & Canc Dispar, Sacramento, CA 95817 USA.
[Dignan, Mark B.] Univ Kentucky, Med Ctr, Lucille P Markey Canc Ctr, Dept Internal Med,Prevent Res Ctr, Lexington, KY 40536 USA.
[Partridge, Edward] Univ Alabama, Ctr Comprehens Canc, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
RP Chu, KC (reprint author), NCI, Ctr Reduce Canc Hlth Dispar, Dispar Res Branch, 6116 Execut Blvd,Room 602,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kc10d@nih.gov
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU Center to Reduce Cancer Health Disparities of the National Cancer
Institute
FX Supported by the Center to Reduce Cancer Health Disparities of the
National Cancer Institute.
NR 16
TC 2
Z9 2
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
BP 2790
EP 2796
DI 10.1002/cncr.23879
PG 7
WC Oncology
SC Oncology
GA 372PV
UT WOS:000260914400021
PM 18780311
ER
PT J
AU Azad, N
Minasian, L
Kohn, E
AF Azad, Nilofer
Minasian, Lori
Kohn, Elise
TI Reply to Lack of Reliability of CA125 Response Criteria With Anti-VEF
Molecularly Targeted Therapy
SO CANCER
LA English
DT Letter
ID CANCER
C1 [Azad, Nilofer; Minasian, Lori; Kohn, Elise] NCI, NIH, Bethesda, MD 20892 USA.
RP Azad, N (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
BP 2833
EP 2834
DI 10.1002/cncr.23894
PG 2
WC Oncology
SC Oncology
GA 372PV
UT WOS:000260914400027
ER
PT J
AU Watson, M
Saraiya, M
Ahmed, F
Cardinez, CJ
Reichman, ME
Weir, HK
Richards, TB
AF Watson, Meg
Saraiya, Mona
Ahmed, Faruque
Cardinez, Cheryll J.
Reichman, Marsha E.
Weir, Hannah K.
Richards, Thomas B.
TI Using Population-based Cancer Registry Data to Assess the Burden of
Human Papillomavirus-associated Cancers in the United States: Overview
of Methods
SO CANCER
LA English
DT Article
DE methods; human papillomavirus; cancer; surveillance
ID SQUAMOUS-CELL CARCINOMA; ANAL CANCER; PARTICLE VACCINE; NATIONAL
PROGRAM; EPIDEMIOLOGY; SURVEILLANCE; ETIOLOGY; WORLDWIDE; INFECTION;
EFFICACY
AB Increased attention to human papillomavirus (HPV)-associated cancers in light of the recent release of an HPV vaccine, as well as increased availability of cancer registry data that now include reporting from a large proportion of the US population, prompted the current assessment of HPV-associated cancers. This article describes methods used to assess the burden of HPV-associated cervical, Vulvar, vaginal, penile, anal, and oral cavity/oropharyngeal cancers in the United States during 1998 through 2003 using cancer registry data, and it provides a brief overview of the epidemiology of these cancers. Cancer 2008;113(10 suppl):2841-54. Published 2008 by the American Cancer Society.*
C1 [Watson, Meg; Saraiya, Mona; Cardinez, Cheryll J.; Weir, Hannah K.; Richards, Thomas B.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA 30341 USA.
[Ahmed, Faruque] Ctr Dis Control & Prevent, Immunizat Serv Div, Atlanta, GA 30341 USA.
[Reichman, Marsha E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Watson, M (reprint author), Ctr Dis Control & Prevent, Div Canc Prevent & Control, 4770 Buford Highway,MS K55, Atlanta, GA 30341 USA.
EM mwatson2@cdc.gov
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 53
TC 97
Z9 98
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 2841
EP 2854
DI 10.1002/cncr.23758
PG 14
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200002
PM 18980203
ER
PT J
AU Ryerson, AB
Peters, ES
Coughlin, SS
Chen, VW
Gillison, ML
Reichman, ME
Wu, XC
Chaturvedi, AK
Kawaoka, K
AF Ryerson, A. Blythe
Peters, Edward S.
Coughlin, Steven S.
Chen, Vivien W.
Gillison, Maura L.
Reichman, Marsha E.
Wu, Xiaocheng
Chaturvedi, Anil K.
Kawaoka, Kelly
TI Burden of Potentially Human Papillomavirus-associated Cancers of the
Oropharynx and Oral Cavity in the US, 1998-2003
SO CANCER
LA English
DT Article
DE cancer; human papillomavirus; oral cancer; oropharyngeal cancer
ID SQUAMOUS-CELL CARCINOMA; UPPER AERODIGESTIVE TRACT; NECK-CANCER;
PHARYNGEAL CANCER; UNITED-STATES; TONSILLAR CANCER; HPV INFECTIONS;
HEAD; EPIDEMIOLOGY; RISK
AB BACKGROUND. As human papillomavirus (HPV) vaccination becomes widely available in the US for cervical cancer prevention, it may also affect the rates of other cancers potentially associated with HPV The objective of the current study was to describe the incidence rates of oropharyngeal and oral cavity cancers in the US with a focus on anatomic sites potentially associated with HPV infection.
METHODS. incident cases diagnosed between 1998 and 2003 identified through 39 population-based registries that participate in the National Program of Cancer Registries and/or the Surveillance, Epidemiology, and End Results Program were examined. The incidence rates of potentially HPV-associated oropharyngeal and oral cavity cancers by various characteristics were estimated. The 1998 through 2003 trends in these rates were also compared with rates for sites not previously shown to be associated with HPV (comparison sites).
RESULTS. In all, 44,160 cases of potentially HPV-associated cancers of the oropharynx and oral cavity were identified, including 19,239 (43.6%) tonsillar, 16,964 (38.4%) base of tongue, and 7957 (18.0%) other oropharyngeal cancers. The incidence rates for these sites were highest among blacks, and higher among non-Hispanics and men than among Hispanics and women. The annual incidence rates of potentially HPV-associated cancers of the tonsil mid base of tongue both increased significantly from 1998 through 2003 (annual percentage change [APC], 3.0; P < .05 for both sites), whereas the incidence rates of cancer at the comparison sites generally decreased.
CONCLUSIONS. The results of the current study provide baseline incidence rates of potentially HPV-associated cancers of the oropharynx and oral cavity that can be compared with rates after the widespread implementation of the HPV vaccination. Cancer 2008;113(10 suppl):2901-9. Published 2008 by the American Cancer Society.*
C1 [Ryerson, A. Blythe; Coughlin, Steven S.; Kawaoka, Kelly] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA 30341 USA.
[Chaturvedi, Anil K.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Reichman, Marsha E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Gillison, Maura L.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Peters, Edward S.; Chen, Vivien W.; Wu, Xiaocheng] Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, Louisiana Tumor Registry,Epidemiol Program, New Orleans, LA USA.
RP Ryerson, AB (reprint author), Ctr Dis Control & Prevent, Div Canc Prevent & Control, Natl Ctr Chron Dis Prevent & Hlth Promot, 4770 Buford Highway NE,K-55, Atlanta, GA 30341 USA.
EM ARyerson@cdc.gov
RI Chaturvedi, Anil/J-2024-2015;
OI Chaturvedi, Anil/0000-0003-2696-8899; /0000-0003-4928-6532
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 50
TC 157
Z9 160
U1 1
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 2901
EP 2909
DI 10.1002/cncr.23745
PG 9
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200008
PM 18980273
ER
PT J
AU Balamurugan, A
Ahmed, F
Saraiya, M
Kosary, C
Schwenn, M
Cokkinides, V
Flowers, L
Pollack, LA
AF Balamurugan, Appathurai
Ahmed, Faruque
Saraiya, Mona
Kosary, Carol
Schwenn, Molly
Cokkinides, Vilma
Flowers, Lisa
Pollack, Lori A.
TI Potential Role of Human Papillomavirus in the Development of Subsequent
Primary In Situ and Invasive Cancers Among Cervical Cancer Survivors
SO CANCER
LA English
DT Article
DE human papillomavirus; human papillomavirus vaccine; cervical cancer;
survivors; prevention; subsequent primary cancer
ID 2ND PRIMARY-CANCER; TEACHABLE MOMENT; RISK; CARCINOMA; VACCINATION;
INFECTION; SMOKING; HEALTH; WOMEN
AB BACKGROUND. The recent licensure of human papillomavirus (HPV) vaccines will likely decrease the development of primary in situ and invasive cervical cancers and possibly other HPV-associated cancers such as vaginal, vulvar, and anal cancers. Because the HPV vaccine has the ability to impact the development of >1 HPV-associated cancer in the same individual, the risk of developing subsequent primary cancers among cervical cancer survivors was examined.
METHODS. Using the 1992 through 2004 data from the Surveillance, Epidemiology, and End Results (SEER) program, 23,509 cervical cancer survivors were followed (mean of 4.8 person-years) for the development of subsequent primary cancers. The observed number (0) of subsequent cancers of all sites were compared with those expected (E) based on age-/race-/year-/site-specific rates in the SEER population. Standardized incidence ratios (SIRs = O/E) were considered statistically significant if they differed from 1, with an a level of 0.05.
RESULTS. Among cervical cancer index cases, there was a significant elevated risk for Subsequent in situ cancers of the vagina and vulva (SIRs of 53.8 and 6.6, respectively); and invasive vaginal, vulvar, and rectal cancers (SIRs of 29.9, 5.7, and 2.2, respectively). Significantly elevated risks were observed across race and ethnic populations for subsequent vaginal in situ (SIR for whites of 49.4; blacks, 52.8; Asian/Pacific Islander [API], 91.4; and Hispanics, 55.7) and invasive cancers (SIR for whites of 25.7; blacks, 34.5; API, 48.5; and Hispanics, 25.2).
CONCLUSIONS. The results of the current Study demonstrate a substantially increased risk of the development of subsequent primary in situ and invasive cancers among cervical cancer survivors and have implications for the development of prevention and early detection strategies as the role of HPV infection becomes evident. Cancer 2008;113(10 suppl):2919-25. Published 2008 by the American Cancer Society.*
C1 [Balamurugan, Appathurai] Arkansas Dept Hlth, Arkansas Cent Canc Registry, Epidemiol Branch, Little Rock, AR 72205 USA.
[Ahmed, Faruque] Ctr Dis Control & Prevent, Immunizat Serv Div, Atlanta, GA USA.
[Saraiya, Mona; Pollack, Lori A.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA USA.
[Kosary, Carol] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Schwenn, Molly] Dept Hlth & Human Serv, Maine Ctr Dis Control & Prevent, Maine Canc Registry, Augusta, ME USA.
[Cokkinides, Vilma] Amer Canc Soc, Dept Epidemiol & Res Surveillance, Atlanta, GA 30329 USA.
[Flowers, Lisa] Emory Univ, Dept Obstet & Gynecol, Atlanta, GA 30322 USA.
RP Balamurugan, A (reprint author), Ctr Publ Hlth Practice, Epidemiol Branch, 4815 W Markham,Slot H-32, Little Rock, AR 72205 USA.
EM Appathurai.Balamurugan@arkansas.gov
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 25
TC 15
Z9 16
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 2919
EP 2925
DI 10.1002/cncr.23746
PG 7
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200010
PM 18980275
ER
PT J
AU Coughlin, SS
Richards, TB
Nasseri, K
Weiss, NS
Wiggins, CL
Saraiya, M
Stinchcomb, DG
Vensor, VM
Nielson, CM
AF Coughlin, Steven S.
Richards, Thomas B.
Nasseri, Kiumarss
Weiss, Nancy S.
Wiggins, Charles L.
Saraiya, Mona
Stinchcomb, David G.
Vensor, Veronica M.
Nielson, Carrie M.
TI Cervical Cancer Incidence in the United States in the US-Mexico Border
Region, 1998-2003
SO CANCER
LA English
DT Article
DE cervical cancer; healthcare access; Hispanics; incidence
ID FOREIGN-BORN WOMEN; AMERICAN WOMEN; METAANALYSIS; BREAST; AGE
AB BACKGROUND. Cervical cancer mortality rates have declined in the United States, primarily because of Papanicolaou testing. However, limited information is available about the incidence of the disease in the US-Mexico border region, where some of the poorest counties in the United States are located. This study was undertaken to help compare the patterns of cervical cancer incidence among women in the US-Mexico border region and other parts of the United States.
METHODS. Age-adjusted cervical cancer incidence rates for border counties in the states bordering Mexico (California, Arizona, New Mexico, Texas) for the years 1998 to 2003 were compared with the rates for nonborder counties of the border states and with those of nonborder states. Differences were examined by age, race, ethnicity, rural residence, educational attainment, poverty, migration, stage of disease, and histology.
RESULTS. Overall, Hispanic women had almost twice the cervical cancer incidence of non-Hispanic women in border counties, and Hispanic women in the border states had higher rates than did non-Hispanic women in nonborder states. In contrast, cervical cancer incidence rates among black women in the border counties were lower than those among black women in the nonborder states. Among white women, however, incidence rates were higher among those in nonborder states. Differences in cervical cancer incidence rates by geographic locality were also evident by age, urban/rural residence, migration from outside the United States, and stage of disease.
CONCLUSIONS. Disparities in cervical cancer incidence in the US-Mexico border counties, when the incidence is compared with that of other counties and geographic regions, are evident. Of particular concern are the higher rates of late-stage cervical cancer diagnosed among women in the border states, especially because such cervical cancer is preventable. Cancer 2008;113(10 suppl):2964-73. Published 2008 by the American Cancer Society.*
C1 [Nielson, Carrie M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Vensor, Veronica M.] Arizona Dept Hlth Serv, Phoenix, AZ 85007 USA.
[Stinchcomb, David G.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Wiggins, Charles L.] Univ New Mexico, New Mexico Tumor Registry, Albuquerque, NM 87131 USA.
[Weiss, Nancy S.] Texas Dept State Hlth Serv, Texas Canc Registry, Austin, TX USA.
[Nasseri, Kiumarss] Calif Canc Registry, Inst Publ Hlth, Santa Barbara, CA USA.
[Coughlin, Steven S.; Richards, Thomas B.; Saraiya, Mona] Ctr Dis Control & Prevent, Epidemiol & Appl Res Branch, Div Canc Prevent & Control, Atlanta, GA USA.
RP Coughlin, SS (reprint author), Dept Vet Affairs, Environm Epidemiol Serv 135, 810 Vermont Ave NW, Washington, DC 20420 USA.
EM steven.coughlin@va.gov
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 27
TC 15
Z9 15
U1 0
U2 8
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 2964
EP 2973
DI 10.1002/cncr.23748
PG 10
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200015
PM 18980280
ER
PT J
AU Tiro, JA
Saraiya, M
Jain, N
Liddon, N
Cokkinides, V
Lai, SM
Breen, N
Wideroff, L
AF Tiro, Jasmin A.
Saraiya, Mona
Jain, Nidhi
Liddon, Nicole
Cokkinides, Vilma
Lai, Sue Min
Breen, Nancy
Wideroff, Louise
TI Human Papillomavirus and Cervical Cancer Behavioral Surveillance in the
US
SO CANCER
LA English
DT Article
DE cervical cancer; behavioral surveillance; human papillomavirus;
Papanicolaou test use
ID 2006 CONSENSUS GUIDELINES; HEALTH INTERVIEW SURVEY; EARLY-DETECTION
PROGRAM; HIGH-SCHOOL-STUDENTS; UNITED-STATES; TELEPHONE SURVEY;
SOCIOECONOMIC-STATUS; SOCIETY GUIDELINE; SEXUAL-BEHAVIOR;
SCREENING-TESTS
AB In the US, federal and state behavioral surveillance systems routinely monitor self-reported sexual behavior and Papanicolaou (Pap) test use to identify high-risk populations, trends, and disparities and to guide and evaluate interventions for cervical cancer prevention and control. Clinical uptake of human papillomavirus (HPV) vaccination and testing necessitates the expansion of behavioral surveillance systems. Cervical disease is the main focus of HPV-related behavioral surveillance because of greater cancer incidence and mortality relative to other susceptible organs, and the availability of effective technologies for prevention and control. In the current Study, a framework is presented for the types of behaviors to monitor, their conceptual and operational definitions, target Populations, and evidence supporting the reliability and validity of self-report measures. An overview is also provided of 8 population-based and 2 provider-based data systems that are nationally representative and accessible for behavioral Surveillance research. Ongoing surveillance at the national, state, and local level is critical for monitoring the dissemination of HPV technologies and their impact on reducing disparities in the detection of precursor lesions, incidence of invasive cancer, and mortality. Cancer 2008;113(10 suppl):3013-30. Published 2008 by the American Cancer Society.*
C1 [Tiro, Jasmin A.] Univ Texas SW Med Ctr Dallas, Dept Clin Sci, Div Behav & Commun Sci, Dallas, TX 75390 USA.
[Saraiya, Mona] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA USA.
[Jain, Nidhi] Ctr Dis Control & Prevent, Immunizat Serv Div, Atlanta, GA USA.
[Liddon, Nicole] Ctr Dis Control & Prevent, Div Sexually Transmitted Dis Prevent, Atlanta, GA USA.
[Cokkinides, Vilma] Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA.
[Lai, Sue Min] Univ Kansas, Med Ctr, Dept Prevent Med, Kansas City, KS 66103 USA.
[Breen, Nancy; Wideroff, Louise] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Tiro, JA (reprint author), Univ Texas SW Med Ctr Dallas, Dept Clin Sci, Div Behav & Commun Sci, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM jasmin.tiro@utsouthwestern.edu
RI Hernandez, Jessica/G-6527-2011;
OI Tiro, Jasmin/0000-0001-8300-0441
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 84
TC 20
Z9 20
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 3013
EP 3030
DI 10.1002/cncr.23760
PG 18
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200020
PM 18980284
ER
PT J
AU Castle, PE
Solomon, D
Saslow, D
Schiffman, M
AF Castle, Philip E.
Solomon, Diane
Saslow, Debbie
Schiffman, Mark
TI Predicting the Effect of Successful Human Papillomavirus Vaccination on
Existing Cervical Cancer Prevention Programs in the United States
SO CANCER
LA English
DT Article
DE cervical abnormalities; colposcopy-guided biopsy; oncogenic human
papillomavirus testing; positive predictive value; prevention;
screening; viral-like particle vaccines
ID RANDOMIZED CONTROLLED-TRIAL; LIQUID-BASED CYTOLOGY; QUADRIVALENT
VACCINE; SOCIETY GUIDELINE; PARTICLE VACCINE; SCREENING-TESTS;
YOUNG-WOMEN; NEOPLASIA; INFECTION; LESIONS
AB The development of a prophylactic human papillomavirus (HPV) vaccine that potentially may eliminate a majority of cervical cancers is a landmark in cancer prevention. Cervical screening, however, will continue to play an important role for the foreseeable future. Maintaining screening at the same intensity and simply adding on the expense of vaccination would result in redundancy of prevention efforts at enormously increased costs without necessarily further reducing cervical cancer mortality. Effectively integrating vaccination and screening efforts will be a critical and evolving challenge over the next decade; this will require understanding not only the impact of vaccination on reducing cervical abnormalities but also the influence of vaccination on screening test performance. Cancer 2008;113(10 suppl):3031-5. Published 2008 by the American Cancer Society.*
C1 [Solomon, Diane] NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Castle, Philip E.; Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Saslow, Debbie] Amer Canc Soc, Atlanta, GA 30329 USA.
RP Solomon, D (reprint author), NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, EPN Room 2130,6130 Execut Blvd, Rockville, MD 20852 USA.
EM ds87v@nih.gov
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04];
National Cancer Institute (NCI)
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).; A National Cancer Institute (NCI)-sponsored clinical trial of
the GlaxoSmithKline (GSK) human papillomavirus vaccine receives vaccine
from the manufacturer (GSK) at no cost. GSK also provides support for
aspects of the trial associated with regulatory submission needs to the
US Federal Drug Administration.
NR 31
TC 14
Z9 14
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 3031
EP 3035
DI 10.1002/cncr.23762
PG 5
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200021
PM 18980285
ER
PT J
AU Gillison, ML
Chaturvedi, AK
Lowy, DR
AF Gillison, Maura L.
Chaturvedi, Anil K.
Lowy, Douglas R.
TI HPV Prophylactic Vaccines and the Potential Prevention of Noncervical
Cancers in Both Men and Women
SO CANCER
LA English
DT Article
DE human papillomavirus; screening; noncervical cancer; HPV vaccine
ID SQUAMOUS-CELL CARCINOMA; HUMAN-PAPILLOMAVIRUS DNA; RANDOMIZED
CONTROLLED-TRIAL; RISK HUMAN-PAPILLOMAVIRUS; VULVAR CARCINOMA; PENILE
CANCER; ANAL CANCER; CERVICAL-CANCER; PROGNOSTIC-SIGNIFICANCE;
QUADRIVALENT VACCINE
AB Human papillomavirus (HPV) is a necessary cause of cervical cancer. In addition, on the basis of the fulfillment of a combination of viral as well as epidemiological criteria, it is currently accepted that a proportion of anal, oropharyngeal, vulvar, and vaginal cancers among women and anal, oropharyngeal, and penile cancers among men are etiologically related to HPV At these noncervical sites with etiologic heterogeneity HPV-associated cancers represent a distinct clinicopathological entity, which is generally characterized by a younger age at onset, basaloid or warty histopathology, association with sexual behavior, and better prognosis, when compared with their HPV-negative counterparts. Currently available estimates indicate that the number of HPV-associated noncervical cancers diagnosed annually in the US roughly approximates the number of cervical cancers, with an equal number of noncervical cancers among men and women. Furthermore, whereas the incidence of cervical cancers has been decreasing over time, the incidence of anal and oropharyngeal cancers, for which there are no effective or widely used screening programs, has been increasing in the US. The efficacy of HPV vaccines in preventing infection at sites other than the cervix, vagina, and vulva should, therefore, be assessed (eg, oral and anal). Given that a substantial proportion of cervical cancers (approximately 70%) and an even greater proportion of HPV-associated noncervical cancers (approximately 86% to 95%) are caused by HPV16 and 18 (HPV types that are targeted by the currently available vaccines), current HPV vaccines may hold great promise (provided equivalent efficacy at all relevant anatomic sites) in reducing the burden of HPV-associated noncervical cancers, in addition to cervical cancers. Cancer 2008;113(10 suppl):3036-46. Published 2008 by the American Cancer Society.*
C1 [Gillison, Maura L.] Johns Hopkins Kimmel Canc Ctr, Div Viral Oncol, Baltimore, MD USA.
[Chaturvedi, Anil K.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lowy, Douglas R.] NCI, Cellular Oncol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Gillison, ML (reprint author), Johns Hopkins Univ, Canc Res Bldg 1,Rm 3M 54A,1650 Orleans St, Baltimore, MD 21231 USA.
EM gillima@jhmi.edu
RI Chaturvedi, Anil/J-2024-2015
OI Chaturvedi, Anil/0000-0003-2696-8899
FU Centers for Disease Control and Prevention (CDC) [U50 DP424071-04]
FX This supplement to Cancer was supported by Cooperative Agreement Number
U50 DP424071-04 from the Centers for Disease Control and Prevention
(CDC).
NR 70
TC 184
Z9 193
U1 1
U2 15
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
SU S
BP 3036
EP 3046
DI 10.1002/cncr.23764
PG 11
WC Oncology
SC Oncology
GA 372QC
UT WOS:000260915200022
PM 18980286
ER
PT J
AU Shin, DM
Shaffer, DJ
Wang, HS
Roopenian, DC
Morse, HC
AF Shin, Dong-Mi
Shaffer, Daniel J.
Wang, Hongsheng
Roopenian, Derry C.
Morse, Herbert C., III
TI NOTCH Is Part of the Transcriptional Network Regulating Cell Growth and
Survival in Mouse Plasmacytomas
SO CANCER RESEARCH
LA English
DT Article
ID ZONE B-CELLS; MALIGNANT PLASMA-CELLS; MULTIPLE-MYELOMA; C-MYC;
GENE-EXPRESSION; IN-VIVO; BONE-MARROW; LYMPHOMA; MICE; DIFFERENTIATION
AB Aside from Myc-activating translocations characteristic of plasmacytomas (PCT), little is known about genetic factors and signaling pathways responsible for the development of spontaneous B-cell lineage lymphomas of mice. Here, we characterized the transcriptional profiles of PCT, centroblastic diffuse large B-cell lymphomas (CBI,), and high-grade splenic marginal zone B-cell lymphoma (MZL++) using high-throughput quantitative reverse transcription-PCR. Expression profiles of CBL and MZL++ were strikingly similar and quite unlike that of PCT. Among the genes expressed at significantly higher levels by PCT were a number involved in NOTCH signaling, a finding supported by gene set enrichment analyses of microarray data. To investigate the importance of this pathway, NOTCH signaling was blocked in PCT cell lines by treatment with a gamma-secretase inhibitor (GSI) or transduction of a dominant-negative mutant of MAMLI. These treatments resulted in reduced expression of NOTCH transcriptional targets in association with impaired proliferation and increased apoptosis. GSI treatment of transformed plasma cells in a primary PCT also induced apoptosis. These results integrate NOTCH activation with oncogenic signaling pathways downstream of translocated Myc in the pathogenesis of mouse PCT, two signaling pathways also implicated in development of human multiple myeloma and T-cell lymphoblastic lymphoma. [Cancer Res 2008;68(22):9202-11]
C1 [Shin, Dong-Mi; Wang, Hongsheng; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
[Shaffer, Daniel J.; Roopenian, Derry C.] Jackson Lab, Bar Harbor, ME 04609 USA.
RP Morse, HC (reprint author), NIAID, Immunopathol Lab, NIH, 5640 Fishers Lane,Room 1421, Rockville, MD 20852 USA.
EM hmorse@niaid.nih.gov
OI Morse, Herbert/0000-0002-9331-3705
FU NIH [DK56597, RO1A128802]; National Institute of Allergy and Infectious
Diseases
FX Grant support: Intramural Research Program of the NIH, National
Institute of Allergy and Infectious Diseases, and NIH grants DK56597 and
RO1A128802) (D.C. Roopenian).; The costs of publication of this article
were defrayed in part by the payment. of page charges. This article must
therefore be hereby marked advertisement in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact.; We thank Drs. Siegfried
Janz. Alexander Kovalchuk. Janet Hartley, and Torgny N. Fredrickson for
providing materials, histologic studies of mouse lymphomas, and many
helpful discussions and Drs. Zohreh Naghashfar and Chang Hoon Lee for
microarray hybridization and technical advice.
NR 50
TC 16
Z9 18
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9202
EP 9211
DI 10.1158/0008-5472.CAN-07-6555
PG 10
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600015
PM 19010892
ER
PT J
AU Cross, AJ
Leitzmann, MF
Subar, AF
Thompson, FE
Hollenbeck, AR
Schatzkin, A
AF Cross, Amanda J.
Leitzmann, Michael F.
Subar, Amy F.
Thompson, Frances E.
Hollenbeck, Albert R.
Schatzkin, Arthur
TI A Prospective Study of Meat and Fat Intake in Relation to Small
Intestinal Cancer
SO CANCER RESEARCH
LA English
DT Article
ID HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; SERVICES-TASK-FORCE;
N-NITROSO COMPOUNDS; COLORECTAL-CANCER; RISK-FACTORS; SMALL-BOWEL;
GASTROINTESTINAL CANCERS; NATIONAL-INSTITUTES; PRIMARY PREVENTION
AB Diets high in red and processed meats are associated with carcinogenesis of the large intestine, but no prospective study has examined meat and fat intake in relation to cancer of the small intestine. We prospectively investigated meat and fat intakes, estimated from a food frequency questionnaire, in relation to small intestinal cancer among half a million men and women enrolled in the NIH-AARP Diet and Health Study. We used Cox proportional hazards regression to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). During up to 8 years of follow-up, 60 adenocarcinomas and 80 carcinoid tumors of the small intestine were diagnosed. Despite slightly elevated HRs for red meat, there were no clear associations for red or processed meat intake and either adenocarcinoma or carcinoid tumors of the small intestine. In contrast, we noted a markedly elevated risk for carcinoid tumors of the small intestine with saturated fat intake in both the categorical (highest versus lowest tertile: HR, 3.18; 95% CI, 1.62-6.25) and continuous data (HR, 3.72; 95% CI, 1.79-7.74 for each 10-g increase in intake per 1,000 kcal). Our findings suggest that the positive associations for meat intake reported in previous case-control studies may partly be explained by saturated fat intake. [Cancer Res 2008;68(22):9274-9]
C1 [Cross, Amanda J.; Leitzmann, Michael F.; Schatzkin, Arthur] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Subar, Amy F.; Thompson, Frances E.] NCI, Risk Factor Methods & Monitoring Branch, Appl Res Program, Div Canc Control & Populat Sci,NIH,Dept Hlth & Hu, Rockville, MD 20852 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Cross, AJ (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM crossa@mail.nih.gov
FU National Cancer Institute; NIH, Department of Health and Human Services
FX Grant support: Intramural Research Program of the National Cancer
Institute, NIH, Department of Health and Human Services.; Cancer
incidence data from the Atlanta metropolitan area were collected by the
Georgia Center for Cancer Statistics, Department of Epidemiology,
Rollins School of Public Health, Emory University. Cancer incidence data
from California were collected 1)), the California Department of Health
Services, Cancer Surveillance Section. Cancer incidence data from the
Detroit metropolitan area were collected by the Michigan Cancer
Surveillance Program, Community Health Administration, State of
Michigan. The Florida cancer incidence data used in this report were
collected by the Florida Cancer Data System tinder contract to the
Department of Health. The views expressed herein are solely those of the
authors and do not necessarily reflect those of the contractor or
Department of Health. Cancer incidence data from Louisiana were
collected by the Louisiana Tumor Registry, Louisiana State University
Medical Center in New Orleans. Cancer incidence data from New Jersey
were collected by the New Jersey State Cancer Registry, Cancer
Fpidemiology Services, New Jersey State Department of Health and Senior
Services. Cancer incidence data from North Carolina were collected by
the North Carolina Central Cancer Registry. Cancer incidence data from
Pennsylvania were Supplied by the Division of Health Statistics and
Research, Pennsylvania Department of Health, Harrisburg, Pennsylvania.
The Pennsylvania Department of Health specifically disclaims
responsibility for any analyses, interpretations or conclusions.; The
costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
advertisement in accordance with IS U.S.C. Section 1734 solely to
indicate this fact.; We thank the participants in the NIH-AARP Diet and
Health Study for their outstanding cooperation.
NR 40
TC 19
Z9 20
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9274
EP 9279
DI 10.1158/0008-5472.CAN-08-2015
PG 6
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600023
PM 19010900
ER
PT J
AU Joshi, BH
Leland, P
Calvo, A
Green, JE
Puri, RK
AF Joshi, Bharat H.
Leland, Pamela
Calvo, Alfonso
Green, Jeffrey E.
Puri, Raj K.
TI Human Adrenomedullin Up-regulates Interleukin-13 Receptor alpha 2 Chain
in Prostate Cancer In vitro and In vivo: A Novel Approach to Sensitize
Prostate Cancer to Anticancer Therapy
SO CANCER RESEARCH
LA English
DT Article
ID CHIMERIC FUSION PROTEINS; CELL CARCINOMA-CELLS; HUMAN GLIOMA-CELLS;
PSEUDOMONAS EXOTOXIN; IL-13 RECEPTOR; SIGNAL-TRANSDUCTION; PANCREATIC
TUMORS; GENE-TRANSFER; MUTATED FORM; EXPRESSION
AB Interleukin-13 (IL-13) receptor alpha 2 (IL-13R alpha 2), a high-affinity IL-13 binding subunit and a tumor antigen, is amplified in a variety of human tumor cell lines and tumors in vivo. By cDNA microarray, we have shown that gene transfer of human and rat adrenomedullin (AM) up-regulates IL-13R alpha 2 in a human prostate tumor cell line. Here, we show that IL-13R alpha 2 mRNA and protein are also up-regulated in PC-3 prostate tumor cells by recombinant AM (rAM) and human synthetic AM peptide in a dose-dependent manner in vitro and in vivo in mouse prostate tumor model. The 8- to 10-fold up-regulation of IL-13R alpha 2 by rAM or AM peptide in prostate tumor cells in vitro and in vivo increased their sensitivity to IL-13PE cytotoxin consisting of IL-13 and a truncated form of Pseudomonas exotoxin. Immunodeficient mice with established prostate tumors transfected with AM or treated with AM peptide showed reduction in tumor size by intra-tumoral administration of IL-13PE in a dose-dependent manner. At the highest dose (three 100 mu g/kg/d every alternate day), >70% reduction of tumor size was observed compared with controls (P <= 0.01). These results indicate that two completely unrelated hormones (AM and IL-13) are closely related to each other and that we have identified a novel role of AM in sensitizing certain types of prostate tumors to IL-13R-directed therapeutic agent. [Cancer Res 2008;68(22):9311-7]
C1 [Joshi, Bharat H.; Leland, Pamela; Puri, Raj K.] US FDA, Tumor Vaccines & Biotechno Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
[Green, Jeffrey E.] NCI, Cell Biol & Genet Lab, NIH, Bethesda, MD 20892 USA.
[Calvo, Alfonso] Univ Navarra, Dept Histol & Pathol, E-31080 Pamplona, Spain.
RP Puri, RK (reprint author), US FDA, Tumor Vaccines & Biotechno Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, NIH Bldg 29B,Room 2NN20,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM raj.puri@fda.hhs.gov
FU Intramural Program of the NIH; Center for Cancer Research; National
Cancer Institute and FDA; Center for Biologies Evaluation and Research
FX Grant support: Intramural Program of the NIH, Center for Cancer
Research, National Cancer Institute and FDA, Center for Biologies
Evaluation and Research.
NR 37
TC 9
Z9 9
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9311
EP 9317
DI 10.1158/0008-5472.CAN-08-2810
PG 7
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600027
PM 19010904
ER
PT J
AU Inthal, A
Krapf, G
Beck, D
Joas, R
Kauer, MO
Orel, L
Fuka, G
Mann, G
Panzer-Grumayer, ER
AF Inthal, Andrea
Krapf, Gerd
Beck, Dominik
Joas, Ruth
Kauer, Max O.
Orel, Lukas
Fuka, Gerhard
Mann, Georg
Panzer-Gruemayer, E. Renate
TI Role of the Erythropoietin Receptor in ETV6/RUNX1-Positive Acute
Lymphoblastic Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CHILDHOOD ACUTE-LEUKEMIA; EXPRESSION PATTERNS; FUSION PROTEIN;
STEM-CELLS; IN-VITRO; TEL-AML1; CANCER; T(12/21); CHILDREN; TEL/AML1
AB Purpose: We explored the mechanisms leading to the distinct overexpression of EPOR as well as the effects of EPO signaling on ETV6/RUNX1-positive acute lymphoblastic leukemias.
Experimental Design: ETV6/RUNX1-expressing model cell lines and leukemic cells were used for real-time PCR of EPOR expression. Proliferation, viability, and apoptosis were analyzed on cells exposed to EPO, prednisone, or inhibitors of EPOR pathways by [3 H]thymidine incorporation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and Annexin V/propidium iodide staining. Western blot analysis was done to detect activation of signaling proteins. Serum EPO levels and sequences of the EPOR (n = 53) as well as hemoglobin levels were taken from children with acute lymphoblastic leukemia enrolled in Austrian protocols.
Results: We show here that ectopic expression of ETV6/RUNX1 induced EPOR up-regulation. Anemia, however, did not appear to influence EPOR expression on leukemic cells, although children with ETV6/RUNX1-positive leukemias had a lower median hemoglobin than controls. Exposure to EPO increased proliferation and survival of ETV6/RUNX1-positive leukemias in vitro, whereas blocking its binding site did not alter cell survival. The latter was not caused by activating mutations in the EPOR but might be triggered by constitutive activation of phosphatidylinositol 3-kinase/Akt, the major signaling pathway of EPOR in these cells. Moreover, prednisone-induced apoptosis was attenuated in the presence of EPO in this genetic subgroup.
Conclusions: Our data suggest that ETV6/RUNX1 leads to EPOR up-regulation and that activation by EPO might be of relevance to the biology of this leukemia subtype. Further studies are, however, needed to assess the clinical implications of its apoptosis-modulating properties.
C1 [Inthal, Andrea; Krapf, Gerd; Beck, Dominik; Joas, Ruth; Kauer, Max O.; Orel, Lukas; Fuka, Gerhard; Panzer-Gruemayer, E. Renate] St Anna Kinderkrebsforsch, Childrens Canc Res Inst, A-1090 Vienna, Austria.
[Mann, Georg; Panzer-Gruemayer, E. Renate] St Anna Childrens Hosp, Vienna, Austria.
[Kauer, Max O.] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Panzer-Grumayer, ER (reprint author), St Anna Kinderkrebsforsch, Childrens Canc Res Inst, Kinderspitalgasse 6, A-1090 Vienna, Austria.
EM renate.panzer@ccri.at
FU Department of Laboratory Medicine, Medical University of Vienna for EPO
analysis; Uli Potschger
FX We thank Prof. Christian Bieglmayer (Department of Laboratory Medicine,
Medical University of Vienna) for EPO analysis, Uli Potschger for
support in statistical evaluations, Andreas Heitger and ldriss
Benanni-Baiti for fruitful discussions, and Marion Zavadil for
proofreading the article.
NR 43
TC 18
Z9 21
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7196
EP 7204
DI 10.1158/1078-0432.CCR-07-5051
PG 9
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500007
PM 19010836
ER
PT J
AU Pastorino, F
Di Paolo, D
Piccardi, F
Nico, B
Ribatti, D
Daga, A
Baio, G
Neumaier, CE
Brignole, C
Loi, M
Marimpietri, D
Pagnan, G
Cilli, M
Lepekhin, EA
Garde, SV
Longhi, R
Corti, A
Allen, TM
Wu, JJ
Ponzoni, M
AF Pastorino, Fabio
Di Paolo, Daniela
Piccardi, Feclerica
Nico, Beatrice
Ribatti, Domenico
Daga, Antonio
Baio, Gabriella
Neumaier, Carlo E.
Brignole, Chiara
Loi, Monica
Marimpietri, Danilo
Pagnan, Gabriella
Cilli, Michele
Lepekhin, Eugene A.
Garde, Seema V.
Longhi, Renato
Corti, Angelo
Allen, Theresa M.
Wu, Jinzi J.
Ponzoni, Mirco
TI Enhanced Antitumor Efficacy of Clinical-Grade Vasculature-Targeted
Liposomal Doxorubicin
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HUMAN NEUROBLASTOMA; BLOOD-VESSELS; THERAPEUTIC-EFFICACY; ANGIOGENIC
SWITCH; CANCER; GROWTH; CHEMOTHERAPY; DRUGS; CELLS; PHARMACOKINETICS
AB Purpose: In vivo evaluation of good manufacturing practice-grade targeted liposomal doxorubicin (TVT-DOX), bound to a CD13 isoform expressed on the vasculature of solid tumors, in human tumor xenografts of neuroblastoma, ovarian cancer, and lung cancer.
Experimental Design: Mice were implanted with lung, ovarian, or neuroblastoma tumor cells via the pulmonary, peritoneal, or orthotopic (adrenal gland) routes, respectively, and treated, at different days post inoculation, with multiple doses of doxorubicin, administered either free or encapsulated in untargeted liposomes (Caelyx) or in TVT-DOX. The effect of TVT-DOX treatment on tumor cell proliferation, viability, apoptosis, and angiogenesis was studied by immunohistochemical analyses of neoplastic tissues and using the chick embryo choriciallantoic membrane assay.
Results: Compared with the three control groups (no doxorubicin, free doxorubicin, or Caelyx), statistically significant improvements in survival was seen in all three animal models following treatment with 5 mg/kg (maximum tolerated dose) of TVT-DOX, with long-term survivors occurring in the neuroblastoma group; increased survival was also seen at a dose of 1.7 mg/kg in mice bearing neuroblastoma or ovarian cancer. Minimal residual disease after surgical removal of neuroblastoma primary mass, and the enhanced response to TVT-DOX, was visualized and quantified by bioluminescence imaging and with magnetic resonance imaging. When treated with TVT-DOX, compared with Caelyx, all three tumor models, as assayed by immunohistochernistry and choriciallantoic membrane, showed statistically significant reductions in cell proliferation, blood vessel density, and microvessel area, showing increased cell apoptosis.
Conclusion: TVT-DOX should be evaluated as a novel angiostatic strategy for adjuvant therapy of solid tumors.
C1 [Pastorino, Fabio; Di Paolo, Daniela; Brignole, Chiara; Loi, Monica; Marimpietri, Danilo; Pagnan, Gabriella; Ponzoni, Mirco] G Gaslini Childrens Hosp, Expt Therapies Unit, Lab Oncol, I-16148 Genoa, Italy.
[Piccardi, Feclerica; Cilli, Michele] Natl Canc Inst, Anim Res Facil, Genoa, Italy.
[Daga, Antonio] Natl Canc Inst, Gene Transfer Lab, Genoa, Italy.
[Baio, Gabriella; Neumaier, Carlo E.] Natl Canc Inst, Dept Radiol, Genoa, Italy.
[Nico, Beatrice; Ribatti, Domenico] Univ Bari, Dept Human Anat, Bari, Italy.
[Lepekhin, Eugene A.; Garde, Seema V.; Wu, Jinzi J.] Ambrilia Biopharma Inc, Verdun, PQ, Canada.
[Longhi, Renato] CNR, Ist Chim Riconoscimento Mol, Milan, Italy.
[Corti, Angelo] Ist Sci San Raffaele, Immunobiotechnol Unit, I-20132 Milan, Italy.
[Allen, Theresa M.] Univ Alberta, Dept Pharmacol, Edmonton, AB, Canada.
RP Pastorino, F (reprint author), G Gaslini Childrens Hosp, Expt Therapies Unit, Lab Oncol, I-16148 Genoa, Italy.
EM fabiopastorino@ospedale-gaslini.ge.it
RI Daga, Antonio/C-3041-2008; Corti, Angelo/F-7046-2012; Baio,
Gabriella/M-7621-2015; Di Paolo, Daniela/J-7681-2016; Ponzoni,
Mirco/J-7713-2016;
OI Corti, Angelo/0000-0002-0893-6191; Baio, Gabriella/0000-0002-8397-5318;
Di Paolo, Daniela/0000-0001-7264-6888; Ponzoni,
Mirco/0000-0002-6164-4286; Subba, Rajkrishna/0000-0003-0051-0062; Daga,
Antonio/0000-0001-5845-8530
FU Fondazione Italiana per la Lotta al Neuroblastoma; Associazione Italiana
Ricerca Cancro; Italian Ministry of Health; Fondazione Italiana per la
Lotta
FX Ambrilia Biopharma, Fondazione Italiana per la Lotta al Neuroblastoma,
Associazione Italiana Ricerca Cancro [MFAG (F. Pastorino) and IG (M.
Ponzoni)], and Italian Ministry of Health; Fondazione Italiana per la
Lotta Neuroblastoma fellowship (F. Pastorino and G. Pagnan); Fondazione
Italiana Ricerca Cancro fellowship (D. Di Paolo); and Master&Back
Regione Autonoma Sardegna fellowship (M. Loi).
NR 52
TC 47
Z9 48
U1 2
U2 19
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7320
EP 7329
DI 10.1158/1078-0432.CCR-08-0804
PG 10
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500020
PM 19010847
ER
PT J
AU Gill, RK
Vazquez, MF
Kramer, A
Hames, M
Zhang, LJ
Heselmeyer-Haddad, K
Ried, T
Shilo, K
Henschke, C
Yankelevitz, D
Jen, J
AF Gill, Rajbir K.
Vazquez, Madeline F.
Kramer, Arin
Hames, Megan
Zhang, Lijuan
Heselmeyer-Haddad, Kerstin
Ried, Thomas
Shilo, Konstantin
Henschke, Claudia
Yankelevitz, David
Jen, Jin
TI The Use of Genetic Markers to Identify Lung Cancer in Fine Needle
Aspiration Samples
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID IN-SITU HYBRIDIZATION; COMPARATIVE GENOMIC HYBRIDIZATION; SQUAMOUS-CELL
CARCINOMAS; INTERPHASE CYTOGENETICS; CHROMOSOME-ABERRATIONS;
COMPUTED-TOMOGRAPHY; TUMOR-CELLS; DNA GAINS; CT; ADENOCARCINOMA
AB Purpose: We seek to establish a genetic test to identify lung cancer using cells obtained through computed tomography-guided fine needle aspiration (FNA).
Experimental Design: We selected regions of frequent copy number gains in chromosomes 1q32, 3q26, 5p15, and 8q24 in non-small cell lung cancer and tested their ability to determine the neoplastic state of cells obtained by FNA using fluorescent in situ hybridization. Two sets of samples were included. The pilot set included six paraffin-embedded, noncancerous lung tissues and 33 formalin-fixed FNA specimens. These 39 samples were used to establish the optimal fixation and single scoring criteria for the samples. The test set included 40 FNA samples. The results of the genetic test were compared with the cytology, pathology, and clinical follow-up for each case to assess the sensitivity and specificity of the genetic test.
Results: Nontumor lung tissues had <= 4 signals per nucleus for all tested markers, whereas tumor samples had >= 5 signals per nucleus in five or more cells for at least one marker. Among the 40 testing cases, 36 of 40 (90%) FNA samples were analyzable. Genetic analysis identified 15 cases as tumor and 21 cases as nontumor. Clinical and pathologic diagnoses confirmed the genetic test in 15 of 16 lung cancer cases regardless of tumor subtype, stage, or size and in 20 of 20 cases diagnosed as benign lung diseases.
Conclusions: A set of only four genetic markers can distinguish the neoplastic state of lung lesion using small samples obtained through computed tomography-guided FNA.
C1 [Gill, Rajbir K.; Hames, Megan; Jen, Jin] NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Heselmeyer-Haddad, Kerstin; Ried, Thomas] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Vazquez, Madeline F.; Kramer, Arin; Zhang, Lijuan; Henschke, Claudia; Yankelevitz, David] Cornell Univ, Weill Med Coll, Early Lung Canc Act Program, New York, NY 10021 USA.
[Vazquez, Madeline F.; Kramer, Arin; Zhang, Lijuan; Henschke, Claudia; Yankelevitz, David] Cornell Univ, Weill Med Coll, Dept Pathol & Lab Med, New York, NY 10021 USA.
[Shilo, Konstantin] Armed Forces Inst Pathol, Washington, DC 20306 USA.
RP Jen, J (reprint author), Mayo Clin & Mayo Fdn, Div Pulm & Crit Care Med & Microarray Share Resou, 200 1st St,SW, Rochester, MN 55905 USA.
EM Jen.Jin@Mayo.edu
RI Shilo, Konstantin/E-4084-2011;
OI S, K/0000-0002-6702-3130
FU Intramural research funds from the Center for Cancer Research; National
Cancer Institute
FX Grant support: Intramural research funds from the Center for Cancer
Research, National Cancer Institute.
NR 40
TC 10
Z9 10
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7481
EP 7487
DI 10.1158/1078-0432.CCR-07-5242
PG 7
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500039
PM 19010865
ER
PT J
AU Greene, MH
Feng, ZD
Gail, MH
AF Greene, Mark H.
Feng, Ziding
Gail, Mitchell H.
TI The Importance of Test Positive Predictive Value in Ovarian Cancer
Screening
SO CLINICAL CANCER RESEARCH
LA English
DT Letter
C1 [Greene, Mark H.] NCI, Clin Genet Branch, Rockville, MD USA.
[Feng, Ziding] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Gail, Mitchell H.] NCI, Biostat Branch, Rockville, MD USA.
RP Greene, MH (reprint author), NCI, Clin Genet Branch, Rockville, MD USA.
NR 5
TC 15
Z9 15
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7574
EP 7575
DI 10.1158/1078-0432.CCR-08-2232
PG 2
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500052
PM 18948386
ER
PT J
AU Kamiya, N
Ye, L
Kobayashi, T
Mochida, Y
Yamauchi, M
Kronenberg, HM
Feng, JQ
Mishina, Y
AF Kamiya, Nobuhiro
Ye, Ling
Kobayashi, Tatsuya
Mochida, Yoshiyuki
Yamauchi, Mitsuo
Kronenberg, Henry M.
Feng, Jian Q.
Mishina, Yuji
TI BMP signaling negatively regulates bone mass through sclerostin by
inhibiting the canonical Wnt pathway
SO DEVELOPMENT
LA English
DT Article
DE BMP receptor IA; Bone mass; Canonical Wnt signaling; Osteoblast;
Osteoclastogenesis; Sclerostin; Mouse
ID RECEPTOR-RELATED PROTEIN-5; TAMOXIFEN-INDUCIBLE FORM;
VAN-BUCHEM-DISEASE; MORPHOGENETIC PROTEIN; BETA-CATENIN; OSTEOBLAST
LINEAGE; OSTEOCLAST DIFFERENTIATION; CELL-DIFFERENTIATION; SOST GENE;
LRP5 GENE
AB Bone morphogenetic proteins (BMPs) are known to induce ectopic bone. However, it is largely unknown how BMP signaling in osteoblasts directly regulates endogenous bone. This study investigated the mechanism by which BMP signaling through the type IA receptor (BMPR1A) regulates endogenous bone mass using an inducible Cre-loxP system. When BMPR1A in osteoblasts was conditionally disrupted during embryonic bone development, bone mass surprisingly was increased with upregulation of canonical Wnt signaling. Although levels of bone formation markers were modestly reduced, levels of resorption markers representing osteoclastogenesis were severely reduced, resulting in a net increase in bone mass. The reduction of osteoclastogenesis was primarily caused by Bmpr1a-deficiency in osteoblasts, at least through the RANKL-OPG pathway. Sclerostin (Sost) expression was downregulated by about 90% and SOST protein was undetectable in osteoblasts and osteocytes, whereas the Wnt signaling was upregulated. Treatment of Bmpr1a-deficient calvariae with sclerostin repressed the Wnt signaling and restored normal bone morphology. By gain of Smad-dependent BMPR1A signaling in mice, Sost expression was upregulated and osteoclastogenesis was increased. Finally, the Bmpr1a-deficient bone phenotype was rescued by enhancing BMPR1A signaling, with restoration of osteoclastogenesis. These findings demonstrate that BMPR1A signaling in osteoblasts restrain endogenous bone mass directly by upregulating osteoclastogenesis through the RANKL-OPG pathway, or indirectly by downregulating canonical Wnt signaling through sclerostin, a Wnt inhibitor and a bone mass mediator.
C1 [Kamiya, Nobuhiro; Mishina, Yuji] NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Mishina, Yuji] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
[Ye, Ling; Feng, Jian Q.] Univ Missouri, Sch Dent, Kansas City, MO 64108 USA.
[Kobayashi, Tatsuya; Kronenberg, Henry M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Kobayashi, Tatsuya; Kronenberg, Henry M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Mochida, Yoshiyuki; Yamauchi, Mitsuo] Univ N Carolina, Dent Res Ctr, Chapel Hill, NC 27599 USA.
RP Mishina, Y (reprint author), NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM mishina@umich.edu
OI Mochida, Yoshiyuki/0000-0002-2115-4303
FU NIH [P01 DK56246, R01 AR051587, R21 AR052824, ES071003- 11]; RIKEN Brain
Science Institute; Lilly Fellowship Foundation
FX We gratefully thank Tomokazu Fukuda and Greg Scott for generation of
caBmpr1a mouse line and Donald Lucas for critical reading of this
manuscript. This work was supported by NIH grants P01 DK56246 (H. K.),
R01 AR051587 (J. F.), R21 AR052824 (M. Y.), ES071003- 11 and a
conditional gift from RIKEN Brain Science Institute (Y. M.) and Lilly
Fellowship Foundation (N. K.).
NR 74
TC 130
Z9 136
U1 0
U2 10
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 NOV 15
PY 2008
VL 135
IS 22
BP 3801
EP 3811
DI 10.1242/dev.025825
PG 11
WC Developmental Biology
SC Developmental Biology
GA 364MV
UT WOS:000260340700016
PM 18927151
ER
PT J
AU Qiao, F
Gao, CY
Tripathi, BK
Zelenka, PS
AF Qiao, Fengyu
Gao, Chun Y.
Tripathi, Brajendra K.
Zelenka, Peggy S.
TI Distinct functions of Cdk5(Y15) phosphorylation and Cdk5 activity in
stress fiber formation and organization
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Cdk5; Adhesion; Stress fibers; Epithelial cells; Cell spreading; Signal
transduction; Src family kinases; Lens
ID CYCLIN-DEPENDENT KINASE-5; LENS EPITHELIAL-CELLS; ACTIN CYTOSKELETON;
NEURITE OUTGROWTH; ADHESION; SRC; DIFFERENTIATION; P35; LOCALIZATION;
ACTIVATION
AB Previous studies have shown that Cdk5 promotes lens epithelia] cell adhesion. Here we use a cell spreading assay to investigate the mechanism of this effect. As cells spread, forming matrix adhesions and stress fibers, Cdk5(Y15) phosphorylation and Cdk5 kinase activity increased. Cdk5 (Y15) phosphorylation was inhibited by PP1, a Src family kinase inhibitor. To identify the PP1-sensitive kinase, we transfected cells with siRNA oligonucleotides for cSrc and related kinases. Only cSrc siRNA oligonucleotides inhibited Cdk5(Y15) phosphorylation. Cdk5(pY15) and its activator, p35, colocalized with actin in stress fibers. To examine Cdk5 function, we inhibited Cdk5 activity under conditions that also prevent phosphorylation at Y15: expression of kinase inactive Mutations Cdk5(Y15F) and Cdk5(K33T), and siRNA Suppression of Cdk5. Stress fiber formation was severely inhibited. To distinguish between a requirement for Cdk5 kinase activity and a possible adaptor role for Cdk5(pY15), we used two methods that inhibit kinase activity without inhibiting phosphorylation at Y15: pharmacological inhibition with olomoucine and expression of the kinase inactive mutation, Cdk5(D144N). Stress fiber organization was altered, but stress fiber formation was not blocked. These findings indicate that Cdk5(Y15) phosphorylation and Cdk5 activity have distinct functions required for stress fiber formation and organization, respectively. Published by Elsevier Inc.
C1 [Qiao, Fengyu; Gao, Chun Y.; Tripathi, Brajendra K.; Zelenka, Peggy S.] NEI, NIH, Bethesda, MD 20892 USA.
RP Zelenka, PS (reprint author), NEI, NIH, 7-102,7 Mem Dr,MSC 0704, Bethesda, MD 20892 USA.
EM zelenkap@nei.nih.gov
FU National Eye Institute Intramural Research Program [Z01-EY000238-20]
FX We thank Dr. John Reddan, Oakland University, for providing the N/N1003A
rabbit lens epithelial cells and FHL124 human lens epithelial cells, and
Drs. Robert Fariss and JenYue Tsai of the NEI Imaging Core for confocal
microscopy. This work was supported by the National Eye Institute
Intramural Research Program Z01-EY000238-20.
NR 34
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
J9 EXP CELL RES
JI Exp. Cell Res.
PD NOV 15
PY 2008
VL 314
IS 19
BP 3542
EP 3550
DI 10.1016/j.yexcr.2008.08.023
PG 9
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 380HQ
UT WOS:000261457200010
PM 18838073
ER
PT J
AU Nola, S
Sebbagh, M
Marchetto, S
Osmani, N
Nourry, C
Audebert, S
Navarro, C
Rachel, R
Montcouquiol, M
Sans, N
Etienne-Manneville, S
Borg, JP
Santoni, MJ
AF Nola, Sebastien
Sebbagh, Michael
Marchetto, Sylvie
Osmani, Nael
Nourry, Claire
Audebert, Stephane
Navarro, Christel
Rachel, Rivka
Montcouquiol, Mireille
Sans, Nathalie
Etienne-Manneville, Sandrine
Borg, Jean-Paul
Santoni, Marie-Josee
TI Scrib regulates PAK activity during the cell migration process
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID TUMOR-SUPPRESSOR SCRIBBLE; BASOLATERAL PDZ PROTEIN; LEUCINE-RICH REPEAT;
BREAST-CANCER CELLS; P21-ACTIVATED KINASE; EPITHELIAL-CELLS; E6
PROTEINS; E-CADHERIN; POLARITY; COMPLEX
AB Genetic studies have highlighted the key role of Scrib in the development of Metazoans. Deficiency in Scrib impairs many aspects of cell polarity and cell movement although the mechanisms involved remain unclear. In mammals, Scrib belongs to a protein complex containing beta PIX, an exchange factor for Rac/Cdc42, and GIT1, a GTPase activating protein for ARF6 implicated in receptor recycling and exocytosis. Here we show that the Scrib complex associates with PAK, a serine-threonine kinase family crucial for cell migration. PAK colocalizes with members of the Scrib complex at the leading edge of heregulin-treated T47D breast cancer cells. We demonstrate that the Scrib complex is required for epithelial cells and primary mouse embryonic fibroblasts to efficiently respond to chemoattractant cues. In Scrib-deficient cells, the pool of cortical PAK is decreased, thereby precluding its proper activation by Rac. Loss of Scrib also impairs the polarized distribution of active Rac at the leading edge and compromises the regulated activation of the GTPase in T47D cells and mouse embryonic fibroblasts. These data underscore the role of Scrib in cell migration and show the strong impact of Scrib in the function of PAK and Rac, two key molecules implicated in this process.
C1 [Borg, Jean-Paul] Univ Aix Marseille 2, Inst J Paoli I Calmettes, INSERM, UMR891,Ctr Rech Cancerol Marseille, F-13009 Marseille, France.
[Nola, Sebastien; Sebbagh, Michael; Marchetto, Sylvie; Nourry, Claire; Audebert, Stephane; Navarro, Christel; Borg, Jean-Paul; Santoni, Marie-Josee] INSERM, U891, Ctr Rech Cancerol Marseille, F-13009 Marseille, France.
[Osmani, Nael; Etienne-Manneville, Sandrine] Inst Pasteur, F-75724 Paris, France.
[Rachel, Rivka] NEI, Neurobiol Neurodegenerat & Repair Lab, Bethesda, MD 20892 USA.
[Montcouquiol, Mireille] Inst Francois Magendie, Avenir U862 Equipe 6, F-33077 Bordeaux, France.
[Sans, Nathalie] Inst Francois Magendie, Avenir U862 Equipe 7, F-33077 Bordeaux, France.
RP Borg, JP (reprint author), Univ Aix Marseille 2, Inst J Paoli I Calmettes, INSERM, UMR891,Ctr Rech Cancerol Marseille, 27 Blvd Lei Roure, F-13009 Marseille, France.
EM jean-paul.borg@inserm.fr
RI OSMANI, Nael/P-5728-2016; Nola, Sebastien/D-6518-2017; Sebbagh,
Michael/E-8502-2017;
OI OSMANI, Nael/0000-0003-1195-753X; Nola, Sebastien/0000-0002-6485-9856;
Sebbagh, Michael/0000-0003-2468-7006; montcouquiol,
mireille/0000-0001-8739-6519
FU Inserm; Institut Paoli-Calmettes; La Ligue Nationale Contre Le Cancer
(Label Ligue); Association pour la Recherche contre le Cancer; Institut
National du Cancer; Region PACA; la Fondation pour la Recherche
Medicale; La Ligue Nationale Contre Le Cancer
FX This work was supported by Inserm, Institut Paoli-Calmettes, La Ligue
Nationale Contre Le Cancer (Label Ligue), Association pour la Recherche
contre le Cancer, Institut National du Cancer and Region PACA. S.N. and
M.S. are recipients of a fellowship from la Fondation pour la Recherche
Medicale and La Ligue Nationale Contre Le Cancer, respectively.
NR 56
TC 47
Z9 56
U1 3
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2008
VL 17
IS 22
BP 3552
EP 3565
DI 10.1093/hmg/ddn248
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 365BV
UT WOS:000260381800011
PM 18716323
ER
PT J
AU Lubet, RA
Fischer, SM
Steele, VE
Juliana, MM
Desmond, R
Grubbs, CJ
AF Lubet, Ronald A.
Fischer, Susan M.
Steele, Vernon E.
Juliana, M. Margaret
Desmond, Renee'
Grubbs, Clinton J.
TI Rosiglitazone, a PPAR gamma agonist: Potent promoter of
hydroxybutyl(butyl)nitrosamine-induced urinary bladder cancers
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE rosiglitazone; urinary bladder; cancer; PPAR gamma agonist
ID PROLIFERATOR-ACTIVATED RECEPTORS; FEMALE FISCHER-344 RATS; PEROXISOME
PROLIFERATORS; POLYPHENON-E; EXPRESSION; MICE; CARCINOGENESIS;
N-BUTYL-N-(4-HYDROXYBUTYL)NITROSAMINE; CHEMOPREVENTION; CELECOXIB
AB In an initial study, to determine if rosiglitazone had chemopreventive activity, Fischer-344 female rats were administered twice weekly doses of hydroxybutyl(butyl)nitrosamine (OH-BBN), a urinary bladder specific carcinogen, for 8 weeks. Two weeks following the last dose of OH-BBN, rats were administered rosiglitazone (50 mg/kg BW) daily by gavage for the remainder of the study (7 months). Only 57% of OH-BBN-treated animals developed palpable urinary bladder cancers during the course of the study, while all of the OH-BBN plus rosiglitazone treated rats developed large cancers (p < 0.01). Surprisingly, examination for PPAR gamma by, immunohistochemistry in the urinary bladders of rats showed that while untreated bladder urothelium and preneoplastic lesions clearly, expressed PPAR gamma, frank carcinomas exhibited significantly lower levels. This was confirmed by employing microarray studies of the same samples. In additional studies, lower doses of rosiglitazone (10, 2 and 0.4 mg/kg BW/day) were administered. The 10 mg/kg BW/day dose greatly enhanced bladder cancer incidence (p < 0.01). The dose of 2 mg/kg BW/day, which is roughly, equivalent to a standard human dose, also significantly increased bladder cancer incidence (controls, 48%; rosiglitazone-treated, 84%). The lowest dose did not significantly increase tumor incidence (rosiglitazone at 0.4 mg/kg BW/day, 64%) or tumor weight in the rats, although there was a trend in that direction. Rosiglitazone alone (10 mg/kg BW/day) given in the absence of OH-BBN did not result in bladder cancer formation when given for 10 months. In summary, rosiglitazone over a wide dose range enhanced urinary, bladder carcinogenesis in the OH-BBN model in rats. Published 2008 Wiley-Liss. Inc. This article is a US Government work, and. its such, is in the public domain in the United States of America.
C1 [Lubet, Ronald A.; Steele, Vernon E.] NCI, Canc Prevent Div, Rockville, MD 20852 USA.
[Fischer, Susan M.] Univ Texas MD Anderson Canc Ctr, Div Sci Pk Res, Smithville, TX USA.
[Juliana, M. Margaret] Univ Alabama, Dept Genet, Birmingham, AL USA.
[Desmond, Renee'] Univ Alabama, Dept Biostat, Birmingham, AL 35294 USA.
[Grubbs, Clinton J.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
RP Lubet, RA (reprint author), NCI, Canc Prevent Div, Execut Plaza N,Suite 2110,6130 Execut Blvd, Rockville, MD 20852 USA.
EM lubetr@mail.nih.gov
FU NCI [HHSN261200433001C]
FX Grant sponsor: NCI; Grant number: HHSN261200433001C.
NR 23
TC 37
Z9 38
U1 1
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2008
VL 123
IS 10
BP 2254
EP 2259
DI 10.1002/ijc.23765
PG 6
WC Oncology
SC Oncology
GA 365XQ
UT WOS:000260443300004
PM 18712722
ER
PT J
AU Palayoor, ST
Mitchell, JB
Cerna, D
DeGraff, W
John-Aryankalayil, M
Coleman, CN
AF Palayoor, Sanjeewani T.
Mitchell, James B.
Cerna, David
DeGraff, William
John-Aryankalayil, Molykutty
Coleman, C. Norman
TI PX-478, an inhibitor of hypoxia-inducible factor-1 alpha, enhances
radiosensitivity of prostate carcinoma cells
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE PX-478; hypoxia; normoxia; HIF-1 alpha; radiosensitivity
ID PREDICTS RADIATION RESPONSE; PHOSPHORYLATED HISTONE H2AX; TUMOR-GROWTH;
CANCER CELLS; IN-VIVO; FACTOR 1-ALPHA; EXPRESSION; HEAD; NECK; PATHWAY
AB Overexpression of hypoxia-inducible factor-1 alpha (HIF-1 alpha) in human tumors is associated with poor prognosis and poor outcome to radiation therapy. Inhibition of HIF-1 alpha is considered as a promising approach in cancer therapy. The purpose of this study was to test the efficacy of a novel HIF-1 alpha inhibitor PX-478 as a radiosensitizer under normoxic and hypoxic conditions in vitro. PC3 and DU 145 prostate carcinoma cells were treated with PX-478 for 20 hr, and HIF-1 alpha protein level and clonogenic cell survival were determined under normoxia and hypoxia. Effects of PX-478 on cell cycle distribution and phosphorylation of H2AX bistone were evaluated. PX-478 decreased HIF-1 alpha protein in PC3 and DU 145 cells. PX-478 produced cytotoxicity in both cell lines with enhanced toxicity under hypoxia for DU-145. PX-478 (20 mu mol/L) enhanced the radiosensitivity of PC3 cells irradiated under normoxic and hypoxic condition with enhancement factor (EF) 1.4 and 1.56, respectively. The drug was less effective in inhibiting HIF-1 alpha and enhancing radiosensitivity of DU 145 cells compared to PC3 cells with EF 1.13 (normoxia) and 1.25 (hypoxia) at 50 mu mol/L concentration. PX-478 induced S/G2M arrest in PC3 but not in DU 145 cells. Treatment of PC3 and DU 145 cells with the drug resulted in phosphorylation of H2AX histone and prolongation of gamma H2AX expression in the irradiated cells. PX-478 is now undergoing Phase I clinical trials as an oral agent. Although the precise mechanism of enhancement of radiosensitivity remains to be identified, this study suggests a potential role for PX-478 as a clinical radiation enhancer.
C1 [Palayoor, Sanjeewani T.; Cerna, David; John-Aryankalayil, Molykutty; Coleman, C. Norman] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mitchell, James B.; DeGraff, William] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Palayoor, ST (reprint author), NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, 9000 Rockville Pike,Bldg 10,Room 3B 49, Bethesda, MD 20892 USA.
EM palayoor@mail.nih.gov
FU Center for Cancer Research; National Cancer Institute; National
Institutes of Health
FX Grant sponsor: Intramural Research Program of the Center for Cancer
Research. National Cancer Institute, National Institutes of Health.
NR 44
TC 43
Z9 45
U1 0
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2008
VL 123
IS 10
BP 2430
EP 2437
DI 10.1002/ijc.23807
PG 8
WC Oncology
SC Oncology
GA 365XQ
UT WOS:000260443300028
PM 18729192
ER
PT J
AU Allan, JM
Shorto, J
Adlard, J
Bury, J
Coggins, R
George, R
Katory, M
Quirke, P
Richman, S
Scott, D
Scott, K
Seymour, M
Travis, LB
Worrillow, LJ
Bishop, DT
Cox, A
AF Allan, James M.
Shorto, Jennifer
Adlard, Julian
Bury, Jonathan
Coggins, Ron
George, Rina
Katory, Mark
Quirke, Philip
Richman, Susan
Scott, Daniel
Scott, Kathryn
Seymour, Matthew
Travis, Lois B.
Worrillow, Lisa J.
Bishop, D. Timothy
Cox, Angela
CA UK NCRI Colorectal Clinical Studie
Colorectal Canc Study Grp
TI MLH1-93G > A promoter polymorphism and risk of mismatch repair deficient
colorectal cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE MLH1; mismatch repair; colorectal; polymorphism; proximal; promoter; dna
repairs; cancer
ID MICROSATELLITE INSTABILITY; HMLH1; MLH1; GENE; SUSCEPTIBILITY;
PREDISPOSITION; ASSOCIATION; MUTATION; VARIANT; POLYPS
AB Rare inherited mutations in the mutL homolog 1 (MLH1) DNA mismatch repair gene can confer an increased susceptibility to colorectal cancer (CRC) with high penetrance where disease frequently develops in the proximal colon. The core promoter of, MLH1 contains a common single nucleotide polymorphism (SNP) (-93G > A, dbSNP ID:rs1800734) located in a region essential for maximum transcriptional activity. We used logistic regression analysis to examine the association between this variant and risk of CRC in patients in the United Kingdom. All statistical tests were 2 sided. In an analysis of 1,518 patients with CRC, homozygosity for the MLH1 -93A variant was associated with a significantly increased 3-fold risk of CRC negative for MLH1 protein by immunohistochemistry (odds ratio (OR): AA vs GG = 3.30, 951 v CI 1.46-7.47, n = 1392, p = 0.004, MLH1 negative vs MLH1 positive CRC) and with a 68% excess of proximal CRC (OR: AA vs GG=1.68, 95% confidence interval (CI) 1.00-2.83, n = 1,518. p = 0.05, proximal vs distal CRC). These findings suggest that the MLHI -93G > A polymorphism defines a low penetrance risk allele for CRC. (C) 2008 Wiley-Liss, Inc.
C1 [Allan, James M.] Newcastle Univ, Sch Med, No Inst Canc Res, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
[Shorto, Jennifer; George, Rina; Katory, Mark; Cox, Angela] Univ Sheffield, Sch Med, Inst Canc Studies, Sheffield, S Yorkshire, England.
[Adlard, Julian] Cookridge Hosp, York Reg Ctr Canc Treatment, Leeds LS16 6QB, W Yorkshire, England.
[Bury, Jonathan] Univ Sheffield, Sch Med, Acad Unit Pathol, Sheffield, S Yorkshire, England.
[Coggins, Ron; Bishop, D. Timothy] Leeds Inst Mol Med, Epidemiol & Biostat Sect, Leeds, W Yorkshire, England.
[Quirke, Philip] Leeds Inst Mol Med, Acad Unit Pathol, Leeds, W Yorkshire, England.
[Richman, Susan; Seymour, Matthew] Canc Res UK Clin Ctr Leeds, Leeds, W Yorkshire, England.
[Scott, Daniel] Harrogate & Dist NHS Fdn Trust, Dept Histopathol, Harrogate, England.
[Scott, Kathryn; Worrillow, Lisa J.] Univ York, Dept Biol, York YO10 5DD, N Yorkshire, England.
[Travis, Lois B.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Allan, JM (reprint author), Newcastle Univ, Sch Med, No Inst Canc Res, Paul OGorman Bldg,Framlington Pl, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
EM james.allan@newcastle.ac.uk
RI Allan, James/B-4448-2009;
OI Katory, Mark/0000-0002-9401-8687; Quirke, Philip/0000-0002-3597-5444;
Bishop, Tim/0000-0002-8752-8785; Cox, Angela/0000-0002-5138-1099
FU White Rose PhD studentship; Yorkshire Cancer Research
FX We thank all the patients who have taken part ill this Study. We also
thank Dr. Simon Cross (University of Sheffield, UK), Mr. Ian Adam and
Mr. Andrew Shorthouse (Sheffield Teaching Hospitals Foundation Trust,
UK) for the identification and recruitment of Sheffield patients with
colon tumours. This work was supported by a White Rose PhD studentship
(to JS) and Yorkshire Cancer Research (to JIMA). AC and MK were also
supported by Yorkshire Cancer Research.
NR 26
TC 32
Z9 32
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2008
VL 123
IS 10
BP 2456
EP 2459
DI 10.1002/ijc.23770
PG 4
WC Oncology
SC Oncology
GA 365XQ
UT WOS:000260443300031
PM 18712731
ER
PT J
AU Esthappan, J
Chaudhari, S
Santanam, L
Mutic, S
Olsen, J
MacDonald, DM
Low, DA
Singh, AK
Grigsby, PW
AF Esthappan, Jacqueline
Chaudhari, Summer
Santanam, Lakshmi
Mutic, Sasa
Olsen, Jeffrey
MacDonald, Dusten M.
Low, Daniel A.
Singh, Anurag K.
Grigsby, Perry W.
TI PROSPECTIVE CLINICAL TRIAL OF POSITRON EMISSION TOMOGRAPHY/COMPUTED
TOMOGRAPHY IMAGE-GUIDED INTENSITY-MODULATED RADIATION THERAPY FOR
CERVICAL CARCINOMA WITH POSITIVE PARA-AORTIC LYMPH NODES
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE IMRT; Cervix cancer; PET/CT; Dose escalation; Treatment planning
ID GYNECOLOGIC MALIGNANCIES; EXTENDED-FIELD; RADIOTHERAPY; TOXICITY;
CANCER; IMRT; IRRADIATION; GUIDELINES; WOMEN; PET
AB Purpose: To describe a more aggressive treatment technique allowing dose escalation to positive para-aortic lymph nodes (PALN) in patients with cervical cancer, by means of positron emission tomography (PET)/computed tomography (CT)-guided intensity-modulated radiation therapy (IMRT). Here, we describe methods for simulation and planning of these treatments and provide objectives for target coverage as well as normal tissue sparing to guide treatment plan evaluation.
Methods and Materials: Patients underwent simulation on a PET/CT scanner. Treatment plans were generated to deliver 60.0 Gy to the T-positive PALN and 50.0 Gy to the PALN and pelvic lymph node beds. Treatment plans were optimized to deliver at least 95% of the prescribed doses to at least 95% of each target volume. Dose-volume histograms were calculated for normal structures.
Results: The plans of 10 patients were reviewed. Target coverage goals were satisfied in all plans. Analysis of dose-volume histograms indicated that treatment plans involved irradiation of approximately 50% of the bowel volume to at least 25.0 Gy, with less than 10% receiving at least 50.0 Gy and less than 1% receiving at least 60.0. With regard to kidney sparing, approximately 50% of the kidney volume received at least 16.0 Gy, less than 5% received at least 50.0 Gy, and less than 1% received at least 60.0 Gy.
Conclusions: We have provided treatment simulation and planning methods as well as guidelines for the evaluation of target coverage and normal tissue sparing that should facilitate the more aggressive treatment of cervical cancer. (C) 2008 Elsevier Inc.
C1 [Esthappan, Jacqueline; Chaudhari, Summer; Santanam, Lakshmi; Mutic, Sasa; Olsen, Jeffrey; MacDonald, Dusten M.; Low, Daniel A.; Grigsby, Perry W.] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63110 USA.
[Singh, Anurag K.] NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA.
RP Esthappan, J (reprint author), Washington Univ, Sch Med, Dept Radiat Oncol, 4921 Parkview Pl,Campus Box 8224, St Louis, MO 63110 USA.
EM esthappan@radonc.wustl.edu
NR 16
TC 48
Z9 51
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2008
VL 72
IS 4
BP 1134
EP 1139
DI 10.1016/j.ijrobp.2008.02.063
PG 6
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 368AB
UT WOS:000260592600024
PM 18472358
ER
PT J
AU Song, M
Wang, L
Zhao, H
Hang, TJ
Wen, AD
Yang, L
Jia, L
AF Song, Min
Wang, Li
Zhao, Hua
Hang, Taijun
Wen, Aidong
Yang, Lin
Jia, Lee
TI Rapid and sensitive liquid chromatography-tandem mass spectrometry:
Assay development, validation and application to a human pharmacokinetic
study
SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL
AND LIFE SCIENCES
LA English
DT Article
DE Rasagiline; Human pharmacokinetics; Urine excretion; LC-MS/MS
ID PARKINSONS-DISEASE; B INHIBITOR; DRUG-METABOLISM; IN-VITRO; RASAGILINE;
PHARMACODYNAMICS; CONDUCT; VIVO
AB Rasagiline is a highly potent, selective and irreversible second-generation monoamine oxidase inhibitor with selectivity for type B of the enzyme (MAO-B). The present studies aimed at developing and validating a rapid and sensitive liquid chromatography-tandem mass spectrometric (LC-MS/MS) method for determination of rasagiline in human plasma and urine. LC-MS/MS analysis was carried out on a Finnigan LC-TSQ Quantum mass spectrometer using positive ion electrospray ionization (ESI(+)) and selected reaction monitoring (SRM). The assay for rasagiline was linear over the range of 0.01-40 ng/mL in plasma and 0.025-40 ng/mL in urine. It took 5.5 min to analyze a sample. The average recoveries in plasma and urine samples were both > 85%. The RSD of precision and bias of accuracy were less than 15% and 10%, respectively, of their nominal values based on the intra- and inter-day analysis. The developed method was proved to be suitable for use in clinical pharmacokinetic study after single oral administration of 0.5, 1 and 2 mg rasagiline mesylate tablets in healthy Chinese volunteers. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Song, Min; Wang, Li; Zhao, Hua; Hang, Taijun] China Pharmaceut Univ, Dept Pharmaceut Anal, Nanjing 210009, Peoples R China.
[Wen, Aidong; Yang, Lin] Fourth Mil Med Univ, Xijing Hosp, Dept Pharm, Xian 710032, Peoples R China.
[Jia, Lee] NCI, Dev Therapeut Program, NIH, Rockville, MD 20852 USA.
RP Hang, TJ (reprint author), China Pharmaceut Univ, Dept Pharmaceut Anal, Nanjing 210009, Peoples R China.
EM hangtj@cpu.edu.cn; adwen-2004@hotmail.com; jiale@mail.nih.gov
NR 19
TC 10
Z9 12
U1 2
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-0232
J9 J CHROMATOGR B
JI J. Chromatogr. B
PD NOV 15
PY 2008
VL 875
IS 2
BP 515
EP 521
DI 10.1016/j.jchromb.2008.10.005
PG 7
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 377TG
UT WOS:000261272900026
PM 18952510
ER
PT J
AU Pandrea, I
Gaufin, T
Brenchley, JM
Gautam, R
Moniure, C
Gautam, A
Coleman, C
Lackner, AA
Ribeiro, RM
Douek, DC
Apetrei, C
AF Pandrea, Ivona
Gaufin, Thaidra
Brenchley, Jason M.
Gautam, Rajeev
Moniure, Christopher
Gautam, Aarti
Coleman, Clint
Lackner, Andrew A.
Ribeiro, Ruy M.
Douek, Daniel C.
Apetrei, Cristian
TI Cutting Edge: Experimentally Induced Immune Activation in Natural Hosts
of Simian Immunodeficiency Virus Induces Significant Increases in Viral
Replication and CD4(+) T Cell Depletion
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID AFRICAN-GREEN MONKEYS; INFECTED SOOTY MANGABEYS; PATHOGENESIS; PROFILES;
AIDS
AB Chronically SIVagm-infected African green monkeys (AGMs) have a remarkably stable nonpathogenic disease course, with levels of immune activation in chronic SIVagm infection similar to those observed in uninfected monkeys and with stable viral loads for long periods of time. In vivo administration of LPS or an IL-2/diphtheria toxin fusion protein (Ontak) to chronically SIVagm-infected AGMs triggered increases in immune activation and subsequently of viral replication and depletion of intestinal CD4(+) T cells. Our study indicates that circulating microbial products can increase viral replication by inducing immune activation and increasing the number of viral target cells, thus demonstrating that immune activation and T cell proliferation are key factors in AIDS pathogenesis. The Journal of Immunology, 2008, 181: 6687-6691.
C1 [Pandrea, Ivona; Gaufin, Thaidra; Gautam, Rajeev; Moniure, Christopher; Gautam, Aarti; Coleman, Clint; Lackner, Andrew A.; Apetrei, Cristian] Tulane Natl Primate Res Ctr, Div Comparat Pathol, Covington, LA 70433 USA.
[Pandrea, Ivona; Gaufin, Thaidra; Gautam, Rajeev; Moniure, Christopher; Gautam, Aarti; Coleman, Clint; Lackner, Andrew A.; Apetrei, Cristian] Tulane Natl Primate Res Ctr, Div Microbiol, Covington, LA 70433 USA.
[Pandrea, Ivona] Tulane Univ, Sch Med, Dept Pathol, New Orleans, LA 70112 USA.
[Gaufin, Thaidra; Coleman, Clint; Lackner, Andrew A.] Tulane Univ, Sch Med, Dept Microbiol & Immunol, New Orleans, LA 70112 USA.
[Brenchley, Jason M.] NIAID, Immunopathogenesis Unit, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Douek, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Ribeiro, Ruy M.] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
[Apetrei, Cristian] Tulane Univ, Sch Publ Hlth, Dept Trop Med, New Orleans, LA 70112 USA.
RP Pandrea, I (reprint author), Tulane Natl Primate Res Ctr, Div Comparat Pathol, Covington, LA 70433 USA.
EM ipandrea@tulane.edu
FU National Institutes of Health/National Institute of Allergy and
Infectious Diseases/National Center [R01 AI064066, R21 AI069935, R01
AI065325, RR-00168]
FX This work was supported by National Institutes of Health/National
Institute of Allergy and Infectious Diseases/National Center for
Research Resources Grants R01 AI064066 and R21 AI069935 (to I.P.), R01
AI065325 (to C.A.), and RR-00168 (to Tulane National Primate Research
Center).
NR 12
TC 80
Z9 81
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 6687
EP 6691
PG 5
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900002
PM 18981083
ER
PT J
AU Kinter, AL
Godbout, EJ
McNally, JP
Sereti, I
Roby, GA
O'Shea, MA
Fauci, AS
AF Kinter, Audrey L.
Godbout, Emily J.
McNally, Jonathan P.
Sereti, Irini
Roby, Gregg A.
O'Shea, Marie A.
Fauci, Anthony S.
TI The Common gamma-Chain Cytokines IL-2, IL-7, IL-15, and IL-21 Induce the
Expression of Programmed Death-1 and Its Ligands
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID T-CELL RESPONSES; HOMEOSTATIC PROLIFERATION; IMMUNE-RESPONSES;
HIV-INFECTION; ACTIVATION; CD8(+); AUTOIMMUNITY; LYMPHOCYTES; EXPANSION;
CD4(+)
AB The programmed death (PD)-1 molecule and its ligands (PD-L1 and PD-L2), negative regulatory members of the B7 family, play an important role in peripheral tolerance. Previous studies have demonstrated that PD-1 is up-regulated on T cells following TCR-mediated activation; however, little is known regarding PD-1 and Ag-independent, cytokine-induced T cell activation. The common gamma-chain (gamma c) cytokines IL-2, IL-7, IL-15, and IL-21, which play an important role in peripheral T cell expansion and survival, were found to up-regulate PD-1 and, with the exception of IL-21, PD-L1 on purified T cells in vitro. This effect was most prominent on memory T cells. Furthermore, these cytokines induced, indirectly, the expression of PD-L1 and PD-L2 on monocytes/macrophages in PBMC. The in vivo correlate of these observations was confirmed on PBMC isolated from HIV-infected individuals receiving IL-2 immunotherapy. Exposure of gamma c cytokine pretreated T cells to PD-1 ligand-IgG had no effect on STAT5 activation, T cell proliferation, or survival driven by gamma c cytokines. However, PD-1 ligand-IgG dramatically inhibited anti-CD3/CD28-driven proliferation and Lck activation. Furthermore, following restimulation with anti-CD3/CD28, cytokine secretion by both gamma c cytokine and anti-CD3/CD28 pretreated T cells was suppressed. These data suggest that gamma c cytokine-induced PD-1 does not interfere with cytokine-driven peripheral T cell expansion/survival, but may act to suppress certain effector functions of cytokine-stimulated cells upon TCR engagement, thereby minimizing immune-mediated damage to the host. The Journal of Immunology, 2008, 181: 6738-6746.
C1 [Kinter, Audrey L.; Godbout, Emily J.; McNally, Jonathan P.; Sereti, Irini; Roby, Gregg A.; O'Shea, Marie A.; Fauci, Anthony S.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Kinter, AL (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10,Room 6A33,MSC-1576,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM AKinter@niaid.nih.gov
NR 54
TC 170
Z9 173
U1 2
U2 13
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 6738
EP 6746
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900010
PM 18981091
ER
PT J
AU Wilson, MS
Pesce, JT
Ramalingam, TR
Thompson, RW
Cheever, A
Wynn, TA
AF Wilson, Mark S.
Pesce, John T.
Ramalingam, Thirumalai R.
Thompson, Robert W.
Cheever, Allen
Wynn, Thomas A.
TI Suppression of Murine Allergic Airway Disease by IL-2:Anti-IL-2
Monoclonal Antibody-Induced Regulatory T Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID RECOMBINANT INTERLEUKIN-2 RIL-2; COLLAGEN-INDUCED ARTHRITIS; RESPONSE
IN-VIVO; DENILEUKIN DIFTITOX; AUTOIMMUNE-DISEASE; IMMUNE-COMPLEXES;
FUSION PROTEIN; IFN-GAMMA; IL-2; INFLAMMATION
AB Regulatory T cells (Treg) play a decisive role in many diseases including asthma and allergen-induced lung inflammation. However, little progress has been made developing new therapeutic strategies for pulmonary disorders. In the current study we demonstrate that cytokine:antibody complexes of IL-2 and anti-IL-2 mAb reduce the severity of allergen-induced inflammation in the lung by expanding Tregs in vivo. Unlike rIL-2 or anti-IL-2 mAb treatment alone, IL-2:anti-IL-2 complexes dampened airway inflammation and eosinophilia while suppressing IL-5 and eotaxin-1 production. Mucus production, airway hyperresponsiveness to methacholine, and parenchymal tissue inflammation were also dramatically reduced following IL-2:anti-IL-2 treatment. The suppression in allergic airway disease was associated with a marked expansion of Tregs (IL-10(+)CD4(+)CD25(+) and Foxp3(+)CD4(+)CD25(+)) in the tissues, with a corresponding decrease in effector T cell responses. The ability of IL-2:anti-IL-2 complexes to suppress airway inflammation was dependent on Treg-derived IL-10, as IL-10(+/+), but not IL-10(-/-) Tregs, were capable of mediating the suppression. Furthermore, a therapeutic protocol using a model of established airway allergy highlighted the ability of IL-2:anti-IL-2 complexes to expand Tregs and prevent successive airway inflammation and airway hyperresponsiveness. This study suggests that endogenous Treg therapy may be a useful tool to combat the rising incidence of allergic airway disease. The Journal of Immunology, 2008, 181: 6942-6954.
C1 [Wynn, Thomas A.] NIAID, Immunopathogenesis Sect, Parasit Dis Lab, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Cheever, Allen] Biomed Res Inst, Rockville, MD 20852 USA.
RP Wynn, TA (reprint author), NIAID, Immunopathogenesis Sect, Parasit Dis Lab, NIH,Dept Hlth & Human Serv, 50 S Dr,Room 6154,Mail Stop Code 8003, Bethesda, MD 20892 USA.
EM twynn@niaid.nih.gov
RI Wynn, Thomas/C-2797-2011
FU Intramural Research Program of the National Institutes of Health;
National Institute of Allergy and Infectious Diseases
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 73
TC 55
Z9 59
U1 1
U2 5
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 6942
EP 6954
PG 13
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900033
PM 18981114
ER
PT J
AU Adoro, S
Erman, B
Sarafova, SD
Van Laethem, F
Park, JH
Feigenbaum, L
Singer, A
AF Adoro, Stanley
Erman, Batu
Sarafova, Sophia D.
Van Laethem, Francois
Park, Jung-Hyun
Feigenbaum, Lionel
Singer, Alfred
TI Targeting CD4 Coreceptor Expression to Postselection Thymocytes Reveals
That CD4/CD8 Lineage Choice Is neither Error-Prone nor Stochastic
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID T-CELLS; POSITIVE SELECTION; GENE-EXPRESSION; COMMITMENT;
DIFFERENTIATION; SPECIFICITY; SIGNALS; THYMUS; TCR; TRANSCRIPTION
AB The mechanism by which CD4/CD8 lineage choice is coordinated with TCR specificity during positive selection remains an unresolved problem in immunology. The stochastic/selection model proposes that CD4/CD8 lineage choice in TCR-signaled CD4(+)CD8(+) thymocytes occurs randomly and therefore is highly error-prone. This perspective is strongly supported by "coreceptor rescue" experiments in which transgenic CD4 coreceptors were ectopically expressed on thymocytes throughout their development and caused significant numbers of cells bearing MHC-II-specific TCR to differentiate into mature, CD8 lineage T cells. However, it is not known if forced coreceptor expression actually rescued positively selected thymocytes making an incorrect lineage choice or if it influenced developing thymocytes into making an incorrect lineage choice. We have now reassessed. coreceptor rescue and the concept that lineage choice is highly error-prone with a novel CD4 transgene (referred to as E8(1)-CD4) that targets expression of transgenic CD4 coreceptors specifically to thymocytes that have already undergone positive selection and adopted a CD8 lineage fate. Unlike previous CD4 transgenes, the E8(1)-CD4 transgene has no effect on early thymocyte development and cannot itself influence CD4/CD8 lineage choice. We report that the E8(1)-CD4 transgene did in fact induce expression of functional CD4 coreceptor proteins on newly arising CD8 lineage thymocytes precisely at the point in thymic development that transgenic CD4 coreceptors would putatively rescue MHC-II-specific thymocytes that incorrectly adopted the CD8 lineage. However, the E8(1)-CD4 transgene did not reveal any MHC-II-selected thymocytes that adopted the CD8 lineage fate. These results demonstrate that CD4/CD8 lineage choice is neither error-prone nor stochastic. The Journal of Immunology, 2008, 181: 6975-6983.
C1 [Adoro, Stanley; Erman, Batu; Sarafova, Sophia D.; Van Laethem, Francois; Park, Jung-Hyun; Singer, Alfred] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA.
[Adoro, Stanley] Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
[Erman, Batu] Sabanci Univ, Biol Sci & Bioengn Program, Fac Engn & Nat Sci, Istanbul, Turkey.
[Sarafova, Sophia D.] Davidson Coll, Dept Biol, Davidson, NC 28035 USA.
[Feigenbaum, Lionel] NCI, Sci Applicat Int Corp, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
RP Singer, A (reprint author), NCI, Expt Immunol Branch, Bldg 10 Room 4B36, Bethesda, MD 20892 USA.
EM singera@nih.gov
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 30
TC 6
Z9 6
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 6975
EP 6983
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900036
PM 18981117
ER
PT J
AU Semnani, RT
Venugopal, PG
Mahapatra, L
Skinner, JA
Meylan, F
Chien, D
Dorward, DW
Chaussabel, D
Siegel, RM
Nutman, TB
AF Semnani, Roshanak Tolouei
Venugopal, Priyanka Goel
Mahapatra, Lily
Skinner, Jason A.
Meylan, Francoise
Chien, Daniel
Dorward, David W.
Chaussabel, Damien
Siegel, Richard M.
Nutman, Thomas B.
TI Induction of TRAIL- and TNF-alpha-Dependent Apoptosis in Human
Monocyte-Derived Dendritic Cells by Microfilariae of Brugia malayi
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CYTOCHROME-C RELEASE; CASPASE ACTIVATION; LEISHMANIA-MAJOR; FILARIAL
PARASITES; T-LYMPHOCYTES; DEATH; PROTEIN; MITOCHONDRIA; MACROPHAGES;
SUPPRESSION
AB Dysregulation of professional APC has been postulated as a major mechanism underlying Ag-specific T cell hyporesponsiveness in patients with patent filarial infection. To address the nature of this dysregulation, dendritic cells (DC) and macrophages generated from elutriated monocytes were exposed to live microfilariae (mf), the parasite stage that circulates in blood and is responsible for most immune dysregulation in filarial infections. DC exposed to mf for 24-96 h showed a marked increase in cell death and caspase-positive cells compared with unexposed DC, whereas mf exposure did not induce apoptosis in macrophages. Interestingly, 48-h exposure of DC to mf induced mRNA expression of the proapoptotic gene TRAIL and both mRNA and protein expression of TNF-alpha. mAb to TRAIL-R2, TNF-R1, or TNF-alpha partially reversed mf-induced cell death in DC, as did knocking down the receptor for TRAIL-R2 using small interfering RNA. The mf also induced gene expression of BH3-interacting domain death agonist and protein expression of cytochrome c in DC; mf-induced cleavage of BH3-interacting domain death agonist could be shown to induce release of cytochrome c, leading to activation of caspase 9. Our data suggest that mf induce DC apoptosis in a TRAIL- and TNF-alpha-dependent fashion. The Journal of Immunology, 2008, 181: 7081-7089.
C1 [Semnani, Roshanak Tolouei; Venugopal, Priyanka Goel; Mahapatra, Lily; Chien, Daniel; Nutman, Thomas B.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20872 USA.
[Meylan, Francoise; Siegel, Richard M.] NIAMSD, Autoimmun Branch, NIH, Bethesda, MD 20872 USA.
[Skinner, Jason A.; Chaussabel, Damien] Baylor Inst Immunol Res, Dallas, TX 75204 USA.
[Dorward, David W.] NIAID, Res Technol Sect, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Semnani, RT (reprint author), NIAID, NIH, 4 Ctr Dr,Room 4-B 105, Bethesda, MD 20892 USA.
EM rsemnani@niaid.nih.gov
OI Siegel, Richard/0000-0001-5953-9893
FU Intramural Research Program of the Division of Intramural Research;
National Institute of Allergy and Infectious Diseases; National
Institutes of Health
FX This work was supported by the Intramural Research Program of the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health. Because R.T.S.,
P.G.V., L.M., F.M., D. C., D.D., R.M.S., and T.B.N. are government
employees and this is a government work, the work is in the public
domain in the United States. Notwithstanding any other agreements, the
National Institutes of Health reserves the right to provide the work to
PubMedCentral for display and use by the public, and PubMeclCentral may
tag or modify the work consistent with its customary practices. Rights
can be established outside of the U.S. Subject to a government use
license.
NR 40
TC 17
Z9 18
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7081
EP 7089
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900047
PM 18981128
ER
PT J
AU Lu, L
Ma, Z
Jokiranta, TS
Whitney, AR
DeLeo, FR
Zhang, JR
AF Lu, Ling
Ma, Zhuo
Jokiranta, T. Sakari
Whitney, Adeline R.
DeLeo, Frank R.
Zhang, Jing-Ren
TI Species-Specific Interaction of Streptococcus pneumoniae with Human
Complement Factor H
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PNEUMOCOCCAL SURFACE PROTEIN; REGULATOR FACTOR-H; RESISTANCE MECHANISMS;
SECRETORY COMPONENT; EPITHELIAL-CELLS; IMMUNE EVASION; IN-VIVO; PSPC;
BINDING; PNEUMOLYSIN
AB Streptococcus pneumoniae naturally colonizes the nasopharynx as a commensal organism and sometimes causes Infections in remote tissue sites. This bacterium is highly capable of resisting host innate immunity during nasopharyngeal colonization and disseminating infections. The ability to recruit complement factor H (FH) by S. pneumoniae has been implicated as a bacterial immune evasion mechanism against complement-mediated bacteria] clearance because FH is a complement alternative pathway inhibitor. S. pneumoniae recruits FH through a previously defined FH binding domain of choline-binding protein A (CbpA), a major surface protein of S. pneumoniae. In this study, we show that CbpA binds to human FH, but not to the FH proteins of mouse and other animal species tested to date. Accordingly, deleting the FH binding domain of CbpA in strain D39 did not result in obvious change in the levels of pneumococcal bacteremia or virulence in a bacteremia mouse model. Furthermore, this species-specific pneumococcal interaction with FH was shown to occur in multiple pneumococcal isolates from the blood and cerebrospinal fluid. Finally, our phagocytosis experiments with human and mouse phagocytes and complement systems provide additional evidence to support our hypothesis that CbpA acts as a bacterial determinant for pneumococcal resistance to complement-mediated host defense in humans. The Journal of Immunology, 2008, 181: 7138-7146.
C1 [Lu, Ling; Ma, Zhuo; Zhang, Jing-Ren] Albany Med Coll, Ctr Immunol & Microbial Dis, Albany, NY 12208 USA.
[Jokiranta, T. Sakari] Univ Helsinki, Dept Bacteriol & Immunol, Haartman Inst, Helsinki, Finland.
[Jokiranta, T. Sakari] Univ Helsinki, HUSLAB, Helsinki, Finland.
[Whitney, Adeline R.; DeLeo, Frank R.] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Zhang, JR (reprint author), Albany Med Coll, Ctr Immunol & Microbial Dis, M-C 151,Room MS453,47 New Scotland Ave, Albany, NY 12208 USA.
EM zhangj@mail.amc.edu
RI Jokiranta, T. Sakari/F-1906-2011;
OI DeLeo, Frank/0000-0003-3150-2516
FU Intramural Research Program of the National Institutes of Health;
National Institute of Allergy and Infectious Diseases; National
Institutes of Health/National Institutes of Deafness and Other
Communication Disorders [DC006917]
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health. National Institute of Allergy and
Infectious Diseases, and by a research grant from the National
Institutes of Health/National Institutes of Deafness and Other
Communication Disorders (DC006917).
NR 66
TC 35
Z9 35
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7138
EP 7146
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900054
PM 18981135
ER
PT J
AU Baranova, IN
Kurlander, R
Bocharov, AV
Vishnyakova, TG
Chen, ZG
Remaley, AT
Csako, G
Patterson, AP
Eggerman, TL
AF Baranova, Irina N.
Kurlander, Roger
Bocharov, Alexander V.
Vishnyakova, Tatyana G.
Chen, Zhigang
Remaley, Alan T.
Csako, Gyorgy
Patterson, Amy P.
Eggerman, Thomas L.
TI Role of Human CD36 in Bacterial Recognition, Phagocytosis, and
Pathogen-Induced JNK-Mediated Signaling
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID INTERLEUKIN-8 GENE-EXPRESSION; CORONARY-HEART-DISEASE; TOLL-LIKE
RECEPTORS; N-TERMINAL KINASE; SCAVENGER RECEPTOR; CHLAMYDIA-PNEUMONIAE;
STAPHYLOCOCCUS-AUREUS; HELICOBACTER-PYLORI; INNATE IMMUNITY;
LIPOPOLYSACCHARIDE
AB Scavenger receptor CD36 mediates Staphylococcus aureus phagocytosis and initiates TLR2/6 signaling. We analyzed the role of CD36 in the uptake and TLR-independent signaling of various bacterium, including Escherichia coli, Klebsiella pneumoniae, Salmonella typhimurium, S. aureus, and Enterococcus faecalis. Expression of human CD36 in HeLa cells increased the uptake of both Gram-positive and Gram-negative bacteria compared with the control mock-transfected cells. Bacterial adhesion was associated with pathogen phagocytosis. Upon CD36 transfection, HEK293 cells, which demonstrate no TLR2/4 expression, acquired LPS responsiveness as assessed by IL-8 production. The cells demonstrated a marked 5- to 15-fold increase in cytokine release upon exposure to Gram-negative bacteria, while the increase was much smaller (1.5- to 3-fold) with Gram-positive bacteria and lipoteichoic acid. CD36 down-regulation utilizing CD36 small interfering RNA reduced cytokine release by 40-50% in human fibroblasts induced by both Gram-negative and Gram-positive bacteria as well as LPS. Of all MAPK signaling cascade inhibitors tested, only the inhibitor of JNK, a stress-activated protein kinase, potently blocked E. coli/LPS-stimulated cytokine production. NF-kappa B inhibitors were ineffective, indicating direct TLR-independent signaling. JNK activation was confirmed by Western blot analyses of phosphorylated JKN1/2 products. Synthetic amphipathic peptides with an a-helical motif were shown to be efficient inhibitors of E. coli- and LPS-induced IL-8 secretion as well as JNK1/2 activation/phosphorylation in CD36-overexpressing cells. These results indicate that CD36 functions as a phagocytic receptor for a variety of bacteria and mediates signaling induced by Gram-negative bacteria and LPS via a JNK-mediated signaling pathway in a TLR2/4-independent manner. The Journal of Immunology, 2008, 181: 7147-7156.
C1 [Eggerman, Thomas L.] NIDDKD, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA.
[Baranova, Irina N.; Kurlander, Roger; Bocharov, Alexander V.; Vishnyakova, Tatyana G.; Chen, Zhigang; Remaley, Alan T.; Csako, Gyorgy; Patterson, Amy P.; Eggerman, Thomas L.] NIDDKD, Dept Lab Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Patterson, Amy P.] NIDDKD, Off Biotechnol Act, Off Sci Policy, Off Director,NIH, Bethesda, MD 20892 USA.
RP Eggerman, TL (reprint author), NIDDKD, Div Diabet Endocrinol & Metab Dis, NIH, 6707 Democracy Blvd,Room 697,MSC 5460, Bethesda, MD 20892 USA.
EM Eggermant@niddk.nih.gov
FU Intramural Research Programs of the Clinical Center; National Institute
of Diabetes and Digestive and Kidney Diseases; National Institute of
Allergy and Infectious Diseases; National Institutes of Health
FX This research was supported by the Intramural Research Programs of the
Clinical Center, National Institute of Diabetes and Digestive and Kidney
Diseases and the National Institute of Allergy and Infectious Diseases,
National Institutes of Health.
NR 48
TC 71
Z9 72
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7147
EP 7156
PG 10
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900055
PM 18981136
ER
PT J
AU Hu, XM
Zhang, D
Pang, H
Caudle, WM
Li, YC
Gao, HM
Liu, YX
Qian, L
Wilson, B
Di Monte, DA
Ali, SF
Zhang, J
Block, ML
Hong, JS
AF Hu, Xiaoming
Zhang, Dan
Pang, Hao
Caudle, W. Michael
Li, Yachen
Gao, Huiming
Liu, Yuxin
Qian, Li
Wilson, Belinda
Di Monte, Donato A.
Ali, Syed F.
Zhang, Jing
Block, Michelle L.
Hong, Jau-Shyong
TI Macrophage Antigen Complex-1 Mediates Reactive Microgliosis and
Progressive Dopaminergic Neurodegeneration in the MPTP Model of
Parkinson's Disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID BETA-2 INTEGRIN CD11B/CD18; NADPH OXIDASE ACTIVATION; SUBSTANTIA-NIGRA;
OXIDATIVE STRESS; NITRIC-OXIDE; CELL-DEATH; IN-VITRO; HLA-DR;
1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; NEUROTOXICITY
AB Neuronal death is known to trigger reactive microgliosis. However, little is known regarding the manner by which microglia are activated by injured neurons and how microgliosis participates in neurodegeneration. In this study we delineate the critical role of macrophage Ag complex-1 (MAC1), a member of the beta(2) integrin family, in mediating reactive microgliosis and promoting dopaminergic (DAergic) neurodegeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. MAC1 deficiency greatly attenuated the DAergic neurodegeneration induced by MPTP or 1-methyl-4-phenyl-pyridium iodide (MPP+) exposure both in vivo and in vitro, respectively. Reconstituted experiments created by adding microglia from MAC1(-/-) or MAC1(+/+) mice back to MAC1(+/+) neuron-enriched cultures showed that microglia with functional MAC1 expression was mandatory for microglia-enhanced neurotoxicity. Both in vivo and in vitro morphological and Western blot studies demonstrated that MPTP/MPP+ produced less microglia activation in MAC1(-/-) mice than MAC1(+/+) mice. Further mechanistic studies revealed that a MPP+-mediated increase in superoxide production was reduced in MAC1(-/-) neuron-glia cultures compared with MAC1(+/+) cultures. The stunted production of superoxide in MAC1(-/-) microglia is likely linked to the lack of translocation of the cytosolic NADPH oxidase (PHOX) subunit (p47(phox)) to the membrane. In addition, the production of PGE(2) markedly decreased in neuron plus MAC1(-/-) microglia cocultures vs neuron plus MAC1(+/+) microglia cocultures. Taken together, these results demonstrate that MAC1 plays a critical role in MPTP/MPP+-induced reactive microgliosis and further support the hypothesis that reactive microgliosis is an essential step in the self-perpetuating cycle leading to progressive DAergic neurodegeneration observed in Parkinson's disease. The Journal of Immunology, 2008, 181: 7194-7204.
C1 [Hu, Xiaoming; Zhang, Dan; Pang, Hao; Li, Yachen; Gao, Huiming; Liu, Yuxin; Qian, Li; Wilson, Belinda; Block, Michelle L.; Hong, Jau-Shyong] NIEHS, Neuropharmacol Sect, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA.
[Caudle, W. Michael; Zhang, Jing] Univ Washington, Dept Pathol, Seattle, WA 98104 USA.
[Di Monte, Donato A.] Parkinsons Inst, Sunnyvale, CA USA.
[Ali, Syed F.] US FDA, Natl Ctr Toxicol Res, Neurochem Lab, Jefferson, AR 72079 USA.
[Block, Michelle L.] Virginia Commonwealth Univ, Dept Anat & Neurobiol, Richmond, VA 23298 USA.
RP Hong, JS (reprint author), NIEHS, Neuropharmacol Sect, Lab Pharmacol & Chem, Mail Drop F1-01,POB 12233, Res Triangle Pk, NC 27709 USA.
EM hong3@niehs.nih.gov
RI gao, huiming/C-8454-2012
FU Intramural Research Program of the National Instrunes of Health;
National Institutes of Health Pathway to Independence Award [NIEHS
IK99ES01549-01]
FX This work was supported by the Intramural Research Program of the
National Instrunes of Health. National Institute of Environmental Health
Sciences. M.L.B. was supported by the National Institutes of Health
Pathway to Independence Award (NIEHS IK99ES01549-01).
NR 60
TC 57
Z9 59
U1 1
U2 7
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7194
EP 7204
PG 11
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900060
PM 18981141
ER
PT J
AU Shi, GP
Cox, CA
Vistica, BP
Tan, CY
Wawrousek, EF
Gery, I
AF Shi, Guangpu
Cox, Catherine A.
Vistica, Barbara P.
Tan, Cuiyan
Wawrousek, Eric F.
Gery, Igal
TI Phenotype Switching by Inflammation-Inducing Polarized Th17 Cells, but
Not by Th1 Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID IL-17-PRODUCING T-CELLS; AUTOIMMUNE ENCEPHALOMYELITIS; OCULAR
INFLAMMATION; NONSPECIFIC CELLS; ROR-ALPHA; TGF-BETA; IL-17; INDUCTION;
LINEAGE; IL-23
AB Th1 and Th17 cells are characterized by their expression of IFN-gamma or IL-17, respectively. The finding of Th cells producing both IL-17 and IFN-gamma suggested, however, that certain Th cells may modify their selective cytokine expression. In this study, we examined changes in cytokine expression in an experimental system in which polarized Th1 or Th17 cells specific against hen egg lysozyme induce ocular inflammation in recipient mice expressing hen egg lysozyme in their eyes. Whereas only IFN-gamma was expressed in eyes of Th1 recipient mice, substantial proportions of donor cells expressed IFN-gamma or both IFN-gamma and IL-17 in Th17 recipient eyes. The possibility that nonpolarized cells in Th17 preparations were responsible for expression of IFN-gamma or IFN-gamma M-17 in Th17 recipient eyes was contradicted by the finding that the proportions of such cells were larger in recipients of Th17 preparations with 20-25% nonpolarized cells than in recipients of 35-40% preparations. Moreover, whereas incubation in vitro of Th1 cells with Th17-polarizing mixture had no effect on their phenotype, incubation of Th17 with Th1-polarizing mixture, or in the absence of cytokines, converted most of these cells into IFN-gamma or IFN-gamma/IL-17-expressing cells. In addition, Th17 incubated with the Th1 mixture expressed T-bet, whereas no ROR-gamma t was detected in Th1 incubated with Th17 mixture. Thus, polarized Th1 cells retain their phenotype in the tested systems, whereas Th17 may switch to express IFN-gamma or IFN-gamma/IL-17 following activation in the absence of cytokines, or exposure to certain cytokine milieus at the inflammation site or in culture. The Journal of Immunology, 2008, 181: 7205-7213.
C1 [Shi, Guangpu; Cox, Catherine A.; Vistica, Barbara P.; Tan, Cuiyan; Gery, Igal] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Wawrousek, Eric F.] NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Cox, Catherine A.] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20814 USA.
RP Gery, I (reprint author), NEI, Immunol Lab, NIH, Bldg 10,Room 10N208, Bethesda, MD 20892 USA.
EM geryi@nei.nih.gov
FU Intramural Research Program of the National Eye Institute; National
Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Eye Institute, National Institutes of Health.
NR 33
TC 96
Z9 97
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7205
EP 7213
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900061
PM 18981142
ER
PT J
AU Barry, JM
Viboud, C
Simonsen, L
AF Barry, John M.
Viboud, Cecile
Simonsen, Lone
TI Cross-Protection between Successive Waves of the 1918-1919 Influenza
Pandemic: Epidemiological Evidence from US Army Camps and from Britain
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID NEW-YORK-CITY; NONPHARMACEUTICAL INTERVENTIONS; CITIES
AB Background. The current worst-case scenario for pandemic influenza planning is based on the catastrophic 1918-1919 pandemic. In this article, we examine the strength of cross-protection between successive waves of the 1918-1919 pandemic, which has remained a long-standing issue of debate.
Method. We studied monthly hospitalization and mortality rates for respiratory illness in 37 army camps, as well as the rates of repeated episodes of influenza infection during January-December 1918 in 8 military and civilian settings in the United States and Britain.
Results. A first wave of respiratory illness occurred in US Army camps during March-May 1918 and in Britain during May-June, followed by a lethal second wave in the fall. The first wave was characterized by high morbidity but had a lower fatality rate than the second wave (1.1% vs. 4.7% among hospitalized soldiers; P <.001). Based on repeated illness data, the first wave provided 35%-94% protection against clinical illness during the second wave and 56%-89% protection against death (P <.001).
Conclusion. Exposure to influenza in the spring and summer of 1918 provided mortality and morbidity protection during the fall pandemic wave. The intensity of the first wave may have differed across US cities and countries and may partly explain geographical variation in pandemic mortality rates in the fall. Pandemic preparedness plans should consider that immune protection could be naturally acquired during a first wave of mild influenza illnesses.
C1 [Barry, John M.] Tulane Univ, Ctr Bioenvironm Res, New Orleans, LA 70112 USA.
[Barry, John M.] Xavier Univ, Ctr Bioenvironm Res, New Orleans, LA 70112 USA.
[Viboud, Cecile] Fogarty Int Ctr, Bethesda, MD USA.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth, Hlth Serv, Washington, DC USA.
RP Barry, JM (reprint author), Tulane Univ, Ctr Bioenvironm Res, New Orleans, LA 70112 USA.
EM jbarry@tulane.edu
OI Simonsen, Lone/0000-0003-1535-8526
FU Intramural NIH HHS
NR 31
TC 65
Z9 69
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2008
VL 198
IS 10
BP 1427
EP 1434
DI 10.1086/592454
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 366HW
UT WOS:000260472400003
PM 18808337
ER
PT J
AU Sandstrom, E
Nilsson, C
Hejdeman, B
Brave, A
Bratt, G
Robb, M
Cox, J
VanCott, T
Marovich, M
Stout, R
Aboud, S
Bakari, M
Pallangyo, K
Ljungberg, K
Moss, B
Earl, P
Michael, N
Birx, D
Mhalu, F
Wahren, B
Biberfeld, G
AF Sandstrom, Eric
Nilsson, Charlotta
Hejdeman, Bo
Brave, Andreas
Bratt, Goran
Robb, Merlin
Cox, Josephine
VanCott, Thomas
Marovich, Mary
Stout, Richard
Aboud, Said
Bakari, Muhammad
Pallangyo, Kisali
Ljungberg, Karl
Moss, Bernard
Earl, Patricia
Michael, Nelson
Birx, Deborah
Mhalu, Fred
Wahren, Britta
Biberfeld, Gunnel
CA HIV Immunogenicity Study 01 02 Tea
TI Broad Immunogenicity of a Multigene, Multiclade HIV-1 DNA Vaccine
Boosted with Heterologous HIV-1 Recombinant Modified Vaccinia Virus
Ankara
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT 6th Annual International AIDS Vaccine Conference
CY AUG 20-23, 2007
CL Seattle, WA
ID CD8(+) T-CELL; COLONY-STIMULATING FACTOR; HEPATITIS-B VACCINATION;
CANDIDATE VACCINE; IMMUNE-RESPONSES; PHASE-1 SAFETY; AIDS RESEARCH;
EPITOPES; REGIMEN; CLADE
AB Background. A human immunodeficiency virus (HIV) vaccine that limits disease and transmission is urgently needed. This clinical trial evaluated the safety and immunogenicity of an HIV vaccine that combines a plasmid-DNA priming vaccine and a modified vaccinia virus Ankara (MVA) boosting vaccine. Methods. Forty healthy volunteers were injected with DNA plasmids containing gp160 of HIV-1 subtypes A, B, and C; rev B; p17/p24 gag A and B, and RTmut B by use of a needle-free injection system. The vaccine was administered intradermally or intramuscularly, with or without recombinant granulocyte macrophage colony-stimulating factor, and boosted with a heterologousMVAcontaining env, gag, and pol of CRF01A_ E. Immune responses were monitored with HIV-specific interferon (IFN)-gamma and interleukin (IL)-2 ELISpot and lymphoproliferative assays (LPAs). Results. Vaccine-related adverse events were mild and tolerable. After receipt of the DNA priming vaccine, 11 (30%) of 37 vaccinees had HIV-specific IFN-gamma responses. After receipt of the MVA boosting vaccine, ELISpot assays showed that 34 (92%) of 37 vaccinees had HIV-specific IFN-gamma responses, 32 (86%) to Gag and 24 ( 65%) to Env. IFN-gamma production was detected in both the CD8(+) T cell compartment ( 5 of 9 selected vaccinees) and the CD4(+) T cell compartment ( 9 of 9). ELISpot results showed that 25 ( 68%) of 37 vaccinees had a positive IL-2 response and 35 ( 92%) of 38 had a positive LPA response. Of 38 subjects, a total of 37 (97%) were responders. One milligram of HIV-1 DNA administered intradermally was as effective as 4mg administered intramuscularly in priming for the MVA boosting vaccine. Conclusion. This HIV-DNA priming-MVA boosting approach is safe and highly immunogenic.
C1 [Ljungberg, Karl] Karolinska Inst, Dept Oncol Pathol, S-11883 Stockholm, Sweden.
[Nilsson, Charlotta; Brave, Andreas; Wahren, Britta; Biberfeld, Gunnel] Karolinska Inst, Swedish Inst Infect Dis Control, S-11883 Stockholm, Sweden.
[Robb, Merlin; Cox, Josephine; VanCott, Thomas; Marovich, Mary; Michael, Nelson; Birx, Deborah] Walter Reed Army Inst Res, Dept Retrovirol, Rockville, MD USA.
[Moss, Bernard; Earl, Patricia] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Stout, Richard] Bioject, Portland, OR USA.
[Aboud, Said; Bakari, Muhammad; Pallangyo, Kisali; Mhalu, Fred] Muhimbili Univ Hlth & Allied Sci, Dar Es Salaam, Tanzania.
[Nilsson, Charlotta; Brave, Andreas; Wahren, Britta; Biberfeld, Gunnel] Karolinska Inst, Dept Microbiol & Tumor & Cell Biol, S-11883 Stockholm, Sweden.
[Sandstrom, Eric; Hejdeman, Bo; Bratt, Goran] Karolinska Inst, Soder Sjukhuset, Dept Clin Sci & Educ, S-11883 Stockholm, Sweden.
RP Wahren, B (reprint author), Karolinska Inst, Soder Sjukhuset, Dept Clin Sci & Educ, S-11883 Stockholm, Sweden.
EM Eric.sandstrom@sodersjukhuset.se; Britta.Wahren@smi.ki.se
OI Ljungberg, Karl/0000-0001-7192-6204
FU Intramural NIH HHS [Z01 AI000416-25]
NR 34
TC 99
Z9 100
U1 2
U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2008
VL 198
IS 10
BP 1482
EP 1490
DI 10.1086/592507
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 366HW
UT WOS:000260472400010
PM 18808335
ER
PT J
AU Houff, SA
Berger, J
Major, EO
AF Houff, Sidney A.
Berger, Joseph
Major, Eugene O.
TI Response to Linberg et al. Natalizumab alters transcriptional expression
profiles of blood cell subpopulations of multiple sclerosis patients
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Letter
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HEMATOPOIETIC PROGENITOR
CELLS; LYMPHOCYTES; ANTIBODY; LATENCY
C1 [Houff, Sidney A.; Berger, Joseph] Univ Kentucky, Dept Neurol, Lexington, KY 40536 USA.
[Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, Bethesda, MD 20892 USA.
RP Houff, SA (reprint author), Univ Kentucky, Dept Neurol, Lexington, KY 40536 USA.
EM sahouf2@uky.edu
NR 14
TC 5
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-5728
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD NOV 15
PY 2008
VL 204
IS 1-2
BP 155
EP 156
DI 10.1016/j.jneuroim.2008.05.007
PG 2
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 377SK
UT WOS:000261270700021
PM 19117088
ER
PT J
AU van Aken, AFJ
Atiba-Davies, M
Marcotti, W
Goodyear, RJ
Bryant, JE
Richardson, GP
Noben-Trauth, K
Kros, CJ
AF van Aken, Alexander F. J.
Atiba-Davies, Margaret
Marcotti, Walter
Goodyear, Richard J.
Bryant, Jane E.
Richardson, Guy P.
Noben-Trauth, Konrad
Kros, Corne J.
TI TRPML3 mutations cause impaired mechano-electrical transduction and
depolarization by an inward-rectifier cation current in auditory hair
cells of varitint-waddler mice
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID ANKLE-LINK COMPLEX; MOUSE COCHLEA; MECHANOTRANSDUCER CHANNEL; SENSORY
CELLS; PROTEIN; DEAFNESS; HEARING; ABNORMALITIES; LOCALIZATION;
STEREOCILIA
AB TRPML3 (mucolipin-3) belongs to one of the transient-receptor-potential (TRP) ion channel families. Mutations in the Trpml3 gene cause disorganization of the stereociliary hair bundle, structural aberrations in outer and inner hair cells and stria vascularis defects, leading to deafness in the varitint-waddler (Va) mouse. Here we refined the stereociliary localization of TRPML3 and investigated cochlear hair cell function in varitint-waddler (Va(J)) mice carrying the TRPML3 < I362T/A419P > mutations. Using a TRPML3-specific antibody we detected a similar to 68 kDa protein with near-equal expression levels in cochlea and vestibule of wild-type and Va(J) mutants. At postnatal days 3 and 5, we observed abundant localization of TRPML3 at the base of stereocilia near the position of the ankle links. This stereociliary localization domain was absent in Va(J) heterozygotes and homozygotes. Electrophysiological recordings revealed reduced mechano-electrical transducer currents in hair cells from Va(J)/+ and Va(J)/Va(J) mice. Furthermore, FM1-43 uptake and [(3)H]gentamicin accumulation were decreased in hair cells in cultured organs of Corti from Va(J)/+ and Va(J)/Va(J) mice. We propose that TRPML3 plays a critical role at the ankle-link region during hair-bundle growth and that an adverse effect of mutant TRPML3 on bundle development and mechano-electrical transduction is the main cause of hearing loss in Va(J)/+ mutant mice. Outer hair cells of Va(J)/Va(J) mice additionally had depolarized resting potentials due to an inwardly rectifying leak conductance formed by the mutant channels, leading over time to hair-cell degeneration and contributing to their deafness. Our findings argue against TRPML3 being a component of the hair-cell transducer channel.
C1 [Atiba-Davies, Margaret; Noben-Trauth, Konrad] Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD 20850 USA.
[van Aken, Alexander F. J.; Marcotti, Walter; Goodyear, Richard J.; Bryant, Jane E.; Richardson, Guy P.; Kros, Corne J.] Univ Sussex, Sch Life Sci, Brighton BN1 9QG, E Sussex, England.
RP Noben-Trauth, K (reprint author), Natl Inst Deafness & Other Commun Disorders, NIH, 5 Res Court, Rockville, MD 20850 USA.
EM nobentk@nidcd.nih.gov; c.j.kros@sussex.ac.uk
FU EU Integrated Project; MRC Programme Grant; Division of Intramural
Research at NIDCD; Wellcome Trust; Royal Society University
FX This work was supported by EuroHear, an EU Integrated Project (C.J.K.
and G.P.R.), an MRC Programme Grant (C.J.K.), the Division of Intramural
Research at NIDCD ( K.N.-T.) and a Wellcome Trust grant (G.P.R.). W.M.
is a Royal Society University Research Fellow. We thank Kuni Iwasa and
Susan Sullivan for comments on earlier versions of this manuscript.
NR 46
TC 42
Z9 42
U1 1
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD NOV 15
PY 2008
VL 586
IS 22
BP 5403
EP 5418
DI 10.1113/jphysiol.2008.156992
PG 16
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 377TX
UT WOS:000261274600015
PM 18801844
ER
PT J
AU Laird, ME
Igarashi, T
Martin, MA
Desrosiers, RC
AF Laird, Melissa E.
Igarashi, Tatsuhiko
Martin, Malcolm A.
Desrosiers, Ronald C.
TI Importance of the V1/V2 Loop Region of Simian-Human Immunodeficiency
Virus Envelope Glycoprotein gp120 in Determining the Strain Specificity
of the Neutralizing Antibody Response
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN MONOCLONAL-ANTIBODY; INTRACHAIN DISULFIDE BONDS; HIV-1/SIV
CHIMERIC VIRUS; FUSION INHIBITOR T-20; TYPE-1 ENVELOPE; RHESUS-MONKEYS;
V3 LOOP; VACCINE DEVELOPMENT; INDUCE ANTIBODIES; HUMORAL IMMUNITY
AB Plasma samples from individuals infected with human immunodeficiency virus type 1 (HIV-1) are known to be highly strain specific in their ability to neutralize HIV-1 infectivity. Such plasma samples exhibit significant neutralizing activity against autologous HIV-1 isolates but typically exhibit little or no activity against heterologous strains, although some cross-neutralizing activity can develop late in infection. Monkeys infected with the simian-human immunodeficiency virus (SHIV) clone DH12 generated antibodies that neutralized SHIV DH12, but not SHIV KB9. Conversely, antibodies from monkeys infected with the SHIV clone KB9 neutralized SHIV KB9, but not SHIV DH12. To investigate the role of the variable loops of the HIV-1 envelope glycoprotein gp120 in determining this strain specificity, variable loops 1 and 2 (V1/V2), V3, or V4 were exchanged individually or in combination between SHIV DH12 and SHIV KB9. Despite the fact that both parental viruses exhibited significant infectivity and good replication in the cell lines examined, 3 of the 10 variable-loop chimeras exhibited such poor infectivity that they could not be used further for neutralization assays. These results indicate that a variable loop that is functional in the context of one particular envelope background will not necessarily function within another. The remaining seven replication-competent chimeras allowed unambiguous assignment of the sequences principally responsible for the strain specificity of the neutralizing activity present in SHIV-positive plasma. Exchange of the V1/V2 loop sequences conferred a dominant loss of sensitivity to neutralization by autologous plasma and a gain of sensitivity to neutralization by heterologous plasma. Substitution of V3 or V4 had little or no effect on the sensitivity to neutralization. These data demonstrate that the V1/V2 region of HIV-1 gp120 is principally responsible for the strain specificity of the neutralizing antibody response in monkeys infected with these prototypic SHIVs.
C1 [Laird, Melissa E.; Desrosiers, Ronald C.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, New England Primate Res Ctr, Southborough, MA 01772 USA.
[Igarashi, Tatsuhiko] Kyoto Univ, Inst Virus Res, Expt Res Ctr Infect Dis, Lab Primate Models, Kyoto 6068507, Japan.
[Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Desrosiers, RC (reprint author), Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, New England Primate Res Ctr, 1 Pine Hill Dr, Southborough, MA 01772 USA.
EM ronald_desrosiers@hms.harvard.edu
FU PHS [AI 025328, RR00168]; International AIDS Vaccine Initiative;
National Institute of Allergy and Infectious Diseases; National
Institutes of Health
FX This work was supported by PHS grants AI 025328 ( R. C. D.) and RR00168
(NEPRC) and by funding from the International AIDS Vaccine Initiative.
Additionally, this work was supported by the Intramural Research Program
of the National Institute of Allergy and Infectious Diseases, National
Institutes of Health ( M. A. M.).; We thank the NEPRC DNA-sequencing
core for technical support and the NEPRC Division of Primate Resources
for experimental monkey infection and blood sampling. We also thank
Thomas Postler, Elizabeth MacKenzie, and Jacqueline Bixby for technical
and editing assistance.
NR 98
TC 18
Z9 19
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11054
EP 11065
DI 10.1128/JVI.01341-08
PG 12
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000009
PM 18768967
ER
PT J
AU Hoelzer, K
Shackelton, LA
Holmes, EC
Parrish, CR
AF Hoelzer, Karin
Shackelton, Laura A.
Holmes, Edward C.
Parrish, Colin R.
TI Within-Host Genetic Diversity of Endemic and Emerging Parvoviruses of
Dogs and Cats
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID FELINE PANLEUKOPENIA VIRUS; CANINE-PARVOVIRUS; MINUTE VIRUS;
NONHOMOLOGOUS RECOMBINATION; EVOLUTIONARY DYNAMICS; SPONTANEOUS
MUTATION; MUTANT FREQUENCY; ANALYSIS REVEALS; DOMESTIC CAT; MURINE CELLS
AB Viral emergence can result from the adaptation of endemic pathogens to new or altered host environments, a process that is strongly influenced by the underlying sequence diversity. To determine the extent and structure of intrahost genetic diversity in a recently emerged single-stranded DNA virus, we analyzed viral population structures during natural infections of animals with canine parvovirus (CPV) or its ancestor, feline panleukopenia virus (FPV). We compared infections that occurred shortly after CPV emerged with more recent infections and examined the population structure of CPV after experimental cross-species transmission to cats. Infections with CPV and FPV showed limited genetic diversity regardless of the analyzed host tissue or year of isolation. Coinfections with genetically distinct viral strains were detected in some cases, and rearranged genomes were seen in both FPV and CPV. The sporadic presence of some sequences with multiple mutations suggested the occurrence of either particularly error-prone viral replication or coinfection by more distantly related strains. Finally, some potentially organ-specific host effects were seen during experimental cross-species transmission, with many of the mutations located in the nonstructural protein NS2. These included residues with evidence of positive selection at the population level, which is compatible with a role of this protein in host adaptation.
C1 [Hoelzer, Karin; Parrish, Colin R.] Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Shackelton, Laura A.; Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, Mueller Lab, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Parrish, CR (reprint author), Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
EM crp3@cornell.edu
RI Hoelzer, Karin/A-8230-2010;
OI Holmes, Edward/0000-0001-9596-3552
FU National Institutes of Health [GM080533, AI028385]
FX We thank Virginia Scarpino, Wendy Weichert, and Melanie Ho for technical
support.; This work was supported by National Institutes of Health
grants GM080533 to E. C. H. and AI028385 to C. R. P. K. H. is supported
by a graduate assistantship from the College of Veterinary Medicine at
Cornell.
NR 47
TC 26
Z9 28
U1 0
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11096
EP 11105
DI 10.1128/JVI.01003-08
PG 10
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000013
PM 18768982
ER
PT J
AU Heiman, EM
McDonald, SM
Barro, M
Taraporewala, ZF
Bar-Magen, T
Patton, JT
AF Heiman, Erica M.
McDonald, Sarah M.
Barro, Mario
Taraporewala, Zenobia F.
Bar-Magen, Tamara
Patton, John T.
TI Group A Human Rotavirus Genomics: Evidence that Gene Constellations Are
Influenced by Viral Protein Interactions
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RNA-RNA HYBRIDIZATION; MOLECULAR CHARACTERIZATION; REGULATORY FACTOR-3;
CAPSID PROTEIN; SUBGROUP-I; STRAINS; SEROTYPE; SPECIFICITY;
IDENTIFICATION; PATTERN
AB Group A human rotaviruses (HRVs) are the major cause of severe viral gastroenteritis in infants and young children. To gain insight into the level of genetic variation among HRVs, we determined the genome sequences for 10 strains belonging to different VP7 serotypes (G types). The HRVs chosen for this study, D, DS-1, P, ST3, IAL28, Se584, 69M, WI61, A64, and L26, were isolated from infected persons and adapted to cell culture to use as serotype references. Our sequencing results revealed that most of the individual proteins from each HRV belong to one of three genotypes (1, 2, or 3) based on their similarities to proteins of genogroup strains (Wa, DS-1, or AU-1, respectively). Strains D, P, ST3, IAL28, and WI61 encode genotype 1 (Wa-like) proteins, whereas strains DS-1 and 69M encode genotype 2 (DS-1-like) proteins. Of the 10 HRVs sequenced, 3 of them (Se584, A64, and L26) encode proteins belonging to more than one genotype, indicating that they are intergenogroup reassortants. We used amino acid sequence alignments to identify residues that distinguish proteins belonging to HRV genotype 1, 2, or 3. These genotype-specific changes cluster in definitive regions within each viral protein, many of which are sites of known protein-protein interactions. For the intermediate viral capsid protein (VP6), the changes map onto the atomic structure at the VP2-VP6, VP4-VP6, and VP7-VP6 interfaces. The results of this study provide evidence that group A HRV gene constellations exist and may be influenced by interactions among viral proteins during replication.
C1 [Heiman, Erica M.; McDonald, Sarah M.; Barro, Mario; Taraporewala, Zenobia F.; Bar-Magen, Tamara; Patton, John T.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Patton, JT (reprint author), NIAID, Infect Dis Lab, NIH, 50 S Dr,MSC 8026,Room 6314, Bethesda, MD 20892 USA.
EM jpatton@niaid.nih.gov
RI Patton, John/P-1390-2014
FU NIH; National Institute of Allergy and Infectious Diseases; Oak Ridge
Associated Universities' Research Associates
FX We express our appreciation to Taka Hoshino for generously providing the
HRVs used in this study and to A1 Kapikian and Jelle Matthijnssens for
insightful comments and critical readings of the manuscript.; This work
was supported by the Intramural Research Program of the NIH, National
Institute of Allergy and Infectious Diseases. E. M. H. was also
supported by the Oak Ridge Associated Universities' Research
Associates/Specialists Program at the NIH.
NR 52
TC 82
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U1 0
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11106
EP 11116
DI 10.1128/JVI.01402-08
PG 11
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000014
PM 18786998
ER
PT J
AU Chan, R
Uchil, PD
Jin, J
Shui, GH
Ott, DE
Mothes, W
Wenk, MR
AF Chan, Robin
Uchil, Pradeep D.
Jin, Jing
Shui, Guanghou
Ott, David E.
Mothes, Walther
Wenk, Markus R.
TI Retroviruses Human Immunodeficiency Virus and Murine Leukemia Virus Are
Enriched in Phosphoinositides
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ROUS-SARCOMA-VIRUS; IONIZATION MASS-SPECTROMETRY; CELL PLASMA-MEMBRANES;
LIPID RAFTS; TYPE-1 GAG; MULTIVESICULAR ENDOSOMES;
QUANTITATIVE-ANALYSIS; PROTEINS; HIV-1; CERAMIDE
AB Retroviruses acquire a lipid envelope during budding from the membrane of their hosts. Therefore, the composition of this envelope can provide important information about the budding process and its location. Here, we present mass spectrometry analysis of the lipid content of human immunodeficiency virus type 1 (HIV-1) and murine leukemia virus (MLV). The results of this comprehensive survey found that the overall lipid content of these viruses mostly matched that of the plasma membrane, which was considerably different from the total lipid content of the cells. However, several lipids are enriched in comparison to the composition of the plasma membrane: (i) cholesterol, ceramide, and GM3; and (ii) phosphoinositides, phosphorylated derivatives of phosphatidylinositol. Interestingly, microvesicles, which are similar in size to viruses and are also released from the cell periphery, lack phosphoinositides, suggesting a different budding mechanism/location for these particles than for retroviruses. One phosphoinositide, phosphatidylinositol 4,5-bisphosphate [ PI( 4,5) P 2], has been implicated in membrane binding by HIV Gag. Consistent with this observation, we found that PI(4,5)P(2) was enriched in HIV-1 and that depleting this molecule in cells reduced HIV-1 budding. Analysis of mutant virions mapped the enrichment of PI(4,5)P(2) to the matrix domain of HIV Gag. Overall, these results suggest that HIV-1 and other retroviruses bud from cholesterol-rich regions of the plasma membrane and exploit matrix/PI(4,5)P(2) interactions for particle release from cells.
C1 [Wenk, Markus R.] Natl Univ Singapore, Yong Loo Lin Sch Med, Ctr Life Sci, Dept Biochem, Singapore 117607, Singapore.
[Wenk, Markus R.] Natl Univ Singapore, Dept Biol Sci, Singapore 117607, Singapore.
[Uchil, Pradeep D.; Jin, Jing; Mothes, Walther] Yale Univ, Sch Med, Dept Microbial Pathogenesis, New Haven, CT USA.
[Ott, David E.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Wenk, MR (reprint author), Natl Univ Singapore, Yong Loo Lin Sch Med, Ctr Life Sci, Dept Biochem, 28 Med Dr,Level 04-21, Singapore 117607, Singapore.
EM bchmrw@nus.edu.sg
RI Wenk, Markus/D-1441-2014
FU Singapore National Research Foundation; National University of Singapore
[R-183000-607-712]; Academic Research Fund [R-183-000-160-112];
Biomedical Research Council of Singapore [R-183-000-134-305]; Novartis
Institute for Tropical Diseases [R-183-000-166-592]; National Institutes
of Health (NIH) [R21 AI065284, ND1-CO-12400]; Anna Fuller Fellowship;
National Cancer Institute
FX We thank Maik Lehmann for initial virus preparations; Donna Beer Stolz
for silica beads; Kunio Nagashima and Marc Pypaert for electron
microscopy; and Pietro de Camilli for valuable suggestions.; M. R. W.
was supported in part by grants from the Singapore National Research
Foundation under CRP award no. 2007-04, the National University of
Singapore via the Office of Life Science (R-183000-607-712), the
Academic Research Fund (R-183-000-160-112), the Biomedical Research
Council of Singapore (R-183-000-134-305), and the Novartis Institute for
Tropical Diseases (R-183-000-166-592). W. M. was supported by a grant
from the National Institutes of Health (NIH) (R21 AI065284), and P. D.
U. was supported by an Anna Fuller Fellowship in Cancer Research. This
project was funded in part with federal funds from the National Cancer
Institute, National Institutes of Health, under contract no.
ND1-CO-12400.
NR 63
TC 158
Z9 159
U1 1
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11228
EP 11238
DI 10.1128/JVI.00981-08
PG 11
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000024
PM 18799574
ER
PT J
AU Bishop, KA
Hickey, AC
Khetawat, D
Patch, JR
Bossart, KN
Zhu, ZY
Wang, LF
Dimitrov, DS
Broder, CC
AF Bishop, Kimberly A.
Hickey, Andrew C.
Khetawat, Dimple
Patch, Jared R.
Bossart, Katharine N.
Zhu, Zhongyu
Wang, Lin-Fa
Dimitrov, Dimiter S.
Broder, Christopher C.
TI Residues in the Stalk Domain of the Hendra Virus G Glycoprotein Modulate
Conformational Changes Associated with Receptor Binding
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NEWCASTLE-DISEASE VIRUS; HEMAGGLUTININ-NEURAMINIDASE PROTEIN; HOMOLOGOUS
FUSION PROTEIN; AMINO-ACID SUBSTITUTIONS; F-SPECIFIC DOMAIN; NIPAH
VIRUS; CELL-FUSION; MEMBRANE-FUSION; MEASLES-VIRUS; HN PROTEIN
AB Hendra virus (HeV) is a member of the broadly tropic and highly pathogenic paramyxovirus genus Henipavirus. HeV is enveloped and infects cells by using membrane-anchored attachment (G) and fusion (F) glycoproteins. G possesses an N-terminal cytoplasmic tail, an external membrane-proximal stalk domain, and a C-terminal globular head that binds the recently identified receptors ephrinB2 and ephrinB3. Receptor binding is presumed to induce conformational changes in G that subsequently trigger F-mediated fusion. The stalk domains of other attachment glycoproteins appear important for oligomerization and F interaction and specificity. However, this region of G has not been functionally characterized. Here we performed a mutagenesis analysis of the HeV G stalk, targeting a series of isoleucine residues within a hydrophobic alpha-helical domain that is well conserved across several attachment glycoproteins. Nine of 12 individual HeV G alanine substitution mutants possessed a complete defect in fusion-promotion activity yet were cell surface expressed and recognized by a panel of conformation-dependent monoclonal antibodies (MAbs) and maintained their oligomeric structure. Interestingly, these G mutations also resulted in the appearance of an additional electrophoretic species corresponding to a slightly altered glycosylated form. Analysis revealed that these G mutants appeared to adopt a receptor-bound conformation in the absence of receptor, as measured with a panel of MAbs that preferentially recognize G in a receptor-bound state. Further, this phenotype also correlated with an inability to associate with F and in triggering fusion even after receptor engagement. Together, these data suggest the stalk domain of G plays an important role in the conformational stability and receptor binding-triggered changes leading to productive fusion, such as the dissociation of G and F.
C1 [Bishop, Kimberly A.; Hickey, Andrew C.; Khetawat, Dimple; Patch, Jared R.; Broder, Christopher C.] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
[Bossart, Katharine N.; Wang, Lin-Fa] CSIRO Livestock Ind, Australian Anim Hlth Lab, Geelong, Vic 3220, Australia.
[Zhu, Zhongyu; Dimitrov, Dimiter S.] NCI, Prot Interact Grp, CCRNP, CCR,NIH, Frederick, MD 21702 USA.
[Zhu, Zhongyu] NCI, BRP, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Broder, CC (reprint author), Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
EM cbroder@usuhs.mil
OI Bossart, Katharine/0000-0001-6886-6896
FU NIH [AI054715, N01-CO-12400]; National Cancer Institute
FX We thank Michael Flora and all his staff at the Biomedical
Instrumentation Center (BIC) of the Uniformed Services University (USU)
for primer synthesis and sequencing. We also thank John White (CSIRO)
for monoclonal antibodies and Erica Ollman Saphire (Scripps) and Rebecca
Dutch (University of Kentucky) for helpful discussions.; This work was
supported by NIH grant AI054715 to C. C. B. This study was also
supported by the NIH intramural biodefense program (D.S.D.). This
project has been funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
N01-CO-12400. This research was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research.; The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U. S. Government. The views
expressed in the manuscript are solely those of the authors, and they do
not represent official views or opinions of the Department of Defense or
The Uniformed Services University of the Health Sciences.
NR 51
TC 53
Z9 56
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11398
EP 11409
DI 10.1128/JVI.02654-07
PG 12
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000039
PM 18799571
ER
PT J
AU Kader, M
Hassan, WM
Eberly, M
Piatak, M
Lifson, JD
Roederer, M
Mattapallil, JJ
AF Kader, Muhamuda
Hassan, Wail M.
Eberly, Matthew
Piatak, Michael
Lifson, Jeffrey D.
Roederer, Mario
Mattapallil, Joseph J.
TI Antiretroviral Therapy prior to Acute Viral Replication Preserves CD4 T
Cells in the Periphery but Not in Rectal Mucosa during Acute Simian
Immunodeficiency Virus Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HIV-1 INFECTION; RHESUS MACAQUES; LYMPHOID-TISSUE;
GASTROINTESTINAL-TRACT; SIV INFECTION; MEMORY; PERSISTENCE; DEPLETION;
RESTORATION; RECHALLENGE
AB The rectal mucosa is a major site for human immunodeficiency virus entry and CD4 T-cell depletion. The early and near-total loss of these cells from the rectal mucosa severely compromises the ability of the mucosal immune system to control various opportunistic infections. Protecting these cells from infection and destruction can delay disease progression, leading to a better long-term outcome. Here we show that effective suppression of viral infection in memory CD4 T cells from the rectal mucosa and peripheral blood to a very low level with antiretroviral therapy (ART) initiated prior to the peak of infection is associated with opposite outcomes in these tissues. A near-total loss of CD4 T cells in the rectal mucosa contrasted with preservation of most memory CD4 T cells in peripheral blood during the course of treatment. Interestingly, ART significantly reduced viral infection in memory CD4 T cells from both rectal mucosa and peripheral blood. Although early ART was of limited value in protecting the CD4 T cells in the rectal mucosa, the significant preservation of peripheral CD4 T cells could contribute to maintaining immune competence, leading to a better long-term outcome.
C1 [Mattapallil, Joseph J.] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
[Piatak, Michael; Lifson, Jeffrey D.] NCI, SAIC, Frederick, MD 21702 USA.
[Roederer, Mario] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Mattapallil, JJ (reprint author), Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Room B4068, Bethesda, MD 20814 USA.
EM jmattapallil@usuhs.mil
OI Hassan, Wail/0000-0002-2960-3927
FU National Institute of Allergy and Infectious Diseases (NIAID)
[K22AI07812]; National Institute of Dental and Craniofacial Research
(NIDCR) [R21DE018339]; National Institutes of Health [NO1-CO-124000]
FX We thank Nancy Miller at the SVEU of NIAID for help with the animals;
Michael Miller at Gilead Sciences, Inc., for providing PMPA and FTC;
Karen Wolcott and Kateryna Lund at the Biomedical Instrumentation Core
facility at USUHS for help with flow cytometry; and Deborah Weiss and
Jim Treece at ABL, Inc., Rockville, MD, for expert assistance with the
animals.; The described project was supported by grant K22AI07812 from
the National Institute of Allergy and Infectious Diseases (NIAID), by
grant R21DE018339 from the National Institute of Dental and Craniofacial
Research (NIDCR) to J.J.M., and in part by federal funds from the
National Cancer Institute, National Institutes of Health, under contract
NO1-CO-124000.; The content is solely the responsibility of the authors
and does not necessarily represent the official views of NIAID, NIDCR,
or the National Institutes of Health.
NR 32
TC 18
Z9 19
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11467
EP 11471
DI 10.1128/JVI.01143-08
PG 5
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000047
PM 18768962
ER
PT J
AU Oh, J
Chang, KW
Hughes, SH
AF Oh, Jangsuk
Chang, Kevin W.
Hughes, Stephen H.
TI Integration of Rous Sarcoma Virus DNA: a CA Dinucleotide Is Not Required
for Integration of the U3 End of Viral DNA
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TYPE-1 POLYPURINE TRACT; RNASE-H CLEAVAGE; IN-VITRO INTEGRATION;
SUBSTRATE-SPECIFICITY; SEQUENCES ADJACENT; RETROVIRAL DNA; PROTEIN;
VIVO; MUTATIONS; DETERMINANTS
AB The two ends of RSV linear DNA are independently inserted into host DNA by integrase in vivo. We previously showed that the range of U3 sequences that are acceptable substrates for integrase appeared to be greater than the range of acceptable U5 sequences in vivo. We have done additional experiments to determine which U3 sequences are good integrase substrates. On the U3 end, there does not appear to be a stringent requirement for the canonical CA, integrase can efficiently remove three nucleotides, and six nucleotides are sufficient to allow integration with reasonable, albeit reduced, efficiency.
C1 [Oh, Jangsuk; Chang, Kevin W.; Hughes, Stephen H.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Oh, Jangsuk] NHLBI, Lab Mol Immunol, Bethesda, MD 20892 USA.
[Chang, Kevin W.] NIH, Off Technol Transfer, Rockville, MD USA.
RP Hughes, SH (reprint author), NCI, HIV Drug Resistance Program, POB B,Bldg 539,Rm 130A, Frederick, MD 21702 USA.
EM hughes@ncifcrf.gov
FU NIH; NIH, National Cancer Institute, Center for Cancer Research
FX We thank Teresa Burdette for help with the preparation of the
manuscript.; This research was supported by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research.
NR 24
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2008
VL 82
IS 22
BP 11480
EP 11483
DI 10.1128/JVI.01353-08
PG 4
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000050
PM 18768972
ER
PT J
AU Zhang, F
Gaur, NA
Hasek, J
Kim, SJ
Qiu, HF
Swanson, MJ
Hinnebusch, AG
AF Zhang, Fan
Gaur, Naseem A.
Hasek, Jiri
Kim, Soon-ja
Qiu, Hongfang
Swanson, Mark J.
Hinnebusch, Alan G.
TI Disrupting Vesicular Trafficking at the Endosome Attenuates
Transcriptional Activation by Gcn4
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID RNA-POLYMERASE-II; SACCHAROMYCES-CEREVISIAE GENOME; AMINO-ACID
BIOSYNTHESIS; IN-VIVO; GENE-EXPRESSION; SRB MEDIATOR; TRANSLATIONAL
CONTROL; CANDIDA-ALBICANS; MASTER REGULATOR; SHUTTLE VECTORS
AB The late endosome (MVB) plays a key role in coordinating vesicular transport of proteins between the Golgi complex, vacuole/lysosome, and plasma membrane. We found that deleting multiple genes involved in vesicle fusion at the MVB (class C/D vps mutations) impairs transcriptional activation by Gcn4, a global regulator of amino acid biosynthetic genes, by decreasing the ability of chromatin-bound Gcn4 to stimulate preinitiation complex assembly at the promoter. The functions of hybrid activators with Gal4 or VP16 activation domains are diminished in class D mutants as well, suggesting a broader defect in activation. Class E vps mutations, which impair protein sorting at the MVB, also decrease activation by Gcn4, provided they elicit rapid proteolysis of MVB cargo proteins in the aberrant late endosome. By contrast, specifically impairing endocytic trafficking from the plasma membrane, or vesicular transport to the vacuole, has a smaller effect on Gcn4 function. Thus, it appears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, and not merely the failure to transport cargo properly to the vacuole or downregulate plasma membrane proteins by endocytosis, is required to attenuate substantially transcriptional activation by Gcn4.
C1 [Zhang, Fan; Gaur, Naseem A.; Kim, Soon-ja; Qiu, Hongfang; Swanson, Mark J.; Hinnebusch, Alan G.] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
[Hasek, Jiri] Acad Sci Czech Republic, Inst Microbiol, Prague, Czech Republic.
RP Hinnebusch, AG (reprint author), NICHHD, Lab Gene Regulat & Dev, NIH, Bldg 6A Room B1A-13, Bethesda, MD 20892 USA.
EM ahinnebusch@nih.gov
RI Hasek, Jiri/H-2427-2014;
OI Gaur, Naseem/0000-0002-1224-8789
FU NIH; LC545; Institutional Research Concept [AV0Z50200510]
FX This work was supported in part by the Intramural Research Program of
the NIH. J.H. was supported by LC545 and Institutional Research Concept
no. AV0Z50200510.
NR 72
TC 13
Z9 13
U1 0
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD NOV 15
PY 2008
VL 28
IS 22
BP 6796
EP 6818
DI 10.1128/MCB.00800-08
PG 23
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 364XC
UT WOS:000260367900006
PM 18794364
ER
PT J
AU Alone, PV
Cao, C
Dever, TE
AF Alone, Pankaj V.
Cao, Chune
Dever, Thomas E.
TI Translation Initiation Factor 2 gamma Mutant Alters Start Codon
Selection Independent of Met-tRNA Binding
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID 40S RIBOSOMAL-SUBUNIT; SACCHAROMYCES-CEREVISIAE; PREINITIATION COMPLEX;
GTP HYDROLYSIS; SITE SELECTION; EF-TU; EIF1; YEAST; MUTATIONS;
RECOGNITION
AB Selection of the AUG start codon for translation in eukaryotes is governed by codon-anticodon interactions between the initiator Met-tRNA(i)(Met) and the mRNA. Translation initiation factor 2 (eIF2) binds Met-tRNA(i)(Met) to the 40S ribosomal subunit, and previous studies identified Sui- mutations in eIF2 that enhanced initiation from a noncanonical UUG codon, presumably by impairing Met-tRNA(i)(Met) binding. Consistently, an eIF2 gamma-N135D GTP-binding domain mutation impairs Met-tRNA(i)(Met) binding and causes a Sui(-) phenotype. Intragenic A208V and A382V suppressor mutations restore Met-tRNA(i)(Met) binding affinity and cell growth; however, only A208V suppresses the Sui(-) phenotype associated with the eIF2 gamma-N135D mutation. An eIF2 gamma-A219T mutation impairs Met-tRNA(i)(Met) binding but unexpectedly enhances the fidelity of initiation, suppressing the Sui(-) phenotype associated with the eIF2 gamma-N135D, A382V mutant. Overexpression of eIF1, which is thought to monitor codon-anticodon interactions during translation initiation, likewise suppresses the Sui(-) phenotype of the eIF2 gamma mutants. We propose that structural alterations in eIF2 gamma subtly alter the conformation of Met-tRNA(i)(Met) on the 40S subunit and thereby affect the fidelity of start codon recognition independent of Met-tRNA(i)(Met) binding affinity.
C1 [Alone, Pankaj V.; Cao, Chune; Dever, Thomas E.] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Dever, TE (reprint author), NICHHD, Lab Gene Regulat & Dev, NIH, Bldg 6A Rm B1A-03,6 Ctr Dr, Bethesda, MD 20892 USA.
EM tdever@nih.gov
OI Dever, Thomas/0000-0001-7120-9678
FU NIH; NICHD
FX This work was supported in part by the Intramural Program of the NIH,
NICHD (T.E.D.).
NR 33
TC 22
Z9 23
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD NOV 15
PY 2008
VL 28
IS 22
BP 6877
EP 6888
DI 10.1128/MCB.01147-08
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 364XC
UT WOS:000260367900012
PM 18794367
ER
PT J
AU Harris, P
Alcantara, DA
Amenta, N
Lopez, OL
Eiriksdottir, G
Sigurosson, S
Gudnason, V
Madsen, S
Thompson, PM
Launer, LJ
Carmichael, OT
AF Harris, Peter
Alcantara, Dan A.
Amenta, Nina
Lopez, Oscar L.
Eiriksdottir, Guony
Sigurosson, Sigurour
Gudnason, Villmundur
Madsen, Sarah
Thompson, Paul M.
Launer, Lenore J.
Carmichael, Owen T.
TI Localized measures of callosal atrophy are associated with late-life
hypertension: AGES-Reykjavik Study
SO NEUROIMAGE
LA English
DT Article
ID MIDLIFE BLOOD-PRESSURE; HUMAN CORPUS-CALLOSUM; WHITE-MATTER LESIONS;
ALZHEIMERS-DISEASE; SEX-DIFFERENCES; COGNITIVE PERFORMANCE; FOLLOW-UP;
ADULTS; RISK; HYPERINTENSITIES
AB Hypertension is highly prevalent in elderly individuals and may be associated with cognitive decline, but the mechanisms by which hypertension may impact brain structure, and thereby modulate the time course of late-life cognitive performance, are not well understood. Therefore we used Localized Components Analysis, a novel computational method, to measure spatially-localized patterns of corpus callosum (CC) atrophy in 28 right-handed female subjects aged 75-79 years in the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik), a large-scale epidemiological study of aging. Localized callosal atrophy in the posterior midbody and splenium was significantly associated with systolic blood pressure in linear statistical models that controlled for age, while associations between blood pressure and anterior CC atrophy measures were not statistically significant. Additionally, overall measures of global CC atrophy were not significantly associated with blood pressure. The posterior CC may be differentially vulnerable to hypertension-associated atrophy, possibly due to its relatively tenuous vascularization. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Harris, Peter; Carmichael, Owen T.] Univ Calif Davis, Dept Neurol, Davis, CA 95616 USA.
[Alcantara, Dan A.; Amenta, Nina; Carmichael, Owen T.] Univ Calif Davis, Dept Comp Sci, Davis, CA 95616 USA.
[Lopez, Oscar L.] Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15260 USA.
[Eiriksdottir, Guony; Sigurosson, Sigurour] Iceland Heart Assoc Res Inst, Hjartavernd, Iceland.
[Madsen, Sarah; Thompson, Paul M.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
[Launer, Lenore J.] NIA, Neuroepidemiol Sect, Bethesda, MD 20892 USA.
RP Carmichael, OT (reprint author), Univ Calif Davis, Dept Neurol, Davis, CA 95616 USA.
EM ocarmichael@ucdavis.edu
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
FU Intramural NIH HHS [Z01 AG007380-02]; NIA NIH HHS [K01 AG030514, K01
AG030514-01A1]
NR 53
TC 7
Z9 7
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2008
VL 43
IS 3
BP 489
EP 496
DI 10.1016/j.neuroimage.2008.07.007
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 392JY
UT WOS:000262300200008
PM 18692143
ER
PT J
AU Alves, G
Yu, YK
AF Alves, Gelio
Yu, Yi-Kuo
TI Statistical characterization of a 1D random potential problem-With
applications in score statistics of MS-based peptide sequencing
SO PHYSICA A-STATISTICAL MECHANICS AND ITS APPLICATIONS
LA English
DT Article
DE Statistical significance; Dynamic programming; Mass spectrometry;
Directed paths in random media; Peptide identification
ID MASS-SPECTROMETRY; RANDOM IMPURITIES; DIRECTED PATHS
AB We provide a complete thermodynamic solution of a 1D hopping model in the presence of a random potential by obtaining the density of states. Since the partition function is related to the density of states by a Laplace transform, the density of states determines completely the thermodynamic behavior of the system. We have also shown that the transfer matrix technique, or the so-called dynamic programming, used to obtain the density of states in the I D hopping model may be generalized to tackle a long-standing problem in statistical significance assessment for one of the most important proteomic tasks-peptide sequencing using tandem mass spectrometry data. Published by Elsevier B.V.
C1 [Alves, Gelio; Yu, Yi-Kuo] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Yu, YK (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM yyu@ncbi.nlm.nih.gov
FU National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Library of Medicine at the National Institutes of Health.
NR 9
TC 9
Z9 9
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-4371
J9 PHYSICA A
JI Physica A
PD NOV 15
PY 2008
VL 387
IS 26
BP 6538
EP 6544
DI 10.1016/j.physa.2008.08.024
PG 7
WC Physics, Multidisciplinary
SC Physics
GA 370AY
UT WOS:000260736300011
PM 19918268
ER
PT J
AU Wullenweber, A
Kroner, O
Kohrman, M
Maier, A
Dourson, M
Rak, A
Wexler, P
Tomljanovic, C
AF Wullenweber, Andrea
Kroner, Oliver
Kohrman, Melissa
Maier, Andrew
Dourson, Michael
Rak, Andrew
Wexler, Philip
Tomljanovic, Chuck
TI Resources for global risk assessment: The International Toxicity
Estimates for Risk (ITER) and Risk Information Exchange (RiskIE)
databases
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Risk values; Risk assessment; TOXNLT; National Library of Medicine;
Database; ITER; RiskIE
AB The rate of chemical synthesis and use has outpaced the development of risk values and the resolution of risk assessment methodology questions. In addition, available risk values derived by different organizations may vary due to scientific judgments, mission of the organization, or use of more recently published data. Further, each organization derives values for a unique chemical list so it can be challenging to locate data on a given chemical. Two Internet resources are available to address these issues. First, the International Toxicity Estimates for Risk (ITER) database (www.tera.org/iter) provides chronic human health risk assessment data from a variety of organizations worldwide in a side-by-side format, explains differences in risk values derived by different organizations, and links directly to each organization's website for more detailed information. It is also the only database that includes risk information from independent parties whose risk values have undergone independent peer review. Second, the Risk Information Exchange (RiskIE) is a database of in progress chemical risk assessment work, and includes non-chemical information related to human health risk assessment, such as training modules, white papers and risk documents. RiskIE is available at http://www.allianceforrisk.org/RiskIE.htm, and will join ITER on National Library of Medicine's TOXNET (http://toxnet.nlm.nih.gov/). Together, ITER and RiskIE provide risk assessors essential tools for easily identifying and comparing available risk data, for sharing in progress assessments, and for enhancing interaction among risk assessment groups to decrease duplication of effort and to harmonize risk assessment procedures across organizations. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Wullenweber, Andrea; Kroner, Oliver; Kohrman, Melissa; Maier, Andrew; Dourson, Michael] TERA, Cincinnati, OH 45211 USA.
[Rak, Andrew] Noblis, Falls Church, VA USA.
[Wexler, Philip] Natl Lib Med, Bethesda, MD USA.
[Tomljanovic, Chuck] CTC, Johnstown, PA USA.
RP Wullenweber, A (reprint author), TERA, 2300 Montana Ave,Suite 409, Cincinnati, OH 45211 USA.
EM wullenweber@tera.org
FU ITER; National Library of Medicine; Noblis and Concurrent Technologies
Corporation (CTC)
FX The ITER database has been developed over the past twelve years by TERA
and is provided to the public free of charge by TERA and the National
Library of Medicine. Funding and in-kind support for ITER has been
provided by a variety of public, private, and non-profit organizations.
A full list of ITER sponsors is located at
http://www.tera.org/iter/sponsors.htm. RiskIE has been in development
for the past two years and funding has been provided by TERA and the
National Library of Medicine. In-kind support has been provided by
Noblis and Concurrent Technologies Corporation (CTC). The authors are
solely responsible for the content of this manuscript. No other sponsors
of the ITER or RiskIE databases have had a role in writing this paper or
in deciding to write it.
NR 0
TC 7
Z9 7
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2008
VL 233
IS 1
BP 45
EP 53
DI 10.1016/j.taap.2007.12.035
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 380PO
UT WOS:000261477800010
PM 18655804
ER
PT J
AU Fostel, JM
AF Fostel, Jennifer M.
TI Towards standards for data exchange and integration and their impact on
a public database such as CEBS (Chemical Effects in Biological Systems)
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Toxicogenomics; Data integration; Data exchange; Database; Ketoconazole;
1-napthyl isothiocyanate; Clotrimazole; Econazole; Carbon tetrachloride;
Ethanol; Valproic acid; Sodium arsenite; Miconazole; Fluconazole;
Itraconazole; Simvastatin; Atorvastatin; N,N-dimethylformamide;
Gemfribrozil; Bezafibrate; Allyl alcohol; Clofibrate; Fenofibrate;
Lovastatin; N-nitrosodiethylamine; Fluvastatin
ID GENE-EXPRESSION PROFILES; MICROARRAY DATA; TOXICITY; REVEALS;
MECHANISMS; PREDICTS
AB Integration, re-use and meta-analysis of high content study data, typical of DNA microarray studies, can increase its scientific utility. Access to study data and design parameters would enhance the mining of data integrated across studies. However, without standards for which data to include in exchange, and common exchange formats, publication of high content data is time-consuming and often prohibitive. The MGED Society (www.mged.org) was formed in response to the widespread publication of microarray data, and the recognition of the utility of data re-use for meta-analysis. The NIEHS has developed the Chemical Effects in Biological Systems (CEBS) database, which can manage and integrate study data and design from biological and biomedical studies. As community standards are developed for study data and metadata it will become increasingly straightforward to publish high content data in CEBS, where they will be available for meta-analysis. Different exchange formats for study data are being developed: Standard for Exchange of Nonclinical Data (SEND; www.cdisc.org);Tox-ML (www.Leadscope.com) and Simple Investigation Formatted Text (SIFT) from the NIEHS. Data integration can be done at the level of conclusions about responsive genes and phenotypes, and this workflow is supported by CEBS. CEBS also integrates raw and preprocessed data within a given platform. The utility and a method for integrating data within and across DNA microarray studies is shown in an example analysis using DrugMatrix data deposited in CEBS by Iconix Pharmaceuticals. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Fostel, Jennifer M.] Natl Inst Environm Hlth Sci, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Fostel, Jennifer M.] SRA Int Inc LLC, Global Hlth Sector, Durham, NC USA.
RP Fostel, JM (reprint author), Natl Inst Environm Hlth Sci, NIH, Dept Hlth & Human Serv, MD F1-05,111 Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM Fostel@niehs.nih.gov
FU Division of Intramural research of the National Institute of
Environmental Health Science [HHSN273200700046U]
FX I would like to acknowledge members of the numerous communities working
on data exchange formats and standards, and Dr. B.A. Merrick for helpful
comments on the manuscript. This work was supported by the Division of
Intramural research of the National Institute of Environmental Health
Science, under contract HHSN273200700046U.
NR 25
TC 12
Z9 12
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 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2008
VL 233
IS 1
BP 54
EP 62
DI 10.1016/j.taap.2008.06.015
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 380PO
UT WOS:000261477800011
PM 18680759
ER
PT J
AU Wexler, P
AF Wexler, Philip
TI Online toxicology resources in support of risk assessment from the US
National Library of Medicine
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
C1 Natl Lib Med, Toxicol & Environm Hlth Informat Program, Bethesda, MD USA.
RP Wexler, P (reprint author), Natl Lib Med, Toxicol & Environm Hlth Informat Program, Bethesda, MD USA.
EM wexlerp@mail.nih.gov
FU Intramural NIH HHS [Z99 LM999999]
NR 0
TC 0
Z9 0
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 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2008
VL 233
IS 1
BP 63
EP 63
DI 10.1016/j.taap.2007.12.034
PG 1
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 380PO
UT WOS:000261477800012
PM 19013304
ER
PT J
AU Sargent, LM
Ensell, MX
Ostvold, AC
Baldwin, KT
Kashon, ML
Lowry, DT
Senft, JR
Jefferson, AM
Johnson, RC
Li, Z
Tyson, FL
Reynolds, SH
AF Sargent, Linda M.
Ensell, Mang X.
Ostvold, Anne-Caring
Baldwin, Kimberly T.
Kashon, Michael L.
Lowry, David T.
Senft, Jamie R.
Jefferson, Amy M.
Johnson, Robert C.
Li, Zhi
Tyson, Frederick L.
Reynolds, Steven H.
TI Chromosomal changes in high- and low-invasive mouse lung adenocarcinoma
cell strains derived from early passage mouse lung adenocarcinoma cell
strains
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Mouse model; Lung adenocarcinoma; Amplification; Chromosome 1; CGH array
ID COMPARATIVE GENOMIC HYBRIDIZATION; BINDING PROTEIN; GENE-EXPRESSION;
PULMONARY INFLAMMATION; TUMOR PROMOTION; UNITED-STATES; BREAST-CANCER;
MICE; SUSCEPTIBILITY; CARCINOMA
AB The incidence of adenocarcinoma of the lung is increasing in the United States, however, the difficulties in obtaining lung cancer families and representative samples of early to late stages of the disease have lead to the study of mouse models for lung cancer. We used Spectral Karyotyping (SKY), mapping with fluorescently labeled genomic clones (FISH), comparative genomic hybridization (CGH) arrays, gene expression arrays. Western immunoblot and real time polymerase chain reaction (PCR) to analyze nine pairs of high-invasive and low-invasive tumor cell strains derived from early passage mouse lung adenocarcinoma cells to detect molecular changes associated with tumor invasion. The duplication of chromosomes I and 15 and deletion of chromosome 8 were significantly associated with a high-invasive phenotype. The duplication of chromosome 1 at band C4 and E1/2-H1 were the most significant chromosomal changes in the high-invasive cell strains. Mapping with FISH and CGH array further narrowed the minimum region of duplication of chromosome I to 71-82 centimorgans (cM). Expression array analysis and confirmation by real time PCR demonstrated increased expression of COX-2, Translin (TB-RBP), DYRK3, MUCKS and Tubulin-alpha 4 genes in the high-invasive cell strains. Elevated expression and copy number of these genes, which are involved in inflammation, cell movement, proliferation, inhibition of apoptosis and telomere elongation, were associated with an invasive phenotype. Similar linkage groups are altered in invasive human lung adenocarcinoma, implying that the mouse is a valid genetic model for the study of the progression of human lung adenocarcinoma. Published by Elsevier Inc.
C1 [Sargent, Linda M.; Baldwin, Kimberly T.; Kashon, Michael L.; Lowry, David T.; Senft, Jamie R.; Jefferson, Amy M.; Reynolds, Steven H.] NIOSH, Morgantown, WV 26505 USA.
[Ensell, Mang X.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Ostvold, Anne-Caring] Univ Oslo, Oslo, Norway.
[Johnson, Robert C.] Spectral Genom Inc, Houston, TX 77054 USA.
[Li, Zhi] Johns Hopkins Univ, Baltimore, MD 21205 USA.
[Tyson, Frederick L.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA.
RP Sargent, LM (reprint author), NIOSH, Morgantown, WV 26505 USA.
EM LSargent@cdc.gov
NR 55
TC 19
Z9 19
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 0041-008X
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2008
VL 233
IS 1
BP 81
EP 91
DI 10.1016/j.taap.2008.01.031
PG 11
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 380PO
UT WOS:000261477800016
PM 18367224
ER
PT J
AU Fowler, BA
Conner, EA
Yamauchi, H
AF Fowler, Bruce A.
Conner, Elizabeth A.
Yamauchi, Hiroshi
TI Proteomic and metabolomic biomarkers for III-V semiconductors: And
prospects for application to nano-materials
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Biomarkers; Proteomic biomarkers; Metabolomic biomarkers; Ill-V
semiconductors; Nanomaterials
ID AMINOLEVULINIC-ACID DEHYDRATASE; MASS-SPECTROMETRY; INDIUM CHLORIDE;
ALTERED REGULATION; QUANTUM DOTS; RAT-KIDNEY; DISCOVERY; EXPOSURE;
METABONOMICS; ARSENATE
AB There has been an increased appreciation over the last 20 years that chemical agents at very low dose levels can produce biological responses in protein expression patterns (proteomic responses) or alterations in sensitive metabolic pathways (metabolomic responses). Marked improvements in analytical methodologies, such as 2-D gel electrophoresis, matrix-assisted laser desorption-time of flight (MALDI-TOF) and surface enhanced laser desorption-time of flight (SELDI-TOF) technologies are capable of identifying specific protein patterns related to exposure to chemicals either alone or as mixtures. The detection and interpretation of early cellular responses to chemical agents have also made great advances through correlative ultrastructural morphometric and biochemical studies. Similarly, advances in analytical technologies such as HPLC, proton NMR, MALDI-TOF, and SELDI-TOF have permitted early detection of changes in a number of essential metabolic pathways following chemical exposures by measurement of alterations in metabolic products from those pathways. Data from these approaches are increasingly regarded as potentially useful biomarkers of chemical exposure and early cellular responses. Validation and establishment of linkages to biological outcomes are needed in order for biomarkers of effect to be established. This short review will cover a number of the above techniques and report data from chemical exposures to two binary III-V semiconductor compounds to illustrate gender differences in proteomic responses. In addition, the use of these methodologies in relation to rapid safety evaluations of nanotechnology products will be discussed. (Supported in part by NIH R01-ES4879). (C) 2008 Published by Elsevier Inc.
C1 [Fowler, Bruce A.] ATSDR, Atlanta, GA USA.
[Fowler, Bruce A.; Conner, Elizabeth A.; Yamauchi, Hiroshi] Univ Maryland, Toxicol Program, Baltimore, MD 21201 USA.
[Conner, Elizabeth A.] NCI, Bethesda, MD 20892 USA.
[Yamauchi, Hiroshi] Kitasato Univ, Tokyo, Japan.
RP Fowler, BA (reprint author), ATSDR, Atlanta, GA USA.
EM bxf9@edc.gov
FU NIEHS NIH HHS [R01-ES4879]
NR 36
TC 5
Z9 5
U1 3
U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2008
VL 233
IS 1
BP 110
EP 115
DI 10.1016/j.taap.2008.01.014
PG 6
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 380PO
UT WOS:000261477800020
PM 18353413
ER
PT J
AU Tekle, E
Wolfe, MD
Oubrahim, H
Chock, PB
AF Tekle, E.
Wolfe, M. D.
Oubrahim, H.
Chock, P. B.
TI Phagocytic clearance of electric field induced 'apoptosis-mimetic' cells
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Electroporation; Phagocytosis; Phosphatidylserine; Apoptosis;
Electropermeabilization; Electric field
ID PHOSPHATIDYLSERINE; EXPOSURE; PHOSPHOLIPIDS; MACROPHAGES; LYMPHOCYTES;
ACTIVATION; MEMBRANES; SURFACE; BLEB
AB Cells undergoing apoptosis lose lipid asymmetry that is often manifested by the exposure of phosphatidylserine (PS) to the outer Surface of the cell membrane. Macrophages and other cell types recognize externalized PS to signal phagocytosis, thereby eliciting a non-inflammatory response. PS exposure is obligatory in the recognition and clearance of apoptotic cells. Here, we find that externally applied moderate electric field induces PS externalization in a mouse B-cell (FOX-NY) membrane without procaspase-3 activation, a major characteristic of apoptotic cells. The field-induced PS inversion is caused as a result of electroporation and/or a process involving membrane reorganizations and recovery that ensues following field exposure. Using a mouse macrophage cell line U7444A.1) from the same strain, we show phagocytic clearance of PS expressing B-cells and demonstrate that this is in part due to the apoptosis mimicry of the field exposed cells. Published by Elsevier Inc.
C1 [Tekle, E.; Wolfe, M. D.; Oubrahim, H.; Chock, P. B.] NHLBI, Ctr Biochem & Biophys, Biochem Lab, NIH, Bethesda, MD 20892 USA.
RP Tekle, E (reprint author), NHLBI, Ctr Biochem & Biophys, Biochem Lab, NIH, Bldg 50,Room 2127,50 South Dr, Bethesda, MD 20892 USA.
EM ephrem@helix.nih.gov
FU NIH; NHLBI
FX The Intramural Research Program of the NIH, NHLBI, supported this
research.
NR 23
TC 13
Z9 13
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 14
PY 2008
VL 376
IS 2
BP 256
EP 260
DI 10.1016/j.bbrc.2008.08.060
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 362KS
UT WOS:000260197200003
PM 18771656
ER
PT J
AU Nyaga, SG
Lohani, A
Evans, MK
AF Nyaga, Simon G.
Lohani, Althaf
Evans, Michele K.
TI Deficient repair of 8-hydroxyguanine in the BxPC-3 pancreatic cancer
cell line
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Pancreatic cancer; Oxidative stress; Oxidative DNA damage; DNA repair;
Base excision repair; Reactive oxygen species; 8-Hydroxyguanine; hOGG1;
Pancreatic cancer risk and antioxidant enzymes
ID 8-OXOGUANINE DNA GLYCOSYLASE; OGG1 PROTEIN; LIGASE-I; HOGG1; MUTATION;
CARCINOGENESIS; MITOCHONDRIA; ADDUCTS; CLONING; LESIONS
AB Elevated levels of oxidatively induced DNA lesions have been reported in malignant pancreatic tissues relative to normal pancreatic tissues. However, the ability of the pancreatic cancer cells to remove these lesions has not previously been addressed. This study analyzed the effectiveness of the pancreatic cancer cell line, BxPC-3 to repair 8-hydroxyguanine (8-OH-Gua) relative to a nonmalignant cell line. We show that BxPC-3 cells repair 8-OH-Gua less effectively than the nonmalignant cells. This repair deficiency correlated with significant downregulation of the hOGG1 protein and the corresponding mRNA (30-fold lower than GAPDH) in BxPC-3 cell line. The repair defect was complemented in vivo by transient transfection of the hOGG1 gene and in vivo by recombinant hOGG1. These results are the first to show a deficiency of 8-OH-Gua repair in BxPC-3 cells, implicating this defect in the risk factor of pancreatic cancer. Published by Elsevier Inc.
C1 [Nyaga, Simon G.; Lohani, Althaf; Evans, Michele K.] NIA, Cellular & Mol Biol Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Evans, MK (reprint author), NIA, Cellular & Mol Biol Lab, NIH, Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM me42v@nih.gov
FU NIH; National Institute on Aging
FX We thank Dr. Dan L. Longo for his useful suggestions especially the
repair complementation experiments. Drs. Sankar Mitra and Tapas Hazra
are thanked for the generous gift of OGG1-containing plasmid. We also
thank summer interns, Erica Reeves and Sabrina Kum for their help with
tissue culture. Dr. Andrzej R. Trzeciak is thanked for help with figures
and statistical analyses. Drs. Myriam Gorospe and Andrea Wurster are
thanked for critically reading the manuscript. This research was
supported by the Intramural Research Program of the NIH, National
Institute on Aging.
NR 29
TC 4
Z9 4
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 14
PY 2008
VL 376
IS 2
BP 336
EP 340
DI 10.1016/j.bbrc.2008.08.134
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 362KS
UT WOS:000260197200018
PM 18774780
ER
PT J
AU Lin, RH
Dai, SS
Irwin, RD
Heinloth, AN
Boorman, GA
Li, LP
AF Lin, Rongheng
Dai, Shuangshuang
Irwin, Richard D.
Heinloth, Alexandra N.
Boorman, Gary A.
Li, Leping
TI Gene set enrichment analysis for non-monotone association and multiple
experimental categories
SO BMC BIOINFORMATICS
LA English
DT Article
ID WIDE EXPRESSION PROFILES; FALSE DISCOVERY RATE; MICROARRAY DATA;
REGRESSION
AB Background: Recently, microarray data analyses using functional pathway information, e. g., gene set enrichment analysis (GSEA) and significance analysis of function and expression ( SAFE), have gained recognition as a way to identify biological pathways/processes associated with a phenotypic endpoint. In these analyses, a local statistic is used to assess the association between the expression level of a gene and the value of a phenotypic endpoint. Then these gene-specific local statistics are combined to evaluate association for pre-selected sets of genes. Commonly used local statistics include t-statistics for binary phenotypes and correlation coefficients that assume a linear or monotone relationship between a continuous phenotype and gene expression level. Methods applicable to continuous non-monotone relationships are needed. Furthermore, for multiple experimental categories, methods that combine multiple GSEA/SAFE analyses are needed.
Results: For continuous or ordinal phenotypic outcome, we propose to use as the local statistic the coefficient of multiple determination (i.e., the square of multiple correlation coefficient) R(2) from fitting natural cubic spline models to the phenotype-expression relationship. Next, we incorporate this association measure into the GSEA/SAFE framework to identify significant gene sets. Unsigned local statistics, signed global statistics and one-sided p-values are used to reflect our inferential interest. Furthermore, we describe a procedure for inference across multiple GSEA/SAFE analyses. We illustrate our approach using gene expression and liver injury data from liver and blood samples from rats treated with eight hepatotoxicants under multiple time and dose combinations. We set out to identify biological pathways/processes associated with liver injury as manifested by increased blood levels of alanine transaminase in common for most of the eight compounds. Potential statistical dependency resulting from the experimental design is addressed in permutation based hypothesis testing.
Conclusion: The proposed framework captures both linear and non-linear association between gene expression level and a phenotypic endpoint and thus can be viewed as extending the current GSEA/SAFE methodology. The framework for combining results from multiple GSEA/SAFE analyses is flexible to address practical inference interests. Our methods can be applied to microarray data with continuous phenotypes with multi-level design or the meta-analysis of multiple microarray data sets.
C1 [Lin, Rongheng; Li, Leping] NIEHS, Biostat Branch, Res Triangle Pk, NC 27713 USA.
[Dai, Shuangshuang] Alpha Gamma Technol Inc, Raleigh, NC 27609 USA.
[Irwin, Richard D.] NIEHS, Environm Toxicol Program, Res Triangle Pk, NC 27713 USA.
[Heinloth, Alexandra N.] NIEHS, Mol Toxicol Lab, Res Triangle Pk, NC 27713 USA.
[Boorman, Gary A.] Covance Inc, Vienna, VA 22066 USA.
RP Lin, RH (reprint author), NIEHS, Biostat Branch, Res Triangle Pk, NC 27713 USA.
EM rlin@schoolph.umass.edu; dai3@niehs.nih.gov; irwin@niehs.nih.gov;
heinloth@gmail.com; Gary.Boorman@covance.com; li3@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences.
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences. We thank the
NCT for the compendium data used in this analysis. We thank Clarice
Weinberg, David Umbach and Grace Kissling for insightful discussion and
for critically reading the manuscript. We thank Shyamal Peddada, Dmitri
Zaykin and Bhanu Singh for helpful discussion. We thank Robert Bass for
creating the web site for R code downloading. We thank the Computational
Biology Facility at NIEHS for computing time. We also thank anonymous
referees for helpful comments which greatly improve our work.
NR 39
TC 9
Z9 9
U1 1
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 14
PY 2008
VL 9
AR 481
DI 10.1186/1471-2105-9-481
PG 12
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Mathematical & Computational Biology
GA 415YK
UT WOS:000263972200001
PM 19014579
ER
PT J
AU Xu, CQ
Gagnon, E
Call, ME
Schnell, JR
Schwieters, CD
Carman, CV
Chou, JJ
Wucherpfennig, KW
AF Xu, Chenqi
Gagnon, Etienne
Call, Matthew E.
Schnell, Jason R.
Schwieters, Charles D.
Carman, Christopher V.
Chou, James J.
Wucherpfennig, Kai W.
TI Regulation of T Cell Receptor Activation by Dynamic Membrane Binding of
the CD3 epsilon Cytoplasmic Tyrosine-Based Motif
SO CELL
LA English
DT Article
ID EFFECTOR DOMAIN; PROTEIN; PHOSPHORYLATION; BICELLES; BILAYER; COMPLEX;
ZAP-70; ZETA
AB Many immune system receptors signal through cytoplasmic tyrosine-based motifs (ITAMs), but how receptor ligation results in ITAM phosphorylation remains unknown. Live-cell imaging studies showed a close interaction of the CD3 epsilon cytoplasmic domain of the T cell receptor (TCR) with the plasma membrane through fluorescence resonance energy transfer between a C-terminal fluorescent protein and a membrane fluorophore. Electrostatic interactions between basic CD3 epsilon residues and acidic phospholipids enriched in the inner leaflet of the plasma membrane were required for binding. The nuclear magnetic resonance structure of the lipid-bound state of this cytoplasmic domain revealed deep insertion of the two key tyrosines into the hydrophobic core of the lipid bilayer. Receptor ligation thus needs to result in unbinding of the CD3 epsilon ITAM from the membrane to render these tyrosines accessible to Src kinases. Sequestration of key tyrosines into the lipid bilayer represents a previously unrecognized mechanism for control of receptor activation.
C1 [Call, Matthew E.; Schnell, Jason R.; Chou, James J.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Xu, Chenqi; Gagnon, Etienne; Wucherpfennig, Kai W.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Carman, Christopher V.] Harvard Univ, Sch Med, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Wucherpfennig, Kai W.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Wucherpfennig, Kai W.] Harvard Univ, Sch Med, Program Immunol, Boston, MA 02115 USA.
[Schwieters, Charles D.] Natl Inst Hlth, Imaging Sci Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Chou, JJ (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
EM james_chou@hms.harvard.edu; kai_wucherpfennig@dfci.harvard.edu
RI Carman, Christopher/L-8108-2016; Chou, James/N-9840-2013
OI Carman, Christopher/0000-0001-7358-2548;
FU Intramural NIH HHS; NIAID NIH HHS [AI054520, R01 AI054520, R01
AI054520-05]
NR 33
TC 182
Z9 188
U1 0
U2 24
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 14
PY 2008
VL 135
IS 4
BP 702
EP 713
DI 10.1016/j.cell.2008.09.044
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 372FG
UT WOS:000260886900020
PM 19013279
ER
PT J
AU Bolland, S
AF Bolland, Silvia
TI An Innate Path to Human B Cell Tolerance
SO IMMUNITY
LA English
DT Editorial Material
ID TOLL-LIKE RECEPTORS
AB Self-reactive B cells are eliminated during development by antibody-affinity selection and receptor-editing mechanisms. Work by Isnardi et al. (2008) in this issue of immunity suggests that removal of autoreactivity from the immature B cell pool also requires innate immunity pathways.
C1 NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
RP Bolland, S (reprint author), NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
EM sbolland@niaid.nih.gov
FU Intramural NIH HHS [ZIA AI000912-08]
NR 9
TC 1
Z9 1
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 667
EP 669
DI 10.1016/j.immuni.2008.10.001
PG 3
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000003
PM 19006689
ER
PT J
AU Isnardi, I
Ng, YS
Srdanovic, I
Motaghedi, R
Rudchenko, S
von Bernuth, H
Zhang, SY
Puel, A
Jouanguy, E
Picard, C
Garty, BZ
Camcioglu, Y
Doffinger, R
Kumararatne, D
Davies, G
Gallin, JI
Haraguchi, S
Day, NK
Casanova, JL
Meffre, E
AF Isnardi, Isabelle
Ng, Yen-Shing
Srdanovic, Iva
Motaghedi, Roja
Rudchenko, Sergei
von Bernuth, Horst
Zhang, Shen-Ying
Puel, Anne
Jouanguy, Emmanuelle
Picard, Capucine
Garty, Ben-Zion
Camcioglu, Yildiz
Doffinger, Rainer
Kumararatne, Dinakantha
Davies, Graham
Gallin, John I.
Haraguchi, Soichi
Day, Noorbibi K.
Casanova, Jean-Laurent
Meffre, Eric
TI IRAK-4-and MyD88-Dependent Pathways Are Essential for the Removal of
Developing Autoreactive B Cells in Humans
SO IMMUNITY
LA English
DT Article
ID TOLL-LIKE RECEPTORS; PLASMACYTOID DENDRITIC CELLS; RECURRENT
BACTERIAL-INFECTIONS; REGULATORY T-CELLS; RHEUMATOID-ARTHRITIS;
MYD88-DEFICIENT MICE; ANTIGEN RECEPTOR; TOLERANCE; DEFICIENCY; IMMUNITY
AB Most autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for interleukin-1 receptor-associated kinase 4 (IRAK-4), myeloid differentiation factor 88 (MyD88), and UNC-93B. Indeed, all TLRs except TLR3 require IRAK-4 and MyD88 to signal, and UNC-93B-deficient cells are unresponsive to TLR3, TLR7, TLR8, and TLR9. All patients suffered from defective central and peripheral B cell tolerance checkpoints, resulting in the accumulation of large numbers of autoreactive mature naive B cells in their blood. Hence, TLR7, TLR8, and TLR9 may prevent the recruitment of developing autoreactive B cells in healthy donors. Paradoxically, IRAK-4-, MyD88-, and UNC-93B-deficient patients did not display autoreactive antibodies in their serum or develop autoimmune diseases, suggesting that IRAK-4, MyD88, and UNC-93B pathway blockade may thwart autoimmunity in humans.
C1 [Isnardi, Isabelle; Ng, Yen-Shing; Srdanovic, Iva; Meffre, Eric] Hosp Special Surg, Lab Biochem & Mol Immunol, New York, NY 10021 USA.
[Motaghedi, Roja] Cornell Univ, Weill Med Coll, Dept Pediat, New York, NY 10021 USA.
[Rudchenko, Sergei] Hosp Special Surg, Flow Cytometry Facil, New York, NY 10021 USA.
[von Bernuth, Horst; Zhang, Shen-Ying; Puel, Anne; Jouanguy, Emmanuelle; Picard, Capucine; Casanova, Jean-Laurent] Univ Paris 05, Lab Genet Humaine Malad Infect, INSERM, Fac Med Necker,U550, F-75015 Paris, France.
[Garty, Ben-Zion] Schneider Childrens Med Ctr Israel, Dept Pediat, IL-49202 Petah Tigva, Israel.
[Camcioglu, Yildiz] Univ Istanbul, Cerrahpasa Med Sch, Dept Pediat, TR-3403 Istanbul, Turkey.
[Doffinger, Rainer; Kumararatne, Dinakantha] Addenbrookes Hosp, Dept Clin Biochem & Immunol, Cambridge CB2 0QQ, England.
[Davies, Graham] Great Ormond St Hosp Sick Children, Dept Immunol, London WC1N 3JH, England.
[Gallin, John I.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Haraguchi, Soichi; Day, Noorbibi K.] Univ S Florida, Div Allergy & Immunol, Dept Pediat, St Petersburg, FL 33701 USA.
[Haraguchi, Soichi; Day, Noorbibi K.] All Childrens Hosp, St Petersburg, FL 33701 USA.
RP Meffre, E (reprint author), Hosp Special Surg, Lab Biochem & Mol Immunol, 535 E 70th St, New York, NY 10021 USA.
EM meffree@hss.edu
OI Picard, Capucine/0000-0001-8788-5056
FU National Institutes of Health [C06-RR12538-01]; National Institutes of
Health-National Institute of Allergy and Infectious Diseases [A1061093,
A1071087]; Fondation pour la Recherche Medicale
FX We thank G. Charvin for help with microscopy analysis; N. Tangsinmankong
for information on IRAK-4-deficient patient 2; M.C. Nussenzweig, S.
Yurasov, and M. Tsuiji for sharing recombinant antibodies; C.-A.
Reynaud, M. Herv6, L. IV16nard, and D. Saadoun for helpful discussions;
and L. Abel, M. Tardieu, F. Rozenberg, V. Sancho-Shimizu, L. Lazaro, M.
Chrabeh, and C.L. Ku for various support. We are very much indebted to
the patients and their families. This investigation was conducted in a
facility constructed with support from Research Facilities Improvement
Program grant number C06-RR12538-01 from the National Center for
Research Resources, National Institutes of Health. This publication was
made possible by grant number A1061093 and A1071087 from the National
Institutes of Health-National Institute of Allergy and Infectious
Diseases (to E.M.) and a grant from Fondation pour la Recherche Medicale
(to I.I.).
NR 53
TC 115
Z9 118
U1 1
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 746
EP 757
DI 10.1016/j.immuni.2008.09.015
PG 12
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000012
PM 19006693
ER
PT J
AU Hill, JA
Hall, JA
Sun, CM
Cai, Q
Ghyselinck, N
Chambon, P
Belkaid, Y
Mathis, D
Benoist, C
AF Hill, Jonathan A.
Hall, Jason A.
Sun, Cheng-Ming
Cai, Qi
Ghyselinck, Norbert
Chambon, Pierre
Belkaid, Yasmine
Mathis, Diane
Benoist, Christophe
TI Retinoic Acid Enhances Foxp3 Induction Indirectly by Relieving
Inhibition from CD4(+)CD44(hi) Cells
SO IMMUNITY
LA English
DT Article
ID REGULATORY T-CELLS; IOXP-FLANKED ALLELE; TRANSCRIPTION FACTOR FOXP3;
TGF-BETA; SIGNALING PATHWAY; NUCLEAR RECEPTORS; DENDRITIC CELLS; ORAL
TOLERANCE; RAR-GAMMA; DIFFERENTIATION
AB CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. This indirect effect was evident in vivo and required the expression of the RA receptor alpha. Thus, cytokine-producing CD44(hi) cells actively restrain TGF-beta-mediated Foxp3 expression in naive T cells, and this balance can be shifted or fine-tuned by RA.
C1 [Hill, Jonathan A.; Mathis, Diane; Benoist, Christophe] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Joslin Diabet Ctr,Sect Immunol & Immunog, Boston, MA 02215 USA.
[Hall, Jason A.; Sun, Cheng-Ming; Belkaid, Yasmine] NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Hall, Jason A.] Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
[Cai, Qi; Ghyselinck, Norbert; Chambon, Pierre] Univ Strasbourg 1, INSERM, CNRS, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France.
RP Mathis, D (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Joslin Diabet Ctr,Sect Immunol & Immunog, Boston, MA 02215 USA.
EM cbdm@joslin.harvard.edu; cbdm@joslin.harvard.edu
RI Cai, Qi/E-4357-2014; GHYSELINCK, Norbert/I-6999-2015
OI Cai, Qi/0000-0002-2598-542X; GHYSELINCK, Norbert/0000-0003-4042-6818
FU Juvenile Diabetes Research Foundation [4-2007-1057]; National Institutes
of Health (NIH) [1R01A151530-5]; Young Chair; National Institute of
Diabetes and Digestive and Kidney Diseases; Canadian Institutes of
Health Research; Division of Intramural Research of the National
Institute of Allergy and Infectious Diseases, NIH
FX We thank S. Vitolo and K. Hattori for assistance with mice, J. LaVecchio
and G. Buruzala for help with cytometry, J. Perez and K. Leatherbee for
microarrays, and C. Laplace for graphics. This work was supported by
grants from the Juvenile Diabetes Research Foundation (4-2007-1057) and
the National Institutes of Health (NIH) (1R01A151530-5), by Young Chair
funds to D.M. and C.B., and by the National Institute of Diabetes and
Digestive and Kidney Diseases-funded Joslin Diabetes and Endocrinology
Research Center core facilities. J.A. Hill was supported by a
postdoctoral fellowship from the Canadian Institutes of Health Research,
and C.M.S. and J.A. Hall were supported by the Division of Intramural
Research of the National Institute of Allergy and Infectious Diseases,
NIH.
NR 54
TC 204
Z9 208
U1 0
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 758
EP 770
DI 10.1016/j.immuni.2008.09.018
PG 13
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000013
PM 19006694
ER
PT J
AU Gri, G
Piconese, S
Frossi, B
Manfroi, V
Merluzzi, S
Tripodo, C
Viola, A
Odom, S
Rivera, J
Colombo, MP
Pucillo, CE
AF Gri, Giorgia
Piconese, Silvia
Frossi, Barbara
Manfroi, Vanessa
Merluzzi, Sonia
Tripodo, Claudio
Viola, Antonella
Odom, Sandra
Rivera, Juan
Colombo, Mario P.
Pucillo, Carlo E.
TI CD4(+)CD25(+) Regulatory T Cells Suppress Mast Cell Degranulation and
Allergic Responses through OX40-OX40L Interaction
SO IMMUNITY
LA English
DT Article
ID OX40 LIGAND; MURINE MODEL; MONOCLONAL-ANTIBODY; CUTTING EDGE; IN-VIVO;
B-CELLS; ACTIVATION; ASTHMA; INFLAMMATION; EXPRESSION
AB T regulatory (Treg) cells play a role in the suppression of immune responses, thus serving to induce tolerance and control autoimmunity. Here, we explored whether Treg cells influence the immediate hypersensitivity response of mast cells (MCs). Treg cells directly inhibited the Fc epsilon RI-dependent MC degranulation through cell-cell contact involving OX40-OX40L interactions between Treg cells and MCs, respectively. When activated in the presence of Treg cells, MCs showed increased cyclic adenosine monophosphate (cAMP) concentrations and reduced Ca2+ influx, independently of phospholipase C (PLC)-gamma 2 or Ca2+ release from intracellular stores. Antagonism of cAMP in MCs reversed the inhibitory effects of Treg cells, restoring normal Ca2+ responses and degranulation. Importantly, the in vivo depletion or inactivation of Treg cells caused enhancement of the anaphylactic response. The demonstrated crosstalk between Treg cells and MCs defines a previously unrecognized mechanism controlling MC degranulation. Loss of this interaction may contribute to the severity of allergic responses.
C1 [Piconese, Silvia; Colombo, Mario P.] Fdn IRCCS, Ist Nazl Tumori, Dept Expt Oncol, Immunotherapy & Gene Therapy Unit, I-20133 Milan, Italy.
[Gri, Giorgia; Frossi, Barbara; Manfroi, Vanessa; Merluzzi, Sonia; Pucillo, Carlo E.] Univ Udine, Dept Biomed Sci & Technol, I-33100 Udine, Italy.
[Gri, Giorgia; Frossi, Barbara; Manfroi, Vanessa; Merluzzi, Sonia; Pucillo, Carlo E.] Univ Udine, MATI Ctr Excellence, I-33100 Udine, Italy.
[Tripodo, Claudio] Univ Palermo, Dept Human Pathol, I-90127 Palermo, Italy.
[Viola, Antonella] Univ Padua, Dept Biomed Sci, I-35129 Padua, Italy.
[Viola, Antonella] Venetian Inst Mol Med, I-35129 Padua, Italy.
[Odom, Sandra; Rivera, Juan] Natl Inst Arthrit Musculoskeletal & Skin Dis, Lab Immune Cell Signaling, NIH, Bethesda, MD 20892 USA.
RP Colombo, MP (reprint author), Fdn IRCCS, Ist Nazl Tumori, Dept Expt Oncol, Immunotherapy & Gene Therapy Unit, I-20133 Milan, Italy.
EM mario.colombo@istitutotumori.mi.it
RI Pucillo, Carlo/A-5515-2008; Tripodo, Claudio/O-4536-2016; Agatea,
Lisa/L-8267-2016;
OI Tripodo, Claudio/0000-0002-0821-6231; Agatea, Lisa/0000-0002-8380-9619;
GRI, Giorgia/0000-0002-2826-0459; Colombo, Mario
Paolo/0000-0003-0042-7955; Pucillo, Carlo/0000-0002-4872-6156
FU Ministero dell'lstruzione Universita e Ricerca; Agenzia Spaziale
Italiana (Progetto OSMA); Associazione Italana Ricerca sul Cancro; LR.11
del Friuli Venezia Giulia; Fondazione Italiana Ricerca sul Cancro;
National Institute of Arthritis, Musculoskeletal and Skin Diseases of
the National Institutes of Health
FX This work was supported by grants from the Ministero dell'lstruzione
Universita e Ricerca (PRIN 2005), Agenzia Spaziale Italiana (Progetto
OSMA), Associazione Italana Ricerca sul Cancro, and LR.11 del Friuli
Venezia Giulia. S.P. is supported by a fellowship from Fondazione
Italiana Ricerca sul Cancro. The work of J.R. and S.O. was supported by
the National Institute of Arthritis, Musculoskeletal and Skin Diseases
of the National Institutes of Health. We thank A.H. Sharpe (Harvard
University) for providing Tnfsf4-/- bone marrow and I. Arioli
for technical assistance. We also thank D. Cesselli and E. Puppato for
cell sorting.
NR 51
TC 198
Z9 208
U1 1
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 771
EP 781
DI 10.1016/j.immuni.2008.08.018
PG 11
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000014
PM 18993084
ER
PT J
AU Antunes, I
Tolaini, M
Kissenpfennig, A
Iwashiro, M
Kuribayashi, K
Malissen, B
Hasenkrug, K
Kassiotis, G
AF Antunes, Ines
Tolaini, Mauro
Kissenpfennig, Adrien
Iwashiro, Michihiro
Kuribayashi, Kagemasa
Malissen, Bernard
Hasenkrug, Kim
Kassiotis, George
TI Retrovirus-Specificity of Regulatory T Cells Is Neither Present nor
Required in Preventing Retrovirus-Induced Bone Marrow Immune Pathology
SO IMMUNITY
LA English
DT Article
ID HEMATOPOIETIC PROGENITOR CELLS; HIV-1 SUBTYPE-C; APLASTIC-ANEMIA;
EFFECTOR FUNCTION; STEM-CELLS; IN-VITRO; INFECTION; CD4(+); MICE; VIRUS
AB Chronic viral infections of the hematopoietic system are associated with bone marrow dysfunction, to which both virus-mediated and immune-mediated effects may contribute. Using unresolving noncytopathic Friend virus (FV) infection in mice, we showed that unregulated CD4+ T cell response to FV caused IFN-gamma-mediated bone marrow pathology and anemia. Importantly, bone marrow pathology was triggered by relative insufficiency in regulatory T (Treg) cells and was prevented by added Treg cells, which suppressed the local IFN-gamma production by FV-specific CD4(+) T cells. We further showed that the T cell receptor (TCR) repertoire of transgenic Treg cells expressing the beta chain of an FV-specific TCR was virtually devoid of FV-specific clones. Moreover, anemia induction by virus-specific CD4(+) T cells was efficiently suppressed by virus-nonspecific Treg cells. Thus, sufficient numbers of polyclonal Treg cells may provide substantial protection against bone marrow pathology in chronic viral infections.
C1 [Antunes, Ines; Kassiotis, George] Natl Inst Med Res, MRC, Div Immunoregulat, London NW7 1AA, England.
[Tolaini, Mauro] Natl Inst Med Res, MRC, Div Mol Immunol, London NW7 1AA, England.
[Hasenkrug, Kim] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Kissenpfennig, Adrien; Malissen, Bernard] Univ Aix Marseille 2, CNRS, INSERM, Ctr Immunol Marseille Luminy, F-13288 Marseille 09, France.
[Kuribayashi, Kagemasa] Tazuke Kofukai Med Res Inst, Osaka 5308480, Japan.
[Iwashiro, Michihiro] Kyoto Univ, Fac Med, Dept Oral & Maxillofacial Surg, Kyoto 6068507, Japan.
RP Kassiotis, G (reprint author), Natl Inst Med Res, MRC, Div Immunoregulat, London NW7 1AA, England.
EM gkassio@nimr.mrc.ac.uk
OI Malissen, Bernard/0000-0003-1340-9342
FU Intramural NIH HHS; Medical Research Council [, MC_U117581330]
NR 52
TC 37
Z9 38
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
EI 1097-4180
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 782
EP 794
DI 10.1016/j.immuni.2008.09.016
PG 13
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000015
PM 19006695
ER
PT J
AU Zhang, SS
Park, CG
Zhang, P
Bartra, SS
Plano, GV
Klena, JD
Skurnik, M
Hinnebusch, BJ
Chen, T
AF Zhang, Shu-sheng
Park, Chae Gyu
Zhang, Pei
Bartra, Sara Schesser
Plano, Gregory V.
Klena, John D.
Skurnik, Mikael
Hinnebusch, B. Joseph
Chen, Tie
TI Plasminogen Activator Pla of Yersinia pestis Utilizes Murine DEC-205
(CD205) as a Receptor to Promote Dissemination
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PRIMARY PNEUMONIC PLAGUE; DENDRITIC CELL SUBSETS; ANTIGEN GENE-CLUSTER;
DC-SIGN CD209; O-ANTIGEN; MYCOBACTERIUM-TUBERCULOSIS; CORE
LIPOPOLYSACCHARIDE; NEISSERIA-GONORRHOEAE; NONINTEGRIN CD209;
ESCHERICHIA-COLI
AB Yersinia pestis, a Gram-negative bacterium that causes bubonic and pneumonic plague, is able to rapidly disseminate to other parts of its mammalian hosts. Y. pestis expresses plasminogen activator (PLA) on its surface, which has been suggested to play a role in bacterial dissemination. It has been speculated that Y. pestis hijacks antigen-presenting cells, such as macrophages (M phi s) and dendritic cells, to be delivered to lymph nodes to initiate dissemination and infection. Both alveolar M phi s and pulmonary dendritic cells express a C-type lectin receptor, DEC-205 (CD205), which mediates antigen uptake and presentation. However, no ligand has been identified for DEC-205. In this study, we show that the invasion of alveolar M phi s by Y. pestis depends both in vitro and in vivo on the expression of PLA. DEC-205-expressing M phi s and transfectants, but not their negative counterparts, phagocytosed PLA-expressing Y. pestis and Escherichia coli K12 more efficiently than PLA-negative controls. The interactions between PLA-expressing bacteria and DEC-205-expressing transfectants or alveolar M phi s could be inhibited by an anti-DEC-205 antibody. Importantly, the blockage of the PLA-DEC-205 interaction reduced the dissemination of Y. pestis in mice. In conclusion, murine DEC-205 is a receptor for PLA of Y. pestis, and this host-pathogen interaction appears to play a key role in promoting bacterial dissemination.
C1 [Zhang, Shu-sheng; Zhang, Pei; Chen, Tie] Univ Illinois, Coll Med Rockford, Dept Biomed Sci, Rockford, IL 61107 USA.
[Park, Chae Gyu] Rockefeller Univ, Chris Browne Ctr Immunol & Immune Dis, Lab Cellular Physiol & Immunol, New York, NY 10065 USA.
[Bartra, Sara Schesser; Plano, Gregory V.] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33101 USA.
[Klena, John D.] Univ Canterbury, Sch Biol Sci, Christchurch 1, New Zealand.
[Bartra, Sara Schesser] Umea Univ, Dept Mol Biol, SE-90187 Umea, Sweden.
[Hinnebusch, B. Joseph] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MN 59840 USA.
[Skurnik, Mikael] Univ Helsinki, Haartman Inst, Dept Bacteriol & Immunol, FIN-00014 Helsinki, Finland.
[Skurnik, Mikael] Univ Helsinki, Cent Hosp Lab Diagnost, FIN-00014 Helsinki, Finland.
RP Chen, T (reprint author), Univ Illinois, Coll Med Rockford, Dept Biomed Sci, 1601 Parkview Ave, Rockford, IL 61107 USA.
EM tiechen@uic.edu
OI Skurnik, Mikael/0000-0001-8791-9260; Park, Chae Gyu/0000-0003-1906-1308
FU National Institutes of Health [AI 057158]; University of Illinois,
College of Medicine, Rockford; Academy of Finland [114075]; [Northeast
Biodefense Center]
FX This work was supported, in whole or in part, by National Institutes of
Health grants (USPHS). This work was also supported in part by a grant
from the University of Illinois, College of Medicine, Rockford (to T.
C.), and work in the Skurnik laboratory was supported by Academy of
Finland Grant 114075. The costs of publication of this article were
defrayed in part by the payment of page charges. This article must
therefore be hereby marked "advertisement" in accordance with 18 U. S.
C. Section 1734 solely to indicate this fact.; Supported by National
Institutes of Health Grant AI 057158 (Northeast Biodefense Center).
NR 70
TC 35
Z9 38
U1 1
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 31511
EP 31521
DI 10.1074/jbc.M804646200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800030
PM 18650418
ER
PT J
AU Mahajan, B
Selvapandiyan, A
Gerald, NJ
Majam, V
Zheng, H
Wickramarachchi, T
Tiwari, J
Fujioka, H
Moch, JK
Kumar, N
Aravind, L
Nakhasi, HL
Kumar, S
AF Mahajan, Babita
Selvapandiyan, Angamuthu
Gerald, Noel J.
Majam, Victoria
Zheng, Hong
Wickramarachchi, Thilan
Tiwari, Jawahar
Fujioka, Hisashi
Moch, J. Kathleen
Kumar, Nirbhay
Aravind, L.
Nakhasi, Hira L.
Kumar, Sanjai
TI Centrins, Cell Cycle Regulation Proteins in Human Malaria Parasite
Plasmodium falciparum
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SPINDLE POLE BODY; CHLAMYDOMONAS-REINHARDTII; CALCIUM-BINDING;
SACCHAROMYCES-CEREVISIAE; LEISHMANIA-DONOVANI; MAXIMUM-LIKELIHOOD;
TRYPANOSOMA-BRUCEI; MURINE CENTRIN; GENE; DUPLICATION
AB Molecules and cellular mechanisms that regulate the process of cell division in malaria parasites remain poorly understood. In this study we isolate and characterize the four Plasmodium falciparum centrins (PfCENs) and, by growth complementation studies, provide evidence for their involvement in cell division. Centrins are cytoskeleton proteins with key roles in cell division, including centrosome duplication, and possess four Ca2+-binding EF hand domains. By means of phylogenetic analysis, we were able to decipher the evolutionary history of centrins in eukaryotes with particular emphasis on the situation in apicomplexans and other alveolates. Plasmodium possesses orthologs of four distinct centrin paralogs traceable to the ancestral alveolate, including two that are unique to alveolates. By real time PCR and/or immunofluorescence, we determined the expression of PfCEN mRNA or protein in sporozoites, asexual blood forms, gametocytes, and in the oocysts developing inside mosquito mid-gut. Immunoelectron microscopy studies showed that centrin is expressed in close proximity with the nucleus of sporozoites and asexual schizonts. Furthermore, confocal and widefield microscopy using the double staining with alpha-tubulin and centrin antibodies strongly suggested that centrin is associated with the parasite centrosome. Following the episomal expression of the four PfCENs in a centrin knock-out Leishmania donovani parasite line that exhibited a severe growth defect, one of the PfCENs was able to partially restore Leishmania growth rate and overcome the defect in cytokinesis in such mutant cell line. To our knowledge, this study is the first characterization of a Plasmodium molecule that is involved in the process of cell division. These results provide the opportunity to further explore the role of centrins in cell division in malaria parasites and suggest novel targets to construct genetically modified, live attenuated malaria vaccines.
C1 [Kumar, Sanjai] US FDA, CBER, DETTD, OBRR, Rockville, MD 20852 USA.
[Tiwari, Jawahar] US FDA, Ctr Biol Evaluat & Res, Div Biostat, Rockville, MD 20852 USA.
[Fujioka, Hisashi] Case Western Reserve Univ, Dept Pharmacol, Cleveland, OH 44106 USA.
[Moch, J. Kathleen] Walter Reed Army Inst Res, Dept Immunol, Silver Spring, MD 20910 USA.
[Kumar, Nirbhay] Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA.
[Aravind, L.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20892 USA.
RP Kumar, S (reprint author), US FDA, CBER, DETTD, OBRR, 1401 Rockville Pike HFM-313, Rockville, MD 20852 USA.
EM sanjai.kumar@fda.hhs.gov
NR 64
TC 20
Z9 21
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 31871
EP 31883
DI 10.1074/jbc.M800028200
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800070
PM 18693242
ER
PT J
AU Shmelzer, Z
Karter, M
Eisenstein, M
Leto, TL
Hadad, N
Ben-Menahem, D
Gitler, D
Banani, S
Wolach, B
Rotem, M
Levy, R
AF Shmelzer, Zeev
Karter, Maria
Eisenstein, Miriam
Leto, Thomas L.
Hadad, Nurit
Ben-Menahem, David
Gitler, Daniel
Banani, Shirly
Wolach, Baruch
Rotem, Meir
Levy, Rachel
TI Cytosolic Phospholipase A(2)alpha Is Targeted to the p47(phox)-PX Domain
of the Assembled NADPH Oxidase via a Novel Binding Site in Its C2 Domain
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PHOSPHORYLATION-INDUCED ACTIVATION; PROTEIN-PROTEIN DOCKING; SRC
HOMOLOGY-3 DOMAINS; ESSENTIAL REQUIREMENT; RESPIRATORY BURST; HUMAN
NEUTROPHILS; INTRAMOLECULAR INTERACTION; DIRECTED MUTAGENESIS;
CRYSTAL-STRUCTURE; CATALYTIC DOMAIN
AB We have previously demonstrated a physical interaction between cytosolic phospholipase A2 alpha (cPLA(2)) and the assembled NADPH oxidase on plasma membranes following neutrophil stimulation. The aim of the present study was to define the exact binding sites between these two enzymes. Here we show, based on blot overlay experiments, Forster resonance energy transfer analysis and studies in neutrophils from patients with chronic granulomatous disease deficient in p67(phox) or p47(phox), that cPLA2 specifically binds to p47(phox) and that p47(phox) is sufficient to anchor cPLA2 to the assembled oxidase on the plasma membranes upon stimulation. Blot overlay and affinity binding experiments using subfragments of cPLA2 and p47(phox) demonstrated that the cPLA(2)-C2 domain and the p47(phox)-PX domain interact to form a complex that is resistant to high salt. Computational docking was used to identify hydrophobic peptides within these two domains that inhibited the association between the two enzymes and NADPH oxidase activity in electro-permeabilized neutrophils. These results were used in new docking computations that produced an interaction model. Based on this model, cPLA(2)-C2 domain mutations were designed to explore its interaction p47(phox) in neutrophillysates. The triple mutant F35A/M38A/L39A of the cPLA(2)-C2 domain caused a slight inhibition of the affinity binding to p47(phox), whereas the single mutant I67A was highly effective. The double mutant M59A/H115A of the p47(phox)-PX domain caused a significant inhibition of the affinity binding to cPLA(2). Thus, Ile(67) of the cPLA(2)-C2 domain is identified as a critical, centrally positioned residue in a hydrophobic interaction in the p47(phox)-PX domain.
C1 [Shmelzer, Zeev; Karter, Maria; Hadad, Nurit; Banani, Shirly; Levy, Rachel] Soroka Univ, Med Ctr, Fac Hlth Sci, Infect Dis Lab,Dept Clin Biochem, IL-84105 Beer Sheva, Israel.
[Ben-Menahem, David] Soroka Univ, Med Ctr, Fac Hlth Sci, Dept Pharmacol, IL-84105 Beer Sheva, Israel.
[Gitler, Daniel] Soroka Univ, Med Ctr, Fac Hlth Sci, Dept Physiol, IL-84105 Beer Sheva, Israel.
Ben Gurion Univ Negev, IL-84105 Beer Sheva, Israel.
[Eisenstein, Miriam] Weizmann Inst Sci, Dept Chem Res Support, IL-76100 Rehovot, Israel.
[Wolach, Baruch] Meir Hosp, Dept Pediat, Lab Leukocyte Funct, IL-44281 Kefar Sava, Israel.
[Rotem, Meir] Ha Emek Hosp, Dept Pediat, IL-18110 Afula, Israel.
[Leto, Thomas L.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
RP Levy, R (reprint author), Soroka Univ, Med Ctr, Fac Hlth Sci, Infect Dis Lab,Dept Clin Biochem, IL-84105 Beer Sheva, Israel.
EM ral@bgu.ac.il
RI Gitler, Daniel/F-1304-2012
OI Gitler, Daniel/0000-0001-9544-3610
FU Israel Sciences Foundation; Israel Academy of Sciences and Humanities
[438/03]
FX This work was supported by the Israel Sciences Foundation founded by the
Israel Academy of Sciences and Humanities (Grant 438/03).
NR 49
TC 14
Z9 14
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 31898
EP 31908
DI 10.1074/jbc.M804674200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800072
PM 18765662
ER
PT J
AU Brzeska, H
Hwang, KJ
Korn, ED
AF Brzeska, Hanna
Hwang, Kae-Jung
Korn, Edward D.
TI Acanthamoeba Myosin IC Colocalizes with Phosphatidylinositol
4,5-Bisphosphate at the Plasma Membrane Due to the High Concentration of
Negative Charge
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PLECKSTRIN HOMOLOGY DOMAINS; ACTIN-BINDING-SITES;
INTRACELLULAR-LOCALIZATION; PHOSPHOINOSITIDE-BINDING; CAPPING PROTEIN;
HEAVY-CHAIN; LIGHT-CHAIN; SH3 DOMAIN; AMINO-ACID; IN-VIVO
AB The tail of Acanthamoeba myosin IC (AMIC) has a basic region (BR), which contains a putative pleckstrin homology (PH) domain, followed by two Gly/Pro/Ala (GPA)-rich regions separated by a Src homology 3 (SH3) domain. Cryoelectron microscopy had shown that the tail is folded back on itself at the junction of BR and GPA1, and nuclear magnetic resonance spectroscopy indicated that the SH3 domain may interact with the putative PH domain. The BR binds to acidic phospholipids, and the GPA region binds to F-actin. We now show that the folded tail does not affect the affinity of AMIC for acidic phospholipids. AMIC binds phosphatidylinositol 4,5-bisphosphate (PIP2) with high affinity (similar to 1 mu M), but binding is not stereospecific. When normalized to net negative charge, AMIC binds with equal affinity to phosphatidylserine (PS) and PIP2. This and other data show that the putative PH domain of AMIC is not a typical PIP2-specific PH domain. We have identified a 13-residue sequence of basic-hydrophobic-basic amino acids within the putative PH domain that may be a major determinant of binding of AMIC to acidic phospholipids. Despite the lack of stereospecificity, AMIC binds 10 times more strongly to vesicles containing 5% PIP2 plus 25% PS than to vesicles containing only 25% PS, suggesting that AMIC may be targeted to PIP2-enriched regions of the plasma membrane. In agreement with this, AMIC colocalizes with PIP2 at dynamic, protrusive regions of the plasma membrane. We discuss the possibility that AMIC binding to PIP2 may initiate the formation of a multiprotein complex at the plasma membrane.
C1 [Brzeska, Hanna; Hwang, Kae-Jung; Korn, Edward D.] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Brzeska, H (reprint author), NHLBI, Cell Biol Lab, NIH, 9000 Rockville Pike,Bldg 50,Rm 2515, Bethesda, MD 20892 USA.
EM brzeskah@mail.nih.gov
RI Korn, Edward/F-9929-2012
FU National Institutes of Health; NHLBI, Division of Intramural Research
FX This work was authored, in whole or in part, by National Institutes of
Health staff. This work was supported, in whole or in part, by the
National Institutes of Health, NHLBI, Division of Intramural Research.
The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section 1734 solely to
indicate this fact.
NR 51
TC 20
Z9 20
U1 1
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 32014
EP 32023
DI 10.1074/jbc.M804828200
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800083
PM 18772133
ER
PT J
AU Dagdug, L
Berezhkovskii, AM
Makhnovskii, YA
Zitserman, VY
AF Dagdug, Leonardo
Berezhkovskii, Alexander M.
Makhnovskii, Yurii A.
Zitserman, Vladimir Yu.
TI Particle size effect on diffusion in tubes with dead ends: Nonmonotonic
size dependence of effective diffusion constant
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
DE diffusion; particle size
AB Diffusion of a spherical particle of radius r in a tube with identical periodic dead ends is analyzed. It is shown that the effective diffusion constant follows the Stokes-Einstein relation, D(eff)(r)proportional to 1/r, only when r is larger or much smaller than the radius of the dead end entrance. In between, D(eff)(r) not only deviates from the 1/r behavior but may also even become a nonmonotonic function, which increases with the particle radius for a certain range of r.
C1 [Dagdug, Leonardo] Univ Autonoma Metropolitana Iztapalapa, Dept Fis, Mexico City 09340, DF, Mexico.
[Berezhkovskii, Alexander M.] Ctr Informat Technol, NIH, Div Computat Biosci, Math Stat & Comp Lab, Bethesda, MD 20892 USA.
[Makhnovskii, Yurii A.] Russian Acad Sci, AV Topchiev Petrochem Synth Inst, Moscow 119991, Russia.
[Zitserman, Vladimir Yu.] Russian Acad Sci, Joint Inst High Temp, Moscow 125412, Russia.
RP Dagdug, L (reprint author), Univ Autonoma Metropolitana Iztapalapa, Dept Fis, Apartado Postal 55-534, Mexico City 09340, DF, Mexico.
EM dll@xanum.uam.mx
RI Makhnovskii, Yurii/B-1223-2014
OI Makhnovskii, Yurii/0000-0002-1517-536X
FU CONACyT [52305]; Russian Foundation for Basic Research [06-0332373];
NIH; Center for Information Technology
FX L. D. thanks CONACyT for partial support by the Grant No. 52305. Yu. A.
M. and V. Yu. Z. thank the Russian Foundation for Basic Research for
support (Grant No. 06-0332373). This study was supported by the
Intramural Research Program of the NIH, Center for Information
Technology.
NR 2
TC 10
Z9 10
U1 1
U2 4
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0021-9606
J9 J CHEM PHYS
JI J. Chem. Phys.
PD NOV 14
PY 2008
VL 129
IS 18
AR 184706
DI 10.1063/1.3010709
PG 5
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 373AV
UT WOS:000260944300045
PM 19045422
ER
PT J
AU Wei, SJ
Williams, JG
Dang, H
Darden, TA
Betz, BL
Humble, MM
Chang, FM
Trempus, CS
Johnson, K
Cannon, RE
Tennant, RW
AF Wei, Sung-Jen
Williams, Jason G.
Dang, Hong
Darden, Thomas A.
Betz, Bryan L.
Humble, Margaret M.
Chang, Fang-Mei
Trempus, Carol S.
Johnson, Katina
Cannon, Ronald E.
Tennant, Raymond W.
TI Identification of a Specific Motif of the DSS1 Protein Required for
Proteasome Interaction and p53 Protein Degradation
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE DSS1; Ubiquitin-proteasome system; RPN3/S3; siRNA; p53
ID SPLIT FOOT MALFORMATION; 26S PROTEASOME; REGULATORY PARTICLE;
SACCHAROMYCES-CEREVISIAE; UBIQUITIN SYSTEM; USTILAGO-MAYDIS; CANDIDATE
GENE; CORE PARTICLE; FISSION YEAST; DNA-REPAIR
AB Deleted in Split hand/Split foot 1 (DSS1) was previously identified as a novel 12-O-tetradecanoylphorbol-13-acetate (TPA)-inducible gene with possible involvement in early event of mouse skin carcinogenesis. The mechanisms by which human DSS1 (HsDSS1) exerts its biological effects via regulation of the ubiquitin-proteasome system (UPS) are currently unknown. Here, we demonstrated that HsDSS1 regulates the human proteasome by associating with it in the cytosol and nucleus via the RPN3/S3 subunit of the 19S regulatory particle (RP). Molecular anatomy of HsDSS1 revealed an RPN3/S3-interacting motif (R3IM), located at amino acid residues 15 to 21 of the NH2 terminus. Importantly, negative charges of the R3IM motif were demonstrated to be required for proteasome interaction and binding to poly-ubiquitinated substrates. Indeed, the R3IM motif of HsDSS1 protein alone was sufficient to replace the ability of intact HsDSS1 protein to pull down proteasome complexes and protein substrates with high-molecular mass ubiquitin conjugates. Interestingly, this interaction is highly conserved throughout evolution from humans to nematodes. Functional study, lowering the levels of the endogenous HsDSS1 using siRNA, indicates that the R3IM/proteasome complex binds and targets p53 for ubiquitin-mediated degradation via gankyrin-MDM2/HDM2 pathway. Most significantly, this work indicates that the R3IM motif of HsDSS1, in conjunction with the complexes of 19S RP and 20S core particle (CP), regulates proteasome interaction through RPN3/S3 molecule, and utilizes a specific subset of poly-ubiquitinated p53 as a substrate. Published by Elsevier Ltd.
C1 [Wei, Sung-Jen; Betz, Bryan L.; Humble, Margaret M.; Chang, Fang-Mei; Trempus, Carol S.; Cannon, Ronald E.; Tennant, Raymond W.] Natl Inst Environm Hlth Sci, Canc Biol Grp, Mol Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Williams, Jason G.; Darden, Thomas A.; Johnson, Katina] Natl Inst Environm Hlth Sci, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Dang, Hong] Alpha Gamma Technol Inc, Raleigh, NC 27609 USA.
[Wei, Sung-Jen; Chang, Fang-Mei] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, Div Med Res, Edinburg Reg Acad Hlth Ctr, Edinburg, TX 78541 USA.
RP Wei, SJ (reprint author), Natl Inst Environm Hlth Sci, Canc Biol Grp, Mol Toxicol Lab, NIH, Bldg 101,Rm F-149,MD F1-05,POB 12233, Res Triangle Pk, NC 27709 USA.
EM wei2@niehs.nih.gov
NR 62
TC 29
Z9 29
U1 0
U2 4
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 14
PY 2008
VL 383
IS 3
BP 693
EP 712
DI 10.1016/j.jmb.2008.08.044
PG 20
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 366TL
UT WOS:000260506200022
PM 18775730
ER
PT J
AU Zerhouni, EA
Potocnik, J
AF Zerhouni, Elias A.
Potocnik, Janez
TI European Union and NIH Collaborate
SO SCIENCE
LA English
DT Letter
C1 [Zerhouni, Elias A.] NIH, Bethesda, MD 20892 USA.
[Potocnik, Janez] Commiss European Communities, Sci & Res European Union, B-1049 Brussels, Belgium.
RP Zerhouni, EA (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM zerhoune@mail.nih.gov; janez.potocnik@ec.europa.eu
NR 0
TC 5
Z9 5
U1 0
U2 1
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 14
PY 2008
VL 322
IS 5904
BP 1048
EP 1048
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 371YD
UT WOS:000260867700010
PM 18974314
ER
PT J
AU Liu, SX
Abbondanzieri, EA
Rausch, JW
Le Grice, SFJ
Zhuang, XW
AF Liu, Shixin
Abbondanzieri, Elio A.
Rausch, Jason W.
Le Grice, Stuart F. J.
Zhuang, Xiaowei
TI Slide into Action: Dynamic Shuttling of HIV Reverse Transcriptase on
Nucleic Acid Substrates
SO SCIENCE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; MURINE LEUKEMIA-VIRUS; STRAND DISPLACEMENT
SYNTHESIS; DEPENDENT DNA-POLYMERASE; RNASE-H; CRYSTAL-STRUCTURE;
ANGSTROM RESOLUTION; ESCHERICHIA-COLI; SINGLE MOLECULES; ENERGY-TRANSFER
AB The reverse transcriptase ( RT) of human immunodeficiency virus ( HIV) catalyzes a series of reactions to convert single- stranded viral RNA into double- stranded DNA for host cell integration. This process requires a variety of enzymatic activities, including DNA polymerization, RNA cleavage, strand transfer, and strand displacement synthesis. We used single- molecule fluorescence resonance energy transfer to probe the interactions between RT and nucleic acid substrates in real time. RT was observed to slide on nucleic acid duplexes, rapidly shuttling between opposite termini of the duplex. Upon reaching the DNA 3' terminus, RT can spontaneously flip into a polymerization orientation. Sliding kinetics were regulated by cognate nucleotides and anti- HIV drugs, which stabilized and destabilized the polymerization mode, respectively. These long- range translocation activities facilitate multiple stages of the reverse transcription pathway, including normal DNA polymerization and strand displacement synthesis.
C1 [Liu, Shixin; Abbondanzieri, Elio A.; Zhuang, Xiaowei] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Zhuang, Xiaowei] Harvard Univ, Dept Phys, Cambridge, MA 02138 USA.
[Zhuang, Xiaowei] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
[Rausch, Jason W.; Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
RP Zhuang, XW (reprint author), Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
EM zhuang@chemistry.harvard.edu
RI Liu, Shixin/A-4560-2012
FU NIH [GM 068518]; Intramural Research Program of the Center for Cancer
Research; National Cancer Institute
FX This work is supported in part by NIH (GM 068518 to X. Z.) and the
Intramural Research Program of the Center for Cancer Research, National
Cancer Institute (to S.F.J.L.G.). X.Z. is a Howard Hughes Medical
Institute investigator. E.A.A. is a Jane Coffin Childs postdoctoral
fellow. Nevirapine was provided through the AIDS Research and Reference
Reagent Program of NIH.
NR 44
TC 96
Z9 97
U1 1
U2 29
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 14
PY 2008
VL 322
IS 5904
BP 1092
EP 1097
DI 10.1126/science.1163108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 371YD
UT WOS:000260867700035
PM 19008444
ER
PT J
AU Choi, EY
Chavakis, E
Czabanka, MA
Langer, HF
Fraemohs, L
Economopoulou, M
Kundu, RK
Orlandi, A
Zheng, YY
Prieto, DA
Ballantyne, CM
Constant, SL
Aird, WC
Papayannopoulou, T
Gahmberg, CG
Udey, MC
Vajkoczy, P
Quertermous, T
Dimmeler, S
Weber, C
Chavakis, T
AF Choi, Eun Young
Chavakis, Emmanouil
Czabanka, Marcus A.
Langer, Harald F.
Fraemohs, Line
Economopoulou, Matina
Kundu, Ramendra K.
Orlandi, Alessia
Zheng, Ying Yi
Prieto, DaRue A.
Ballantyne, Christie M.
Constant, Stephanie L.
Aird, William C.
Papayannopoulou, Thalia
Gahmberg, Carl G.
Udey, Mark C.
Vajkoczy, Peter
Quertermous, Thomas
Dimmeler, Stefanie
Weber, Christian
Chavakis, Triantafyllos
TI Del-1, an Endogenous Leukocyte-Endothelial Adhesion Inhibitor, Limits
Inflammatory Cell Recruitment
SO SCIENCE
LA English
DT Article
ID EXTRACELLULAR-MATRIX; INTEGRINS; MIGRATION; PROTEIN; MOLECULE-1; ICAM-1;
LFA-1
AB Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte- endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 ( developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA- 1- dependent leukocyte adhesion in vitro and in vivo. Del-1(-/-) mice displayed significantly higher neutrophil accumulation in lipopolysaccharide- induced lung inflammation in vivo, which was reversed in Del- /LFA-1 double- deficient mice. Thus, Del- 1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte- endothelial interactions in disease.
C1 [Choi, Eun Young; Langer, Harald F.; Zheng, Ying Yi; Chavakis, Triantafyllos] NCI, Expt Immunol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Chavakis, Emmanouil; Orlandi, Alessia; Dimmeler, Stefanie] Univ Frankfurt, Dept Internal Med 3, Frankfurt, Germany.
[Czabanka, Marcus A.; Vajkoczy, Peter] Charite Univ Med Berlin, Dept Neurosurg, D-13353 Berlin, Germany.
[Fraemohs, Line; Weber, Christian] Rhein Westfal TH Aachen, Univ Hosp, Inst Mol Cardiovasc Res, Aachen, Germany.
[Economopoulou, Matina] NCI, Lab Cellular Oncol, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Kundu, Ramendra K.; Quertermous, Thomas] Stanford Univ, Sch Med, Div Cardiovasc Med, Palo Alto, CA 94304 USA.
[Prieto, DaRue A.] NCI, Lab Proteom & Anal Technol, SAIC Frederick, Frederick, MD 21701 USA.
[Ballantyne, Christie M.] Baylor Coll Med, Houston, TX 77030 USA.
[Ballantyne, Christie M.] Methodist DeBakey Heart & Vasc Ctr, Ctr Cardiovasc Dis Prevent, Houston, TX 77030 USA.
[Constant, Stephanie L.] George Washington Univ, Dept Microbiol Immunol & Trop Med, Washington, DC USA.
[Aird, William C.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Papayannopoulou, Thalia] Univ Washington, Dept Med Hematol, Seattle, WA 98195 USA.
[Gahmberg, Carl G.] Univ Helsinki, Div Biochem, Fac Biosci, Helsinki, Finland.
[Udey, Mark C.] NCI, Dermatol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Chavakis, T (reprint author), NCI, Expt Immunol Branch, Canc Res Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM chavakist@mail.nih.gov
OI Gahmberg, Carl/0000-0001-9892-9296; Weber, Christian/0000-0003-4610-8714
FU Intramural Research Program; NIH [AI067254, RO1 HL082927]; NCI; Deutsche
Forschungsgemeinschaft [FOR809, TP6, TR-SFB23, Exc 147/1]
FX We thank X. Feng and M. Sardy for generating the Del-1-Fc protein, N.
Hogg for the antibody mAb24, Valentis Inc. for recombinant Del- 1 and
the antibody to mouse Del- 1, T. Veenstra for help with mass
spectrometry, D. Winkler for help with genotyping, I. Okwumabua for
technical assistance, and D. Singer for critically reading the
manuscript. This research was supported by the Intramural Research
Program of the NIH, NCI (T.C. and M.C.U.); by NIH grants AI067254
(S.L.C.) and RO1 HL082927 (W.C.A.); and by the Deutsche
Forschungsgemeinschaft (grants FOR809 and TP6 to C.W.; TR-SFB23 and Exc
147/1 to S.D. and E.C.). A patent application on the anti- inflammatory
actions of Del-1 has been filed.
NR 23
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U1 0
U2 17
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 14
PY 2008
VL 322
IS 5904
BP 1101
EP 1104
DI 10.1126/science.1165218
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 371YD
UT WOS:000260867700037
PM 19008446
ER
PT J
AU Nelson, RG
Paukov, ME
Hanson, RL
Knowler, WC
AF Nelson, Robert G.
Paukov, Meda E.
Hanson, Robert L.
Knowler, William C.
TI Changing course of diabetic nephropathy in the Pima Indians
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article; Proceedings Paper
CT International Symposium on Diabetic Nephropathy
CY 2008
CL Shiga, JAPAN
DE Type 2 diabetes; Diabetic nephropathy; Epidemiology; Pima Indians;
Secular trends
ID STAGE RENAL-DISEASE; TYPE-2 DIABETES/; PREVALENCE; MELLITUS; MORTALITY;
CHILDREN; OBESITY; PROTEINURIA; ANTIBODIES; IRBESARTAN
AB Pima Indians from the Gila River Indian Community in Arizona have a high incidence rate of type 2 diabetes, and kidney disease attributable to diabetes is a major cause of morbidity and mortality in this population. Since 1965, each member of the population at least 5 years of age is invited to participate in a research examination every other year. During the past 43 years, the overall incidence of diabetes in the Pima Indians has not changed, but the incidence of diabetes among those less than 15 years of age has increased nearly 6-fold, as an increasing prevalence and degree of obesity in the youth have shifted the onset of diabetes to younger ages, The rising frequency of diabetes in the youth has led, in turn, to the emergence in mid-life of the major complications of diabetes, including kidney disease. On the other hand, the introduction and widespread use of medicines to control blood pressure, reduce hyperglycemia, and block the renin-angiotensin system (RAS) have lead to improvements in the average blood pressure and glycosylated hemoglobin levels in the diabetic population. These countervailing forces have influenced the course of diabetic nephropathy in a generally favorable direction in the past few years, as evidenced by the decline in the overall incidence of end-stage kidney disease since 1990. A continued increase in the incidence of type 2 diabetes in youth, however, threatens to reverse this trend. Published by Elsevier Ireland Ltd.
C1 [Nelson, Robert G.; Paukov, Meda E.; Hanson, Robert L.; Knowler, William C.] NIDDK, NIH, Phoenix Epidemiol & Clin Res Branch, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ 85014 USA.
RP Nelson, RG (reprint author), NIDDK, NIH, Phoenix Epidemiol & Clin Res Branch, Diabet Epidemiol & Clin Res Sect, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA.
EM rgnelson@mail.nih.gov
RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU Intramural NIH HHS [Z01 DK069036-18, Z99 DK999999]
NR 33
TC 3
Z9 4
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD NOV 13
PY 2008
VL 82
SU 1
BP S10
EP S14
DI 10.1016/j.diabres.2008.09.014
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 381RM
UT WOS:000261553600003
PM 18842316
ER
PT J
AU Bosmans, F
Martin-Eauclaire, MF
Swartz, KJ
AF Bosmans, Frank
Martin-Eauclaire, Marie-France
Swartz, Kenton J.
TI Deconstructing voltage sensor function and pharmacology in sodium
channels
SO NATURE
LA English
DT Article
ID DEPENDENT K+ CHANNEL; ALPHA-SCORPION TOXIN; PERFORMANCE
LIQUID-CHROMATOGRAPHY; GATING MODIFIER TOXINS; GATED ION CHANNELS;
POTASSIUM CHANNEL; SKELETAL-MUSCLE; MOLECULAR DETERMINANTS; FAST
INACTIVATION; TARANTULA TOXINS
AB Voltage- activated sodium (Na(v)) channels are crucial for the generation and propagation of nerve impulses, and as such are widely targeted by toxins and drugs. The four voltage sensors in Na(v) channels have distinct amino acid sequences, raising fundamental questions about their relative contributions to the function and pharmacology of the channel. Here we use four- fold symmetric voltage- activated potassium ( K(v)) channels as reporters to examine the contributions of individual S3b-S4 paddle motifs within Na(v) channel voltage sensors to the kinetics of voltage sensor activation and to forming toxin receptors. Our results uncover binding sites for toxins from tarantula and scorpion venom on each of the four paddle motifs in Nav channels, and reveal how paddle- specific interactions can be used to reshape Na(v) channel activity. One paddle motif is unique in that it slows voltage sensor activation, and toxins selectively targeting this motif impede Na(v) channel inactivation. This reporter approach and the principles that emerge will be useful in developing new drugs for treating pain and Na(v) channelopathies.
C1 [Bosmans, Frank; Swartz, Kenton J.] NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
[Bosmans, Frank] Catholic Univ Louvain, Toxicol Lab, B-3000 Louvain, Belgium.
[Martin-Eauclaire, Marie-France] Univ Aix Marseille 2, CNRS, Inst Jean Roche, UMR 6231,CRN2M, Marseille, France.
RP Swartz, KJ (reprint author), NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
EM swartzk@ninds.nih.gov
RI Bosmans, Frank/A-9660-2013
OI Bosmans, Frank/0000-0002-6476-235X
FU Intramural Research Program; NINDS; NIH; NIH- FWO postdoctoral
fellowship
FX We thank J.W. Kyle, D.A. Hanck and A.L. Goldin for the
rNav1.2a, rNav1.4 and beta1 clones, C.
Deutsch for Kv1.3, M.M. Smith for GxTx-1E, K.M. Blumenthal
and J.B. Herrington for ProTx-II, L.D. Possani for a sample of TsVII,
the NINDS DNA sequencing facility for DNA sequencing, and the NINDS
protein sequencing facility for mass spectrometry and peptide
sequencing. We thank A.A. Alabi for helping with Kv and Nav channel
alignments and T.-H. Chang for assistance with Nav channel mutants. We
also thank A. A. Alabi, M. Holmgren, M. Mayer, M. Milescu, J. Mindell,
A. Plested, S. Silberberg and members of the Swartz laboratory for
discussions. This work was supported by the Intramural Research Program
of the NINDS, NIH (K.J.S.) and by an NIH- FWO postdoctoral fellowship
(F.B.).
NR 62
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U1 5
U2 23
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 13
PY 2008
VL 456
IS 7219
BP 202
EP U28
DI 10.1038/nature07473
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374JJ
UT WOS:000261039300032
PM 19005548
ER
PT J
AU Liu, Y
Borchert, GL
Surazynski, A
Phang, JM
AF Liu, Y.
Borchert, G. L.
Surazynski, A.
Phang, J. M.
TI Proline oxidase, a p53-induced gene, targets COX-2/PGE(2) signaling to
induce apoptosis and inhibit tumor growth in colorectal cancers
SO ONCOGENE
LA English
DT Article
DE proline oxidase; COX-2; signaling cross talk; colorectal cancer; tumor
suppressor
ID FACTOR RECEPTOR; COLON-CANCER; POSTTRANSCRIPTIONAL CONTROL;
CYCLOOXYGENASE-2; EXPRESSION; CARCINOGENESIS; PATHWAY; OXYGEN; CELLS;
CHEMOPREVENTION
AB Proline oxidase (POX), a flavoenzyme localized at the inner mitochondrial membrane, catalyzes the first step of proline degradation by converting proline to pyrroline-5-carboxylate (P5C). POX is markedly elevated during p53-induced apoptosis and generates proline-dependent reactive oxygen species (ROS), specifically superoxide radicals, to induce apoptosis through both mitochondrial and death receptor pathways. These previous studies also showed suppression of the mitogen-activated protein kinase pathway leading us to broaden our exploration of proliferative signaling. In our current report, we used DLD-1 colorectal cancer cells stably transfected with the POX gene under the control of a tetracycline-inducible promoter and found that three pathways which cross talk with each other were downregulated by POX: the cyclooxygenase-2(COX-2) pathway, the epidermal growth factor receptor (EGFR) pathway and the Wnt/beta-catenin pathway. First, POX markedly reduced COX-2 expression, suppressed the production of prostaglandin E2 (PGE2) and importantly, the growth inhibition by POX was partially reversed by treatment with PGE2. Phosphorylation of EGFR was decreased with POX expression and the addition of EGF partially reversed the POX-dependent downregulation of COX-2. Wnt/beta-catenin signaling was decreased by POX in that phosphorylation of glycogen synthase kinase-3 beta (GSK-3 beta) was decreased on the one hand and phosphorylation of beta-catenin was increased on the other. There changes led to decreased accumulation of beta-catenin and decreased beta-catenin/TCF/LEF-mediated transcription. Our newly described POX-mediated suppression of proliferative signaling together with the previously reported induction of apoptosis suggested that POX could function as a tumor suppressor. Indeed, in human colorectal tissue samples, immunohistochemically-monitored POX was dramatically decreased in tumors compared with normal counterparts. Thus, POX metabolism of substrate proline affects multiple signaling pathways, modulating both apoptosis and tumor growth, and could be an attractive target to metabolically control the cancer phenotypes.
C1 [Liu, Y.; Borchert, G. L.] NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Surazynski, A.; Phang, J. M.] NCI, Ctr Canc Res, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
RP Liu, Y (reprint author), NCI, Basic Res Program, SAIC Frederick Inc, Bldg 538,Room 144, Frederick, MD 21702 USA.
EM liuy@ncifcrf.gov
FU NIH [N01-CO-12400]; National Cancer Institute; Center for Cancer
Research
FX This research is supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. This project
also has been funded in part with Federal funds from the National Cancer
Institute, National Institutes of Health under Contract No.
N01-CO-12400. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the US Government.
NR 38
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U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD NOV 13
PY 2008
VL 27
IS 53
BP 6729
EP 6737
DI 10.1038/onc.2008.322
PG 9
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 371XO
UT WOS:000260866200003
PM 18794809
ER
PT J
AU Biggar, RJ
Lee, TH
Wen, L
Broadhead, R
Kumwenda, N
Taha, TE
Busch, MP
AF Biggar, Robert J.
Lee, Tzong-Hae
Wen, Li
Broadhead, Robin
Kumwenda, Newton
Taha, E. Taha
Busch, Michael P.
TI The role of transplacental microtransfusions of maternal lymphocytes in
HIV transmission to newborns
SO AIDS
LA English
DT Article
DE Africa; childbirth; children; genome; human immunodeficiency virus;
Malawi; placenta; retrovirus; sensitivity
ID TO-CHILD TRANSMISSION; BLOOD COMPONENTS; CLINICAL-TRIAL; FILTER-PAPER;
CLASS-I; PLASMA; DNA; MICROCHIMERISM; INTERVENTION; CONCORDANCE
AB Background: Perinatal HIV transmission could occur via microtransfused maternal blood during delivery. If so, detecting maternal cells in umbilical cord blood should correlate with infection risk. Objective: To develop sensitive assays for maternal DNA in infant's blood stored as dried blood spots (DBS) and examine the correlation between microtransfusion and perinatal HIV infection risk.
Methods: Blood-in-blood serial dilutions were prepared as DBS. Extracted DNA was amplified for unique minor-population sequences using 24 allele-specific polymerase chain reaction assays. Using newborns born to HIV+ mothers, paired mother-infant samples were similarly examined to identify unique maternal sequences targeted by allele-specific polymerase chain reaction of DNA extracted from cord blood DES. Cord-blood PCR-negative infants were categorized as uninfected or perinatally infected by HIV PCR on samples collected 4-8 weeks after birth.
Results: Sequences from added cells were detected at less than 1 : 1000 dilutions in 19 of 20 aliquots, and less than 1 : 10000 dilutions in seven of 20 aliquots; the median limit of detection (probit analysis) was one added genomic sequence in 9500 background sequences of amplifiable DNA. Maternal sequences were detected in cord-blood DBS of 50% of infected infants (N=18) and 44% of uninfected infants (N=43). Infection did not correlate with more frequent detection of maternal sequences.
Conclusion: This semiquantitative assay reliably detected maternal DNA sequences in DBS at levels of less than 1 : 1000 cells. Maternal sequences were frequently detected but did not correlate infection risk with detection or level of maternal DNA in umbilical cord blood. Therefore, we could not demonstrate that microtransfusions at parturition were responsible for perinatal HIV transmission. (C) 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
C1 [Biggar, Robert J.] State Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
[Biggar, Robert J.] NCI, Infect & Immun Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lee, Tzong-Hae; Wen, Li; Busch, Michael P.] Blood Syst Res Inst, San Francisco, CA USA.
[Broadhead, Robin; Kumwenda, Newton] Univ Malawi, Sch Med, Blantyre, Malawi.
[Taha, E. Taha] Johns Hopkins Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Busch, Michael P.] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
RP Biggar, RJ (reprint author), State Serum Inst, Dept Epidemiol Res, Artillersvej 5, DK-2300 Copenhagen, Denmark.
EM rjbiggar@gmail.com
FU National Heart, Lung and Blood Institute, National Institutes of Health
[# R01-HL-08838]; Blood Systems Research Institute, San Francisco, and
California
FX This work was supported by a grant (NHLBI grant # R01-HL-08838) from the
National Heart, Lung and Blood Institute, National Institutes of Health
to Dr Michael Busch (Principal Investigator) and colleagues at Blood
Systems Research Institute, San Francisco, and California.
NR 25
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Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 12
PY 2008
VL 22
IS 17
BP 2251
EP 2256
DI 10.1097/QAD.0b013e328314e36b
PG 6
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 377SH
UT WOS:000261270400004
PM 18981764
ER
PT J
AU Brown, E
Chi, BH
Read, JS
Taha, TE
Sharma, U
Hoffman, IF
Pikora, C
Goldenberg, R
Fiscus, SA
AF Brown, Elizabeth
Chi, Benjamin H.
Read, Jennifer S.
Taha, Taha E.
Sharma, Usha
Hoffman, Irving F.
Pikora, Cheryl
Goldenberg, Robert
Fiscus, Susan A.
TI Determining an optimal testing strategy for infants at risk for
mother-to-child transmission of HIV-1 during the late postnatal period
SO AIDS
LA English
DT Article
DE breastfeeding; HIV infant diagnosis; late postnatal transmission
ID IMMUNODEFICIENCY-VIRUS TYPE-1; RANDOMIZED CONTROLLED-TRIAL;
NATURAL-HISTORY; AFRICAN CHILDREN; CLINICAL-TRIAL; SOUTH-AFRICA;
INFECTION; ZIDOVUDINE; MORTALITY; PREVENTION
AB Objectives: To determine the optimal time for a second HIV-1 nucleic acid amplification assay to detect late postnatal transmission of HIV-1 (first negative test at 4-8 weeks of age) in resource-limited settings.
Design: A longitudinal analysis of data from HIV Prevention Trial Network trial 024.
Methods: Children born to HIV-1-infected mothers enrolled in the HIV Prevention Trial Network trial 024 were tested for HIV-1 infection at six intervals within the first year of life. Mothers and infants received nevirapine prophylaxis. We estimated the probability of being alive and having a positive test in each interval after 4-8 weeks and at 30 days after weaning, conditional on having acquired HIV during the late postnatal period. The interval with the highest probability was taken to be the optimal visit interval.
Results: A total of 1609 infants from HIV Prevention Trial Network trial 024 had at least one HIV-1 diagnostic test and were included in the analysis. We found that testing at 1 month after weaning or 12 months of age (whichever comes first) identified 81% of those infected during the late postnatal period (after 4-8 weeks) through breastfeeding. In total, 93% (95% confidence interval 89, 98) of all infected infants would be detected if tests were performed at these two time points.
Conclusion: In resource-limited settings, HIV-1 PCR testing at 4-8 weeks followed by a second test at 1 month after weaning or at 1 year of age (whichever comes first), led to the identification of the vast majority of HIV-1-infected infants. (C) 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
C1 [Fiscus, Susan A.] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA.
[Brown, Elizabeth] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Brown, Elizabeth] Fred Hutchinson Canc Res Ctr, SCHARP, Seattle, WA 98104 USA.
[Chi, Benjamin H.] Ctr Infect Dis Res Zambia, Lusaka, Zambia.
[Read, Jennifer S.] DHHS, Pediat Adolescent & Maternal AIDS Branch, CRMC, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Taha, Taha E.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Sharma, Usha] DHHS, Div AIDS, NIAID, Bethesda, MD USA.
[Hoffman, Irving F.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Pikora, Cheryl] Kendle Int Inc, Cincinnati, OH USA.
[Goldenberg, Robert] Drexel Coll Med, Dept Obstet & Gynecol, Philadelphia, PA USA.
RP Fiscus, SA (reprint author), Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA.
RI Brown, Elizabeth/A-8984-2008
FU U.S. National Institute of Allergy and Infections Diseases (NIAID),
National Institute of Health (NIH) [NO1-AI-35173, NO1-AI-45200,
NO1-AI-35173-117/412]; Eunice Kennedy Shriver National Institute of
Child Health and Human Development; National Institute on Drug Abuse;
National Institutes of Mental Health; Office of AIDS Research of the
National Institutes of Health; U.S. Department of Health and Human
Services, Harvard University [U01-AI-48006]; Johns Hopkins University
[U01-AI-48005]; University of Alabama at Birmingham [U01-AI-47972];
[HPTN]
FX The HPTN024 Trial was supported by the HIVNET and sponsored by the U.S.
National Institute of Allergy and Infections Diseases (NIAID), National
Institute of Health (NIH), Department of Health and Human Services,
through contracts NO1-AI-35173 with Family Health International,
NO1-AI-45200 with Fred Hutchinson Cancer Research Center, and
subcontract NO1-AI-35173-117/412 with Johns Hopkins University. In
addition, the trial was supported by the HPTN and sponsored by NIAID,
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institute on Drug Abuse, the National Institutes
of Mental Health, and the Office of AIDS Research of the National
Institutes of Health, U.S. Department of Health and Human Services,
Harvard University (U01-AI-48006), Johns Hopkins University
(U01-AI-48005), and the University of Alabama at Birmingham
(U01-AI-47972). Nevirapine (Viramune) for the study was provided by
Boebringer Ingelheim Pharmaceuticals, Inc. The conclusion and opinions
expressed in this study are those of the authors and do not necessarily
reflect those of the funding agencies and participating institutions.
NR 26
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U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
EI 1473-5571
J9 AIDS
JI Aids
PD NOV 12
PY 2008
VL 22
IS 17
BP 2341
EP 2346
DI 10.1097/QAD.0b013e328317cc15
PG 6
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 377SH
UT WOS:000261270400013
PM 18981773
ER
PT J
AU Nakamura, M
Choe, SK
Runko, AP
Gardner, PD
Sagerstrom, CG
AF Nakamura, Mako
Choe, Seong-Kyu
Runko, Alexander P.
Gardner, Paul D.
Sagerstroem, Charles G.
TI Nlz1/Znf703 acts as a repressor of transcription
SO BMC DEVELOPMENTAL BIOLOGY
LA English
DT Article
ID ZINC-FINGER PROTEINS; ZEBRAFISH HINDBRAIN; GENE-EXPRESSION;
EMBRYONIC-DEVELOPMENT; FGF SIGNALS; FACTOR SP1; DOMAINS; FAMILY; VHNF1;
ACTIVATION
AB Background: Members of the NET subfamily of zinc-finger proteins are related to the Sp-family of transcription factors and are required during embryogenesis. In particular, Nlz1/Znf703 and Nlz2/Znf503 are required for formation of rhombomere 4 of the vertebrate hindbrain. While NET family proteins have been hypothesized to regulate transcription, it remains unclear if they function as activators or repressors of transcription.
Results: Here we demonstrate that Nlz proteins repress transcription both in cell lines and in developing zebrafish embryos. We first use standard cell culture-based reporter assays to demonstrate that Nlz1/Znf703 represses transcription of a luciferase reporter in four different cell lines. Structure-function analyses and pharmacological inhibition further reveal that Nlz1-mediated repression requires histone deacetylase activity. We next generate a stable transgenic zebrafish reporter line to demonstrate that Nlz1 promotes histone deacetylation at the transgenic promoter and repression of transgene expression during embryogenesis. Lastly, taking a genetic approach we find that endogenous Nlz proteins are required for formation of hindbrain rhombomere 4 during zebrafish embryogenesis by repressing expression of non-rhombomere 4 genes.
Conclusion: We conclude that Nlz1/Znf703 acts as a repressor of transcription and hypothesize that other NET family members function in a similar manner.
C1 [Nakamura, Mako; Choe, Seong-Kyu; Runko, Alexander P.; Sagerstroem, Charles G.] Univ Massachusetts, Sch Med, Dept Mol Pharmacol & Biochem, Worcester, MA 01605 USA.
[Gardner, Paul D.] Univ Massachusetts, Sch Med, Dept Psychiat, Worcester, MA 01655 USA.
[Nakamura, Mako] Kyushu Univ, Fac Agr, Fukuoka 812, Japan.
[Runko, Alexander P.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Sagerstrom, CG (reprint author), Univ Massachusetts, Sch Med, Dept Mol Pharmacol & Biochem, Worcester, MA 01605 USA.
EM mako_n@agr.kyushu-u.ac.jp; seong-kyu.choe@umassmed.edu;
runkoa@ninds.nih.gov; paul.gardner@umassmed.edu;
charles.sagerstrom@umassmed.edu
FU March of Dimes [FY04-105, FY07-430]
FX The authors thank Dr Scot Wolfe for helpful discussions about zinc
finger proteins and Letitiah Etheridge for expert assistance in
preparation of the TG(UAS-SV40:Luciferase) line. We are grateful to
Yasuyuki Ohkawa and Anthony Imbalzano for assistance with the ChIP
assays ant Cecilia Moens for fgf plasmids. We acknowledge Dr Nancy
Hopkins for providing the vhnflhi2169 strain. This work was
funded by grants FY04-105 and FY07-430 from the March of Dimes.
NR 40
TC 15
Z9 16
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-213X
J9 BMC DEV BIOL
JI BMC Dev. Biol.
PD NOV 12
PY 2008
VL 8
AR 108
DI 10.1186/1471-213X-8-108
PG 12
WC Developmental Biology
SC Developmental Biology
GA 381SX
UT WOS:000261557300001
PM 19014486
ER
PT J
AU Saha, A
Kim, SJ
Zhang, ZJ
Lee, YC
Sarkar, C
Tsai, PC
Mukherjee, AB
AF Saha, Arjun
Kim, Sung-Jo
Zhang, Zhongjian
Lee, Yi-Ching
Sarkar, Chinmoy
Tsai, Pei-Chih
Mukherjee, Anil B.
TI RAGE signaling contributes to neuroinflammation in infantile neuronal
ceroid lipofuscinosis
SO FEBS LETTERS
LA English
DT Article
DE Neuroinflammation; Neurodegeneration; Infantile neuronal ceroid
lipofuscinosis; Batten disease; Palmitoyl-protein thioesterase-1
ID PALMITOYL-PROTEIN THIOESTERASE; NF-KAPPA-B; GLYCATION END-PRODUCTS;
ALZHEIMERS-DISEASE; OXIDATIVE STRESS; ACTIVATION; RECEPTOR;
NEURODEGENERATION; INFLAMMATION; APOPTOSIS
AB Palmitoyl-protein thioesterase-1 (PPT1) deficiency causes infantile neuronal ceroid lipofuscinosis (INCL), a devastating childhood neurodegenerative storage disorder. We previously reported that neuronal apoptosis in INCL is mediated by endoplasmic reticulum-stress. ER-stress disrupts Ca(2+)-homeostasis and stimulates the expression of Ca(2+)-binding proteins. We report here that in the PPT1-deficient human and mouse brain the levels of S100B, a Ca(2+)-binding protein, and its receptor, RAGE (receptor for advanced glycation end-products) are elevated. We further demonstrate that activation of RAGE signaling in astroglial cells mediates pro-inflammatory cytokine production, which is inhibited by SiRNA-mediated suppression of RAGE expression. We propose that RAGE signaling contributes to neuroinflammation in INCL. (C) 2008 Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.
C1 [Saha, Arjun; Kim, Sung-Jo; Zhang, Zhongjian; Lee, Yi-Ching; Sarkar, Chinmoy; Tsai, Pei-Chih; Mukherjee, Anil B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Dev Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Mukherjee, AB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Dev Genet, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
EM mukherja@exchange.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 45
TC 16
Z9 16
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-5793
J9 FEBS LETT
JI FEBS Lett.
PD NOV 12
PY 2008
VL 582
IS 27
BP 3823
EP 3831
DI 10.1016/j.febslet.2008.10.015
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 377EP
UT WOS:000261234800020
PM 18948101
ER
PT J
AU Levens, ED
DeCherney, AH
AF Levens, Eric D.
DeCherney, Alan H.
TI Human Oocyte Research The Ethics of Donation and Donor Protection
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID STEM-CELL RESEARCH; EGGS; IVF
C1 [Levens, Eric D.; DeCherney, Alan H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Levens, ED (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bldg 10,CRC,Room E1-3140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM levense@mail.nih.gov
FU Intramural NIH HHS
NR 15
TC 8
Z9 8
U1 1
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 12
PY 2008
VL 300
IS 18
BP 2174
EP 2176
DI 10.1001/jama.2008.601
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 370WM
UT WOS:000260793800028
PM 19001629
ER
PT J
AU Jiang, Y
Langley, B
Lubin, FD
Renthal, W
Wood, MA
Yasui, DH
Kumar, A
Nestler, EJ
Akbarian, S
Beckel-Mitchener, AC
AF Jiang, Yan
Langley, Brett
Lubin, Farah D.
Renthal, William
Wood, Marcelo A.
Yasui, Dag H.
Kumar, Arvind
Nestler, Eric J.
Akbarian, Schahram
Beckel-Mitchener, Andrea C.
TI Epigenetics in the Nervous System
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE epigenetics; chromatin; DNA methylation; histone; transcription; gene
ID LONG-TERM-MEMORY; HISTONE DEACETYLASE INHIBITOR; CREB-BINDING PROTEIN;
RUBINSTEIN-TAYBI-SYNDROME; TRANSGENIC MOUSE MODEL; SYNAPTIC PLASTICITY;
NEUROTROPHIC-FACTOR; RETT-SYNDROME; GENE-EXPRESSION; LYSINE-9
METHYLATION
AB It is becoming increasingly clear that epigenetic modifications are critical factors in the regulation of gene expression. With regard to the nervous system, epigenetic alterations play a role in a diverse set of processes and have been implicated in a variety of disorders. Gaining a more complete understanding of the essential components and underlying mechanisms involved in epigenetic regulation could lead to novel treatments for a number of neurological and psychiatric conditions.
C1 [Beckel-Mitchener, Andrea C.] NIMH, NIH, NSC, Bethesda, MD 20892 USA.
[Jiang, Yan; Akbarian, Schahram] Univ Massachusetts, Sch Med, Brudnick Neuropsychiat Res Inst, Worcester, MA 01604 USA.
[Langley, Brett] Cornell Univ, Weill Med Coll, Burke Med Res Inst, White Plains, NY 10021 USA.
[Lubin, Farah D.] Univ Alabama, Evelyn F McKnight Brain Inst, Dept Neurobiol, Birmingham, AL 35294 USA.
[Renthal, William; Kumar, Arvind; Nestler, Eric J.] Univ Texas SW Med Ctr Dallas, Dept Psychiat & Neurosci, Dallas, TX 75390 USA.
[Wood, Marcelo A.] Univ Calif Irvine, Ctr Neurobiol Learning & Memory, Dept Neurobiol & Behav, Irvine, CA 92697 USA.
[Yasui, Dag H.] Univ Calif Davis, Sch Med, Dept Med Microbiol, Rowe Program Human Genet, Davis, CA 95616 USA.
[Yasui, Dag H.] Univ Calif Davis, Sch Med, Dept Immunol, Rowe Program Human Genet, Davis, CA 95616 USA.
RP Beckel-Mitchener, AC (reprint author), NIMH, NIH, NSC, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM amitchen@mail.nih.gov
RI Jiang, yan/C-7126-2011; Wood, Marcelo/G-9527-2012
FU NCRR NIH HHS [S10 RR024747, S10 RR024747-01]; NICHD NIH HHS [R01
HD048799-03, R01 HD048799, R01 HD041462-06A2, R01 HD041462]; NIDA NIH
HHS [R37 DA007359, T32 DA007290-14, T32 DA007290, R37 DA007359-15]; NIMH
NIH HHS [R01 MH086509, K99 MH082106, K99 MH082106-01, R01 MH074114, R01
MH074114-01, R01 MH081004, R01 MH081004-01A1]
NR 87
TC 112
Z9 120
U1 1
U2 19
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 12
PY 2008
VL 28
IS 46
BP 11753
EP 11759
DI 10.1523/JNEUROSCI.3797-08.2008
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600003
PM 19005036
ER
PT J
AU Eisch, AJ
Cameron, HA
Encinas, JM
Meltzer, LA
Ming, GL
Overstreet-Wadiche, LS
AF Eisch, Amelia J.
Cameron, Heather A.
Encinas, Juan M.
Meltzer, Leslie A.
Ming, Guo-Li
Overstreet-Wadiche, Linda S.
TI Adult Neurogenesis, Mental Health, and Mental Illness: Hope or Hype?
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE neural stem cell; epilepsy; learning; depression; addiction;
schizophrenia
ID TEMPORAL-LOBE EPILEPSY; NEWLY GENERATED NEURONS; CENTRAL-NERVOUS-SYSTEM;
GFP TRANSGENIC MICE; HIPPOCAMPAL NEUROGENESIS; NUCLEUS-ACCUMBENS; RAT
HIPPOCAMPUS; DENTATE GYRUS; PROGENITOR CELLS; NEURAL STEM
AB Psychiatric and neurologic disorders take an enormous toll on society. Alleviating the devastating symptoms and consequences of neuropsychiatric disorders such as addiction, depression, epilepsy, and schizophrenia is a main force driving clinical and basic researchers alike. By elucidating these disease neuromechanisms, researchers hope to better define treatments and preventive therapies. Research suggests that regulation of adult hippocampal neurogenesis represents a promising approach to treating and perhaps preventing mental illness. Here we appraise the role of adult hippocampal neurogenesis in major psychiatric and neurologic disorders within the essential framework of recent progress made in understanding "normal" adult neurogenesis. Topics addressed include the following: the life cycle of an adult hippocampal stem cell and the implications for aging; links between learning and hippocampal neurogenesis; the reciprocal relationship between cocaine self-administration and adult hippocampal neurogenesis; the role of adult neurogenesis in an animal model of depression and response to antidepressant exposure; the impact of neonatal seizures on dentate gyrus neurogenesis; and the contribution of a schizophrenia-susceptibility gene to adult hippocampal neurogenesis. These topics are discussed in light of the regulation of adult neurogenesis, the relationship to normal neurogenesis in adulthood and aging, and, importantly, the manipulation of neurogenesis to promote mental health and treat mental illness.
C1 [Eisch, Amelia J.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Cameron, Heather A.] NIMH, Unit Neuroplast, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA.
[Encinas, Juan M.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
[Meltzer, Leslie A.] Stanford Univ, Dept Bioengn, Stanford, CA 94305 USA.
[Ming, Guo-Li] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21205 USA.
[Ming, Guo-Li] Johns Hopkins Univ, Dept Neurosci, Baltimore, MD 21205 USA.
[Overstreet-Wadiche, Linda S.] Univ Alabama, Dept Neurobiol, Birmingham, AL 35294 USA.
RP Eisch, AJ (reprint author), Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
EM amelia.eisch@utsouthwestern.edu
RI Encinas, Juan/E-3625-2010; Ming, Guo-li/J-7880-2013; Cameron,
Heather/E-6221-2011;
OI Cameron, Heather/0000-0002-3245-5777; Wadiche, Linda/0000-0001-7367-5998
FU National Institute on Drug Abuse [RO1 DA016765, K02 DA023555]; National
Institutes of Health [NS0488271, MH084018]; Intramural Research Program
of the National Institute on Mental Health [Z01-MH002784]
FX This work was supported by National Institute on Drug Abuse Grants RO1
DA016765 and K02 DA023555 (A.J.E.), National Institutes of Health Grants
NS0488271 and MH084018 (G.L.M.), Intramural Research Program of the
National Institute on Mental Health Grant Z01-MH002784 (H.A.C.), a
National Alliance for Research on Schizophrenia and Depression Young
Investigator Award (J.M.E.), a Stanford Bio-X Graduate Fellowship
(L.A.M.), a Klingenstein Fellowship Award in the Neurosciences, the
March of Dimes, the Alfred P. Sloan Foundation and Adelson Medical
Research Foundation (all to G. L. M.), and the Epilepsy Foundation
(L.S.O.-W.). A.J.E. thanks Dr. Diane Lagace, Nathan DeCarolis, Michele
Noonan, Dr. Shveta Malhotra, and her coauthors for their significant
intellectual contributions to this article during its preparation.
A.J.E. particularly acknowledges the skill and effort of Jessica L.
Ables in crafting
NR 89
TC 165
Z9 169
U1 0
U2 12
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 12
PY 2008
VL 28
IS 46
BP 11785
EP 11791
DI 10.1523/JNEUROSCI.3798-08.2008
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600007
PM 19005040
ER
PT J
AU Hikosaka, O
Sesack, SR
Lecourtier, L
Shepard, PD
AF Hikosaka, Okihide
Sesack, Susan R.
Lecourtier, Lucas
Shepard, Paul D.
TI Habenula: Crossroad between the Basal Ganglia and the Limbic System
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE reward; motivation; cognition; dopamine; striatum; serotonin;
depression; schizophrenia
ID MIDBRAIN DOPAMINE NEURONS; DORSAL RAPHE NUCLEUS; LATERAL HABENULA; RAT;
REWARD; LESIONS; TRANSMISSION; ACCUMBENS; COMPLEX; STIMULATION
AB There is a growing awareness that emotion, motivation, and reward values are important determinants of our behavior. The habenula is uniquely positioned both anatomically and functionally to participate in the circuit mediating some forms of emotive decision making. In the last few years there has been a surge of interest in this structure, especially the lateral habenula (LHb). The new studies suggest that the LHb plays a pivotal role in controlling motor and cognitive behaviors by influencing the activity of dopamine and serotonin neurons. Further, dysfunctions of the LHb have also been implicated in psychiatric disorders, such as depression, schizophrenia, and drug-induced psychosis.
C1 [Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
[Sesack, Susan R.] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA.
[Sesack, Susan R.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Lecourtier, Lucas] Univ Strasbourg 1, CNRS, UMR 7191, Lab Imagerie & Neurosci Cognit, F-67000 Strasbourg, France.
[Shepard, Paul D.] Univ Maryland, Sch Med, Dept Psychiat, Baltimore, MD 21228 USA.
[Shepard, Paul D.] Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA.
RP Hikosaka, O (reprint author), NEI, Sensorimotor Res Lab, NIH, Bldg 49,Room 2A50,49 Convent Dr, Bethesda, MD 20892 USA.
EM oh@lsr.nei.nih.gov
FU National Eye Institute; United States Public Health Service [MH-067937,
R37-MH48404, MH-072647]
FX This work was supported by the intramural research program of the
National Eye Institute to O.H. and by United States Public Health
Service Grants MH-067937 to S. R. S., R37-MH48404 (principal
investigator: B. Moghaddam) to L. L., and MH-072647 to P. D. S.
(co-principal investigator: J. Gold).
NR 57
TC 166
Z9 173
U1 3
U2 15
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 12
PY 2008
VL 28
IS 46
BP 11825
EP 11829
DI 10.1523/JNEUROSCI.3463-08.2008
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600014
PM 19005047
ER
PT J
AU Wax, MB
Tezel, G
Yang, J
Peng, G
Patil, RV
Agarwal, N
Sappington, RM
Calkins, DJ
AF Wax, Martin B.
Tezel, Guelguen
Yang, Junjie
Peng, Guanghua
Patil, Rajkumar V.
Agarwal, Neeraj
Sappington, Rebecca M.
Calkins, David J.
TI Induced Autoimmunity to Heat Shock Proteins Elicits Glaucomatous Loss of
Retinal Ganglion Cell Neurons via Activated T-Cell-Derived Fas-Ligand
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE autoimmunity; glaucoma; microglia; T-cells; FasL; heat shock proteins
ID CENTRAL-NERVOUS-SYSTEM; NORMAL-PRESSURE GLAUCOMA; ENDOTOXIN-INDUCED
UVEITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS;
IMMUNE SURVEILLANCE; SERUM AUTOANTIBODIES; OCULAR HYPERTENSION; CLASS-I;
MICROGLIA
AB Glaucomatous optic neuropathy causes blindness through the degeneration of retinal ganglion cells (RGCs) and their axons, which comprise the optic nerve. Glaucoma traditionally is associated with elevated intraocular pressure, but often occurs or may progress with intraocular pressure in the normal range. Like other diseases of the CNS, a subset of glaucoma has been proposed to involve an autoimmune component to help explain the loss of RGCs in the absence of elevated intraocular pressure. One hypothesis involves heat shock proteins (HSPs), because increased serum levels of HSP autoantibodies are prominent in some glaucoma patients with normal pressures. In the first direct support of this hypothesis, we found that HSP27 and HSP60 immunization in the Lewis rat induced RGC degeneration and axon loss 1-4 months later in vivo in a pattern with similarities to human glaucoma, including topographic specificity of cell loss. Infiltration of increased numbers of T-cells in the retina occurred much earlier, 14-21 d after HSP immunization, and appeared to be transient. In vitro studies found that T-cells activated by HSP immunization induced RGC apoptosis via the release of the inflammatory cytokine FasL, whereas HSP immunization induced activation of microglia cells and upregulation of the FasL receptor in RGCs. In summary, our results suggest that RGC degeneration in glaucoma for selected individuals likely involves failed immunoregulation of the T-cell-RGC axis and is thus a disturbance of both proapoptotic and protective pathways.
C1 [Wax, Martin B.] Univ Texas Southwestern Med Sch, Dept Ophthalmol, Dallas, TX 75390 USA.
[Wax, Martin B.; Yang, Junjie; Patil, Rajkumar V.] Alcon Corp, Ophthalmol Discovery Res, Ft Worth, TX 76134 USA.
[Tezel, Guelguen] Univ Louisville, Dept Ophthalmol & Visual Sci, Louisville, KY 40202 USA.
[Tezel, Guelguen] Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA.
[Peng, Guanghua] Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, St Louis, MO 63110 USA.
[Agarwal, Neeraj] NEI, Div Extramural Res, Bethesda, MD 20892 USA.
[Sappington, Rebecca M.; Calkins, David J.] Vanderbilt Univ, Med Ctr, Vanderbilt Eye Inst, Nashville, TN 37232 USA.
RP Wax, MB (reprint author), Univ Texas Southwestern Med Sch, Dept Ophthalmol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM mbw817@yahoo.com
RI Sappington, Rebecca/F-8183-2010
FU National Eye Institute (Bethesda, MD) [EY12314]; Glaucoma Research
Foundation (San Francisco, CA); Research to Prevent Blindness (New York,
NY)
FX This work was supported in part by EY12314 (M. B. W.) from the National
Eye Institute (Bethesda, MD), the Glaucoma Research Foundation (San
Francisco, CA), and Research to Prevent Blindness (New York, NY). We
thank Byron Li, Shutong Cao, Bing Li, and Yoseph Yaacobi for their
excellent technical assistance in the preparation of this manuscript.
NR 68
TC 83
Z9 87
U1 0
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 12
PY 2008
VL 28
IS 46
BP 12085
EP 12096
DI 10.1523/JNEUROSCI.3200-08.2008
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600040
PM 19005073
ER
PT J
AU Shiels, A
Bennett, TM
Knopf, HLS
Maraini, G
Li, AR
Jiao, XD
Hejtmancik, JF
AF Shiels, Alan
Bennett, Thomas M.
Knopf, Harry L. S.
Maraini, Giovanni
Li, Anren
Jiao, Xiaodong
Hejtmancik, J. Fielding
TI The EPHA2 gene is associated with cataracts linked to chromosome 1p
SO MOLECULAR VISION
LA English
DT Article
ID DOMINANT CONGENITAL CATARACT; AGE-RELATED CATARACT; SIGNIFICANT FAMILIAL
AGGREGATION; SHARED ENVIRONMENTAL-FACTORS; POSTERIOR POLAR CATARACT;
MISSENSE MUTATION; CORTICAL CATARACT; NUCLEAR CATARACT; OLDER
POPULATION; JUVENILE-ONSET
AB Purpose: Cataracts are a clinically and genetically heterogeneous disorder affecting the ocular lens, and the leading cause of treatable vision loss and blindness worldwide. Here we identify a novel gene linked with a rare autosomal dominant form of childhood cataracts segregating in a four generation pedigree, and further show that this gene is likely associated with much more common forms of age-related cataracts in a case-control cohort.
Methods: Genomic DNA was prepared from blood leukocytes, and genotyping was performed by means of single nucleotide polymorphism (SNP) markers, and short tandem repeat (STR) markers. Linkage analyses were performed with the GeneHunter and MLINK programs, and association analyses were performed with the Haploview and Exemplar programs. Mutation detection was achieved by PCR amplification of exons and di-deoxy cycle-sequencing.
Results: Genome-wide linkage analysis with SNP markers, identified a likely disease-haplotype interval on chromosome 1p (rs707455-[similar to 10 Mb]-rs477558). Linkage to chromosome 1p was confirmed using STR markers D1S2672 (LOD score left perpendicularZright perpendicular=3.56, recombination distance left perpendicular theta right perpendicular=0), and D1S2697 (Z=2.92,theta=0). Mutation profiling of positional-candidate genes detected a heterozygous transversion (c.2842G>T) in exon 17 of the gene coding for Eph-receptor type-A2 (EPHA2) that cosegregated with the disease. This missense change was predicted to result in the non-conservative substitution of a tryptophan residue for a phylogenetically conserved glycine residue at codon 948 (p.G948W), within a conserved cytoplasmic domain of the receptor. Candidate gene association analysis further identified SNPs in the EPHA2 region of chromosome 1p that were suggestively associated with age-related cataracts (p=0.007 for cortical cataracts, and p=0.01 for cortical and/or nuclear cataracts).
Conclusions: These data provide the first evidence that EPHA2, which functions in the Eph-ephrin bidirectional signaling pathway of mammalian cells, plays a vital role in maintaining lens transparency.
C1 [Shiels, Alan; Bennett, Thomas M.; Knopf, Harry L. S.] Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, St Louis, MO 63110 USA.
[Shiels, Alan] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA.
[Maraini, Giovanni] Univ Parma, Dept Ophthalmol, I-43100 Parma, Italy.
[Li, Anren; Jiao, Xiaodong; Hejtmancik, J. Fielding] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
RP Shiels, A (reprint author), Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, Campus Box 8096,660 S Euclid Ave, St Louis, MO 63110 USA.
EM shiels@vision.wustl.edu
FU NIH/NEI [EY012284, EY02687]; FIL
FX We thank family and case-control members for participating in this
study, Dr. Olivera Boskovska for help with ascertaining family Mu, Dr.
Donna Mackay for preliminary linkage analysis, Raffaella Aldigeri and
Francesca Grassi for DNA preparation from the Italian case-control
cohort, and the Microarray Core Facility at Washington University Genome
Center, St. Louis, MO for SNP genotyping. This work was supported by
NIH/NEI grants EY012284 (to A. S.) and EY02687, and FIL 2002-2003 grants
(to G. M.).
NR 52
TC 80
Z9 83
U1 0
U2 6
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD NOV 12
PY 2008
VL 14
IS 241
BP 2042
EP 2055
PG 14
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 406WK
UT WOS:000263325400001
PM 19005574
ER
PT J
AU Lu, X
McDonald, SM
Tortorici, MA
Tao, YJ
Carpio, RVD
Nibert, ML
Patton, JT
Harrison, SC
AF Lu, Xiaohui
McDonald, Sarah M.
Tortorici, M. Alejandra
Tao, Yizhi Jane
Carpio, Rodrigo Vasquez-Del
Nibert, Max L.
Patton, John T.
Harrison, Stephen C.
TI Mechanism for Coordinated RNA Packaging and Genome Replication by
Rotavirus Polymerase VP1
SO STRUCTURE
LA English
DT Article
ID HEPATITIS-C VIRUS; MINUS-STRAND SYNTHESIS; CRYSTAL-STRUCTURE;
GUANYLYLTRANSFERASE ACTIVITY; ANGSTROM RESOLUTION; PROTEIN MODELS;
SYSTEM; SEQUENCE; DNA; IDENTIFICATION
AB Rotavirus RNA-dependent RNA polymerase VP1 catalyzes RNA synthesis within a subviral particle. This activity depends on core shell protein VP2. A conserved sequence at the 3' end of plus-strand RNA templates is important for polymerase association and genome replication. We have determined the structure of VP1 at 2.9 angstrom resolution, as apoenzyme and in complex with RNA. The cage-like enzyme is similar to reovirus lambda 3, with four tunnels leading to or from a central, catalytic cavity. A distinguishing characteristic of VP1 is specific recognition, by conserved features of the template-entry channel, of four bases, UGUG, in the conserved 3' sequence. Well-defined interactions with these bases position the RNA so that its 3' end overshoots the initiating register, producing a stable but catalytically inactive complex. We propose that specific 3' end recognition selects rotavirus RNA for packaging and that VP2 activates the autoinhibited VP1/RNA complex to coordinate packaging and genome replication.
C1 [Lu, Xiaohui; Tao, Yizhi Jane; Harrison, Stephen C.] Childrens Hosp, Mol Med Lab, Boston, MA 02115 USA.
[McDonald, Sarah M.; Tortorici, M. Alejandra; Carpio, Rodrigo Vasquez-Del; Patton, John T.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Nibert, Max L.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Harrison, Stephen C.] Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA.
RP Harrison, SC (reprint author), Childrens Hosp, Mol Med Lab, 300 Longwood Ave, Boston, MA 02115 USA.
EM harrison@crystal.harvard.edu
RI Patton, John/P-1390-2014
FU NIH [CA13202, AI47904]; National Institutes of Allergy and Infectious
Diseases
FX We thank Teresa Broering, Sophia Rits-Volloch, Rachelle Gaudet, Kelly
Arnett, Hongyan Yang, Harsh Ramanathan, and Tamara Bar-Magen for
technical assistance, and Philip Dormitzer, Ethan Settembre, and Piotr
Sliz for advice. We also express our appreciation to the staff at ALS
(beamlines 7.2.1 and 7.2.2) and APS (beamlines ID-19 and ID-24) for help
in data collection. This work was supported by NIH grants CA13202 (to
S.C.H.) and AI47904 (to M.L.N.), and by the Intramural Research Program
of the NIH, National Institutes of Allergy and Infectious Diseases
(J.T.P., S.M.M., M.A.T., and R.V.-D.C.). S.C.H. is an Investigator in
the Howard Hughes Medical Institute.
NR 41
TC 66
Z9 70
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD NOV 12
PY 2008
VL 16
IS 11
BP 1678
EP 1688
DI 10.1016/j.str.2008.09.006
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 374GQ
UT WOS:000261032200011
PM 19000820
ER
PT J
AU Madani, N
Schon, A
Princiotto, AM
LaLonde, JM
Courter, JR
Soeta, T
Ng, D
Wang, LP
Brower, ET
Xiang, SH
Do Kwon, Y
Huang, CC
Wyatt, R
Kwong, PD
Freire, E
Smith, AB
Sodroski, J
AF Madani, Navid
Schoen, Arne
Princiotto, Amy M.
LaLonde, Judith M.
Courter, Joel R.
Soeta, Takahiro
Ng, Danny
Wang, Liping
Brower, Evan T.
Xiang, Shi-Hua
Do Kwon, Young
Huang, Chih-Chin
Wyatt, Richard
Kwong, Peter D.
Freire, Ernesto
Smith, Amos B., III
Sodroski, Joseph
TI Small-Molecule CD4 Mimics Interact with a Highly Conserved Pocket on
HIV-1 gp120
SO STRUCTURE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ENVELOPE GLYCOPROTEIN; RECEPTOR-BINDING;
MONOCLONAL-ANTIBODY; ACCURATE DOCKING; SITE; NEUTRALIZATION; DESIGN;
CCR5; MINIPROTEIN
AB Human immunodeficiency virus (HIV-1) interaction with the primary receptor, CD4, induces conformational changes in the viral envelope glycoproteins that allow binding to the CCR5 second receptor and virus entry into the host cell. The small molecule NBD-556 mimics CD4 by binding the gp120 exterior envelope glycoprotein, moderately inhibiting virus entry into CD4-expressing target cells and enhancing CCR5 binding and virus entry into CCR5-expressing cells lacking CD4. Studies of NBD-556 analogs and gp120 mutants suggest that (1) NBD-556 binds within the Phe 43 cavity, a highly conserved, functionally important pocket formed as gp120 assumes the CD4-bound conformation; (2) the NBD-556 phenyl ring projects into the Phe 43 cavity; (3) enhancement of CD4-independent infection by NBD-556 requires the induction of conformational changes in gp120; and (4) increased affinity of NBD-556 analogs for gp120 improves antiviral potency during infection of CD4-expressing cells.
C1 [Madani, Navid; Princiotto, Amy M.; Wang, Liping; Xiang, Shi-Hua; Sodroski, Joseph] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Madani, Navid; Sodroski, Joseph] Harvard Univ, Sch Med, Dept Pathol, Div AIDS, Boston, MA 02115 USA.
[Schoen, Arne; Brower, Evan T.; Freire, Ernesto] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
[LaLonde, Judith M.] Bryn Mawr Coll, Dept Chem, Bryn Mawr, PA 19010 USA.
[Courter, Joel R.; Soeta, Takahiro; Ng, Danny; Smith, Amos B., III] Univ Penn, Dept Chem, Philadelphia, PA 19104 USA.
[Do Kwon, Young; Huang, Chih-Chin; Wyatt, Richard; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Sodroski, Joseph] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Sodroski, J (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu
RI Kwon, Young Do/A-6957-2010; SOETA, Takahiro/E-7060-2015
OI SOETA, Takahiro/0000-0001-9883-4772
FU National Institutes of Health [GM56550, AI24755I60354]; International
AIDS Vaccine Initiative; William F. McCarty-Cooper
FX We thank Wayne Hendrickson and Irwin Chaiken for valuable discussion. We
thank Yvette McLaughlin and Elizabeth Carpelan for manuscript
preparation, and Jonathan Stuckey for preparation of figures. This study
was supported by the National Institutes of Health (Grants GM56550,
AI24755, and AI60354), the International AIDS Vaccine Initiative, and
William F. McCarty-Cooper.
NR 39
TC 100
Z9 102
U1 0
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD NOV 12
PY 2008
VL 16
IS 11
BP 1689
EP 1701
DI 10.1016/j.str.2008.09.005
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 374GQ
UT WOS:000261032200012
PM 19000821
ER
PT J
AU Liang, W
Hoang, Q
Clark, RB
Fishman, PH
AF Liang, Wei
Hoang, Quang
Clark, Richard B.
Fishman, Peter H.
TI Accelerated Dephosphorylation of the beta(2)-Adrenergic Receptor by
Mutation of the C-Terminal Lysines: Effects on Ubiquitination,
Intracellular Trafficking, and Degradation
SO BIOCHEMISTRY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; HUMAN BETA(1)-ADRENERGIC RECEPTOR;
AGONIST-PROMOTED UBIQUITINATION; MEDIATED DOWN-REGULATION;
BETA-ARRESTIN; INTERNALIZATION; RESENSITIZATION; DESENSITIZATION;
ENDOCYTOSIS; SEQUESTRATION
AB Agonist-mediated ubiquitination regulates some G protein-coupled receptors by targeting them to lysosomes for degradation. Phosphorylation also regulates receptor endocytosis and trafficking to lysosomes. To explore the roles of the two post-translational modifications, we mutated the three C-terminal lysines to arginines in the human beta(2)-adrenergic receptor (beta(2)AR) (K348/372/375R). The level of agonist-mediated ubiquitination of the mutant (3K/R) was greatly reduced compared to that of wild-type (WT) beta(2)AR in whole cells and in cell-free assays. Downregulation of 3K/R also was attenuated compared to that of the WT, whereas internalization and recycling were more similar. During endocytosis, WT and 3K/R appeared in different vesicles and WT, but not 3K/R, was transported to lysosomes. Both were rapidly phosphorylated in agonist-stimulated cells, but upon agonist removal, the rate of dephosphorylation of 3K/R initially was similar to 5 times faster than that of WT. The increased rate also was observed in a cell-free, soluble assay and, thus, was not due to differences in receptor trafficking. Okadaic acid, a potent phosphatase inhibitor, reduced the level of dephosphorylation and increased the levels of lysosomal targeting and degradation of 3K/R. The reduced level of ubiquitination and rapid dephosphorylation of 3K/R appear to prevent it from being sorted to lysosomes in contrast to the phosphorylated and ubiquitinated WT beta(2)AR. Our findings indicate that both phosphorylation and ubiquitination are involved in the intracellular sorting Of beta(2)AR between pathways of recycling to the plasma membrane and degradation in lysosomes, and that the rate of dephosphorylation may be another mechanism of regulating the sorting.
C1 [Liang, Wei; Hoang, Quang; Fishman, Peter H.] NINDS, NIH, Mol & Cellular Neurobiol Lab, Membrane Biochem Sect, Bethesda, MD 20892 USA.
[Clark, Richard B.] Univ Texas Hlth Sci Ctr Houston, Sch Med, Dept Integrat Biol & Pharmacol, Houston, TX 77030 USA.
RP Fishman, PH (reprint author), NINDS, NIH, Mol & Cellular Neurobiol Lab, Membrane Biochem Sect, Bethesda, MD 20892 USA.
EM fishmanp@mail.nih.gov
FU National Institute of Neurological Disorders and Stroke; National
Institutes of Health; National Institutes of Health [GM031208]
FX Supported in part by the Intramural Research Program of the National
Institute of Neurological Disorders and Stroke, National Institutes of
Health (W.L., Q.H., and P.H.F.), and National Institutes of Health Grant
GM031208 (R.B.C.).
NR 46
TC 10
Z9 10
U1 0
U2 0
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 11
PY 2008
VL 47
IS 45
BP 11750
EP 11762
DI 10.1021/bi800219q
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 368JH
UT WOS:000260616900007
PM 18841999
ER
PT J
AU Korde, LA
Premkumar, A
Mueller, C
Rosenberg, P
Soho, C
Bratslavsky, G
Greene, MH
AF Korde, L. A.
Premkumar, A.
Mueller, C.
Rosenberg, P.
Soho, C.
Bratslavsky, G.
Greene, M. H.
TI Increased prevalence of testicular microlithiasis in men with familial
testicular cancer and their relatives
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE testicular microlithiasis; germ cell tumour; familial predisposition;
genetic susceptibility; ultrasound; testicular cancer
ID GERM-CELL TUMOR; ASYMPTOMATIC POPULATION; RISK; SUSCEPTIBILITY;
ASSOCIATION; EXPERIENCE; TESTIS
AB Testicular germ cell tumours (TGCT) cluster in families, but responsible genes remain unidentified. The association between testicular microlithiasis (TM) and testicular carcinoma in situ (CIS) suggests that TM may be a TC risk factor. We report testicular ultrasound findings in men with familial TGCT (FTGCT) and their unaffected relatives. A total of 81 men (48 affected and 33 unaffected) from 31 families with >= 2 TC cases underwent testicular ultrasound. Testicular microlithiasis was defined as either 'classic' (>= 5 microliths) or 'limited' (< 5 microliths). Statistical analyses used Fisher's exact test and permutation testing. Testicular microlithiasis was more frequent in the contralateral testicles of men with a history of TGCT (affected men) than in unaffected men (48 vs 24%, P = 0.04). The association appeared stronger for classic TM (21 vs 9%) than for limited TM (27 vs 15%). Testicular microlithiases were bilateral in six out of seven (87%) unaffected men. Among affected men, TM was not associated with histology, age at diagnosis or cancer treatment. Of the 31 families, 10 accounted for a majority (61%) of the TM cases identified (P = 0.11). Testicular microlithiasis was more prevalent among FTGCT family members than described previously in the general population, and was more common among FTGCT cases vs unaffected blood relatives. Testicular microlithiasis appeared to cluster in certain families. These findings suggest both a familial predisposition to TM and an association between TM and FTGCT. If proven, this could be clinically important to men in FTGCT families, and may be useful in identifying specific genes involved in FTGCT.
C1 [Korde, L. A.; Mueller, C.; Greene, M. H.] NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD 20852 USA.
[Premkumar, A.] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
[Rosenberg, P.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Soho, C.] Westat Corp, Rockville, MD USA.
[Bratslavsky, G.] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Korde, LA (reprint author), NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, 6120 Execut Blvd,Rm 7030, Rockville, MD 20852 USA.
EM kordel@mail.nih.gov
FU Intramural NIH HHS [Z01 CP010144-09, Z01 SC006659-25]; NCI NIH HHS
[N02-CP-11019-50, N02-CP-65504-50, N02CP11019, N02CP65504]
NR 29
TC 24
Z9 25
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 11
PY 2008
VL 99
IS 10
BP 1748
EP 1753
DI 10.1038/sj.bjc.6604704
PG 6
WC Oncology
SC Oncology
GA 371LI
UT WOS:000260832400027
PM 18841155
ER
PT J
AU Velagaleti, RS
Pencina, MJ
Murabito, JM
Wang, TJ
Parikh, NI
D'Agostino, RB
Levy, D
Kannel, WB
Vasan, RS
AF Velagaleti, Raghava S.
Pencina, Michael J.
Murabito, Joanne M.
Wang, Thomas J.
Parikh, Nisha I.
D'Agostino, Ralph B.
Levy, Daniel
Kannel, William B.
Vasan, Ramachandran S.
TI Long-Term Trends in the Incidence of Heart Failure After Myocardial
Infarction
SO CIRCULATION
LA English
DT Article
DE heart failure; myocardial infarction; prognosis; risk factors;
epidemiology
ID LEFT-VENTRICULAR DYSFUNCTION; TEMPORAL TRENDS; FRAMINGHAM; DISEASE;
EPIDEMIOLOGY; PERSPECTIVE; MORTALITY; SURVIVAL; RATES; DEATH
AB Background - Although mortality after myocardial infarction (MI) has declined in the United States in recent decades, there have been few community-based investigations of the long-term trends in the incidence of heart failure after MI, and their results appear to be conflicting.
Methods and Results - We evaluated 676 Framingham Heart Study participants between 45 and 85 years of age (mean age 67 years, 34% women) who developed a first MI between 1970 and 1999. We assessed the incidence rates of heart failure and of death without heart failure in each of 3 decades (1970 to 1979, 1980 to 1989, and 1990 to 1999). We estimated the multivariable-adjusted risk of events in the latter 2 decades, with the period 1970 to 1979 serving as the referent. The 30-day incidence of heart failure after MI rose from 10% in 1970 to 1979 to 23.1% in 1990 to 1999 (P for trend 0.003), whereas 30-day mortality after MI declined from 12.2% (1970 to 1979) to 4.1% (1990 to 1999). The 5-year incidence of heart failure after MI rose from 27.6% in 1970 to 1979 to 31.9% in 1990 to 1999 (P for trend 0.02), whereas 5-year mortality after MI declined from 41.1% (1970 to 1979) to 17.3% (1990 to 1999). In multivariable analyses, compared with the period 1970 to 1979, we observed higher 30-day (risk ratio 2.05, 95% confidence interval 1.25 to 3.36) and 5-year (risk ratio 1.74, 95% confidence interval 1.07 to 2.84) risks of heart failure in the decade 1990 to 1999. These trends were accompanied by lower 30-day (risk ratio 0.21, 95% confidence interval 0.09 to 0.47) and 5-year (risk ratio 0.31, 95% confidence interval 0.18 to 0.54) mortality rates in 1990 to 1999.
Conclusions - In the present community-based sample, we observed an increase in the incidence of heart failure in recent decades that paralleled the decrease in mortality after MI. (Circulation. 2008; 118: 2057-2062.)
C1 [Velagaleti, Raghava S.; Pencina, Michael J.; Murabito, Joanne M.; Wang, Thomas J.; Parikh, Nisha I.; D'Agostino, Ralph B.; Levy, Daniel; Kannel, William B.; Vasan, Ramachandran S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
[Wang, Thomas J.] Harvard Univ, Sch Med, Dept Med, Massachusetts Gen Hosp,Div Cardiol, Boston, MA USA.
[Pencina, Michael J.; D'Agostino, Ralph B.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Levy, Daniel; Vasan, Ramachandran S.] Boston Univ, Sch Med, Prevent Med Sect, Boston Med Ctr, Boston, MA 02118 USA.
[Levy, Daniel; Vasan, Ramachandran S.] Boston Univ, Sch Med, Cardiol Sect, Boston Med Ctr, Boston, MA 02118 USA.
[Murabito, Joanne M.] Boston Univ, Sch Med, Gen Internal Med Sect, Boston Med Ctr, Boston, MA 02118 USA.
RP Vasan, RS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave, Framingham, MA 01702 USA.
EM vasan@bu.edu
OI Murabito, Joanne/0000-0002-0192-7516; Ramachandran,
Vasan/0000-0001-7357-5970
FU National Institutes of Health/National Heart, Lung, and Blood Institute
[N01-HC-25195, 2K24HL4334]
FX This work was supported by National Institutes of Health/National Heart,
Lung, and Blood Institute contract No. N01-HC-25195 and 2K24HL4334 (Dr
Vasan).
NR 23
TC 187
Z9 196
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 11
PY 2008
VL 118
IS 20
BP 2057
EP 2062
DI 10.1161/CIRCULATIONAHA.108.784215
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 370XG
UT WOS:000260795800007
PM 18955667
ER
PT J
AU Chakraborty, P
Wang, YM
Wei, JH
van Deursen, J
Yu, HT
Malureanu, L
Dasso, M
Forbes, DJ
Levy, DE
Seemann, J
Fontoura, BMA
AF Chakraborty, Papia
Wang, Yaming
Wei, Jen-Hsuan
van Deursen, Jan
Yu, Hongtao
Malureanu, Liviu
Dasso, Mary
Forbes, Douglass J.
Levy, David E.
Seemann, Joachim
Fontoura, Beatriz M. A.
TI Nucleoporin Levels Regulate Cell Cycle Progression and Phase-Specific
Gene Expression
SO DEVELOPMENTAL CELL
LA English
DT Article
ID NUCLEAR-PORE COMPLEX; MESSENGER-RNA EXPORT; NUP107-160 COMPLEX;
BIOGENESIS PATHWAY; SUBCOMPLEX; NUP145P; NUP96; D3; KINETOCHORES;
CONTRIBUTES
AB The Nup107-160 complex, the largest subunit of the nuclear pore, is multifunctional. It mediates mRNA export in interphase, and has roles in kinetochore function, spindle assembly, and postmitotic nuclear pore assembly. We report here that the levels of constituents of the Nup107-160 complex are coordinately cell cycle-regulated. At mitosis, however a member of the complex, Nup96, is preferentially downregulated. This occurs via the ubiquitin-proteasome pathway. When the levels of Nup96 are kept high, a significant delay in G1/S progression occurs. Conversely, in cells of Nup96(+/-) mice, which express low levels of Nup96, cell cycle progression is accelerated. These lowered levels of Nup96 yield specific defects in nuclear export of certain mRNAs and protein expression, among which are key cell cycle regulators. Thus, Nup96 levels regulate differential gene expression in a phase-specific manner, setting the stage for proper cell cycle progression.
C1 [Chakraborty, Papia; Wei, Jen-Hsuan; Seemann, Joachim; Fontoura, Beatriz M. A.] Univ Texas SW Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
[Wang, Yaming; Levy, David E.] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA.
[van Deursen, Jan; Malureanu, Liviu] Mayo Clin, Dept Pediat & Adolescent Med, Rochester, MN 55905 USA.
[Yu, Hongtao] Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
[Dasso, Mary] NICHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
[Forbes, Douglass J.] Univ Calif San Diego, Sect Cell & Dev Biol, La Jolla, CA 92093 USA.
RP Fontoura, BMA (reprint author), Univ Texas SW Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
EM beatriz.fontoura@utsouthwestern.edu
OI Dasso, Mary/0000-0002-5410-1371; Levy, David/0000-0002-7320-7788
FU NIH [R01A128900, U54AI5715801, R01 GM07159-01]
FX We thank A. Levay, D.R. Nussenzveig, and K. Jeganathan for assistance.
We thank R. Basavappa, Z. Nawaz, and M. Matunis for reagents. This work
was supported by NIH R01A128900 and U54AI5715801 to D.E.L., and R01
GM07159-01 to B.M.A.F.
NR 52
TC 52
Z9 53
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
J9 DEV CELL
JI Dev. Cell
PD NOV 11
PY 2008
VL 15
IS 5
BP 657
EP 667
DI 10.1016/j.devcel.2008.08.020
PG 11
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 371XW
UT WOS:000260867000007
PM 19000832
ER
PT J
AU Lin, L
Zhang, JH
Panicker, LM
Simonds, WF
AF Lin, Ling
Zhang, Jian-Hua
Panicker, Leelamma M.
Simonds, William F.
TI The parafibromin tumor suppressor protein inhibits cell proliferation by
repression of the c-myc proto-oncogene
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE HRPT2; hyperparathyroidism; parathyroid cancer; PAF1 complex
ID FAMILIAL ISOLATED HYPERPARATHYROIDISM; SPORADIC PARATHYROID TUMORS;
RNA-POLYMERASE-II; HEREDITARY HYPERPARATHYROIDISM; GENETIC ANALYSES;
HRPT2 MUTATION; HUMAN PAF1; GERMLINE; TRANSCRIPTION; EXPRESSION
AB Parafibromin is a tumor suppressor protein encoded by HRPT2, a gene recently implicated in the hereditary hyperparathyroidism-jaw tumor syndrome, parathyroid cancer, and a subset of kindreds with familial isolated hyperparathyroidism. Human parafibromin binds to RNA polymerase II as part of a PAF1 transcriptional regulatory complex. The physiologic targets of parafibromin and the mechanism by which its loss of function can lead to neoplastic transformation are poorly understood. We show here that RNA interference with the expression of parafibromin or Paf1 stimulates cell proliferation and increases levels of the c-myc protooncogene product, a DNA-binding protein and established regulator of cell growth. This effect results from both c-myc protein stabilization and activation of the c-myc promoter, without alleviation of the c-myc transcriptional pause. Chromatin immunoprecipitation demonstrates the occupancy of the c-myc promoter by parafibromin and other PAF1 complex subunits in native cells. Knockdown of c-myc blocks the proliferative effect of RNA interference with parafibromin or Paf1 expression. These experiments provide a previously uncharacterized mechanism for the anti-proliferative action of the parafibromin tumor suppressor protein resulting from PAF1 complex-mediated inhibition of the c-myc proto-oncogene.
C1 [Lin, Ling; Zhang, Jian-Hua; Panicker, Leelamma M.; Simonds, William F.] NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Simonds, WF (reprint author), NIDDK, Metab Dis Branch, NIH, Bldg 10 Room 8C-101, Bethesda, MD 20892 USA.
EM wfs@helix.nih.gov
FU NIH; NIDDK
FX We are grateful to Sunita Agarwal and Stephen Marx for encouragement and
helpful discussion. This research was supported by the Intramural
Research Program of the NIH, NIDDK to W.F.S.
NR 30
TC 48
Z9 51
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 11
PY 2008
VL 105
IS 45
BP 17420
EP 17425
DI 10.1073/pnas.0710725105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 373OP
UT WOS:000260981800047
PM 18987311
ER
PT J
AU Derrick, SC
Perera, LP
Dheenadhayalan, V
Yang, A
Kolibab, K
Morris, SL
AF Derrick, Steven C.
Perera, L. P.
Dheenadhayalan, Veerabadran
Yang, Amy
Kolibab, Kristopher
Morris, Sheldon L.
TI The safety of post-exposure vaccination of mice infected with
Mycobacterium tuberculosis
SO VACCINE
LA English
DT Article
DE Tuberculosis; Vaccine; Safety
ID DNA VACCINATION; PROTECTIVE IMMUNITY; FUSION PROTEIN; MOUSE MODEL;
GUINEA-PIGS; VACCINES; BCG; EFFICACY; DISEASE
AB New post-exposure tuberculosis vaccination strategies are being developed to prevent disease in individuals latently infected with Mycobacterium tuberculosis. However, concerns about the potential induction of deleterious Koch-like reactions after immunization of persons with latent tuberculosis has limited progress in assessing the effectiveness of post-exposure vaccination. To evaluate the safety of immunization after M. tuberculosis infection, two mouse models were established, a drug treatment low bacterial burden model and an active disease model. Twelve different M. tuberculosis antigen preparations and vaccines (including DNA, subunit, viral vectored, and live, attenuated vaccines) were evaluated using these mouse models. In the low bacterial burden model, post-exposure vaccination did not induce significant reactivational disease and only injection of BCG evoked increases in]Ling inflammatory responses at I month after the immunizations. Additionally, although significant increases in lung inflammation were seen for animals injected with the hps65 DNA vaccine or a M. tuberculosis culture supernatant preparation, no differences in the survival periods were detected between vaccinated and non-vaccinated mice at 10 months post-immunization using the low bacterial burden model. For the active disease model, significantly more lung inflammation was observed at I month after administration of the hsp65 DNA vaccine but none of the antigen preparations tested increased the lung bacterial burdens at this early time point. Furthermore, vaccination of diseased mice with BCG or TB DNA vaccines did not significantly affect mortality rates compared to non-vaccinated controls at 10 months post-immunization. Overall, these data suggest that while the potential risk of inducing Koch-like reactions is low after immunization of persons with latent tuberculosis, extreme caution is still needed as post-exposure vaccines progress from pre-clinical experiments into the initial phases of clinical testing. Published by Elsevier Ltd.
C1 [Derrick, Steven C.; Yang, Amy; Kolibab, Kristopher; Morris, Sheldon L.] US FDA, Ctr Biol Evaluat & Res, Lab Mycobacterial Dis & Cellular Immunol, Bethesda, MD 20892 USA.
[Perera, L. P.] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Dheenadhayalan, Veerabadran] Aeras Global TB Vaccine Fdn, Rockville, MD 20850 USA.
RP Derrick, SC (reprint author), Bldg 29,Room 509,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM steven.derrick@fda.hhs.gov
NR 29
TC 14
Z9 17
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 11
PY 2008
VL 26
IS 48
BP 6092
EP 6098
DI 10.1016/j.vaccine.2008.09.011
PG 7
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 381LS
UT WOS:000261538200009
PM 18809446
ER
PT J
AU Rossouw, JE
Cushman, M
Greenland, P
Lloyd-Jones, DM
Bray, P
Kooperberg, C
Pettinger, M
Robinson, J
Hendrix, S
Hsia, J
AF Rossouw, Jacques E.
Cushman, Mary
Greenland, Philip
Lloyd-Jones, Donald M.
Bray, Paul
Kooperberg, Charles
Pettinger, Mary
Robinson, Jennifer
Hendrix, Susan
Hsia, Judith
TI Inflammatory, Lipid, Thrombotic, and Genetic Markers of Coronary Heart
Disease Risk in the Women's Health Initiative Trials of Hormone Therapy
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID ESTROGEN PLUS PROGESTIN; RANDOMIZED CONTROLLED-TRIAL;
CARDIOVASCULAR-DISEASE; POSTMENOPAUSAL WOMEN; FIBRINOGEN
AB Background: Clinical trials of postmenopausal hormone therapy (HT) have shown increased risk of coronary heart disease (CHD) in the first few years after initiation of therapy and no overall benefit.
Methods: This nested case-control study evaluates a range of inflammatory, lipid, thrombotic, and genetic markers for their association with CHD in the 4 years after randomization and assesses whether any of these markers modified or mediated the initially increased risk associated with HT in postmenopausal women aged 50 to 79 years at baseline. Conjugated equine estrogens, 0.625 mg/d, or placebo was given to 10 739 hysterectomized women, and the same estrogen plus medroxyprogesterone acetate, 2.5 mg/d, was given to 16 608 women with an intact uterus.
Results: In multivariate-adjusted analyses of 359 cases and 820 controls in the combined trials, baseline levels of 12 of the 23 biomarkers studied were associated with CHD events: interleukin 6, matrix metalloproteinase 9, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, triglycerides, D-dimer, factor VIII, von Willebrand factor, leukocyte count, homocysteine, and fasting insulin. Biomarkers tended to be more strongly associated with CHD in the initial 2 years after randomization. The genetic polymorphism glycoprotein IIIa leu33pro was significantly associated with CHD. Baseline low-density lipoprotein cholesterol interacted significantly with HT so that women with higher levels were at higher risk for CHD when given HT (P = .03 for interaction). The levels of several biomarkers were changed by HT, but these changes did not seem to be associated with future CHD events.
Conclusions: Several thrombotic, inflammatory, and lipid biomarkers were associated with CHD events in postmenopausal women, but only low-density lipoprotein cholesterol modified the effect of HT. Further research is needed to identify the mechanisms by which HT increases the risk of CHD.
Trial Registration: clinicaltrials. gov Identifier: NCT00000611
C1 [Rossouw, Jacques E.] NHLBI, Womens Hlth Initiat Branch, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Cushman, Mary] Univ Vermont, Dept Med, Burlington, VT 05405 USA.
[Cushman, Mary] Univ Vermont, Dept Pathol, Burlington, VT 05405 USA.
[Greenland, Philip; Lloyd-Jones, Donald M.] Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
[Bray, Paul] Thomas Jefferson Univ, Jefferson Med Coll, Dept Med, Philadelphia, PA 19107 USA.
[Kooperberg, Charles; Pettinger, Mary] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Robinson, Jennifer] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Hendrix, Susan] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Hsia, Judith] George Washington Univ, Dept Med, Washington, DC USA.
RP Rossouw, JE (reprint author), NHLBI, Womens Hlth Initiat Branch, Div Prevent & Populat Sci, 6701 Rockledge Dr,Rockledge 2 Bldg,Ste 10018, Bethesda, MD 20892 USA.
EM rossouwj@nih.gov
RI Lloyd-Jones, Donald/C-5899-2009
FU National Heart, Lung, and Blood Institute, National Institutes of Health
[N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115,
32118-32119, 32122, 42107-26, 4212932, 44221]
FX The WHI program is funded by contracts N01WH22110, 24152, 32100-2,
32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26,
4212932, and 44221 from the National Heart, Lung, and Blood Institute,
National Institutes of Health.
NR 17
TC 54
Z9 54
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD NOV 10
PY 2008
VL 168
IS 20
BP 2245
EP 2253
DI 10.1001/archinte.168.20.2245
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 370XS
UT WOS:000260797000010
PM 19001202
ER
PT J
AU Grady, C
Seidenfeld, J
Horstmann, E
Emanuel, EJ
AF Grady, Christine
Seidenfeld, Justine
Horstmann, Elizabeth
Emanuel, Ezekiel J.
TI Participants in Phase 1 Oncology Research Trials Are Vulnerable In reply
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Grady, Christine] NIH, Dept Clin Bioeth, Bethesda, MD 20892 USA.
RP Grady, C (reprint author), NIH, Dept Clin Bioeth, 10 Ctr Dr,Room 1C118, Bethesda, MD 20892 USA.
EM cgrady@cc.nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD NOV 10
PY 2008
VL 168
IS 20
BP 2288
EP 2288
DI 10.1001/archinte.168.20.2288
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 370XS
UT WOS:000260797000022
ER
PT J
AU Dudley, ME
Yang, JC
Sherry, R
Hughes, MS
Royal, R
Kammula, U
Robbins, PF
Huang, J
Citrin, DE
Leitman, SF
Wunderlich, J
Restifo, NP
Thomasian, A
Downey, SG
Smith, FO
Klapper, J
Morton, K
Laurencot, C
White, DE
Rosenberg, SA
AF Dudley, Mark E.
Yang, James C.
Sherry, Richard
Hughes, Marybeth S.
Royal, Richard
Kammula, Udai
Robbins, Paul F.
Huang, JianPing
Citrin, Deborah E.
Leitman, Susan F.
Wunderlich, John
Restifo, Nicholas P.
Thomasian, Armen
Downey, Stephanie G.
Smith, Franz O.
Klapper, Jacob
Morton, Kathleen
Laurencot, Carolyn
White, Donald E.
Rosenberg, Steven A.
TI Adoptive Cell Therapy for Patients With Metastatic Melanoma: Evaluation
of Intensive Myeloablative Chemoradiation Preparative Regimens
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID CD8(+) T-CELLS; TUMOR-INFILTRATING LYMPHOCYTES; IMMUNOTHERAPY;
LYMPHODEPLETION; REGRESSION; EXPANSION; AUGMENTS; ANTIGEN
AB Purpose
The two approved treatments for patients with metastatic melanoma, interleukin (IL)-2 and dacarbazine, mediate objective response rates of 12% to 15%. We previously reported that adoptive cell therapy (ACT) with autologous antitumor lymphocytes in lymphodepleted hosts mediated objective responses in 51% of 35 patients. Here, we update that study and evaluate the safety and efficacy of two increased-intensity myeloablative lymphodepleting regimens.
Patients and Methods
We performed two additional sequential trials of ACT with autologous tumor-infiltrating lymphocytes (TIL) in patients with metastatic melanoma. Increasing intensity of host preparative lymphodepletion consisting of cyclophosphamide and fludarabine with either 2 (25 patients) or 12 Gy (25 patients) of total-body irradiation (TBI) was administered before cell transfer. Objective response rates by Response Evaluation Criteria in Solid Tumors (RECIST) and survival were evaluated. Immunologic correlates of effective treatment were studied.
Results
Although nonmyeloablative chemotherapy alone showed an objective response rate of 49%, when 2 or 12 Gy of TBI was added, the response rates were 52% and 72% respectively. Responses were seen in all visceral sites including brain. There was one treatment-related death in the 93 patients. Host lymphodepletion was associated with increased serum levels of the lymphocyte homeostatic cytokines IL-7 and IL-15. Objective responses were correlated with the telomere length of the transferred cells.
Conclusion
Host lymphodepletion followed by autologous TIL transfer and IL-2 results in objective response rates of 50% to 70% in patients with metastatic melanoma refractory to standard therapies.
C1 [Dudley, Mark E.] NCI, Surg Branch, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Dudley, ME (reprint author), NCI, Surg Branch, Radiat Oncol Branch, NIH, CRC 3W-5752,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Mark_Dudley@nih.gov
RI Restifo, Nicholas/A-5713-2008;
OI Restifo, Nicholas P./0000-0003-4229-4580
FU Intramural NIH HHS [Z01 SC003811-33]
NR 18
TC 698
Z9 713
U1 1
U2 23
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2008
VL 26
IS 32
BP 5233
EP 5239
DI 10.1200/JCO.2008.16.5449
PG 7
WC Oncology
SC Oncology
GA 369MK
UT WOS:000260698400016
PM 18809613
ER
PT J
AU Varga, T
Palkovits, M
Usdin, TB
Dobolyi, A
AF Varga, Tamas
Palkovits, Miklos
Usdin, Ted Bjoern
Dobolyi, Arpad
TI The Medial Paralemniscal Nucleus and Its Afferent Neuronal Connections
in Rat
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE tuberoinfundibular peptide of 39 residues; cytoarchitectonic
description; brainstem auditory nuclei; neuronal projection; retrograde
and anterograde tracer; cholera toxin beta subunit
ID ECHOLOCATING HORSESHOE BATS; CENTRAL-NERVOUS-SYSTEM; BRAIN-STEM NUCLEI;
TUBEROINFUNDIBULAR PEPTIDE; INFERIOR COLLICULUS; 39 RESIDUES;
TOPOGRAPHIC ORGANIZATION; SUPERIOR COLLICULUS; RETICULAR-FORMATION;
AUDITORY-CORTEX
AB Previously, we described a cell group expressing tuberoinfundibular peptide of 39 residues (TIP39) in the lateral pontomesencephalic tegmenturn, and referred to it as the medial paralemniscal nucleus (MPL). To identify this nucleus further in rat, we have now characterized the MPL cytoarchitectonically on coronal, sagittal, and horizontal serial sections. Neurons in the MPL have a columnar arrangement distinct from adjacent areas. The MPL is bordered by the intermediate nucleus of the lateral lemniscus nucleus laterally, the oral pontine reticular formation medially, and the rubrospinal tract ventrally, whereas the A7 noradrenergic cell group is located immediately mediocaudal to the MPL. TIP39-immunoreactive neurons are distributed throughout the cytoarchitectonically defined MPL and constitute 75% of its neurons as assessed by double labeling of TIP39 with a fluorescent Nissl dye or NeuN. Furthermore, we investigated the neuronal inputs to the MPL by using the retrograde tracer cholera toxin B subunit. The MPL has afferent neuronal connections distinct from adjacent brain regions including major inputs from the auditory cortex, medial part of the medial geniculate body, superior colliculus, external and dorsal cortices of the inferior colliculus, periolivary area, lateral preoptic area, hypothalamic ventromedial nucleus, lateral and dorsal hypothalamic areas, subparafascicular and posterior intralaminar thalamic nuclei, periaqueductal gray, and cuneiform nucleus. In addition, injection of the anterograde tracer biotinylated dextran amine into the auditory cortex and the hypothalamic ventromedial nucleus confirmed projections from these areas to the distinct MPL. The afferent neuronal connections of the MPL suggest its involvement in auditory and reproductive functions. J. Comp. Neurol. 511:221-237, 2008. (C) 2008 Wiley-Liss, Inc.
C1 [Varga, Tamas; Palkovits, Miklos; Dobolyi, Arpad] Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol & Neuroendocrine Res Lab, H-1094 Budapest, Hungary.
[Varga, Tamas; Palkovits, Miklos; Dobolyi, Arpad] Hungarian Acad Sci, H-1094 Budapest, Hungary.
[Usdin, Ted Bjoern] NIMH, Sect Fundamental Neurosci, Bethesda, MD 20892 USA.
RP Dobolyi, A (reprint author), Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol Lab, Tuzolto 58, H-1094 Budapest, Hungary.
EM dobolyi@ana.sote.hu
RI Palkovits, Miklos/F-2707-2013;
OI Palkovits, Miklos/0000-0003-0578-0387
FU Hungarian Science Foundation [NKTH-OTKA K67646, OTKA TS49861]; National
Institute of Mental Health Intramural Research Program; Bolyai Janos
Scholarship
FX Grant sponsor: the Hungarian Science Foundation; Grant numbers:
NKTH-OTKA K67646 (to A.D.) and OTKA TS49861 (to M.P.); Grant sponsor:
the National Institute of Mental Health Intramural Research Program (to
T.B.U.); Grant sponsor: the Bolyai Janos Scholarship (to A.D.).
NR 82
TC 15
Z9 15
U1 0
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD NOV 10
PY 2008
VL 511
IS 2
BP 221
EP 237
DI 10.1002/cne.21829
PG 17
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA 362JA
UT WOS:000260192800004
PM 18770870
ER
PT J
AU Christie, LA
Saunders, RC
Kowalska, DM
MacKay, WA
Head, E
Cotman, CW
AF Christie, Lori-Ann
Saunders, Richard C.
Kowalska, Danuta M.
MacKay, William A.
Head, Elizabeth
Cotman, Carl W.
TI Rhinal and Dorsolateral Prefrontal Cortex Lesions Produce Selective
Impairments in Object and Spatial Learning and Memory in Canines
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE object recognition; spatial; medial temporal lobe; entorhinal cortex;
perirhinal cortex; dorsolateral prefrontal cortex; frontal lobe; canine;
delayed nonmatching to sample; delayed nonmatching to position
ID POSITRON-EMISSION-TOMOGRAPHY; FRONTAL ASSOCIATION CORTEX; BETA-AMYLOID
ACCUMULATION; VISUAL WORKING-MEMORY; AGED BEAGLE DOGS; RECOGNITION
MEMORY; ENTORHINAL CORTEX; RHESUS-MONKEYS; TEMPORAL-LOBE; PERIRHINAL
CORTEX
AB To examine the effects of rhinal and dorsolateral prefrontal cortex lesions on object and spatial recognition memory in canines, we used a protocol in which both an object (delayed nonmatching to sample, or DNMS) and a spatial (delayed nonmatching to position or DNMP) recognition task were administered daily. The tasks used similar procedures such that only the type of stimulus information to be remembered differed. Rhinal cortex (RC) lesions produced a selective deficit on the DNMS task, both in retention of the task rules at short delays and in object recognition memory. By contrast, performance on the DNMP task remained intact at both short and long delay intervals in RC animals. Subjects who received dorsolateral prefrontal cortex (dlPFC) lesions were impaired on a spatial task at a short, 5-second delay, suggesting disrupted retention of the general task rules; however, this impairment was transient, and long-term spatial memory performance was unaffected in dlPFC subjects. The present results provide support for the involvement of the RC in object, but not visuospatial, processing and recognition memory, whereas the dlPFC appears to mediate retention of a nonmatching rule. These findings support theories of functional specialization within the medial temporal lobe and frontal cortex and suggest that rhinal and dorsolateral prefrontal cortices in canines are functionally similar to analogous regions in other mammals. J. Comp. Neurol. 511:257-270, 2008. (C) 2008 Wiley-Liss, Inc.
C1 [Christie, Lori-Ann; Head, Elizabeth; Cotman, Carl W.] Univ Calif Irvine, Inst Brain Aging & Dementia, Irvine, CA 92697 USA.
[Saunders, Richard C.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Kowalska, Danuta M.] M Nencki Inst Expt Biol, Dept Neurophysiol, PL-02093 Warsaw, Poland.
[MacKay, William A.] Univ Toronto, Dept Physiol, Toronto, ON M5S 1A8, Canada.
RP Christie, LA (reprint author), Univ Calif Irvine, Inst Brain Aging & Dementia, 1226 Gillespie NRF, Irvine, CA 92697 USA.
EM lori@uci.edu
FU National Institute on Aging [AG12694]; Natural Sciences and Engineering
Research Council of Canada; National Institute of Mental Health
Intramural Research Program
FX Grant sponsor: National Institute on Aging; Grant number: AG12694 (to
C.W.C.); Grant sponsor: Natural Sciences and Engineering Research
Council of Canada (to L.-A.C.); Grant sponsor: National Institute of
Mental Health Intramural Research Program.
NR 82
TC 3
Z9 3
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD NOV 10
PY 2008
VL 511
IS 2
BP 257
EP 270
DI 10.1002/cne.21821
PG 14
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA 362JA
UT WOS:000260192800006
PM 18792072
ER
PT J
AU Huang, L
Pickle, LW
Das, B
AF Huang, Lan
Pickle, Linda W.
Das, Barnali
TI Evaluating spatial methods for investigating global clustering and
cluster detection of cancer cases
SO STATISTICS IN MEDICINE
LA English
DT Article
DE spatial statistic comparison; spatial clustering and cluster detection;
cancer cases
ID MORANS-I; POPULATION-DENSITY; UNITED-STATES; DISEASE; TESTS; POWER; RISK
AB There have been articles on comparing methods for global clustering evaluation and cluster detection in disease surveillance, but power and sample size (SS) requirements have not been explored for spatially correlated data in this area. We are developing such requirements for tests of spatial clustering and cluster detection for regional cancer cases. We compared global clustering methods including Moran's I, Tango's and Besag-Newell's R statistics, and cluster detection methods including circular and elliptic spatial scan statistics (SaTScan), flexibly shaped spatial scan statistics, Turnbull's Cluster evaluation permutation procedure, local indicators of spatial association, and upper-level set scan statistics. We identified eight geographic patterns that are representative of patterns of mortality due to various types of cancer in the U.S. from 1998 to 2002. We then evaluated the selected spatial methods based on state- and county-level data simulated from these different spatial patterns in terms of geographic locations and relative risks, and varying SSs using the 2000 population in each county. The comparison provides insight into the performance of the spatial methods when applied to varying cancer count data in terms of power and precision of cluster detection. Copyright (C) 2008 John Wiley & Sons, Ltd.
C1 [Huang, Lan; Pickle, Linda W.; Das, Barnali] NCI, SRAB, SRP, DCCPS, Rockville, MD 20852 USA.
RP Huang, L (reprint author), NCI, SRAB, SRP, DCCPS, 6116 Execut Blvd,Rm 5043, Rockville, MD 20852 USA.
EM huangla@mail.nih.gov
FU Intramural NIH HHS [NIH0011917195]; PHS HHS [NIH0011917195]
NR 38
TC 26
Z9 27
U1 0
U2 13
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2008
VL 27
IS 25
BP 5111
EP 5142
DI 10.1002/sim.3342
PG 32
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 368RS
UT WOS:000260640800002
PM 18712778
ER
PT J
AU Freedman, LS
Midthune, D
Carroll, RJ
Kipnis, V
AF Freedman, Laurence S.
Midthune, Douglas
Carroll, Raymond J.
Kipnis, Victor
TI A comparison of regression calibration, moment reconstruction and
imputation for adjusting for covariate measurement error in regression
SO STATISTICS IN MEDICINE
LA English
DT Article
DE differential measurement error; moment reconstruction; multiple
imputation; non-differential measurement error; regression calibration
ID HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; LOGISTIC-REGRESSION;
MULTIPLE-IMPUTATION; NATIONAL-INSTITUTES; MODELS
AB Regression calibration (RC) is a popular method for estimating regression coefficients when one or more continuous explanatory variables, X, are measured with an error. In this method, the mismeasured covariate, W, is substituted by the expectation E(X I W), based on the assumption that the error in the measurement of X is non-differential. Using simulations, we compare three versions of RC with two other 'substitution' methods, moment reconstruction (MR) and imputation (TM), neither of which rely on the non-differential error assumption. We investigate studies that have an internal calibration sub-study. For RC, we consider (i) the usual version of RC, (ii) RC applied only to the 'marker' information in the calibration study, and (iii) an 'efficient' version (ERC) in which the estimators (i) and (ii) are combined. Our results show that ERC is preferable when there is non-differential measurement error. Under this condition, there are cases where ERC is less efficient than MR or TM, but they rarely occur in epidemiology. We show that the efficiency gain of usual RC and ERC over the other methods can sometimes be dramatic. The usual version of RC carries similar efficiency gains to ERC over MR and IM, but becomes unstable as measurement error becomes large, leading to bias and poor precision. When differential measurement error does pertain, then MR and IM have considerably less bias than RC, but can have much larger variance. We demonstrate our findings with an analysis of dietary fat intake and mortality in a large cohort study. Copyright (C) 2008 John Wiley & Sons, Ltd.
C1 [Freedman, Laurence S.] Gertner Inst Epidemiol & Hlth Policy Res, IL-52161 Tel Hashomer, Israel.
[Midthune, Douglas; Kipnis, Victor] NCI, Canc Prevent Div, Biometry Res Grp, Bethesda, MD 20892 USA.
[Carroll, Raymond J.] Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA.
RP Freedman, LS (reprint author), Gertner Inst Epidemiol & Hlth Policy Res, IL-52161 Tel Hashomer, Israel.
EM lsf@actcom.co.il
FU National Cancer Institute [CA-57030]
FX Contract/grant sponsor: National Cancer Institute; contract/grant
number: CA-57030
NR 15
TC 24
Z9 24
U1 2
U2 10
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2008
VL 27
IS 25
BP 5195
EP 5216
DI 10.1002/sim.3361
PG 22
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 368RS
UT WOS:000260640800006
PM 18680172
ER
PT J
AU Ansarah-Sobrinho, C
Nelson, S
Jost, CA
Whitehead, SS
Pierson, TC
AF Ansarah-Sobrinho, Camilo
Nelson, Steevenson
Jost, Christiane A.
Whitehead, Stephen S.
Pierson, Theodore C.
TI Temperature-dependent production of pseudoinfectious dengue reporter
virus particles by complementation
SO VIROLOGY
LA English
DT Article
DE Flavivirus; West Nile virus; Dengue; Reporter virus; Antibody-mediated
neutralization
ID WEST-NILE-VIRUS; BORNE-ENCEPHALITIS-VIRUS; ANTIBODY-MEDIATED
NEUTRALIZATION; HUMAN DENDRITIC CELLS; HEMORRHAGIC-FEVER; ENVELOPE
PROTEINS; YELLOW-FEVER; IN-VITRO; JAPANESE ENCEPHALITIS; SUBGENOMIC
REPLICONS
AB Dengue Virus (DENV) is a mosquito-borne flavivirus responsible for 50 to 100 million human infections each year, highlighting the need for a safe and effective vaccine. In this study, we describe the production of pseudoinfectious DENV reporter virus particles (RVPs) using two different genetic complementation approaches, including the creation of cell lines that release reporter viruses in an inducible fashion. In Contrast to Studies with West Nile virus (WNV), production of infectious DENV RVPs was temperature-dependent; the yield Of infectious DENV RVPs at 37 degrees C is significantly reduced in comparison to experiments conducted at lower temperatures Or With WNV. This reflects both a significant reduction in the late Of infectious DENV RVP release over time, and the more rapid decay of infectious DENV RVPs at 37 degrees C. Optimized production approaches allow the production of DENV RVPs with titers Suitable for the study Of DENV entry, assembly, and the analysis of the humoral immune response of infected and vaccinated individuals. (C) 2008 Published by Elsevier Inc
C1 [Ansarah-Sobrinho, Camilo; Nelson, Steevenson; Jost, Christiane A.; Pierson, Theodore C.] Natl Inst Hlth, Viral Pathogenesis Sect, Viral Dis Lab, Bethesda, MD 20892 USA.
[Whitehead, Stephen S.] Natl Inst Hlth, Infect Dis Lab, Bethesda, MD USA.
RP Pierson, TC (reprint author), Natl Inst Hlth, Viral Pathogenesis Sect, Viral Dis Lab, Bethesda, MD 20892 USA.
EM piersontc@mail.nih.gov
FU NIH; National Institutes of Allergy and Infectious Diseases (NIAID);
Pediatric Dengue Vaccine Initiative (PDVI)
FX This work Was Supported by the Intramural Research Program of the NIH,
National Institutes of Allergy and Infectious Diseases (NIAID) and by
the Pediatric Dengue Vaccine Initiative (PDVI). We are grateful to Qing
Xu for technical Support and Dr. Bridget Puffer for providing the DENV
C-pi-M-E expression vectors Used throughout this Study, for excellent
technical assistance, and productive discussions. We thank Drs.
Christopher Buck, Subhajit Poddar, and Michael Diamond for useful
discussions and then, comments on the manuscript.
NR 56
TC 53
Z9 54
U1 2
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 10
PY 2008
VL 381
IS 1
BP 67
EP 74
DI 10.1016/j.virol.2008.08.021
PG 8
WC Virology
SC Virology
GA 368BB
UT WOS:000260595200010
PM 18801552
ER
PT J
AU Belyakov, IM
Ahlers, JD
Nabel, GJ
Moss, B
Berzofsky, JA
AF Belyakov, Igor M.
Ahlers, Jeffrey D.
Nabel, Gary J.
Moss, Bernard
Berzofsky, Jay A.
TI Generation of functionally active HIV-1 specific CD8(+) CTL in
intestinal mucosa following mucosal, systemic or mixed prime-boost
immunization
SO VIROLOGY
LA English
DT Article
DE Recombinant modified vaccinia virus Ankara; Recombinant adenovirus;
Mucosal immunity; CD8+CTL avidity
ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-CELL RESPONSES; RECOMBINANT VACCINIA
VIRUS; INFECTED RHESUS-MONKEYS; HIGH-AVIDITY; IMMUNE-RESPONSES;
GASTROINTESTINAL-TRACT; ENVELOPE GLYCOPROTEIN; PROTECTIVE IMMUNITY; AIDS
VACCINE
AB Gastrointestinal and vaginal mucosa are major sites of entry in natural HIV infection and therefore the preferred sites to elicit high-avidity CD8(+) CTL by vaccination. We directly compare systemic and mucosal immunization in mice after DNA priming and boosting with rgp160 env expressed either in MVA or Ad for their ability to induce mucosal as well as systemic HIV-specific CTL. The optimal CTL response in the gut mucosa was observed after priming with the HIV-1 gp160 env DNA vaccine and boosting with rMVA or rAd encoding the same envelope gene all administered intrarectally (IR). Maximum levels of high-avidity CD8(+) T cells were seen in intestinal lamina propria following this regimen. When the prime and boost routes were distinct, the delivery site of the boost had a greater impact than the DNA priming. IM DNA prime and IR FMVA boost were more effective than IR DNA prime and IM rMVA boost for eliciting mucosal CD8(+) T cell avidity. A systemic DNA-prime-followed by systemic rMVA boost induced high levels of high-avidity CD8(+) T cells systemically, but responses were undetectable in mucosal sites. A single systemic immunization with rMVA Was Sufficient to induce high-avidity IFN-gamma secreting CD8(+) T cells in systemic organs, whereas a single mucosal immunization with rMVA was not Sufficient to elicit high-avidity CD8(+) T cells In mucosa. Thus, a heterologous mucosal DNA prime-viral vectored boost strategy was needed. The requirement for a heterologous DNA prime-recombinant viral boost strategy for generation of high-avidity CD8(+) T cells in mucosal sites in mice may be more stringent than for the induction of high-avidity CD8(+) T cells in systemic compartments. Published by Elsevier Inc.
C1 [Belyakov, Igor M.; Ahlers, Jeffrey D.; Berzofsky, Jay A.] NCI, Mol Immunogenet & Vaccine Res Sect, Vaccine Branch, CCR,NIH, Bethesda, MD 20892 USA.
[Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Belyakov, Igor M.] Midwest Res Inst, Frederick, MD 21702 USA.
RP Belyakov, IM (reprint author), NCI, Mol Immunogenet & Vaccine Res Sect, Vaccine Branch, CCR,NIH, Bethesda, MD 20892 USA.
EM igorbelyakov@yahoo.com
FU Center for Cancer Research, National Cancer Institute; National
Institute of Allergy and Infectious Diseases; Vaccine Research Center,
National Institute of Allergy and Infectious Diseases, NIH
FX We thank Dr. David Margulies for critical comments oil the manuscript
and helpful Suggestions. We thank Drs. Linda Wyatt and Patricia Earl for
providing MVA/HXB2env, and Drs. Ling Xu, Zhi-Yong Yang, and Wing Kong
for generating and providing rAd vectors. This work was carried Out With
the support of the intramural programs of the Center for Cancer
Research, National Cancer Institute, the National Institute of Allergy
and Infectious Diseases, and the Vaccine Research Center, National
Institute of Allergy and Infectious Diseases, NIH.
NR 78
TC 40
Z9 42
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 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 10
PY 2008
VL 381
IS 1
BP 106
EP 115
DI 10.1016/j.virol.2008.08.019
PG 10
WC Virology
SC Virology
GA 368BB
UT WOS:000260595200015
PM 18793787
ER
PT J
AU Tuleuova, N
An, CI
Ramanculov, E
Revzin, A
Yokobayashi, Y
AF Tuleuova, Nazgul
An, Chung-Il
Ramanculov, Erlan
Revzin, Alexander
Yokobayashi, Yohei
TI Modulating endogenous gene expression of mammalian cells via RNA-small
molecule interaction
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE RNA interference; aptamer; gene silencing; theophylline
ID INTERFERENCE; SIRNAS; DISCRIMINATION; DELIVERY; SEQUENCE
AB RNA interference (RNAi) has emerged as a powerful technology to silence arbitrary genes by designing small RNA constructs based on the targeted messenger RNA sequences. We recently developed a small molecule-controlled RNAi gene switch that combined the molecular recognition by in vitro selected RNA aptamers with versatile gene silencing by small interfering RNAs, and demonstrated for the first time, posttranscriptional modulation of RNAi through direct RNA-small molecule interaction. In this report, we describe the first application of this technology to regulate an endogenous gene in mammalian cells. As a proof-of-concept demonstration we chose to modulate expression of albumin-serum protein produced by the liver. We designed and constructed a theophylline aptamer-fused short hairpin RNA (shRNA) expression vector targeting albumin mRNA in hepatic (HepG2) cells. Transfection of HepG2 cells with the aptamer-shRNA expression vector allowed to control albumin gene expression by adding theophylline into the culture media in dose dependent fashion. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Tuleuova, Nazgul; An, Chung-Il; Revzin, Alexander; Yokobayashi, Yohei] Univ Calif Davis, Dept Biomed Engn, Davis, CA 95616 USA.
[Tuleuova, Nazgul; Ramanculov, Erlan] Natl Biotechnol Ctr, Astana, Kazakhstan.
RP Revzin, A (reprint author), Univ Calif Davis, Dept Biomed Engn, 451 Hlth Sci Dr, Davis, CA 95616 USA.
EM arevzin@ucdavis.edu; yoko@ucdavis.edu
RI Yokobayashi, Yohei/B-5898-2009
OI Yokobayashi, Yohei/0000-0002-2417-1934
FU National Institutes of Health [DK073901]; National Science Foundation
[CBET 0755053]; National Center for Biotechnology, Republic of
Kazakhstan
FX This work was supported in part by National Institutes of Health grant
(DK073901) awarded to A.R. and National Science Foundation grant (CBET
0755053) awarded to Y.Y. N.T. was supported through a Biotechnology
Fellowship from the National Center for Biotechnology, Republic of
Kazakhstan.
NR 23
TC 30
Z9 31
U1 1
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 7
PY 2008
VL 376
IS 1
BP 169
EP 173
DI 10.1016/j.bbrc.2008.08.112
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 356NC
UT WOS:000259783900034
PM 18765226
ER
PT J
AU Wright, DG
Zhang, Y
Murphy, JR
AF Wright, Daniel G.
Zhang, Ying
Murphy, John R.
TI Effective delivery of antisense peptide nucleic acid oligomers into
cells by anthrax protective antigen
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE peptide nucleic acid; antisense; anthrax protective antigen
ID GENE-EXPRESSION; DIPHTHERIA-TOXIN; CATALYTIC DOMAIN; PNA;
OLIGONUCLEOTIDES; RECEPTOR; DNA; INTERLEUKIN-2; TRANSLOCATION;
THERAPEUTICS
AB Peptide nucleic acid (PNA) is highly stable and binds to complementary RNA and DNA with high affinity, but it resists cellular uptake, thereby limiting its bioavailability. We investigated whether protective antigen (PA, a non-toxic component of anthrax toxin) could transport antisense PNA oligomers into reporter cells that contain luciferase transgenes with mutant beta-globin IVS2 intronic inserts, which permit aberrant pre-mRNA splicing and impair luciferase expression. PNA oligomers antisense to mutant splice sites in these IVS2 inserts induced luciferase expression when effectively delivered into the cells. PNA 18-mers with C-terminal poly-lysine tails [PNA(Lys)(8)] demonstrated modest sequence-specific antisense activity by themselves at micromolar concentrations in luc-IVS2 reporter cell cultures. However, this activity was greatly amplified by PA. Antisense PNA(Lys)(8) with but not without PA also corrected the IVS2-654 beta-globin splice defect in cultured erythroid precursor cells from a patient with beta-thalassemia [genotype, IVS2-654(beta(O)/beta(E))], providing further evidence that anthrax PA can effectively transport antisense PNA oligomers into cells. Published by Elsevier Inc.
C1 [Wright, Daniel G.; Zhang, Ying; Murphy, John R.] Boston Univ, Sch Med, Dept Med, Mol Med Sect, Boston, MA 02118 USA.
RP Wright, DG (reprint author), NIDDK, Mol Med Branch, NIH, 10 Ctr Dr,Bldg 10 Room 9N314 MS1822, Bethesda, MD 20892 USA.
EM dw341u@nih.gov
FU National Cancer Institute, NIH [R21CA11228]
FX The authors are indebted to Dr. David Chui, Professor of Medicine and
Pathology, Boston University Medical Center, and to Dr. Edmond S.K. Ma,
Assoc. Professor of Medicine, Division of Haematology, University of
Hong Kong, Queen Mary Hospital, Hong Kong, PRC, for helping us obtain a
blood sample from an untransfused patient with beta-thalassemia
intermedia [IVS2-654(betaO)/betaE genotype] for
study. This work was supported in part by a grant from the National
Cancer Institute, NIH: R21CA11228.
NR 34
TC 5
Z9 5
U1 2
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 7
PY 2008
VL 376
IS 1
BP 200
EP 205
DI 10.1016/j.bbrc.2008.08.124
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 356NC
UT WOS:000259783900040
PM 18774771
ER
PT J
AU Garcia-Pino, A
Christensen-Dalsgaard, M
Wyns, L
Yarmolinsky, M
Magnuson, RD
Gerdes, K
Loris, R
AF Garcia-Pino, Abel
Christensen-Dalsgaard, Mikkel
Wyns, Lode
Yarmolinsky, Michael
Magnuson, Roy David
Gerdes, Kenn
Loris, Remy
TI Doc of Prophage P1 Is Inhibited by Its Antitoxin Partner Phd through
Fold Complementation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PLASMID ADDICTION SYSTEM; PROGRAMMED CELL-DEATH; ESCHERICHIA-COLI;
CRYSTAL-STRUCTURE; STRUCTURAL BASIS; MESSENGER-RNAS; CYCLIC-AMP; TOXIN;
PROTEIN; ANTIDOTE
AB Prokaryotic toxin-antitoxin modules are involved in major physiological events set in motion under stress conditions. The toxin Doc (death on curing) from the phd/doc module on phage P1 hosts the C-terminal domain of its antitoxin partner Phd (prevents host death) through fold complementation. This Phd domain is intrinsically disordered in solution and folds into an alpha-helix upon binding to Doc. The details of the interactions reveal the molecular basis for the inhibitory action of the antitoxin. The complex resembles the Fic (filamentation induced by cAMP) proteins and suggests a possible evolutionary origin for the phd/doc operon. Doc induces growth arrest of Escherichia coli cells in a reversible manner, by targeting the protein synthesis machinery. Moreover, Doc activates the endogenous E. coli RelE mRNA interferase but does not require this or any other known chromosomal toxin-antitoxin locus for its action in vivo.
C1 [Garcia-Pino, Abel; Wyns, Lode; Loris, Remy] Vrije Univ Brussels, Lab Ultrastruct, B-1050 Brussels, Belgium.
[Garcia-Pino, Abel; Wyns, Lode; Loris, Remy] Vlaams Interuniv Inst Biotechnol VIB, Dept Mol & Cellular Interact, B-1050 Brussels, Belgium.
[Christensen-Dalsgaard, Mikkel; Gerdes, Kenn] Univ Newcastle, Sch Med, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England.
[Christensen-Dalsgaard, Mikkel] Univ So Denmark, Dept Biochem & Mol Biol, DK-5230 Odense M, Denmark.
[Yarmolinsky, Michael] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Magnuson, Roy David] Univ Alabama, Dept Biol Sci, Huntsville, AL 35899 USA.
RP Loris, R (reprint author), Vrije Univ Brussels, Lab Ultrastruct, Pl Laan 2, B-1050 Brussels, Belgium.
EM reloris@vub.ac.be
RI Gerdes, Kenn/M-2420-2014;
OI Gerdes, Kenn/0000-0002-7462-4612; Garcia-Pino, Abel/0000-0002-0634-0300
FU National Institutes of Health [2 R15 GM67668-03]; National Institutes of
Health Intramural Research Training Award; VIB; Fonds voor
Wetenschappelijk Onderzoek Vlaanderen; Centre for mRNP Biogenesis and
Metabolism of the Danish National Research Foundation; Onderzoeksraad of
the Vrije Universiteit Brussel
FX This work was supported, in whole or in part, by National Institutes of
Health Grant 2 R15 GM67668-03 from the NIGMS (to R. D. M.) and a
National Institutes of Health Intramural Research Training Award grant.
This work was also supported by grants from the VIB, the Fonds voor
Wetenschappelijk Onderzoek Vlaanderen, the Centre for mRNP Biogenesis
and Metabolism of the Danish National Research Foundation, and the
Onderzoeksraad of the Vrije Universiteit Brussel. The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked " advertisement"
in accordance with 18 U. S. C. Section 1734 solely to indicate this
fact.
NR 40
TC 62
Z9 65
U1 2
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 7
PY 2008
VL 283
IS 45
BP 30821
EP 30827
DI 10.1074/jbc.M805654200
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 367ID
UT WOS:000260544800037
PM 18757857
ER
PT J
AU Tsai, CJ
Sauna, ZE
Kimchi-Sarfaty, C
Ambudkar, SV
Gottesman, MM
Nussinov, R
AF Tsai, Chung-Jung
Sauna, Zuben E.
Kimchi-Sarfaty, Chava
Ambudkar, Suresh V.
Gottesman, Michael M.
Nussinov, Ruth
TI Synonymous Mutations and Ribosome Stalling Can Lead to Altered Folding
Pathways and Distinct Minima
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Review
DE synonymous mutations; protein folding; kinetics; multidrug resistance
gene; ABC transporter
ID TRANSMEMBRANE CONDUCTANCE REGULATOR; MULTIDRUG-BINDING PROTEIN; BLOOD
MONONUCLEAR-CELLS; ESCHERICHIA-COLI; ENDOPLASMIC-RETICULUM; MDR1 GENE;
CODON USAGE; INTRAMOLECULAR CHAPERONES; C3435T POLYMORPHISM;
TRANSLATIONAL PAUSE
AB How can we understand a case in which a given amino acid sequence folds into structurally and functionally distinct molecules? Synonymous single-nucleoticle polymorphisms in the MDR1 (multidrug resistance 1 or ABCB1) gene involving frequent-to-rare codon substitutions lead to identical protein sequences. Remarkably, these alternative sequences give a protein product with similar but different structures and functions. Here, we propose that long-enough ribosomal pause time scales may lead to alternate folding pathways and distinct minima on the folding free energy surface. While the conformational and functional differences between the native and alternate states may be minor, the MDR1 case illustrates that the barriers may nevertheless constitute sufficiently high hurdles in physiological time scales, leading to kinetically trapped states with altered structures and functions. Different folding pathways leading to conformationally similar trapped states may be due to swapping of (fairly symmetric) segments. Domain swapping is more likely in the no-pause case in which the chain elongates and folds simultaneously; on the other hand, sufficiently long pause times between such segments may be expected to lessen the chances of swapping events. Here, we review the literature in this light. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Tsai, Chung-Jung; Nussinov, Ruth] SAIC Frederick Inc, Basic Res Program, Ctr Canc Res Nanobiol Program, NCI Frederick, Frederick, MD 21702 USA.
[Sauna, Zuben E.; Kimchi-Sarfaty, Chava; Ambudkar, Suresh V.; Gottesman, Michael M.] NCI, Ctr Canc Res, Cell Biol Lab, Bethesda, MD 20892 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Sackler Inst Mol Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), SAIC Frederick Inc, Basic Res Program, Ctr Canc Res Nanobiol Program, NCI Frederick, Frederick, MD 21702 USA.
EM ruthn@ncifcrf.gov
FU National Cancer Institute; National Institutes of Health [N01-CO-12400];
National Institutes of Health
FX The contents of this publication do not necessarily reflect the views or
policies of the Department of Health and Human Services; neither does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government. This project has been funded in
whole or in part with federal funds from the National Cancer Institute,
National Institutes of Health, under contract number N01-CO-12400. This
research was supported in part by the Intramural Research Program of the
Center for Cancer Research of the National Cancer Institute, National
Institutes of Health. We thank Dr. H. Robert Guy (Laboratory of Cell
Biology, National Cancer Institute) for comments on the manuscript.
NR 86
TC 118
Z9 121
U1 1
U2 12
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 7
PY 2008
VL 383
IS 2
BP 281
EP 291
DI 10.1016/j.jmb.2008.08.012
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 369AN
UT WOS:000260665100001
PM 18722384
ER
PT J
AU Landis, S
Insel, TR
AF Landis, Story
Insel, Thomas R.
TI The "Neuro" in Neurogenetics
SO SCIENCE
LA English
DT Editorial Material
C1 [Landis, Story] NINDS, NIH, Bethesda, MD 20892 USA.
[Insel, Thomas R.] NIMH, NIH, Bethesda, MD 20892 USA.
RP Landis, S (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 6
Z9 6
U1 0
U2 1
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 7
PY 2008
VL 322
IS 5903
BP 821
EP 821
DI 10.1126/science.1167707
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 369DI
UT WOS:000260674100001
PM 18988812
ER
PT J
AU Gupta, SN
Ries, M
Murray, GJ
Quirk, JM
Brady, RO
Lidicker, JR
Schiffmann, R
Moore, DF
AF Gupta, Surya N.
Ries, Markus
Murray, Gary J.
Quirk, Jane M.
Brady, Roscoe O.
Lidicker, Jeffrey R.
Schiffmann, Raphael
Moore, David F.
TI Skin-impedance in Fabry Disease: A prospective, controlled,
non-randomized clinical study
SO BMC NEUROLOGY
LA English
DT Article
ID ENZYME REPLACEMENT THERAPY; STRATUM-CORNEUM
AB Background: We previously demonstrated improved sweating after enzyme replacement therapy (ERT) in Fabry disease using the thermo-regularity sweat and quantitative sudomotor axon reflex tests. Skin-impedance, a measure skin-moisture (sweating), has been used in the clinical evaluation of burns and pressure ulcers using the portable dynamic dermal impedance monitor (DDIM) system.
Methods: We compared skin impedance measurements in hemizygous patients with Fabry disease (22 post 3-years of bi-weekly ERT and 5 ERT naive) and 22 healthy controls. Force compensated skin-moisture values were used for statistical analysis. Outcome measures included 1) moisture reading of the 100(th) repetitive reading, 2) rate of change, 3) average of 60-110(th) reading and 4) overall average of all readings.
Results: All outcome measures showed a significant difference in skin-moisture between Fabry patients and control subjects (p < 0.0001). There was no difference between Fabry patients on ERT and patients naive to ERT. Increased skin-impedance values for the four skin-impedance outcome measures were found in a small number of dermatome test-sites two days post-enzyme infusions.
Conclusion: The instrument portability, ease of its use, a relatively short time required for the assessment, and the fact that DDIM system was able to detect the difference in skin-moisture renders the instrument a useful clinical tool.
C1 [Ries, Markus; Murray, Gary J.; Quirk, Jane M.; Brady, Roscoe O.; Schiffmann, Raphael] Natl Inst Neurol Disorders & Stroke, NIH, Dev & Metab Neurol Branch, Bethesda, MD USA.
[Gupta, Surya N.] Penn State Univ, Coll Med, Dept Pediat, Div Pediat Neurol, Hershey, PA 17033 USA.
[Lidicker, Jeffrey R.] Temple Univ, Sch Med, Ctr Stat & Informat Sci, Philadelphia, PA 19122 USA.
[Moore, David F.] Univ Manitoba, Dept Internal Med, Neurol Sect, Winnipeg, MB, Canada.
[Ries, Markus] Shire Human Genet Therapies, Cambridge, MA USA.
[Schiffmann, Raphael] Baylor Res Inst, Inst Metab Dis, Dallas, TX 75226 USA.
RP Schiffmann, R (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, Dev & Metab Neurol Branch, Bethesda, MD USA.
EM suryangupta@rediffmail.com; markus.ries@alumni.duke.edu;
murrayg@ninds.nih.gov; quirkj@ninds.nih.gov; brayr@ninds.nih.gov;
jlidicker@Yahoo.com; raphael.schiffmann@baylorhealth.edu;
mooredf@mac.com
OI Ries, Markus/0000-0002-5054-5741
FU National Institutes of Health (NINDS)
FX The authors wish to acknowledge Michelle Ashmus for organizing the
results of alpha-galactosidase A assay for analysis, James Mitkon, NOVA
Technology Corporation, for his technical support, and Cheryl Hipple for
having coordinated the examinations. We are indebted to our patients for
their participation in this study. This work was funded by the
Intramural Program of the National Institutes of Health (NINDS) and was
conducted as an investigator-initiated project parallel to a clinical
trial sponsored by Shire Human Genetic Therapies.
NR 22
TC 8
Z9 8
U1 0
U2 2
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.
PD NOV 6
PY 2008
VL 8
AR 41
DI 10.1186/1471-2377-8-41
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 379II
UT WOS:000261389500001
PM 18990229
ER
PT J
AU Chen, S
Ross, TJ
Zhan, W
Myers, CS
Chuang, KS
Heishman, SJ
Stein, EA
Yang, YH
AF Chen, Sharon
Ross, Thomas J.
Zhan, Wang
Myers, Carol S.
Chuang, Keh-Shih
Heishman, Stephen J.
Stein, Elliot A.
Yang, Yihong
TI Group independent component analysis reveals consistent resting-state
networks across multiple sessions
SO BRAIN RESEARCH
LA English
DT Article
DE Default-mode; Dimensionality; fMRI; Longitudinal studies
ID INTRINSIC BRAIN ACTIVITY; FUNCTIONAL CONNECTIVITY; DEFAULT MODE; FMRI
DATA; BLIND SEPARATION; WORKING-MEMORY; MOTOR CORTEX; MRI;
REPRODUCIBILITY; FLUCTUATIONS
AB Group independent component analysis (gICA) was performed on resting-state data from 14 healthy subjects scanned on 5 fMRI scan sessions across 16 days. The data were reduced and aggregated in 3 steps using Principal Components Analysis (PCA, within scan, within session and across session) and subjected to gICA procedures. The amount of reduction was estimated by an improved method that utilizes a first-order autoregressive fitting technique to the PCA spectrum. Analyses were performed using all sessions in order to maximize sensitivity and alleviate the problem of component identification across session. Across-session consistency was examined by three methods, all using back-reconstruction of the single-session or single-subject/session maps from the grand (5-session) maps. The gICA analysis produced 55 spatially independent maps. Obvious artifactual maps were eliminated and the remainder were grouped based upon physiological recognizability. Biologically relevant component maps were found, including sensory, motor and a 'default-mode' map. All analysis methods showed that components were remarkably consistent across session. Critically, the components with the most obvious physiological relevance were the most consistent. The consistency of these maps suggests that, at least over a period of several weeks, these networks would be useful to follow longitudinal treatment-related manipulations. Published by Elsevier B.V.
C1 [Chen, Sharon; Ross, Thomas J.; Zhan, Wang; Stein, Elliot A.; Yang, Yihong] Natl Inst Drug Abuse, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
[Myers, Carol S.; Heishman, Stephen J.] Natl Inst Drug Abuse, Clin Pharmacol & Therapeut Branch, NIH, Baltimore, MD 21224 USA.
[Chuang, Keh-Shih] Natl Tsing Hua Univ, Dept Biomed Engn & Environm Sci, Hsinchu, Taiwan.
[Chen, Sharon] Kaohsiung Med Univ, Fac Med Radiol, Kaohsiung, Taiwan.
RP Yang, YH (reprint author), Natl Inst Drug Abuse, Neuroimaging Res Branch, NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM yihongyang@intra.nida.nih.gov
RI Ross, Thomas/B-7469-2008
OI Ross, Thomas/0000-0002-7745-3572
FU NIH; National Institute on Drug Abuse
FX This work was supported by the Intramural Research Program of the NIH,
National Institute on Drug Abuse.
NR 44
TC 65
Z9 65
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 6
PY 2008
VL 1239
BP 141
EP 151
DI 10.1016/j.brainres.2008.08.028
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 373DA
UT WOS:000260950000016
PM 18789314
ER
PT J
AU Flores-Ortega, A
Casanovas, J
Nussinov, R
Aleman, C
AF Flores-Ortega, Alejandra
Casanovas, Jordi
Nussinov, Ruth
Aleman, Carlos
TI Conformational Preferences of beta- and gamma-Aminated Proline Analogues
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID CIS-TRANS ISOMERIZATION; PROTEIN BUILDING-BLOCKS; NANOSTRUCTURE DESIGN;
AQUEOUS-SOLUTION; DIPEPTIDE ANALOGS; SOLVATION MODEL; PEPTIDE MODELS;
AMINO-ACIDS; SIDE-CHAIN; GAS-PHASE
AB Quantum mechanical calculations have been used to investigate how the incorporation of an amino group to the C-beta- or C-gamma-positions of the pyrrolidine ring affects the intrinsic conformational properties of the proline. Specifically, a conformational study of the N-acetyl-N'-methylamide derivatives of four isomers of aminoproline, which differ not only in the beta- or gamma-position of the substituent but also in its cis or trans relative disposition, has been performed. To further understand the role of the intramolecular hydrogen bonds between the backbone carbonyl groups and the amino side group, a conformational study was also performed on the corresponding four analogues of (dimethylamino)proline. In addition, the effects of solvation on aminoproline and (dimethylamino)proline dipeptides have been evaluated using a self-consistent reaction field model, and considering four different solvents (carbon tetrachloride, chloroform, methanol and water). Results indicate that the incorporation of the amino substituent into the pyrrolidine e ring affects the conformational properties, with backbone...side chain intramolecular hydrogen bonds detected when it is incorporated in a cis relative disposition. In general, the incorporation of the amino side group tends to stabilize those structures where the peptide bond involving the pyrrolidine nitrogen is arranged in cis. The aminoproline isomer with the substituent attached to the C-gamma-position with a cis relative disposition is the most stable in the gas phase and in chloroform, methanol and water solutions. Replacement of the amino side group by the dimethylamino substituent produces significant changes in the potential energy surfaces of the four investigated (dimethylamino)proline-containing dipeptides. Thus, these changes affect not only the number of minima, which increases considerably, but also the backbone and pseudorotational preferences. In spite of these effects, comparison of the conformational preferences, i.e., the more favored conformers, calculated for different isomers of aminoproline and (dimethylamino)proline dipeptides showed a high degree of consistency for the two families of compounds.
C1 [Casanovas, Jordi] Univ Lleida, Escola Politecn Super, Dept Quim, Lleida 25001, Spain.
[Flores-Ortega, Alejandra; Aleman, Carlos] Univ Politecn Cataluna, Dept Engn Quim, ETS Engn Ind Barcelona, E-08028 Barcelona, Spain.
[Nussinov, Ruth] NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res,Nanobiol Program, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sch Med, Dept Human Genet Sackler, IL-69978 Tel Aviv, Israel.
RP Casanovas, J (reprint author), Univ Lleida, Escola Politecn Super, Dept Quim, C Jaume 2 69, Lleida 25001, Spain.
EM jcasanovas@quimica.udl.cat; carlos.aleman@upc.edu
RI Casanovas, Jordi/B-5435-2013
OI Casanovas, Jordi/0000-0002-4914-9194
FU National Cancer Institute, National Institutes of Health [N01-CO-12400];
NIH, National Cancer Institute, Center for Cancer Research
FX Acknowledgment. Gratitude is expressed to the Centre de Supercomputacio
de Catalunya (CESCA) and to the Universitat de Lleida for computational
facilities. This project has been funded in whole or in part with
Federal funds from the National Cancer Institute, National Institutes of
Health, under contract number N01-CO-12400. The content of this
publication does not necessarily reflect the view of the policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organization imply endorsement by the
U.S. Government. This research was supported [in part] by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research.
NR 64
TC 11
Z9 11
U1 1
U2 20
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD NOV 6
PY 2008
VL 112
IS 44
BP 14045
EP 14055
DI 10.1021/jp807638p
PG 11
WC Chemistry, Physical
SC Chemistry
GA 367DQ
UT WOS:000260533100042
PM 18842022
ER
PT J
AU Shaikh, AG
Miura, K
Optican, LM
Ramat, S
Tripp, RM
Zee, DS
AF Shaikh, Aasef G.
Miura, Kenichiro
Optican, Lance M.
Ramat, Stefano
Tripp, Robert M.
Zee, David S.
TI Hypothetical membrane mechanisms in essential tremor
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID ACTIVATED CATION CURRENT; THALAMIC RELAY NEURONS; PLACEBO-CONTROLLED
TRIAL; IN-VITRO; ELECTROPHYSIOLOGICAL PROPERTIES; PACEMAKER CHANNELS;
RETICULAR NUCLEUS; GLOBUS-PALLIDUS; DOUBLE-BLIND; CYCLIC-AMP
AB Background: Essential tremor (ET) is the most common movement disorder and its pathophysiology is unknown. We hypothesize that increased membrane excitability in motor circuits has a key role in the pathogenesis of ET. Specifically, we propose that neural circuits controlling ballistic movements are inherently unstable due to their underlying reciprocal innervation. Such instability is enhanced by increased neural membrane excitability and the circuit begins to oscillate. These oscillations manifest as tremor.
Methods: Postural limb tremor was recorded in 22 ET patients and then the phenotype was simulated with a conductance-based neuromimetic model of ballistic movements. The model neuron was Hodgkin-Huxley type with added hyperpolarization activated cation current (I(h)), low threshold calcium current (I(T)), and GABA and glycine mediated chloride currents. The neurons also featured the neurophysiological property of rebound excitation after release from sustained inhibition (post-inhibitory rebound). The model featured a reciprocally innervated circuit of neurons that project to agonist and antagonist muscle pairs.
Results: Neural excitability was modulated by changing I(h) and/or I(T). Increasing I(h) and/or I(T) further depolarized the membrane and thus increased excitability. The characteristics of the tremor from all ET patients were simulated when I(h) was increased to similar to 10(x) the range of physiological values. In contrast, increasing other membrane conductances, while keeping I(h) at a physiological value, did not simulate the tremor. Increases in I(h) and I(T) determined the frequency and amplitude of the simulated oscillations.
Conclusion: These simulations support the hypothesis that increased membrane excitability in potentially unstable, reciprocally innervated circuits can produce oscillations that resemble ET. Neural excitability could be increased in a number of ways. In this study membrane excitability was increased by up-regulating I(h) and I(T). This approach suggests new experimental and clinical ways to understand and treat common tremor disorders.
C1 [Shaikh, Aasef G.; Zee, David S.] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
[Optican, Lance M.] NEI, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Ramat, Stefano] Univ Pavia, I-27100 Pavia, Italy.
[Tripp, Robert M.] FlexAble Syst, Fountain Hills, AZ USA.
[Miura, Kenichiro] Kyoto Univ, Grad Sch Med, Kyoto, Japan.
RP Shaikh, AG (reprint author), Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
EM ashaikh@dizzy.med.jhu.edu; kmiura@brain.med.kyoto-u.ac.jp;
lanceoptican@nih.gov; steram@bioing.unipv.it; bob@flexable.com;
dzee@dizzy.med.jhu.edu
RI Ramat, Stefano/E-6495-2011
OI Ramat, Stefano/0000-0001-5932-186X
FU NIH [EY01849]; Gustavus and Louise Pfeiffer Foundation;
Ataxia-telangiectasia Children's Project
FX The work was supported by grants from NIH EY01849, Intramural Division
of the National Eye Institute (NIH, DHHS), Gustavus and Louise Pfeiffer
Foundation, and Ataxia-telangiectasia Children's Project. The authors
thank Mr. Dale Roberts and Mr. Adrian Lasker for comments and support.
NR 47
TC 17
Z9 17
U1 1
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD NOV 6
PY 2008
VL 6
AR 68
DI 10.1186/1479-5876-6-68
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 393KW
UT WOS:000262373200001
PM 18990221
ER
PT J
AU Bentley, DR
Balasubramanian, S
Swerdlow, HP
Smith, GP
Milton, J
Brown, CG
Hall, KP
Evers, DJ
Barnes, CL
Bignell, HR
Boutell, JM
Bryant, J
Carter, RJ
Cheetham, RK
Cox, AJ
Ellis, DJ
Flatbush, MR
Gormley, NA
Humphray, SJ
Irving, LJ
Karbelashvili, MS
Kirk, SM
Li, H
Liu, XH
Maisinger, KS
Murray, LJ
Obradovic, B
Ost, T
Parkinson, ML
Pratt, MR
Rasolonjatovo, IMJ
Reed, MT
Rigatti, R
Rodighiero, C
Ross, MT
Sabot, A
Sankar, SV
Scally, A
Schroth, GP
Smith, ME
Smith, VP
Spiridou, A
Torrance, PE
Tzonev, SS
Vermaas, EH
Walter, K
Wu, XL
Zhang, L
Alam, MD
Anastasi, C
Aniebo, IC
Bailey, DMD
Bancarz, IR
Banerjee, S
Barbour, SG
Baybayan, PA
Benoit, VA
Benson, KF
Bevis, C
Black, PJ
Boodhun, A
Brennan, JS
Bridgham, JA
Brown, RC
Brown, AA
Buermann, DH
Bundu, AA
Burrows, JC
Carter, NP
Castillo, N
Catenazzi, MCE
Chang, S
Cooley, RN
Crake, NR
Dada, OO
Diakoumakos, KD
Dominguez-Fernandez, B
Earnshaw, DJ
Egbujor, UC
Elmore, DW
Etchin, SS
Ewan, MR
Fedurco, M
Fraser, LJ
Fajardo, KVF
Furey, WS
George, D
Gietzen, KJ
Goddard, CP
Golda, GS
Granieri, PA
Green, DE
Gustafson, DL
Hansen, NF
Harnish, K
Haudenschild, CD
Heyer, NI
Hims, MM
Ho, JT
Horgan, AM
Hoschler, K
Hurwitz, S
Ivanov, DV
Johnson, MQ
James, T
Jones, TAH
Kang, GD
Kerelska, TH
Kersey, AD
Khrebtukova, I
Kindwall, AP
Kingsbury, Z
Kokko-Gonzales, PI
Kumar, A
Laurent, MA
Lawley, CT
Lee, SE
Lee, X
Liao, AK
Loch, JA
Lok, M
Luo, SJ
Mammen, RM
Martin, JW
McCauley, PG
McNitt, P
Mehta, P
Moon, KW
Mullens, JW
Newington, T
Ning, ZM
Ng, BL
Novo, SM
O'Neill, MJ
Osborne, MA
Osnowski, A
Ostadan, O
Paraschos, LL
Pickering, L
Pike, AC
Pike, AC
Pinkard, DC
Pliskin, DP
Podhasky, J
Quijano, VJ
Raczy, C
Rae, VH
Rawlings, SR
Rodriguez, AC
Roe, PM
Rogers, J
Bacigalupo, MCR
Romanov, N
Romieu, A
Roth, RK
Rourke, NJ
Ruediger, ST
Rusman, E
Sanches-Kuiper, RM
Schenker, MR
Seoane, JM
Shaw, RJ
Shiver, MK
Short, SW
Sizto, NL
Sluis, JP
Smith, MA
Sohna, JES
Spence, EJ
Stevens, K
Sutton, N
Szajkowski, L
Tregidgo, CL
Turcatti, G
vandeVondele, S
Verhovsky, Y
Virk, SM
Wakelin, S
Walcott, GC
Wang, JW
Worsley, GJ
Yan, JY
Yau, L
Zuerlein, M
Rogers, J
Mullikin, JC
Hurles, ME
McCooke, NJ
West, JS
Oaks, FL
Lundberg, PL
Klenerman, D
Durbin, R
Smith, AJ
AF Bentley, David R.
Balasubramanian, Shankar
Swerdlow, Harold P.
Smith, Geoffrey P.
Milton, John
Brown, Clive G.
Hall, Kevin P.
Evers, Dirk J.
Barnes, Colin L.
Bignell, Helen R.
Boutell, Jonathan M.
Bryant, Jason
Carter, Richard J.
Cheetham, R. Keira
Cox, Anthony J.
Ellis, Darren J.
Flatbush, Michael R.
Gormley, Niall A.
Humphray, Sean J.
Irving, Leslie J.
Karbelashvili, Mirian S.
Kirk, Scott M.
Li, Heng
Liu, Xiaohai
Maisinger, Klaus S.
Murray, Lisa J.
Obradovic, Bojan
Ost, Tobias
Parkinson, Michael L.
Pratt, Mark R.
Rasolonjatovo, Isabelle M. J.
Reed, Mark T.
Rigatti, Roberto
Rodighiero, Chiara
Ross, Mark T.
Sabot, Andrea
Sankar, Subramanian V.
Scally, Aylwyn
Schroth, Gary P.
Smith, Mark E.
Smith, Vincent P.
Spiridou, Anastassia
Torrance, Peta E.
Tzonev, Svilen S.
Vermaas, Eric H.
Walter, Klaudia
Wu, Xiaolin
Zhang, Lu
Alam, Mohammed D.
Anastasi, Carole
Aniebo, Ify C.
Bailey, David M. D.
Bancarz, Iain R.
Banerjee, Saibal
Barbour, Selena G.
Baybayan, Primo A.
Benoit, Vincent A.
Benson, Kevin F.
Bevis, Claire
Black, Phillip J.
Boodhun, Asha
Brennan, Joe S.
Bridgham, John A.
Brown, Rob C.
Brown, Andrew A.
Buermann, Dale H.
Bundu, Abass A.
Burrows, James C.
Carter, Nigel P.
Castillo, Nestor
Catenazzi, Maria Chiara E.
Chang, Simon
Cooley, R. Neil
Crake, Natasha R.
Dada, Olubunmi O.
Diakoumakos, Konstantinos D.
Dominguez-Fernandez, Belen
Earnshaw, David J.
Egbujor, Ugonna C.
Elmore, David W.
Etchin, Sergey S.
Ewan, Mark R.
Fedurco, Milan
Fraser, Louise J.
Fajardo, Karin V. Fuentes
Furey, W. Scott
George, David
Gietzen, Kimberley J.
Goddard, Colin P.
Golda, George S.
Granieri, Philip A.
Green, David E.
Gustafson, David L.
Hansen, Nancy F.
Harnish, Kevin
Haudenschild, Christian D.
Heyer, Narinder I.
Hims, Matthew M.
Ho, Johnny T.
Horgan, Adrian M.
Hoschler, Katya
Hurwitz, Steve
Ivanov, Denis V.
Johnson, Maria Q.
James, Terena
Jones, T. A. Huw
Kang, Gyoung-Dong
Kerelska, Tzvetana H.
Kersey, Alan D.
Khrebtukova, Irina
Kindwall, Alex P.
Kingsbury, Zoya
Kokko-Gonzales, Paula I.
Kumar, Anil
Laurent, Marc A.
Lawley, Cynthia T.
Lee, Sarah E.
Lee, Xavier
Liao, Arnold K.
Loch, Jennifer A.
Lok, Mitch
Luo, Shujun
Mammen, Radhika M.
Martin, John W.
McCauley, Patrick G.
McNitt, Paul
Mehta, Parul
Moon, Keith W.
Mullens, Joe W.
Newington, Taksina
Ning, Zemin
Ng, Bee Ling
Novo, Sonia M.
O'Neill, Michael J.
Osborne, Mark A.
Osnowski, Andrew
Ostadan, Omead
Paraschos, Lambros L.
Pickering, Lea
Pike, Andrew C.
Pike, Alger C.
Pinkard, D. Chris
Pliskin, Daniel P.
Podhasky, Joe
Quijano, Victor J.
Raczy, Come
Rae, Vicki H.
Rawlings, Stephen R.
Rodriguez, Ana Chiva
Roe, Phyllida M.
Rogers, John
Bacigalupo, Maria C. Rogert
Romanov, Nikolai
Romieu, Anthony
Roth, Rithy K.
Rourke, Natalie J.
Ruediger, Silke T.
Rusman, Eli
Sanches-Kuiper, Raquel M.
Schenker, Martin R.
Seoane, Josefina M.
Shaw, Richard J.
Shiver, Mitch K.
Short, Steven W.
Sizto, Ning L.
Sluis, Johannes P.
Smith, Melanie A.
Sohna, Jean Ernest Sohna
Spence, Eric J.
Stevens, Kim
Sutton, Neil
Szajkowski, Lukasz
Tregidgo, Carolyn L.
Turcatti, Gerardo
vandeVondele, Stephanie
Verhovsky, Yuli
Virk, Selene M.
Wakelin, Suzanne
Walcott, Gregory C.
Wang, Jingwen
Worsley, Graham J.
Yan, Juying
Yau, Ling
Zuerlein, Mike
Rogers, Jane
Mullikin, James C.
Hurles, Matthew E.
McCooke, Nick J.
West, John S.
Oaks, Frank L.
Lundberg, Peter L.
Klenerman, David
Durbin, Richard
Smith, Anthony J.
TI Accurate whole human genome sequencing using reversible terminator
chemistry
SO NATURE
LA English
DT Article
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; STRUCTURAL VARIATION; HAPLOTYPE MAP;
PROJECT; IDENTIFICATION; CHROMATIN
AB DNA sequence information underpins genetic research, enabling discoveries of important biological or medical benefit. Sequencing projects have traditionally used long ( 400 - 800 base pair) reads, but the existence of reference sequences for the human and many other genomes makes it possible to develop new, fast approaches to re- sequencing, whereby shorter reads are compared to a reference to identify intraspecies genetic variation. Here we report an approach that generates several billion bases of accurate nucleotide sequence per experiment at low cost. Single molecules of DNA are attached to a flat surface, amplified in situ and used as templates for synthetic sequencing with fluorescent reversible terminator deoxyribonucleotides. Images of the surface are analysed to generate high- quality sequence. We demonstrate application of this approach to human genome sequencing on flow- sorted X chromosomes and then scale the approach to determine the genome sequence of a male Yoruba from Ibadan, Nigeria. We build an accurate consensus sequence from. 303 average depth of paired 35- base reads. We characterize four million single- nucleotide polymorphisms and four hundred thousand structural variants, many of which were previously unknown. Our approach is effective for accurate, rapid and economical whole- genome re- sequencing and many other biomedical applications.
C1 [Bentley, David R.; Swerdlow, Harold P.; Smith, Geoffrey P.; Milton, John; Brown, Clive G.; Hall, Kevin P.; Evers, Dirk J.; Barnes, Colin L.; Bignell, Helen R.; Boutell, Jonathan M.; Bryant, Jason; Carter, Richard J.; Cheetham, R. Keira; Cox, Anthony J.; Ellis, Darren J.; Gormley, Niall A.; Humphray, Sean J.; Irving, Leslie J.; Liu, Xiaohai; Maisinger, Klaus S.; Murray, Lisa J.; Obradovic, Bojan; Ost, Tobias; Parkinson, Michael L.; Rasolonjatovo, Isabelle M. J.; Rigatti, Roberto; Rodighiero, Chiara; Ross, Mark T.; Sabot, Andrea; Smith, Mark E.; Smith, Vincent P.; Spiridou, Anastassia; Torrance, Peta E.; Wu, Xiaolin; Anastasi, Carole; Aniebo, Ify C.; Bailey, David M. D.; Bancarz, Iain R.; Barbour, Selena G.; Benoit, Vincent A.; Benson, Kevin F.; Bevis, Claire; Black, Phillip J.; Boodhun, Asha; Brennan, Joe S.; Brown, Rob C.; Brown, Andrew A.; Bundu, Abass A.; Catenazzi, Maria Chiara E.; Cooley, R. Neil; Crake, Natasha R.; Dada, Olubunmi O.; Diakoumakos, Konstantinos D.; Dominguez-Fernandez, Belen; Earnshaw, David J.; Egbujor, Ugonna C.; Fraser, Louise J.; Fajardo, Karin V. Fuentes; Goddard, Colin P.; Green, David E.; Harnish, Kevin; Heyer, Narinder I.; Hims, Matthew M.; Horgan, Adrian M.; Hoschler, Katya; James, Terena; Jones, T. A. Huw; Kang, Gyoung-Dong; Kersey, Alan D.; Kingsbury, Zoya; Kokko-Gonzales, Paula I.; Kumar, Anil; Lee, Sarah E.; Loch, Jennifer A.; Mammen, Radhika M.; McCauley, Patrick G.; Mehta, Parul; Newington, Taksina; Novo, Sonia M.; Osborne, Mark A.; Osnowski, Andrew; Pickering, Lea; Pike, Andrew C.; Raczy, Come; Rae, Vicki H.; Rawlings, Stephen R.; Rodriguez, Ana Chiva; Roe, Phyllida M.; Rogers, John; Bacigalupo, Maria C. Rogert; Romanov, Nikolai; Rourke, Natalie J.; Ruediger, Silke T.; Sanches-Kuiper, Raquel M.; Schenker, Martin R.; Shaw, Richard J.; Smith, Melanie A.; Sohna, Jean Ernest Sohna; Stevens, Kim; Sutton, Neil; Szajkowski, Lukasz; Tregidgo, Carolyn L.; vandeVondele, Stephanie; Wang, Jingwen; Worsley, Graham J.; McCooke, Nick J.; Smith, Anthony J.] Illumina Cambridge Ltd, Saffron Walden CB10 1XL, Essex, England.
[Balasubramanian, Shankar; Barnes, Colin L.; Liu, Xiaohai; Earnshaw, David J.; Furey, W. Scott; Osborne, Mark A.; Klenerman, David] Univ Cambridge, Dept Chem, Univ Chem Lab, Cambridge CB2 1EW, England.
[Flatbush, Michael R.; Karbelashvili, Mirian S.; Kirk, Scott M.; Pratt, Mark R.; Reed, Mark T.; Sankar, Subramanian V.; Schroth, Gary P.; Tzonev, Svilen S.; Vermaas, Eric H.; Zhang, Lu; Alam, Mohammed D.; Banerjee, Saibal; Baybayan, Primo A.; Bridgham, John A.; Buermann, Dale H.; Burrows, James C.; Castillo, Nestor; Chang, Simon; Elmore, David W.; Etchin, Sergey S.; Ewan, Mark R.; George, David; Golda, George S.; Granieri, Philip A.; Gustafson, David L.; Haudenschild, Christian D.; Ho, Johnny T.; Hurwitz, Steve; Ivanov, Denis V.; Johnson, Maria Q.; Kerelska, Tzvetana H.; Khrebtukova, Irina; Kindwall, Alex P.; Lee, Xavier; Liao, Arnold K.; Lok, Mitch; Luo, Shujun; Martin, John W.; McNitt, Paul; Moon, Keith W.; Mullens, Joe W.; O'Neill, Michael J.; Ostadan, Omead; Paraschos, Lambros L.; Pike, Alger C.; Pinkard, D. Chris; Pliskin, Daniel P.; Podhasky, Joe; Quijano, Victor J.; Roth, Rithy K.; Rusman, Eli; Seoane, Josefina M.; Shiver, Mitch K.; Short, Steven W.; Sizto, Ning L.; Sluis, Johannes P.; Spence, Eric J.; Verhovsky, Yuli; Virk, Selene M.; Wakelin, Suzanne; Walcott, Gregory C.; Yan, Juying; Yau, Ling; Zuerlein, Mike; West, John S.; Oaks, Frank L.; Lundberg, Peter L.] Illumina Hayward, Hayward, CA 94343 USA.
[Li, Heng; Scally, Aylwyn; Walter, Klaudia; Carter, Nigel P.; Ning, Zemin; Ng, Bee Ling; Rogers, Jane; Hurles, Matthew E.; Durbin, Richard] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England.
[Fedurco, Milan; Romieu, Anthony; Turcatti, Gerardo] Manteia Predict Med SA, CH-1267 Coinsins, Switzerland.
[Gietzen, Kimberley J.; Laurent, Marc A.; Lawley, Cynthia T.; Ostadan, Omead] Illumina Inc, Corp Headquarters, San Diego, CA 92121 USA.
[Hansen, Nancy F.; Mullikin, James C.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Bentley, DR (reprint author), Illumina Cambridge Ltd, Chesterford Res Pk, Saffron Walden CB10 1XL, Essex, England.
EM dbentley@illumina.com
RI Balasubramanian, Shankar/C-1671-2009; Li, Heng/D-9344-2011; Sincan,
Murat /A-3794-2010; Ning, Zemin/D-2411-2013;
OI Li, Heng/0000-0003-4874-2874; Durbin, Richard/0000-0002-9130-1006;
Klenerman, David/0000-0001-7116-6954; Ning, Zemin/0000-0003-4359-776X;
Walter, Klaudia/0000-0003-4448-0301
FU The Wellcome Trust; Biotechnology and Biological Sciences Research
Council; BBSRC Applied Genomics LINK Programme; Intramural Research
Program of the National Human Genome Research Institute; National
Institutes of Health
FX The authors acknowledge the advice of A. Williamson, T. Rink, S.
Benkovic, J. Berriman, J. Todd, R. Waterston, S. Eletr, W. Jack, M.
Cooper, T. Brown, C. Reece and R. Cook during this work; E. Margulies
for assistance with data analysis; M. Shumway for assistance with data
submission; and the contributions of the administrative and support
staff at all the institutions. This research was supported in part by
The Wellcome Trust (to H.L., A.Sc., K.W., N.P.C, B.N.L., J.R., M.E.H.
and R.D.), the Biotechnology and Biological Sciences Research Council
(BBSRC) (to S.B. and D.K.), the BBSRC Applied Genomics LINK Programme
(to A.Sp. and C.L.B.) and the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health
(to N.F.H. and J.C.M.). S. Balasubramanian and D. Klenerman are
inventors and founders of Solexa Ltd.
NR 33
TC 1611
Z9 1654
U1 36
U2 307
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 6
PY 2008
VL 456
IS 7218
BP 53
EP 59
DI 10.1038/nature07517
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 369DH
UT WOS:000260674000039
PM 18987734
ER
PT J
AU Richards, C
Tao, W
Hamer, D
AF Richards, Chris
Tao, Wang
Hamer, Dean
TI Cellulose Sulfate for Prevention of HIV Infection
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Richards, Chris; Tao, Wang; Hamer, Dean] NIH, Bethesda, MD 20892 USA.
RP Richards, C (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM deanh@helix.nih.gov
NR 3
TC 0
Z9 0
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 6
PY 2008
VL 359
IS 19
BP 2067
EP 2067
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 368OW
UT WOS:000260632700019
ER
PT J
AU Stoney, CM
Coates, P
Briggs, JP
AF Stoney, Catherine M.
Coates, Paul
Briggs, Josephine P.
TI Integrity of Active Components of Botanical Products Used in
Complementary and Alternative Medicine
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Stoney, Catherine M.; Briggs, Josephine P.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Coates, Paul] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
RP Stoney, CM (reprint author), NIH, Natl Ctr Complementary & Alternat Med, Bldg 10, Bethesda, MD 20892 USA.
EM stoneyc@mail.nih.gov
RI Briggs, Josephine/B-9394-2009
OI Briggs, Josephine/0000-0003-0798-1190
NR 4
TC 2
Z9 2
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 5
PY 2008
VL 300
IS 17
BP 1995
EP 1995
DI 10.1001/jama.2008.557
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 368EX
UT WOS:000260605400012
PM 18984883
ER
EF