FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Ma, KK
Mele, L
Landon, MB
Spong, CY
Ramin, SM
Casey, B
Wapner, RJ
Varner, MW
Rouse, DJ
Thorp, JM
Sciscione, A
Catalano, P
Harper, M
Saade, G
Caritis, SN
Sorokin, Y
Peaceman, AM
AF Ma, Kimberly K.
Mele, Lisa
Landon, Mark B.
Spong, Catherine Y.
Ramin, Susan M.
Casey, Brian
Wapner, Ronald J.
Varner, Michael W.
Rouse, Dwight J.
Thorp, John M., Jr.
Sciscione, Anthony
Catalano, Patrick
Harper, Margaret
Saade, George
Caritis, Steve N.
Sorokin, Yoram
Peaceman, Alan M.
CA Eunice Kennedy Shriver Natl Inst
TI The Obstetric and Neonatal Implications of a Low Value on the 50-g
Glucose Screening Test
SO AMERICAN JOURNAL OF PERINATOLOGY
LA English
DT Article
DE low glucose screening test; neonatal hypoglycemia
ID INTRAUTERINE GROWTH-RETARDATION; TOLERANCE-TEST; ORAL GLUCOSE;
HYPOGLYCEMIA; METABOLISM; PREGNANCY
AB Objective To assess the relationship between a low 50-g 1-hour glucose loading test (GLT) and maternal and neonatal outcomes in women without diabetes.
Study Design This was a secondary analysis of a multicenter observational cohort from a randomized trial of treatment for mild gestational diabetes. Maternal and neonatal outcomes were compared between women with GLT values < 90 mg/dL and those with results 90 to 119 mg/dL.
Results Of 436 enrolled women, 297 (68.1%) had a GLT result of 90 to 119 mg/dL and 139 (31.9%) had a result of < 90 mg/dL. There was a lower incidence of neonatal hypoglycemia in those with a GLT < 90 mg/dL (5.7% versus 16.5%, p = 0.006). Other outcomes were not associated with test results.
Conclusion A GLT result < 90 mg/dL compared with 90 to 119 mg/dL is associated with a lower risk of neonatal hypoglycemia, but no other significant findings.
C1 [Ma, Kimberly K.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Mele, Lisa] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Landon, Mark B.] Ohio State Univ, Columbus, OH 43210 USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Casey, Brian] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Wapner, Ronald J.] Columbia Univ, New York, NY USA.
[Varner, Michael W.] Univ Utah, Salt Lake City, UT USA.
[Rouse, Dwight J.] Univ Alabama Birmingham, Birmingham, AL USA.
[Thorp, John M., Jr.] Univ N Carolina, Chapel Hill, NC USA.
[Sciscione, Anthony] Drexel Univ, Philadelphia, PA 19104 USA.
[Catalano, Patrick] Case Western Reserve Univ, MetroHlth Med Ctr, Cleveland, OH 44106 USA.
[Harper, Margaret] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Saade, George] Univ Texas Med Branch, Galveston, TX 77555 USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Peaceman, Alan M.] Northwestern Univ, Chicago, IL 60611 USA.
RP Ma, KK (reprint author), 1959 NE Pacific St,Box 356460, Seattle, WA 98195 USA.
EM kkma@uw.edu
RI Varner, Michael/K-9890-2013
OI caritis, steve/0000-0002-2169-0712; Peaceman, Alan/0000-0002-4515-4850;
Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HD27915, HD34116, HD40485, HD34208, HD27869, HD40500,
HD40560, HD34136, HD40544, HD27860, HD40545, HD53097, HD21410, HD27917,
HD40512, HD53118, HD36801]; General Clinical Research Centers Grant
[M01-RR00034]; National Center for Research Resources [UL1-RR024989,
M01-RR00080, UL1-RR025764, C06-RR11234]
FX The project described was supported by grants from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(HD27915, HD34116, HD40485, HD34208, HD27869, HD40500, HD40560, HD34136,
HD40544, HD27860, HD40545, HD53097, HD21410, HD27917, HD40512, HD53118,
HD36801), General Clinical Research Centers Grant (M01-RR00034), and the
National Center for Research Resources (UL1-RR024989, M01-RR00080,
UL1-RR025764, C06-RR11234) and does not necessarily represent the
official views of the Eunice Kennedy Shriver National Institute of Child
Health and Human Development or the National Institutes of Health.
NR 21
TC 2
Z9 2
U1 0
U2 0
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0735-1631
EI 1098-8785
J9 AM J PERINAT
JI Am. J. Perinatol.
PD OCT
PY 2013
VL 30
IS 9
BP 714
EP 720
DI 10.1055/s-0032-1331027
PG 7
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 217WI
UT WOS:000324392900002
ER
PT J
AU Londhe, VA
Nolen, TL
Das, A
Higgins, RD
Tyson, JE
Oh, W
Devaskar, SU
AF Londhe, Vedang A.
Nolen, Tracy L.
Das, Abhik
Higgins, Rosemary D.
Tyson, Jon E.
Oh, William
Devaskar, Sherin U.
CA Eunice Kennedy Shriver Natl Inst
TI Vitamin A Supplementation in Extremely Low-Birth-Weight Infants:
Subgroup Analysis in Small-for-Gestational-Age Infants
SO AMERICAN JOURNAL OF PERINATOLOGY
LA English
DT Article
DE vitamin A; IUGRintrauterine growth restriction; BPDbronchopulmonary
dysplasia; SGAsmall for gestational age; AGAappropriate for gestational
age
ID INTRAUTERINE GROWTH-RETARDATION; LUNG-FUNCTION; NEWBORN
AB Objective Preterm infants with intrauterine growth restriction are at increased risk of respiratory distress syndrome and bronchopulmonary dysplasia (BPD). A randomized clinical trial by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Neonatal Research Network demonstrated that vitamin A supplementation in extremely low-birth-weight (ELBW) preterm infants requiring early respiratory support decreased the risk of developing BPD.
Study Design A subgroup analysis of small-for-gestational-age (SGA) infants from the original NICHD trial was performed to test the hypothesis that in infants requiring early respiratory support, vitamin A supplementation decreases the relative risk of BPD or death in premature SGA infants to a greater extent than in gestational age-equivalent vitamin A-treated appropriate-for-gestational-age (AGA) infants.
Results Although vitamin A supplementation significantly increased serum retinol concentrations in AGA ELBW infants (median [5th percentile, 95th percentile]: 16.3 [-7.0, 68.8] versus 2.4 [-13.9, 55.1]; p < 0.001), no increases were noted in SGA ELBW infants.
Conclusions Given the limited power of this analysis due to a low number of SGA infants, these data did not provide evidence to support the hypothesis that vitamin A supplementation in preterm SGA infants requiring early respiratory support decreases the relative risk of BPD or death as compared with preterm AGA infants.
C1 [Londhe, Vedang A.; Devaskar, Sherin U.] Univ Calif Los Angeles, David Geffen Sch Med, Div Neonatol & Dev Biol, Dept Pediat,Neonatal Res Ctr, Los Angeles, CA 90095 USA.
[Nolen, Tracy L.; Das, Abhik] RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Tyson, Jon E.] Univ Texas Med Sch Houston, Dept Pediat, Houston, TX USA.
[Oh, William] Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02908 USA.
RP Londhe, VA (reprint author), Dept Pediat, Div Neonatol & Dev Biol, 175217,B2-375 MDCC,10833 Le Conte Ave, Los Angeles, CA 90095 USA.
EM vlondhe@mednet.ucla.edu
FU National Institutes of Health; NICHD; National Center for Research
Resources; National Center for Advancing Translational Sciences through
UCLA CTSI [UL1TR000124]
FX The National Institutes of Health, the NICHD, and the National Center
for Research Resources provided grant support for the Neonatal Research
Network's Vitamin A Trial.; Yale University and Yale-New Haven
Children's Hospital (U10HD27871, M01 RR6022): Richard A. Ehrenkranz, MD;
Patricia Gettner, RN; Monica Konstantino, RN, BSN; JoAnn Poulsen, RN;
Sherin U. Devaskar was supported by the National Center for Advancing
Translational Sciences through UCLA CTSI Grant UL1TR000124
NR 21
TC 4
Z9 4
U1 0
U2 3
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0735-1631
EI 1098-8785
J9 AM J PERINAT
JI Am. J. Perinatol.
PD OCT
PY 2013
VL 30
IS 9
BP 770
EP 778
DI 10.1055/s-0032-1333410
PG 9
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 217WI
UT WOS:000324392900011
ER
PT J
AU Manasyan, A
Saleem, S
Koso-Thomas, M
Althabe, F
Pasha, O
Chomba, E
Goudar, SS
Patel, A
Esamai, F
Garces, A
Kodkany, B
Belizan, J
McClure, EM
Derman, RJ
Hibberd, P
Liechty, EA
Hambidge, KM
Carlo, WA
Buekens, P
Moore, J
Wright, LL
Goldenberg, RL
AF Manasyan, Albert
Saleem, Sarah
Koso-Thomas, Marion
Althabe, Fernando
Pasha, Omrana
Chomba, Elwyn
Goudar, Shivaprasad S.
Patel, Archana
Esamai, Fabian
Garces, Ana
Kodkany, Bhala
Belizan, Jose
McClure, Elizabeth M.
Derman, Richard J.
Hibberd, Patricia
Liechty, Edward A.
Hambidge, K. Michael
Carlo, Waldemar A.
Buekens, Pierre
Moore, Janet
Wright, Linda L.
Goldenberg, Robert L.
CA EmONC Trial Grp
TI Assessment of Obstetric and Neonatal Health Services in Developing
Country Health Facilities
SO AMERICAN JOURNAL OF PERINATOLOGY
LA English
DT Article
DE emergency obstetric and neonatal care; developing countries; perinatal
mortality
ID MATERNAL MORTALITY; CARE SERVICES; QUALITY
AB Objective To describe the staffing and availability of medical equipment and medications and the performance of procedures at health facilities providing maternal and neonatal care at African, Asian, and Latin American sites participating in a multicenter trial to improve emergency obstetric/neonatal care in communities with high maternal and perinatal mortality.
Study Design In 2009, prior to intervention, we surveyed 136 hospitals and 228 clinics in 7 sites in Africa, Asia, and Latin America regarding staffing, availability of equipment/medications, and procedures including cesarean section.
Results The coverage of physicians and nurses/midwives was poor in Africa and Latin America. In Africa, only 20% of hospitals had full-time physicians. Only 70% of hospitals in Africa and Asia had performed cesarean sections in the last 6 months. Oxygen was unavailable in 40% of African hospitals and 17% of Asian hospitals. Blood was unavailable in 80% of African and Asian hospitals.
Conclusions Assuming that adequate facility services are necessary to improve pregnancy outcomes, it is not surprising that maternal and perinatal mortality rates in the areas surveyed are high. The data presented emphasize that to reduce mortality in these areas, resources that result in improved staffing and sufficient equipment, supplies, and medication, along with training, are required.
C1 [Manasyan, Albert; Chomba, Elwyn; Carlo, Waldemar A.] Ctr Infect Dis Zambia, Lusaka, Zambia.
[Manasyan, Albert; Chomba, Elwyn] Univ Alabama Birmingham, Dept Pediat, Birmingham, AL USA.
[Saleem, Sarah; Pasha, Omrana] Aga Khan Univ, Dept Community Hlth Sci, Karachi, Pakistan.
[Koso-Thomas, Marion] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol & Pregnancy Branch, Bethesda, MD USA.
[Althabe, Fernando; Belizan, Jose] Inst Clin Effectiveness & Hlth Policy, Dept Mother & Child Hlth Res, Buenos Aires, DF, Argentina.
[Chomba, Elwyn] Univ Zambia, Dept Pediat, Lusaka, Zambia.
[Goudar, Shivaprasad S.] KLEs Jawaharlal Nehru Med Coll, Dept Physiol, Belgaum, India.
[Patel, Archana] Indira Gandhi Govt Med Coll, Clin Epidemiol Unit, Nagpur, Maharashtra, India.
[Esamai, Fabian] Moi Univ, Dept Pediat, Eldoret, Kenya.
[Garces, Ana] Francisco Marroquin Univ, IMSALUD, Guatemala City, Guatemala.
[Kodkany, Bhala] KLEs Jawaharlal Nehru Med Coll, Dept Obstet, Belgaum, India.
[McClure, Elizabeth M.; Moore, Janet] Res Triangle Inst, Durham, NC 27709 USA.
[Derman, Richard J.] Christiana Hlth Care, Dept Obstet, Newark, DE USA.
[Hibberd, Patricia] Indiana Univ, Dept Pediat, Indianapolis, IN 46204 USA.
[Liechty, Edward A.] Massachusetts Gen Hosp Children, Dept Pediat, Boston, MA USA.
[Hambidge, K. Michael] Univ Colorado, Dept Pediat, Denver, CO 80202 USA.
[Buekens, Pierre] Tulane Sch Publ Hlth & Trop Med, New Orleans, LA USA.
[Wright, Linda L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Ctr Res Mothers & Children, Bethesda, MD USA.
[Goldenberg, Robert L.] Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
RP McClure, EM (reprint author), Res Triangle Inst, Durham, NC 27709 USA.
EM mcclure@rti.org
OI GOUDAR, SHIVAPRASAD/0000-0002-8680-7053; Belizan,
Jose/0000-0002-8412-3010
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [U01 HD040477, U01 HD043464, U01 HD040657, U01 HD042372, U01
HD040607, U01 HD058322, U01 HD058326, U01 HD040636]
FX This study was funded by grants from the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (U01 HD040477, U01
HD043464, U01 HD040657, U01 HD042372, U01 HD040607, U01 HD058322, U01
HD058326, and U01 HD040636). The authors declare that they have no
conflicts of interest.
NR 16
TC 13
Z9 13
U1 4
U2 7
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0735-1631
EI 1098-8785
J9 AM J PERINAT
JI Am. J. Perinatol.
PD OCT
PY 2013
VL 30
IS 9
BP 787
EP 793
DI 10.1055/s-0032-1333409
PG 7
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 217WI
UT WOS:000324392900013
PM 23329566
ER
PT J
AU Abulaban, K
Rovin, BH
Nelson, S
Song, HJ
Kimmel, P
Kusek, J
Feldman, H
Ramachandran, V
Bennett, M
Ying, J
Brunner, H
AF Abulaban, Khalid
Rovin, Brad H.
Nelson, Shannen
Song, Huijuan
Kimmel, Paul
Kusek, John
Feldman, Harold
Ramachandran, Vasan
Bennett, Michael
Ying, Jun
Brunner, Hermine
TI Candidate Urinary Biomarkers May Predict The Future Development Of Renal
Functional Loss With Lupus Nephritis In Children and Adults
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Abulaban, Khalid; Bennett, Michael; Brunner, Hermine] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Rovin, Brad H.; Song, Huijuan] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Nelson, Shannen] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Kimmel, Paul; Kusek, John] NIDDK, NIH, Bethesda, MD USA.
[Feldman, Harold] Univ Penn, Philadelphia, PA 19104 USA.
[Ramachandran, Vasan] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Ying, Jun] Univ Cincinnati, Cincinnati, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 590
BP S254
EP S255
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202102
ER
PT J
AU Aggarwal, R
Ruperto, N
Erman, B
Feroz, S
Vencovsky, J
Huber, A
Oliveira, SK
Pistorio, A
Pilkington, C
Ravelli, A
Feldman, BM
Rockette, H
Miller, FW
Lachenbruch, PA
Rider, LG
AF Aggarwal, Rohit
Ruperto, Nicolino
Erman, Brian
Feroz, Saad
Vencovsky, Jiri
Huber, Adam
Oliveira, Sheila K.
Pistorio, Angela
Pilkington, Clarissa
Ravelli, Angelo
Feldman, Brian M.
Rockette, Howard
Miller, Frederick W.
Lachenbruch, Peter A.
Rider, Lisa G.
TI Good Inter-Rater Reliability Of Myositis Experts In Assessing Clinical
Improvement
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Aggarwal, Rohit; Rockette, Howard] Univ Pittsburgh, Pittsburgh, PA USA.
[Ruperto, Nicolino] IRCCS G Gaslini, PRINTO, Genoa, Italy.
[Erman, Brian] NIH, Bethesda, DC USA.
[Feroz, Saad; Miller, Frederick W.; Lachenbruch, Peter A.; Rider, Lisa G.] NIEHS, NIH, Bethesda, MD USA.
[Vencovsky, Jiri] Inst Rheumatol, Prague, Czech Republic.
[Huber, Adam] IWK Hlth Ctr, Halifax, NS, Canada.
[Oliveira, Sheila K.] Univ Fed Rio de Janeiro, IPPMG, Rio de Janeiro, Brazil.
[Pistorio, Angela] PRINTO, Genoa, Italy.
[Pilkington, Clarissa] Great Ormond St Hosp Sick Children, London, England.
[Ravelli, Angelo] Ist Giannina Gaslini, I-16148 Genoa, Italy.
[Feldman, Brian M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
RI Oliveira, Sheila/F-5213-2016
OI Oliveira, Sheila/0000-0002-2426-716X
NR 0
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2061
BP S879
EP S879
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205009
ER
PT J
AU Aranow, C
Cush, JJ
Bolster, MB
Striebich, CC
Dall'Era, M
Mackay, M
Olech, E
Frech, TM
Box, J
Keating, RM
Wasko, MCM
St Clair, EW
Kivitz, A
Diamond, B
Davidson, A
Spychala, M
Goldmuntz, EA
AF Aranow, Cynthia
Cush, John J.
Bolster, Marcy B.
Striebich, Christopher C.
Dall'Era, Maria
Mackay, Meggan
Olech, Ewa
Frech, Tracy M.
Box, J.
Keating, Richard M.
Wasko, Mary Chester M.
St Clair, E. William
Kivitz, Alan
Diamond, Betty
Davidson, Anne
Spychala, Meagan
Goldmuntz, Ellen A.
CA Autoimmunity Ctr Excellence
TI A Double-Blind Randomized Placebo-Controlled Trial Of Lovastatin in
Patients with Rheumatoid Arthritis.
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Aranow, Cynthia; Mackay, Meggan; Diamond, Betty; Davidson, Anne] Feinstein Inst Med Res, Manhasset, NY USA.
[Cush, John J.] Baylor Res Inst, Dallas, TX USA.
[Cush, John J.] Baylor Univ, Med Ctr, Dallas, TX USA.
[Bolster, Marcy B.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Striebich, Christopher C.] Univ Colorado Denver, Aurora, CO USA.
[Dall'Era, Maria] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Olech, Ewa] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Frech, Tracy M.] Univ Utah, Sch Med, Salt Lake City, UT USA.
[Box, J.] Carolina Bone & Joint, Charlotte, NC USA.
[Keating, Richard M.] Univ Chicago, Chicago, IL 60637 USA.
[Wasko, Mary Chester M.] Temple Univ, Sch Med, Pittsburgh, PA USA.
[St Clair, E. William] Duke Univ, Med Ctr, Durham, NC USA.
[Kivitz, Alan] Altoona Ctr Clin Res, Duncansville, PA USA.
[Spychala, Meagan] Rho Inc, Chapel Hill, NC USA.
[Goldmuntz, Ellen A.] NIAID, NIH, Bethesda, MD 20892 USA.
[Autoimmunity Ctr Excellence] NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2765
BP S1181
EP S1182
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206194
ER
PT J
AU Barron, KS
Ombrello, AK
Goldsmith, DP
Aksentijevich, I
Jones, A
Kastner, DL
AF Barron, Karyl S.
Ombrello, Amanda K.
Goldsmith, Donald P.
Aksentijevich, Ivona
Jones, Anne
Kastner, Daniel L.
TI Single MVK Mutation and Recurrent Fevers
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Barron, Karyl S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ombrello, Amanda K.; Aksentijevich, Ivona; Jones, Anne; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Goldsmith, Donald P.] St Christophers Hosp Children, Drexel Coll Med, Philadelphia, PA 19133 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2172
BP S926
EP S926
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205120
ER
PT J
AU Barron, KS
Ombrello, AK
Aksentijevich, I
Jones, A
Kastner, DL
AF Barron, Karyl S.
Ombrello, Amanda K.
Aksentijevich, Ivona
Jones, Anne
Kastner, Daniel L.
TI Clinical Variation In Children With Mutations In MEFV
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Barron, Karyl S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ombrello, Amanda K.; Aksentijevich, Ivona; Jones, Anne; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1781
BP S758
EP S758
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204240
ER
PT J
AU Cudrici, C
Bourla, A
Pelletier, M
Billingham, L
Ombrello, AK
Murphy, M
Kastner, DL
Siegel, RM
AF Cudrici, Cornelia
Bourla, Ariel
Pelletier, Martin
Billingham, Leah
Ombrello, Amanda K.
Murphy, Michael
Kastner, Daniel L.
Siegel, Richard M.
TI Oxidative Stress As a Disease Marker and Therapeutic Target In Patients
With Tumor Necrosis Factor Receptor Associated Periodic Fever Syndrome
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Cudrici, Cornelia; Bourla, Ariel; Pelletier, Martin; Billingham, Leah] Autoimmun Branch, Immunoregulat Sect, Bethesda, MD USA.
[Ombrello, Amanda K.; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Murphy, Michael] Med Res Council Mitochondria Biol Unit Cambridge, Cambridge, England.
[Siegel, Richard M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1160
BP S491
EP S492
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203144
ER
PT J
AU de Jesus, AA
Niemela, J
Liu, Y
Boyden, S
Aksentijevich, I
Kastner, DL
Fleisher, TA
Goldbach-Mansky, R
Deng, ZM
AF de Jesus, Adriana Almeida
Niemela, Julie
Liu, Yin
Boyden, Steven
Aksentijevich, Ivona
Kastner, Daniel L.
Fleisher, Thomas A.
Goldbach-Mansky, Raphaela
Deng, Zuoming
TI Whole Exome Sequencing In Pediatric Patients With Early Onset Rare
Immunodysregulatory Diseases That Present With Fever and Systemic
Inflammation
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [de Jesus, Adriana Almeida; Liu, Yin; Goldbach-Mansky, Raphaela; Deng, Zuoming] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Niemela, Julie; Fleisher, Thomas A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Boyden, Steven; Aksentijevich, Ivona; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2864
BP S1227
EP S1228
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206291
ER
PT J
AU Edwan, JH
Chae, JJ
Goldbach-Mansky, RT
Colbert, RA
AF Edwan, Jehad H.
Chae, Jae Jin
Goldbach-Mansky, Raphaela T.
Colbert, Robert A.
TI Evidence That STAT3 controls NLRP3 inflammasome-dependent Release Of
IL-1 beta and Pyronecrosis Through Regulation of mitochondrial activity
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Edwan, Jehad H.; Colbert, Robert A.] NIAMS, NIH, Bethesda, MD USA.
[Chae, Jae Jin] NHGRI, NIH, Bethesda, MD 20892 USA.
[Goldbach-Mansky, Raphaela T.] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2741
BP S1170
EP S1170
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206170
ER
PT J
AU Endres, T
Hofer, F
Goldbach-Mansky, RT
Hoffman, HM
Blank, N
Krause, K
Rietschel, C
Horneff, G
Lohse, P
Kuemmerle-Deschner, JB
AF Endres, Theresa
Hofer, Ferdinand
Goldbach-Mansky, Raphaela T.
Hoffman, Hal M.
Blank, Norbert
Krause, Karoline
Rietschel, Christoph
Horneff, Gerd
Lohse, Peter
Kuemmerle-Deschner, Jasmin B.
TI Low-Penetrance NLRP3-Variants
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Endres, Theresa; Hofer, Ferdinand; Kuemmerle-Deschner, Jasmin B.] Univ Tubingen Hosp, Tubingen, Germany.
[Goldbach-Mansky, Raphaela T.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Hoffman, Hal M.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Blank, Norbert] Heidelberg Univ, Heidelberg, Germany.
[Krause, Karoline] Charite, Dept Dermatol & Allergy, Allergie Ctr Charite, D-13353 Berlin, Germany.
[Rietschel, Christoph] Clementine Kinderhosp, Frankfurt, Germany.
[Horneff, Gerd] Asklepios Klin St Augustin, St Augustin, Germany.
[Lohse, Peter] Inst Lab Med & Humangenet, Singen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1213
BP S513
EP S513
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203197
ER
PT J
AU Fava, A
Cimbro, R
Rosen, A
Liu, QR
Wigley, FM
Boin, F
AF Fava, Andrea
Cimbro, Raffaello
Rosen, Antony
Liu, Qing-Rong
Wigley, Fredrick M.
Boin, Francesco
TI Topoisomerase-1 Specific T Cells Exhibit a Proinflammatory Th17
Phenotype and Are Associated With Interstitial Lung Disease In
Scleroderma
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Fava, Andrea; Cimbro, Raffaello; Rosen, Antony] Johns Hopkins Univ, Baltimore, MD USA.
[Liu, Qing-Rong] NIDA, NIH, Baltimore, MD USA.
[Wigley, Fredrick M.; Boin, Francesco] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 661
BP S283
EP S284
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202171
ER
PT J
AU Feroz, S
Ruperto, N
Vencovsky, J
Lachenbruch, PA
Erman, B
Huber, A
Feldman, BM
Lundberg, IE
Pistorio, A
Rockette, H
Miller, FW
Aggarwal, R
Rider, LG
Ravelli, A
Pilkington, C
Oliveira, SK
AF Feroz, Saad
Ruperto, Nicolino
Vencovsky, Jiri
Lachenbruch, Peter A.
Erman, Brian
Huber, Adam
Feldman, Brian M.
Lundberg, Ingrid E.
Pistorio, Angela
Rockette, Howard
Miller, Frederick W.
Aggarwal, Rohit
Rider, Lisa G.
Ravelli, Angelo
Pilkington, Clarissa
Oliveira, Sheila K.
CA ACR-EULAR Myositis Response
TI Developing International Consensus Definitions Of Improvement For Adult
and Juvenile Dermatomyositis and Polymyositis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Feroz, Saad; Lachenbruch, Peter A.; Miller, Frederick W.; Rider, Lisa G.; ACR-EULAR Myositis Response] NIEHS, NIH, Bethesda, MD USA.
[Ruperto, Nicolino] IRCCS G Gaslini, PRINTO, Genoa, Italy.
[Vencovsky, Jiri] Charles Univ Prague, Fac Med 1, Dept Clin & Expt Rheumatol, Inst Rheumatol, Prague, Czech Republic.
[Erman, Brian] SRA Int, Res Triangle Pk, NC USA.
[Huber, Adam] IWK Hlth Ctr, Halifax, NS, Canada.
[Feldman, Brian M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Lundberg, Ingrid E.] Karolinska Inst, Karolinska Univ Hosp Solna, Dept Med, Rheumatol Unit, Stockholm, Sweden.
[Pistorio, Angela] PRINTO, Genoa, Italy.
[Rockette, Howard; Aggarwal, Rohit] Univ Pittsburgh, Pittsburgh, PA USA.
[Ravelli, Angelo] Ist Giannina Gaslini, Paediat Rheumatol Int Trials Org PRINTO, I-16148 Genoa, Italy.
[Pilkington, Clarissa] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Oliveira, Sheila K.] Univ Fed Rio de Janeiro, IPPMG, Rio De Janeiro, Brazil.
RI Oliveira, Sheila/F-5213-2016
OI Oliveira, Sheila/0000-0002-2426-716X
NR 0
TC 1
Z9 1
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1981
BP S844
EP S845
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204439
ER
PT J
AU Gallo, A
Jang, SI
Danielides, S
Cotrim, AP
Alevizos, I
AF Gallo, Alessia
Jang, Shih-Ing
Danielides, Stamatina
Cotrim, Ana Paola
Alevizos, Ilias
TI Comparative Study Of The Transcriptome Of Minor Salivary Gland Of
Sjogren's Syndrome Patients Versus Healthy Controls Based On RNA-Seq
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Gallo, Alessia] NIDCR, Bethesda, MD USA.
[Jang, Shih-Ing; Danielides, Stamatina; Cotrim, Ana Paola] NIH, Bethesda, MD 20892 USA.
[Alevizos, Ilias] NIDCR NIH 10 1N110, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1490
BP S633
EP S633
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203468
ER
PT J
AU Gallo, A
Tandon, M
Danielides, S
Cotrim, AP
Alevizos, I
AF Gallo, Alessia
Tandon, Mayank
Danielides, Stamatina
Cotrim, Ana Paola
Alevizos, Ilias
TI Discovery and Validation Of Novel Micrornas In Minor Salivary Glands Of
Sjogren's Syndrome Patients
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Gallo, Alessia; Tandon, Mayank] NIDCR, Bethesda, MD USA.
[Danielides, Stamatina; Cotrim, Ana Paola] NIH, Bethesda, MD 20892 USA.
[Alevizos, Ilias] NIDCR NIH 10 1N110, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1491
BP S633
EP S633
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203469
ER
PT J
AU Gensler, LS
Ward, MM
Lee, M
Rahbar, M
Brown, MA
Reveille, JD
Weisman, MH
AF Gensler, Lianne S.
Ward, Michael M.
Lee, MinJae
Rahbar, Mohammad
Brown, Matthew A.
Reveille, John D.
Weisman, Michael H.
TI Cardiovascular Disease Is Associated With Worse Functional Outcomes In
Ankylosing Spondylitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Ward, Michael M.] NIAMS, NIH, Bethesda, MD USA.
[Lee, MinJae; Rahbar, Mohammad; Reveille, John D.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Brown, Matthew A.] Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
[Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2448
BP S1047
EP S1047
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205394
ER
PT J
AU Gensler, LS
Reveille, JD
Lee, M
Rahbar, M
Ardjomand-Hessabi, M
Brown, MA
Weisman, MH
Ward, MM
AF Gensler, Lianne S.
Reveille, John D.
Lee, MinJae
Rahbar, Mohammad
Ardjomand-Hessabi, Manouchehr
Brown, Matthew A.
Weisman, Michael H.
Ward, Michael M.
TI Regular Exercise Is Associated With Better Functional Outcomes In
Ankylosing Spondylitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Reveille, John D.; Lee, MinJae; Rahbar, Mohammad; Ardjomand-Hessabi, Manouchehr] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Brown, Matthew A.] Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
[Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Ward, Michael M.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1542
BP S654
EP S655
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204007
ER
PT J
AU Grayson, PC
Monach, PA
Cuthbertson, D
Carette, S
Hoffman, GS
Khalidi, NA
Koening, CL
Langford, CA
Maksimowicz-McKinnon, K
Pagnoux, C
Seo, P
Specks, U
Ytterberg, SR
Merkel, PA
AF Grayson, Peter C.
Monach, Paul A.
Cuthbertson, David
Carette, Simon
Hoffman, Gary S.
Khalidi, Nader A.
Koening, C. L.
Langford, Carol A.
Maksimowicz-McKinnon, Kathleen
Pagnoux, Christian
Seo, Philip
Specks, Ulrich
Ytterberg, Steven R.
Merkel, Peter A.
TI Clinical Value Of Commonly-Measured Laboratory Tests In Eosinophilic
Granulomatosis With Polyangiitis (Churg-Strauss)
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Grayson, Peter C.] NIH, Bethesda, MD 20892 USA.
[Monach, Paul A.] Boston Univ, Boston, MA 02215 USA.
[Cuthbertson, David] Univ S Florida, Tampa, FL USA.
[Carette, Simon] UHN MSH, Toronto, ON, Canada.
[Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Khalidi, Nader A.] McMaster Univ, Hamilton, ON, Canada.
[Koening, C. L.] Salt Lake City Vet Adm, Salt Lake City, UT USA.
[Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Maksimowicz-McKinnon, Kathleen] Henry Ford Hosp, Detroit, MI 48202 USA.
[Pagnoux, Christian] Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada.
[Seo, Philip] Johns Hopkins Vasculitis Ctr, Baltimore, MD USA.
[Specks, Ulrich; Ytterberg, Steven R.] Mayo Clin, Rochester, MN USA.
[Merkel, Peter A.] Univ Penn, Philadelphia, PA 19104 USA.
NR 0
TC 1
Z9 1
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 756
BP S319
EP S319
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202261
ER
PT J
AU Gupta, S
Tatouli, IP
Rosen, LB
Hasni, SA
Siegel, RM
Holland, SM
Moutsopopoulos, HM
Browne, SK
AF Gupta, Sarthak
Tatouli, Ioanna P.
Rosen, Lindsey B.
Hasni, Sarfaraz A.
Siegel, Richard M.
Holland, Steven M.
Moutsopopoulos, Haralampos M.
Browne, Sarah K.
TI Rheumatoid Arthritis, Sjogren's Syndrome and Systemic Lupus
Erythematosus Patients Have a Distinct Spectrum Of Serum Anticytokine
Autoantibodies
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Gupta, Sarthak; Rosen, Lindsey B.; Holland, Steven M.; Browne, Sarah K.] NIAID, NIH, Bethesda, MD 20892 USA.
[Tatouli, Ioanna P.; Moutsopopoulos, Haralampos M.] Natl Univ Athens, Sch Med, Athens, Greece.
[Hasni, Sarfaraz A.; Siegel, Richard M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1844
BP S787
EP S787
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204303
ER
PT J
AU Hasni, SA
Illei, GG
Nikolov, NP
Hakim, F
Leitman, S
Balow, JE
Austin, HA
Gea-Banacloche, J
Oh, U
Muraro, P
Sportes, C
Lipsky, PE
Gress, R
Pavletic, S
Grammer, A
AF Hasni, Sarfaraz A.
Illei, Gabor G.
Nikolov, Nikolay P.
Hakim, Francis
Leitman, Susan
Balow, James E.
Austin, Howard A.
Gea-Banacloche, Juan
Oh, Unsong
Muraro, Paulo
Sportes, Claude
Lipsky, Peter E.
Gress, Ronald
Pavletic, Steve
Grammer, Amrie
TI Lymphoablation Including B Cell Depletion and Autologous Hematopoietic
Stem Cell Transplantation Leads To Long Remissions In
Treatment-Resistant Systemic Lupus Erythematosus Patients
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Hasni, Sarfaraz A.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Illei, Gabor G.; Nikolov, Nikolay P.] NIDCR, NIH, Bethesda, MD USA.
[Hakim, Francis; Leitman, Susan; Gea-Banacloche, Juan; Sportes, Claude; Gress, Ronald; Pavletic, Steve] NCI, NIH, Bethesda, MD 20892 USA.
[Balow, James E.] NIH, Bethesda, MD 20892 USA.
[Austin, Howard A.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Oh, Unsong; Muraro, Paulo] NINDS, NIH, Bethesda, MD 20892 USA.
[Lipsky, Peter E.; Grammer, Amrie] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1610
BP S683
EP S684
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204074
ER
PT J
AU Isenberg, DA
Wofsy, D
Li, Y
Licu, D
Wax, SD
Gordon, C
Rossi, CP
AF Isenberg, David A.
Wofsy, David
Li, Yong
Licu, Daiana
Wax, Stephen D.
Gordon, Caroline
Rossi, Claudia Pena
TI Pharmacodynamics and Predictive Biomarkers In Patients Treated With
Atacicept: Data From The APRIL-SLE Trial
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Isenberg, David A.] UCL, London, England.
[Wofsy, David] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wofsy, David] NIAID Autoimmun Ctr Excellence, San Francisco, CA USA.
[Li, Yong; Wax, Stephen D.] EMD Serono, Rockland, MA USA.
[Licu, Daiana; Rossi, Claudia Pena] Merck Serono SA, Geneva, Switzerland.
[Gordon, Caroline] Univ Birmingham, Birmingham, W Midlands, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2551
BP S1089
EP S1089
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205496
ER
PT J
AU Kim, H
de Jesus, AA
Liu, Y
Huang, Y
Montealegre, G
Chapelle, D
Plass, N
Tsai, WX
Gadina, M
Rider, LG
Vanderver, A
Goldbach-Mansky, R
AF Kim, Hanna
de Jesus, Adriana Almeida
Liu, Yin
Huang, Yan
Montealegre, Gina
Chapelle, Dawn
Plass, Nicole
Tsai, Wanxia
Gadina, Massimo
Rider, Lisa G.
Vanderver, Adeline
Goldbach-Mansky, Raphaela
TI Clinical and Immunologic Description Of Pediatric Conditions With
Interferon-Regulated Gene Signatures (Chronic Atypical Neutrophilic
Dermatosis Lipodystrophy Elevated Tempature, Aicardi Goutieres Syndrome,
Juvenile Dermatomyositis, Juvenile Systemic Lupus Erythematosus)
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Kim, Hanna; Huang, Yan; Plass, Nicole; Goldbach-Mansky, Raphaela] NIAMSD, NIH, Bethesda, MD 20892 USA.
[de Jesus, Adriana Almeida; Liu, Yin; Montealegre, Gina; Chapelle, Dawn; Tsai, Wanxia] NIAMS, NIH, Bethesda, MD USA.
[Gadina, Massimo] NIAMSD, Bethesda, MD 20892 USA.
[Rider, Lisa G.] NIEHS, NIH, Bethesda, MD USA.
[Vanderver, Adeline] Childrens Natl Med Ctr, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2190
BP S933
EP S934
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205138
ER
PT J
AU Kwon, G
Yang, E
Sikora, KA
Srinivasalu, H
Layh-Schmitt, G
Colbert, RA
AF Kwon, Grace
Yang, Eva
Sikora, Keith A.
Srinivasalu, Hemalatha
Layh-Schmitt, Gerlinde
Colbert, Robert A.
TI Evidence For Enhanced Induction Of Unfolded Protein Response Target
Genes In Peripheral Blood Mononuclear Cells From Spondyloarthritis
Patients
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Kwon, Grace; Yang, Eva; Sikora, Keith A.; Srinivasalu, Hemalatha; Layh-Schmitt, Gerlinde; Colbert, Robert A.] NIAMS NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 525
BP S230
EP S231
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202038
ER
PT J
AU Mamyrova, G
Rider, LG
Jones, O
Ehrlich, A
Pachman, LM
Nickeson, R
Criscione-Schreiber, LG
Miller, FW
Jung, LK
Katz, JD
AF Mamyrova, Gulnara
Rider, Lisa G.
Jones, Olcay
Ehrlich, Alison
Pachman, Lauren M.
Nickeson, Robert
Criscione-Schreiber, Lisa G.
Miller, Frederick W.
Jung, Lawrence K.
Katz, James D.
TI Environmental Factors Associated With Disease Flare In Juvenile and
Adult Dermatomyositis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Mamyrova, Gulnara; Ehrlich, Alison; Katz, James D.] George Washington Univ, Washington, DC USA.
[Rider, Lisa G.; Miller, Frederick W.] NIEHS, NIH, Bethesda, MD USA.
[Jones, Olcay] Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
[Pachman, Lauren M.] Northwestern Univ, Feinberg Sch Med, Div Pediat Rheumatol, Chicago, IL 60611 USA.
[Nickeson, Robert] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Criscione-Schreiber, Lisa G.] Duke Univ, Sch Med, Durham, NC USA.
[Jung, Lawrence K.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2083
BP S888
EP S888
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205031
ER
PT J
AU Miloslavsky, E
Specks, U
Merkel, PA
Seo, P
Spiera, RF
Langford, CA
Hoffman, GS
Kallenberg, CGM
St Clair, EW
Tchao, N
Ding, L
Ikle, D
Jepson, B
Brunetta, P
Stone, JH
AF Miloslavsky, Eli
Specks, Ulrich
Merkel, Peter A.
Seo, Philip
Spiera, Robert F.
Langford, Carol A.
Hoffman, Gary S.
Kallenberg, Cees G. M.
St Clair, E. William
Tchao, Nadia
Ding, Linna
Ikle, David
Jepson, Brett
Brunetta, Paul
Stone, John H.
TI Retreatment With Rituximab In The Rituximab In ANCA-Associated
Vasculitis (RAVE) Trial
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Miloslavsky, Eli] Massachusetts Gen Hopsital, Boston, MA USA.
[Specks, Ulrich] Mayo Clin, Rochester, MN USA.
[Merkel, Peter A.] Univ Penn, Philadelphia, PA 19104 USA.
[Merkel, Peter A.] VA Med Ctr, Philadelphia, PA USA.
[Seo, Philip] Johns Hopkins Vasculitis Ctr, Baltimore, MD USA.
[Spiera, Robert F.] Hosp Special Surg, New York, NY 10021 USA.
[Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Kallenberg, Cees G. M.] Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[St Clair, E. William] Duke Unvers Med Ctr, Durham, NC USA.
[Tchao, Nadia] Immune Tolerance Network, Bethesda, MD USA.
[Ding, Linna] NIAID, Bethesda, MD 20892 USA.
[Ikle, David; Jepson, Brett] Rho, Chapel Hill, NC USA.
[Brunetta, Paul] Genentech Inc, So San Francisco, CA USA.
[Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2782
BP S1190
EP S1190
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206211
ER
PT J
AU Miloslavsky, E
Specks, U
Merkel, PA
Seo, P
Spiera, RF
Langford, CA
Hoffman, GS
Kallenberg, CGM
St Clair, EW
Tchao, N
Ding, LN
Ikle, D
Jepson, B
Brunetta, P
Stone, JH
AF Miloslavsky, Eli
Specks, Ulrich
Merkel, Peter A.
Seo, Philip
Spiera, Robert F.
Langford, Carol A.
Hoffman, Gary S.
Kallenberg, Cees G. M.
St Clair, E. William
Tchao, Nadia
Ding, Linna
Ikle, David
Jepson, Brett
Brunetta, Paul
Stone, John H.
TI Efficacy Of Glucocorticoids To Treat Limited Flares In ANCA-Associated
Vasculitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Miloslavsky, Eli] Massachusetts Gen Hopsital, Boston, MA USA.
[Specks, Ulrich] Mayo Clin, Rochester, MN USA.
[Merkel, Peter A.] Univ Penn, Philadelphia, PA 19104 USA.
[Seo, Philip] Johns Hopkins Vasculitis Ctr, Baltimore, MD USA.
[Spiera, Robert F.] Hosp Special Surg, New York, NY 10021 USA.
[Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Kallenberg, Cees G. M.] Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[St Clair, E. William] Duke Univ, Med Ctr, Durham, NC USA.
[Tchao, Nadia] Immune Tolerance Network, Bethesda, MD USA.
[Ding, Linna] NIAID, Bethesda, MD 20892 USA.
[Ikle, David; Jepson, Brett] Rho, Chapel Hill, NC USA.
[Brunetta, Paul] Genentech Inc, So San Francisco, CA USA.
[Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 747
BP S315
EP S316
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202252
ER
PT J
AU Miloslavsky, E
Specks, U
Merkel, PA
Seo, P
Spiera, RF
Langford, CA
Hoffman, GS
Kallenberg, CGM
St Clair, EW
Tchao, N
Ding, LN
Ikle, D
Jepson, B
Brunetta, P
Stone, JH
AF Miloslavsky, Eli
Specks, Ulrich
Merkel, Peter A.
Seo, Philip
Spiera, Robert F.
Langford, Carol A.
Hoffman, Gary S.
Kallenberg, Cees G. M.
St Clair, E. William
Tchao, Nadia
Ding, Linna
Ikle, David
Jepson, Brett
Brunetta, Paul
Stone, John H.
TI Safety Of Remission Induction With Rituximab Versus Cyclosphosphamide In
Patients 65 and Older With Severe ANCA-Associated Vasculitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Miloslavsky, Eli; Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Specks, Ulrich] Mayo Clin, Rochester, MN USA.
[Merkel, Peter A.] Univ Penn, Philadelphia, PA 19104 USA.
[Merkel, Peter A.] VA Med Ctr, Philadelphia, PA USA.
[Seo, Philip] Johns Hopkins Vasculitis Ctr, Baltimore, MD USA.
[Spiera, Robert F.] Hosp Special Surg, New York, NY 10021 USA.
[Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Kallenberg, Cees G. M.] Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[St Clair, E. William] Duke Univ, Med Ctr, Durham, NC USA.
[Tchao, Nadia] Immune Tolerance Network, Bethesda, MD USA.
[Ding, Linna] NIAID, Bethesda, MD 20892 USA.
[Ikle, David; Jepson, Brett] Rho, Chapel Hill, NC USA.
[Brunetta, Paul] Genentech Inc, So San Francisco, CA USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 742
BP S313
EP S313
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202247
ER
PT J
AU Ogdie, A
Yu, YD
Haynes, K
Maliha, S
Love, T
Troxel, A
Hennessy, S
Margolis, D
Kimmel, S
Mehta, NN
Choi, HK
Gelfand, J
AF Ogdie, Alexis
Yu, Yiding
Haynes, Kevin
Maliha, Samantha
Love, Thorvardur
Troxel, Andrea
Hennessy, Sean
Margolis, David
Kimmel, Stephen
Mehta, Nehal N.
Choi, Hyon K.
Gelfand, Joel
TI Risk Of Cardiovascular Events In Patients With Psoriatic Arthritis,
Psoriasis, and Rheumatoid Arthritis: A General Population-Based Cohort
Study
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Ogdie, Alexis; Haynes, Kevin; Maliha, Samantha; Troxel, Andrea; Hennessy, Sean; Margolis, David; Kimmel, Stephen; Gelfand, Joel] Univ Penn, Philadelphia, PA 19104 USA.
[Yu, Yiding] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Love, Thorvardur] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Mehta, Nehal N.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Choi, Hyon K.] Boston Univ, Sch Med, Boston, MA 02118 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 303
BP S128
EP S128
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359201302
ER
PT J
AU Ombrello, AK
Barron, KS
Hoffmann, PM
Jones, A
Stone, D
Kastner, DL
AF Ombrello, Amanda K.
Barron, Karyl S.
Hoffmann, Patrycja M.
Jones, Anne
Stone, Deborah
Kastner, Daniel L.
TI An Escalating Dose Of Anakinra In Patients With Autoinflammatory Disease
Is a Safe and Reasonable Therapeutic Option
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Ombrello, Amanda K.; Hoffmann, Patrycja M.; Jones, Anne; Stone, Deborah; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Barron, Karyl S.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1203
BP S509
EP S509
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203187
ER
PT J
AU Ombrello, MJ
Remmers, EF
Tachmazidou, I
Grom, AA
Foll, D
Martini, A
Gattorno, M
Ozen, S
Prahalad, S
Bohnsack, JF
Ilowite, NT
Mellins, ED
Russo, RAG
Len, CA
Oliveira, SK
Yeung, RSM
Wedderburn, LR
Anton, J
Langefeld, CD
Thompson, SD
Zeggini, E
Thomson, W
Kastner, DL
Woo, P
AF Ombrello, Michael J.
Remmers, Elaine F.
Tachmazidou, Ioanna
Grom, Alexei A.
Foell, Dirk
Martini, Alberto
Gattorno, Marco
Ozen, Seza
Prahalad, Sampath
Bohnsack, John F.
Ilowite, Norman T.
Mellins, Elizabeth D.
Russo, Ricardo A. G.
Len, Claudio A.
Oliveira, Sheila K.
Yeung, Rae S. M.
Wedderburn, Lucy R.
Anton, Jordi
Langefeld, Carl D.
Thompson, Susan D.
Zeggini, Eleftheria
Thomson, Wendy
Kastner, Daniel L.
Woo, Patricia
CA Int Childhood Arthrit Genetics
TI Genome Wide Association Meta-Analysis Implicates HLA-DRB1, The
BTNL2/HLA-DRA region, and a Novel Susceptibility Locus On Chromosome 1
In Systemic Juvenile Idiopathic Arthritis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Ombrello, Michael J.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Remmers, Elaine F.; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Tachmazidou, Ioanna; Zeggini, Eleftheria] Wellcome Trust Sanger Inst, Cambridge, England.
[Grom, Alexei A.; Thompson, Susan D.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Foell, Dirk] Univ Munster, D-48149 Munster, Germany.
[Martini, Alberto] Ist Giannina Gaslini, I-16148 Genoa, Italy.
[Gattorno, Marco] G Gaslini Inst Children, Genoa, Italy.
[Ozen, Seza] Hacettepe Univ, Ankara, Turkey.
[Prahalad, Sampath] Emory Childrens Ctr, Atlanta, GA USA.
[Bohnsack, John F.] Univ Utah, Salt Lake City, UT USA.
[Ilowite, Norman T.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Mellins, Elizabeth D.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Russo, Ricardo A. G.] Hosp Pediat Garrahan, Buenos Aires, DF, Argentina.
[Len, Claudio A.] Univ Fed Sao Paulo UNIFESP, Sao Paulo, Brazil.
[Oliveira, Sheila K.] Univ Fed Rio de Janeiro, IPPMG, Rio De Janeiro, Brazil.
[Yeung, Rae S. M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Yeung, Rae S. M.] Univ Toronto, Toronto, ON, Canada.
[Wedderburn, Lucy R.] UCL, Great Ormond St Hosp Children, Arthrit Res UK Ctr Adolescent Rheumatol, London, England.
[Wedderburn, Lucy R.] UCL, UCLH, London, England.
[Anton, Jordi] Hosp St Joan de Deu, Barcelona, Spain.
[Langefeld, Carl D.] Wake Forest Sch Med, Winston Salem, NC USA.
[Thomson, Wendy] Univ Manchester, Manchester Acad Hlth Sci Ctr, Inst Inflammat & Repair, Arthrit Res UK Epidemiol Unit, Manchester, Lancs, England.
[Woo, Patricia] UCL, London, England.
[Int Childhood Arthrit Genetics] INCHARGE, London, England.
RI Oliveira, Sheila/F-5213-2016
OI Oliveira, Sheila/0000-0002-2426-716X
NR 0
TC 2
Z9 2
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2198
BP S937
EP S937
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205146
ER
PT J
AU Ombrello, MJ
Kirino, Y
de Bakker, P
Gul, A
Remmers, EF
Kastner, DL
AF Ombrello, Michael J.
Kirino, Yohei
de Bakker, Paul
Gul, Ahmet
Remmers, Elaine F.
Kastner, Daniel L.
TI Major Histocompatibility Complex Class I Molecules Contribute To
Behcet's Disease Risk Through Both Innate and Adaptive Immune
Interactions
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Ombrello, Michael J.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Kirino, Yohei; Remmers, Elaine F.; Kastner, Daniel L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[de Bakker, Paul] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Gul, Ahmet] Istanbul Univ, Istanbul Fac Med, Istanbul, Turkey.
RI de Bakker, Paul/B-8730-2009; zhang, jun/D-7782-2015
OI de Bakker, Paul/0000-0001-7735-7858;
NR 0
TC 0
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1879
BP S800
EP S801
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204338
ER
PT J
AU Parks, CG
D'Aloisio, A
Sandler, D
AF Parks, Christine G.
D'Aloisio, Aimee
Sandler, Dale
TI Perinatal and Early Life Risk Factors For Systemic Lupus Erythematosus
In a National Cohort Of Women
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Parks, Christine G.; D'Aloisio, Aimee; Sandler, Dale] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1059
BP S452
EP S452
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203045
ER
PT J
AU Patwardhan, A
Lintner, K
Rider, LG
Miller, FW
O'Hanlon, T
Wu, YL
Zhou, B
Wang, HY
Newsom, D
White, P
Spencer, CH
Yu, CY
AF Patwardhan, Anjali
Lintner, Katherine
Rider, Lisa G.
Miller, Frederick W.
O'Hanlon, Terrance
Wu, Yee Ling
Zhou, Bi
Wang, Huanyu
Newsom, David
White, Peter
Spencer, Charles H.
Yu, C. Yung
TI Copy Number Variations Of Complement C4A and C4B Genes Are Genetic Risk
Factor and Disease Modification Factor, Respectively, For Juvenile
Dermatomyositis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Patwardhan, Anjali; Lintner, Katherine; Wu, Yee Ling; Zhou, Bi; Wang, Huanyu; Newsom, David; White, Peter; Yu, C. Yung] Nationwide Childrens Hosp, Res Inst, Columbus, OH USA.
[Patwardhan, Anjali; Lintner, Katherine; Wu, Yee Ling; Zhou, Bi; Wang, Huanyu; Newsom, David; White, Peter; Yu, C. Yung] Ohio State Univ, Columbus, OH 43210 USA.
[Rider, Lisa G.; Miller, Frederick W.; O'Hanlon, Terrance] NIEHS, NIH, Bethesda, MD USA.
[Spencer, Charles H.] Nationwide Childrens Hosp, Columbus, OH USA.
RI Yu, Chack-Yung/E-4360-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2863
BP S1227
EP S1227
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206290
ER
PT J
AU Perez-Aso, M
Fernandez, P
Mediero, A
Chan, ESL
Cronstein, BN
AF Perez-Aso, Miguel
Fernandez, Patricia
Mediero, Aranzazu
Chan, Edwin S. L.
Cronstein, Bruce N.
TI Adenosine 2A Receptor Promotes Collagen Production By Human Fibroblasts
Via Smad2/3-Independent Pathways Involving Cyclic AMP and AKT
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Perez-Aso, Miguel; Mediero, Aranzazu; Chan, Edwin S. L.] NYU, Sch Med, New York, NY USA.
[Fernandez, Patricia] NCI, NIH, Bethesda, MD 20892 USA.
[Cronstein, Bruce N.] NYU, Sch Med, Div Rheumatol, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1851
BP S790
EP S790
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204310
ER
PT J
AU Reveille, JD
Ward, MM
Lee, M
Rahbar, M
Ardjomand-Hessabi, M
Diekman, LA
Brown, MA
Gensler, LS
Weisman, MH
AF Reveille, John D.
Ward, Michael M.
Lee, MinJae
Rahbar, Mohammad
Ardjomand-Hessabi, Manouchehr
Diekman, Laura A.
Brown, Matthew A.
Gensler, Lianne S.
Weisman, Michael H.
TI Opiate Use In Patients With Ankylosing Spondylitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Reveille, John D.; Lee, MinJae; Rahbar, Mohammad; Ardjomand-Hessabi, Manouchehr; Diekman, Laura A.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Ward, Michael M.] NIAMS, NIH, Bethesda, MD USA.
[Brown, Matthew A.] Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
[Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2446
BP S1046
EP S1046
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205392
ER
PT J
AU Ringold, S
Weiss, PF
Colbert, RA
DeWitt, EM
Lee, TC
Onel, K
Prahalad, S
Schneider, R
Shenoi, S
Vehe, RK
Kimura, Y
AF Ringold, Sarah
Weiss, Pamela F.
Colbert, Robert A.
DeWitt, Esi Morgan
Lee, Tzielan C.
Onel, Karen
Prahalad, Sampath
Schneider, Rayfel
Shenoi, Susan
Vehe, Richard K.
Kimura, Yukiko
TI Childhood Arthritis and Rheumatology Research Alliance (CARRA)
Standardized Consensus Treatment Plans for New Onset Polyarticular
Juvenile Idiopathic Arthritis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Ringold, Sarah] Seattle Childrens Hosp, Seattle, WA USA.
[Weiss, Pamela F.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Colbert, Robert A.] NIAMS, NIH, Bethesda, MD USA.
[DeWitt, Esi Morgan] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Lee, Tzielan C.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Onel, Karen] PRCSG, Cincinnati, OH USA.
[Prahalad, Sampath] Emory Childrens Ctr, Atlanta, GA USA.
[Schneider, Rayfel] PRCSG, Cincinnati, OH USA.
[Shenoi, Susan] Univ Washington, Seattle Childrens Hosp, Seattle, WA 98195 USA.
[Vehe, Richard K.] Univ Minnesota, Minneapolis, MN USA.
[Kimura, Yukiko] Hackensack Univ, Med Ctr, Joseph M Sanzari Childrens Hosp, Hackensack, NJ USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 277
BP S116
EP S116
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359201276
ER
PT J
AU Sanchez, GAM
Reinhardt, AL
Brogan, P
Berkun, Y
Brown, D
Chira, P
Gao, L
Chapelle, DC
Plass, N
Kim, H
Davis, M
de Jesus, AA
Liu, Y
Huang, Y
Hadigan, C
Heller, T
Zlotogorski, Z
O'Shea, JJ
Lee, CC
Hill, SC
Rother, K
Gadina, M
Goldbach-Mansky, RT
AF Sanchez, Gina A. Montealegre
Reinhardt, Adam L.
Brogan, Paul
Berkun, Yackov
Brown, Diane
Chira, Peter
Gao, Ling
Chapelle, Dawn C.
Plass, Nicole
Kim, Hanna
Davis, Michael
de Jesus, Adriana Almeida
Liu, Yin
Huang, Yan
Hadigan, Colleen
Heller, Theo
Zlotogorski, Zlotogorski
O'Shea, John J.
Lee, Chyi-chia
Hill, Suvimol C.
Rother, Kristina
Gadina, Massimo
Goldbach-Mansky, Raphaela T.
TI Chronic Atypical Neutrophilic Dermatosis With Lipodystrophy and Elevated
Temperatures (CANDLE): Clinical Characterization and Initial Response To
Janus Kinase Inhibition With Baricitinib
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Sanchez, Gina A. Montealegre; Chapelle, Dawn C.; Plass, Nicole; Kim, Hanna; Davis, Michael; de Jesus, Adriana Almeida; Liu, Yin; Huang, Yan; O'Shea, John J.; Gadina, Massimo; Goldbach-Mansky, Raphaela T.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Reinhardt, Adam L.] Childrens Hosp Omaha UNMC, Omaha, NE USA.
[Brogan, Paul] Ist Giannina Gaslini, Paediat Rheumatol Int Trials Org PRINTO, I-16148 Genoa, Italy.
[Berkun, Yackov] Hadassah Med Ctr, IL-91120 Jerusalem, Israel.
[Brown, Diane] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Chira, Peter] Indiana Univ Sch Med, Riley Hosp Children, Indianapolis, IN 46202 USA.
[Gao, Ling] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Hadigan, Colleen] NIAID, NIH, Bethesda, MD 20892 USA.
[Heller, Theo; Rother, Kristina] NIDDK, NIH, Bethesda, MD USA.
[Zlotogorski, Zlotogorski] Hadassah Hebrew Univ Med Ctr, Dept Dermatol, Jerusalem, Israel.
[Lee, Chyi-chia] NCI, NIH, Bethesda, MD 20892 USA.
[Hill, Suvimol C.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1782
BP S758
EP S759
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204241
ER
PT J
AU Saxena, P
Loeser, RF
Pathmasiri, W
Sumner, S
Beavers, D
Hunter, DJ
Messier, SP
AF Saxena, Puja
Loeser, Richard F.
Pathmasiri, Wimal
Sumner, Susan
Beavers, Daniel
Hunter, David J.
Messier, Stephen P.
TI Metabolomics For The Identification Of Urinary Biomarkers In Knee
Osteoarthritis Progression.
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Saxena, Puja; Beavers, Daniel] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Loeser, Richard F.] Wake Forest Sch Med, Winston Salem, NC USA.
[Pathmasiri, Wimal; Sumner, Susan] NIH Eastern Reg Comprehens Metabol Resource Core, Res Triangle Pk, NC USA.
[Hunter, David J.] Univ Sydney, Sydney, NSW 2006, Australia.
[Messier, Stephen P.] Wake Forest Univ, Winston Salem, NC 27109 USA.
RI Beavers, Daniel/G-5338-2016
NR 0
TC 0
Z9 0
U1 2
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2757
BP S1177
EP S1177
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206186
ER
PT J
AU Schiffenbauer, A
Turkbey, E
Rider, LG
Hill, S
Whitt, IZ
Liu, ST
Bluemke, DA
Miller, FW
AF Schiffenbauer, Adam
Turkbey, Evrim
Rider, Lisa G.
Hill, Suvimol
Whitt, Irene Z.
Liu, Songtao
Bluemke, David A.
Miller, Frederick W.
TI Comparison Of Whole Body Versus Targeted Magnetic Resonance Imaging For
Assessing Disease Activity and Damage In Idiopathic Inflammatory
Myopathies.
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Schiffenbauer, Adam; Rider, Lisa G.; Miller, Frederick W.] NIEHS, NIH, Bethesda, MD USA.
[Turkbey, Evrim; Hill, Suvimol; Liu, Songtao; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Whitt, Irene Z.] Duke, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 222
BP S90
EP S91
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359201221
ER
PT J
AU Schwartz, DM
Wang, RS
Barron, KS
Kastner, DL
Ombrello, AK
AF Schwartz, Daniella M.
Wang, Runsheng
Barron, Karyl S.
Kastner, Daniel L.
Ombrello, Amanda K.
TI The Interleukin-1 Receptor Antagonist Anakinra Is Effective In The
Treatment Of Undifferentiated Periodic Fever Syndromes
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Schwartz, Daniella M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Wang, Runsheng] NIAMS, NIH, Rheumatol Fellowship & Training Branch, Bethesda, MD USA.
[Barron, Karyl S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Kastner, Daniel L.; Ombrello, Amanda K.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2173
BP S926
EP S927
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205121
ER
PT J
AU Shahzad, A
Jafri, F
Rizvi, B
Zhao, XC
Waldman, M
Hasni, SA
AF Shahzad, Ali
Jafri, Farheen
Rizvi, Bisharah
Zhao, Xiongce
Waldman, Meryl
Hasni, Sarfaraz A.
TI Cyclophosphamide and Rituximab Combination Treatment For Severe Systemic
Lupus erythematosus is Effective and Well Tolerated
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Shahzad, Ali] NIAMS, NIH, Bethesda, MD USA.
[Jafri, Farheen; Rizvi, Bisharah] R Res, Hamilton, NJ USA.
[Zhao, Xiongce; Waldman, Meryl] NIDDK, NIH, Bethesda, MD USA.
[Hasni, Sarfaraz A.] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1559
BP S662
EP S662
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204024
ER
PT J
AU Sharif, R
Parekh, TM
Gensler, LS
Lee, M
Rahbar, M
Diekman, LA
Weisman, MH
Ward, MM
Assassi, S
Reveille, JD
AF Sharif, Roozbeh
Parekh, Trisha M.
Gensler, Lianne S.
Lee, MinJae
Rahbar, Mohammad
Diekman, Laura A.
Weisman, Michael H.
Ward, Michael M.
Assassi, Shervin
Reveille, John D.
TI Predictors Of Spinal Mobility Progression In A Multi-ethnic Cohort Of
Patients With Ankylosing Spondylitis.
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Sharif, Roozbeh; Parekh, Trisha M.] Univ Texas Med Branch, Galveston, TX 77555 USA.
[Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Lee, MinJae; Rahbar, Mohammad; Diekman, Laura A.; Assassi, Shervin; Reveille, John D.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Ward, Michael M.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2840
BP S1217
EP S1217
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206268
ER
PT J
AU Sibley, C
Hatemi, G
Yazici, Y
Liu, Y
Brooks, S
Yazici, H
Goldbach-Mansky, R
AF Sibley, Cailin
Hatemi, Gulen
Yazici, Yusuf
Liu, Yin
Brooks, Steve
Yazici, Hasan
Goldbach-Mansky, Raphaela
TI Systems Approach To The Study Of the Microbiome and Inflammatory
Pathways In Oral Ulcer Tissue From Patients With Active Behcet's
Syndrome (BS)
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Sibley, Cailin; Liu, Yin; Brooks, Steve] NIAMS, NIH, Bethesda, MD USA.
[Hatemi, Gulen] Istanbul Univ, Cerrahpasa Med Fac, Istanbul, Turkey.
[Yazici, Yusuf] NYU, Hosp Joint Dis, New York, NY USA.
[Yazici, Yusuf] NYU, Sch Med, New York, NY USA.
[Yazici, Hasan] Istanbul Univ, Cerrahpasa Med Fac, Istanbul, Turkey.
[Goldbach-Mansky, Raphaela] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 1
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1165
BP S493
EP S493
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203149
ER
PT J
AU Takeuchi, M
Mizuki, N
Meguro, A
Ombrello, MJ
Satorius, C
Kirino, Y
Kawagoe, T
Ustek, D
Tugal-tutkun, I
Seyahi, E
Ozyazgan, Y
Ohno, S
Ueda, A
Ishigatsubo, Y
Gul, A
Kastner, DL
Remmers, E
AF Takeuchi, Masaki
Mizuki, Nobuhisa
Meguro, Akira
Ombrello, Michael J.
Satorius, Colleen
Kirino, Yohei
Kawagoe, Tatsukata
Ustek, Duran
Tugal-tutkun, Ilknur
Seyahi, Emire
Ozyazgan, Yilmaz
Ohno, Shigeaki
Ueda, Atsuhisa
Ishigatsubo, Yoshiaki
Gul, Ahmet
Kastner, Daniel L.
Remmers, Elaine
TI High Density Genotyping Of Immune-Related Disease Genes Identifies 7 New
Susceptibility Loci For Behcets Disease
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Takeuchi, Masaki; Satorius, Colleen; Kastner, Daniel L.; Remmers, Elaine] NHGRI, NIH, Bethesda, MD 20892 USA.
[Mizuki, Nobuhisa; Meguro, Akira; Kirino, Yohei; Kawagoe, Tatsukata; Ueda, Atsuhisa; Ishigatsubo, Yoshiaki] Yokohama City Univ, Grad Sch Med, Yokohama, Kanagawa 232, Japan.
[Ombrello, Michael J.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Ustek, Duran] Istanbul Univ, Inst Expt Med, Istanbul, Turkey.
[Tugal-tutkun, Ilknur; Gul, Ahmet] Istanbul Univ, Istanbul Fac Med, Istanbul, Turkey.
[Seyahi, Emire; Ozyazgan, Yilmaz] Istanbul Univ, Cerrahpasa Fac Med, Istanbul, Turkey.
[Ohno, Shigeaki] Hokkaido Univ, Grad Sch Med, Sapporo, Hokkaido 060, Japan.
RI Ustek, Duran/C-3484-2009
OI Ustek, Duran/0000-0002-0060-2859
NR 0
TC 0
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1703
BP S721
EP S722
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204164
ER
PT J
AU Tan, S
Dasgupta, A
Yao, JH
Flynn, JA
Yao, L
Ward, MM
AF Tan, Sovira
Dasgupta, Abhijit
Yao, Jianhua
Flynn, John A.
Yao, Lawrence
Ward, Michael M.
TI Syndesmophyte Distribution Along The Vertebral Rim In Ankylosing
Spondylitis Is Non-Random
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Tan, Sovira; Dasgupta, Abhijit; Ward, Michael M.] NIAMS, NIH, Bethesda, MD USA.
[Yao, Jianhua; Yao, Lawrence] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Flynn, John A.] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2434
BP S1040
EP S1040
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359205380
ER
PT J
AU Teos, LY
Swaim, B
Cotrim, AP
Grisius, M
Bebris, L
Ambudkar, I
Illei, GG
Alevizos, I
AF Teos, Leyla Y.
Swaim, Bill
Cotrim, Ana Paola
Grisius, Margaret
Bebris, Lolita
Ambudkar, Indu
Illei, Gabor G.
Alevizos, Ilias
TI Hypofunction In Intact Cell Lobules Reflect Salivary Flow Rates In
Sjogren's Patients
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Teos, Leyla Y.; Cotrim, Ana Paola; Grisius, Margaret] NIH, Bethesda, MD 20892 USA.
[Swaim, Bill; Bebris, Lolita] NIDCR, NIH, Bethesda, MD USA.
[Ambudkar, Indu] NIDCR, Bethesda, MD USA.
[Illei, Gabor G.] MedImmune LLC, Gaithersburg, MD USA.
[Alevizos, Ilias] NIDCR NIH 10 1N110, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1498
BP S635
EP S635
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359203475
ER
PT J
AU Tran, TM
Hong, S
Colbert, RA
AF Tran, Tri M.
Hong, Sohee
Colbert, Robert A.
TI Effects Of ERAP1 Knockdown On HLA Class I and HLA-B27 Expression In
Human Monocytic U937 Cells
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Tran, Tri M.; Hong, Sohee; Colbert, Robert A.] NIAMS NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 539
BP S235
EP S236
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202051
ER
PT J
AU Wang, RS
Meylan, F
Zou, JZ
Rao, M
Siegel, RM
AF Wang, Runsheng
Meylan, Francoise
Zou, Jizhong
Rao, Mahendra
Siegel, Richard M.
TI Mesenchymal Stem Cells and Skin Fibroblasts Both Suppress Early Steps In
T Cell Activation In a Nitric-Oxide Dependent Manner
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Wang, Runsheng] NIAMS, NIH, Rheumatol Fellowship & Training Branch, Bethesda, MD USA.
[Meylan, Francoise] NIAMS, NIH, Autoimmun Branch, Bethesda, MD USA.
[Zou, Jizhong; Rao, Mahendra] NIAMS, NIH, Ctr Regenerat Med, Bethesda, MD USA.
[Siegel, Richard M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 718
BP S304
EP S305
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202224
ER
PT J
AU Weiss, PF
Chauvin, N
Klink, AJ
Localio, RA
Feudtner, C
Jaramillo, D
Colbert, RA
Sherry, DD
Keren, R
AF Weiss, Pamela F.
Chauvin, Nancy
Klink, Andrew J.
Localio, Russell A.
Feudtner, Chris
Jaramillo, Diego
Colbert, Robert A.
Sherry, David D.
Keren, Ron
TI Detection Of Enthesitis In Children With Enthesitis-Related Arthritis:
Dolorimeter Examination Compared To Ultrasonography
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Weiss, Pamela F.; Chauvin, Nancy; Klink, Andrew J.; Jaramillo, Diego; Sherry, David D.; Keren, Ron] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Localio, Russell A.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Feudtner, Chris] Childrens Hosp Philadelphia, Div Gen Pediat, Philadelphia, PA 19104 USA.
[Feudtner, Chris] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Colbert, Robert A.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1715
BP S726
EP S727
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204175
ER
PT J
AU Wessel, A
Hsu, A
Zilberman-Rudenko, J
Goldbach-Mansky, R
Siegel, RM
Hanson, E
AF Wessel, Alex
Hsu, Amy
Zilberman-Rudenko, Jevgenia
Goldbach-Mansky, Raphaela
Siegel, Richard M.
Hanson, Eric
TI Inflammatory Disease Due To Dysregulated Nuclear Factor-kappa B
Activation and Impaired Type I Interferon Response Resulting From a De
Novo Human NEMO Hypomorphic Mutation
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Wessel, Alex; Zilberman-Rudenko, Jevgenia; Goldbach-Mansky, Raphaela; Siegel, Richard M.; Hanson, Eric] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Hsu, Amy] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 764
BP S323
EP S323
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202269
ER
PT J
AU Wofsy, D
Isenberg, DA
Licu, D
Li, Y
Rossi, CP
Gordon, C
AF Wofsy, David
Isenberg, David A.
Licu, Daiana
Li, Yong
Rossi, Claudia Pena
Gordon, Caroline
TI Efficacy and Safety Of Atacicept For Prevention Of Flares In Subjects
With Moderate To Severe Systemic Lupus Erythematosus (SLE)
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Wofsy, David] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wofsy, David] NIAID, Autoimmun Ctr Excellence, San Francisco, CA USA.
[Isenberg, David A.] UCL, London, England.
[Licu, Daiana; Rossi, Claudia Pena] Merck Serono SA, Geneva, Switzerland.
[Li, Yong] EMD Serono, Rockland, MA USA.
[Gordon, Caroline] Univ Birmingham, Birmingham, W Midlands, England.
NR 0
TC 3
Z9 3
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 1591
BP S675
EP S675
PG 1
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359204055
ER
PT J
AU Wofsy, D
Askanase, A
Cagnoli, PC
Chatham, WW
Contreras, G
Dall'Era, M
Dooley, MA
Fragoso-Loyo, H
Karp, DR
Jolly, M
Kalunian, K
Kamen, DL
Lee, I
Levesque, MC
Lim, SS
Mackay, M
Ramos-Remus, C
Rovin, BH
Utset, TO
Venuturupalli, S
Winchester, R
Ding, LN
Gao, WD
Keyes-Elstein, L
Tosta, P
AF Wofsy, David
Askanase, Anca
Cagnoli, Patricia C.
Chatham, W. Winn
Contreras, Gabriel
Dall'Era, Maria
Dooley, Mary Anne
Fragoso-Loyo, Hilda
Karp, David R.
Jolly, Meenakshi
Kalunian, Kenneth
Kamen, Diane L.
Lee, Iris
Levesque, Marc C.
Lim, S. Sam
Mackay, Meggan
Ramos-Remus, Cesar
Rovin, Brad H.
Utset, Tammy O.
Venuturupalli, Swamy
Winchester, Robert
Ding, Linna
Gao, Wendy
Keyes-Elstein, Lynette
Tosta, Patti
TI Treatment Of Lupus Nephritis With Abatacept Plus Low-Dose Pulse
Cyclophosphamide Followed By Azathioprine (the Euro-Lupus Regimen):
Twenty-Four Week Data From a Double-Blind Controlled Trial
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Wofsy, David] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wofsy, David] NIAID Autoimmun Ctr Excellence, San Francisco, CA USA.
[Askanase, Anca] NYU, Sch Med, New York, NY USA.
[Cagnoli, Patricia C.] Univ Michigan Hlth, Ann Arbor, MI USA.
[Chatham, W. Winn; Tosta, Patti] Univ Alabama Birmingham, Birmingham, AL USA.
[Contreras, Gabriel] Univ Miami, Miami, FL USA.
[Dall'Era, Maria] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Dooley, Mary Anne] Univ N Carolina, Chapel Hill, NC USA.
[Fragoso-Loyo, Hilda] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Mexico City, DF, Mexico.
[Karp, David R.] UT Southwestern Med Ctr, Dallas, TX USA.
[Karp, David R.] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Jolly, Meenakshi] UCSD Sch Med, La Jolla, CA USA.
[Kalunian, Kenneth] Med Univ S Carolina, Charleston, SC 29425 USA.
[Kamen, Diane L.] Temple Univ, Philadelphia, PA 19122 USA.
[Lee, Iris] Univ Pittsburgh, Pittsburgh, PA USA.
[Levesque, Marc C.] Emory Univ, Atlanta, GA 30322 USA.
[Lim, S. Sam] Feinstein Inst Med Res, Manhasset, NY USA.
[Mackay, Meggan] Unidad Invest Enfermedades Cronicodegenerat, Guadalajara, Mexico.
[Ramos-Remus, Cesar] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Rovin, Brad H.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Utset, Tammy O.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Venuturupalli, Swamy] Columbia Univ, New York, NY USA.
[Winchester, Robert; Ding, Linna; Gao, Wendy] NIAID, Bethesda, MD 20892 USA.
[Keyes-Elstein, Lynette] Rho Fed Syst Inc, Chapel Hill, NC USA.
[Tosta, Patti] Immune Tolerance Network, San Francisco, CA USA.
NR 0
TC 7
Z9 7
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 884
BP S379
EP S380
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202389
ER
PT J
AU Yang, E
Kwon, G
Colbert, RA
Layh-Schmitt, G
AF Yang, Eva
Kwon, Grace
Colbert, Robert A.
Layh-Schmitt, Gerlinde
TI HLA-B27 Expression Prevents Tnf alpha-Induced Inhibition Of Bone
Formation in Vitro In IFN gamma/Tnf alpha-Treated Osteoblasts.
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Yang, Eva; Kwon, Grace; Colbert, Robert A.; Layh-Schmitt, Gerlinde] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 2694
BP S1151
EP S1152
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359206124
ER
PT J
AU Zhou, Q
Yang, D
Zavialov, A
Ombrello, A
Kuehn, H
Chae, JJ
Zavialov, A
Chin, D
Stone, D
Toro, C
Milner, J
Lee, CC
Cowen, E
Candotti, F
Remmers, E
Moir, S
Sood, R
Burgess, S
Gadina, M
Rosenzweig, S
Hershfield, M
Kastner, DL
Boehm, M
Aksentijevich, I
AF Zhou, Qing
Yang, Dan
Zavialov, Andrey
Ombrello, Amanda
Kuehn, Hyesun
Chae, Jae Jin
Zavialov, Anton
Chin, David
Stone, Deborah
Toro, Camilo
Milner, Joshua
Lee, Chyi-chia
Cowen, Edward
Candotti, Fabio
Remmers, Elaine
Moir, Susan
Sood, Raman
Burgess, Shawn
Gadina, Massimo
Rosenzweig, Sergio
Hershfield, Michael
Kastner, Daniel L.
Boehm, Manfred
Aksentijevich, Ivona
TI Intermittent Fever, Immune Dysregulation, and Systemic Vasculopathy Due
To Loss-Of-Function Mutations In Adenosine Deaminase2
SO ARTHRITIS AND RHEUMATISM
LA English
DT Meeting Abstract
CT 77th Annual Meeting of the American-College-of-Rheumatology / 48th
Annual Meeting of the Association-of-Rheumatology-Health-Professionals
CY OCT 25-30, 2013
CL San Diego, CA
SP Amer Coll Rheumatol, Assoc Rheumatol Hlth Profess
C1 [Zhou, Qing; Ombrello, Amanda; Chae, Jae Jin; Chin, David; Stone, Deborah; Toro, Camilo; Candotti, Fabio; Remmers, Elaine; Sood, Raman; Burgess, Shawn; Kastner, Daniel L.; Aksentijevich, Ivona] NHGRI, NIH, Bethesda, MD 20892 USA.
[Yang, Dan; Boehm, Manfred] NHLBI, NIH, Bethesda, MD 20892 USA.
[Zavialov, Andrey; Zavialov, Anton] Univ Turku, Turku, Finland.
[Kuehn, Hyesun] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Milner, Joshua; Moir, Susan; Rosenzweig, Sergio] NIAID, NIH, Bethesda, MD 20892 USA.
[Lee, Chyi-chia; Cowen, Edward] NCI, NIH, Bethesda, MD 20892 USA.
[Gadina, Massimo] NIAMSD, Bethesda, MD 20892 USA.
[Hershfield, Michael] Duke Univ, Med Ctr, Durham, NC USA.
RI Zavialov, Anton/C-7664-2015
OI Zavialov, Anton/0000-0001-6191-5931
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
SU 10
SI SI
MA 894
BP S383
EP S384
PG 2
WC Rheumatology
SC Rheumatology
GA 230RF
UT WOS:000325359202399
ER
PT J
AU Schweitzer, CJ
Liang, TJ
AF Schweitzer, Cameron J.
Liang, T. Jake
TI Impact of host and virus genome variability on HCV replication and
response to interferon
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID HEPATITIS-C-VIRUS; RIBAVIRIN COMBINATION THERAPY; AMINO-ACID
SUBSTITUTIONS; NONSTRUCTURAL PROTEIN 5A; CORE PROTEIN;
GENETIC-VARIATION; PEGYLATED-INTERFERON; INTERLEUKIN 28B; GENOTYPE 1B;
IL28B GENOTYPE
AB Since the discovery of hepatitis C virus (HCV), treatment has proven difficult and the regimen of pegylated interferon-alpha and ribavirin is only effective for half of patients. Evidence suggests that host and viral genome variations play a role in either viral clearance or persistence. Powerful genomic technologies have made it possible to study genome-wide associations with treatment response, which yielded critical genetic polymorphisms that predict treatment response. This has important implications for treatment of HCV infection and opened the door to the possibility of genetic marker-guided treatment (personalized medicine). This review will focus on the recent advances in understanding host and viral genetic variations with regards to treatment and the importance for future therapeutic intervention
C1 [Schweitzer, Cameron J.; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
RP Schweitzer, CJ (reprint author), NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
EM cameron.schweitzer@NIH.gov; jakel@bdg10.niddk.nih.gov
FU Intramural NIH HHS [Z99 DK999999, ZIA DK054504-16, ZIA DK054511-05, ZIA
DK054505-15, ZIA DK054504-15, ZIA DK054511-06, ZIA DK054505-16]
NR 76
TC 4
Z9 4
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD OCT
PY 2013
VL 3
IS 5
BP 501
EP 507
DI 10.1016/j.coviro.2013.06.005
PG 7
WC Virology
SC Virology
GA 240ZN
UT WOS:000326136300004
PM 23835049
ER
PT J
AU Koonin, EV
Dolja, VV
AF Koonin, Eugene V.
Dolja, Valerian V.
TI A virocentric perspective on the evolution of life
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID GENOME EVOLUTION; MOBILE ELEMENTS; REPLICATOR SYSTEMS; IMMUNE EVASION;
CELLULAR GENES; VIRAL WORLD; DNA VIRUSES; ORIGIN; EUKARYOTES; DIVERSITY
AB Viruses and/or virus-like selfish elements are associated with all cellular life forms and are the most abundant biological entities on Earth, with the number of virus particles in many environments exceeding the number of cells by one to two orders of magnitude. The genetic diversity of viruses is commensurately enormous and might substantially exceed the diversity of cellular organisms. Unlike cellular organisms with their uniform replication-expression scheme, viruses possess either RNA or DNA genomes and exploit all conceivable replication-expression strategies. Although viruses extensively exchange genes with their hosts, there exists a set of viral hallmark genes that are shared by extremely diverse groups of viruses to the exclusion of cellular life forms. Coevolution of viruses and host defense systems is a key aspect in the evolution of both viruses and cells, and viral genes are often recruited for cellular functions. Together with the fundamental inevitability of the emergence of genomic parasites in any evolving replicator system, these multiple lines of evidence reveal the central role of viruses in the entire evolution of life.
C1 [Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[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.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
FU US Department of Health and Human Services
FX EVK is supported by intramural funds of the US Department of Health and
Human Services (to the National Library of Medicine, NIH).
NR 88
TC 48
Z9 48
U1 4
U2 42
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD OCT
PY 2013
VL 3
IS 5
BP 546
EP 557
DI 10.1016/j.coviro.2013.06.008
PG 12
WC Virology
SC Virology
GA 240ZN
UT WOS:000326136300011
PM 23850169
ER
PT J
AU Lado, WE
Zhang, DP
Mennigen, JA
Zamora, JM
Popesku, JT
Trudeau, VL
AF Lado, Wudu E.
Zhang, Dapeng
Mennigen, Jan A.
Zamora, Jacob M.
Popesku, Jason T.
Trudeau, Vance L.
TI Rapid modulation of gene expression profiles in the telencephalon of
male goldfish following exposure to waterborne sex pheromones
SO GENERAL AND COMPARATIVE ENDOCRINOLOGY
LA English
DT Article
DE Microarray; Ependymin; Calmodulin; Aldolase C; GnRH; Pheromones; Sperm
release
ID GONADOTROPIN-RELEASING-HORMONE; NR2B-CONTAINING NMDA RECEPTORS;
AMINO-ACID NEUROTRANSMITTERS; CARASSIUS-AURATUS; SPAWNING BEHAVIOR;
FEMALE GOLDFISH; DIFFERENTIAL ROLES; KAINATE RECEPTORS; GABA(A)
RECEPTORS; MICROARRAY DATA
AB Sex pheromones rapidly affect endocrine physiology and behaviour, but little is known about their effects on gene expression in the neural tissues that mediate olfactory processing. In this study, we exposed male goldfish for 6 h to waterborne 17,20 beta P (4.3 nM) and PGF(2 alpha) (3 nM), the main pre-ovulatory and post-ovulatory pheromones, respectively. Both treatments elevated milt volume (P = 0.001). Microarray analysis of male telencephalon following PGF(2 alpha), treatment identified 71 unique transcripts that were differentially expressed (q < 5%; 67 up, 4 down). Functional annotation of these regulated genes indicates that PGF(2 alpha),1 pheromone exposure affects diverse biological processes including nervous system functions, energy metabolism, cholesterol/lipoprotein transport, translational regulation, transcription and chromatin remodelling, protein processing, cytoskeletal organization, and signalling. By using real-time RT-PCR, we further validated three candidate genes, ependymin-II, calmodulin-A and aldolase C, which exhibited 3-5-fold increase in expression following PGF(2 alpha), exposure. Expression levels of some other genes that are thought to be important for reproduction were also determined using real-time RT-PCR. Expression of sGnRH was increased by PGF(2 alpha), but not 17,20 beta P, whereas cGnRH expression was increased by 17,20 beta P but not PGF2a. In contrast, both pheromones increase the expression of glutamate (GluR2a, NR2A) and gamma-aminobutyric acid (GABA(A) gamma 2) receptor subunit mRNAs. Milt release and rapid modulation of neuronal transcription are part of the response of males to female sex pheromones. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Lado, Wudu E.; Zamora, Jacob M.; Trudeau, Vance L.] Univ Ottawa, Dept Biol, Ottawa, ON, Canada.
[Zhang, Dapeng] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Mennigen, Jan A.] UR Nutr Aquaculture & Genom Nutr Metab & Aquacult, Inst Natl Rech Agron, F-64310 Quartier Ibarron, St Pee Sur Nive, France.
[Popesku, Jason T.] Univ British Columbia, Inst Life Sci, Dept Cellular & Physiol Sci, Vancouver, BC V6T 1Z3, Canada.
RP Trudeau, VL (reprint author), Univ Ottawa, Dept Biol, Ottawa, ON, Canada.
EM trudeauv@uottawa.ca
OI Trudeau, Vance/0000-0002-0845-9444
FU University of Ottawa International scholarship; Ontario Graduate
Scholarships; National Sciences and Engineering Research Council (NSERC)
summer scholarship; Discovery programs
FX This work was supported by a University of Ottawa International
scholarship (DZ, JAM), Ontario Graduate Scholarships (WEL, JTP),
National Sciences and Engineering Research Council (NSERC) summer
scholarship (JMZ) and Discovery programs (VLT).
NR 66
TC 4
Z9 4
U1 2
U2 16
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0016-6480
EI 1095-6840
J9 GEN COMP ENDOCR
JI Gen. Comp. Endocrinol.
PD OCT 1
PY 2013
VL 192
BP 204
EP 213
DI 10.1016/j.ygcen.2013.06.015
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 235QS
UT WOS:000325736400023
PM 23800560
ER
PT J
AU Walker, L
Curry, M
Nayak, A
Lange, N
Pierpaoli, C
AF Walker, Lindsay
Curry, Michael
Nayak, Amritha
Lange, Nicholas
Pierpaoli, Carlo
CA Brain Dev Cooperative Grp
TI A framework for the analysis of phantom data in multicenter diffusion
tensor imaging studies
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE diffusion tensor imaging; DTI; multicenter; reproducibility; accuracy;
pediatric
ID NORMAL BRAIN-DEVELOPMENT; FRACTIONAL ANISOTROPY; DISTORTION CORRECTION;
WEIGHTED MRI; SPIN-ECHO; NIH MRI; NOISE; RELIABILITY; IMAGES;
OPTIMIZATION
AB Diffusion tensor imaging (DTI) is commonly used for studies of the human brain due to its inherent sensitivity to the microstructural architecture of white matter. To increase sampling diversity, it is often desirable to perform multicenter studies. However, it is likely that the variability of acquired data will be greater in multicenter studies than in single-center studies due to the added confound of differences between sites. Therefore, careful characterization of the contributions to variance in a multicenter study is extremely important for meaningful pooling of data from multiple sites. We propose a two-step analysis framework for first identifying outlier datasets, followed by a parametric variance analysis for identification of intersite and intrasite contributions to total variance. This framework is then applied to phantom data from the NIH MRI study of normal brain development (PedsMRI). Our results suggest that initial outlier identification is extremely important for accurate assessment of intersite and intrasite variability, as well as for early identification of problems with data acquisition. We recommend the use of the presented framework at frequent intervals during the data acquisition phase of multicenter DTI studies, which will allow investigators to identify and solve problems as they occur. Hum Brain Mapp 34:2439-2454, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Walker, Lindsay; Curry, Michael; Nayak, Amritha; Pierpaoli, Carlo] NICHD, Program Pediat Imaging & Tissue Sci, NIH, Bethesda, MD USA.
[Walker, Lindsay; Nayak, Amritha] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Lange, Nicholas] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Lange, Nicholas] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Walker, L (reprint author), Bldg 13,Rm 3W16D,13 South Dr, Bethesda, MD 20892 USA.
EM walkerlin@mail.nih.gov
FU National Institute of Neurological Disorders and Stroke [N01-HD02-3343,
N01-MH9-0002, N01-NS-9-2314, N01-NS-9-2315, N01-NS-9-2316,
N01-NS-9-2317, N01-NS-9-2319, N01-NS-9-2320, NS34783]; National
Institute of Child Health and Human Development; National Institute on
Drug Abuse; National Institute of Mental Health
FX Contract grant sponsor: National Institute of Neurological Disorders and
Stroke; Contract grant numbers: N01-HD02-3343, N01-MH9-0002,
N01-NS-9-2314, N01-NS-9-2315, N01-NS-9-2316, N01-NS-9-2317,
N01-NS-9-2319, N01-NS-9-2320, NS34783; Contract grant sponsors: National
Institute of Child Health and Human Development; the National Institute
on Drug Abuse; the National Institute of Mental Health.
NR 39
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U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD OCT
PY 2013
VL 34
IS 10
BP 2439
EP 2454
DI 10.1002/hbm.22081
PG 16
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 216TI
UT WOS:000324306900007
PM 22461391
ER
PT J
AU Chakravarty, MM
Steadman, P
van Eede, MC
Calcott, RD
Gu, V
Shaw, P
Raznahan, A
Collins, DL
Lerch, JP
AF Chakravarty, M. Mallar
Steadman, Patrick
van Eede, Matthijs C.
Calcott, Rebecca D.
Gu, Victoria
Shaw, Philip
Raznahan, Armin
Collins, D. Louis
Lerch, Jason P.
TI Performing label-fusion-based segmentation using multiple automatically
generated templates
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE segmentation; label-fusion; multi-atlas; subcortical anatomy; striatum;
globus pallidus; thalamus; small animal imaging; mouse imaging; atlases;
nonlinear registration
ID DEFORMATION-BASED MORPHOMETRY; MODEL-BASED SEGMENTATION; HUMAN BRAIN;
PROBABILISTIC ATLAS; MOUSE-BRAIN; IMAGE SEGMENTATION; MR-IMAGES;
NEUROANATOMICAL STRUCTURES; AUTOMATED SEGMENTATION; HIPPOCAMPAL
SUBFIELDS
AB Classically, model-based segmentation procedures match magnetic resonance imaging (MRI) volumes to an expertly labeled atlas using nonlinear registration. The accuracy of these techniques are limited due to atlas biases, misregistration, and resampling error. Multi-atlas-based approaches are used as a remedy and involve matching each subject to a number of manually labeled templates. This approach yields numerous independent segmentations that are fused using a voxel-by-voxel label-voting procedure. In this article, we demonstrate how the multi-atlas approach can be extended to work with input atlases that are unique and extremely time consuming to construct by generating a library of multiple automatically generated templates of different brains (MAGeT Brain). We demonstrate the efficacy of our method for the mouse and human using two different nonlinear registration algorithms (ANIMAL and ANTs). The input atlases consist a high-resolution mouse brain atlas and an atlas of the human basal ganglia and thalamus derived from serial histological data. MAGeT Brain segmentation improves the identification of the mouse anterior commissure (mean Dice Kappa values (kappa = 0.801), but may be encountering a ceiling effect for hippocampal segmentations. Applying MAGeT Brain to human subcortical structures improves segmentation accuracy for all structures compared to regular model-based techniques (kappa = 0.845, 0.752, and 0.861 for the striatum, globus pallidus, and thalamus, respectively). Experiments performed with three manually derived input templates suggest that MAGeT Brain can approach or exceed the accuracy of multi-atlas label-fusion segmentation (kappa = 0.894, 0.815, and 0.895 for the striatum, globus pallidus, and thalamus, respectively). Hum Brain Mapp 34:2635-2654, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Chakravarty, M. Mallar; Steadman, Patrick; van Eede, Matthijs C.; Calcott, Rebecca D.; Gu, Victoria; Lerch, Jason P.] Hosp Sick Children, Mouse Imaging Ctr, Toronto, ON M5G 1X8, Canada.
[Chakravarty, M. Mallar] Ctr Addict & Mental Hlth, Kimel Family Translat Imaging Genet Res Lab, Toronto, ON, Canada.
[Chakravarty, M. Mallar] Univ Toronto, Dept Psychiat, Toronto, ON M5S 1A1, Canada.
[Steadman, Patrick; Lerch, Jason P.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Shaw, Philip] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA.
[Raznahan, Armin] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Collins, D. Louis] McGill Univ, Montreal Neurol Inst, Brain Imaging Ctr, Montreal, PQ, Canada.
RP Chakravarty, MM (reprint author), Hosp Sick Children, Mouse Imaging Ctr, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM mallar_chakravarty@camh.net
OI Steadman, Patrick/0000-0002-5814-4977
FU Canada Foundation for Innovation under the auspices of Compute Canada;
Government of Ontario; Ontario Research Fund - Research Excellence;
University of Toronto
FX Computations were performed on the SciNet supercomputer at the SciNet
HPC Consortium. SciNet is funded by the Canada Foundation for Innovation
under the auspices of Compute Canada, the Government of Ontario, Ontario
Research Fund - Research Excellence and the University of Toronto. MMC
would also like to thank G. Clinton, E. Hazel, and B. Worrell for
inspiring this work.
NR 69
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U1 2
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD OCT
PY 2013
VL 34
IS 10
BP 2635
EP 2654
DI 10.1002/hbm.22092
PG 20
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 216TI
UT WOS:000324306900021
PM 22611030
ER
PT J
AU Wei, HJ
Viallon, M
Delattre, BMA
Wang, LH
Pai, VM
Wen, H
Xue, H
Guetter, C
Croisille, P
Zhu, YM
AF Wei, Hongjiang
Viallon, Magalie
Delattre, Benedicte M. A.
Wang, Lihui
Pai, Vinay M.
Wen, Han
Xue, Hui
Guetter, Christoph
Croisille, Pierre
Zhu, Yuemin
TI Assessment of Cardiac Motion Effects on the Fiber Architecture of the
Human Heart In Vivo
SO IEEE TRANSACTIONS ON MEDICAL IMAGING
LA English
DT Article
DE Diffusion tensor imaging (DTI); fiber architecture; in vivo heart;
motion; polarized light imaging
ID DIFFUSION-TENSOR MRI; IMAGING MATHEMATICS; ANISOTROPY; NOISE;
LIMITATIONS; INFARCTION; STRAIN; ECHOES
AB The use of diffusion tensor imaging (DTI) for studying the human heart in vivo is very challenging due to cardiac motion. This paper assesses the effects of cardiac motion on the human myocardial fiber architecture. To this end, a model for analyzing the effects of cardiac motion on signal intensity is presented. A Monte-Carlo simulation based on polarized light imaging data is then performed to calculate the diffusion signals obtained by the displacement of water molecules, which generate diffusion weighted (DW) images. Rician noise and in vivo motion data obtained from DENSE acquisition are added to the simulated cardiac DW images to produce motion-induced datasets. An algorithm based on principal components analysis filtering and temporal maximum intensity projection (PCATMIP) is used to compensate for motion-induced signal loss. Diffusion tensor parameters derived from motion-reduced DW images are compared to those derived from the original simulated DW images. Finally, to assess cardiac motion effects on in vivo fiber architecture, in vivo cardiac DTI data processed by PCATMIP are compared to those obtained from one trigger delay (TD) or one single phase acquisition. The results showed that cardiac motion produced overestimated fractional anisotropy and mean diffusivity as well as a narrower range of fiber angles. The combined use of shifted TD acquisitions and postprocessing based on image registration and PCATMIP effectively improved the quality of in vivo DW images and subsequently, the measurement accuracy of fiber architecture properties. This suggests new solutions to the problems associated with obtaining in vivo human myocardial fiber architecture properties in clinical conditions.
C1 [Wei, Hongjiang; Viallon, Magalie; Delattre, Benedicte M. A.; Wang, Lihui; Croisille, Pierre; Zhu, Yuemin] CNRS, INSERM, CREATIS, UMR 5220,U1044, F-69100 Villeurbanne, France.
[Wei, Hongjiang; Viallon, Magalie; Delattre, Benedicte M. A.; Wang, Lihui; Croisille, Pierre; Zhu, Yuemin] INSA Lyon, F-69100 Villeurbanne, France.
[Wei, Hongjiang; Viallon, Magalie; Delattre, Benedicte M. A.; Wang, Lihui; Croisille, Pierre; Zhu, Yuemin] Univ Lyon, F-69100 Villeurbanne, France.
[Pai, Vinay M.] NIBIB, Div Appl Sci & Technol, NIH, Bethesda, MD 20892 USA.
[Wen, Han] NHLBI, Phys Lab, NIH, Bethesda, MD 20892 USA.
[Xue, Hui; Guetter, Christoph] Siemens Corp, Corp Technol, Princeton, NJ 08540 USA.
RP Wei, HJ (reprint author), CNRS, INSERM, CREATIS, UMR 5220,U1044, F-69100 Villeurbanne, France.
RI Croisille, Pierre/H-4928-2014; Magalie, Viallon/H-4471-2014; Wen,
Han/G-3081-2010
OI Croisille, Pierre/0000-0003-4019-3460; Magalie,
Viallon/0000-0001-9118-0438; Wen, Han/0000-0001-6844-2997
FU French ANR [ANR-09-BLAN-0372-01]
FX This work was supported by the French ANR 2009 (under
ANR-09-BLAN-0372-01).
NR 44
TC 12
Z9 12
U1 0
U2 16
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0278-0062
EI 1558-254X
J9 IEEE T MED IMAGING
JI IEEE Trans. Med. Imaging
PD OCT
PY 2013
VL 32
IS 10
BP 1928
EP 1938
DI 10.1109/TMI.2013.2269195
PG 11
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Engineering, Electrical & Electronic; Imaging Science &
Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Imaging Science & Photographic
Technology; Radiology, Nuclear Medicine & Medical Imaging
GA 230YV
UT WOS:000325380300015
PM 23797241
ER
PT J
AU Prescott, J
Safronetz, D
Haddock, E
Robertson, S
Scott, D
Feldmann, H
AF Prescott, Joseph
Safronetz, David
Haddock, Elaine
Robertson, Shelly
Scott, Dana
Feldmann, Heinz
TI The adaptive immune response does not influence hantavirus disease or
persistence in the Syrian hamster
SO IMMUNOLOGY
LA English
DT Article
DE hantavirus; hantavirus cardiopulmonary syndrome; infectious disease; T
cells; zoonosis
ID SIN-NOMBRE-VIRUS; PEROMYSCUS-MANICULATUS MODEL; PULMONARY SYNDROME;
T-CELLS; HEMORRHAGIC-FEVER; SEOUL-VIRUS; NONPATHOGENIC HANTAVIRUSES;
CARDIOPULMONARY SYNDROME; ENDOTHELIAL-CELLS; RENAL SYNDROME
AB Summary
Pathogenic New World hantaviruses cause severe disease in humans characterized by a vascular leak syndrome, leading to pulmonary oedema and respiratory distress with case fatality rates approaching 40%. Hantaviruses infect microvascular endothelial cells without conspicuous cytopathic effects, indicating that destruction of the endothelium is not a mechanism of disease. In humans, high levels of inflammatory cytokines are present in the lungs of patients that succumb to infection. This, along with other observations, suggests that disease has an immunopathogenic component. Currently the only animal model available to study hantavirus disease is the Syrian hamster, where infection with Andes virus (ANDV), the primary agent of disease in South America, results in disease that closely mimics that seen in humans. Conversely, inoculation of hamsters with a passaged Sin Nombre virus (SNV), the virus responsible for most cases of disease in North America, results in persistent infection with high levels of viral replication. We found that ANDV elicited a stronger innate immune response, whereas SNV elicited a more robust adaptive response in the lung. Additionally, ANDV infection resulted in significant changes in the blood lymphocyte populations. To determine whether the adaptive immune response influences infection outcome, we depleted hamsters of CD4(+) and CD8(+) T cells before infection with hantaviruses. Depletion resulted in inhibition of virus-specific antibody responses, although the pathogenesis and replication of these viruses were unaltered. These data show that neither hantavirus replication, nor pathogenesis caused by these viruses, is influenced by the adaptive immune response in the Syrian hamster.
C1 [Prescott, Joseph; Safronetz, David; Haddock, Elaine; Robertson, Shelly; Feldmann, Heinz] NIAID, Virol Lab, DIR, NIH,Rocky Mt Lab, Hamilton, MT 59840 USA.
[Scott, Dana] NIAID, Rocky Mt Vet Branch, Div Intramural Res, NIH,Rocky Mt Labs, Hamilton, MT 59840 USA.
RP Prescott, J (reprint author), NIAID, Virol Lab, DIR, NIH,Rocky Mt Lab, 903 South 4th St, Hamilton, MT 59840 USA.
EM prescottjb@niaid.nih.gov; feldmannh@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Disease, National Institutes of Health
FX We would like to thank Dan Long, Tina Thomas and Rebecca Rosenke for
histopathology work. We would also like to thank Anita Mora for the
preparation of graphics. This work was supported by the Division of
Intramural Research, National Institute of Allergy and Infectious
Disease, National Institutes of Health.
NR 42
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U1 1
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD OCT
PY 2013
VL 140
IS 2
BP 168
EP 178
DI 10.1111/imm.12116
PG 11
WC Immunology
SC Immunology
GA 216SB
UT WOS:000324303200003
PM 23600567
ER
PT J
AU Bernstein, M
Garnett-Benson, C
Zhang, H
Hodge, JW
Guha, C
AF Bernstein, M.
Garnett-Benson, C.
Zhang, H.
Hodge, J. W.
Guha, C.
TI Radiation Therapy Alters Tumor Cell Phenotypes and Enhances the Immune
Response
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Bernstein, M.; Zhang, H.; Guha, C.] Montefiore Med Ctr, Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Garnett-Benson, C.] Georgia State Univ, Atlanta, GA 30303 USA.
[Hodge, J. W.] NCI, NIH, Bethesda, MD 20892 USA.
RI Hodge, James/D-5518-2015
OI Hodge, James/0000-0001-5282-3154
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S110
EP S110
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503600270
ER
PT J
AU Dan, T
Simone, B
Simone, C
Scuito, L
Smith, S
Danforth, D
Camphausen, K
Simone, N
AF Dan, T.
Simone, B.
Simone, C.
Scuito, L.
Smith, S.
Danforth, D.
Camphausen, K.
Simone, N.
TI Cosmetic Outcomes and Quality of Life are Similar in Patients Receiving
Breast Conservation Versus Mastectomy: 25-Year Follow-up of the NCI
Randomized Trial
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Dan, T.; Simone, B.; Simone, N.] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
[Simone, C.] Univ Penn, Philadelphia, PA 19104 USA.
[Scuito, L.; Smith, S.; Danforth, D.; Camphausen, K.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S48
EP S48
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503600115
ER
PT J
AU Fasola, C
Jones, JC
Huang, D
Le, Q
Hoppe, RT
AF Fasola, C.
Jones, J. C.
Huang, D.
Le, Q.
Hoppe, R. T.
TI Low-Dose Radiation Therapy (2 Gy x 2) in the Treatment of Non-Hodgkin
Lymphoma of the Ocular Adnexa
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Fasola, C.; Le, Q.; Hoppe, R. T.] Stanford Canc Ctr, Stanford, CA USA.
[Jones, J. C.] NCI, Bethesda, MD 20892 USA.
[Huang, D.] Univ Calif Los Angeles Olive View, Sylmar, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S59
EP S60
PG 2
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503600144
ER
PT J
AU Lautenschlaeger, T
Perry, I
Peereboom, D
White, J
Steeg, P
Mehta, M
Chakravarti, A
AF Lautenschlaeger, T.
Perry, I.
Peereboom, D.
White, J.
Steeg, P.
Mehta, M.
Chakravarti, A.
TI Cilengitide Inhibits Proliferation and Shows Combined Effects With
Radiation in Breast Cancer Cell Lines
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Lautenschlaeger, T.; Perry, I.; White, J.; Chakravarti, A.] Ohio State Univ, Columbus, OH 43210 USA.
[Peereboom, D.] Cleveland Clin, Cleveland, OH 44106 USA.
[Steeg, P.] NCI, Bethesda, MD 20892 USA.
[Mehta, M.] Univ Maryland, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S658
EP S658
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503602391
ER
PT J
AU Lin, SH
Zhang, J
Giri, U
Stephan, C
Sobieski, MM
Nguyen, N
Davies, P
Komaki, R
Yoo, SS
Heymach, JV
AF Lin, S. H.
Zhang, J.
Giri, U.
Stephan, C.
Sobieski, M. M.
Nguyen, N.
Davies, P.
Komaki, R.
Yoo, S. S.
Heymach, J. V.
TI High Throughput Clonogenic Survival Screen Identifies Novel Radiation
Sensitizers for K-ras Mutant Non-Small Cell Lung Cancer
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Lin, S. H.; Zhang, J.; Giri, U.; Komaki, R.; Heymach, J. V.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Stephan, C.; Sobieski, M. M.; Nguyen, N.; Davies, P.] Texas A&M Hlth Sci Ctr, Houston, TX USA.
[Yoo, S. S.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S651
EP S651
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503602370
ER
PT J
AU Logan, JK
Hoang, AN
Walton-Diaz, A
Truong, H
Citrin, DE
Turkbey, B
Choyke, PL
Wood, BJ
Pinto, PA
AF Logan, J. K.
Hoang, A. N.
Walton-Diaz, A.
Truong, H.
Citrin, D. E.
Turkbey, B.
Choyke, P. L.
Wood, B. J.
Pinto, P. A.
TI Salvage MR-Guided Focal Laser Ablation of Prostate Cancer After
Brachytherapy
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Logan, J. K.; Hoang, A. N.; Walton-Diaz, A.; Truong, H.; Pinto, P. A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Citrin, D. E.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Turkbey, B.; Choyke, P. L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Wood, B. J.; Pinto, P. A.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S349
EP S350
PG 2
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503601298
ER
PT J
AU Matsuo, M
Matsumoto, S
Saito, K
Takakusagi, Y
Morris, D
Munasinghe, J
Devasahayam, N
Subramanian, S
Mitchell, J
Krishna, M
AF Matsuo, M.
Matsumoto, S.
Saito, K.
Takakusagi, Y.
Morris, D.
Munasinghe, J.
Devasahayam, N.
Subramanian, S.
Mitchell, J.
Krishna, M.
TI Hypoxic and Acute Hypoxic Intratumor Mapping by pO(2) Imaging
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Matsuo, M.; Matsumoto, S.; Saito, K.; Takakusagi, Y.; Morris, D.; Munasinghe, J.; Devasahayam, N.; Subramanian, S.; Mitchell, J.; Krishna, M.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S644
EP S645
PG 2
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503602354
ER
PT J
AU Schlaff, CD
Arscott, WT
Gordon, I
Tandle, A
Tofilon, P
Camphausen, K
AF Schlaff, C. D.
Arscott, W. T.
Gordon, I.
Tandle, A.
Tofilon, P.
Camphausen, K.
TI Radiosensitization Effects of Novel Triple-Inhibitor CUDC-101 in
Glioblastoma Multiforme and Breast Cancer Cells In Vitro
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Schlaff, C. D.; Arscott, W. T.; Gordon, I.; Tandle, A.; Tofilon, P.; Camphausen, K.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S650
EP S650
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503602369
ER
PT J
AU Simone, B
Jin, L
Dan, T
Savage, J
Minassian, H
Lim, M
Rosenberg, A
Palazzo, J
Simone, NL
AF Simone, B.
Jin, L.
Dan, T.
Savage, J.
Minassian, H.
Lim, M.
Rosenberg, A.
Palazzo, J.
Simone, N. L.
TI Caloric Restriction Coupled With Radiation Increases Overall Survival in
a Metastatic Breast Cancer Model
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Simone, B.; Jin, L.; Dan, T.; Minassian, H.; Lim, M.; Rosenberg, A.; Palazzo, J.; Simone, N. L.] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
[Savage, J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S649
EP S649
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503602365
ER
PT J
AU Tran, PT
Bellovin, DI
Adam, S
Gentles, A
Roessler, S
Thiyagarajan, S
Aziz, K
Chettiar, S
Luong, R
Plevritis, S
AF Tran, P. T.
Bellovin, D. I.
Adam, S.
Gentles, A.
Roessler, S.
Thiyagarajan, S.
Aziz, K.
Chettiar, S.
Luong, R.
Plevritis, S.
TI Twist1 Induces the Step-Wise Malignant Progression of Liver Cancer in
Transgenic Mice Revealing a Prognostic 19-Gene Signature for Humans
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
(ASTRO)
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
C1 [Tran, P. T.; Thiyagarajan, S.; Aziz, K.; Chettiar, S.] Johns Hopkins Med, Baltimore, MD USA.
[Bellovin, D. I.; Adam, S.; Gentles, A.; Luong, R.; Plevritis, S.] Stanford Univ, Stanford, CA 94305 USA.
[Roessler, S.] NCI, Bethesda, MD 20892 USA.
RI Chettiar, Sivarajan/K-2766-2014
OI Chettiar, Sivarajan/0000-0002-6864-7308
NR 0
TC 0
Z9 0
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
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD OCT 1
PY 2013
VL 87
IS 2
SU S
BP S169
EP S169
PG 1
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 219JY
UT WOS:000324503600419
ER
PT J
AU Wickerham, DL
Julian, TB
AF Wickerham, D. Lawrence
Julian, Thomas B.
TI Ductal Carcinoma In Situ: A Rose by Any Other Name
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID BREAST-CANCER; PROGRESSION; TAMOXIFEN; MARKERS; TRIAL
C1 [Wickerham, D. Lawrence; Julian, Thomas B.] Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
[Wickerham, D. Lawrence; Julian, Thomas B.] Allegheny Gen Hosp, Allegheny Canc Ctr, Pittsburgh, PA 15212 USA.
RP Wickerham, DL (reprint author), Four Allegheny Ctr, Natl Surg Adjuvant Breast & Bowel Project, 5th Fl, Pittsburgh, PA 15212 USA.
EM larry.-wickerham@nsabp.org
FU NCI NIH HHS [U10-CA-12027, U10-CA-37377, U10-CA-69651, U10-CA-69974]
NR 18
TC 8
Z9 8
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 20
BP 1521
EP 1522
DI 10.1093/jnci/djt268
PG 2
WC Oncology
SC Oncology
GA 239RS
UT WOS:000326043700003
PM 24068770
ER
PT J
AU Safaeian, M
Sherman, ME
AF Safaeian, Mahboobeh
Sherman, Mark E.
TI From Papanicolaou to Papillomaviruses: Evolving Challenges in Cervical
Cancer Screening in the Era of Human Papillomavirus Vaccination
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID UNITED-STATES; MORTALITY; TRENDS; WOMEN; RISK
C1 [Safaeian, Mahboobeh] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Sherman, Mark E.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Safaeian, M (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 9609 Med Ctr Dr,6E224,MSC 9767, Bethesda, MD 20892 USA.
EM safaeianm@mail.nih.gov
FU Intramural NIH HHS
NR 13
TC 4
Z9 4
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 20
BP 1524
EP 1526
DI 10.1093/jnci/djt267
PG 3
WC Oncology
SC Oncology
GA 239RS
UT WOS:000326043700005
PM 24096622
ER
PT J
AU Forsythe, LP
Parry, C
Alfano, CM
Kent, EE
Leach, CR
Haggstrom, DA
Ganz, PA
Aziz, N
Rowland, JH
AF Forsythe, Laura P.
Parry, Carla
Alfano, Catherine M.
Kent, Erin E.
Leach, Corinne R.
Haggstrom, David A.
Ganz, Patricia A.
Aziz, Noreen
Rowland, Julia H.
TI Use of Survivorship Care Plans in the United States: Associations With
Survivorship Care
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID FOLLOW-UP CARE; CANCER SURVIVORS; OUTCOMES RESEARCH; BREAST-CANCER;
PHYSICIANS; HEALTH; VIEWS; RECOMMENDATIONS; ONCOLOGISTS; INFORMATION
AB Survivorship care plans (SCPs), including a treatment summary and follow-up plan, intend to promote coordination of posttreatment cancer care; yet, little is known about the provision of these documents by oncologists to primary care physicians (PCPs). This study compared self-reported oncologist provision and PCP receipt of treatment summaries and follow-up plans, characterized oncologists who reported consistent provision of these documents to PCPs, and examined associations between PCP receipt of these documents and survivorship care.
A nationally representative sample of medical oncologists (n 1130) and PCPs (n 1020) were surveyed regarding follow-up care for breast and colon cancer survivors. All statistical tests were two-sided. Multivariable regression models identified factors associated with oncologist provision of treatment summaries and SCPs to PCPs (always/almost always vs less frequent).
Nearly half of oncologists reported always/almost always providing treatment summaries, whereas 20.2% reported always/almost always providing SCPs (treatment summary follow-up plan). Approximately one-third of PCPs indicated always/almost always receiving treatment summaries; 13.4% reported always/almost always receiving SCPs. Oncologists who reported training in late- and long-term effects of cancer and use of electronic medical records were more likely to report SCP provision (P < .05). PCP receipt of SCPs was associated with better PCP-reported care coordination, physicianphysician communication, and confidence in survivorship care knowledge compared to receipt of neither treatment summaries nor SCPs (P < .05).
Providing SCPs to PCPs may enhance survivorship care coordination, physicianphysician communication, and PCP confidence. However, considerable progress will be necessary to achieve implementation of sharing SCPs among oncologists and PCPs.
C1 [Forsythe, Laura P.; Parry, Carla; Alfano, Catherine M.; Kent, Erin E.; Rowland, Julia H.] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Forsythe, Laura P.; Kent, Erin E.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Leach, Corinne R.] Amer Canc Soc, Behav Res Ctr, Atlanta, GA 30329 USA.
[Haggstrom, David A.] Vet Affairs Hlth Serv Res & Dev Ctr Excellence Im, Indianapolis, IN USA.
[Haggstrom, David A.] Indiana Univ Sch Med, Dept Med, Div Gen Internal Med & Geriatr, Indianapolis, IN 46202 USA.
[Haggstrom, David A.] Indiana Univ, Ctr Hlth Serv & Outcomes Res, Regenstrief Inst Inc, Indianapolis, IN 46204 USA.
[Ganz, Patricia A.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Ganz, Patricia A.] Jonsson Comprehens Canc Ctr, Sch Publ Hlth, Div Canc Prevent & Control Res, Los Angeles, CA 90034 USA.
[Aziz, Noreen] NINR, Off Extramural Programs, NIH, Bethesda, MD 20892 USA.
RP Forsythe, LP (reprint author), 1828 L St NW,Suite 900, Washington, DC 20036 USA.
EM lforsythe@pcori.org
FU National Cancer Institute [HHSN261200700068C]; American Cancer Society
Behavioral Research Center Intramural Research funds
FX This study was supported by the National Cancer Institute (contract
number HHSN261200700068C) and the American Cancer Society Behavioral
Research Center Intramural Research funds.
NR 37
TC 36
Z9 36
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 20
BP 1579
EP 1587
DI 10.1093/jnci/djt258
PG 9
WC Oncology
SC Oncology
GA 239RS
UT WOS:000326043700012
PM 24096621
ER
PT J
AU Wuthrich, M
LeBert, V
Galles, K
Hu-Li, J
Ben-Sasson, SZ
Paul, WE
Klein, BS
AF Wuethrich, Marcel
LeBert, Vanessa
Galles, Kevin
Hu-Li, Jane
Ben-Sasson, Shlomo Z.
Paul, William E.
Klein, Bruce S.
TI Interleukin 1 Enhances Vaccine-Induced Antifungal T-Helper 17 Cells and
Resistance Against Blastomyces dermatitidis Infection
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE IL-1; adjuvant; T-cell priming; vaccine immunity; fungi
ID IMMUNE-DEFICIENT HOSTS; ANTIGEN; FUNGI; TH17; INDUCTION; MICE;
COCCIDIOIDOMYCOSIS; DIFFERENTIATION; REQUIREMENTS; EXPANSION
AB Vaccine-induced T-helper 17 (Th17) cells are necessary and sufficient to protect against fungal infection. Although live fungal vaccines are efficient in driving protective Th17 responses and immunity, attenuated fungi may not be safe for human use. Heat-inactivated formulations and subunit vaccines are safer but less potent and require adjuvant to increase their efficacy. Here, we show that interleukin 1 (IL-1) enhances the capacity of weak vaccines to induce protection against lethal Blastomyces dermatitidis infection in mice and is far more effective than lipopolysaccharide. While IL-1 enhanced expansion and differentiation of fungus-specific T cells by direct action on those cells, cooperation with non-T cells expressing IL-1R1 was necessary to maximize protection. Mechanistically, IL-17 receptor signaling was required for the enhanced protection induced by IL-1. Thus, IL-1 enhances the efficacy of safe but inefficient vaccines against systemic fungal infection in part by increasing the expansion of CD4(+) T cells, allowing their entry into the lungs, and inducing their differentiation to protective Th17 cells.
C1 [Wuethrich, Marcel; LeBert, Vanessa; Galles, Kevin; Klein, Bruce S.] Univ Wisconsin, Univ Wisconsin Hosp & Clin, Sch Med, Dept Pediat, Madison, WI 53706 USA.
[Klein, Bruce S.] Univ Wisconsin, Univ Wisconsin Hosp & Clin, Sch Med, Dept Internal Med, Madison, WI 53706 USA.
[Klein, Bruce S.] Univ Wisconsin, Univ Wisconsin Hosp & Clin, Sch Med, Dept Med Microbiol & Immunol, Madison, WI 53706 USA.
[Hu-Li, Jane; Ben-Sasson, Shlomo Z.; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Ben-Sasson, Shlomo Z.] Hebrew Univ Jerusalem, Hadassah Med Ctr, Lautenberg Ctr Gen & Tumor Immunol, Jerusalem, Israel.
RP Wuthrich, M (reprint author), Univ Wisconsin, Microbial Sci Bldg,1550 Linden Dr, Madison, WI 53706 USA.
EM mwuethri@wisc.edu
FU National Institutes of Health (NIH) [R01 AI093553, R01 AI40996];
Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, NIH
FX This work was supported by that National Institutes of Health (NIH;
grants R01 AI093553 [to M. W.] and R01 AI40996 [to B. K.]) and the
Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, NIH (to W. E. P.).
NR 30
TC 9
Z9 9
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT 1
PY 2013
VL 208
IS 7
BP 1175
EP 1182
DI 10.1093/infdis/jit283
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 239ST
UT WOS:000326046400016
PM 23788728
ER
PT J
AU Durbin, AP
Whitehead, SS
AF Durbin, Anna P.
Whitehead, Stephen S.
TI Analyzing the Development of Vaccines for Flavivirus-Endemic Scenarios:
The Case of Dengue and Dengue Vaccine in Peru Response
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Letter
ID TRIAL
C1 [Durbin, Anna P.; Whitehead, Stephen S.] Johns Hopking Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Whitehead, Stephen S.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Durbin, AP (reprint author), 624 N Broadway,Room 214, Baltimore, MD 21205 USA.
EM adurbin@jhsph.edu
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 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT 1
PY 2013
VL 208
IS 7
DI 10.1093/infdis/jit298
PG 1
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 239ST
UT WOS:000326046400018
ER
PT J
AU Jones, KA
Kim, PD
Patel, BB
Kelsen, SG
Braverman, A
Swinton, DJ
Gafken, PR
Jones, LA
Lane, WS
Neveu, JM
Leung, HCE
Shaffer, SA
Leszyk, JD
Stanley, BA
Fox, TE
Stanley, A
Hall, MJ
Hampel, H
South, CD
de la Chapelle, A
Burt, RW
Jones, DA
Kopelovich, L
Yeung, AT
AF Jones, Kelly A.
Kim, Phillip D.
Patel, Bhavinkumar B.
Kelsen, Steven G.
Braverman, Alan
Swinton, Derrick J.
Gafken, Philip R.
Jones, Lisa A.
Lane, William S.
Neveu, John M.
Leung, Hon-Chiu E.
Shaffer, Scott A.
Leszyk, John D.
Stanley, Bruce A.
Fox, Todd E.
Stanley, Anne
Hall, Michael J.
Hampel, Heather
South, Christopher D.
de la Chapelle, Albert
Burt, Randall W.
Jones, David A.
Kopelovich, Levy
Yeung, Anthony T.
TI Immunodepletion Plasma Proteomics by TripleTOF 5600 and Orbitrap
Elite/LTQ-Orbitrap Velos/Q Exactive Mass Spectrometers
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE immunodepletion; Seppro; IgY14; iTRAQ; EMMOL normalization; TripleTOF;
Orbitrap; Q Exactive
ID FINE-NEEDLE-ASPIRATION; FAMILIAL ADENOMATOUS POLYPOSIS; PANCREATIC
CYSTIC NEOPLASMS; ISOBARIC TAGS; CANCER; ITRAQ; PROTEINS; CYTOLOGY;
SEARCH; FLUID
AB Plasma proteomic experiments performed rapidly and economically using several of the latest high-resolution mass spectrometers were compared. Four quantitative hyperfractionated plasma proteomics experiments were analyzed in replicates by two AB SCIEX TripleTOF 5600 and three Thermo Scientific Orbitrap (Elite/LTQ-Orbitrap Velos/Q Exactive) instruments. Each experiment compared two iTRAQ isobaric-labeled immunodepleted plasma proteomes, provided as 30 labeled peptide fractions, and 480 LC-MS/MS runs delivered >250 GB of data in 2 months. Several analysis algorithms were compared. At 1% false discovery rate, the relative comparative findings concluded that the Thermo Scientific Q Exactive Mass Spectrometer resulted in the highest number of identified proteins and unique sequences with iTRAQ quantitation. The confidence of iTRAQ fold-change for each protein is dependent on the overall ion statistics (Mascot Protein Score) attainable by each instrument. The benchmarking also suggested how to further improve the mass spectrometry parameters and HPLC conditions. Our findings highlight the special challenges presented by the low abundance peptide ions of iTRAQ plasma proteome because the dynamic range of plasma protein abundance is uniquely high compared with cell lysates, necessitating high instrument sensitivity.
C1 [Jones, Kelly A.; Kim, Phillip D.; Patel, Bhavinkumar B.; Hall, Michael J.; Yeung, Anthony T.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Kelsen, Steven G.; Braverman, Alan] Temple Univ, Sch Med, Philadelphia, PA 19140 USA.
[Swinton, Derrick J.] Lincoln Univ, Lincoln, PA 19352 USA.
[Gafken, Philip R.; Jones, Lisa A.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Lane, William S.; Neveu, John M.] Harvard Univ, Mass Spectrometry & Prote Resource Lab, Cambridge, MA 02138 USA.
[Leung, Hon-Chiu E.] Baylor Coll Med, Mass Spectrometry & Prote Core Facil, Houston, TX 77030 USA.
[Shaffer, Scott A.; Leszyk, John D.] Univ Massachusetts, Sch Med, Prote & Mass Spectrometry Facil, Worcester, MA 01545 USA.
[Stanley, Bruce A.; Fox, Todd E.; Stanley, Anne] Penn State Coll Med, Mass Spectrometry Core, Hershey, PA 17033 USA.
[Hampel, Heather; South, Christopher D.; de la Chapelle, Albert] Ohio State Univ, Human Canc Genet Program, Columbus, OH 43210 USA.
[Burt, Randall W.; Jones, David A.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Yeung, AT (reprint author), Fox Chase Canc Ctr, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
EM anthony.yeung@fccc.edu
OI Stanley, Bruce/0000-0003-1338-2928
FU NIH [RC2 HL101713, CA138017]; NCI [N01-CN-43309]; Driskill Foundation;
Institutional Core Grants [P30 CA06927, P30 CA16058]; PA Dept. of Health
FX We acknowledge John Cottrell for optimizing the peak-picking parameters
for Mascot Distiller for this study. This work was partially supported
by NIH grant RC2 HL101713, CA138017, the NCI Work Assignment 16 of
N01-CN-43309, the Driskill Foundation, PA Dept. of Health, and
Institutional Core Grants P30 CA06927 and P30 CA16058. We acknowledge
the FCCC Biorepository, and Darshna Bhatt, Hopethe Hubbard, and Danielle
J. Culbert of OSU, for assistance in the collection of some of the
plasma samples. The authors received free demo licenses and advice from
Thermo Scientific, AB SCIEX, and Matrix Science using their software.
NR 36
TC 23
Z9 26
U1 5
U2 73
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD OCT
PY 2013
VL 12
IS 10
BP 4351
EP 4365
DI 10.1021/pr400307u
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 243MK
UT WOS:000326320300008
PM 24004147
ER
PT J
AU Balsam, J
Bruck, HA
Rasooly, A
AF Balsam, Joshua
Bruck, Hugh Alan
Rasooly, Avraham
TI Orthographic projection capillary array fluorescent sensor for mHealth
SO METHODS
LA English
DT Article
DE mHealth; Capillary; Telecentric lens; Orthographic projection;
Fluorescence; Mobile and smart phone; Camera
ID CELL-PHONE; PLATFORM; HEALTH; POINT
AB TO overcome the limited sensitivity of phone cameras for mobile health (mHealth) fluorescent detection, we have previously developed a capillary array which enables a similar to 100x increase in detection sensitivity. However, for an effective detection platform, the optical configuration must allow for uniform measurement sensitivity between channels when using such a capillary array sensor. This is a challenge due to the parallax inherent in imaging long parallel capillary tubes with typical lens configurations.
To enable effective detection, we have developed an orthographic projection system in this work which forms parallel light projection images from the capillaries using an object-space telecentric lens configuration. This optical configuration results in a significantly higher degree of uniformity in measurement between channels, as well as a significantly reduced focal distance, which enables a more compact sensor.
A plano-convex lens (f = 150 mm) was shown to produce a uniform orthographic projection when properly combined with the phone camera's built in lens (f = 4 mm), enabling measurements of long capillaries (125 mm) to be made from a distance of 160 mm. The number of parallel measurements which can be made is determined by the size of the secondary lens. Based on these results, a more compact configuration with shorter 32 mm capillaries and a plano-convex lens with a shorter focal length (f = 10 mm) was constructed.
This optical system was used to measure serial dilutions of fluorescein with a limit of detection (LOD) of 10 nM, similar to the LOD of a commercial plate reader. However, many plate readers based on standard 96 well plate requires sample volumes of 100 Ill for measurement, while the capillary array requires a sample volume of less than 10 mu l.
This optical configuration allows for a device to make use of the similar to 100x increase in fluorescent detection sensitivity produced by capillary amplification while maintaining a compact size and capability to analyze extremely small sample volumes. Such a device based on a phone or other optical mHealth technology will have the sensitivity of a conventional plate reader but have greater mHealth clinical utility, especially for telemedicine and for resource-poor settings and global health applications. Published by Elsevier Inc.
C1 [Balsam, Joshua; Rasooly, Avraham] FDA, Div Biol, Off Sci & Engn, Silver Spring, MD 20993 USA.
[Balsam, Joshua; Bruck, Hugh Alan] Univ Maryland, College Pk, MD 20742 USA.
[Rasooly, Avraham] NCI, Div Canc Biol, Bethesda, MD 20892 USA.
RP Balsam, J (reprint author), NCI, Div Canc Biol, Bethesda, MD 20892 USA.
EM rasoolya@mail.nih.gov
FU FDA's Center for Devices and Radiological Health, Division of Biology;
National Cancer Institute
FX This work was supported by the FDA's Center for Devices and Radiological
Health, Division of Biology and the National Cancer Institute. The views
expressed are those of the authors and do not represent those of the
U.S. Government.
NR 22
TC 2
Z9 2
U1 0
U2 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-2023
EI 1095-9130
J9 METHODS
JI Methods
PD OCT
PY 2013
VL 63
IS 3
BP 276
EP 281
DI 10.1016/j.ymeth.2013.07.044
PG 6
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 240ZI
UT WOS:000326135800010
PM 24018203
ER
PT J
AU Bruck, HA
Yang, MH
Kostov, Y
Rasooly, A
AF Bruck, Hugh Alan
Yang, Minghui
Kostov, Yordan
Rasooly, Avraham
TI Electrical percolation based biosensors
SO METHODS
LA English
DT Article
DE Biosensor; Semiconductor; Carbon nanotubes; Electrical percolation;
Antibody
ID STAPHYLOCOCCAL-ENTEROTOXIN-B; CARBON NANOTUBES; FOOD; FUNCTIONALIZATION;
IMMUNODETECTION; IMMUNOASSAY; COMPOSITES; SENSORS; CONDUCTIVITY; WIRES
AB A new approach to label free biosensing has been developed based on the principle of "electrical percolation". In electrical percolation, long-range electrical connectivity is formed in randomly oriented and distributed systems of discrete elements. By applying this principle to biological interactions, it is possible to measure biological components both directly and electronically. The main element for electrical percolation biosensor is the biological semiconductor (BSC) which is a multi-layer 3-D carbon nano-tube-antibody network. In the BSC, molecular interactions, such as binding of antigens to the antibodies, disrupt the network continuity causing increased resistance of the network. BSCs can be fabricated by immobilizing conducting elements, such as pre-functionalized single-walled carbon nanotubes (SWNTs)-antibody complex, directly onto a substrate, such as a Poly(methyl methacrylate) (PMMA) surface (also known as plexi-glass or Acrylic).
BSCs have been demonstrated for direct (label-free) electronic measurements of antibody-antigen binding using SWNTs. If the concentration of the SWNT network is slightly above the electrical percolation threshold, then binding of a specific antigen to the pre-functionalized SWNT dramatically increases the electrical resistance due to changes in the tunneling between the SWNTs. Using anti-staphylococcal enterotoxin B (SEB) IgG as a "gate" and SEB as an "actuator", it was demonstrated that the BSC was able to detect SEB at concentrations of 1 ng/ml. Based on this concept, an automated configuration for BSCs is described here that enables real time continuous detection. The new BSC configuration may permit assembly of multiple sensors on the same chip to create "biological central processing units (CPUs)" with multiple biological elements, capable of processing and sorting out information on multiple analytes simultaneously. Published by Elsevier Inc.
C1 [Bruck, Hugh Alan] Univ Maryland, College Pk, MD 20742 USA.
[Yang, Minghui] Cent S Univ, Coll Chem & Chem Engn, Changsha 410083, Hunan, Peoples R China.
[Kostov, Yordan] Univ Maryland Baltimore Cty, Baltimore, MD 21250 USA.
[Rasooly, Avraham] US FDA, Div Biol, Off Sci & Engn, Silver Spring, MD 20993 USA.
[Rasooly, Avraham] NCI, Rockville, MD 20850 USA.
RP Rasooly, A (reprint author), NCI, NIH, 9609 Med Ctr Dr, Rockville, MD 20850 USA.
EM rasoolya@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 43
TC 2
Z9 2
U1 1
U2 20
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-2023
EI 1095-9130
J9 METHODS
JI Methods
PD OCT
PY 2013
VL 63
IS 3
BP 282
EP 289
DI 10.1016/j.ymeth.2013.08.031
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 240ZI
UT WOS:000326135800011
PM 24041756
ER
PT J
AU Huang, JH
Doria-Rose, NA
Longo, NS
Laub, L
Lin, CL
Turk, E
Kang, BH
Migueles, SA
Bailer, RT
Mascola, JR
Connors, M
AF Huang, Jinghe
Doria-Rose, Nicole A.
Longo, Nancy S.
Laub, Leo
Lin, Chien-Li
Turk, Ellen
Kang, Byong H.
Migueles, Stephen A.
Bailer, Robert T.
Mascola, John R.
Connors, Mark
TI Isolation of human monoclonal antibodies from peripheral blood B cells
SO NATURE PROTOCOLS
LA English
DT Article
ID NEUTRALIZING ANTIBODIES; POTENT NEUTRALIZATION; PLASMA-CELLS; HIV-1;
BROAD; GENERATION; ANTIGENS; CLONING
AB Isolation of monoclonal antibodies is an important technique for understanding the specificities and characteristics of antibodies that underlie the humoral immune response to a given antigen. Here we describe a technique for isolating monoclonal antibodies from human peripheral blood mononuclear cells. The protocol includes strategies for the isolation of switch-memory B cells from peripheral blood, the culture of B cells, the removal of the supernatant for screening and the lysis of B cells in preparation for immunoglobulin heavy-chain and light-chain amplification and cloning. We have observed that the addition of cytokines IL-2, IL-21 and irradiated 3T3-msCD40L feeder cells can successfully stimulate switch-memory B cells to produce high concentrations of IgG in the supernatant. The supernatant may then be screened by appropriate assays for binding or for other functions. This protocol can be completed in 2 weeks. It is adaptable to use in other species and enables the efficient isolation of antibodies with a desired functional characteristic without prior knowledge of specificity.
C1 [Huang, Jinghe; Laub, Leo; Kang, Byong H.; Migueles, Stephen A.; Connors, Mark] NIAID, HIV Specif Immun Sect, Immunoregulat Lab, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
[Doria-Rose, Nicole A.; Longo, Nancy S.; Lin, Chien-Li; Turk, Ellen; Bailer, Robert T.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Connors, M (reprint author), NIAID, HIV Specif Immun Sect, Immunoregulat Lab, US Natl Inst Hlth NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM mconnors@nih.gov
RI Huang, Jinghe/O-1986-2015
FU Intramural Research Programs of the NIAID
FX This project has been funded in part with federal funds from the
Intramural Research Programs of the NIAID. The content of this
publication does not necessarily reflect the views or policies of the US
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 25
Z9 25
U1 3
U2 23
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-2189
EI 1750-2799
J9 NAT PROTOC
JI Nat. Protoc.
PD OCT
PY 2013
VL 8
IS 10
BP 1907
EP 1915
DI 10.1038/nprot.2013.117
PG 9
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 241JQ
UT WOS:000326163400006
PM 24030440
ER
PT J
AU Horner, AE
Heath, CJ
Hvoslef-Eide, M
Kent, BA
Kim, CH
Nilsson, SRO
Alsio, J
Oomen, CA
Holmes, A
Saksida, LM
Bussey, TJ
AF Horner, Alexa E.
Heath, Christopher J.
Hvoslef-Eide, Martha
Kent, Brianne A.
Kim, Chi Hun
Nilsson, Simon R. O.
Alsioe, Johan
Oomen, Charlotte A.
Holmes, Andrew
Saksida, Lisa M.
Bussey, Timothy J.
TI The touchscreen operant platform for testing learning and memory in rats
and mice
SO NATURE PROTOCOLS
LA English
DT Article
ID CONDITIONAL VISUAL-DISCRIMINATION; PAVLOVIAN APPROACH BEHAVIOR; ANTERIOR
CINGULATE CORTEX; NUCLEUS-ACCUMBENS CORE; SPATIAL-PATTERN SEPARATION;
COMPUTER-GRAPHIC STIMULI; MEDIAL PREFRONTAL CORTEX; DORSAL STRIATAL
SYSTEM; HIPPOCAMPAL-LESIONS; ALZHEIMERS-DISEASE
AB An increasingly popular method of assessing cognitive functions in rodents is the automated touchscreen platform, on which a number of different cognitive tests can be run in a manner very similar to touchscreen methods currently used to test human subjects. This methodology is low stress (using appetitive rather than aversive reinforcement), has high translational potential and lends itself to a high degree of standardization and throughput. Applications include the study of cognition in rodent models of psychiatric and neurodegenerative diseases (e. g., Alzheimer's disease, schizophrenia, Huntington's disease, frontotemporal dementia), as well as the characterization of the role of select brain regions, neurotransmitter systems and genes in rodents. This protocol describes how to perform four touchscreen assays of learning and memory: visual discrimination, object-location paired-associates learning, visuomotor conditional learning and autoshaping. It is accompanied by two further protocols (also published in this issue) that use the touchscreen platform to assess executive function, working memory and pattern separation.
C1 [Horner, Alexa E.] Synome Ltd, Cambridge, England.
[Horner, Alexa E.; Heath, Christopher J.; Hvoslef-Eide, Martha; Kent, Brianne A.; Kim, Chi Hun; Nilsson, Simon R. O.; Alsioe, Johan; Oomen, Charlotte A.; Saksida, Lisa M.; Bussey, Timothy J.] Univ Cambridge, Dept Psychol, Cambridge, England.
[Horner, Alexa E.; Heath, Christopher J.; Hvoslef-Eide, Martha; Kent, Brianne A.; Kim, Chi Hun; Nilsson, Simon R. O.; Alsioe, Johan; Oomen, Charlotte A.; Saksida, Lisa M.; Bussey, Timothy J.] Univ Cambridge, Behav & Clin Neurosci Inst, Cambridge, England.
[Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, US Natl Inst Hlth, Bethesda, MD USA.
RP Horner, AE (reprint author), Synome Ltd, Babraham Res Campus, Cambridge, England.
EM alexa.horner@cantab.net
RI Oomen, Charlotte/K-5259-2014; Bussey, Timothy/M-2758-2016; Saksida,
Lisa/M-2753-2016;
OI Bussey, Timothy/0000-0001-7518-4041; Saksida, Lisa/0000-0002-8416-8171;
Kent, Brianne/0000-0003-0074-028X
FU European Federation of Pharmaceutical Industries [115008]; European
Union [241995, 242167]; Wellcome Trust/Medical Research Council
[089703/Z/09/Z]; Alzheimer's Research UK [ART/PG2006/5]; Swedish Academy
of Pharmaceutical Sciences; NIAAA Intramural Research Program
FX The protocols described here are those that are currently used in our
laboratory, and they were written by current members of the group.
However, many researchers have contributed to the development of
touchscreen tasks, and we gratefully acknowledge their contribution.
They include S. Bartko, J. Brigman, S. Forwood, C. Graybeal, A.
Izquierdo, L. Lyon, A. Marti, K. McAllister, S. McTighe, J.
Nithianantharajah, C. Romberg, J. Talpos and B. Winters. The research
leading to these results has received support from the Innovative
Medicine Initiative Joint Undertaking under grant agreement no. 115008,
of which resources are composed of a European Federation of
Pharmaceutical Industries and Associations in-kind contribution and
financial contribution from the European Union's Seventh Framework
Programme (FP7/2007-2013); the Wellcome Trust/Medical Research Council
(089703/Z/09/Z) and Alzheimer's Research UK (ART/PG2006/5). A.E.H.
receives funding from the European Union Seventh Framework Programme
under grant agreement nos. 241995 (Project 'GENCODYS') and 242167
(Project 'SYNSYS'). J.A. was supported by the Swedish Academy of
Pharmaceutical Sciences. A.H. was supported by the NIAAA Intramural
Research Program.
NR 126
TC 54
Z9 54
U1 0
U2 42
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-2189
EI 1750-2799
J9 NAT PROTOC
JI Nat. Protoc.
PD OCT
PY 2013
VL 8
IS 10
BP 1961
EP 1984
DI 10.1038/nprot.2013.122
PG 24
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 241JQ
UT WOS:000326163400010
PM 24051959
ER
PT J
AU Mar, AC
Horner, AE
Nilsson, SRO
Alsio, J
Kent, BA
Kim, CH
Holmes, A
Saksida, LM
Bussey, TJ
AF Mar, Adam C.
Horner, Alexa E.
Nilsson, Simon R. O.
Alsioe, Johan
Kent, Brianne A.
Kim, Chi Hun
Holmes, Andrew
Saksida, Lisa M.
Bussey, Timothy J.
TI The touchscreen operant platform for assessing executive function in
rats and mice
SO NATURE PROTOCOLS
LA English
DT Article
ID REACTION-TIME-TASK; PREFRONTAL SEROTONIN DEPLETION; SPATIAL
WORKING-MEMORY; REVERSAL-LEARNING TASK; FRONTAL-LOBE LESIONS;
ORBITOFRONTAL CORTEX; VISUAL-DISCRIMINATION; FEAR EXTINCTION; COGNITIVE
INFLEXIBILITY; SUSTAINED ATTENTION
AB This protocol details a subset of assays developed within the touchscreen platform to measure various aspects of executive function in rodents. Three main procedures are included: extinction, measuring the rate and extent of curtailing a response that was previously, but is no longer, associated with reward; reversal learning, measuring the rate and extent of switching a response toward a visual stimulus that was previously not, but has become, associated with reward (and away from a visual stimulus that was previously, but is no longer, rewarded); and the 5-choice serial reaction time (5-CSRT) task, gauging the ability to selectively detect and appropriately respond to briefly presented, spatially unpredictable visual stimuli. These protocols were designed to assess both complementary and overlapping constructs including selective and divided visual attention, inhibitory control, flexibility, impulsivity and compulsivity. The procedures comprise part of a wider touchscreen test battery assessing cognition in rodents with high potential for translation to human studies.
C1 [Mar, Adam C.; Horner, Alexa E.; Nilsson, Simon R. O.; Alsioe, Johan; Kent, Brianne A.; Kim, Chi Hun; Saksida, Lisa M.; Bussey, Timothy J.] Univ Cambridge, Dept Psychol, Cambridge, England.
[Mar, Adam C.; Horner, Alexa E.; Nilsson, Simon R. O.; Alsioe, Johan; Kent, Brianne A.; Kim, Chi Hun; Saksida, Lisa M.; Bussey, Timothy J.] Univ Cambridge, Behav & Clin Neurosci Inst, Cambridge, England.
[Horner, Alexa E.] Synome Ltd, Cambridge, England.
[Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, NIH, Bethesda, MD 90034 USA.
RP Mar, AC (reprint author), Univ Cambridge, Dept Psychol, Cambridge, England.
EM am682@cam.ac.uk
RI Bussey, Timothy/M-2758-2016; Saksida, Lisa/M-2753-2016;
OI Bussey, Timothy/0000-0001-7518-4041; Saksida, Lisa/0000-0002-8416-8171;
Kent, Brianne/0000-0003-0074-028X
FU European Union [241995, 242167]; Wellcome Trust/Medical Research Council
[089703/Z/09/Z]; Alzheimer's Research UK [ART/PG2006/5]; Swedish Academy
of Pharmaceutical Sciences; NIAAA Intramural Research Program
FX The protocols described here are those currently used in our laboratory
and were written by current members of the group. However, many
researchers have contributed to the development of touchscreen tasks and
we would like to gratefully acknowledge their contribution. They include
S. Bartko, J. Brigman, S. Forwood, C. Graybeal, A. Izquierdo, L. Lyon,
A. Marti, K. McAllister, S. McTighe, J. Nithianantharajah, C. Romberg,
J. Talpos and B. Winters. We also thank M. Hvoslef-Eide for her
assistance in creating and modifying the mask schematics and flow
charts. The research leading to these results has received support from
the Innovative Medicine Initiative Joint Undertaking under grant
agreement no. 115008, of which resources are composed of an European
Federation of Pharmaceutical Industries and Associations in-kind
contribution and financial contribution from the European Union's
Seventh Framework Programme (FP7/2007-2013); from the Wellcome
Trust/Medical Research Council (089703/Z/09/Z) and from Alzheimer's
Research UK (ART/PG2006/5). A.E.H. receives funding from the European
Union Seventh Framework Programme under grant agreement nos. 241995
(Project 'GENCODYS') and 242167 (Project 'SYNSYS'). J.A. was supported
by the Swedish Academy of Pharmaceutical Sciences. A.E.H. was supported
by the NIAAA Intramural Research Program.
NR 102
TC 45
Z9 45
U1 2
U2 38
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-2189
EI 1750-2799
J9 NAT PROTOC
JI Nat. Protoc.
PD OCT
PY 2013
VL 8
IS 10
BP 1985
EP 2005
DI 10.1038/nprot.2013.123
PG 21
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 241JQ
UT WOS:000326163400011
PM 24051960
ER
PT J
AU Wegienka, G
Baird, D
Cooper, T
Woodcroft, K
Havstad, S
AF Wegienka, Ganesa
Baird, Donna
Cooper, Tracy
Woodcroft, Kimberley
Havstad, Suzanne
TI Authors' Reply: Cytokines and Uterine Leiomyoma - A Novel Trustful
Pathway?
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Letter
C1 [Wegienka, Ganesa; Woodcroft, Kimberley; Havstad, Suzanne] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Baird, Donna] Natl Inst Environm Hlth Sci, Epidemiol Branch, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC USA.
[Cooper, Tracy] Henry Ford Hosp, Dept Diagnost Radiol, Div Ultrasound, Detroit, MI 48202 USA.
RP Wegienka, G (reprint author), Henry Ford Hlth Syst, Dept Publ Hlth Sci, 1 Ford Pl,3E, Detroit, MI 48202 USA.
EM gwegien1@hfhs.org
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
NR 5
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
EI 1600-0897
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD OCT
PY 2013
VL 70
IS 4
BP 263
EP 263
DI 10.1111/aji.12147
PG 1
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 217SD
UT WOS:000324379800001
PM 23845097
ER
PT J
AU Lee, J
Romero, R
Chaiworapongsa, T
Dong, Z
Tarca, AL
Xu, Y
Chiang, PJ
Kusanovic, JP
Hassan, SS
Yeo, L
Yoon, BH
Than, NG
Kim, CJ
AF Lee, JoonHo
Romero, Roberto
Chaiworapongsa, Tinnakorn
Dong, Zhong
Tarca, Adi L.
Xu, Yi
Chiang, Po Jen
Pedro Kusanovic, Juan
Hassan, Sonia S.
Yeo, Lami
Yoon, Bo Hyun
Than, Nandor Gabor
Kim, Chong Jai
TI Characterization of the Fetal Blood Transcriptome and Proteome in
Maternal Anti-Fetal Rejection: Evidence of a Distinct and Novel Type of
Human Fetal Systemic Inflammatory Response
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Apolipoprotein C-III; CD 34; chronic placental inflammation; CXCL10;
pregnancy
ID PRETERM PREMATURE RUPTURE; AMNIOTIC-FLUID INTERLEUKIN-6; LEUKOCYTE
ANTIGEN ANTIBODIES; PRETRANSPLANT SERUM CXCL10; NECROSIS-FACTOR-ALPHA;
VERSUS-HOST-DISEASE; TOLL-LIKE RECEPTORS; REGULATORY T-CELLS; CHRONIC
CHORIOAMNIONITIS; INTRAAMNIOTIC INFLAMMATION
AB Background
The human fetus is able to mount a systemic inflammatory response when exposed to microorganisms. This stereotypic response has been termed the 'fetal inflammatory response syndrome' (FIRS), defined as an elevation of fetal plasma interleukin-6 (IL-6). FIRS is frequently observed in patients whose preterm deliveries are associated with intra-amniotic infection, acute inflammatory lesions of the placenta, and a high rate of neonatal morbidity. Recently, a novel form of fetal systemic inflammation, characterized by an elevation of fetal plasma CXCL10, has been identified in patients with placental lesions consistent with 'maternal anti-fetal rejection'. These lesions include chronic chorioamnionitis, plasma cell deciduitis, and villitis of unknown etiology. In addition, positivity for human leukocyte antigen (HLA) panel-reactive antibodies (PRA) in maternal sera can also be used to increase the index of suspicion for maternal anti-fetal rejection. The purpose of this study was to determine (i) the frequency of pathologic lesions consistent with maternal anti-fetal rejection in term and spontaneous preterm births; (ii) the fetal serum concentration of CXCL10 in patients with and without evidence of maternal anti-fetal rejection; and (iii) the fetal blood transcriptome and proteome in cases with a fetal inflammatory response associated with maternal anti-fetal rejection.
Method of study
Maternal and fetal sera were obtained from normal term (n = 150) and spontaneous preterm births (n = 150). A fetal inflammatory response associated with maternal anti-fetal rejection was diagnosed when the patients met two or more of the following criteria: (i) presence of chronic placental inflammation; (ii) >= 80% of maternal HLA class I PRA positivity; and (iii) fetal serum CXCL10 concentration > 75th percentile. Maternal HLA PRA was analyzed by flow cytometry. The concentrations of fetal CXCL10 and IL-6 were determined by ELISA. Transcriptome analysis was undertaken after the extraction of total RNA from white blood cells with a whole-genome DASL assay. Proteomic analysis of fetal serum was conducted by two-dimensional difference gel electrophoresis. Differential gene expression was considered significant when there was a P < 0.01 and a fold-change > 1.5.
Results
(i) The frequency of placental lesions consistent with maternal anti-fetal rejection was higher in patients with preterm deliveries than in those with term deliveries (56% versus 32%; P < 0.001); (ii) patients with spontaneous preterm births had a higher rate of maternal HLA PRA class I positivity than those who delivered at term (50% versus 32%; P = 0.002); (iii) fetuses born to mothers with positive maternal HLA PRA results had a higher median serum CXCL10 concentration than those with negative HLA PRA results (P < 0.001); (iv) the median serum CXCL10 concentration (but not IL-6) was higher in fetuses with placental lesions associated with maternal anti-fetal rejection than those without such lesions (P < 0.
1); (v) a whole-genome DASL assay of fetal blood RNA demonstrated differential expression of 128 genes between fetuses with and without lesions associated with maternal anti-fetal rejection; and (vi) comparison of the fetal serum proteome demonstrated 20 proteins whose abundance differed between fetuses with and without lesions associated with maternal anti-fetal rejection.
Conclusion
We describe a systemic inflammatory response in human fetuses born to mothers with evidence of maternal anti-fetal rejection. The transcriptome and proteome of this novel type of fetal inflammatory response were different from that of FIRS type I (which is associated with acute infection/inflammation).
C1 [Lee, JoonHo; Romero, Roberto; Chaiworapongsa, Tinnakorn; Dong, Zhong; Tarca, Adi L.; Xu, Yi; Chiang, Po Jen; Pedro Kusanovic, Juan; Hassan, Sonia S.; Yeo, Lami; Than, Nandor Gabor; Kim, Chong Jai] NICHD, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Lee, JoonHo; Romero, Roberto; Chaiworapongsa, Tinnakorn; Dong, Zhong; Tarca, Adi L.; Xu, Yi; Chiang, Po Jen; Pedro Kusanovic, Juan; Hassan, Sonia S.; Yeo, Lami; Than, Nandor Gabor; Kim, Chong Jai] NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI 48201 USA.
[Chaiworapongsa, Tinnakorn; Hassan, Sonia S.; Yeo, Lami; Than, Nandor Gabor] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Tarca, Adi L.] Wayne State Univ, Dept Comp Sci, Detroit, MI 48202 USA.
[Pedro Kusanovic, Juan] Hosp Dr Sotero del Rio, Dept Obstet & Gynecol, Santiago, Chile.
[Pedro Kusanovic, Juan] Pontificia Univ Catolica Chile, Sch Med, Dept Obstet & Gynecol, Santiago, Chile.
[Yoon, Bo Hyun] Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul, South Korea.
[Kim, Chong Jai] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, Seoul 138736, South Korea.
RP Romero, R (reprint author), NICHD, Perinatol Res Branch, NIH, DHHS,Hutzel Womens Hosp, 3990 John R St, Detroit, MI 48201 USA.
EM romeror@mail.nih.gov; ckim@amc.seoul.kr
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services (NICHD/NIH); NICHD, NIH [HHSN275201300006C]
FX This research was supported, in part, by the Perinatology Research
Branch, Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services (NICHD/NIH); and, in
part, with Federal funds from NICHD, NIH under Contract No.
HHSN275201300006C. The authors are grateful to the patients who agreed
to participate in our studies; to the nurses, laboratory staff, and
clinicians who made this work possible; and to Maureen McGerty and
Andrea Bernard (Wayne State University) for their critical readings of
the manuscript.
NR 171
TC 13
Z9 13
U1 0
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
EI 1600-0897
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD OCT
PY 2013
VL 70
IS 4
BP 265
EP 284
DI 10.1111/aji.12142
PG 20
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 217SD
UT WOS:000324379800003
PM 23905683
ER
PT J
AU Romero, R
Whitten, A
Korzeniewski, SJ
Than, NG
Chaemsaithong, P
Miranda, J
Dong, Z
Hassan, SS
Chaiworapongsa, T
AF Romero, Roberto
Whitten, Amy
Korzeniewski, Steven J.
Than, Nandor Gabor
Chaemsaithong, Piya
Miranda, Jezid
Dong, Zhong
Hassan, Sonia S.
Chaiworapongsa, Tinnakorn
TI Maternal Floor Infarction/Massive Perivillous Fibrin Deposition: A
Manifestation of Maternal Antifetal Rejection?
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Fibrinoid deposition; HLA; plasma cell deciduitis; stillbirth; villitis;
pregnancy; chorioamnionitis; VUE; PRA; CXCL; MPFD; MFI
ID REGULATORY T-CELLS; RENAL-ALLOGRAFT REJECTION; VERSUS-HOST-DISEASE;
LEUKOCYTE ANTIGEN ANTIBODIES; SOLID-ORGAN TRANSPLANTATION; CHEMOKINE
RECEPTOR CXCR3; CHRONIC CHORIOAMNIONITIS; CLINICAL-SIGNIFICANCE; UNKNOWN
ETIOLOGY; FETAL TOLERANCE
AB Objective
Massive perivillous fibrin deposition (MPFD) and maternal floor infarction (MFI) are related placental lesions often associated with fetal death and fetal growth restriction. A tendency to recur in subsequent pregnancies has been reported. This study was conducted to determine whether this complication of pregnancy could reflect maternal antifetal rejection.
Methods
Pregnancies with MPFD were identified (n=10). Controls consisted of women with uncomplicated pregnancies who delivered at term without MPFD (n=175). Second-trimester maternal plasma was analyzed for panel-reactive anti-HLA class I and class II antibodies. The prevalence of chronic chorioamnionitis, villitis of unknown etiology, and plasma cell deciduitis was compared between cases and controls. Immunohistochemistry was performed on available umbilical vein segments from cases with MPFD (n=4) to determine whether there was evidence of complement activation (C4d deposition). Specific maternal HLA-antibody and fetal HLA-antigen status were also determined in paired specimens (n=6). Plasma CXCL-10 concentrations were measured in longitudinal samples of cases (n=28 specimens) and controls (n=749 specimens) by ELISA. Linear mixed-effects models were used to test for differences in plasma CXCL-10 concentration.
Results
(i) The prevalence of plasma cell deciduitis in the placenta was significantly higher in cases with MPFD than in those with uncomplicated term deliveries (40% versus 8.6%, P=0.01), (ii) patients with MPFD had a significantly higher frequency of maternal anti-HLA class I positivity during the second trimester than those with uncomplicated term deliveries (80% versus 36%, P=0.01); (iii) strongly positive C4d deposition was observed on umbilical vein endothelium in cases of MPFD, (iv) a specific maternal antibody against fetal HLA antigen class I or II was identified in all cases of MPFD; and 5) the mean maternal plasma concentration of CXCL-10 was higher in patients with evidence of MPFD than in those without evidence of MFPD (P<0.001).
Conclusion
A subset of patients with MPFD has evidence of maternal antifetal rejection.
C1 [Romero, Roberto; Whitten, Amy; Korzeniewski, Steven J.; Than, Nandor Gabor; Chaemsaithong, Piya; Miranda, Jezid; Dong, Zhong; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI USA.
[Romero, Roberto; Whitten, Amy; Korzeniewski, Steven J.; Than, Nandor Gabor; Chaemsaithong, Piya; Miranda, Jezid; Dong, Zhong; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] NICHD, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Whitten, Amy; Korzeniewski, Steven J.; Than, Nandor Gabor; Chaemsaithong, Piya; Miranda, Jezid; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
RP Romero, R (reprint author), Wayne State Univ, Hutzel Womens Hosp, Perinatol Res Branch, NICHD,NIH,DHHS, 3990 John R,Box 4, Detroit, MI 48201 USA.
EM romeror@mail.nih.gov
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services (NICHD/NIH); NICHD, NIH [HSN275201300006C]
FX This research was supported, in part, by the Perinatology Research
Branch, Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services (NICHD/NIH); and, in
part, with Federal funds from NICHD, NIH under Contract No.
HSN275201300006C.
NR 116
TC 12
Z9 12
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
EI 1600-0897
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD OCT
PY 2013
VL 70
IS 4
BP 285
EP 298
DI 10.1111/aji.12143
PG 14
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 217SD
UT WOS:000324379800004
PM 23905710
ER
PT J
AU Wegienka, G
Baird, DD
Cooper, T
Woodcroft, KJ
Havstad, S
AF Wegienka, Ganesa
Baird, Donna Day
Cooper, Tracy
Woodcroft, Kimberley J.
Havstad, Suzanne
TI Cytokine Patterns Differ Seasonally between Women with and without
Uterine Leiomyomata
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE chemokines; cytokines; growth factors; inflammation; leiomyoma
ID REPRODUCTIVE FACTORS; MONONUCLEAR-CELLS; FIBROIDS; RISK; INFLAMMATION;
HYPOTHESIS; CANCER; SUSCEPTIBILITY; ENDOMETRIOSIS; HYSTERECTOMY
AB Problem
Uterine leiomyomata are the most common reproductive tumor in women, and their cause is not known.
Methods of Study
Plasma samples from 155 women (74 with and 81 without ultrasound-confirmed leiomyoma) from a new study of leiomyoma risk factors in the Detroit, Michigan area, were examined for any cross-sectional associations between commonly examined cytokines and leiomyoma presence.
Results
Associations varied by season of sample collection defined a priori as winter (December-February) and non-winter seasons. In the winter months, interleukin (IL)13 and IL17 were positively and IP10 was inversely associated with having a leiomyoma. In the non-winter samples, VEGF, G-CSF, and IP10 were positively associated and Monocyte chemotactic protein-1, IL13, and IL17 were inversely associated with having a leiomyoma. Associations were not changed by adjustment for age or BMI.
Conclusions
These data suggest that new insight into leiomyoma formation may be acquired through investigation of the immune system.
C1 [Wegienka, Ganesa; Woodcroft, Kimberley J.; Havstad, Suzanne] Henry Ford Hosp, Dept Publ Hlth Sci, Detroit, MI 48202 USA.
[Baird, Donna Day] Natl Inst Environm Hlth Sci, Epidemiol Branch, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC USA.
[Cooper, Tracy] Henry Ford Hosp, Dept Diagnost Radiol, Div Ultrasound, Detroit, MI 48202 USA.
RP Wegienka, G (reprint author), 1 Ford Pl,3E, Detroit, MI 48202 USA.
EM gwegien1@hfhs.org
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU intramural program at the National Institute of Environmental Health
Sciences, NIH
FX Dr. Christie Barker-Cummings manages the Study of Environment Lifestyle
and Fibroids. Project management at Henry Ford Health System was led by
Karen Bourgeois, LPN, and Kyra Jones, MEd. Data collection was funded by
the intramural program at the National Institute of Environmental Health
Sciences, NIH.
NR 41
TC 2
Z9 2
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
EI 1600-0897
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD OCT
PY 2013
VL 70
IS 4
BP 327
EP 335
DI 10.1111/aji.12127
PG 9
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 217SD
UT WOS:000324379800008
PM 23614810
ER
PT J
AU Andreopoulou, E
Vigoda, IS
Valero, V
Hershman, DL
Raptis, G
Vahdat, LT
Han, HS
Wright, JJ
Pellegrino, CM
Cristofanilli, M
Alvarez, RH
Fehn, K
Fineberg, S
Sparano, JA
AF Andreopoulou, Eleni
Vigoda, Ivette S.
Valero, Vicente
Hershman, Dawn L.
Raptis, George
Vahdat, Linda T.
Han, Hyo S.
Wright, John J.
Pellegrino, Christine M.
Cristofanilli, Massimo
Alvarez, Ricardo H.
Fehn, Karen
Fineberg, Susan
Sparano, Joseph A.
TI Phase I-II study of the farnesyl transferase inhibitor tipifarnib plus
sequential weekly paclitaxel and doxorubicin-cyclophosphamide in
HER2/neu-negative inflammatory carcinoma and non-inflammatory estrogen
receptor-positive breast carcinoma
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Farnesyl transferase inhibitor; Tipifarnib; Ras; Breast cancer;
Neoadjuvant chemotherapy; Inflammatory breast cancer
ID PATHOLOGICAL COMPLETE RESPONSE; BIPOLAR SPINDLE FORMATION; RAS
TRANSGENIC MICE; FARNESYLTRANSFERASE INHIBITOR; NEOADJUVANT
CHEMOTHERAPY; CANCER CELLS; TUMOR-CELLS; EXPRESSION; R115777; KINASE
AB Tipifarnib (T) is a farnesyl transferase inhibitor (FTI) that enhances the antineoplastic effects of cytotoxic therapy in vitro, has activity in metastatic breast cancer, and enhances the pathologic complete response (pCR) rate to neoadjuvant doxorubicin-cyclophosphamide (AC) chemotherapy. We, therefore, performed a phase I-II trial of T plus neoadjuvant sequential weekly paclitaxel and 2-week AC chemotherapy in locally advanced breast cancer. Eligible patients with HER2-negative clinical stage IIB-IIIC breast cancer received 12 weekly doses of paclitaxel (80 mg/m(2)) followed by AC (60/600 mg/m(2) every 2 weeks and filgrastim), plus T (100 or 200 mg PO on days 1-3 of each P dose, and 200 mg PO on days 2-7 of each AC cycle). The trial was powered to detect an improvement in breast pCR rate from 15 to 35 % (alpha = 0.10, beta = 0.10) in two strata, including ER and/or PR-positive, non-inflammatory (stratum A) and inflammatory carcinoma (stratum B). Of the 60 patients accrued, there were no dose-limiting toxicities among the first six patients treated at the first T dose level (100 mg BID; N = 3) or second T dose level (200 mg BID; N = 3) plus paclitaxel. Breast pCR occurred in 6/33 patients (18 %, 95 % confidence intervals (CI) 7-36 %) and 1/22 patients (4 %, 95 % CI 0-8 %) in stratum B. Combination of the FTI T with weekly paclitaxel-AC is unlikely to be associated with a breast pCR rate of 35 % or higher in patients with locally advanced HER2/neu-negative inflammatory or non-inflammatory ER- and/or PR-positive breast carcinoma.
C1 [Andreopoulou, Eleni; Vigoda, Ivette S.; Pellegrino, Christine M.; Fehn, Karen; Fineberg, Susan; Sparano, Joseph A.] Albert Einstein Coll Med, Montefiore Med Ctr, Dept Oncol, Weiler Div, Bronx, NY 10461 USA.
[Valero, Vicente; Alvarez, Ricardo H.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Hershman, Dawn L.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
[Raptis, George] North Shore LIJ Canc Inst, Manhasset, NY USA.
[Vahdat, Linda T.] Weill Cornell Med Coll, New York, NY USA.
[Han, Hyo S.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Wright, John J.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Cristofanilli, Massimo] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
RP Sparano, JA (reprint author), Albert Einstein Coll Med, Montefiore Med Ctr, Dept Oncol, Weiler Div, 2 South,1825 Eastchester Rd, Bronx, NY 10461 USA.
EM jsparano@montefiore.org
OI Vahdat, Linda/0000-0002-3522-7382
FU United States Department of Health and Human Service [N01-CM-62204];
[RO1CA98473]
FX Supported by United States Department of Health and Human Service
contract N01-CM-62204 (P. I. Joseph A. Sparano, MD) and Grant RO1CA98473
(P. I. Said Sebti, PhD, co-PI: Joseph A. Sparano, MD).
NR 40
TC 4
Z9 5
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD OCT
PY 2013
VL 141
IS 3
BP 429
EP 435
DI 10.1007/s10549-013-2704-x
PG 7
WC Oncology
SC Oncology
GA 239QS
UT WOS:000326041100011
PM 24068539
ER
PT J
AU Phan, GQ
Rosenberg, SA
AF Phan, Giao Q.
Rosenberg, Steven A.
TI Adoptive Cell Transfer for Patients With Metastatic Melanoma: The
Potential and Promise of Cancer Immunotherapy
SO CANCER CONTROL
LA English
DT Article
ID TUMOR-INFILTRATING LYMPHOCYTES; CD8(+) T-CELLS; RECOMBINANT
INTERLEUKIN-2 THERAPY; HIGH-DOSE INTERLEUKIN-2; ACTIVATED KILLER-CELLS;
AUTOLOGOUS TUMOR; MALIGNANT-MELANOMA; CLINICAL-TRIAL; ADVERSE EVENT;
REGRESSION
AB Background: Current FDA-approved therapeutic options for patients with metastatic melanoma include dacarbazine, interleukin 2, ipilimumab, vemurafenib, dabrafenib, and trametinib, but long-term tumor regression using available agents remains out of reach for most patients. Adoptive cell transfer (ACT) with autologous tumor-infiltrating lymphocytes (TILs) has shown encouraging results in clinical trials, with evidence of durable ongoing complete responses in patients with advanced melanoma. Emerging techniques to engineer T-cell receptors (TCRs) or chimeric antigen receptors (CARs) using lymphocytes from peripheral blood may offer new tactics in ACT
Methods: We reviewed the literature to provide a synopsis on the development and clinical trial results of ACT, as well as the future outlook for using ACT in patients with metastatic melanoma.
Results: ACT with TILs as part of a lymphodepleting regimen has been shown in clinical trials to cause objective clinical responses in approximately 40% to 72% of patients with metastatic melanoma, with up to 40% of those patients experiencing complete responses lasting up to 7 years ongoing. Pilot trials using TCR-engineered cells against melanoma-associated antigens MART-1 and gp100 and the cancer-testis antigen NY-ESO-1 have shown clinical responses in patients with melanoma. CAR cells directed against melanoma have been tested only in preclinical models; however, CAR cells targeting other histologies such as lymphoma have elicited antitumor responses in patients.
Conclusions: An example of state-of-the-art personalized medicine, ACT is a potentially curative therapy for patients with metastatic melanoma. Ongoing trials aiming to simplify the regimens may allow a broader range of patients to be treated and enable ACT to be offered by academic cancer centers.
C1 [Phan, Giao Q.; Rosenberg, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Phan, GQ (reprint author), NCI, Surg Branch, NIH, Bldg 10-CRC,Room 3-5760,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Giao.Phan@nih.gov
NR 66
TC 37
Z9 40
U1 0
U2 14
PU H LEE MOFFITT CANCER CENTER & RESEARCH INST
PI TAMPA
PA 12902 MAGNOLIA DR, TAMPA, FL 33612 USA
SN 1073-2748
J9 CANCER CONTROL
JI Cancer Control
PD OCT
PY 2013
VL 20
IS 4
BP 289
EP 297
PG 9
WC Oncology
SC Oncology
GA 234RV
UT WOS:000325662900006
PM 24077405
ER
PT J
AU Yutin, N
Galperin, MY
AF Yutin, Natalya
Galperin, Michael Y.
TI A genomic update on clostridial phylogeny: Gram-negative spore formers
and other misplaced clostridia
SO ENVIRONMENTAL MICROBIOLOGY
LA English
DT Article
ID RIBOSOMAL-RNA ANALYSIS; SP-NOV.; GEN. NOV.; HUMAN FECES; POSITIVE
BACTERIA; OUTER-MEMBRANE; COMB. NOV; SEQUENCE; SPORULATION; DATABASE
AB The class Clostridia in the phylum Firmicutes (formerly low-G+C Gram-positive bacteria) includes diverse bacteria of medical, environmental and biotechnological importance. The Selenomonas-Megasphaera-Sporomusa branch, which unifies members of the Firmicutes with Gram-negative-type cell envelopes, was recently moved from Clostridia to a separate class Negativicutes. However, draft genome sequences of the spore-forming members of the Negativicutes revealed typically clostridial sets of sporulation genes. To address this and other questions in clostridial phylogeny, we have compared a phylogenetic tree for a concatenated set of 50 widespread ribosomal proteins with the trees for beta subunits of the RNA polymerase (RpoB) and DNA gyrase (GyrB) and with the 16S rRNA-based phylogeny. The results obtained by these methods showed remarkable consistency, suggesting that they reflect the true evolutionary history of these bacteria. These data put the Selenomonas-Megasphaera-Sporomusa group back within the Clostridia. They also support placement of Clostridium difficile and its close relatives within the family Peptostreptococcaceae; we suggest resolving the long-standing naming conundrum by renaming it Peptoclostridium difficile. These data also indicate the existence of a group of cellulolytic clostridia that belong to the family Ruminococcaceae. As a tentative solution to resolve the current taxonomical problems, we propose assigning 78 validly described Clostridium species that clearly fall outside the family Clostridiaceae to six new genera: Peptoclostridium, Lachnoclostridium, Ruminiclostridium, Erysipelatoclostridium, Gottschalkia and Tyzzerella. This work reaffirms that 16S rRNA and ribosomal protein sequences are better indicators of evolutionary proximity than phenotypic traits, even such key ones as the structure of the cell envelope and Gram-staining pattern.
C1 [Yutin, Natalya; Galperin, Michael Y.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Galperin, MY (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
EM galperin@ncbi.nlm.nih.gov
OI Galperin, Michael/0000-0002-2265-5572
FU NIH Intramural Research Program at the National Library of Medicine
FX We thank Drs. Boris Belitsky, Elizaveta Bonch-Osmolovskaya, Ilya
Borovok, Jean Paul Euzeby, William B. Whitman and Juergen Wiegel for
critically reading the manuscript and many helpful comments and Drs.
Yuri Wolf and Eugene Koonin for advice on the phylogenetic trees. This
work was supported by the NIH Intramural Research Program at the
National Library of Medicine.
NR 59
TC 116
Z9 119
U1 8
U2 57
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-2912
EI 1462-2920
J9 ENVIRON MICROBIOL
JI Environ. Microbiol.
PD OCT
PY 2013
VL 15
IS 10
BP 2631
EP 2641
DI 10.1111/1462-2920.12173
PG 11
WC Microbiology
SC Microbiology
GA 230TY
UT WOS:000325367200001
PM 23834245
ER
PT J
AU Hankee, LD
Preis, SR
Beiser, AS
Devine, SA
Liu, YL
Seshadri, S
Wolf, PA
Au, R
AF Hankee, Lisa D.
Preis, Sarah R.
Beiser, Alexa S.
Devine, Sherral A.
Liu, Yulin
Seshadri, Sudha
Wolf, Philip A.
Au, Rhoda
TI QUALITATIVE NEUROPSYCHOLOGICAL MEASURES: NORMATIVE DATA ON EXECUTIVE
FUNCTIONING TESTS FROM THE FRAMINGHAM OFFSPRING STUDY
SO EXPERIMENTAL AGING RESEARCH
LA English
DT Article
ID WHITE-MATTER HYPERINTENSITIES; MILD COGNITIVE IMPAIRMENT;
ALZHEIMERS-DISEASE; OLDER-ADULTS; RISK PROFILE; BRAIN; AGE; ASSOCIATION;
POPULATION; ATTENTION
AB Background/Study Context: Studies have found that executive functioning is affected early in the pathophysiological processes associated with Alzheimer's disease and vascular dementia. There also exists a range of functioning on executive tasks during normal aging. Although qualitative data are commonly utilized in clinical practice for evaluating subtle changes in cognitive functioning and diagnostic discernment, it is not clear whether error responses used in clinical practice are also evident as normative behavior. Methods: As part of an extensive battery of neuropsychological tests, executive functioning measures (i.e., Trail Making Test Part B, Similarities and Verbal Fluency tests) were administered via standardized administration prescript. Regression analyses were used to determine associations between vascular aging indices and qualitative performance measures. Descriptive statistics are included for 1907 cognitively normal individuals. Results: Results suggest that although qualitative errors do occur, they are relatively infrequent within a presumably cognitively normal sample. Error commission rates on executive functioning tests are significantly associated with both age and education. Conclusion: Provided is a baseline profile of errors committed on tests of executive function across a range of age and educational levels. The normative data sets are included, stratified by age and educational achievement, for which to compare qualitative test performance of clinical and research populations.
C1 [Hankee, Lisa D.; Beiser, Alexa S.; Devine, Sherral A.; Liu, Yulin; Seshadri, Sudha; Wolf, Philip A.; Au, Rhoda] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Hankee, Lisa D.; Preis, Sarah R.; Beiser, Alexa S.; Devine, Sherral A.; Liu, Yulin; Seshadri, Sudha; Wolf, Philip A.; Au, Rhoda] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Preis, Sarah R.; Beiser, Alexa S.] Boston Univ, Sch Publ Hlth, Boston, MA 02118 USA.
RP Au, R (reprint author), Boston Univ, Dept Neurol, Sch Med, 72 E Concord St,B-6, Boston, MA 02118 USA.
EM rhodaau@bu.edu
OI Beiser, Alexa/0000-0001-8551-7778
FU Framingham Heart Study's National Heart, Lung, and Blood Institute
[N01-HC-25195]; National Institute on Aging [R01-AG16495, R01-AG08122,
R01-AG033040]; National Institute of Neurological Disorders and Stroke
[R01-NS17950]
FX This work was supported by the Framingham Heart Study's National Heart,
Lung, and Blood Institute contract (N01-HC-25195), by grants
(R01-AG16495, R01-AG08122, R01-AG033040) from the National Institute on
Aging, and by grant (R01-NS17950) from the National Institute of
Neurological Disorders and Stroke.
NR 44
TC 4
Z9 4
U1 0
U2 12
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0361-073X
EI 1096-4657
J9 EXP AGING RES
JI Exp. Aging Res.
PD OCT 1
PY 2013
VL 39
IS 5
BP 515
EP 535
DI 10.1080/0361073X.2013.839029
PG 21
WC Geriatrics & Gerontology; Psychology
SC Geriatrics & Gerontology; Psychology
GA 239HH
UT WOS:000326012700003
PM 24151914
ER
PT J
AU Wright, PW
Huehn, A
Cichocki, F
Li, H
Sharma, N
Dang, H
Lenvik, TR
Woll, P
Kaufman, D
Miller, JS
Anderson, SK
AF Wright, P. W.
Huehn, A.
Cichocki, F.
Li, H.
Sharma, N.
Dang, H.
Lenvik, T. R.
Woll, P.
Kaufman, D.
Miller, J. S.
Anderson, S. K.
TI Identification of a KIR antisense lncRNA expressed by progenitor cells
SO GENES AND IMMUNITY
LA English
DT Article
DE human NK cells; KIR; antisense; transcription; lncRNA
ID ZINC-FINGER GENE; DNA METHYLATION; NK CELLS; TRANSCRIPTION; REPERTOIRE;
PROMOTERS; PATTERNS; ELEMENT; BINDING; FAMILY
AB Human NK cells express cell surface class I MHC receptors (killer cell immunoglobulin-like receptor, KIR) in a probabilistic manner. Previous studies have shown that a distal promoter acts in conjunction with a proximal bidirectional promoter to control the selective activation of KIR genes. We report here the presence of an intron 2 promoter in several KIR genes that produce a spliced antisense transcript. This long noncoding RNA (lncRNA) transcript contains antisense sequence complementary to KIR-coding exons 1 and 2 as well as the proximal promoter region of the KIR genes. The antisense promoter contains myeloid zinc finger 1 (MZF-1)-binding sites, a transcription factor found in hematopoietic progenitors and myeloid precursors. The KIR antisense lncRNA was detected only in progenitor cells or pluripotent cell lines, suggesting a function that is specific for stem cells. Overexpression of MZF-1 in developing NK cells led to decreased KIR expression, consistent with a role for the KIR antisense lncRNA in silencing KIR gene expression early in development.
C1 [Wright, P. W.; Li, H.; Anderson, S. K.] SAIC Frederick Inc, Frederick Natl Lab, Expt Immunol Lab, Frederick, MD 21702 USA.
[Huehn, A.; Sharma, N.; Dang, H.; Anderson, S. K.] NCI, Canc & Inflammat Program, CCR, Frederick, MD 21701 USA.
[Cichocki, F.; Lenvik, T. R.; Miller, J. S.] Univ Minnesota, Div Hematol Oncol & Transplantat, Minneapolis, MN USA.
[Woll, P.; Kaufman, D.] Univ Minnesota, Stem Cell Inst, Minneapolis, MN USA.
RP Anderson, SK (reprint author), SAIC Frederick Inc, Frederick Natl Lab, Expt Immunol Lab, Bldg 560,Room 31-93, Frederick, MD 21702 USA.
EM andersonst@mail.nih.gov
RI Anderson, Stephen/B-1727-2012;
OI Anderson, Stephen/0000-0002-7856-4266; Miller, Jeffrey
S/0000-0002-0339-4944; Woll, Petter S./0000-0002-2340-2526
FU National Cancer Institute (NCI), NIH [HHSN261200800001E]; NCI [P01
111412]; Intramural Research Program of the NIH, NCI, Center for Cancer
Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute (NCI), NIH, under contract
HHSN261200800001E and NCI grant P01 111412 (JSM, SKA). This research was
supported in part by the Intramural Research Program of the NIH, NCI,
Center for Cancer Research.
NR 27
TC 9
Z9 9
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
EI 1476-5470
J9 GENES IMMUN
JI Genes Immun.
PD OCT
PY 2013
VL 14
IS 7
BP 427
EP 433
DI 10.1038/gene.2013.36
PG 7
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 240LR
UT WOS:000326098300003
PM 23863987
ER
PT J
AU Gottesman, O
Kuivaniemi, H
Tromp, G
Faucett, WA
Li, RL
Manolio, TA
Sanderson, SC
Kannry, J
Zinberg, R
Basford, MA
Brilliant, M
Carey, DJ
Chisholm, RL
Chute, CG
Connolly, JJ
Crosslin, D
Denny, JC
Gallego, CJ
Haines, JL
Hakonarson, H
Harley, J
Jarvik, GP
Kohane, I
Kullo, IJ
Larson, EB
McCarty, C
Ritchie, MD
Roden, DM
Smith, ME
Bottinger, EP
Williams, MS
AF Gottesman, Omri
Kuivaniemi, Helena
Tromp, Gerard
Faucett, W. Andrew
Li, Rongling
Manolio, Teri A.
Sanderson, Saskia C.
Kannry, Joseph
Zinberg, Randi
Basford, Melissa A.
Brilliant, Murray
Carey, David J.
Chisholm, Rex L.
Chute, Christopher G.
Connolly, John J.
Crosslin, David
Denny, Joshua C.
Gallego, Carlos J.
Haines, Jonathan L.
Hakonarson, Hakon
Harley, John
Jarvik, Gail P.
Kohane, Isaac
Kullo, Iftikhar J.
Larson, Eric B.
McCarty, Catherine
Ritchie, Marylyn D.
Roden, Dan M.
Smith, Maureen E.
Bottinger, Erwin P.
Williams, Marc S.
CA eMerge Network
TI The Electronic Medical Records and Genomics (eMERGE) Network: past,
present, and future
SO GENETICS IN MEDICINE
LA English
DT Review
DE collaborative research; electronic medical records; genetics and
genomics; genome-wide association studies; personalized medicine
ID DECISION-SUPPORT-SYSTEMS; WIDE ASSOCIATION; PRACTITIONER PERFORMANCE;
PATIENT OUTCOMES; CLINICAL IMPACT; PHENOME-WIDE; BASE-PAIRS; HEALTH;
VARIANTS; DISCOVERIES
AB The Electronic Medical Records and Genomics Network is a National Human Genome Research Institute-funded consortium engaged in the development of methods and best practices for using the electronic medical record as a tool for genomic research. Now in its sixth year and second funding cycle, and comprising nine research groups and a coordinating center, the network has played a major role in validating the concept that clinical data derived from electronic medical records can be used successfully for genomic research. Current work is advancing knowledge in multiple disciplines at the intersection of genomics and health. care informatics, particularly for electronic phenotyping, genome-wide association studies, genomic medicine implementation, and the ethical and regulatory issues associated with genomics research and returning results to study participants. Here, we describe the evolution, accomplishments, opportunities, and challenges of the network from its inception as a five-group consortium focused on genotype-phenotype associations for genomic discovery to its current form as a nine-group consortium pivoting toward the implementation of genomic medicine.
C1 [Gottesman, Omri; Sanderson, Saskia C.; Kannry, Joseph; Zinberg, Randi; Bottinger, Erwin P.] Mt Sinai Sch Med, New York, NY 10029 USA.
[Kuivaniemi, Helena; Tromp, Gerard; Faucett, W. Andrew; Carey, David J.; Williams, Marc S.] Weis Ctr Res, Geisinger Clin, Danville, PA 17822 USA.
[Li, Rongling; Manolio, Teri A.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Basford, Melissa A.; Denny, Joshua C.; Haines, Jonathan L.; Roden, Dan M.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Brilliant, Murray] Marshfield Clin Res Fdn, Marshfield, WI USA.
[Chisholm, Rex L.; Smith, Maureen E.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Chute, Christopher G.; Kullo, Iftikhar J.] Mayo Clin, Rochester, MN USA.
[Connolly, John J.; Hakonarson, Hakon] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Crosslin, David; Gallego, Carlos J.; Jarvik, Gail P.] Univ Washington, Med Ctr, Seattle, WA 98195 USA.
[Harley, John] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Kohane, Isaac] Boston Childrens Hosp, Boston, MA USA.
[Larson, Eric B.] Grp Hlth Res Inst, Seattle, WA USA.
[McCarty, Catherine] Essentia Inst Rural Hlth, Duluth, MN USA.
[Ritchie, Marylyn D.] Penn State Univ, University Pk, PA 16802 USA.
RP Gottesman, O (reprint author), Mt Sinai Sch Med, New York, NY 10029 USA.
EM omri.gottesman@mssm.edu; shkuivaniemi@geisinger.edu
RI Jarvik, Gail/N-6476-2014; Hulot, Jean-Sebastien/A-2278-2016; Wagner,
Michael/E-6273-2016; Tromp, Gerard/B-2677-2017;
OI Jarvik, Gail/0000-0002-6710-8708; Hulot,
Jean-Sebastien/0000-0001-5463-6117; Overby, Casey/0000-0001-9302-5968;
Wagner, Michael/0000-0003-3421-4763; Tromp, Gerard/0000-0002-7761-0806;
Pan, Vivian/0000-0002-1666-9273; Williams, Marc/0000-0001-6165-8701;
Kuivaniemi, Helena/0000-0001-5753-8766
FU NHGRI; National Institute of General Medical Sciences [U01HG004438,
U01HG004424, U01HG004610, U01HG006375, U01HG004608, U01HG006389,
U01HG04599, U01HG006379, U01HG004609, U01HG006388, U01HG04603,
U01HG006378, U01HG006385, U01HG006382, U01HG006380, U01HG006830,
U01HG006828]; Pennsylvania Commonwealth Universal Research Enhancement
Program; Ben Franklin Technology Development Fund of PA; National
Institutes of Health [P30DK072488, R01DK088231, R01DK091601]; Geisinger
Clinical Research Fund; American Heart Association; Northwest Institute
of Genetic Medicine; Washington State Life Sciences Discovery funds
[265508]
FX The eMERGE Network is funded by the NHGRI, with additional funding from
the National Institute of General Medical Sciences through the following
grants: U01HG004438 to Johns Hopkins University; U01HG004424 to the
Broad Institute; U01HG004438 to Center for Inherited Disease Research;
U01HG004610 and U01HG006375 to Group Health Cooperative; U01HG004608 to
Marshfield Clinic; U01HG006389 to Essentia Institute of Rural Health;
U01HG04599 and U01HG006379 to Mayo Clinic; U01HG004609 and U01HG006388
to Northwestern University; U01HG04603 and U01HG006378 to Vanderbilt
University; U01HG006385 to the Coordinating Center; U01HG006382 to
Geisinger Clinic; U01HG006380 to Mount Sinai School of Medicine;
U01HG006830 to The Children's Hospital of Philadelphia; and U01HG006828
to Cincinnati Children's Hospital and Boston Children's Hospital.; The
biobanking and genotyping at Geisinger Clinic was funded by the
Pennsylvania Commonwealth Universal Research Enhancement Program, the
Ben Franklin Technology Development Fund of PA, grants from the National
Institutes of Health (P30DK072488, R01DK088231, and R01DK091601), the
Geisinger Clinical Research Fund, and a grant-in-aid from the American
Heart Association.; The Group Health subject collection was part of an
ongoing National Institute on Aging project, Adult Changes in Thoughts
(ACT) study (AG06781) and was also supported in part by the Northwest
Institute of Genetic Medicine with funds from the Washington State Life
Sciences Discovery funds (grant 265508).
NR 52
TC 140
Z9 143
U1 2
U2 39
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2013
VL 15
IS 10
BP 761
EP 771
DI 10.1038/gim.2013.72
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 234SQ
UT WOS:000325665000002
PM 23743551
ER
PT J
AU Tarczy-Hornoch, P
Amendola, L
Aronson, SJ
Garraway, L
Gray, S
Grundmeier, RW
Hindorff, LA
Jarvik, G
Karavite, D
Lebo, M
Plon, SE
Van Allen, E
Weck, KE
White, PS
Yang, YP
AF Tarczy-Hornoch, Peter
Amendola, Laura
Aronson, Samuel J.
Garraway, Levi
Gray, Stacy
Grundmeier, Robert W.
Hindorff, Lucia A.
Jarvik, Gail
Karavite, Dean
Lebo, Matthew
Plon, Sharon E.
Van Allen, Eliezer
Weck, Karen E.
White, Peter S.
Yang, Yaping
TI A survey of informatics approaches to whole-exome and whole-genome
clinical reporting in the electronic health record
SO GENETICS IN MEDICINE
LA English
DT Article
DE clinical decision support; clinical sequencing; decision support rules;
electronic health record; electronic medical record; next-generation
sequencing
ID MEDICAL-RECORDS; GENETIC-VARIANTS; DECISION-SUPPORT; KNOWLEDGE;
INTEGRATION
AB Purpose: Genome-scale clinical sequencing is being adopted more broadly in medical practice. The National Institutes of Health developed the Clinical Sequencing Exploratory Research (CSER) program to guide implementation and dissemination of best practices for the integration of sequencing into clinical care. This study describes and compares the state of the art of incorporating whole-exome and whole-genome sequencing results into the electronic health record, including approaches to decision support across the six current CSER sites.
Methods: The CSER Medical Record Working Group collaboratively developed and completed an in-depth survey to assess the communication of genome-scale data into the electronic health record. We summarized commonalities and divergent approaches.
Results: Despite common sequencing platform (Illumina) adoptions, there is a great diversity of approaches to annotation tools and workflow, as well as to report generation. At all sites, reports are human-readable structured documents available as passive decision support in the electronic health record. Active decision support is in early implementation at two sites.
Conclusion: The parallel efforts across CSER sites in the creation of systems for report generation and integration of reports into the electronic health record, as well as the lack of standardized approaches to interfacing with variant databases to create active clinical decision support, create opportunities for cross-site and vendor collaborations.
C1 [Tarczy-Hornoch, Peter; Amendola, Laura; Aronson, Samuel J.; Garraway, Levi; Grundmeier, Robert W.; Hindorff, Lucia A.; Karavite, Dean; Plon, Sharon E.; Van Allen, Eliezer; Weck, Karen E.; White, Peter S.] NHGRI, NIH, Clin Sequencing Exploratory Res Elect Med Records, Bethesda, MD 20892 USA.
[Tarczy-Hornoch, Peter; Amendola, Laura; Jarvik, Gail] Univ Washington, Seattle, WA 98195 USA.
[Aronson, Samuel J.; Lebo, Matthew] Partners HealthCare Ctr Personalized Genet Med, Boston, MA USA.
[Garraway, Levi; Gray, Stacy; Van Allen, Eliezer] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Garraway, Levi; Gray, Stacy; Grundmeier, Robert W.; Lebo, Matthew; White, Peter S.] Harvard Univ, Sch Med, Boston, MA USA.
[Gray, Stacy; Van Allen, Eliezer] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Grundmeier, Robert W.; Karavite, Dean; White, Peter S.] Childrens Hosp Philadelphia, Ctr Biomed Informat, Philadelphia, PA 19104 USA.
[Hindorff, Lucia A.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Lebo, Matthew] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Plon, Sharon E.; Yang, Yaping] Baylor Coll Med, Houston, TX 77030 USA.
[Weck, Karen E.] Univ N Carolina, Chapel Hill, NC USA.
RP Tarczy-Hornoch, P (reprint author), NHGRI, NIH, Clin Sequencing Exploratory Res Elect Med Records, Bethesda, MD 20892 USA.
EM pth@uw.edu
RI Jarvik, Gail/N-6476-2014;
OI Jarvik, Gail/0000-0002-6710-8708; Weck, Karen/0000-0002-8516-333X; Van
Allen, Eliezer/0000-0002-0201-4444; Tarczy-Hornoch,
Peter/0000-0003-1047-179X; Lebo, Matthew/0000-0002-9733-5207
FU National Institutes of Health [U01HG006507, U01HG00637, U01HG006500,
U01HG606492, U01HG006487, U01HG006485, U01HG006546, KG100355,
RC1LM010526, UL1RR02574, UL1TR000423, U01HL098188, 275200800001C-2-0-1];
Susan G. Komen foundation; Washington State Life Sciences Discovery
Fund; Northwest Institute for Genetic Medicine; Dana-Farber Cancer
Institute Leadership Council
FX All the authors contributed equally to the writing of the this article.
The authors thank the members of the Clinical Sequencing Exploratory
Research (CSER) consortium, in particular all additional members of the
informatics teams at each of the six current CSER sites. The following
sources of funding supported parts of the work described in this
article: National Institutes of Health extramural projects U01HG006507,
U01HG00637, U01HG006500, U01HG606492, U01HG006487, U01HG006485,
U01HG006546, KG100355, RC1LM010526, UL1RR02574, UL1TR000423,
U01HL098188, and 275200800001C-2-0-1; the Susan G. Komen foundation; the
Washington State Life Sciences Discovery Fund; the Northwest Institute
for Genetic Medicine; and the Dana-Farber Cancer Institute Leadership
Council. L.A.H. is a member of the National Human Genome Research
Institute CSER staff team, responsible for scientific program management
of the CSER program.
NR 25
TC 22
Z9 22
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2013
VL 15
IS 10
BP 824
EP 832
DI 10.1038/gim.2013.120
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 234SQ
UT WOS:000325665000010
PM 24071794
ER
PT J
AU Melnick, RL
Ward, JM
Huff, J
AF Melnick, Ronald L.
Ward, Jerrold M.
Huff, James
TI War on Carcinogens: Industry Disputes Human Relevance of Chemicals
Causing Cancer in Laboratory Animals Based on Unproven Hypotheses, Using
Kidney Tumors as an Example
SO INTERNATIONAL JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH
LA English
DT Editorial Material
DE carcinogenicity; chronic progressive nephropathy; human relevance;
kidney; rats; renal tubule tumors; risk assessment
ID CHRONIC PROGRESSIVE NEPHROPATHY; NATIONAL TOXICOLOGY PROGRAM; HUMAN
RISK-ASSESSMENT; MALE F344 RATS; CHRONIC TOXICITY; IARC MONOGRAPHS;
PUBLIC-HEALTH; ASSOCIATION; DISEASE; REEVALUATION
AB Evidence from studies in animals is essential for identifying chemicals likely to cause or contribute to many diseases in humans, including cancers. Yet, to avoid or delay the implementation of protective public health standards, the chemical industry typically denies cancer causation by agents they produce. The spurious arguments put forward to discount human relevance are often based on inadequately tested hypotheses or modes of action that fail to meet Bradford Hill criteria for causation. We term the industry attacks on the relevance of animal cancer findings as the "War on Carcinogens.'' Unfortunately, this tactic has been effective in preventing timely and appropriate health protective actions on many economically important yet carcinogenic chemicals, including: arsenic, asbestos, benzene, 1,3-butadiene, formaldehyde, methylene chloride, phthalates, tobacco usage, trichloroethylene [TCE], and others. Recent examples of the "War on Carcinogens'' are chemicals causing kidney cancer in animals. Industry consultants argue that kidney tumor findings in rats with exacerbated chronic progressive nephropathy (CPN) are not relevant to humans exposed to these chemicals. We dispute and dismiss this unsubstantiated claim with data and facts, and divulge unprofessional actions from a leading toxicology journal.
C1 [Melnick, Ronald L.] Ron Melnick Consulting LLC, North Logan, UT 84341 USA.
[Ward, Jerrold M.] Global VetPathol, Montgomery Village, MD 20886 USA.
[Huff, James] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Melnick, RL (reprint author), Ron Melnick Consulting LLC, 274 E 2280 N,B, North Logan, UT 84341 USA.
NR 40
TC 2
Z9 2
U1 0
U2 10
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 1077-3525
EI 2049-3967
J9 INT J OCCUP ENV HEAL
JI Int. J. Occup. Environ. Health
PD OCT
PY 2013
VL 19
IS 4
BP 255
EP 260
DI 10.1179/1077352513Z.00000000090
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 235XK
UT WOS:000325755700001
PM 24588032
ER
PT J
AU An, CL
Beard, WA
Chen, DS
Wilson, SH
Makridakis, NM
AF An, Changlong
Beard, William A.
Chen, Desheng
Wilson, Samuel H.
Makridakis, Nick M.
TI Understanding the loss-of-function in a triple missense mutant of DNA
polymerase beta found in prostate cancer
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE DNA repair; polymerase; enzyme activity; expression analysis
ID BASE EXCISION-REPAIR; CELLULAR-TRANSFORMATION; CRYSTAL-STRUCTURES;
NUCLEAR EXTRACT; XENOPUS OOCYTES; ACTIVE-SITE; FIDELITY; MUTATIONS;
MECHANISM; CELLS
AB Human DNA polymerase (pol) beta is essential for base excision repair. We previously reported a triple somatic mutant of pol beta (p.P261L/T292A/I298T) found in an early onset prostate tumor. This mutation abolishes polymerase activity, and the wild-type allele was not present in the tumor, indicating a complete deficiency in pol beta function. The effect on polymerase activity is unexpected because the point mutations that comprise the triple mutant are not part of the active site. Herein, we demonstrate the mechanism of this loss-of-function. In order to understand the effect of the individual point mutations we biochemically analyzed all single and double mutants that comprise the triple mutant. We found that the p.I298T mutation is responsible for a marked instability of the triple mutant protein at 37 degrees C. At room temperature the triple mutant's low efficiency is also due to a decrease in the apparent binding affinity for the dNTP substrate, which is due to the p.T292A mutation. Furthermore, the triple mutant displays lower fidelity for transversions in vitro, due to the p.T292A mutation. We conclude that distinct mutations of the triple pol beta mutant are responsible for the loss of activity, lower fidelity, and instability observed in vitro.
C1 [An, Changlong; Chen, Desheng; Makridakis, Nick M.] Tulane Univ, Dept Epidemiol, New Orleans, LA 70112 USA.
[An, Changlong; Chen, Desheng; Makridakis, Nick M.] Tulane Univ, Tulane Canc Ctr, New Orleans, LA 70112 USA.
[Beard, William A.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Makridakis, NM (reprint author), 1700 Tulane Ave,Rm 811, New Orleans, LA 70112 USA.
EM nmakrida@tulane.edu
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01-ES050158, Z01-ES050161]; National Institutes of
Health [1U19CA105010, P20RR020152-06]; Department of Defense [PC094628];
NIH [P41 RR-01081]
FX This research was supported by Research Project Numbers Z01-ES050158 and
Z01-ES050161 in the Intramural Research Program of the National
Institutes of Health, National Institute of Environmental Health
Sciences and was in association with the National Institutes of Health
Grant 1U19CA105010. NMM is supported by grant number P20RR020152-06 from
the National Institutes of Health, and PC094628 from the Department of
Defense. Molecular graphics images were produced using the Chimera
package (35) from the Resource for Biocomputing, Visualization, and
Informatics at the University of California, San Francisco (supported by
NIH P41 RR-01081).
NR 36
TC 1
Z9 1
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD OCT
PY 2013
VL 43
IS 4
BP 1131
EP 1140
DI 10.3892/ijo.2013.2022
PG 10
WC Oncology
SC Oncology
GA 220RF
UT WOS:000324603900021
PM 23877444
ER
PT J
AU Zhu, Y
Wang, HS
Sun, Y
Yan, M
Joo, J
Sun, JF
Chen, WP
Qi, CF
Lv, NH
Morse, H
AF Zhu, Yin
Wang, Hongsheng
Sun, Yan
Yan, Ming
Joo, Jungsoo
Sun, Jiafang
Chen, Weiping
Qi, Chenfeng
Lv, Nonghua
Morse, Herbertcarpenter, III
TI Identifying the role of interferon regulatory factor 8 in helicobacter
pylori-induced inflammatory responses
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Meeting Abstract
DE Helicobacter pylori; IRF8
C1 NIDDK, NIH, Bethesda, MD 20892 USA.
NanChang Univ, Aiilated Hosp 1, Dept Gastroenterol, Nanchang, Peoples R China.
NIAID, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD OCT
PY 2013
VL 28
SU 3
BP 552
EP 552
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 226ER
UT WOS:000325017803229
ER
PT J
AU Myers, M
Parchen, D
Geraci, M
Brenholtz, R
Knisely-Carrigan, D
Hastings, C
AF Myers, Mary
Parchen, Debra
Geraci, Marilla
Brenholtz, Roger
Knisely-Carrigan, Denise
Hastings, Clare
TI Using a Shared Governance Structure to Evaluate the Implementation of a
New Model of Care
SO JOURNAL OF NURSING ADMINISTRATION
LA English
DT Article
ID PATIENT-SATISFACTION; OUTCOMES
AB Sustaining change in the behaviors and habits of experienced practicing nurses can be frustrating and daunting, even when changes are based on evidence. Partnering with an active shared governance structure to communicate change and elicit feedback is an established method to foster partnership, equity, accountability, and ownership. Few recent exemplars in the literature link shared governance, change management, and evidence-based practice to transitions in care models. This article describes an innovative staff-driven approach used by nurses in a shared governance performance improvement committee to use evidence-based practice in determining the best methods to evaluate the implementation of a new model of care.
C1 NIH, Ctr Clin, Nursing Serv, Bethesda, MD 20892 USA.
NIH, Ctr Clin, Patient Care Serv, Bethesda, MD 20892 USA.
RP Myers, M (reprint author), NIH, Ctr Clin, 9000 Rockville Pike,Bldg 10 Room 5-5441, Bethesda, MD 20892 USA.
EM mmyers@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 37
TC 3
Z9 3
U1 2
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-0443
EI 1539-0721
J9 J NURS ADMIN
JI J. Nurs. Adm.
PD OCT
PY 2013
VL 43
IS 10
BP 509
EP 516
DI 10.1097/NNA.0b013e3182a3e7ff
PG 8
WC Nursing
SC Nursing
GA 229NA
UT WOS:000325271900006
PM 24061583
ER
PT J
AU Jeon, HS
Choi, YY
Fukuoka, J
Fujii, M
Lyakh, LA
Song, SH
Travis, WD
Park, JY
Jen, J
AF Jeon, Hyo-Sung
Choi, Yi Young
Fukuoka, Junya
Fujii, Makiko
Lyakh, Lyudmila A.
Song, Sang-Hyun
Travis, William D.
Park, Jae Yong
Jen, Jin
TI High expression of SNIP1 correlates with poor prognosis in Non-small
cell lung cancer and SNIP1 interferes with the recruitment of HDAC1 to
RB in vitro
SO LUNG CANCER
LA English
DT Article
DE SNIP1; RB; HDAC1; Prognosis; Lung cancer
ID RETINOBLASTOMA PROTEIN; HISTONE DEACETYLASE; REPRESS TRANSCRIPTION;
DOMAIN; CYCLE
AB The Rb tumor suppressor gene performs a critical role in controlling cell proliferation and tumorigenesis; it recruits HDAC1 protein into the E2F complexes to repress transcription. In this study, we demonstrate that SNIP1, RB and HDAC1 were significantly expressed in same lung cancer tissues in a tissue microarray (TMA) containing 300 non-small cell lung cancers (NSCLC). High expression level of SNIP) in tumor patients was significantly correlated with poor prognosis in NSCLC (log-rank P for OS = 0.01, log-rank P for DFS = 0.001). Functionally, SNIP1 competes with HDAC1 for binding to RB and reduces HDAC activity in vitro. Knockdown of SNIP1 reduced colony formation ability of lung cancer cells. These findings may indicate the involvement of SNIP1 in progression of lung cancer by regulating the RB/HDAC1 interaction. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Jeon, Hyo-Sung; Choi, Yi Young; Park, Jae Yong] Kyungpook Natl Univ, Sch Med, Dept Biochem & Cell Biol, Taegu 700422, South Korea.
[Fukuoka, Junya] Toyama Univ Hosp, Toyama Tissue Microarray Lab, Anat Pathol Lab, Toyama 9300194, Japan.
[Fujii, Makiko] Aichi Canc Ctr, Res Inst, Div Mol Oncol, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
[Lyakh, Lyudmila A.] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Song, Sang-Hyun] Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea.
[Travis, William D.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Jen, Jin] Mayo Clin, Dept Med, Div Pulm & Crit Care Med, Rochester, MN 55905 USA.
RP Jeon, HS (reprint author), Kyungpook Natl Univ, Med Ctr, Lung Canc Ctr, 474 Hakjeongdong, Taegu 702210, South Korea.
EM jeonh@knu.ac.kr; Jen.Jin@mayo.edu
FU National Research Foundation of Korea (NRF); Ministry of Education,
Science, and Technology [NRF2010-0004700]
FX This work was supported by Basic Science Research Program through the
National Research Foundation of Korea (NRF) funded by the Ministry of
Education, Science, and Technology (NRF2010-0004700).
NR 24
TC 2
Z9 2
U1 1
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD OCT
PY 2013
VL 82
IS 1
BP 24
EP 30
DI 10.1016/j.lungcan.2013.07.015
PG 7
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 236XU
UT WOS:000325833600004
PM 23932364
ER
PT J
AU Ciribilli, Y
Monti, P
Bisio, A
Nguyen, HT
Ethayathulla, AS
Ramos, A
Foggetti, G
Menichini, P
Menendez, D
Resnick, MA
Viadiu, H
Fronza, G
Inga, A
AF Ciribilli, Yari
Monti, Paola
Bisio, Alessandra
Nguyen, H. Thien
Ethayathulla, Abdul S.
Ramos, Ana
Foggetti, Giorgia
Menichini, Paola
Menendez, Daniel
Resnick, Michael A.
Viadiu, Hector
Fronza, Gilberto
Inga, Alberto
TI Transactivation specificity is conserved among p53 family proteins and
depends on a response element sequence code
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DNA-BINDING DOMAIN; CRYSTAL-STRUCTURE; CORE DOMAIN; TRANSCRIPTION
FACTOR; FUNCTIONAL ASSAY; APOPTOSIS INDUCTION; SPONTANEOUS TUMORS;
GENE-EXPRESSION; TARGET GENES; MUTANT P53
AB Structural and biochemical studies have demonstrated that p73, p63 and p53 recognize DNA with identical amino acids and similar binding affinity. Here, measuring transactivation activity for a large number of response elements (REs) in yeast and human cell lines, we show that p53 family proteins also have overlapping transactivation profiles. We identified mutations at conserved amino acids of loops L1 and L3 in the DNA-binding domain that tune the transactivation potential nearly equally in p73, p63 and p53. For example, the mutant S139F in p73 has higher transactivation potential towards selected REs, enhanced DNA-binding cooperativity in vitro and a flexible loop L1 as seen in the crystal structure of the protein-DNA complex. By studying, how variations in the RE sequence affect transactivation specificity, we discovered a RE-transactivation code that predicts enhanced transactivation; this correlation is stronger for promoters of genes associated with apoptosis.
C1 [Ciribilli, Yari; Bisio, Alessandra; Inga, Alberto] Univ Trento, Lab Transcript Networks, Ctr Integrat Biol CIBIO, I-38060 Trento, TN, Italy.
[Monti, Paola; Foggetti, Giorgia; Menichini, Paola; Fronza, Gilberto] IRCSS Azienda Osped Univ San Martino IST, Ist Nazl Ric Canc, Mol Mutagenesis & DNA Repair Unit, I-16132 Genoa, Italy.
[Nguyen, H. Thien; Ethayathulla, Abdul S.; Ramos, Ana; Viadiu, Hector] Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
[Menendez, Daniel; Resnick, Michael A.] NIEHS, Chromosome Stabil Grp, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Viadiu, H (reprint author), Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA.
EM viadiu@ucsd.edu; gilberto.fronza@istge.it; inga@science.unitn.it
FU Italian Association for Cancer Research (in part) (Associazione Italiana
per la Ricerca sul Cancro), AIRC [IG9086, 5506]; CIBIO start-up funds;
NIEHS intramural research funds [Z01-ES065079];
Marie-Curie/Autonomous-Province-of-Trento [40101712]; Department of
Energy and National Institutes of Health [P41RR001209]
FX Funding for open access charge: Italian Association for Cancer Research
(in part) (Associazione Italiana per la Ricerca sul Cancro), AIRC
[#IG9086 to AI and IG#5506 to G.F.] and CIBIO start-up funds; NIEHS
intramural research funds (to M.A.R. and D.M.) project [Z01-ES065079 to
M.A.R.]; Marie-Curie/Autonomous-Province-of-Trento (to Y.C.) (PAT)
cofund grant [#40101712]; Diffraction data were collected at BL7-1 of
the Stanford/Stanford Synchrotron Radiation Lightsource supported by the
Department of Energy and National Institutes of Health [P41RR001209].
NR 85
TC 15
Z9 15
U1 0
U2 8
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 OCT
PY 2013
VL 41
IS 18
BP 8637
EP 8653
DI 10.1093/nar/gkt657
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 236EG
UT WOS:000325776600029
PM 23892287
ER
PT J
AU Kenyon, JC
Prestwood, LJ
Le Grice, SFJ
Lever, AML
AF Kenyon, Julia C.
Prestwood, Liam J.
Le Grice, Stuart F. J.
Lever, Andrew M. L.
TI In-gel probing of individual RNA conformers within a mixed population
reveals a dimerization structural switch in the HIV-1 leader
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID PRIMER ACTIVATION SIGNAL; VIRUS TYPE-1 GENOME; PACKAGING SIGNAL; REVERSE
TRANSCRIPTION; SHAPE CHEMISTRY; 5' REGION; INITIATION; PROTEIN; LOOP;
GAG
AB Definitive secondary structural mapping of RNAs in vitro can be complicated by the presence of more than one structural conformer or multimerization of some of the molecules. Until now, probing a single structure of conformationally flexible RNA molecules has typically relied on introducing stabilizing mutations or adjusting buffer conditions or RNA concentration. Here, we present an in-gel SHAPE (selective 2'OH acylation analysed by primer extension) approach, where a mixed structural population of RNA molecules is separated by non-denaturing gel electrophoresis and the conformers are individually probed within the gel matrix. Validation of the technique using a well-characterized RNA stem-loop structure, the HIV-1 trans-activation response element, showed that authentic structure was maintained and that the method was accurate and highly reproducible. To further demonstrate the utility of in-gel SHAPE, we separated and examined monomeric and dimeric species of the HIV-1 packaging signal RNA. Extensive differences in acylation sensitivity were seen between monomer and dimer. The results support a recently proposed structural switch model of RNA genomic dimerization and packaging, and demonstrate the discriminatory power of in-gel SHAPE.
C1 [Kenyon, Julia C.; Prestwood, Liam J.; Lever, Andrew M. L.] Univ Cambridge, Addenbrookes Hosp, Dept Med, Cambridge CB2 0QQ, England.
[Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Lever, AML (reprint author), Univ Cambridge, Addenbrookes Hosp, Dept Med, Hills Rd, Cambridge CB2 0QQ, England.
EM amll1@medschl.cam.ac.uk
FU Biomedical Research Centre and the Medical Research Council [G0800142];
Intramural Research Program of the National Institutes of Health,
National Cancer Institute; Medical Research Council [G0800142]
FX Biomedical Research Centre and the Medical Research Council [G0800142 to
A. L.] and the Intramural Research Program of the National Institutes of
Health, National Cancer Institute [to S. Le G.]. Funding for open access
charge: Medical Research Council [G0800142].
NR 47
TC 20
Z9 20
U1 1
U2 14
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 OCT
PY 2013
VL 41
IS 18
AR e174
DI 10.1093/nar/gkt690
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 236EG
UT WOS:000325776600005
PM 23935074
ER
PT J
AU Rodgers, JE
Sueta, CA
Kucharska-Newton, A
Stearns, S
Chang, P
Ni, HY
Beyhaghi, H
Zhou, L
Blair, EA
Federspiel, J
AF Rodgers, Jo E.
Sueta, Carla A.
Kucharska-Newton, Anna
Stearns, Sally
Chang, Patricia
Ni, Hanyu
Beyhaghi, Hadi
Zhou, Lei
Blair, Elizabeth A.
Federspiel, Jerome
TI Predictors of medication adherence: results from the Atherosclerosis
Risk in Communities Study
SO PHARMACOTHERAPY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-College-of-Clinical-Pharmacy (ACCP)
CY OCT 13-16, 2013
CL Albuquerque, NM
SP Amer Coll Clin Pharm
C1 [Rodgers, Jo E.; Blair, Elizabeth A.] Univ N Carolina, Div Pharmacotherapy & Expt Therapeut, Eshelman Scool Pharm, Chapel Hill, NC USA.
[Sueta, Carla A.] Univ N Carolina, Div Cardiol, Sch Med, Chapel Hill, NC USA.
[Kucharska-Newton, Anna] UNC Gillings Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Stearns, Sally; Beyhaghi, Hadi; Zhou, Lei; Federspiel, Jerome] UNC Gillings Sch Publ Hlth, Chapel Hill, NC USA.
[Chang, Patricia] Univ North Carolina Hlth Care, Div Cardiol, Dept Med, Chapel Hill, NC USA.
[Ni, Hanyu] NHLBI, Dept Epidemiol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-0008
EI 1875-9114
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD OCT
PY 2013
VL 33
IS 10
MA 32
BP E191
EP E192
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 230RM
UT WOS:000325360100060
ER
PT J
AU Elman, I
Borsook, D
Volkow, ND
AF Elman, Igor
Borsook, David
Volkow, Nora D.
TI Pain and suicidality: Insights from reward and addiction neuroscience
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
DE Anti-reward; Homeostasis; Allostasis; Habenula; Stress;
Cross-sensitization; Aberrant learning
ID POSTTRAUMATIC-STRESS-DISORDER; MAJOR DEPRESSIVE DISORDER;
SELF-INJURIOUS-BEHAVIOR; INTERPERSONAL-PSYCHOLOGICAL THEORY;
NATIONAL-COMORBIDITY-SURVEY; IRRITABLE-BOWEL-SYNDROME; DEFICIENCY
SYNDROME RDS; OPPONENT-PROCESS THEORY; FREELY MOVING RATS; CHRONIC
BACK-PAIN
AB Suicidality is exceedingly prevalent in pain patients. Although the pathophysiology of this link remains unclear, it may be potentially related to the partial congruence of physical and emotional pain systems. The latter system's role in suicide is also conspicuous during setbacks and losses sustained in the context of social attachments. Here we propose a model based on the neural pathways mediating reward and anti-reward (i.e., allostatic adjustment to recurrent activation of the reward circuitry); both are relevant etiologic factors in pain, suicide and social attachments. A comprehensive literature search on neurobiology of pain and suicidality was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) physical and emotional pain, (2) emotional pain and social attachments, (3) pain-and suicide-related alterations of the reward and anti-reward circuits as compared to addiction, which is the premier probe for dysfunction of these circuits and (4) mechanistically informed treatments of co-occurring pain and suicidality. Pain-, stress- and analgesic drugs-induced opponent and proponent states of the mesolimbic dopaminergic pathways may render reward and anti-reward systems vulnerable to sensitization, cross-sensitization and aberrant learning of contents and contexts associated with suicidal acts and behaviors. These findings suggest that pain patients exhibit alterations in the brain circuits mediating reward (depressed function) and anti-reward (sensitized function) that may affect their proclivity for suicide and support pain and suicidality classification among other "reward deficiency syndromes" and a new proposal for "enhanced anti-reward syndromes". We suggest that interventions aimed at restoring the balance between the reward and anti-reward networks in patients with chronic pain may help decreasing their suicide risk. Published by Elsevier Ltd.
C1 [Elman, Igor] Harvard Univ, Sch Med, Providence VA Med Ctr, Somerville, MA 02143 USA.
[Elman, Igor] Harvard Univ, Sch Med, Cambridge Hlth Alliance, Somerville, MA 02143 USA.
[Borsook, David] Boston Childrens Hosp, PAIN Grp, Dept Anesthesiol, Boston, MA USA.
[Borsook, David] Massachusetts Gen Hosp, Dept Radiol, Dept Psychiat & Radiol, Boston, MA 02114 USA.
[Borsook, David] Harvard Univ, Sch Med, Dept Psychiat, McLean Hosp, Boston, MA 02115 USA.
[Volkow, Nora D.] Natl Inst Drug Abuse, Bethesda, MD USA.
RP Elman, I (reprint author), Harvard Univ, Sch Med, Providence VA Med Ctr, 26 Cent St, Somerville, MA 02143 USA.
EM ielman@cha.harvard.edu
FU Mayday Fund/Herlands Fund for Pain Systems Neuroscience Research;
Providence VA Medical Center
FX The authors gratefully acknowledge Ms. Adriana Johnson for her help with
the preparation of the manuscript and support from the Mayday
Fund/Herlands Fund for Pain Systems Neuroscience Research (DB).; This
study was supported with resources and the use of facilities at the
Providence VA Medical Center. The views expressed in this article are
those of the authors and do not necessarily reflect the position or
policy of the Department of Veterans Affairs or the United States
Government.
NR 467
TC 42
Z9 42
U1 7
U2 54
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD OCT
PY 2013
VL 109
BP 1
EP 27
DI 10.1016/j.pneurobio.2013.06.003
PG 27
WC Neurosciences
SC Neurosciences & Neurology
GA 238AO
UT WOS:000325913000001
PM 23827972
ER
PT J
AU Riedl, R
Engels, EA
Warren, JL
Berghold, A
Ricker, W
Pfeiffer, RM
AF Riedl, Regina
Engels, Eric A.
Warren, Joan L.
Berghold, Andrea
Ricker, Winnie
Pfeiffer, Ruth M.
TI Blood transfusions and the subsequent risk of cancers in the United
States elderly
SO TRANSFUSION
LA English
DT Article
ID EPIDEMIOLOGY; METAANALYSIS; POPULATION; RECIPIENTS; ANEMIA; ADULTS
AB BackgroundBlood transfusions are common in older adults and also may modulate the immune system. However, the impact of transfusion on cancer risk in the elderly has not been studied.
Study Design and MethodsCancer risk after blood transfusion was evaluated in a US population-based case-control study using 552,951 elderly cases identified from cancer registries and 100,000 frequency-matched controls. Transfusions received 0 to 12, 13 to 30, and 31 to 48 months before cancer diagnosis or selection date were identified using Medicare claims. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression models. A Bonferroni correction adjusted for multiple testing.
ResultsTransfusions received 0 to 12 months before cancer diagnosis and/or selection were associated with significantly elevated risk of cancer overall (OR,2.05; 95% CI, 1.95-2.16) and cancer of the stomach; cancer of the colon; cancer of the liver, kidney, renal pelvis, and/or ureter; lymphoma; myeloma; and leukemia. No significant associations for cancer overall were observed for the two earlier intervals. No site was associated with transfusions received 13 to 30 or 31 to 48 months before diagnosis and/or selection. Nonetheless, overall cancer risk increased with the number of transfused periods (p-trend<0.0001).
ConclusionRisk of overall cancer and specific sites was elevated 0 to 12 months after blood transfusion and associated with multiple transfusions, possibly due to reverse causation, that is, incipient cancers or cancer precursors causing anemia.
C1 Med Univ Graz, Inst Med Informat Stat & Documentat, Graz, Austria.
NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
Informat Management Serv Inc, Rockville, MD USA.
RP Pfeiffer, RM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, HHS, 6120 Execut Blvd,EPS RM 8030, Bethesda, MD 20892 USA.
EM pfeiffer@mail.nih.gov
FU National Institute of Health, Division of Cancer Epidemiology and
Genetics
FX This research was supported by the Intramural Research Program of the
National Institute of Health, Division of Cancer Epidemiology and
Genetics.
NR 23
TC 2
Z9 3
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
EI 1537-2995
J9 TRANSFUSION
JI Transfusion
PD OCT
PY 2013
VL 53
IS 10
BP 2198
EP 2206
DI 10.1111/trf.12071
PG 9
WC Hematology
SC Hematology
GA 230WP
UT WOS:000325374300018
PM 23320915
ER
PT J
AU Cosson, P
Perrin, J
Bonifacino, JS
AF Cosson, Pierre
Perrin, Jackie
Bonifacino, Juan S.
TI Anchors aweigh: protein localization and transport mediated by
transmembrane domains
SO TRENDS IN CELL BIOLOGY
LA English
DT Review
DE transmembrane domains; protein sorting; protein traffic; lipid domains;
transmembrane receptors; endomembrane system
ID GOLGI RETENTION SIGNAL; ENDOPLASMIC-RETICULUM; MEMBRANE-PROTEINS;
UBIQUITIN LIGASE; RETRIEVAL RECEPTOR; PLASMA-MEMBRANE; DOWN-REGULATION;
CELL-SURFACE; DEGRADATION; DETERMINANTS
AB The transmembrane domains (TMDs) of integral membrane proteins have emerged as major determinants of intracellular localization and transport in the secretory and endocytic pathways. Unlike sorting signals in cytosolic domains, TMD sorting determinants are not conserved amino acid sequences but physical properties such as the length and hydrophilicity of the transmembrane span. The underlying sorting machinery is still poorly characterized, but several mechanisms have been proposed, including TMD recognition by transmembrane sorting receptors and partitioning into membrane lipid domains. Here we review the nature of TMD sorting determinants and how they may dictate transmembrane protein localization and transport.
C1 [Cosson, Pierre; Perrin, Jackie] Ctr Med Univ Geneva, Dept Physiol Cellulaire & Metab, CH-1211 Geneva 4, Switzerland.
[Bonifacino, Juan S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
RP Cosson, P (reprint author), Ctr Med Univ Geneva, Dept Physiol Cellulaire & Metab, 1 Rue Michel Servet, CH-1211 Geneva 4, Switzerland.
EM Pierre.Cosson@unige.ch; bonifacinoj@mail.nih.gov
OI Bonifacino, Juan S./0000-0002-5673-6370
FU Intramural NIH HHS [ZIA HD001607-21]
NR 63
TC 14
Z9 14
U1 4
U2 18
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0962-8924
J9 TRENDS CELL BIOL
JI Trends Cell Biol.
PD OCT
PY 2013
VL 23
IS 10
BP 511
EP 517
DI 10.1016/j.tcb.2013.05.005
PG 7
WC Cell Biology
SC Cell Biology
GA 233SD
UT WOS:000325588900006
PM 23806646
ER
PT J
AU Voss, MW
Vivar, C
Kramer, AF
van Praag, H
AF Voss, Michelle W.
Vivar, Carmen
Kramer, Arthur F.
van Praag, Henriette
TI Bridging animal and human models of exercise-induced brain plasticity
SO TRENDS IN COGNITIVE SCIENCES
LA English
DT Review
ID ADULT HIPPOCAMPAL NEUROGENESIS; TRANSGENIC MOUSE MODEL; GROWTH-FACTOR-I;
ENHANCED SYNAPTIC PLASTICITY; ACTIVITY-DEPENDENT SECRETION; VOLUNTARY
PHYSICAL-EXERCISE; NEUROTROPHIC FACTOR LEVELS; MILD COGNITIVE
IMPAIRMENT; OBJECT RECOGNITION MEMORY; APOLIPOPROTEIN-E GENOTYPE
AB Significant progress has been made in understanding the neurobiological mechanisms through which exercise protects and restores the brain. In this feature review, we integrate animal and human research, examining physical activity effects across multiple levels of description (neurons up to inter-regional pathways). We evaluate the influence of exercise on hippocampal structure and function, addressing common themes such as spatial memory and pattern separation, brain structure and plasticity, neurotrophic factors, and vasculature. Areas of research focused more within species, such as hippocampal neurogenesis in rodents, also provide crucial insight into the protective role of physical activity. Overall, converging evidence suggests exercise benefits brain function and cognition across the mammalian lifespan, which may translate into reduced risk for Alzheimer's disease (AD) in humans.
C1 [Voss, Michelle W.] Univ Iowa, Dept Psychol, Iowa City, IA 52242 USA.
[Vivar, Carmen; van Praag, Henriette] NIA, NIH, Neurosci Lab, Neuroplast & Behav Unit,Intramural Res Program, Baltimore, MD 21224 USA.
[Kramer, Arthur F.] Univ Illinois, Dept Psychol, Urbana, IL 61801 USA.
[Kramer, Arthur F.] Univ Illinois, Beckman Inst Adv Sci & Technol, Urbana, IL 61801 USA.
[Voss, Michelle W.] Univ Iowa, AMBI, Iowa City, IA 52242 USA.
RP Voss, MW (reprint author), Univ Iowa, Dept Psychol, Iowa City, IA 52242 USA.
EM michelle-voss@uiowa.edu; vanpraagh@mail.nih.gov
RI van Praag, Henriette/F-3939-2015
OI van Praag, Henriette/0000-0002-5727-434X
FU Intramural Research Program of the National Institute on Aging; NIA
[5R37AG025667]; University of Iowa
FX This work was supported in part by the Intramural Research Program of
the National Institute on Aging. A.F.K. was supported by 5R37AG025667
from the NIA. M.W.V. was supported by start-up funds from the University
of Iowa. We thank Linda Kitabayashi for preparation of the
photomicrograph and Dr Justin Rhodes and Martina Mustroph for sharing
images.
NR 298
TC 155
Z9 157
U1 14
U2 88
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1364-6613
J9 TRENDS COGN SCI
JI TRENDS COGN. SCI.
PD OCT
PY 2013
VL 17
IS 10
BP 525
EP 544
DI 10.1016/j.tics.2013.08.001
PG 20
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 233SE
UT WOS:000325589000010
PM 24029446
ER
PT J
AU Gasser, DL
Winkler, CA
Peng, M
An, P
McKenzie, LM
Kirk, GD
Shi, YC
Xie, LTX
Marbois, BN
Clarke, CF
Kopp, JB
AF Gasser, David L.
Winkler, Cheryl A.
Peng, Min
An, Ping
McKenzie, Louise M.
Kirk, Gregory D.
Shi, Yuchen
Xie, Letian X.
Marbois, Beth N.
Clarke, Catherine F.
Kopp, Jeffrey B.
TI Focal segmental glomerulosclerosis is associated with a PDSS2 haplotype
and, independently, with a decreased content of coenzyme Q(10)
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE nephrotic syndrome; collapsing glomerulopathy; focal segmental
glomerulosclerosis; mitochondria; ubiquinone
ID DIPHOSPHATE SYNTHASE SUBUNIT-2; INDUCED MITOCHONDRIAL INJURY;
HIV-ASSOCIATED NEPHROPATHY; KIDNEY-DISEASE; KD/KD MICE; NEPHROTIC
SYNDROME; PROXIMAL TUBULES; TUBULOINTERSTITIAL NEPHRITIS;
SACCHAROMYCES-CEREVISIAE; HYPOXIA-REOXYGENATION
AB Gasser DL, Winkler CA, Peng M, An P, McKenzie LM, Kirk GD, Shi Y, Xie LX, Marbois BN, Clarke CF, Kopp JB. Focal segmental glomerulosclerosis is associated with a PDSS2 haplotype and, independently, with a decreased content of coenzyme Q(10). Am J Physiol Renal Physiol 305: F1228-F1238, 2013. First published August 7, 2013; doi:10.1152/ajprenal.00143.2013.-Focal segmental glomerulosclerosis (FSGS) and collapsing glomerulopathy are common causes of nephrotic syndrome. Variants in >20 genes, including genes critical for mitochondrial function, have been associated with these podocyte diseases. One such gene, PDSS2, is required for synthesis of the decaprenyl tail of coenzyme Q(10) (Q(10)) in humans. The mouse gene Pdss2 is mutated in the kd/kd mouse model of collapsing glomerulopathy. We examined the hypothesis that human PDSS2 polymorphisms are associated with podocyte diseases. We genotyped 377 patients with primary FSGS or collapsing glomerulopathy, together with 900 controls, for 9 single-nucleotide polymorphisms in the PDSS2 gene in a case-control study. Subjects included 247 African American (AA) and 130 European American (EA) patients and 641 AA and 259 EA controls. Among EAs, a pair of proxy SNPs was significantly associated with podocyte disease, and patients homozygous for one PDSS2 haplotype had a strongly increased risk for podocyte disease. By contrast, the distribution of PDSS2 genotypes and haplotypes was similar in AA patients and controls. Thus a PDSS2 haplotype, which has a frequency of 13% in the EA control population and a homozygote frequency of 1.2%, is associated with a significantly increased risk for FSGS and collapsing glomerulopathy in EAs. Lymphoblastoid cell lines from FSGS patients had significantly less Q(10) than cell lines from controls; contrary to expectation, this finding was independent of PDSS2 haplotype. These results suggest that FSGS patients have Q(10) deficiency and that this deficiency is manifested in patient-derived lymphoblastoid cell lines.
C1 [Gasser, David L.; Peng, Min] Univ Penn, Sch Med, Dept Genet, Philadelphia, PA 19104 USA.
[Winkler, Cheryl A.; An, Ping; McKenzie, Louise M.] SAIC Frederick, Frederick Natl Lab Canc Res, Basic Res Lab, Ctr Canc Res, Frederick, MD USA.
[Kirk, Gregory D.] Johns Hopkins Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Shi, Yuchen; Xie, Letian X.; Marbois, Beth N.; Clarke, Catherine F.] Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90024 USA.
[Shi, Yuchen; Xie, Letian X.; Marbois, Beth N.; Clarke, Catherine F.] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90024 USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD USA.
RP Gasser, DL (reprint author), Univ Penn, Sch Med, Dept Genet, 415 Curie Blvd, Philadelphia, PA 19104 USA.
EM gasserd@mail.med.upenn.edu
OI Kopp, Jeffrey/0000-0001-9052-186X
FU National Cancer Institute [HHSN26120080001E]; Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research; National Institute of Diabetes and Digestive and Kidney
Diseases; NIH [R01 DK-55852, R01 GM-45952]; National Cancer Institute
Division of Cancer Treatment and Diagnosis [N01 CO-12400]; Ruth L.
Kirschstein National Service Award [GM-007185]; National Center for
Research Resources Grant [S10 RR-024605]; National Institute on Drug
Abuse [R01-DA-04334]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute under Contract HHSN26120080001E. Research
was supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research, and National
Institute of Diabetes and Digestive and Kidney Diseases Intramural
Research Programs and was supported by NIH Grants R01 DK-55852 (D. L.
Gasser), R01 GM-45952 (C. F. Clarke), and National Cancer Institute
Division of Cancer Treatment and Diagnosis under contract N01 CO-12400.
L. X. Xie was supported by the Ruth L. Kirschstein National Service
Award GM-007185. The HPLC-MS/MS determination of quinones was supported
in part by National Center for Research Resources Grant S10 RR-024605.
Recruitment of controls through the ALIVE study was supported by
National Institute on Drug Abuse Grant R01-DA-04334.
NR 67
TC 13
Z9 15
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
EI 1522-1466
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD OCT
PY 2013
VL 305
IS 8
BP F1228
EP F1238
DI 10.1152/ajprenal.00143.2013
PG 11
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 236RF
UT WOS:000325816200017
PM 23926186
ER
PT J
AU Miller, PE
McKinnon, RA
Krebs-Smith, SM
Subar, AF
Chriqui, J
Kahle, L
Reedy, J
AF Miller, Paige E.
McKinnon, Robin A.
Krebs-Smith, Susan M.
Subar, Amy F.
Chriqui, Jamie
Kahle, Lisa
Reedy, Jill
TI Sugar-Sweetened Beverage Consumption in the US Novel Assessment
Methodology
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID SOFT DRINK CONSUMPTION; METABOLIC SYNDROME; DIET QUALITY; RISK-FACTORS;
WEIGHT-GAIN; BODY-WEIGHT; CHILDREN; ADOLESCENTS; ADULTS; YOUNG
AB Background: Sugar-sweetened beverage (SSB) consumption has been linked with poor diet quality, weight gain, and increased risk for obesity, diabetes, and cardiovascular disease. Previous studies have been hampered by inconsistent definitions and a failure to capture all types of SSBs.
Purpose: To comprehensively examine total SSB consumption in the U.S. using an all-encompassing definition that includes beverages calorically sweetened after purchase in addition to presweetened beverages.
Methods: Data from the 2005-2008 National Health and Nutrition Examination Survey (N=17,078) were analyzed in September 2012 and used to estimate calories (kilocalories) of added sugars from SSBs and to identify top sources of SSBs.
Results: On average, Americans aged >= 2 years consumed 171 kcal (8% of total kcal) per day from added sugars in SSBs; the top sources were soda, fruit drinks, tea, coffee, energy/sports drinks, and flavored milks. Male adolescents (aged 12-19 years) had the highest mean intakes (293 kcal/day; 12% of total kcal).
Conclusions: Americans consume more calories from added sugars in beverages than previously reported. The methodology presented in this paper allows for more-comprehensive estimates than those previously used regarding the extent to which SSBs provide calories from added sugars. (C) 2013 American Journal of Preventive Medicine. All rights reserved.
C1 [Miller, Paige E.] NCI, Canc Prevent Fellowship Program, Rockville, MD USA.
[McKinnon, Robin A.; Krebs-Smith, Susan M.; Subar, Amy F.; Reedy, Jill] NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
[Kahle, Lisa] Informat Management Serv Inc, Calverton, MD USA.
[Miller, Paige E.] Exponent Inc, Ctr Epidemiol Biostat & Computat Biol, Chicago, IL 60661 USA.
[Chriqui, Jamie] Univ Illinois, Inst Hlth Res & Policy, Chicago, IL USA.
RP Miller, PE (reprint author), Exponent Inc, 525 West Monroe St,Suite 1050, Chicago, IL 60661 USA.
EM pmiller@exponent.com
FU Cancer Prevention Fellowship Program of the National Cancer Institute
FX This research was supported by the Cancer Prevention Fellowship Program
of the National Cancer Institute.
NR 36
TC 21
Z9 21
U1 1
U2 31
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD OCT
PY 2013
VL 45
IS 4
BP 416
EP 421
DI 10.1016/j.amepre.2013.05.014
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 228NQ
UT WOS:000325193900006
PM 24050417
ER
PT J
AU Fleischhacker, SE
Evenson, KR
Sharkey, J
Pitts, SBJ
Rodriguez, DA
AF Fleischhacker, Sheila E.
Evenson, Kelly R.
Sharkey, Joseph
Pitts, Stephanie B. Jilcott
Rodriguez, Daniel A.
TI Validity of Secondary Retail Food Outlet Data A Systematic Review
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Review
ID COMMERCIAL DATA SOURCES; PHYSICAL-ACTIVITY; FIELD VALIDATION;
NEIGHBORHOOD ENVIRONMENTS; NORTH-CAROLINA; HEALTHY FOODS; GOOGLE EARTH;
ACCESS; STORES; URBAN
AB Context: Improving access to healthy foods is a promising strategy to prevent nutrition-related chronic diseases. To characterize retail food environments and identify areas with limited retail access, researchers, government programs, and community advocates have primarily used secondary retail food outlet data sources (e.g., InfoUSA or government food registries). To advance the state of the science on measuring retail food environments, this systematic review examined the evidence for validity reported for secondary retail food outlet data sources for characterizing retail food environments.
Evidence acquisition: A literature search was conducted through December 31, 2012, to identify peer-reviewed published literature that compared secondary retail food outlet data sources to primary data sources (i.e., field observations) for accuracy of identifying the type and location of retail food outlets. Data were analyzed in 2013.
Evidence synthesis: Nineteen studies met the inclusion criteria. The evidence for validity reported varied by secondary data sources examined, primary data-gathering approaches, retail food outlets examined, and geographic and sociodemographic characteristics. More than half of the studies (53%) did not report evidence for validity by type of food outlet examined and by a particular secondary data source.
Conclusions: Researchers should strive to gather primary data but if relying on secondary data sources, InfoUSA and government food registries had higher levels of agreement than reported by other secondary data sources and may provide sufficient accuracy for exploring these associations in large study areas. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Fleischhacker, Sheila E.] NIDDK, Div Nutr Res Coordinat, NIH, Bethesda, MD 20892 USA.
[Evenson, Kelly R.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Rodriguez, Daniel A.] Univ N Carolina, Dept City & Reg Planning, Chapel Hill, NC USA.
[Pitts, Stephanie B. Jilcott] E Carolina Univ, Dept Publ Hlth, Greenville, NC USA.
[Sharkey, Joseph] Texas A&M Hlth Sci Ctr, Sch Rural Publ Hlth, College Stn, TX USA.
RP Fleischhacker, SE (reprint author), NIDDK, Div Nutr Res Coordinat, NIH, DHHS, 2 Democracy Plaza,Room 635,6707 Democracy Blvd,MS, Bethesda, MD 20892 USA.
EM sheila.fleisch-hacker@nih.gov
FU Health-e NC, an initiative of the University Cancer Research Fund at the
University of North Carolina-Chapel Hill; Healthy Eating Research, a
national program of the Robert Wood Johnson Foundation (RWJF) [66958]
FX Support for preliminary work on this project was provided by the
Health-e NC, an initiative of the University Cancer Research Fund at the
University of North Carolina-Chapel Hill and by Healthy Eating Research,
a national program of the Robert Wood Johnson Foundation (RWJF), ID
#66958. The content is solely the responsibility of the authors and does
not necessarily represent the official views of the NIH, Health-e NC, or
RWJF. Heather D'Angelo, MHS, Robin McKinnon, PhD, MPA, Margaret
McDowell, PhD, MPH, RD, and Van Hubbard, MD, PhD, as well as members of
the CDC's Nutrition and Obesity Policy Research and Evaluation Network
Rural Food Access Working Group provided feedback on the paper.
NR 51
TC 17
Z9 17
U1 0
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD OCT
PY 2013
VL 45
IS 4
BP 462
EP 473
DI 10.1016/j.amepre.2013.06.009
PG 12
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 228NQ
UT WOS:000325193900012
PM 24050423
ER
PT J
AU Gronley, J
Gerber, L
Rasch, EK
AF Gronley, JoAnne
Gerber, Lynn
Rasch, Elizabeth K.
TI In Memoriam: A Tribute to Jacqueline Perry
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Biographical-Item
C1 [Gronley, JoAnne] Rancho Los Amigos Natl Rehabil Ctr, Pathokinesiol Lab, Downey, CA 90242 USA.
[Gerber, Lynn] George Mason Univ, Ctr Study Chron Illness & Disabil, Fairfax, VA 22030 USA.
[Rasch, Elizabeth K.] NIH, Dept Rehabil Med, Clin Res Ctr, Bethesda, MD 20892 USA.
RP Gronley, J (reprint author), Rancho Los Amigos Natl Rehabil Ctr, Pathokinesiol Lab, Downey, CA 90242 USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
EI 1532-821X
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD OCT
PY 2013
VL 94
IS 10
BP 2036
EP 2037
DI 10.1016/j.apmr.2013.07.001
PG 2
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 231TU
UT WOS:000325442100027
ER
PT J
AU Terracciano, A
Chan, W
AF Terracciano, Antonio
Chan, Wayne
TI Personality traits, national character stereotypes, and climate-economic
conditions
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
ID UNITED-STATES; CULTURES
AB Cross-cultural personality research suggests that individuals from wealthier countries tend to be more open-minded. This openness to values may support more democratic governments and the expansion of fundamental freedoms. The link between wealth and freedom is evident in cold-to-temperate climates, but not across wealthy nations in hot climates. Furthermore, temperature and economic conditions shape perceptions of national character stereotypes.
C1 [Terracciano, Antonio] Florida State Univ, Coll Med, Dept Geriatr, Tallahassee, FL 32306 USA.
[Terracciano, Antonio; Chan, Wayne] NIA, NIH, Baltimore, MD 21224 USA.
RP Terracciano, A (reprint author), Florida State Univ, Coll Med, Dept Geriatr, Tallahassee, FL 32306 USA.
EM antonio.terracciano@med.fsu.edu; wayne.chan@rutgers.edu
OI Chan, Wayne/0000-0001-5061-1713
FU Intramural NIH HHS
NR 12
TC 2
Z9 2
U1 1
U2 7
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD OCT
PY 2013
VL 36
IS 5
BP 501
EP 502
DI 10.1017/S0140525X1300023X
PG 2
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA 234YR
UT WOS:000325681000024
PM 23985221
ER
PT J
AU Ito, S
Pophali, P
Wu, CO
Koklanaris, EK
Superata, J
Fahle, GA
Childs, R
Battiwalla, M
Barrett, AJ
AF Ito, S.
Pophali, P.
Wu, C. O.
Koklanaris, E. K.
Superata, J.
Fahle, G. A.
Childs, R.
Battiwalla, M.
Barrett, A. J.
TI CMV reactivation is associated with a lower incidence of relapse after
allo-SCT for CML
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE HSCT; relapse; CMV reactivation; CML
ID STEM-CELL TRANSPLANTATION; ACUTE MYELOID-LEUKEMIA;
BONE-MARROW-TRANSPLANTATION; CORD BLOOD TRANSPLANTATION;
POLYMERASE-CHAIN-REACTION; CYTOMEGALOVIRUS-INFECTION;
LYMPHOCYTE-PROLIFERATION; MOLECULAR REMISSION; PREEMPTIVE THERAPY;
PERIPHERAL-BLOOD
AB Preemptive therapy at CMV reactivation has diminished post-transplant CMV mortality. Furthermore, recent studies suggest a favorable 'virus-versus-leukemia' effect from reactivating CMV, reducing relapse of AML after SCT. We studied the relationship of CMV reactivation with leukemic relapse in 110 patients with CML receiving HLA-identical sibling SCT between 1993 and 2008. Of these, 79 (72%) were in chronic phase, 5 in second chronic phase, 17 in accelerated phase and 9 in blast phase. A total of 97 patients (88%) received a myeloablative conditioning regimen, 97 received 4-log ex vivo T cell-depleted grafts and 13 received T-replete grafts. CMV reactivation before day 100 was observed in 72 patients (65.5%). At a median follow-up of 6.2 years, CMV reactivation < day 100 as a time-dependent covariate was an independent factor associated with decreased relapse. We conclude that CMV reactivation may contribute to a beneficial GVL effect in CML transplant recipients.
C1 [Ito, S.; Pophali, P.; Koklanaris, E. K.; Superata, J.; Childs, R.; Battiwalla, M.; Barrett, A. J.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Wu, C. O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[Fahle, G. A.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Ito, S (reprint author), NHLBI, Hematol Branch, NIH, 10 CRC Room 3E-5288,10 Ctr Dr, Bethesda, MD 20892 USA.
EM itos2@mail.nih.gov
RI Pophali, Priyanka/P-8646-2016
FU National institutes of Health, at the National Heart, Lung, and Blood
Institute
FX This research was supported by the Intramural Research Program of the
National institutes of Health, at the National Heart, Lung, and Blood
Institute.
NR 26
TC 37
Z9 39
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2013
VL 48
IS 10
BP 1313
EP 1316
DI 10.1038/bmt.2013.49
PG 4
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 234KW
UT WOS:000325643700009
PM 23562969
ER
PT J
AU Fitzhugh, CD
Weitzel, RP
Hsieh, MM
Phang, OA
Madison, C
Luznik, L
Powell, JD
Tisdale, JF
AF Fitzhugh, C. D.
Weitzel, R. P.
Hsieh, M. M.
Phang, O. A.
Madison, C.
Luznik, L.
Powell, J. D.
Tisdale, J. F.
TI Sirolimus and post transplant Cy synergistically maintain mixed
chimerism in a mismatched murine model
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE sirolimus; Cy; CSA; mixed chimerism; murine
ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; STEM-CELL
TRANSPLANTATION; TOTAL-BODY IRRADIATION; REGULATORY T-CELLS;
POSTTRANSPLANTATION CYCLOPHOSPHAMIDE; HEMATOLOGIC MALIGNANCIES;
HEMATOPOIETIC CHIMERISM; DOSE CYCLOPHOSPHAMIDE; ANTILYMPHOCYTE-SERUM
AB Because of the toxicity associated with myeloablative conditioning, nonmyeloablative regimens are increasingly being used in vulnerable patient populations. For patients with sickle cell disease, stable mixed chimerism has proven sufficient to reverse the phenotype. Because the vast majority of patients do not have an HLA-matched sibling, a safe nonmyeloablative regimen that could be applied to the haploidentical setting would be ideal. We employed a mismatched mouse model using BALB/c donors and C57BL/6 recipients. Recipient mice were conditioned with 200 cGy TBI and sirolimus or CSA with or without post transplant Cy (PT-Cy). Our data show that when sirolimus or PT-Cy alone is given to C57BL/6 recipients, donor cells are not detected. However, when sirolimus is administered for 15 or 31 days starting 1 day before or up to 6 days after transplant with PT-Cy, all mice maintain stable mixed chimerism. In contrast, conventional therapy employing CSA with or without PT-Cy does not result in stable mixed chimerism. Lastly, mice with stable mixed chimerism after sirolimus display decreased reactivity to donor Ag both in vitro and in vivo. These data identify a novel strategy for inducing mixed chimerism for the treatment of nonmalignant hematologic diseases.
C1 [Fitzhugh, C. D.; Weitzel, R. P.; Hsieh, M. M.; Phang, O. A.; Madison, C.; Tisdale, J. F.] Natl Inst Diabet & Digest & Kidney Dis, NIH, NHLBI, Mol & Cellular Hematol Branch, Bethesda, MD 20892 USA.
[Luznik, L.; Powell, J. D.] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
RP Tisdale, JF (reprint author), Natl Inst Diabet & Digest & Kidney Dis, NIH, NHLBI, Mol & Cellular Hematol Branch, 9000 Rockville Pike,Bldg 10,Room 9N-112, Bethesda, MD 20892 USA.
EM johntis@nhlbi.nih.gov
FU Intramural NIH HHS [Z99 HL999999, ZIA HL006007-06]
NR 42
TC 9
Z9 9
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2013
VL 48
IS 10
BP 1335
EP 1341
DI 10.1038/bmt.2013.60
PG 7
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 234KW
UT WOS:000325643700013
PM 23604009
ER
PT J
AU Wood, WA
Deal, AM
Reeve, BB
Abernethy, AP
Basch, E
Mitchell, SA
Shatten, C
Kim, YH
Whitley, J
Serody, JS
Shea, T
Battaglini, C
AF Wood, W. A.
Deal, A. M.
Reeve, B. B.
Abernethy, A. P.
Basch, E.
Mitchell, S. A.
Shatten, C.
Kim, Y. Hie
Whitley, J.
Serody, J. S.
Shea, T.
Battaglini, C.
TI Cardiopulmonary fitness in patients undergoing hematopoietic SCT: a
pilot study
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE cardiopulmonary fitness; symptoms; health-related quality of life;
hematopoietic SCT
ID QUALITY-OF-LIFE; STEM-CELL TRANSPLANTATION; ACUTE MYELOID-LEUKEMIA;
COMORBIDITY INDEX; AEROBIC EXERCISE; RANDOMIZED-TRIAL; OLDER PATIENTS;
LUNG-CANCER; PERFORMANCE; MORTALITY
AB Hematopoietic cell transplantation (HCT) is a life-saving treatment for patients with high-risk hematological malignancies. Prognostic measures to determine fitness for HCT are needed to inform decision-making and interventions. VO2peak is obtained by measuring gas exchange during cycle ergometry and has not been studied as a prognostic factor in HCT. Thirty-two autologous and allogeneic HCT patients underwent VO2peak and 6 Minute Walk (6MW) testing before HCT, and provided weekly symptom and health-related quality of life (HRQOL) assessments before HCT and concluding at Day 100. Twenty-nine patients completed pre-HCT testing. Pre-HCT VO2peak was positively correlated with pre-HCT 6MW (r=0.65, P<0.001) and negatively correlated with number of chemotherapy regimens and months of chemotherapy. Patients with lower VO2peak reported higher symptom burden and inferior HRQOL at baseline and during early post-HCT period. Patients with pre-HCT VO2peak <16 mL/kg/min had higher risk of mortality post HCT (entire cohort: hazard ratio (HR) 9.1 (1.75-47.0), P=0.01; allogeneic HCT patients only: HR 6.70 (1.29-34.75), P=0.02) and more hospitalized days before Day 100 (entire cohort: median 33 vs 19, P=0.003; allogeneic HCT patients only: median 33 vs 21, P=0.004). VO2peak pre-HCT is feasible and might predict symptom severity, HRQOL and mortality. Additional studies are warranted.
C1 [Wood, W. A.; Basch, E.; Shatten, C.; Whitley, J.; Serody, J. S.; Shea, T.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Deal, A. M.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Biostat Core Facil, Chapel Hill, NC 27599 USA.
[Reeve, B. B.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Hlth Policy & Management, Chapel Hill, NC 27599 USA.
[Abernethy, A. P.] Duke Univ, Med Ctr, Duke Canc Inst, Div Med Oncol, Durham, NC USA.
[Mitchell, S. A.] Natl Canc Inst, Div Canc Control & Populat Sci, Outcomes Res Branch, Bethesda, MD USA.
[Kim, Y. Hie] E Carolina Univ, Brody Sch Med, Greenville, NC USA.
[Battaglini, C.] Univ N Carolina, Dept Exercise & Sport Sci, Chapel Hill, NC USA.
RP Wood, WA (reprint author), Univ N Carolina, Lineberger Comprehens Canc Ctr, Div Hematol & Oncol, Campus Box 7305,3rd Floor,Physicians Off Bldg,170, Chapel Hill, NC 27599 USA.
EM wwood@unch.unc.edu
OI Wood, William/0000-0001-7439-2543; Serody, Jonathan/0000-0003-4568-1092
FU National Institutes of Health [KL2TR000084]
FX This work was supported by the National Institutes of Health Grant
KL2TR000084.
NR 35
TC 18
Z9 18
U1 3
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2013
VL 48
IS 10
BP 1342
EP 1349
DI 10.1038/bmt.2013.58
PG 8
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 234KW
UT WOS:000325643700014
PM 23584437
ER
PT J
AU Ellis, MJ
Gillette, M
Carr, SA
Paulovich, AG
Smith, RD
Rodland, KK
Townsend, RR
Kinsinger, C
Mesri, M
Rodriguez, H
Liebler, DC
AF Ellis, Matthew J.
Gillette, Michael
Carr, Steven A.
Paulovich, Amanda G.
Smith, Richard D.
Rodland, Karin K.
Townsend, R. Reid
Kinsinger, Christopher
Mesri, Mehdi
Rodriguez, Henry
Liebler, Daniel C.
CA CPTAC
TI Connecting Genomic Alterations to Cancer Biology with Proteomics: The
NCI Clinical Proteomic Tumor Analysis Consortium
SO CANCER DISCOVERY
LA English
DT Editorial Material
ID MASS-SPECTROMETRY; CELL-LINES; QUANTIFICATION; PROTEINS
AB The National Cancer Institute (NCI) Clinical Proteomic Tumor Analysis Consortium is applying the latest generation of proteomic technologies to genomically annotated tumors from The Cancer Genome Atlas (TCGA) program, a joint initiative of the NCI and the National Human Genome Research Institute. By providing a fully integrated accounting of DNA, RNA, and protein abnormalities in individual tumors, these datasets will illuminate the complex relationship between genomic abnormalities and cancer phenotypes, thus producing biologic insights as well as a wave of novel candidate biomarkers and therapeutic targets amenable to verifi cation using targeted mass spectrometry methods. (C) 2013 AACR.
C1 [Ellis, Matthew J.] Washington Univ, Sch Med, Dept Med, Div Oncol, St Louis, MO 63110 USA.
[Townsend, R. Reid] Washington Univ, Sch Med, Dept Med, Div Endocrinol & Metab, St Louis, MO 63110 USA.
[Gillette, Michael; Carr, Steven A.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Paulovich, Amanda G.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Smith, Richard D.; Rodland, Karin K.] Pacific NW Natl Lab, Div Biol Sci, Richland, WA 99352 USA.
[Kinsinger, Christopher; Mesri, Mehdi; Rodriguez, Henry] NCI, Off Canc Clin Prote Res, NIH, Bethesda, MD 20892 USA.
[Liebler, Daniel C.] Vanderbilt Ingram Canc Ctr, Jim Ayers Inst Canc Detect & Diag, Nashville, TN USA.
RP Liebler, DC (reprint author), Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Jim Ayers Inst Canc Detect & Diag, U1213 MRBIII,465 21st Ave South, Nashville, TN 37232 USA.
EM mellis@dom.wustl.edu; daniel.liebler@vanderbilt.edu
RI Smith, Richard/J-3664-2012;
OI Smith, Richard/0000-0002-2381-2349; Liebler, Daniel/0000-0002-7873-3031
FU NCI NIH HHS [U24 CA159988, U24 CA160019, U24 CA160034, U24 CA160035, U24
CA160036, U24CA159988, U24CA160019, U24CA160034, U24CA160035,
U24CA160036]
NR 20
TC 48
Z9 49
U1 2
U2 13
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD OCT
PY 2013
VL 3
IS 10
BP 1108
EP 1112
DI 10.1158/2159-8290.CD-13-0219
PG 5
WC Oncology
SC Oncology
GA 235WH
UT WOS:000325751600021
PM 24124232
ER
PT J
AU Rabin, BA
Gaglio, B
Sanders, T
Nekhlyudov, L
Dearing, JW
Bull, S
Glasgow, RE
Marcus, A
AF Rabin, Borsika A.
Gaglio, Bridget
Sanders, Tristan
Nekhlyudov, Larissa
Dearing, James W.
Bull, Sheana
Glasgow, Russell E.
Marcus, Alfred
TI Predicting Cancer Prognosis Using Interactive Online Tools: A Systematic
Review and Implications for Cancer Care Providers
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID OF-THE-LITERATURE; DECISION AIDS; HEALTH INFORMATION; PROSTATE-CANCER;
BREAST-CANCER; COMMUNICATION; RISK; PREFERENCES; THERAPY; MODEL
AB Cancer prognosis is of keen interest for patients with cancer, their caregivers, and providers. Prognostic tools have been developed to guide patient-physician communication and decision-making. Given the proliferation of prognostic tools, it is timely to review existing online cancer prognostic tools and discuss implications for their use in clinical settings. Using a systematic approach, we searched the Internet, Medline, and consulted with experts to identify existing online prognostic tools. Each was reviewed for content and format. Twenty-two prognostic tools addressing 89 different cancers were identified. Tools primarily focused on prostate (n = 11), colorectal (n = 10), breast (n = 8), and melanoma (n = 6), although at least one tool was identified for most malignancies. The input variables for the tools included cancer characteristics (n = 22), patient characteristics (n = 18), and comorbidities (n = 9). Effect of therapy on prognosis was included in 15 tools. The most common predicted outcome was cancer-specific survival/mortality (n = 17). Only a few tools (n = 4) suggested patients as potential target users. A comprehensive repository of online prognostic tools was created to understand the state-of-the-art in prognostic tool availability and characteristics. Use of these tools may support communication and understanding about cancer prognosis. Dissemination, testing, refinement of existing, and development of new tools under different conditions are needed. (C) 2013 AACR.
C1 [Rabin, Borsika A.; Dearing, James W.] Inst Hlth Res, Canc Res Network, Canc Commun Res Ctr, Denver, CO USA.
[Sanders, Tristan] Kaiser Permanente Colorado, Denver, CO 80231 USA.
[Bull, Sheana; Marcus, Alfred] Univ Colorado, Denver, CO 80202 USA.
[Gaglio, Bridget] Kaiser Permanente, Mid Atlantic Permanente Res Inst, Rockville, MD USA.
[Glasgow, Russell E.] NCI, Rockville, MD USA.
[Nekhlyudov, Larissa] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
[Nekhlyudov, Larissa] Harvard Vanguard Med Associates, Dept Med, Boston, MA USA.
RP Rabin, BA (reprint author), Kaiser Permanente Colorado, Legacy Highlands Bldg,10065 E Harvard Ave,Suite 3, Denver, CO 80231 USA.
EM borsika.a.rabin@gmail.com
FU National Cancer Institute [P20 CA137219]
FX This work was supported by the National Cancer Institute (P20 CA137219).
The authors of this manuscript (all except R.E. Glasgow) have received
financial support from the National Cancer Institute to evaluate the
feasibility and small-scale implementation of one of the cancer
prognostic tools (Cancer Survival Query System) included in this review.
NR 35
TC 9
Z9 11
U1 3
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2013
VL 22
IS 10
BP 1645
EP 1656
DI 10.1158/1055-9965.EPI-13-0513
PG 12
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 234GT
UT WOS:000325631200001
PM 23956026
ER
PT J
AU Palmer, NRA
Geiger, AM
Lu, LY
Case, LD
Weaver, KE
AF Palmer, Nynikka R. A.
Geiger, Ann M.
Lu, Lingyi
Case, L. Douglas
Weaver, Kathryn E.
TI Impact of Rural Residence on Forgoing Healthcare after Cancer Because of
Cost
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID MEDICARE BENEFICIARIES; AMERICAN SOCIETY; UNITED-STATES; ACCESS;
DISPARITIES; URBAN; POPULATION; SURVIVORS; ADULTS; BARRIERS
AB Background: Routine follow-up care is recommended to promote the well-being of cancer survivors, but financial difficulties may interfere. Rural-urban disparities in forgoing healthcare due to cost have been observed in the general population; however, it is unknown whether this disparity persists among survivors. The purpose of this study was to examine rural-urban disparities in forgoing healthcare after cancer due to cost.
Methods: We analyzed data from 7,804 cancer survivors in the 2006 to 2010 National Health Interview Survey. Logistic regression models, adjusting for sociodemographic and clinical characteristics, were used to assess rural-urban disparities in forgoing medical care, prescription medications, and dental care due to cost, stratified by age (younger: 18-64, older: 65+).
Results: Compared with urban survivors, younger rural survivors were more likely to forgo medical care (P < 0.001) and prescription medications (P < 0.001) due to cost; older rural survivors were more likely to forgo medical (P < 0.001) and dental care (P = 0.05). Rural-urban disparities did not persist among younger survivors in adjusted analyses; however, older rural survivors remained more likely to forgo medical [OR = 1.66, 95% confidence interval (CI) = 1.11-2.48] and dental care (OR = 1.54, 95%CI = 1.08-2.20).
Conclusions: Adjustment for health insurance and other sociodemographic characteristics attenuates rural-urban disparities in forgoing healthcare among younger survivors, but not older survivors. Financial factors relating to healthcare use among rural survivors should be a topic of continued investigation.
Impact: Addressing out-of-pocket costs may be an important step in reducing rural-urban disparities in healthcare, especially for older survivors. It will be important to monitor how healthcare reform efforts impact disparities observed in this vulnerable population. (C) 2013 AACR.
C1 [Palmer, Nynikka R. A.; Geiger, Ann M.; Weaver, Kathryn E.] Wake Forest Sch Med, Winston Salem, NC 27157 USA.
[Lu, Lingyi; Case, L. Douglas] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
[Geiger, Ann M.] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Weaver, KE (reprint author), Wake Forest Sch Med, Dept Social Sci & Hlth Policy, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM keweaver@wakehealth.edu
OI Palmer, Nynikka/0000-0002-5311-447X
FU National Cancer Institute at the National Institutes of Health [R03
CA156641-01]; Wake Forest School of Medicine Cancer Prevention and
Control Training Program [5R25CA122061]
FX This work was financially supported by the National Cancer Institute at
the National Institutes of Health (grant no. R03 CA156641-01). N.R.A.
Palmer is supported by the Wake Forest School of Medicine Cancer
Prevention and Control Training Program-5R25CA122061.
NR 42
TC 7
Z9 7
U1 4
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2013
VL 22
IS 10
BP 1668
EP 1676
DI 10.1158/1055-9965.EPI-13-0421
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 234GT
UT WOS:000325631200003
PM 24097196
ER
PT J
AU Zhang, W
Xiang, YB
Li, HL
Yang, G
Cai, H
Ji, BT
Gao, YT
Zheng, W
Shu, XO
AF Zhang, Wei
Xiang, Yong-Bing
Li, Hong-Lan
Yang, Gong
Cai, Hui
Ji, Bu-Tian
Gao, Yu-Tang
Zheng, Wei
Shu, Xiao-Ou
TI Vegetable-based dietary pattern and liver cancer risk: Results from the
Shanghai Women's and Men's Health Studies
SO CANCER SCIENCE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; HEPATITIS-B; COLORECTAL-CANCER; STOMACH
CANCERS; CONSUMPTION; CHINA; METAANALYSIS; COHORT; FRUIT;
REPRODUCIBILITY
AB Although dietary patterns, specific foods, and their constituents have been linked to cancer risk, the role of dietary patterns and specific food groups in liver cancer risk has not been investigated. In the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS), two cohort studies of 132837 Chinese women and men, we evaluated the relationship between dietary patterns, food groups, and liver cancer risk. Through in-person interviews, dietary information intake over the preceding year was collected by using a validated food-frequency questionnaire. Cox regression model was used to estimate hazard ratios and 95% confidence intervals with adjustment for potential confounders. During an average follow-up of 10.9 (SWHS) or 5.5 (SMHS) years, 267 incident liver cancer cases were identified after the first 2years of study enrolment. Three dietary patterns were derived by factor analysis. A vegetable-based dietary pattern was inversely associated with liver cancer; hazard ratios (95% confidence intervals) for the lowest to highest quartiles were: 1.00; 0.98 (0.71-1.35); 0.93 (0.67-1.29); and 0.58 (0.40-0.84); P-trend=0.01. The association was stronger among participants with a history of chronic liver disease. Further analyses showed high intakes of celery, mushrooms, allium vegetables, composite vegetables (including asparagus lettuce and garland chrysanthemum), legumes and legume products were associated with reduced liver cancer risk (all P-trend<0.05). Fruit- and meat-based dietary patterns were not associated with liver cancer risk. Our study suggests that a vegetable-based dietary pattern is associated with reduced liver cancer risk.
C1 [Zhang, Wei; Xiang, Yong-Bing; Li, Hong-Lan] Shanghai Jiao Tong Univ, Sch Med, Shanghai Canc Inst, State Key Lab Oncogene & Related Genes,Renji Hosp, Shanghai 200030, Peoples R China.
[Zhang, Wei; Xiang, Yong-Bing; Li, Hong-Lan; Gao, Yu-Tang] Shanghai Jiao Tong Univ, Sch Med, Shanghai Canc Inst, Dept Epidemiol,Renji Hosp, Shanghai 200030, Peoples R China.
[Yang, Gong; Cai, Hui; Zheng, Wei; Shu, Xiao-Ou] Vanderbilt Univ, Sch Med, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37212 USA.
[Ji, Bu-Tian] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Xiang, YB (reprint author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Canc Inst, State Key Lab Oncogene & Related Genes,Renji Hosp, Shanghai 200030, Peoples R China.
EM ybxiang@shsci.org
FU State Key Project Specialized for Infectious Diseases of China
[2008ZX10002-015, 2012ZX10002008-002]; Shanghai Municipal Bureau of
Public Health [2008144]; US National Institutes of Health [R37 CA070867,
R01 CA82729]; Fogarty International Center [D43 TW008313]
FX The authors thank the participants and research staff of the SWHS and
SMHS for their contributions to this article. We also thank Dr. Shenghui
Wu for verifying the statistical analysis and Ms. Bethanie Rammer and
Mrs. Jacqueline Stern for their technical assistance in editing and
preparing the manuscript. This study was supported by the funds of the
State Key Project Specialized for Infectious Diseases of China (No.
2008ZX10002-015 and No. 2012ZX10002008-002 to Y-B Xiang), the research
fund of the Shanghai Municipal Bureau of Public Health (No. 2008144 to
W. Zhang), as well as grants (R37 CA070867 to W. Zheng) and R01 CA82729
to X-O Shu) from the US National Institutes of Health for the parent
studies. Wei Zhang was supported by a training grant from the Fogarty
International Center (D43 TW008313 to X-O Shu). The funding organization
played no role in the design or conduct of the study, collection,
management, analysis, or interpretation of the data, or the preparation,
review, or approval of the manuscript. Drs. Xiang and Shu had full
access to all data in the study and take responsibility for the
integrity of the data and the accuracy of the data analysis.
NR 42
TC 10
Z9 10
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD OCT
PY 2013
VL 104
IS 10
BP 1353
EP 1361
DI 10.1111/cas.12231
PG 9
WC Oncology
SC Oncology
GA 234ZK
UT WOS:000325683200012
PM 23841909
ER
PT J
AU Ramamoorthy, M
May, A
Tadokoro, T
Popuri, V
Seidman, MM
Croteau, DL
Bohr, VA
AF Ramamoorthy, Mahesh
May, Alfred
Tadokoro, Takashi
Popuri, Venkateswarlu
Seidman, Michael M.
Croteau, Deborah L.
Bohr, Vilhelm A.
TI The RecQ helicase RECQL5 participates in psoralen-induced interstrand
cross-link repair
SO CARCINOGENESIS
LA English
DT Article
ID NUCLEOTIDE EXCISION-REPAIR; RNA-POLYMERASE-II; WERNER-SYNDROME PROTEIN;
INDUCED DNA-DAMAGE; BLOOM-SYNDROME; CELLULAR-RESPONSES;
COCKAYNE-SYNDROME; REPLICATION FORK; HUMAN RECQ5-BETA; FANCONI-ANEMIA
AB Interstrand cross-links (ICLs) are very severe lesions as they are absolute blocks of replication and transcription. This property of interstrand cross-linking agents has been exploited clinically for the treatment of cancers and other diseases. ICLs are repaired in human cells by specialized DNA repair pathways including components of the nucleotide excision repair pathway, double-strand break repair pathway and the Fanconi anemia pathway. In this report, we identify the role of RECQL5, a member of the RecQ family of helicases, in the repair of ICLs. Using laser-directed confocal microscopy, we demonstrate that RECQL5 is recruited to ICLs formed by trioxalen (a psoralen-derived compound) and ultraviolet irradiation A. Using single-cell gel electrophoresis and proliferation assays, we identify the role of RECQL5 in the repair of ICL lesions. The domain of RECQL5 that recruits to the site of ICL was mapped to the KIX region between amino acids 500 and 650. Inhibition of transcription and of topoisomerases did not affect recruitment, which was inhibited by DNA-intercalating agents, suggesting that the DNA structure itself may be responsible for the recruitment of RECQL5 to the sites of ICLs.
C1 [Ramamoorthy, Mahesh; May, Alfred; Tadokoro, Takashi; Popuri, Venkateswarlu; Seidman, Michael M.; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Biomed Res Ctr, Lab Mol Gerontol, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Biomed Res Ctr, Lab Mol Gerontol, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
OI Ramamoorthy, Mahesh/0000-0002-2359-5647
FU National Institutes of Health Intramural Program of the National
Institute on Aging [Z01-AG000726-17]
FX National Institutes of Health Intramural Program of the National
Institute on Aging (Z01-AG000726-17).
NR 61
TC 7
Z9 8
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2013
VL 34
IS 10
BP 2218
EP 2230
DI 10.1093/carcin/bgt183
PG 13
WC Oncology
SC Oncology
GA 232IH
UT WOS:000325486200004
PM 23715498
ER
PT J
AU Koutros, S
Meyer, TE
Fox, SD
Issaq, HJ
Veenstra, TD
Huang, WY
Yu, K
Albanes, D
Chu, LW
Andriole, G
Hoover, RN
Hsing, AW
Berndt, SI
AF Koutros, Stella
Meyer, Tamra E.
Fox, Stephen D.
Issaq, Haleem J.
Veenstra, Timothy D.
Huang, Wen-Yi
Yu, Kai
Albanes, Demetrius
Chu, Lisa W.
Andriole, Gerald
Hoover, Robert N.
Hsing, Ann W.
Berndt, Sonja I.
TI Prospective evaluation of serum sarcosine and risk of prostate cancer in
the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial
SO CARCINOGENESIS
LA English
DT Article
ID RECTAL EXAMINATION FAILS; DIABETES-MELLITUS; SMOKING; URINE; MARKER;
IDENTIFICATION; METAANALYSIS; BIOMARKER; PROFILES; COHORT
AB Metabolomic profiling has identified, sarcosine, a derivative of the amino acid glycine, as an important metabolite involved in the etiology or natural history of prostate cancer. We examined the association between serum sarcosine levels and risk of prostate cancer in 1122 cases (813 non-aggressive and 309 aggressive) and 1112 controls in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Sarcosine was quantified using high-throughput liquid chromatographymass spectrometry. A significantly increased risk of prostate cancer was observed with increasing levels of sarcosine (odds ratio [OR] for the highest quartile of exposure [Q4] versus the lowest quartile [Q1] 1.30, 95% confidence interval [CI]: 1.02, 1.65; P-trend 0.03). When stratified by disease aggressiveness, we observed a stronger association for non-aggressive cases (OR for Q4 versus Q1 1.44, 95% CI: 1.11, 1.88; P-trend 0.006) but no association for aggressive prostate cancer (OR for Q4 versus Q1 1.03, 95% CI: 0.73, 1.47; P-trend 0.89). Although not statistically significant, temporal analyses showed a stronger association between sarcosine and prostate cancer for serum collected closer to diagnosis, suggesting that sarcosine may be an early biomarker of disease. Interestingly, the association between sarcosine and prostate cancer risk was stronger among men with diabetes (OR 2.66, 95% CI: 1.04, 6.84) compared with those without reported diabetes (OR 1.23, 95% CI: 0.951.59, P-interaction 0.01). This study found that elevated levels of serum sarcosine are associated with an increased prostate cancer risk and evidence to suggest that sarcosine may be an early biomarker for this disease.
C1 [Koutros, Stella; Huang, Wen-Yi; Yu, Kai; Albanes, Demetrius; Hoover, Robert N.; Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Meyer, Tamra E.] Off Surg Gen, Dept Army, Silver Spring, MD 20910 USA.
[Fox, Stephen D.; Issaq, Haleem J.; Veenstra, Timothy D.] Frederick Natl Lab Canc Res, SAIC Frederick, Adv Technol Program, Lab Prote & Analyt Technol, Frederick, MD 21701 USA.
[Chu, Lisa W.; Hsing, Ann W.] Stanford Canc Inst, Canc Prevent Inst Calif, Fremont, CA 94538 USA.
[Andriole, Gerald] Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63110 USA.
RP Koutros, S (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8112,MSC 7240, Rockville, MD 20852 USA.
EM KoutrosS@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Division of Cancer Epidemiology and Genetics
[Z01 CP010152]
FX Intramural Research Program of the National Institutes of Health,
National Cancer Institute and Division of Cancer Epidemiology and
Genetics (Z01 CP010152).
NR 35
TC 14
Z9 14
U1 1
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2013
VL 34
IS 10
BP 2281
EP 2285
DI 10.1093/carcin/bgt176
PG 5
WC Oncology
SC Oncology
GA 232IH
UT WOS:000325486200011
PM 23698636
ER
PT J
AU Izzotti, A
Balansky, R
D'Agostini, F
Longobardi, M
Cartiglia, C
La Maestra, S
Micale, RT
Camoirano, A
Ganchev, G
Iltcheva, M
Steele, VE
De Flora, S
AF Izzotti, Alberto
Balansky, Roumen
D'Agostini, Francesco
Longobardi, Mariagrazia
Cartiglia, Cristina
La Maestra, Sebastiano
Micale, Rosanna T.
Camoirano, Anna
Ganchev, Gancho
Iltcheva, Marietta
Steele, Vernon E.
De Flora, Silvio
TI Relationships between pulmonary micro-RNA and proteome profiles,
systemic cytogenetic damage and lung tumors in cigarette smoke-exposed
mice treated with chemopreventive agents
SO CARCINOGENESIS
LA English
DT Article
ID MOUSE LUNG; PHENETHYL ISOTHIOCYANATE; N-ACETYLCYSTEINE; TOBACCO-SMOKE;
EXPRESSION; CARCINOGENESIS; PREVENTION; TUMORIGENESIS; PIOGLITAZONE;
COMBINATION
AB Assessing the correlation between molecular endpoints and cancer induction or prevention aims at validating the use of intermediate biomarkers. We previously developed murine models that are suitable to detect both the carcinogenicity of mainstream cigarette smoke (MCS) and the induction of molecular alterations. In this study, we used 931 Swiss mice in two parallel experiments and in a preliminary toxicity study. The chemopreventive agents included vorinostat, myo-inositol, bexarotene, pioglitazone and a combination of bexarotene and pioglitazone. Pulmonary micro-RNAs and proteins were evaluated by microarray analyses at 10 weeks of age in male and female mice, either unexposed or exposed to MCS since birth, and either untreated or receiving each one of the five chemopreventive regimens with the diet after weaning. At 4 months of age, the frequency of micronucleated normochromatic erythrocytes was evaluated. At 7 months, the lungs were subjected to standard histopathological analysis. The results showed that exposure to MCS significantly downregulated the expression of 79 of 694 lung micro-RNAs (11.4%) and upregulated 66 of 1164 proteins (5.7%). Administration of chemopreventive agents modulated the baseline micro-RNA and proteome profiles and reversed several MCS-induced alterations, with some intergender differences. The stronger protective effects were produced by the combination of bexarotene and pioglitazone, which also inhibited the MCS-induced clastogenic damage and the yield of malignant tumors. Pioglitazone alone increased the yield of lung adenomas. Thus, micro-RNAs, proteins, cytogenetic damage and lung tumors were closely related. The molecular biomarkers contributed to evaluate both protective and adverse effects of chemopreventive agents and highlighted the mechanisms involved.
C1 [Izzotti, Alberto; Balansky, Roumen; D'Agostini, Francesco; Longobardi, Mariagrazia; Cartiglia, Cristina; La Maestra, Sebastiano; Micale, Rosanna T.; Camoirano, Anna; De Flora, Silvio] Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy.
[Balansky, Roumen; Ganchev, Gancho; Iltcheva, Marietta] Natl Oncol Ctr, Lab Chem Mutagenesis & Carcinogenesis, Sofia 1756, Bulgaria.
[Steele, Vernon E.] NCI, Chemoprevent Agent Dev Res Program, Canc Prevent Div, Bethesda, MD 20892 USA.
RP De Flora, S (reprint author), Univ Genoa, Dept Hlth Sci, Via A Pastore 1, I-16132 Genoa, Italy.
EM sdf@unige.it
OI izzotti, alberto/0000-0002-8588-0347
FU United States National Cancer Institute [N01-CN 53301]; Bulgarian
Ministry of Education, Youth and Science (National Science Foundation);
Hasumi International Research Foundation (Bulgaria)
FX United States National Cancer Institute (Contract N01-CN 53301);
Bulgarian Ministry of Education, Youth and Science (National Science
Foundation); Hasumi International Research Foundation (Bulgaria).
NR 40
TC 18
Z9 18
U1 0
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2013
VL 34
IS 10
BP 2322
EP 2329
DI 10.1093/carcin/bgt178
PG 8
WC Oncology
SC Oncology
GA 232IH
UT WOS:000325486200017
PM 23708261
ER
PT J
AU Kim, DW
Walker, RL
Meltzer, PS
Cheng, SY
AF Kim, Dong Wook
Walker, Robert L.
Meltzer, Paul S.
Cheng, Sheue-yann
TI Complex temporal changes in TGF oncogenic signaling drive thyroid
carcinogenesis in a mouse model
SO CARCINOGENESIS
LA English
DT Article
ID GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL TRANSITION; HORMONE
RECEPTOR-BETA; BREAST-CANCER CELLS; TRANSFORMING GROWTH-FACTOR-BETA-1;
GENE-EXPRESSION; E-CADHERIN; TRANSCRIPTIONAL REGULATION; MESANGIAL
CELLS; COLLAGEN-III
AB Despite recent advances, understanding of molecular genetic alterations underlying thyroid carcinogenesis remains unclear. One key question is how dynamic temporal changes in global genomic expression affect carcinogenesis as the disease progresses. To address this question, we used a mouse model that spontaneously develops follicular thyroid cancer similar to human cancer (Thrb(PV/PV) mice). Using complementary DNA microarrays, we compared global gene expression profiles of thyroid tumors of Thrb(PV/PV) mice with the age- and gender-matched thyroids of wild-type mice at 3 weeks and at 2, 4, 6 and 14 months. These time points covered the pathological progression from early hyperplasia to capsular invasion, vascular invasion and eventual metastasis. Microarray data indicated that 462 genes were upregulated (Up-cluster genes) and 110 genes were downregulated (Down-cluster genes). Three major expression patterns (trending up, cyclical and spiking up and then down) and two (trending down and cyclical) were apparent in the Up-cluster and Down-cluster genes, respectively. Functional clustering of tumor-related genes followed by Ingenuity Pathways Analysis identified the transforming growth factor (TGF )-mediated network as key signaling pathways. Further functional analyses showed sustained activation of TGF receptorpSMAD2/3 signaling, leading to decreased expression of E-cadherin and increased expression of fibronectin, vimentin, collagens and laminins. These TGF-induced changes facilitated epithelial-to-mesenchymal transition, which promotes cancer invasion and migration. Thus, complex temporal changes in gene expression patterns drive thyroid cancer progression, and persistent activation of TGFTGFRIIpSMAD2/3 signaling leads to EMT, thus promoting metastasis. This study provides new understanding of progression and metastatic spread of human thyroid cancer.
C1 [Kim, Dong Wook; Cheng, Sheue-yann] NCI, Gene Regulat Sect, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Walker, Robert L.; Meltzer, Paul S.] NCI, Mol Genet Sect, Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Cheng, SY (reprint author), NCI, Gene Regulat Sect, Mol Biol Lab, NIH, Room 5128,37 Convent Dr MSC 4264, Bethesda, MD 20892 USA.
EM chengs@mail.nih.gov
FU Intramural Research Program at the Center for Cancer Research, National
Cancer Institute, National Institutes of Health
FX Intramural Research Program at the Center for Cancer Research, National
Cancer Institute, National Institutes of Health.
NR 74
TC 5
Z9 6
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2013
VL 34
IS 10
BP 2389
EP 2400
DI 10.1093/carcin/bgt175
PG 12
WC Oncology
SC Oncology
GA 232IH
UT WOS:000325486200024
PM 23698635
ER
PT J
AU Liu, Y
Wan, B
Yin, J
Horvath, K
Sarkar, J
Lu, J
Lei, M
AF Liu, Y.
Wan, B.
Yin, J.
Horvath, K.
Sarkar, J.
Lu, J.
Lei, M.
TI SLX4 AND TRF2 INTERACTION IS REQUIRED FOR TELOMERE STRUCTURE AND LENGTH
REGULATION
SO CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
LA English
DT Meeting Abstract
CT 4th Meeting of the
Australia-Chinese-Association-for-Biomedical-Sciences-Inc (ACABS)
CY OCT 10-13, 2013
CL Hangzhou, PEOPLES R CHINA
SP Australia Chinese Assoc Biomed Sci Inc
C1 [Liu, Y.; Yin, J.; Horvath, K.; Sarkar, J.; Lu, J.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Wan, B.; Lei, M.] Chinese Acad Sci, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1440-1681
J9 CLIN EXP PHARMACOL P
JI Clin. Exp. Pharmacol. Physiol.
PD OCT
PY 2013
VL 40
SU 1
SI SI
BP 30
EP 30
PG 1
WC Pharmacology & Pharmacy; Physiology
SC Pharmacology & Pharmacy; Physiology
GA 234MA
UT WOS:000325647200078
ER
PT J
AU McCullough, PA
Barnard, D
Clare, R
Ellis, SJ
Fleg, JL
Fonarow, GC
Franklin, BA
Kilpatrick, RD
Kitzman, DW
O'Connor, CM
Pina, IL
Thadani, U
Thohan, V
Whellan, DJ
AF McCullough, Peter A.
Barnard, Denise
Clare, Robert
Ellis, Stephen J.
Fleg, Jerome L.
Fonarow, Gregg C.
Franklin, Barry A.
Kilpatrick, Ryan D.
Kitzman, Dalane W.
O'Connor, Christopher M.
Pina, Ileana L.
Thadani, Udho
Thohan, Vinay
Whellan, David J.
CA HF-ACTION Investigators
TI Anemia and Associated Clinical Outcomes in Patients With Heart Failure
Due to Reduced Left Ventricular Systolic Function
SO CLINICAL CARDIOLOGY
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; SURVEY NHANES 1999-2004; EVALUATION PROGRAM
KEEP; NATIONAL-HEALTH; HF-ACTION; CARDIOVASCULAR RISK; CONTROLLED-TRIAL;
NUTRITION; CKD; DYSFUNCTION
AB Background: Anemia is associated with decreased functional capacity, reduced quality of life, and worsened outcomes among patients with heart failure (HF) due to reduced left ventricular ejection fraction (HFREF). We sought to evaluate the independent effect of anemia on clinical outcomes among those with HFREF.
HypothesisAnemia is associated with cardiovascular events in patients with heart failure.
MethodsThe HF-ACTION trial was a prospective, randomized trial of exercise therapy vs usual care in 2331 patients with HFREF. Patients with New York Heart Association class II to IV HF and left ventricular ejection fractions of 35% were recruited. Hemoglobin (Hb) was measured up to 1 year prior to entry and was stratified by quintile. Anemia was defined as baseline Hb <13 g/dL and <12 g/dL in men and women, respectively. Hemoglobin was assessed in 2 models: a global prediction model that had been previously developed, and a modified model including variables associated with anemia and the studied outcomes.
ResultsHemoglobin was available at baseline in 1763 subjects (76% of total study population); their median age was 59.0 years, 73% were male, and 62% were Caucasian. The prevalence of anemia was 515/1763 (29%). Older age, female sex, African American race, diabetes, hypertension, and lower estimated glomerular filtration rates were all more frequent in lower Hb quintiles. Over a median follow-up of 30 months, the primary outcome of all-cause mortality or all-cause hospitalization occurred in 78% of those with anemia and 64% in those without (P < 0.001). The secondary outcomes of all-cause mortality alone,cardiovascular (CV) mortality or CV hospitalization, and CV mortality or HF hospitalization occurred in 23% vs 15%, 67% vs 54%, and 44 vs 29%, respectively (P < 0.001). Heart failure hospitalizations occurred in 36% vs 22%, and urgent outpatient visits for HF exacerbations occurred in 67% and 55%, respectively (P < 0.001). For the global model, there was an association observed for anemia and all-cause mortality or hospitalization (adjusted hazard ratio [HR]: 1.15, 95% confidence interval [CI]: 1.01-1.32, P = 0.04), but other outcomes were not significant at P < 0.05. In the modified model, the adjusted HR for anemia and the primary outcome of all-cause mortality or all-cause hospitalization was 1.25 (95% CI: 1.10-1.42, P < 0.001). There were independent associations between anemia and all-cause death (HR: 1.11, 95% CI: 0.87-1.42, P = 0.38), CV death or CV hospitalization (HR: 1.16, 95% CI: 1.01-1.33, P = 0.035), and CV death and HF hospitalization (HR: 1.27, 95% CI: 1.06-1.51, P = 0.008).
ConclusionsAnemia modestly is associated with increased rates of death, hospitalization, and HF exacerbation in patients with chronic HFREF. After adjusting for other important covariates, anemia is independently associated with an excess hazard for all-cause mortality and all-cause hospitalization. Anemia is also associated with combinations of CV death and CV/HF hospitalizations as composite endpoints.
C1 [McCullough, Peter A.] St John Providence Hlth Syst, Dept Cardiovasc Med, Warren, MI USA.
[McCullough, Peter A.] St John Hosp & Med Ctr, Detroit, MI USA.
[McCullough, Peter A.] St John Hosp Macomb Oakland Ctr, Madison Hts, MI USA.
[McCullough, Peter A.] Providence Hosp & Med Ctr, Southfield, MI USA.
[McCullough, Peter A.] Providence Hosp & Med Ctr, Novi, MI USA.
[McCullough, Peter A.] Providence Pk Heart Inst, Novi, MI USA.
[Barnard, Denise] Univ Calif San Diego, Sch Med, Dept Cardiol, UCSD Hlth Syst, San Diego, CA 92103 USA.
[Clare, Robert; Ellis, Stephen J.; O'Connor, Christopher M.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Fleg, Jerome L.] NHLBI, Bethesda, MD 20892 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Sch Med, Dept Cardiol, Los Angeles, CA USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Sch Med, Ahmanson UCLA Cardiomyopathy Ctr, Los Angeles, CA USA.
[Franklin, Barry A.] Oakland Univ, William Beaumont Hosp, William Beaumont Sch Med, Dept Cardiac Rehabil, Royal Oak, MI USA.
[Kilpatrick, Ryan D.] Amgen Inc, Thousand Oaks, CA 91320 USA.
[Kitzman, Dalane W.; Thohan, Vinay] Wake Forest Baptist Hlth, Adv Cardiac Care & Heart Transplant Program, Winston Salem, NC USA.
[Pina, Ileana L.] Albert Einstein Coll Med, Montefiore Med Ctr, Div Cardiol, Heart Failure Transplant Program, New York, NY USA.
[Thadani, Udho] Univ Oklahoma, Hlth Sci Ctr, Dept Cardiol, Oklahoma City, OK USA.
[Thadani, Udho] Vet Adm Med Ctr, Oklahoma City, OK 73104 USA.
[Whellan, David J.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Med, Philadelphia, PA 19107 USA.
RP McCullough, PA (reprint author), Providence Pk Heart Inst, 47601 Grand River Ave,Suite B-125, Novi, MI 48374 USA.
EM peteramccullough@gmail.com
FU National Heart, Lung, and Blood Institute of the National Institutes of
Health; Amgen, Inc.
FX This work was funded by the National Heart, Lung, and Blood Institute of
the National Institutes of Health. The authors acknowledge the HF-ACTION
Trial and Amgen, Inc., for partial support of statistical analyses and
manuscript preparation and finalization. Dr. Kilpatrick is an employee
and stockholder of Amgen, Inc., which provided funding for this
analysis. ClinicalTrials.gov identifier: NCT00047437.
NR 36
TC 7
Z9 7
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0160-9289
EI 1932-8737
J9 CLIN CARDIOL
JI Clin. Cardiol.
PD OCT
PY 2013
VL 36
IS 10
BP 611
EP 620
DI 10.1002/clc.22181
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 232KZ
UT WOS:000325493900014
PM 23929781
ER
PT J
AU Sacks, DB
AF Sacks, David B.
TI Reporting Hemoglobin A(1c): Do the Units Matter?
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
ID DIABETES-MELLITUS; STANDARDIZATION; CARE; COMPLICATIONS; BLOOD; A1C
C1 [Sacks, David B.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Sacks, DB (reprint author), Dept Lab Med, Bldg 10,Rm 2C306,10 Ctr Dr, Bethesda, MD 20892 USA.
EM sacksdb@mail.nih.gov
OI Sacks, David/0000-0003-3100-0735
FU Intramural NIH HHS
NR 15
TC 0
Z9 1
U1 0
U2 3
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD OCT
PY 2013
VL 59
IS 10
BP 1427
EP 1429
DI 10.1373/clinchem.2013.211227
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 231FG
UT WOS:000325399800001
PM 23877379
ER
PT J
AU Berg, RA
Sutton, RM
Holubkov, R
Nicholson, CE
Dean, JM
Harrison, R
Heidemann, S
Meert, K
Newth, C
Moler, F
Pollack, M
Dalton, H
Doctor, A
Wessel, D
Berger, J
Shanley, T
Carcillo, J
Nadkarni, VM
AF Berg, Robert A.
Sutton, Robert M.
Holubkov, Richard
Nicholson, Carol E.
Dean, J. Michael
Harrison, Rick
Heidemann, Sabrina
Meert, Kathleen
Newth, Christopher
Moler, Frank
Pollack, Murray
Dalton, Heidi
Doctor, Allan
Wessel, David
Berger, John
Shanley, Thomas
Carcillo, Joseph
Nadkarni, Vinay M.
CA Eunice Kennedy Shriver Natl Inst C
Amer Heart Assoc
TI Ratio of PICU Versus Ward Cardiopulmonary Resuscitation Events Is
Increasing
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE cardiac arrest; cardiopulmonary resuscitation; children; intensive care;
pediatrics
ID AMERICAN-HEART-ASSOCIATION; HOSPITAL CARDIAC-ARREST; MEDICAL EMERGENCY
TEAM; INTENSIVE-CARE UNITS; CHILDREN; OUTCOMES; MORTALITY; DISCHARGE;
ICU
AB Objectives: The aim of this study was to evaluate the relative frequency of pediatric in-hospital cardiopulmonary resuscitation events occurring in ICUs compared to general wards. We hypothesized that the proportion of pediatric cardiopulmonary resuscitation provided in ICUs versus general wards has increased over the past decade, and this shift is associated with improved resuscitation outcomes.
Design: Prospective and observational study.
Setting: Total of 315 hospitals in the American Heart Association's Get With The Guidelines-Resuscitation database.
Patients: Total of 5,870 pediatric cardiopulmonary resuscitation events between January 1, 2000 and September 14, 2010. Cardiopulmonary resuscitation events were defined as external chest compressions longer than 1 minute.
Interventions: None.
Measurements and Main Results: The primary outcome was proportion of total ICU versus general ward cardiopulmonary resuscitation events over time evaluated by chi-square test for trend. Secondary outcome included return of spontaneous circulation following the cardiopulmonary resuscitation event. Among 5,870 pediatric cardiopulmonary resuscitation events, 5,477 (93.3%) occurred in ICUs compared to 393 (6.7%) in inpatient wards. Over time, significantly more of these cardiopulmonary resuscitation events occurred in the ICU compared to the wards (test for trend: p < 0.01), with a prominent shift noted between 2003 and 2004 (2000-2003: 87-91% vs 2004-2010: 94-96%). In a multivariable model controlling for within center variability and other potential confounders, return of spontaneous circulation increased in 2004-2010 compared with 2000-2003 (relative risk, 1.08; 95% CI, 1.03-1.13).
Conclusions: In-hospital pediatric cardiopulmonary resuscitation is much more commonly provided in ICUs than in wards, and the proportion has increased significantly over the past decade, with concomitant increases in return of spontaneous circulation.
C1 [Berg, Robert A.; Sutton, Robert M.; Nadkarni, Vinay M.] Childrens Hosp Philadelphia, Dept Anesthesiol & Crit Care, Div Crit Care Med, Philadelphia, PA 19104 USA.
[Berg, Robert A.; Sutton, Robert M.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Holubkov, Richard; Dean, J. Michael] Univ Utah, Dept Pediat, Salt Lake City, UT USA.
[Nicholson, Carol E.] NICHHD, Div Crit Care Med, Dept Pediat, Bethesda, MD 20892 USA.
[Harrison, Rick] Univ Calif Los Angeles, Dept Pediat, Div Crit Care Med, Los Angeles, CA 90024 USA.
[Heidemann, Sabrina; Meert, Kathleen] Childrens Hosp Michigan, Dept Pediat, Div Crit Care Med, Detroit, MI 48201 USA.
[Newth, Christopher] Childrens Hosp Los Angeles, Dept Anesthesiol & Crit Care, Div Crit Care Med, Los Angeles, CA 90027 USA.
[Moler, Frank; Shanley, Thomas] Univ Michigan, Dept Pediat, Div Crit Care Med, Ann Arbor, MI 48109 USA.
[Moler, Frank; Shanley, Thomas] Mott Childrens Hosp, Ann Arbor, MI USA.
[Pollack, Murray; Dalton, Heidi] Phoenix Childrens Hosp, Div Crit Care Med, Dept Pediat, Phoenix, AZ USA.
[Doctor, Allan] Washington Univ, Sch Med, Dept Pediat, Div Crit Care Med, St Louis, MO 63110 USA.
[Wessel, David; Berger, John] Childrens Natl Med Ctr, Dept Pediat, Div Crit Care Med, Washington, DC 20010 USA.
[Carcillo, Joseph] UPMC, Childrens Hosp Pittsburgh, Dept Crit Care Med, Pittsburgh, PA USA.
RP Berg, RA (reprint author), Childrens Hosp Philadelphia, Dept Anesthesiol & Crit Care, Div Crit Care Med, Philadelphia, PA 19104 USA.
EM bergra@email.chop.edu
OI Doctor, Allan/0000-0002-6096-6400
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), National Institutes of Health (NIH), Department of
Health and Human Services (DHHS) [U10-HD050012, U10-HD050096,
U10-HD063108, U10-HD049983, U10-HD049981, U10-HD063114, U10-HD063106];
National Institutes of Health (NIH); NIH NICHD; Collaborative Pediatric
Critical Care Research Network; NIH
FX Supported, in part, by the following cooperative agreements from the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), National Institutes of Health (NIH), Department of
Health and Human Services (DHHS): U10-HD050012, U10-HD050096,
U10-HD063108, U10-HD049983, U10-HD049981, U10-HD063114, and
U10-HD063106.; Drs. Berg, Holubkov, Nicholson, Dean, Harrison, Meert,
Newth, Moler, Pollack, Dalton, Doctor, Wessel, Berger, and Carcillo
received funding from the National Institutes of Health (NIH). Dr.
Sutton received grant support from NIH NICHD (K3 Career Development
Award). Dr. Sabrina Heidemann received grant support from the
Collaborative Pediatric Critical Care Research Network and funding from
NIH. Dr. Shanley received grant support from NIH, served as a board
member for the Society of Pediatric Research (Secretary/Treasurer),
received textbook royalties from Springer, and received support for
travel from the University of Cincinnati and Case Western Reserve
(external advisory boards). Dr. Nadkarni disclosed that he does not have
any potential conflicts of interest.
NR 18
TC 21
Z9 22
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD OCT
PY 2013
VL 41
IS 10
BP 2292
EP 2297
DI 10.1097/CCM.0b013e31828cf0c0
PG 6
WC Critical Care Medicine
SC General & Internal Medicine
GA 225AP
UT WOS:000324935000024
PM 23921270
ER
PT J
AU Qiu, P
Cui, XZ
Sun, JF
Welsh, J
Natanson, C
Eichacker, PQ
AF Qiu, Ping
Cui, Xizhong
Sun, Junfeng
Welsh, Judith
Natanson, Charles
Eichacker, Peter Q.
TI Antitumor Necrosis Factor Therapy Is Associated With Improved Survival
in Clinical Sepsis Trials: A Meta-Analysis
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE sepsis; septic shock; treatment; tumor necrosis factor
ID FACTOR ANTIBODY-FRAGMENT; PLACEBO-CONTROLLED TRIAL; RECEPTOR FUSION
PROTEIN; SEPTIC SHOCK; FACTOR-ALPHA; MONOCLONAL-ANTIBODY; DOUBLE-BLIND;
MULTICENTER; EFFICACY; SAFETY
AB Objectives: Sepsis is a lethal syndrome annually affecting approximately 900,000 patients in the United States alone. Despite their benefit in rheumatoid disease, selective antitumor necrosis factor agents failed to improve outcome in early sepsis trials in the 1990s. However, data from additional sepsis trials testing these agents are now available. We therefore sought to determine the effect on survival of selective antitumor necrosis factor agents in randomized clinical sepsis trials..
Data Sources: PubMed, Scopus, Embase, and Web of Science.
Study Selection: Randomized human sepsis trials of selective antitumor necrosis factor agents reporting survival rates.
Data Extraction: Two investigators independently collected relevant data on study characteristics, treatment interventions, and patients from each study.
Data Synthesis: Antitumor necrosis factor agents in 15 sepsis trials (n = 8,896 patients) meeting inclusion criteria had similar effects (I-2 = 0, p = 0.84) and compared with controls (placebo in 14 trials or a lower dose in one trial) overall decreased the relative risk of death (95% CI) (0.93 [0.88-0.98], p = 0.01). In subgroup analysis, tumor necrosis factor monoclonal antibodies (10 trials, n = 6,818) alone produced a significant survival benefit (0.93 [0.87, 0.99], p = 0.02) (I-2 = 0, p = 0.83). Tumor necrosis factor polyclonal antibodies (two trials, n = 151) and low-molecular-weight soluble receptor (two trials, n = 1,786) had similar beneficial effects to antitumor necrosis factor agents overall (0.82 [0.49-1.37], p = 0.45; 0.93 [0.81-1.08], p = 0.33, respectively). The effect of tumor necrosis factor high-molecular-weight soluble receptor (one trial, n = 141) was not significantly different from other agents but was on the side of harm (1.50 [0.86-2.61], p = 0.16).
Conclusion: Antitumor necrosis factor agents produced a modest but significant decrease in the risk of dying with sepsis. Prior individual trials failed to demonstrate benefit, likely because they were underpowered. A definitive trial demonstrating the potential benefit of such agents might require 10,000 or more patients with sepsis.
C1 [Qiu, Ping; Cui, Xizhong; Sun, Junfeng; Natanson, Charles; Eichacker, Peter Q.] NIH, Crit Care Med Dept, Ctr Clin, Bethesda, MD 20892 USA.
[Welsh, Judith] NIH, Natl Inst Hlth Lib, Ctr Clin, Bethesda, MD 20892 USA.
RP Eichacker, PQ (reprint author), NIH, Crit Care Med Dept, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM peichacker@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health (NIH);
NIH Clinical Center, Bethesda, MD; National Institutes of Health
FX Supported, in part, by the Intramural Research Program of the National
Institutes of Health (NIH) and the NIH Clinical Center, Bethesda, MD.;
Drs. Eichacker, Qiu, Cui, Sun, and Natanson received funding from the
National Institutes of Health. Dr. Welsh disclosed that she does not
have any potential conflicts of interest.
NR 32
TC 9
Z9 9
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD OCT
PY 2013
VL 41
IS 10
BP 2419
EP 2429
DI 10.1097/CCM.0b013e3182982add
PG 11
WC Critical Care Medicine
SC General & Internal Medicine
GA 225AP
UT WOS:000324935000038
PM 23887234
ER
PT J
AU Mbulaiteye, SM
Kemp, T
Gage, JC
Ajenifuja, KO
Kiruthu, C
Wentzensen, NA
Adepiti, C
Wacholder, S
Burk, RD
Schiffman, M
Pinto, L
AF Mbulaiteye, S. M.
Kemp, T.
Gage, J. C.
Ajenifuja, K. O.
Kiruthu, C.
Wentzensen, N. A.
Adepiti, C.
Wacholder, S.
Burk, R. D.
Schiffman, M.
Pinto, L.
TI Plasma cytokine levels and human papillomavirus infection at the cervix
in rural Nigerian women
SO CYTOKINE
LA English
DT Article
DE Cytokines; Cervical cancer; Inflammation; Plasmodium falciparum malaria
ID CANCER; INFLAMMATION; PREVALENCE; AFRICANS; LESIONS; GUINEA; GRADE; RISK
AB Introduction: We conducted a study to test the hypothesis that systemic dysregulation of Th1/Th2 cytokine levels was associated with detection of carcinogenic or overall human papillomavirus (HPV) at the cervix among 964 women residing in a rural village in Nigeria.
Methods: Levels in plasma were measured for 19 cytokines, including Th1-like cytokines IL-2, IL-12 (p40), TNF-a, IFN-g; Th2-like cytokines IL-4, IL-5, IL-6, IL-10, IL-13; innate/inflammation cytokines IL-1a, IL-1b, IL-8, eotaxin, MCP-1, MIP-1a, and IL-7; and cell development cytokines G-CSF, VEGF, and IL-17. Analysis was restricted to 5 cytokines, TNF-alpha, (Th1), IL-8 (Th2), eotaxin and MCP-1 (innate/inflammation), and G-CSF (cell development), whose levels were detected in 80% or more of the samples measured as well as had a coefficient of variation of <30%.
Results: Strong correlations were noted between levels of eotaxin and TNF-alpha (r = 0.75), IL-8 and MCP-1 (r = 0.60), eotaxin and G-CSF (r = 0.44), and G-CSF and IFN-gamma (r = 0.43). Detection of carcinogenic or non-carcinogenic HPV DNA was unrelated to cytokine levels, except for levels of eotaxin and TNF-alpha, which were inversely correlated, albeit weakly, with detection of any carcinogenic HPV (P = 0.048 and P = 0.067, respectively). In analyses stratified by age group, levels of eotaxin were inversely correlated with detection of any HPV DNA (P = 0.026) and carcinogenic HPV (P = 0.042) in older, but not younger, women.
Conclusions: Our results do not support the hypothesis of association between systemic cytokine dysregulation and detection of HPV at the cervix in Nigerian women, but subgroup analyses raise questions about inverse associations between eotaxin and TNF-alpha in older women. Published by Elsevier Ltd.
C1 [Mbulaiteye, S. M.; Gage, J. C.; Kiruthu, C.; Wentzensen, N. A.; Wacholder, S.; Schiffman, M.] NCI, NIH, Div Canc Epidemiol & Genet, DHHS, Bethesda, MD 20892 USA.
[Kemp, T.; Pinto, L.] Sci Applicat Int Corp, Frederick, MD USA.
[Ajenifuja, K. O.; Adepiti, C.] Obafemi Awolowo Univ, Dept Obstet Gynaecol & Perinatol, Ife, Nigeria.
[Burk, R. D.] Yeshiva Univ, Albert Einstein Coll Med, The Bronx, NY USA.
RP Mbulaiteye, SM (reprint author), NCI, NIH, DCEG, Infect & Immunoepidemiol Branch, 9609 Med Ctr Dr Rm 6E118 MSC 9704, Bethesda, MD 20892 USA.
EM mbulaits@mail.nih.gov
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health,
Department of Health and Human Services NIH [5U01CA078527-13,
HHSN261200900303P]
FX We would like to thank Mr. David Check at the Biostatistics Branch at
the National Cancer Institute (Rockville, Maryland) for help drawing the
graphs. The study was supported by the Intramural Research Program of
the Division of Cancer Epidemiology and Genetics, National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services NIH Grant # 5U01CA078527-13 & NIH contract HHSN261200900303P.
The CareHPV equipment and supplies used in this study were donated by
Qiagen Corporation (Gaithersburg, MD); CareHPV is not the subject of
this report. The authors report no conflicts of interest.
NR 21
TC 6
Z9 8
U1 0
U2 4
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2013
VL 64
IS 1
BP 146
EP 151
DI 10.1016/j.cyto.2013.07.028
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 231UA
UT WOS:000325442700025
PM 23972725
ER
PT J
AU Berlin, I
Singleton, EG
Heishman, SJ
AF Berlin, Ivan
Singleton, Edward G.
Heishman, Stephen J.
TI Predicting smoking relapse with a multidimensional versus a single-item
tobacco craving measure
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Tobacco craving; Smoking relapse; Prognostic markers; Screening
ID MAXIMUM-LIKELIHOOD-ESTIMATION; TRANSCRANIAL MAGNETIC STIMULATION;
NICOTINE WITHDRAWAL SYMPTOMS; BINORMAL ROC CURVES; CIGARETTE WITHDRAWAL;
MYOCARDIAL-INFARCTION; OUTCOME EXPECTANCIES; PROGNOSTIC MODELS; FRENCH
VERSION; QUIT SMOKING
AB Background: Research suggests that craving is a predictor of smoking relapse. Craving can be assessed by multiple item or multifactorial scales or by single items. However, no systematic comparisons of their prognostic validity or accuracy have been published.
Methods: The French versions of the 12-item Tobacco Craving Questionnaire (FTCQ-12) and the single craving item on the Minnesota Nicotine Withdrawal Scale (MNWS) are brief, valid, and reliable self-report measures of tobacco craving. In this secondary study, we analyzed data from French smokers with health-related problems enrolled in the Adjustment of DOses of Nicotine in Smoking (ADONIS) cessation trial. We estimated prediction models for each measure and compared their ability to distinguish correctly participants who relapsed from those who did not at 1-8 weeks after their quit date.
Results: Adjusted for all potential confounders FTCQ-12 risk score (RS; Factor 2, Expectancy plus Factor 4, Purposefulness) and MNWS craving were valid predictors of smoking relapse at endpoints measured 1-7 weeks apart. Prognostic accuracy of FTCQ-12 RS was greatest at 1-2 weeks follow-up compared to only 1 week for MNWS craving. Sensitivity for FTCQ-12 RS and MNWS craving was 85% and 53%, respectively.
Conclusions: FTCQ-12 RS suggests a relapse process involving urges and desires in anticipation of the positive benefits of smoking linked with intent and planning to smoke. Findings also suggest that FTCQ-12 RS may be a better predictor instrument for smoking relapse than MNWS craving. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Berlin, Ivan] Univ Paris 06, INSERM, Hop La Pitie Salpetriere, Dept Pharmacol,Fac Med,U669, Paris, France.
[Singleton, Edward G.] MayaTech Corp, Silver Spring, MD USA.
[Heishman, Stephen J.] NIDA, Nicotine Psychopharmacol Sect, Intramural Res Program, NIH, Baltimore, MD USA.
RP Berlin, I (reprint author), Hop La Pitie Salpetriere, Dept Pharmacol, 47 Bd Hop, F-75013 Paris, France.
EM ivan.berlin@psl.aphp.fr
OI Singleton, Edward G./0000-0003-3442-877X
FU French Ministry of Health Programme Hospitalier de Recherche Clinique
Loco-regional [AOR04001//P040406, 050558]; Agence francaise de securite
sanitaire des produits de sante, Convention Pharmacologie Clinique et
Therapeutique [RAF02020]; Intramural Research Program (IRP) of the
National Institutes of Health, National Institute on Drug Abuse;
Assistance publique-Hopitaux de Paris, France [AOR04001-FAP11014,
P040406]
FX This study was supported by the French Ministry of Health Programme
Hospitalier de Recherche Clinique Loco-regional 2004 (AOR04001//P040406,
registration number: 050558); by the Agence francaise de securite
sanitaire des produits de sante, Convention Pharmacologie Clinique et
Therapeutique 2003, RAF02020 and the Intramural Research Program (IRP)
of the National Institutes of Health, National Institute on Drug Abuse.
Contribution of E.G. Singleton was partly funded by the research grant
AOR04001-FAP11014, P040406 of Assistance publique-Hopitaux de Paris,
France. The authors thank Mrs. Shoreh Azimi, research coordinator, for
her assistance with the study.
NR 84
TC 16
Z9 18
U1 3
U2 21
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
EI 1879-0046
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD OCT 1
PY 2013
VL 132
IS 3
BP 513
EP 520
DI 10.1016/j.drugalcdep.2013.03.017
PG 8
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 232RC
UT WOS:000325510700017
PM 23623506
ER
PT J
AU Eckelman, WC
Jones, AG
Duatti, A
Reba, RC
AF Eckelman, William C.
Jones, Alun G.
Duatti, Adriano
Reba, Richard C.
TI Progress using Tc-99m radiopharmaceuticals for measuring high capacity
sites and low density sites
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID MEMBRANE ANTIGEN; IMAGING AGENT; TECHNETIUM-99M; PERFUSION; INHIBITORS;
SPECT; COMPLEXES; ACID; TRACERS; NUCLEAR
AB Technetium-99m (Tc-99m) has long been a mainstay in clinical nuclear medicine, primarily monitoring biological processes in the heart, kidney, liver, and brain. More recently, Tc-99m chelates have been used as the reporter in targeted nuclear medicine probes that monitor changes in specific protein expression products. The strengths remain the inexpensive source of Tc-99m from the Mo-99/Tc-99m generator, its rich chemistry, high-yield kit formulation, and its widespread availability. Hardware and software advances, such as OSEM reconstructions with scatter and attenuation corrections, have led to quantitation of the injected radioactivity in terms of kBq/cm.
C1 [Eckelman, William C.] Mol Tracer LLC, Bethesda, MD 20814 USA.
[Jones, Alun G.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Duatti, Adriano] Univ Ferrara, I-44121 Ferrara, Italy.
[Reba, Richard C.] NIAID Integrated Res Facil, Frederick, MD 21702 USA.
RP Eckelman, WC (reprint author), Mol Tracer LLC, Bethesda, MD 20814 USA.
EM wceckelman@verizon.net
OI Duatti, Adriano/0000-0001-6567-6245
NR 58
TC 8
Z9 8
U1 0
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
EI 1878-5832
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD OCT
PY 2013
VL 18
IS 19-20
BP 984
EP 991
DI 10.1016/j.drudis.2013.06.008
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 232QX
UT WOS:000325510200009
PM 23806975
ER
PT J
AU Williams, RV
Margossian, R
Lu, MM
Atz, AM
Bradley, TJ
Campbell, MJ
Colan, SD
Gallagher, D
Lai, WW
Pearson, GD
Prakash, A
Shirali, G
Cohen, MS
AF Williams, Richard V.
Margossian, Renee
Lu, Minmin
Atz, Andrew M.
Bradley, Timothy J.
Campbell, Michael Jay
Colan, Steven D.
Gallagher, Dianne
Lai, Wyman W.
Pearson, Gail D.
Prakash, Ashwin
Shirali, Girish
Cohen, Meryl S.
CA Pediat Heart Network Investigators
TI Factors Impacting Echocardiographic Imaging after the Fontan Procedure:
A Report from the Pediatric Heart Network Fontan Cross-Sectional Study
SO ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED
TECHNIQUES
LA English
DT Article
DE Fontan procedure; echocardiographic quality
ID MAGNETIC-RESONANCE; MULTICENTER; DISEASE
AB Echocardiographic image quality in Fontan survivors may be limited by a variety of factors. We sought to describe echocardiographic quality and factors associated with study quality in subjects participating in the Pediatric Heart Network Fontan Cross-Sectional Study. Echocardiograms were obtained at 7 clinical sites using a standard protocol. Quality grading and analysis were performed by a core laboratory. Univariate and multivariable modeling were performed to assess factors associated with quality and ability to obtain images sufficient for prespecified quantitative analysis. A total of 543 echocardiograms were obtained. The quality of echocardiograms improved over the duration of the study. The great arteries, systemic veins, and pulmonary veins were less likely to be adequately imaged than other cardiac structures. Quantitative analysis of ventricular volume was possible in 76% overall, but only 41% of those with mixed ventricular morphology. Factors independently associated with better quality included younger age, levocardia, acquisition of the echocardiogram at a longer time since the beginning of enrollment, absence of a pulmonary artery stent, and clinical site. Patient and center-specific factors are associated with echocardiographic quality after the Fontan procedure. Increased familiarity and experience with a standard imaging protocol is likely to result in improved quality.
C1 [Williams, Richard V.] Univ Utah, Salt Lake City, UT 84113 USA.
[Margossian, Renee; Colan, Steven D.; Prakash, Ashwin] Childrens Hosp Boston, Boston, MA USA.
[Lu, Minmin; Gallagher, Dianne] New England Res Inst, Watertown, MA 02172 USA.
[Atz, Andrew M.; Shirali, Girish] Med Univ S Carolina, Charleston, SC 29425 USA.
[Bradley, Timothy J.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Campbell, Michael Jay] Duke Univ, Durham, NC USA.
[Lai, Wyman W.] Columbia Univ, New York, NY USA.
[Pearson, Gail D.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Cohen, Meryl S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
RP Williams, RV (reprint author), Univ Utah, 100 North Mario Capecchi Dr, Salt Lake City, UT 84113 USA.
EM richard.williams@imail.org
RI Hurwitz Koweek, lynne/N-1351-2015
OI Hurwitz Koweek, lynne/0000-0001-9990-3397
FU National Heart, Lung, and Blood Institute [HL068269, HL068270, HL068279,
HL068281, HL068285, HL068292, HL068290, HL068288]
FX Supported by U01 grants from the National Heart, Lung, and Blood
Institute (HL068269, HL068270, HL068279, HL068281, HL068285, HL068292,
HL068290, HL068288). The contents of this publication are solely the
responsibility of the authors and do not necessarily represent the
official views of the NHLBI.
NR 16
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0742-2822
EI 1540-8175
J9 ECHOCARDIOGR-J CARD
JI Echocardiography-J. Cardiovasc. Ultrasound Allied Tech.
PD OCT
PY 2013
VL 30
IS 9
BP 1098
EP 1106
DI 10.1111/echo.12219
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 232IC
UT WOS:000325485700028
PM 23614708
ER
PT J
AU Xekouki, P
Mastroyiannis, SA
Avgeropoulos, D
Sierra, MDL
Trivellin, G
Gourgari, EA
Lyssikatos, C
Quezado, M
Patronas, N
Kanaka-Gantenbein, C
Chrousos, GP
Stratakis, CA
AF Xekouki, Paraskevi
Mastroyiannis, Spyridon A.
Avgeropoulos, Dimitrios
Sierra, Maria de la Luz
Trivellin, Giampaolo
Gourgari, Evgenia A.
Lyssikatos, Charalampos
Quezado, Martha
Patronas, Nicholas
Kanaka-Gantenbein, Christina
Chrousos, George P.
Stratakis, Constantine A.
TI Familial pituitary apoplexy as the only presentation of a novel AIP
mutation
SO ENDOCRINE-RELATED CANCER
LA English
DT Letter
ID ADENOMAS; HEMORRHAGE; GENE
C1 [Xekouki, Paraskevi; Mastroyiannis, Spyridon A.; Avgeropoulos, Dimitrios; Sierra, Maria de la Luz; Trivellin, Giampaolo; Gourgari, Evgenia A.; Lyssikatos, Charalampos; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet PDEGEN, NIH,NIH Clin Res Ctr, Bethesda, MD 20892 USA.
[Xekouki, Paraskevi; Mastroyiannis, Spyridon A.; Avgeropoulos, Dimitrios; Sierra, Maria de la Luz; Trivellin, Giampaolo; Gourgari, Evgenia A.; Lyssikatos, Charalampos; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Endocrinol Inter Inst Training Program, NIH, NIH Clin Res Ctr, Bethesda, MD 20892 USA.
[Quezado, Martha] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Patronas, Nicholas] NIH, Dept Diagnost Radiol, Clin Res Ctr, Bethesda, MD 20892 USA.
[Kanaka-Gantenbein, Christina; Chrousos, George P.] Univ Athens, Aghia Sophia Childrens Hosp, Dept Pediat 1, Endocrine Unit, Athens, Greece.
RP Stratakis, CA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet PDEGEN, NIH,NIH Clin Res Ctr, 10 Ctr Dr,Bldg 10,Room 1-3330,MSC1103, Bethesda, MD 20892 USA.
EM stratakc@mail.nih.gov
RI Trivellin, Giampaolo/J-6583-2016
OI Trivellin, Giampaolo/0000-0003-2384-4153
FU Intramural NIH HHS [ZIA HD008920-01]
NR 10
TC 6
Z9 6
U1 0
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 1351-0088
EI 1479-6821
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD OCT
PY 2013
VL 20
IS 5
BP L11
EP L14
DI 10.1530/ERC-13-0218
PG 4
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA 234HP
UT WOS:000325633800002
PM 24025584
ER
PT J
AU Major, EO
Douek, DC
Frohman, EM
Walsh, DR
AF Major, Eugene O.
Douek, Daniel C.
Frohman, Elliot M.
Walsh, Declan R.
TI Two demyelinating diseases in the brain of a single patient, PML and MS:
how to minimize 'one' while treating the 'other'
SO EXPERT REVIEW OF CLINICAL IMMUNOLOGY
LA English
DT Editorial Material
DE demyelinating diseases; JCV; natalizumab; patients
ID JC VIRUS; PATHOGENESIS
C1 [Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
[Douek, Daniel C.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Frohman, Elliot M.] Univ Texas SW Med Ctr Dallas, Dept Neurol, Dallas, TX 75390 USA.
[Frohman, Elliot M.] Univ Texas SW Med Ctr Dallas, Dept Ophthalmol, Dallas, TX 75390 USA.
[Walsh, Declan R.] DeFerno Trust, Sligo, Ireland.
RP Major, EO (reprint author), NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
EM majorg@ninds.nih.gov
NR 11
TC 0
Z9 0
U1 0
U2 0
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1744-666X
EI 1744-8409
J9 EXPERT REV CLIN IMMU
JI Expert Rev. Clin. Immunol.
PD OCT
PY 2013
VL 9
IS 10
BP 887
EP 890
DI 10.1586/1744666X.2013.841559
PG 4
WC Immunology
SC Immunology
GA 234IV
UT WOS:000325637500002
PM 24128152
ER
PT J
AU Berzofsky, JA
Wood, LV
Terabe, M
AF Berzofsky, Jay A.
Wood, Lauren V.
Terabe, Masaki
TI Cancer vaccines: 21st century approaches to harnessing an ancient
modality to fight cancer
SO EXPERT REVIEW OF VACCINES
LA English
DT Editorial Material
DE beta-mannosylceramide; cancer immunotherapy; cancer vaccines; epitope
enhancement; NK T cells; prostate cancer; TARP antigen; transforming
growth factor-beta
ID CD8(+) T-CELLS; TUMOR IMMUNOSURVEILLANCE; SUPPRESSOR-CELLS; NKT CELL;
IMMUNITY; EFFICACY; IMMUNOTHERAPY; PROSTATE; IL-13; HELP
C1 [Berzofsky, Jay A.; Wood, Lauren V.; Terabe, Masaki] NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Berzofsky, JA (reprint author), NCI, Vaccine Branch, Ctr Canc Res, NIH, Bldg 41 Room D702D,41 Medlars Dr, Bethesda, MD 20892 USA.
EM berzofsj@mail.nih.gov
NR 34
TC 3
Z9 3
U1 0
U2 3
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1476-0584
EI 1744-8395
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD OCT
PY 2013
VL 12
IS 10
BP 1115
EP 1118
DI 10.1586/14760584.2013.836906
PG 4
WC Immunology
SC Immunology
GA 234GM
UT WOS:000325630400003
PM 24124874
ER
PT J
AU Rees, J
Schlom, J
AF Rees, Jenaid
Schlom, Jeffrey
TI Recombinant cancer vaccines and new vaccine targets
SO EXPERT REVIEW OF VACCINES
LA English
DT Editorial Material
AB Interview by Jenaid Rees, Commissioning Editor Jeffrey Schlom obtained his PhD from Rutgers University (NJ, USA). After obtaining his PhD, he worked at Columbia University (NY, USA) before moving in 1973 to the National Cancer Institute, National Institutes of Health (MD, USA). Since then he has served as the Chief of several sections, including his present position as the Chief of the Laboratory of Tumor Immunology and Biology in the Center for Cancer Research which he has held for the past 30 years. During this period, he has worked as an Adjunct Professor at George Washington University (Washington, DC, USA), served on the Editorial Board of several journals and holds membership in a number of committees. He holds over 30 patents and patent applications in the areas of vaccines, tumor antigens and monoclonal antibodies and has received honors and awards throughout his career. Jeffrey Schlom has been involved in translational research involving the immunotherapy of a range of carcinomas and predominantly works in the areas of tumor immunology, mechanisms of tumor cell-immune cell interactions and immune mechanisms. He has recently been working on the design and characterization of recombinant vaccines for cancer therapy.
C1 [Schlom, Jeffrey] NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM js141c@nih.gov
NR 0
TC 1
Z9 1
U1 0
U2 3
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1476-0584
EI 1744-8395
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD OCT
PY 2013
VL 12
IS 10
BP 1121
EP 1124
DI 10.1586/14760584.2013.836913
PG 4
WC Immunology
SC Immunology
GA 234GM
UT WOS:000325630400007
ER
PT J
AU Ali, T
Choyke, PL
Kobayashi, H
AF Ali, Towhid
Choyke, Peter L.
Kobayashi, Hisataka
TI Endoscopic molecular imaging of cancer
SO FUTURE ONCOLOGY
LA English
DT Article
DE cancer; fluorescence endoscopy; imaging probe; molecular imaging
ID CONFOCAL LASER ENDOMICROSCOPY; GROWTH-FACTOR RECEPTOR; CERVICAL
INTRAEPITHELIAL NEOPLASIA; HIGH-GRADE DYSPLASIA; LOWER-GI TRACT;
IN-VIVO; COLORECTAL-CANCER; INDOCYANINE GREEN; BARRETTS-ESOPHAGUS;
OVARIAN-CANCER
AB White light endoscopy has proven to be a very powerful tool in oncology. There is still, however, a need for better endoscopic techniques to overcome the current limitations of white light optics. New technologies that allow higher sensitivity, improved microanatomy and molecular characterization have been available for in vitro microscopy and are now being translated into in vivo endoscopy. Endoscopic molecular imaging is still in its infancy but holds the promise for enhancing sensitivity for early lesions, thus allowing earlier diagnosis and enabling early image-guided endoscopic intervention. A key feature of endoscopic molecular imaging is its increased sensitivity and specificity, which will be illustrated in this article, as well as describing perspectives on its future use in oncologic surgery.
C1 [Ali, Towhid; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM kobayash@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; NIH
FX The authors are employees of the NIH. This work was supported by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. This work was made possible through the NIH
Medical Research Scholars Program, a public-private partnership
supported jointly by the NIH and generous contributions to the
Foundation for the NIH from Pfizer Inc., The Leona M and Harry B
Helmsley Charitable Trust, and the Howard Hughes Medical Institute, as
well as other private donors. For a complete list, please visit the
Foundation website at
www.fnih.org/work/programs-development/medical-research-scholars-program
. The authors have no other relevant affiliations or financial
involvement with any organization or entity with a financial interest in
or financial conflict with the subject matter or materials discussed in
the manuscript apart from those disclosed.
NR 80
TC 1
Z9 1
U1 4
U2 9
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD OCT
PY 2013
VL 9
IS 10
BP 1501
EP 1513
DI 10.2217/fon.13.123
PG 13
WC Oncology
SC Oncology
GA 231IT
UT WOS:000325410600017
PM 24106901
ER
PT J
AU Koonin, EV
AF Koonin, Eugene V.
TI A flea has smaller fleas that on him prey: giant viruses, their
parasites and evolutionary networks
SO FUTURE VIROLOGY
LA English
DT Article
DE giant viruses; transposable elements; transpovirons; virophages; virus
evolution
ID ORTHOLOGOUS GENES; DNA TRANSPOSONS; VIROPHAGE; MIMIVIRUS;
RECONSTRUCTION; TRANSPOVIRONS; CLUSTERS; GENOMES; ORIGIN
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
NR 20
TC 0
Z9 0
U1 1
U2 16
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1746-0794
EI 1746-0808
J9 FUTURE VIROL
JI Future Virol.
PD OCT
PY 2013
VL 8
IS 10
BP 937
EP 940
DI 10.2217/fvl.13.79
PG 4
WC Virology
SC Virology
GA 218IL
UT WOS:000324425900002
ER
PT J
AU Flood, TF
Gorczyca, M
White, BH
Ito, K
Yoshihara, M
AF Flood, Thomas F.
Gorczyca, Michael
White, Benjamin H.
Ito, Kei
Yoshihara, Motojiro
TI A Large-Scale Behavioral Screen to Identify Neurons Controlling Motor
Programs in the Drosophila Brain
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE command neurons; Drosophila; Gal4; TRPM8; TrpA1
ID SWIMMERET MOVEMENTS; DECISION NETWORK; COURTSHIP SONG; MELANOGASTER;
SYSTEMS; INTERNEURONS; NEUROBIOLOGY; CRAYFISH; EXPRESSION; PROTEIN
AB Drosophila is increasingly used for understanding the neural basis of behavior through genetically targeted manipulation of specific neurons. The primary approach in this regard has relied on the suppression of neuronal activity. Here, we report the results of a novel approach to find and characterize neural circuits by expressing neuronal activators to stimulate subsets of neurons to induce behavior. Classical electrophysiological studies demonstrated that stimulation of command neurons could activate neural circuits to trigger fixed action patterns. Our method was designed to find such command neurons for diverse behaviors by screening flies in which random subsets of brain cells were activated. We took advantage of the large collection of Gal4 lines from the NP project and crossed 835 Gal4 strains with relatively limited Gal4 expression in the brain to flies carrying a UAS transgene encoding TRPM8, a cold-sensitive ion channel. Low temperatures opened the TRPM8 channel in Gal4- expressing cells, leading to their excitation, and in many cases induced overt behavioral changes in adult flies. Paralysis was reproducibly observed in the progeny of crosses with 84 lines, whereas more specific behaviors were induced with 24 other lines. Stimulation performed using the heat-activated channel, TrpA1, resulted in clearer and more robust behaviors, including flight, feeding, and egg-laying. Through follow-up studies starting from this screen, we expect to find key components of the neural circuits underlying specific behaviors, thus providing a new avenue for their functional analysis.
C1 [Flood, Thomas F.; Gorczyca, Michael; Yoshihara, Motojiro] Univ Massachusetts, Sch Med, Dept Neurobiol, Worcester, MA USA.
[White, Benjamin H.] NIMH, Mol Biol Lab, Bethesda, MD 20892 USA.
[Ito, Kei] Univ Tokyo, Inst Mol & Cellular Biosci, Tokyo, Japan.
RP Yoshihara, M (reprint author), MIT, Picower Inst Learning & Memory, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM motojiro@mit.edu
FU National Institute of Mental Health [MH85958]; Worcester Foundation;
Japan Society for the Promotion of Science/National Science Foundation;
National Institute of Mental Health Intramural Research Program
FX We thank S. Waddell for critical discussion, S. Waddell, T. Lee, M.
Alkema, and T. Ip for discussions, members of the NP consortium for NP
lines, S. Waddell, T. Lee, and P. Garrity for fly stocks, and K. Ikeda
for technical advice. This work was supported by National Institute of
Mental Health Grant MH85958, the Worcester Foundation (to M.Y.),
fellowship of the Japan Society for the Promotion of Science/National
Science Foundation (to T.F.F.), grant-in-aid for the Promotion of
Science (to K.I.), and the National Institute of Mental Health
Intramural Research Program (to B.H.W.)
NR 44
TC 5
Z9 5
U1 0
U2 18
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD OCT 1
PY 2013
VL 3
IS 10
BP 1629
EP 1637
DI 10.1534/g3.113.006205
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 232IJ
UT WOS:000325486500002
PM 23934998
ER
PT J
AU Lai, XN
Beilharz, T
Au, WC
Hammet, A
Preiss, T
Basrai, MA
Heierhorst, J
AF Lai, Xianning
Beilharz, Traude
Au, Wei-Chun
Hammet, Andrew
Preiss, Thomas
Basrai, Munira A.
Heierhorst, Joerg
TI Yeast hEST1A/B (SMG5/6)-Like Proteins Contribute to Environment-Sensing
Adaptive Gene Expression Responses
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE hEST1; SMG5; SMG6; gene expression; genetic interactions
ID MESSENGER-RNA DECAY; CARBON METABOLISM REGULON; 18S RIBOSOMAL-RNA;
SACCHAROMYCES-CEREVISIAE; QUALITY-CONTROL; TELOMERE MAINTENANCE;
MAMMALIAN TELOMERES; INTERACTING PROTEIN; POLY(A) POLYMERASE;
CELL-SURFACE
AB During its natural life cycle, budding yeast (Saccharomyces cerevisiae) has to adapt to drastically changing environments, but how environmental-sensing pathways are linked to adaptive gene expression changes remains incompletely understood. Here, we describe two closely related yeast hEST1A-B (SMG5-6)-like proteins termed Esl1 and Esl2 that contain a 14-3-3-like domain and a putative PilT N-terminus ribonuclease domain. We found that, unlike their metazoan orthologs, Esl1 and Esl2 were not involved in nonsense-mediated mRNA decay or telomere maintenance pathways. However, in genomewide expression array analyses, absence of Esl1 and Esl2 led to more than two-fold deregulation of similar to 50 transcripts, most of which were expressed inversely to the appropriate metabolic response to environmental nutrient supply; for instance, normally glucose-repressed genes were derepressed in esl1 Delta esl2 Delta double mutants during growth in a high-glucose environment. Likewise, in a genome-wide synthetic gene array screen, esl1 Delta esl2 Delta double mutants were synthetic sick with null mutations for Rim8 and Dfg16, which form the environmental-sensing complex of the Rim101 pH response gene expression pathway. Overall, these results suggest that Esl1 and Esl2 contribute to the regulation of adaptive gene expression responses of environmental sensing pathways.
C1 [Lai, Xianning; Hammet, Andrew; Heierhorst, Joerg] St Vincents Inst Med Res, Melbourne, Vic 3065, Australia.
[Lai, Xianning; Heierhorst, Joerg] Univ Melbourne, St Vincents Hosp, Dept Med, Melbourne, Vic 3065, Australia.
[Beilharz, Traude; Preiss, Thomas] Victor Chang Cardiac Res Inst, Sydney, NSW 2010, Australia.
[Au, Wei-Chun; Basrai, Munira A.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20889 USA.
RP Heierhorst, J (reprint author), St Vincents Inst Med Res, 9 Princes St, Melbourne, Vic 3065, Australia.
EM jheierhorst@svi.edu.au
OI Beilharz, Traude/0000-0002-8942-9502; Preiss, Thomas/0000-0001-6273-784X
FU NHMRC; Victorian Government's Operational Infrastructure Support
Program; Melbourne International Research Scholarship; Melbourne
International Fee Remission Scholarship; ARC discovery project;
Australian Research Fellowship [DP0878224]
FX Supported by NHMRC project grants and NHMRC Senior Research Fellowships
(J.H. and T.P.), the Victorian Government's Operational Infrastructure
Support Program (J.H.), a Melbourne International Research Scholarship
and Melbourne International Fee Remission Scholarship (X.L.), an ARC
discovery project (T.P.), and Australian Research Fellowship (DP0878224)
(T.H.B.).
NR 54
TC 2
Z9 4
U1 2
U2 6
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD OCT 1
PY 2013
VL 3
IS 10
BP 1649
EP 1659
DI 10.1534/g3.113.006924
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 232IJ
UT WOS:000325486500004
PM 23893744
ER
PT J
AU Klar, AJS
AF Klar, Amar J. S.
TI Schizosaccharomyces japonicus Yeast Poised to Become a Favorite
Experimental Organism for Eukaryotic Research
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE Schizosaccharomyces japonicus; fission yeast; fast growing; rapid
meiotic analysis; organism conducive for research
ID TRANSFORMATION; MECHANISM
AB Both budding yeast Saccharomyces cerevisiae and fission yeast Schizosaccahromyces pombe have been very popular organisms used for biological research with eukaryotes for many decades. Judging from the fission yeast Schizosaccharomyces japonicus DNA sequence determined 2 years ago, this species is evolutionarily very much unrelated to the commonly used yeasts for research. Indicating evolutionary divergence, the S. japonicus makes 8-spored asci and mitosis occurs with a partial breakdown of nuclear membrane whereas the other yeasts make 4-spored asci and cells divide without nuclear breakdown. The commonly used yeast species exhibit a generation time between 1.5 and 2.0 hr, and their genetic cross takes a period of more than 7 working d. As described here, a generation time of only 63 min and meiotic analysis completed in just 2.5 d, the S. japonicus fission yeast is predicted to become a choice organism for future research on the biology of eukaryotes.
C1 NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Klar, AJS (reprint author), NCI, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res, NIH, Bldg 539,Room 154, Frederick, MD 21702 USA.
EM klara@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
FX I thank Michael Bonaduce for providing technical support and Dr. C.
Cagliero for helping to take photographs of yeast cells. Dr. H. Niki
(National Institute of Genetics, Japan) is thanked for providing strains
of japonicus variety. The Intramural Research Program of the National
Cancer Institute, National Institutes of Health, supports this research.
NR 21
TC 3
Z9 3
U1 0
U2 9
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD OCT 1
PY 2013
VL 3
IS 10
BP 1869
EP 1873
DI 10.1534/g3.113.007187
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 232IJ
UT WOS:000325486500026
PM 23934997
ER
PT J
AU Song, PH
Reiter, KL
Weiner, BJ
Minasian, L
McAlearney, AS
AF Song, Paula H.
Reiter, Kristin L.
Weiner, Bryan J.
Minasian, Lori
McAlearney, Ann Scheck
TI The business case for provider participation in clinical trials
research: An application to the National Cancer Institute's community
clinical oncology program
SO HEALTH CARE MANAGEMENT REVIEW
LA English
DT Article
DE business case; clinical trials; oncology; provider-based research
network; return on investment
ID TRANSLATING RESEARCH; RESEARCH-NETWORKS; DIFFUSION; QUALITY; SYSTEM
AB Background: Provider-based research networks (PBRNs) make clinical trials available in community-based practice settings, where most people receive their care, but provider participation requires both financial and in-kind contributions.
Purpose: The aim of this study was to explore whether providers believe there is a business case for participating in PBRNs and what factors contribute to the business case.
Methodology/Approach: We use a multiple case study methodology approach to examine the National Cancer Institute's community clinical oncology program, a long-standing federally funded PBRN. Interviews with 41 key informants across five sites, selected on the basis of organizational maturity, were conducted using a semistructured interview guide. We analyzed interview transcripts using an iterative, deductive process to identify themes and subthemes in the data.
Findings: We found that a business case for provider participation in PBRNs may exist if both direct and indirect financial benefits are identified and included in the analysis and if the time horizon is long enough to allow those benefits to be realized. We identified specific direct and indirect financial benefits that were perceived as important contributors to the business case and the perceived length of time required for a positive return to accrue.
Practice Implications: As the lack of a business case may result in provider reluctance to participate in PBRNs, knowledge of the benefits we identified may be crucial to encouraging and sustaining participation, thereby preserving patient access to innovative community-based treatments. The results are also relevant to federally funded PBRNs outside of oncology or to providers considering participation in any clinical trials research.
C1 [Song, Paula H.; McAlearney, Ann Scheck] Ohio State Univ, Coll Publ Hlth, Div Hlth Serv Management & Policy, Columbus, OH 43210 USA.
[Reiter, Kristin L.; Weiner, Bryan J.] Univ N Carolina, Dept Hlth Policy & Management, Chapel Hill, NC USA.
[Minasian, Lori] NCI, Community Oncol & Prevent Trials Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
[McAlearney, Ann Scheck] Ohio State Univ, Coll Med, Dept Family Med, Columbus, OH 43210 USA.
RP Song, PH (reprint author), Ohio State Univ, Coll Publ Hlth, Div Hlth Serv Management & Policy, Columbus, OH 43210 USA.
EM psong@cph.osu.edu; reiter@email.unc.edu; weiner@email.unc.edu;
minasilo@mail.nih.gov; Ann.McAlearney@osumc.edu
FU NCI NIH HHS [R01CA124402, R01 CA124402]
NR 27
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0361-6274
EI 1550-5030
J9 HEALTH CARE MANAGE R
JI Health Care Manage. Rev.
PD OCT-DEC
PY 2013
VL 38
IS 4
BP 284
EP 294
DI 10.1097/HMR.0b013e31827292fc
PG 11
WC Health Policy & Services
SC Health Care Sciences & Services
GA 222TO
UT WOS:000324754700003
PM 23044836
ER
PT J
AU Daniels, MLA
Leigh, MW
Davis, SD
Armstrong, MC
Carson, JL
Hazucha, M
Dell, SD
Eriksson, M
Collins, FS
Knowles, MR
Zariwala, MA
AF Daniels, M. Leigh Anne
Leigh, Margaret W.
Davis, Stephanie D.
Armstrong, Michael C.
Carson, Johnny L.
Hazucha, Milan
Dell, Sharon D.
Eriksson, Maria
Collins, Francis S.
Knowles, Michael R.
Zariwala, Maimoona A.
TI Founder Mutation in RSPH4A Identified in Patients of Hispanic Descent
with Primary Ciliary Dyskinesia
SO HUMAN MUTATION
LA English
DT Article
DE cilia; Kartagener syndrome; sequencing; RSPH4A
ID MTDNA
AB Primary ciliary dyskinesia (PCD) is a rare, autosomal recessive, genetically heterogeneous disorder characterized by ciliary dysfunction resulting in chronic oto-sino-pulmonary disease, respiratory distress in term neonates, laterality (situs) defects, and bronchiectasis. Diagnosis has traditionally relied on ciliary ultrastructural abnormalities seen by electron microscopy. Mutations in radial spoke head proteins occur in PCD patients with central apparatus defects. Advances in genetic testing have been crucial in addressing the diagnostic challenge. Here, we describe a novel splice-site mutation (c.921+3_6delAAGT) in RSPH4A, which leads to a premature translation termination signal in nine subjects with PCD (seven families). Loss-of-function was confirmed with quantitative ciliary ultrastructural analysis, measurement of ciliary beat frequency and waveform, and transcript analysis. All nine individuals carrying c.921+3_6delAAGT splice-site mutation in RSPH4A were Hispanic with ancestry tracing to Puerto Rico. This mutation is a founder mutation and a common cause of PCD without situs abnormalities in patients of Puerto Rican descent. Published 2013 Wiley Periodicals, Inc.
C1 [Daniels, M. Leigh Anne; Armstrong, Michael C.; Hazucha, Milan; Knowles, Michael R.] UNC Sch Med, Dept Med, Chapel Hill, NC 27599 USA.
[Leigh, Margaret W.; Davis, Stephanie D.; Carson, Johnny L.] UNC Sch Med, Dept Pediat, Chapel Hill, NC 27599 USA.
[Dell, Sharon D.] Univ Toronto, Hosp Sick Children, Dept Pediat, Toronto, ON M5G 1X8, Canada.
[Eriksson, Maria] Karolinska Inst, Ctr Biosci, Dept Biosci & Nutr, Huddinge, Sweden.
[Collins, Francis S.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Zariwala, Maimoona A.] UNC Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
RP Zariwala, MA (reprint author), UNC Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
EM Knowles@med.unc.edu; zariwala@med.unc.edu
FU US National Institute of Health (NIH) Office of the Director; Office of
Rare Diseases Research (ORDR); National Heart, Lung, and Blood Institute
(NHLBI); US National Institutes of Health (NIH)-National Heart, Lung,
and Blood Institute (NHLBI) [5R01HL071798]; T32 Research Training
Program "Multidisciplinary Research Training in Pulmonary Diseases" [T32
HL007106]; National Human Genome Research Institute (NHGRI); National
Center for Advancing Translational Sciences (NCATS) [UL1 TR000083, CFF
R026-CR07]; ORDR; NHLBI; NHGRI; NCATS; NIH Office of Rare Diseases
Research (ORDR) at the National Center for Advancing Translational
Science (NCATS); National Heart Lung and Blood Institute; [5 U54
HL096458-06]
FX Contract grant sponsors: US National Institute of Health (NIH) Office of
the Director; Office of Rare Diseases Research (ORDR); National Heart,
Lung, and Blood Institute (NHLBI); (5 U54 HL096458-06); US National
Institutes of Health (NIH)-National Heart, Lung, and Blood Institute
(NHLBI) (5R01HL071798); T32 Research Training Program "Multidisciplinary
Research Training in Pulmonary Diseases" (T32 HL007106); National Human
Genome Research Institute (NHGRI); National Center for Advancing
Translational Sciences (NCATS) (UL1 TR000083, CFF R026-CR07); ORDR;
NHLBI; NHGRI; NCATS. The Genetic Disorders of Mucociliary Clearance
(U54HL096458) is a part of the National Institutes of Health (NIH) Rare
Disease Clinical Research Network (RDCRN), supported through
collaboration between the NIH Office of Rare Diseases Research (ORDR) at
the National Center for Advancing Translational Science (NCATS), and the
National Heart Lung and Blood Institute. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health.
NR 20
TC 7
Z9 8
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-7794
EI 1098-1004
J9 HUM MUTAT
JI Hum. Mutat.
PD OCT
PY 2013
VL 34
IS 10
BP 1352
EP 1356
DI 10.1002/humu.22371
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 222SW
UT WOS:000324752700006
PM 23798057
ER
PT J
AU Landoure, G
Zhu, PP
Lourenco, CM
Johnson, JO
Toro, C
Bricceno, KV
Rinaldi, C
Meilleur, KG
Sangare, M
Diallo, O
Pierson, TM
Ishiura, H
Tsuji, S
Hein, N
Fink, JK
Stoll, M
Nicholson, G
Gonzalez, MA
Speziani, F
Durr, A
Stevanin, G
Biesecker, LG
Accardi, J
Landis, DMD
Gahl, WA
Traynor, BJ
Marques, W
Zuchner, S
Blackstone, C
Fischbeck, KH
Burnett, BG
AF Landoure, Guida
Zhu, Peng-Peng
Lourenco, Charles M.
Johnson, Janel O.
Toro, Camilo
Bricceno, Katherine V.
Rinaldi, Carlo
Meilleur, Katherine G.
Sangare, Modibo
Diallo, Oumarou
Pierson, Tyler M.
Ishiura, Hiroyuki
Tsuji, Shoji
Hein, Nichole
Fink, John K.
Stoll, Marion
Nicholson, Garth
Gonzalez, Michael A.
Speziani, Fiorella
Duerr, Alexandra
Stevanin, Giovanni
Biesecker, Leslie G.
Accardi, John
Landis, Dennis M. D.
Gahl, William A.
Traynor, Bryan J.
Marques, Wilson, Jr.
Zuechner, Stephan
Blackstone, Craig
Fischbeck, Kenneth H.
Burnett, Barrington G.
CA NIH Intramural Sequencing Ctr
TI Hereditary Spastic Paraplegia Type 43 (SPG43) is Caused by Mutation in
C19orf12
SO HUMAN MUTATION
LA English
DT Article
DE SPG43; NBIA; C19orf12; hereditary spastic paraplegia
ID BRAIN IRON ACCUMULATION; NEURODEGENERATION; PREVALENCE; SUBTYPE;
PROTEIN; LOCUS; NBIA; FORM
AB We report here the genetic basis for a form of progressive hereditary spastic paraplegia (SPG43) previously described in two Malian sisters. Exome sequencing revealed a homozygous missense variant (c.187G>C; p.Ala63Pro) in C19orf12, a gene recently implicated in neurodegeneration with brain iron accumulation (NBIA). The same mutation was subsequently also found in a Brazilian family with features of NBIA, and we identified another NBIA patient with a three-nucleotide deletion (c.197_199del; p.Gly66del). Haplotype analysis revealed that the p.Ala63Pro mutations have a common origin, but MRI scans showed no brain iron deposition in the Malian SPG43 subjects. Heterologous expression of these SPG43 and NBIA variants resulted in similar alterations in the subcellular distribution of C19orf12. The SPG43 and NBIA variants reported here as well as the most common C19orf12 missense mutation reported in NBIA patients are found within a highly conserved, extended hydrophobic domain in C19orf12, underscoring the functional importance of this domain. Published 2013 Wiley Periodicals, Inc.
C1 [Landoure, Guida] Ctr Hosp Univ Point G, Serv Neurol, Bamako, Mali.
[Landoure, Guida; Zhu, Peng-Peng; Bricceno, Katherine V.; Rinaldi, Carlo; Sangare, Modibo; Diallo, Oumarou; Pierson, Tyler M.; Blackstone, Craig; Fischbeck, Kenneth H.; Burnett, Barrington G.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Lourenco, Charles M.; Marques, Wilson, Jr.] Univ Sao Polo, Sch Med Ribeirao Preto, Dept Neurosci & Behav Sci, Sao Polo, Brazil.
[Johnson, Janel O.; Traynor, Bryan J.] NIA, Lab Neurogenet, NIH, Bethesda, MD 20892 USA.
[Toro, Camilo; Pierson, Tyler M.; Accardi, John; Landis, Dennis M. D.; Gahl, William A.] NIH, NIH Undiagnosed Dis Program, NIH Common Fund, Off Director, Bethesda, MD 20892 USA.
[Meilleur, Katherine G.] NINR, Tissue Injury Branch, NIH, Bethesda, MD 20892 USA.
[Ishiura, Hiroyuki; Tsuji, Shoji] Univ Tokyo, Dept Neurol, Grad Sch Med, Tokyo, Japan.
[Hein, Nichole; Fink, John K.] Univ Michigan, Sch Med, Dept Neurol, Ann Arbor, MI USA.
[Fink, John K.] Univ Michigan, Ann Arbor Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Ann Arbor, MI 48109 USA.
[Stoll, Marion; Nicholson, Garth] Univ Sydney, ANZAC Res Inst, Northcott Neurosci Lab, Sydney, NSW 2006, Australia.
[Gonzalez, Michael A.; Speziani, Fiorella; Zuechner, Stephan] Univ Miami, Miller Sch Med, Dept Human Genet, Miami, FL 33136 USA.
[Gonzalez, Michael A.; Speziani, Fiorella; Zuechner, Stephan] Univ Miami, Miller Sch Med, John P Hussman Inst Human Genom, Miami, FL 33136 USA.
[Duerr, Alexandra; Stevanin, Giovanni] Hop La Pitie Salpetriere, Dept Genet & Cytogenet, AP HP, Paris, France.
[Duerr, Alexandra; Stevanin, Giovanni] Hop La Pitie Salpetriere, CNRS UMR7225, INSERM UPMC UMRS975, Ctr Rech Inst Cerveau & Moelle Epiniere, Paris, France.
[Stevanin, Giovanni] EPHE, F-75006 Paris, France.
[Biesecker, Leslie G.] NIH, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Biesecker, Leslie G.] NIH, NIH Intramural Sequencing Ctr, Bethesda, MD 20892 USA.
RP Landoure, G (reprint author), Ctr Hosp Univ Point G, Serv Neurol, POB 333, Bamako, Mali.
EM landoureg@ninds.nih.gov
RI Traynor, Bryan/G-5690-2010; Lourenco, Charles/O-2731-2013; Marques,
Wilson/G-4240-2012; Stevanin, Giovanni/E-5038-2016;
OI Marques, Wilson/0000-0002-4589-2749; Stevanin,
Giovanni/0000-0001-9368-8657
FU NIH/NINDS Intramural Research Funds [1ZIA NS002974-13]; NHGRI; NIH
[R01NS072248, R01NS054132]; l'Agence Nationale pour la Recherche (SPAX);
VERUM Foundation; Association Strumpell-Lorrain
FX Contract grant sponsors: NIH/NINDS Intramural Research Funds (1ZIA
NS002974-13); NHGRI; NIH (R01NS072248, R01NS054132); l'Agence Nationale
pour la Recherche (SPAX); VERUM Foundation and Association
Strumpell-Lorrain.
NR 17
TC 23
Z9 24
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-7794
EI 1098-1004
J9 HUM MUTAT
JI Hum. Mutat.
PD OCT
PY 2013
VL 34
IS 10
BP 1357
EP 1360
DI 10.1002/humu.22378
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 222SW
UT WOS:000324752700007
PM 23857908
ER
PT J
AU Brinton, LA
Westhoff, CL
Scoccia, B
Lamb, EJ
Trabert, B
Niwa, S
Moghissi, KS
AF Brinton, Louise A.
Westhoff, Carolyn L.
Scoccia, Bert
Lamb, Emmet J.
Trabert, Britton
Niwa, Shelley
Moghissi, Kamran S.
TI Fertility drugs and endometrial cancer risk: results from an extended
follow-up of a large infertility cohort
SO HUMAN REPRODUCTION
LA English
DT Article
DE endometrial cancer; risk; infertility; clomiphene citrate;
gonadotrophins
ID IN-VITRO FERTILIZATION; GYNECOLOGIC CANCERS; OVULATION INDUCTION;
UTERINE-CANCER; BREAST; THERAPY; WOMEN
AB Do fertility drugs influence the subsequent risk of endometrial cancer in a manner that is independent of other risk predictors, such as parity?
In this follow-up of a large cohort of women evaluated for infertility and for whom information was captured on fertility drugs, indications for usage and other risk factors that might influence cancer risk, we found no evidence for a substantial relationship between fertility drug use and endometrial cancer risk.
Although the hormonal etiology of endometrial cancer has been well established, it remains unclear whether the use of fertility drugs has an influence on risk. Results regarding the effects of fertility drugs on endometrial cancer risk have been inconsistent, although several studies have shown some evidence for possible increases in risk. The relationship is of particular interest given that clomiphene, a commonly prescribed drug, is a selective estrogen receptor modulator, with chemical properties similar to tamoxifen, another drug linked to an increase in endometrial cancer risk.
In a retrospective cohort of 12 193 women evaluated for infertility between 1965 and 1988 at five US sites, follow-up was pursued through 2010 via both passive as well as active (questionnaire) means.
Among the 9832 subjects for whom follow-up was allowed and achieved, 259 346 at-risk person-years (i.e. prior to hysterectomy) were accrued, and 118 invasive endometrial cancers identified. Cox regression determined hazard ratios (HRs) and 95 confidence intervals (CIs) for fertility treatments adjusted for endometrial cancer risk factors and causes of infertility.
Although we observed slight increases in endometrial cancer risk associated with clomiphene (HR 1.39, 95 CI: 0.962.01) and the less commonly prescribed gonadotrophins (1.34, 0.762.37), there were no convincing relationships of risk with either cycles of use or cumulative exposures for either drug. A statistically significant risk associated with the use of clomiphene among women who began use at younger ages (30) (1.93, 1.243.00) may have reflected indications for drug usage rather than the effect of the drug itself. Women who received clomiphene followed by gonadotrophins were at a non-significantly elevated risk (1.77, 0.983.19).
Like most studies of endometrial cancer, we were limited by sample sizes, particularly for evaluating subgroup associations. We were also unable to follow all women and were not able to obtain complete risk factor information (including hysterectomy status) for the entire cohort.
Although we found no support for a relationship between fertility drugs and endometrial cancer risk, the association should continue to be monitored given that our study population was still young and had not yet reached the age of peak endometrial cancer incidence.
This project was supported in part by funds from the intramural research program of the National Cancer Institute, National Institutes of Health. None of the authors has any conflicting interests to declare.
C1 [Brinton, Louise A.; Trabert, Britton] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Westhoff, Carolyn L.] Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
[Scoccia, Bert] Univ Illinois, Dept Obstet & Gynecol, Chicago, IL 60612 USA.
[Lamb, Emmet J.] Stanford Univ, Stanford, CA 94305 USA.
[Niwa, Shelley] Westat Corp, Rockville, MD USA.
[Moghissi, Kamran S.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
RP Brinton, LA (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
EM brinton@nih.gov
RI Brinton, Louise/G-7486-2015; Trabert, Britton/F-8051-2015
OI Brinton, Louise/0000-0003-3853-8562;
FU National Cancer Institute, National Institutes of Health
FX This project was supported in part by funds from the intramural research
program of the National Cancer Institute, National Institutes of Health.
NR 22
TC 9
Z9 10
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0268-1161
EI 1460-2350
J9 HUM REPROD
JI Hum. Reprod.
PD OCT
PY 2013
VL 28
IS 10
BP 2813
EP 2821
DI 10.1093/humrep/det323
PG 9
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 223UI
UT WOS:000324836300024
PM 23943795
ER
PT J
AU Jukic, AM
Baird, DD
Weinberg, CR
McConnaughey, DR
Wilcox, AJ
AF Jukic, A. M.
Baird, D. D.
Weinberg, C. R.
McConnaughey, D. R.
Wilcox, A. J.
TI Length of human pregnancy and contributors to its natural variation
SO HUMAN REPRODUCTION
LA English
DT Article
DE gestational length; pregnancy; variability; implantation; corpus luteum
ID BASAL BODY-TEMPERATURE; CHORIONIC-GONADOTROPIN; OVULATION DETECTION;
CORPUS-LUTEUM; RHESUS-MONKEY; RISK-FACTORS; WOMANS LIFE; BIRTH;
IMPLANTATION; PROBABILITY
AB How variable is the length of human pregnancy, and are early hormonal events related to gestational length?
Among natural conceptions where the date of conception (ovulation) is known, the variation in pregnancy length spanned 37 days, even after excluding women with complications or preterm births.
Previous studies of length of gestation have either estimated gestational age by last menstrual period (LMP) or ultrasound (both imperfect measures) or included pregnancies conceived through assisted reproductive technology.
The Early Pregnancy Study was a prospective cohort study (198285) that followed 130 singleton pregnancies from unassisted conception to birth, with detailed hormonal measurements through the conception cycle; 125 of these pregnancies were included in this analysis.
We calculated the length of gestation beginning at conception (ovulation) in 125 naturally conceived, singleton live births. Ovulation, implantation and corpus luteum (CL) rescue pattern were identified with urinary hormone measurements. We accounted for events that artificially shorten the natural length of gestation (Cesarean delivery or labor induction, i.e. censoring) using KaplanMeier curves and proportional hazards models. We examined hormonal and other factors in relation to length of gestation. We did not have ultrasound information to compare with our gold standard measure.
The median time from ovulation to birth was 268 days (38 weeks, 2 days). Even after excluding six preterm births, the gestational length range was 37 days. The coefficient of variation was higher when measured by LMP (4.9) than by ovulation (3.7), reflecting the variability of time of ovulation. Conceptions that took longer to implant also took longer from implantation to delivery (P 0.02). CL rescue pattern (reflecting ovarian response to implantation) was predictive (P 0.006): pregnancies with a rapid progesterone rise were longer than those with delayed rise (a 12-day difference in the median gestational length). Mothers with longer gestations were older (P 0.02), had longer pregnancies in other births (P 0.0001) and were heavier at birth (P 0.01). We did not see an association between the length of gestation and several factors that have been associated with gestational length in previous studies: body mass index, alcohol intake, parity or offspring sex.
The sample size was small and some exposures were rare, reducing power to detect weak associations.
Human gestational length varies considerably even when measured exactly (from ovulation). An individual womans deliveries tend to occur at similar gestational ages. Events in the first 2 weeks after conception are predictive of subsequent pregnancy length, and may suggest pathways underlying the timing of delivery.
This research was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences. None of the authors has any conflict of interest to declare.
C1 [Jukic, A. M.; Baird, D. D.; Wilcox, A. J.] NIEHS, Epidemiol Branch, Durham, NC 27709 USA.
[Weinberg, C. R.] NIEHS, Biostat Branch, Durham, NC 27709 USA.
[McConnaughey, D. R.] Westat Corp, Durham, NC 27709 USA.
RP Jukic, AM (reprint author), NIEHS, Epidemiol Branch, POB 12233, Durham, NC 27709 USA.
EM jukica@niehs.nih.gov
RI Baird, Donna/D-5214-2017;
OI Baird, Donna/0000-0002-5544-2653; Wilcox, Allen/0000-0002-3376-1311
FU Intramural Research Program of the 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.
NR 36
TC 26
Z9 26
U1 2
U2 31
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0268-1161
EI 1460-2350
J9 HUM REPROD
JI Hum. Reprod.
PD OCT
PY 2013
VL 28
IS 10
BP 2848
EP 2855
DI 10.1093/humrep/det297
PG 8
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 223UI
UT WOS:000324836300028
PM 23922246
ER
PT J
AU McBride, CM
Persky, S
Wagner, LK
Faith, MS
Ward, DS
AF McBride, C. M.
Persky, S.
Wagner, L. K.
Faith, M. S.
Ward, D. S.
TI Effects of providing personalized feedback of child's obesity risk on
mothers' food choices using a virtual reality buffet
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE genomic risk; parents; communication; family health history
ID INFORMATION-SEEKING; PREDICTING OBESITY; PARENTAL OBESITY;
FAMILY-HISTORY; PUBLIC-HEALTH; BEHAVIORS; PERSPECTIVE; DISEASE;
COMMUNICATION; ADOLESCENTS
AB BACKGROUND: Providing personalized genetic-risk feedback of a child's susceptibility to adult-onset health conditions is a topic of considerable debate. Family health history (FHH), specifically parental overweight/obesity status, is a useful assessment for evaluating a child's genetic and environmental risk of becoming obese. It is unclear whether such risk information may influence parents' efforts to reduce their child's risk of obesity.
PURPOSE: To evaluate whether telling mothers the magnitude of their child's risk of becoming obese based on personal FHH influenced food choices for their young child from a virtual reality-based buffet restaurant.
METHODS: Overweight/obese mothers of a child aged 4-5 years who met eligibility criteria (N=221) were randomly assigned to one of three experimental arms, which emphasized different health information: arm 1, food safety control (Control); arm 2, behavioral-risk information (BRI) alone or arm 3, behavioral-risk information plus personal FHH-based risk assessment (BRI + FHH). Mothers donned a head-mounted display to be immersed in a virtual restaurant buffet, where they selected virtual food and beverages as a lunch for their child.
RESULTS: Mothers who were randomized to BRI + FHH filled the index child's plate with an average of 45 fewer calories than those in the Control arm (P<0.05); those in the BRI arm filled the plate with 35 fewer calories than the Control arm, a non-significant difference. Calorie restriction was greatest among mothers in the BRI + FHH arm who received the weaker-risk message (that is, only one overweight parent).
CONCLUSIONS: The influence of communicating a child's inherited risk of obesity on mothers' feeding practices may vary by the risk level conveyed. High-risk messages may best be coupled with strategies to increase mother's perceptions that efforts can be undertaken to reduce risk and build requisite behavioral skills to reduce risk.
C1 [McBride, C. M.; Persky, S.; Wagner, L. K.] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA.
[Faith, M. S.; Ward, D. S.] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA.
RP McBride, CM (reprint author), NHGRI, Social & Behav Res Branch, Bldg 31,MSC 2073,31 Ctr Dr,Room B1B54, Bethesda, MD 20892 USA.
EM cmcbride@mail.nih.gov
NR 35
TC 6
Z9 6
U1 1
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD OCT
PY 2013
VL 37
IS 10
BP 1322
EP 1327
DI 10.1038/ijo.2013.87
PG 6
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 233CG
UT WOS:000325542200005
PM 23736369
ER
PT J
AU Jones, RE
Zheng, W
McKew, JC
Chen, CZ
AF Jones, Raisa E.
Zheng, Wei
McKew, John C.
Chen, Catherine Z.
TI An Alternative Direct Compound Dispensing Method Using the HP D300
Digital Dispenser
SO JALA
LA English
DT Article
DE compound dispenser; liquid handler; compound screen; serial dilution;
direct dilution
AB Evaluation of compound activity in vitro is crucial to drug discovery efforts and require that the compounds be accurately and reliably titrated and dispensed to the assay wells. The HP D300 dispenser uses inkjet technology to achieve small-volume dispensing that allows concentration-response testing using the direct dilution paradigm. Although inkjet technology has been long in existence, it is new to the field of screening and drug development. We have evaluated the D300 dispenser in a biochemical assay, a cell-based reporter gene assay, and a cytotoxicity assay. The software for this instrument is user friendly, and the compound-dispensing process is streamlined. However, a limitation is that this dispenser is currently applicable to only 96-well and 384-well plate formats and not to 1536-well high-density plates. Our results indicate that the D300 generates clean and reproducible results that correlate with those produced with more commonly used instruments such as the pin tool. We found that the instrument is useful and can improve the throughput of compound dispensing in 96-well and 384-well plates.
C1 [Jones, Raisa E.; Zheng, Wei; McKew, John C.; Chen, Catherine Z.] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
RP Chen, CZ (reprint author), NIH, Natl Ctr Adv Translat Sci, 9800 Med Ctr Dr,MSC 3370, Bethesda, MD 20892 USA.
EM chenc4@mail.nih.gov
OI Zheng, Wei/0000-0003-1034-0757
FU Intramural Research Program of the Therapeutics for Rare and Neglected
Diseases, National Center for Advancing Translational Sciences, NIH
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: This work was
supported by the Intramural Research Program of the Therapeutics for
Rare and Neglected Diseases, National Center for Advancing Translational
Sciences, NIH.
NR 9
TC 6
Z9 6
U1 2
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 2211-0682
EI 1540-2452
J9 JALA-J LAB AUTOM
JI JALA
PD OCT
PY 2013
VL 18
IS 5
BP 367
EP 374
DI 10.1177/2211068213491094
PG 8
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 220YM
UT WOS:000324623400003
PM 23708834
ER
PT J
AU Annunziata, CM
Kohn, EC
AF Annunziata, Christina M.
Kohn, Elise C.
TI Novel Facts About FAK: New Connections to Drug Resistance?
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID FOCAL ADHESION KINASE; MARKER NANOG; CANCER-CELLS; EXPRESSION;
PACLITAXEL; INHIBITOR; CD44; GENE; MDR1
C1 [Annunziata, Christina M.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Kohn, Elise C.] NCI, Clin Invest Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Kohn, EC (reprint author), NCI, Canc Therapy Evaluat Program, NIH, 9609 Med Ctr Dr MSC 5W426 MSC9737, Rockville, MD 20850 USA.
EM kohne@mail.nih.gov
RI Annunziata, Christina/L-3219-2016
OI Annunziata, Christina/0000-0003-2033-6532
NR 21
TC 3
Z9 3
U1 0
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 19
BP 1430
EP 1431
DI 10.1093/jnci/djt255
PG 3
WC Oncology
SC Oncology
GA 232GZ
UT WOS:000325482100006
PM 24062526
ER
PT J
AU Barsevick, AM
Irwin, MR
Hinds, P
Miller, A
Berger, A
Jacobsen, P
Ancoli-Israel, S
Reeve, BB
Mustian, K
O'Mara, A
Lai, JS
Fisch, M
Cella, D
AF Barsevick, Andrea M.
Irwin, Michael R.
Hinds, Pamela
Miller, Andrew
Berger, Ann
Jacobsen, Paul
Ancoli-Israel, Sonia
Reeve, Bryce B.
Mustian, Karen
O'Mara, Ann
Lai, Jin-Shei
Fisch, Michael
Cella, David
TI Recommendations for High-Priority Research on Cancer-Related Fatigue in
Children and Adults
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID PATIENT-REPORTED OUTCOMES; QUALITY-OF-LIFE; SIGNIFICANTLY IMPROVES
FATIGUE; PROPOSED DIAGNOSTIC-CRITERIA; COGNITIVE-BEHAVIORAL THERAPY;
METASTATIC COLORECTAL-CANCER; RANDOMIZED CLINICAL-TRIAL; PRIMARY
BREAST-CANCER; PHYSICAL-ACTIVITY; FUNCTIONAL ASSESSMENT
AB Over the past decades, some scientific progress has been made in understanding and treating cancer-related fatigue (CRF). However, three major problems have limited further progress: lack of agreement about measurement, inadequate understanding of the underlying biology, and problems in the conduct of clinical trials for CRF. This commentary reports the recommendations of a National Cancer Institute Clinical Trials Planning Meeting and an ongoing National Cancer Institute working group to address these problems so that high-priority research and clinical trials can be conducted to advance the science of CRF and its treatment. Recommendations to address measurement issues included revising the current case definition to reflect more rigorous criteria, adopting the Patient Reported Outcomes Measurement Information System fatigue scales as standard measures of CRF, and linking legacy measures to the scales. With regard to the biology of CRF, the group identified the need for longitudinal research to examine biobehavioral mechanisms underlying CRF and testing mechanistic hypotheses within the context of intervention research. To address clinical trial issues, recommendations included using only placebo-controlled trial designs. setting eligibility to minimize sample heterogeneity or enable subgroup analysis, establishing a CRF severity threshold for participation in clinical trials, conducting dissemination trials of efficacious interventions (such as exercise), and combining nonpharmacologic and pharmacologic interventions to exploit the potential synergy between these approaches. Accomplishing these goals has the potential to advance the science of CRF and improve the clinical management of this troubling symptom.
C1 [Barsevick, Andrea M.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Irwin, Michael R.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Hinds, Pamela] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Miller, Andrew] Emory Univ, Atlanta, GA 30322 USA.
[Berger, Ann] Univ Nebraska Med Ctr, Omaha, NE USA.
[Jacobsen, Paul] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Ancoli-Israel, Sonia] Univ Calif San Diego, San Diego, CA 92103 USA.
Univ N Carolina, Chapel Hill, NC USA.
[Mustian, Karen] Univ Rochester, Rochester, NY USA.
[O'Mara, Ann] NCI, Bethesda, MD 20892 USA.
[Lai, Jin-Shei; Cella, David] Northwestern Univ, Chicago, IL 60611 USA.
[Fisch, Michael] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Barsevick, AM (reprint author), Thomas Jefferson Univ, 834 Chestnut St,Suite 314, Philadelphia, PA 19107 USA.
EM Andrea.barsevick@jefferson.edu
RI Irwin, Michael/H-4870-2013;
OI Irwin, Michael/0000-0002-1502-8431; Barsevick,
Andrea/0000-0003-1829-6826
FU NCI NIH HHS [P30 CA016086, R25 CA102618, U10 CA037420]
NR 138
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U1 6
U2 22
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 19
BP 1432
EP 1440
DI 10.1093/jnci/djt242
PG 9
WC Oncology
SC Oncology
GA 232GZ
UT WOS:000325482100007
PM 24047960
ER
PT J
AU Citrin, DE
Shankavaram, U
Horton, JA
Shield, W
Zhao, SP
Asano, H
White, A
Sowers, A
Thetford, A
Chung, EJ
AF Citrin, Deborah E.
Shankavaram, Uma
Horton, Jason A.
Shield, William, III
Zhao, Shuping
Asano, Hiroaki
White, Ayla
Sowers, Anastasia
Thetford, Angela
Chung, Eun Joo
TI Role of Type II Pneumocyte Senescence in Radiation-Induced Lung Fibrosis
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID IDIOPATHIC PULMONARY-FIBROSIS; EPITHELIAL-CELL SENESCENCE; NORMAL HUMAN
FIBROBLASTS; GROWTH ARREST; OXIDATIVE STRESS; GENE-EXPRESSION; TGF-BETA;
INJURY; TOXICITY; MUTATIONS
AB Background Radiation is a commonly delivered therapeutic modality for cancer. The causes underlying the chronic, progressive nature of radiation injury in the lung are poorly understood.
Methods C57Bl/6NCr mice were exposed to thoracic irradiation (n = 3 per dose and time point for tissue collection). Microarray analysis of gene expression from irradiated murine lung was performed using one-way analysis of variance with post hoc Scheffe analysis. Senescence and type II airway epithelial cell (AECII) count were assayed in irradiated murine lung tissue (n = 3 per condition). Irradiated mice were treated with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase (NOX), and fibrosis was assessed by collagen assays. All statistical tests were two-tailed.
Results Gene expression in lung tissue from mice irradiated to 17.5 Gy clustered with that of aged unirradiated mice. Only fibrogenic exposures led to AECII senescence (0 Gy: 0.66% +/- 0.67%; 5 Gy: 4.5% +/- 1.19%; 17.5 Gy: 18.7% +/- 3.05; P = .007) and depletion (0 Gy: 2.89 per alveolus +/- 0.26; 5 Gy: 2.41 +/- 0.19; 17.5 Gy: 1.6 +/- 0.14; P < .001) at 30 weeks. Treatment of irradiated mice with DPI for 16 weeks markedly reduced collagen accumulation (5 x 6 Gy: 57.26 mu g/lung +/- 9.91; 5 x 6 Gy +/- DPI: 36.54 mu g/lung +/- 4.39; P = .03) and AECII senescence (5 x 6 Gy: 37.61% +/- 4.82%; 5 x 6 Gy +/- DPI: 12.38% +/- 2.78; P < .001).
Conclusions These studies identify senescence as an important process in AECII in vivo and indicate that NOX is a critical mediator of radiation-induced AECII senescence and pulmonary fibrosis.
C1 [Citrin, Deborah E.; Shankavaram, Uma; Horton, Jason A.; Shield, William, III; Zhao, Shuping; Asano, Hiroaki; Chung, Eun Joo] NIH, Radiat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Sowers, Anastasia; Thetford, Angela] NIH, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Citrin, DE (reprint author), NCI, Radiat Oncol Branch, Bldg 10 CRC,B2-3500, Bethesda, MD USA.
EM citrind@mail.nih.gov
FU National Institutes of Health, National Cancer Institute
FX All authors were supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 41
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U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD OCT
PY 2013
VL 105
IS 19
BP 1474
EP 1484
DI 10.1093/jnci/djt212
PG 11
WC Oncology
SC Oncology
GA 232GZ
UT WOS:000325482100011
PM 24052614
ER
PT J
AU Ho, JE
Chen, WY
Chen, MH
Larson, MG
McCabe, EL
Cheng, SS
Ghorbani, A
Coglianese, E
Emilsson, V
Johnson, AD
Walter, S
Franceschini, N
O'Donnell, CJ
Dehghan, A
Lu, C
Levy, D
Newton-Cheh, C
Lin, HH
Felix, JF
Schreiter, ER
Vasan, RS
Januzzi, JL
Lee, RT
Wang, TJ
AF Ho, Jennifer E.
Chen, Wei-Yu
Chen, Ming-Huei
Larson, Martin G.
McCabe, Elizabeth L.
Cheng, Susan
Ghorbani, Anahita
Coglianese, Erin
Emilsson, Valur
Johnson, Andrew D.
Walter, Stefan
Franceschini, Nora
O'Donnell, Christopher J.
Dehghan, Abbas
Lu, Chen
Levy, Daniel
Newton-Cheh, Christopher
Lin, Honghuang
Felix, Janine F.
Schreiter, Eric R.
Vasan, Ramachandran S.
Januzzi, James L.
Lee, Richard T.
Wang, Thomas J.
CA CARDIoGRAM Consortium
CHARGE Inflammation Working Grp
CHARGE Heart Failure Working Grp
TI Common genetic variation at the IL1RL1 locus regulates IL-33/ST2
signaling
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID RECEPTOR FAMILY-MEMBER; DECOMPENSATED HEART-FAILURE; SOLUBLE ST2;
MYOCARDIAL-INFARCTION; NATRIURETIC PEPTIDE; CELIAC-DISEASE; ACUTE
DYSPNEA; SERUM-LEVELS; LARGE-SCALE; MAST-CELLS
AB The suppression of turnorigenicity 2/IL-33 (ST2/IL-33) pathway has been implicated in several immune and inflammatory diseases. ST2 is produced as 2 isoforms. The membrane-bound isoform (ST2L) induces an immune response when bound to its ligand, IL-33. The other isoform is a soluble protein (sST2) that is thought to be a decoy receptor for IL-33 signaling. Elevated sST2 levels in serum are associated with an increased risk for cardiovascular disease. We investigated the determinants of sST2 plasma concentrations in 2,991 Framingham Offspring Cohort participants. While clinical and environmental factors explained some variation in sST2 levels, much of the variation in sST2 production was driven by genetic factors. In a genome-wide association study (GWAS), multiple SNPs within IL1RL1 (the gene encoding ST2) demonstrated associations with sST2 concentrations. Five missense variants of IL1RL1 correlated with higher sST2 levels in the GWAS and mapped to the intracellular domain of ST2, which is absent in sST2. In a cell culture model, IL1RL1 missense variants increased sST2 expression by inducing IL-33 expression and enhancing IL-33 responsiveness (via ST2L). Our data suggest that genetic variation in IL1RL1 can result in increased levels of sST2 and alter immune and inflammatory signaling through the ST2/IL-33 pathway.
C1 [Ho, Jennifer E.; Chen, Ming-Huei; Larson, Martin G.; Cheng, Susan; Johnson, Andrew D.; O'Donnell, Christopher J.; Levy, Daniel; Newton-Cheh, Christopher; Lin, Honghuang; Vasan, Ramachandran S.; Wang, Thomas J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Ho, Jennifer E.; Chen, Ming-Huei; Larson, Martin G.; Cheng, Susan; Johnson, Andrew D.; O'Donnell, Christopher J.; Levy, Daniel; Newton-Cheh, Christopher; Lin, Honghuang; Vasan, Ramachandran S.; Wang, Thomas J.] Boston Univ, Sch Med, Framingham, MA USA.
[Ho, Jennifer E.] Boston Univ, Sch Med, Dept Med, Cardiovasc Med Sect, Boston, MA 02118 USA.
[Chen, Wei-Yu; Cheng, Susan; Lee, Richard T.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Cardiol, Boston, MA USA.
[Chen, Ming-Huei] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Larson, Martin G.; Lu, Chen] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[McCabe, Elizabeth L.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Ghorbani, Anahita; O'Donnell, Christopher J.; Newton-Cheh, Christopher; Januzzi, James L.; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Coglianese, Erin] Loyola Univ Hlth Syst, Chicago, IL USA.
[Emilsson, Valur] Iceland Heart Assoc, Kopavogur, Iceland.
[Walter, Stefan] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Walter, Stefan] Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
[Walter, Stefan; Dehghan, Abbas; Felix, Janine F.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Franceschini, Nora] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Newton-Cheh, Christopher] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Lin, Honghuang; Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Schreiter, Eric R.] Univ Puerto Rico, Dept Chem, San Juan, PR 00936 USA.
[Schreiter, Eric R.] Howard Hughes Med Inst, Ashburn, VA USA.
[Wang, Thomas J.] Vanderbilt Univ, Dept Med, Div Cardiovasc Med, Nashville, TN 37232 USA.
RP Wang, TJ (reprint author), Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, 2220 Pierce Ave,383 Preston Res Bldg, Nashville, TN 37232 USA.
EM rlee@partners.org; thomas.j.wang@vanderbilt.edu
RI Altshuler, David/A-4476-2009; Schreiber, Stefan/B-6748-2008; Willenborg,
Christina/D-2668-2012; Lu, Chen/D-8514-2015; Boehm,
Bernhard/F-8750-2015; Gudnason, Vilmundur/K-6885-2015; Meitinger,
Thomas/O-1318-2015; Johnson, Andrew/G-6520-2013;
OI Kleber, Marcus/0000-0003-0663-7275; Dehghan, Abbas/0000-0001-6403-016X;
Lin, Honghuang/0000-0003-3043-3942; Ramachandran,
Vasan/0000-0001-7357-5970; Altshuler, David/0000-0002-7250-4107;
Schreiber, Stefan/0000-0003-2254-7771; Willenborg,
Christina/0000-0001-5217-6882; Gudnason, Vilmundur/0000-0001-5696-0084;
Felix, Janine/0000-0002-9801-5774
FU National Heart, Lung and Blood Institute's Framingham Heart Study
[N01-HC-25195]; Affymetrix Inc. for genotyping services [N02-HL-6-4278];
NIH [R01-NS017950-28, R01-HL093328-01, R01 HL092930, R01-HL086875,
1K23-HL116780]; Boston University School of Medicine Department of
Medicine Career Investment Award; Ellison Foundation; Taiwan National
Science Council [101-2917-I-564-057]; AHA postdoctoral fellowship
[13POST16940030]; NWO grant (veni) [916.12.154]; EUR fellowship; Robert
Dawson Evans Endowment of the Department of Medicine at Boston
University School of Medicine; Boston Medical Center
FX This work was partially supported by the National Heart, Lung and Blood
Institute's Framingham Heart Study (N01-HC-25195), its contract with
Affymetrix Inc. for genotyping services (N02-HL-6-4278), and NIH grants
R01-NS017950-28 and R01-HL093328-01 (to R.S. Vasan), R01 HL092930 (to
R.T. Lee), R01-HL086875 (to T.J. Wang), and 1K23-HL116780 (to J.E. Ho).
J.E. Ho is supported by a Boston University School of Medicine
Department of Medicine Career Investment Award. Measurement of sST2 was
performed by Critical Diagnostics Inc. S. Cheng is supported by an award
from the Ellison Foundation. W.-Y. Chen is supported by awards from the
Taiwan National Science Council (101-2917-I-564-057) and an AHA
postdoctoral fellowship (13POST16940030). A. Dehghan is supported by a
NWO grant (veni, 916.12.154) and the EUR fellowship. The analyses
reflect intellectual input and resource development from the Framingham
Heart Study investigators participating in the SNP Health Association
Resource (SHARe) project. A portion of this research used the Linux
Cluster for Genetic Analysis (LinGA-II) funded by the Robert Dawson
Evans Endowment of the Department of Medicine at Boston University
School of Medicine and Boston Medical Center. Please see Supplemental
Acknowledgments for CHARGE and CARDIoGRAM consortium details.
NR 50
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U2 11
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2013
VL 123
IS 10
BP 4208
EP 4218
DI 10.1172/JCI67119
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 231UE
UT WOS:000325443100017
PM 23999434
ER
PT J
AU Wang, TJ
Ngo, D
Psychogios, N
Dejam, A
Larson, MG
Vasan, RS
Ghorbani, A
O'Sullivan, J
Cheng, S
Rhee, EP
Sinha, S
McCabe, E
Fox, CS
O'Donnell, CJ
Ho, JE
Florez, JC
Magnusson, M
Pierce, KA
Souza, AL
Yu, Y
Carter, C
Light, PE
Melander, O
Clish, CB
Gerszten, RE
AF Wang, Thomas J.
Ngo, Debby
Psychogios, Nikolaos
Dejam, Andre
Larson, Martin G.
Vasan, Ramachandran S.
Ghorbani, Anahita
O'Sullivan, John
Cheng, Susan
Rhee, Eugene P.
Sinha, Sumita
McCabe, Elizabeth
Fox, Caroline S.
O'Donnell, Christopher J.
Ho, Jennifer E.
Florez, Jose C.
Magnusson, Martin
Pierce, Kerry A.
Souza, Amanda L.
Yu, Yi
Carter, Christian
Light, Peter E.
Melander, Olle
Clish, Clary B.
Gerszten, Robert E.
TI 2-Aminoadipic acid is a biomarker for diabetes risk
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; INSULIN-RESISTANCE; LIFE-STYLE; MELLITUS;
METABOLISM; SECRETION; FREQUENCY; OXIDATION; MARKER
AB Improvements in metabolite-profiling techniques are providing increased breadth of coverage of the human metabolome and may highlight biomarkers and pathways in common diseases such as diabetes. Using a metabolomics platform that analyzes intermediary organic acids, purines, pyrimidines, and other compounds, we performed a nested case-control study of 188 individuals who developed diabetes and 188 propensity-matched controls from 2,422 normoglycemic participants followed for 12 years in the Framingham Heart Study. The metabolite 2-aminoadipic acid (2-AAA) was most strongly associated with the risk of developing diabetes. Individuals with 2-AAA concentrations in the top quartile had greater than a 4-fold risk of developing diabetes. Levels of 2-AAA were not well correlated with other metabolite biomarkers of diabetes, such as branched chain amino acids and aromatic amino acids, suggesting they report on a distinct pathophysiological pathway. In experimental studies, administration of 2-AAA lowered fasting plasma glucose levels in mice fed both standard chow and high-fat diets. Further, 2-AAA treatment enhanced insulin secretion from a pancreatic beta cell line as well as murine and human islets. These data highlight a metabolite not previously associated with diabetes risk that is increased up to 12 years before the onset of overt disease. Our findings suggest that 2-AAA is a marker of diabetes risk and a potential modulator of glucose homeostasis in humans.
C1 [Wang, Thomas J.; Ngo, Debby; Psychogios, Nikolaos; Dejam, Andre; O'Sullivan, John; Rhee, Eugene P.; Sinha, Sumita; Gerszten, Robert E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02115 USA.
[Wang, Thomas J.; Ghorbani, Anahita; O'Donnell, Christopher J.; Gerszten, Robert E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02115 USA.
[Wang, Thomas J.; Larson, Martin G.; Vasan, Ramachandran S.; Ghorbani, Anahita; Cheng, Susan; Fox, Caroline S.; O'Donnell, Christopher J.; Ho, Jennifer E.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Wang, Thomas J.; Larson, Martin G.; Vasan, Ramachandran S.; Ghorbani, Anahita; Cheng, Susan; Fox, Caroline S.; O'Donnell, Christopher J.; Ho, Jennifer E.] Boston Univ, Sch Med, Framingham, MA USA.
[Wang, Thomas J.] Vanderbilt Univ, Div Cardiovasc Med, Nashville, TN 37235 USA.
[Ngo, Debby] Harvard Univ, Sch Med, Div Pulm, Boston, MA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Vasan, Ramachandran S.; Ho, Jennifer E.] Boston Univ, Dept Med, Prevent Med Sect, Boston, MA 02215 USA.
[Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc, Boston, MA 02115 USA.
[Rhee, Eugene P.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Renal, Boston, MA USA.
[Rhee, Eugene P.; Florez, Jose C.; Pierce, Kerry A.; Souza, Amanda L.; Clish, Clary B.; Gerszten, Robert E.] MIT, Broad Inst, Cambridge, MA 02139 USA.
[Rhee, Eugene P.; Florez, Jose C.; Pierce, Kerry A.; Souza, Amanda L.; Clish, Clary B.; Gerszten, Robert E.] Harvard, Cambridge, MA USA.
[McCabe, Elizabeth] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
[Fox, Caroline S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol, Boston, MA 02115 USA.
[Fox, Caroline S.; O'Donnell, Christopher J.] NHLBI, Div Intramural Res, Bethesda, MD 20892 USA.
[Florez, Jose C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Diabets Unit, Boston, MA USA.
[Florez, Jose C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Human Genet Res, Boston, MA USA.
[Magnusson, Martin] Skane Univ Hosp, Dept Cardiol, Malmo, Sweden.
[Magnusson, Martin; Melander, Olle] Lund Univ, Dept Clin Sci, Malmo, Sweden.
[Yu, Yi; Carter, Christian; Light, Peter E.] Univ Alberta, Dept Pharmacol, Alberta Diabet Inst, Edmonton, AB, Canada.
[Melander, Olle] Skane Univ Hosp, Ctr Emergency Med, Malmo, Sweden.
RP Gerszten, RE (reprint author), Massachusetts Gen Hosp, Div Cardiol, 185 Cambridge St, Boston, MA 02114 USA.
EM thomas.j.wang@vanderbilt.edu; rgerszten@partners.org
OI Ho, Jennifer/0000-0002-7987-4768; Psychogios,
Nikolaos/0000-0002-2747-6012; Magnusson, Martin/0000-0003-1710-5936;
Ramachandran, Vasan/0000-0001-7357-5970
FU NIH [NO1-HC-25195, R01-DK-HL081572]; Leducq Foundation; Canadian
Institutes of Health Research; American Heart Association
FX This work was supported by NIH contract NO1-HC-25195, R01-DK-HL081572,
the Leducq Foundation, the Canadian Institutes of Health Research, and
the American Heart Association.
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PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2013
VL 123
IS 10
BP 4309
EP 4317
DI 10.1172/JCI64801
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 231UE
UT WOS:000325443100026
PM 24091325
ER
PT J
AU Sukumar, M
Liu, J
Ji, Y
Subramanian, M
Crompton, JG
Yu, ZY
Roychoudhuri, R
Palmer, DC
Muranski, P
Karoly, ED
Mohney, RP
Klebanoff, CA
Lal, A
Finkel, T
Restifo, NP
Gattinoni, L
AF Sukumar, Madhusudhanan
Liu, Jie
Ji, Yun
Subramanian, Murugan
Crompton, Joseph G.
Yu, Zhiya
Roychoudhuri, Rahul
Palmer, Douglas C.
Muranski, Pawel
Karoly, Edward D.
Mohney, Robert P.
Klebanoff, Christopher A.
Lal, Ashish
Finkel, Toren
Restifo, Nicholas P.
Gattinoni, Luca
TI Inhibiting glycolytic metabolism enhances CD8(+) T cell memory and
antitumor function
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID EFFECTOR FUNCTIONS; DIFFERENTIATION; IMMUNOTHERAPY; IMMUNITY;
MAINTENANCE; LYMPHOCYTES; ACTIVATION; MIGRATION; BINDING; LIFE
AB Naive CD8(+) T cells rely upon oxidation of fatty acids as a primary source of energy. After antigen encounter, T cells shift to a glycolytic metabolism to sustain effector function. It is unclear, however, whether changes in glucose metabolism ultimately influence the ability of activated. T cells to become long-lived memory cells. We used a fluorescent glucose analog, 2-NBDG, to quantify glucose uptake in activated CD8(+) T cells. We found that cells exhibiting limited glucose incorporation had a molecular profile characteristic of memory precursor cells and an increased capacity to enter the memory pool compared with cells taking up high amounts of glucose. Accordingly, enforcing glycolytic metabolism by overexpressing the glycolytic enzyme phosphoglycerate mutase-1 severely impaired the ability of CD8(+) T cells to form long-term memory. Conversely, activation of CD8(+) T cells in the presence of an inhibitor of glycolysis, 2-deoxyglucose, enhanced the generation of memory cells and antitumor functionality. Our data indicate that augmenting glycolytic flux drives CD8(+) T cells toward a terminally differentiated state, while its inhibition preserves the formation of long-lived memory CD8(+) T cells. These results have important implications for improving the efficacy of T cell-based therapies against chronic infectious diseases and cancer.
C1 [Sukumar, Madhusudhanan; Crompton, Joseph G.; Yu, Zhiya; Roychoudhuri, Rahul; Palmer, Douglas C.; Muranski, Pawel; Klebanoff, Christopher A.; Restifo, Nicholas P.] NCI, Ctr Canc Res, Surg Branch, Bethesda, MD 20892 USA.
[Liu, Jie; Finkel, Toren] NHLBI, Ctr Mol Med, Bethesda, MD 20892 USA.
[Ji, Yun; Gattinoni, Luca] NCI, Ctr Canc Res, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Subramanian, Murugan; Lal, Ashish] NIH, Ctr Mol Genet, Bethesda, MD 20892 USA.
[Karoly, Edward D.; Mohney, Robert P.] Metabolon Inc, Durham, NC USA.
[Klebanoff, Christopher A.] NCI, Clin Investigator Dev Program, NIH, Bethesda, MD 20892 USA.
RP Sukumar, M (reprint author), NCI, Ctr Canc Res, Surg Branch, NIH,Clin Res Ctr, Room 3W-5816, Bethesda, MD 20892 USA.
EM sukumarm2@mail.nih.gov; gattinol@mail.nih.gov
RI Gattinoni, Luca/A-2281-2008; Ji, Yun/B-7245-2009; Palmer,
Douglas/B-9454-2008; Roychoudhuri, Rahul/A-7442-2010;
OI Gattinoni, Luca/0000-0003-2239-3282; Ji, Yun/0000-0001-6340-7009;
Palmer, Douglas/0000-0001-5018-5734; Roychoudhuri,
Rahul/0000-0002-5392-1853; Restifo, Nicholas P./0000-0003-4229-4580
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. The authors
thank N. Acquavella, D. Clever, E. Tran, and M. Rao for critical review
of the manuscript; A. Mixon, S. Farid, and G. Wiegand of the Flow
Cytometry Unit for help with cell sorting; and D. Goldstein and M. Malik
for catalyzing interactions with Metabolon. We sincerely thank Steven A.
Rosenberg for his continuous support.
NR 55
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PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2013
VL 123
IS 10
BP 4479
EP 4488
DI 10.1172/JCI69389
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 231UE
UT WOS:000325443100040
PM 24091329
ER
PT J
AU Duncan, BB
Highfill, SL
Qin, HY
Bouchkouj, N
Larabee, S
Zhao, P
Woznica, I
Liu, YX
Li, YH
Wu, WG
Lai, JH
Jones, B
Mackall, CL
Bachovchin, WW
Fry, TJ
AF Duncan, Brynn B.
Highfill, Steven L.
Qin, Haiying
Bouchkouj, Najat
Larabee, Shannon
Zhao, Peng
Woznica, Iwona
Liu, Yuxin
Li, Youhua
Wu, Wengen
Lai, Jack H.
Jones, Barry
Mackall, Crystal L.
Bachovchin, William W.
Fry, Terry J.
TI A Pan-Inhibitor of DASH Family Enzymes Induces Immune-mediated
Regression of Murine Sarcoma and Is a Potent Adjuvant to Dendritic Cell
Vaccination and Adoptive T-cell Therapy
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE adjuvant; postproline cleaving enzymes; dipeptidyl peptidases;
rhabdomyosarcoma; immunotherapy
ID TUMOR-ASSOCIATED ANTIGENS; ACTIVATION PROTEIN-ALPHA; DIPEPTIDYL
PEPTIDASE IV; SUPPRESSOR-CELLS; CANCER-IMMUNOTHERAPY; CHILDHOOD-CANCER;
BEARING MICE; IN-VIVO; RHABDOMYOSARCOMA; RESPONSES
AB Multimodality therapy consisting of surgery, chemotherapy, and radiation will fail in approximately 40% of patients with pediatric sarcomas and result in substantial long-term morbidity in those who are cured. Immunotherapeutic regimens for the treatment of solid tumors typically generate antigen-specific responses too weak to overcome considerable tumor burden and tumor suppressive mechanisms and are in need of adjuvant assistance. Previous work suggests that inhibitors of DASH (dipeptidyl peptidase IV activity and/or structural homologs) enzymes can mediate tumor regression by immune-mediated mechanisms. Herein, we demonstrate that the DASH inhibitor, ARI-4175, can induce regression and eradication of well-established solid tumors, both as a single agent and as an adjuvant to a dendritic cell (DC) vaccine and adoptive cell therapy (ACT) in mice implanted with the M3-9-M rhabdomyosarcoma cell line. Treatment with effective doses of ARI-4175 correlated with recruitment of myeloid (CD11b(+)) cells, particularly myeloid DCs, to secondary lymphoid tissues and with reduced frequency of intratumoral monocytic (CD11b(+)Ly6-C(hi)Ly6-G(lo)) myeloid-derived suppressor cells. In immunocompetent mice, combining ARI-4175 with a DC vaccine or ACT with tumor-primed T cells produced significant improvements in tumor responses against well-established M3-9-M tumors. In M3-9-M-bearing immunodeficient (Rag1(-/-)) mice, ACT combined with ARI-4175 produced greater tumor responses and significantly improved survival compared with either treatment alone. These studies warrant the clinical investigation of ARI-4175 for treatment of sarcomas and other malignancies, particularly as an adjuvant to tumor vaccines and ACT.
C1 [Duncan, Brynn B.; Highfill, Steven L.; Qin, Haiying; Bouchkouj, Najat; Larabee, Shannon; Mackall, Crystal L.; Fry, Terry J.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Bouchkouj, Najat] MedStar Georgetown Univ Hosp, Div Pediat Hematol Oncol, Dept Pediat, Washington, DC USA.
[Zhao, Peng; Woznica, Iwona; Liu, Yuxin; Li, Youhua; Wu, Wengen; Lai, Jack H.; Jones, Barry; Bachovchin, William W.] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA.
RP Fry, TJ (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bldg 10,Room 1-3940,10 Ctr Dr, Bethesda, MD 20892 USA.
EM fryt@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; Arasaph Pharmaceuticals
FX This study was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research.; B.J. and W.W.B.
receive consulting fees and grant support from Arasaph Pharmaceuticals.
All the remaining authors have declared there are no financial conflicts
of interest in regard to this work.
NR 53
TC 2
Z9 3
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1524-9557
EI 1537-4513
J9 J IMMUNOTHER
JI J. Immunother.
PD OCT
PY 2013
VL 36
IS 8
BP 400
EP 411
DI 10.1097/CJI.0b013e3182a80213
PG 12
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA 220YJ
UT WOS:000324623100002
PM 23994886
ER
PT J
AU Schaffer, AA
AF Schaeffer, Alejandro A.
TI Digenic inheritance in medical genetics
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Review
DE Digenic inheritance; protein-protein interactions; high-throughput
sequencing; epistatis; facioscapulohumeral muscular dystrophy
ID BARDET-BIEDL-SYNDROME; LONG-QT SYNDROME; FAMILIAL EXUDATIVE
VITREORETINOPATHY; GENOTYPE-PHENOTYPE CORRELATION; 2-TRAIT-LOCUS LINKAGE
ANALYSIS; RECESSIVE OCULAR ALBINISM; MARIE-TOOTH-DISEASE; HEARING
IMPAIRMENT; 2-LOCUS MODELS; HYPOGONADOTROPIC HYPOGONADISM
AB Digenic inheritance (DI) is the simplest form of inheritance for genetically complex diseases. By contrast with the thousands of reports that mutations in single genes cause human diseases, there are only dozens of human disease phenotypes with evidence for DI in some pedigrees. The advent of high-throughput sequencing (HTS) has made it simpler to identify monogenic disease causes and could similarly simplify proving DI because one can simultaneously find mutations in two genes in the same sample. However, through 2012, I could find only one example of human DI in which HTS was used; in that example, HTS found only the second of the two genes. To explore the gap between expectation and reality, I tried to collect all examples of human DI with a narrow definition and characterise them according to the types of evidence collected, and whether there has been replication. Two strong trends are that knowledge of candidate genes and knowledge of protein-protein interactions (PPIs) have been helpful in most published examples of human DI. By contrast, the positional method of genetic linkage analysis, has been mostly unsuccessful in identifying genes underlying human DI. Based on the empirical data, I suggest that combining HTS with growing networks of established PPIs may expedite future discoveries of human DI and strengthen the evidence for them.
C1 NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, US Dept HHS, Bethesda, MD 20894 USA.
RP Schaffer, AA (reprint author), NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, US Dept HHS, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM schaffer@helix.nih.gov
FU National Institutes of Health
FX National Institutes of Health, Intramural Research Program.
NR 125
TC 33
Z9 33
U1 3
U2 11
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 2013
VL 50
IS 10
BP 641
EP 652
DI 10.1136/jmedgenet-2013-101713
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 221FO
UT WOS:000324643400001
PM 23785127
ER
PT J
AU Bondy, C
Bakalov, VK
Cheng, C
Olivieri, L
Rosing, DR
Arai, AE
AF Bondy, Carolyn
Bakalov, Vladimir K.
Cheng, Clara
Olivieri, Laura
Rosing, Douglas R.
Arai, Andrew E.
TI Bicuspid aortic valve and aortic coarctation are linked to deletion of
the X chromosome short arm in Turner syndrome
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Aneuploidy; Congenital heart disease; Chromosomal; Developmental
ID PULMONARY VENOUS DRAINAGE; HYPOPLASTIC LEFT-HEART; CARDIOVASCULAR
MALFORMATIONS; Y-CHROMOSOME; DISEASE; PREVALENCE; ASSOCIATION;
LYMPHEDEMA; ANOMALIES; MONOSOMY
AB Background Congenital heart disease (CHD) is a cardinal feature of X chromosome monosomy, or Turner syndrome (TS). Haploinsufficiency for gene(s) located on Xp have been implicated in the short stature characteristic of the syndrome, but the chromosomal region related to the CHD phenotype has not been established.
Design We used cardiac MRI to diagnose cardiovascular abnormalities in four non-mosaic karyotype groups based on 50-metaphase analyses: 45,X (n=152); 46,X,del(Xp) (n=15); 46,X,del(Xq) (n=4); and 46,X,i(Xq) (n=14) from peripheral blood cells.
Results Bicuspid aortic valves (BAV) were found in 52/152 (34%) 45,X study subjects and aortic coarctation (COA) in 19/152 (12.5%). Isolated anomalous pulmonary veins (APV) were detected in 15/152 (10%) for the 45,X study group, and this defect was not correlated with the presence of BAV or COA. BAVs were present in 28.6% of subjects with Xp deletions and COA in 6.7%. APV were not found in subjects with Xp deletions. The most distal break associated with the BAV/COA trait was at cytologic band Xp11.4 and ChrX:41,500000. One of 14 subjects (7%) with the 46,X,i(Xq) karyotype had a BAV and no cases of COA or APV were found in this group. No cardiovascular defects were found among four patients with Xq deletions.
Conclusions The high prevalence of BAV and COA in subjects missing only the X chromosome short arm indicates that haploinsufficiency for Xp genes contributes to abnormal aortic valve and aortic arch development in TS.
C1 [Bondy, Carolyn; Bakalov, Vladimir K.; Cheng, Clara] NICHHD, Sect Epigenet & Dev, Bethesda, MD 20892 USA.
[Olivieri, Laura; Rosing, Douglas R.; Arai, Andrew E.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Bondy, C (reprint author), NICHHD, Sect Epigenet & Dev, NIH, CRC 1-3330,10 Ctr Dr, Bethesda, MD 20892 USA.
EM bondyc@mail.nih.gov
FU Nationals Institutes of Health Division of Intramural Research
FX This work was supported the Nationals Institutes of Health Division of
Intramural Research.
NR 38
TC 17
Z9 19
U1 0
U2 6
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 2013
VL 50
IS 10
BP 662
EP 665
DI 10.1136/jmedgenet-2013-101720
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 221FO
UT WOS:000324643400003
PM 23825392
ER
PT J
AU Li, JM
Foo, JN
Schoof, N
Varghese, JS
Fernandez-Navarro, P
Gierach, GL
Quek, ST
Hartman, M
Nord, S
Kristensen, VN
Pollan, M
Figueroa, JD
Thompson, DJ
Li, Y
Khor, CC
Humphreys, K
Liu, JJ
Czene, K
Hall, P
AF Li, Jingmei
Foo, Jia Nee
Schoof, Nils
Varghese, Jajini S.
Fernandez-Navarro, Pablo
Gierach, Gretchen L.
Quek, Swee Tian
Hartman, Mikael
Nord, Silje
Kristensen, Vessela N.
Pollan, Marina
Figueroa, Jonine D.
Thompson, Deborah J.
Li, Yi
Khor, Chiea Chuen
Humphreys, Keith
Liu, Jianjun
Czene, Kamila
Hall, Per
TI Large-scale genotyping identifies a new locus at 22q13.2 associated with
female breast size
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Cancer: breast; Epidemiology; Genetic epidemiology; Genome-wide; Complex
traits
ID GENOME-WIDE ASSOCIATION; CANCER RISK; MEGAKARYOBLASTIC LEUKEMIA;
PRINCIPAL-COMPONENTS; VARIANTS; WOMEN; ADJUSTMENT; PROJECT; IMPACT;
STATES
AB Background Individual differences in breast size are a conspicuous feature of variation in human females and have been associated with fecundity and advantage in selection of mates. To identify common variants that are associated with breast size, we conducted a large-scale genotyping association meta-analysis in 7169 women of European descent across three independent sample collections with digital or screen film mammograms.
Methods The samples consisted of the Swedish KARMA, LIBRO-1 and SASBAC studies genotyped on iCOGS, a custom illumina iSelect genotyping array comprising of 211155 single nucleotide polymorphisms (SNPs) designed for replication and fine mapping of common and rare variants with relevance to breast, ovary and prostate cancer. Breast size of each subject was ascertained by measuring total breast area (mm(2)) on a mammogram.
Results We confirm genome-wide significant associations at 8p11.23 (rs10086016, p=1.3x10(-14)) and report a new locus at 22q13 (rs5995871, p=3.2x10(-8)). The latter region contains the MKL1 gene, which has been shown to impact endogenous oestrogen receptor transcriptional activity and is recruited on oestradiol sensitive genes. We also replicated previous genome-wide association study findings for breast size at four other loci.
Conclusions A new locus at 22q13 may be associated with female breast size.
C1 [Li, Jingmei; Foo, Jia Nee; Li, Yi; Khor, Chiea Chuen; Liu, Jianjun] Genome Inst Singapore, Singapore, Singapore.
[Schoof, Nils; Humphreys, Keith; Czene, Kamila; Hall, Per] Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden.
[Varghese, Jajini S.; Thompson, Deborah J.] Univ Cambridge, Ctr Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
[Varghese, Jajini S.] Royal Free Hosp, Plast Surg Unit, London NW3 2QG, England.
[Fernandez-Navarro, Pablo; Pollan, Marina] Carlos III Inst Hlth, Canc & Environm Epidemiol Unit, Natl Ctr Epidemiol, Madrid, Spain.
[Fernandez-Navarro, Pablo; Pollan, Marina] CIBERESP, Consortium Biomed Res Epidemiol & Publ Hlth, Madrid, Spain.
[Gierach, Gretchen L.; Figueroa, Jonine D.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Quek, Swee Tian] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Diagnost Radiol, Singapore 117595, Singapore.
[Hartman, Mikael; Liu, Jianjun] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore.
[Hartman, Mikael; Liu, Jianjun] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Surg, Singapore 117595, Singapore.
[Nord, Silje; Kristensen, Vessela N.] Radiumhospitalet, Inst Canc Res, Dept Genet, Oslo Univ Hosp, Oslo, Norway.
[Kristensen, Vessela N.] Akershus Univ Hosp, Div Med, Dept Clin Mol Biol, Ahus, Norway.
RP Hall, P (reprint author), Karolinska Inst, Dept Med Epidemiol & Biostat, Box 281, S-17177 Stockholm, Sweden.
EM Per.Hall@ki.se
RI Li, Jingmei/I-2904-2012; Hartman, Mikael/B-4324-2011; Pollan,
Marina/M-3259-2014; Foo, Jia Nee/D-6069-2014; Gierach,
Gretchen/E-1817-2016; Nord, Silje/R-5212-2016;
OI Pollan, Marina/0000-0002-4328-1565; Li, Jingmei/0000-0001-8587-7511;
Foo, Jia Nee/0000-0001-9899-2308; Gierach, Gretchen/0000-0002-0165-5522;
Nord, Silje/0000-0002-3271-5356; Czene, Kamila/0000-0002-3233-5695;
Khor, Chiea Chuen/0000-0002-1128-4729
FU Marit and Hans Rausings Initiative Against Breast Cancer; Cancer Risk
Prediction Center (CRisP); Linneus Centre [70867902]; Swedish Research
Council; Agency for Science, Technology and Research of Singapore
(A*STAR); US National Institute of Health (NIH); Susan G Komen Breast
Cancer Foundation; European Community [223175 (HEALTH-F2-2009-223175)];
European Union [HEALTH-F2-2009-223175]; Cancer Research UK
[C1287/A10710, C1287/A10118, C1287/A12014]; Canadian Institutes of
Health Research (CIHR); Ministry of Economic Development, Innovation and
Export Trade of Quebec [PSR-SIIRI-701]; US National Institutes of Health
(NIH) Cancer Post-Cancer GWAS initiative [1 U19 CA 148065-01]; US
National Cancer Institute, Department of Health and Human Services, USA
FX KARMA was supported by Marit and Hans Rausings Initiative Against Breast
Cancer. KARMA and LIBRO-1 were supported the Cancer Risk Prediction
Center (CRisP; www.crispcenter.org), a Linneus Centre (Contract ID
70867902) financed by the Swedish Research Council. SASBAC was supported
by funding from the Agency for Science, Technology and Research of
Singapore (A*STAR), the US National Institute of Health (NIH) and the
Susan G Komen Breast Cancer Foundation. All three studies are genotyped
as part of the Collaborative Oncological Gene-environment Study (COGS),
which is supported by the European Community's Seventh Framework
Programme under grant agreement 223175 (HEALTH-F2-2009-223175) (COGS).
Genotyping of the iCOGS array was funded by the European Union
(HEALTH-F2-2009-223175), Cancer Research UK (C1287/A10710), the Canadian
Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks
of Breast Cancer program and the Ministry of Economic Development,
Innovation and Export Trade of Quebec (grant PSR-SIIRI-701). BCAC is
funded by Cancer Research UK (C1287/A10118 and C1287/A12014). Combining
the GWAS data was supported in part by the US National Institutes of
Health (NIH) Cancer Post-Cancer GWAS initiative grant 1 U19 CA 148065-01
(DRIVE, part of the GAME-ON initiative). This work was also supported,
in part, by the Intramural Research Program of the US National Cancer
Institute, Department of Health and Human Services, USA.
NR 36
TC 6
Z9 6
U1 0
U2 18
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 2013
VL 50
IS 10
BP 666
EP 673
DI 10.1136/jmedgenet-2013-101708
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 221FO
UT WOS:000324643400004
PM 23825393
ER
PT J
AU Wu, F
Kirmaier, A
Ourmanov, I
Goeken, R
Matsuda, K
Whitted, S
Buckler-White, A
Tomioka, K
Plishka, R
Johnson, WE
Hirsch, VM
AF Wu, Fan
Kirmaier, Andrea
Ourmanov, Ilnour
Goeken, Robert
Matsuda, Kenta
Whitted, Sonya
Buckler-White, Alicia
Tomioka, Keiko
Plishka, Ronald
Johnson, Welkin E.
Hirsch, Vanessa M.
TI ESCAPE OF SIVSME543 FROM TRIM5 ALPHA RESTRICTION IN RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Wu, Fan; Ourmanov, Ilnour; Goeken, Robert; Matsuda, Kenta; Whitted, Sonya; Buckler-White, Alicia; Tomioka, Keiko; Plishka, Ronald; Hirsch, Vanessa M.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD USA.
[Kirmaier, Andrea; Johnson, Welkin E.] Harvard Univ, Sch Med, New England Primate Res Ctr, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 1
BP 254
EP 254
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000007
ER
PT J
AU Del Prete, GQ
Scarlotta, M
Kreis, L
Parodi, LM
Roser, JD
Oswald, K
Miller, CJ
Desrosiers, RC
Barouch, DH
Pal, R
Piatak, M
Chertova, E
O'Connor, DH
Giavedoni, LD
Lifson, JD
Keele, BF
AF Del Prete, Gregory Q.
Scarlotta, Matthew
Kreis, Laura
Parodi, Laura M.
Roser, James D.
Oswald, Kelli
Miller, Christopher J.
Desrosiers, Ronald C.
Barouch, Dan H.
Pal, Ranajit
Piatak, Michael, Jr.
Chertova, Elena
O'Connor, David H.
Giavedoni, Luis D.
Lifson, Jeffrey D.
Keele, Brandon F.
TI COMPARATIVE CHARACTERIZATION OF TRANSFECTION-AND INFECTION-DERIVED SIV
CHALLENGE STOCKS FOR IN VIVO NONHUMAN PRIMATE STUDIES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Del Prete, Gregory Q.; Kreis, Laura; Roser, James D.; Oswald, Kelli; Piatak, Michael, Jr.; Chertova, Elena; Lifson, Jeffrey D.; Keele, Brandon F.] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Scarlotta, Matthew; O'Connor, David H.] Univ Wisconsin Madison, Dept Pathol & Lab Med, Wisconsin Natl Primate Res Ctr, Madison, WI USA.
[Miller, Christopher J.] Univ Calif Davis, Ctr Comparat Med, Davis, CA 95616 USA.
[Miller, Christopher J.] Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
[Desrosiers, Ronald C.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, New England Primate Res Ctr, Cambridge, MA 02138 USA.
[O'Connor, David H.] Univ Wisconsin Madison, Wisconsin Natl Primate Res Ctr, Madison, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 3
BP 255
EP 255
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000009
ER
PT J
AU Keele, BF
DelPrete, GQ
Park, H
Reid, C
Oswald, K
Estes, JD
Kahl, C
Macallister, R
Smedley, J
Piatak, M
Lifson, JD
Picker, LJ
AF Keele, Brandon F.
DelPrete, Gregory Q.
Park, Haesun
Reid, Carolyn
Oswald, Kelli
Estes, Jacob D.
Kahl, Christoph
Macallister, Rhonda
Smedley, Jeremy
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Picker, Louis J.
TI SUCCESSFUL IN VIVO TITRATION FOLLOWING INTRARECTAL AND INTRAVENOUS
CHALLENGE WITH MOLECULARLY-TAGGED SIVMAC239 USING 293T TRANSFECTION
PRODUCED VIRUS AND RHPBMC EXPANDED VIRUS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Keele, Brandon F.; DelPrete, Gregory Q.; Reid, Carolyn; Oswald, Kelli; Estes, Jacob D.; Piatak, Michael, Jr.; Lifson, Jeffrey D.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, AIDS & Canc Virus Program, Frederick, MD USA.
[Park, Haesun; Kahl, Christoph; Picker, Louis J.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Oregon Natl Primate Res Ctr, Portland, OR 97201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 10
BP 257
EP 257
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000016
ER
PT J
AU Estes, JD
Brenchley, JM
Vinton, C
Tabb, B
Hao, XP
Connick, E
Pairidini, M
Lifson, JD
Silvestri, G
AF Estes, Jacob D.
Brenchley, Jason M.
Vinton, Carol
Tabb, Brian
Hao, Xing Pei
Connick, Elizabeth
Pairidini, Mirko
Lifson, Jeffrey D.
Silvestri, Guido
TI DIFFERENTIAL INFECTION PATTERNS OF CD4+T CELLS AND LYMPHOID TISSUE VIRAL
BURDEN DISTINGUISH PROGRESSIVE AND NONPROGRESSIVE LENTIVIRAL INFECTIONS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Estes, Jacob D.; Tabb, Brian; Lifson, Jeffrey D.] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Brenchley, Jason M.; Vinton, Carol] NIAID, Program Barrier Immun & Repair, NIH, Bethesda, MD 20892 USA.
[Brenchley, Jason M.; Vinton, Carol] NIAID, Immunopathogenesis Unit, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Brenchley, Jason M.; Vinton, Carol] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Hao, Xing Pei] SAIC Frederick Inc, Pathol & Histotechnol Lab, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Connick, Elizabeth] Univ Colorado Denver, Div Infect Dis, Aurora, CO USA.
[Pairidini, Mirko; Silvestri, Guido] Emory Univ, Div Microbiol & Immunol, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 11
BP 258
EP 258
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000017
ER
PT J
AU Henning, TC
Butler, K
Mitchell, J
Bachman, S
Deyounks, F
Farshy, C
Phillips, C
Papp, J
Caldwell, H
Sturdevant, G
McNicholl, J
Kersh, E
AF Henning, Tara C.
Butler, Katherine
Mitchell, James
Bachman, Shanon
Deyounks, Frank
Farshy, Carol
Phillips, Christi
Papp, John
Caldwell, Harlan
Sturdevant, Gail
McNicholl, Janet
Kersh, Ellen
TI DEVELOPMENT OF A RECTAL SEXUALLY TRANSMITTED INFECTION (STI) - HIV
COINFECTION MACAQUE MODEL UTILIZING CHLAMYDIA TRACHOMATIS AND
SHIVSF162P3
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Henning, Tara C.; Butler, Katherine; Mitchell, James; Bachman, Shanon; Deyounks, Frank; Farshy, Carol; Phillips, Christi; McNicholl, Janet; Kersh, Ellen] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, Atlanta, GA USA.
[Papp, John] Ctr Dis Control & Prevent, Div Sexually Transmitted Dis Prevent, Atlanta, GA USA.
[Caldwell, Harlan; Sturdevant, Gail] NIAID, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 14
BP 259
EP 259
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000020
ER
PT J
AU Okoye, AA
Rohankhedkar, M
Konfe, A
Fukazawa, Y
Lum, R
Park, H
Axthelm, IB
Legasse, A
Axthelm, MK
Oswald, K
Estes, J
Wai, J
Piatak, M
Lifson, JD
Chomont, N
Hazuda, D
Sekaly, RP
Picker, LJ
AF Okoye, Afam A.
Rohankhedkar, Mukta
Konfe, Audrie
Fukazawa, Yoshinori
Lum, Richard
Park, Haesun
Axthelm, Isaac B.
Legasse, Alfred
Axthelm, Michael K.
Oswald, Kelli
Estes, Jacob
Wai, John
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Chomont, Nicolas
Hazuda, Daria
Sekaly, Rafick P.
Picker, Louis J.
TI MODULATION OF THE PD-1 PATHWAY TO ENHANCE VIRUS PRODUCTION AND
ELIMINATION OF LATENTLY INFECTED T CELLS IN SIV-INFECTED RHESUS MACAQUES
ON HIGHLY ACTIVE ANTIRETROVIRAL THERAPY (HAART)
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Okoye, Afam A.; Rohankhedkar, Mukta; Konfe, Audrie; Fukazawa, Yoshinori; Lum, Richard; Park, Haesun; Axthelm, Isaac B.; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR 97006 USA.
[Okoye, Afam A.; Rohankhedkar, Mukta; Konfe, Audrie; Fukazawa, Yoshinori; Lum, Richard; Park, Haesun; Axthelm, Isaac B.; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Beaverton, OR 97006 USA.
[Oswald, Kelli; Estes, Jacob; Piatak, Michael, Jr.; Lifson, Jeffrey D.] Frederick Natl Lab Canc Res, SAIC Frederick, AIDS & Canc Virus Program, Frederick, MD USA.
[Chomont, Nicolas; Sekaly, Rafick P.] Vaccine & Gene Therapy Inst Florida, Port St Lucie, FL 34987 USA.
[Wai, John; Hazuda, Daria] Merck Res Labs, White Horse Junction, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 17
BP 260
EP 260
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000023
ER
PT J
AU DeGottardi, MQ
Okoye, AA
Rohankhedkar, M
Konfe, A
Turner, J
Legasse, A
Estes, J
Piatak, M
Lifson, JD
Axthelm, MK
Picker, LJ
AF DeGottardi, M. Quinn
Okoye, Afam A.
Rohankhedkar, Mukta
Konfe, Audrie
Turner, John
Legasse, Alfred
Estes, Jake
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Axthelm, Michael K.
Picker, Louis J.
TI UNDERSTANDING THE ROLE OF IL-15 IN SIV PATHOGENESIS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [DeGottardi, M. Quinn; Okoye, Afam A.; Rohankhedkar, Mukta; Konfe, Audrie; Turner, John; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR 97006 USA.
[DeGottardi, M. Quinn; Okoye, Afam A.; Rohankhedkar, Mukta; Konfe, Audrie; Turner, John; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Beaverton, OR 97006 USA.
[Estes, Jake; Piatak, Michael, Jr.; Lifson, Jeffrey D.] Frederick Natl Lab Canc Res, SAIC Frederick, AIDS & Canc Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 19
BP 261
EP 261
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000025
ER
PT J
AU Klatt, NR
Canary, LA
Vinton, CL
Morcock, D
Pierce, J
Estes, JD
Brenchley, JM
AF Klatt, Nichole R.
Canary, Lauren A.
Vinton, Carol L.
Morcock, David
Pierce, Jordan
Estes, Jacob D.
Brenchley, Jason M.
TI RATE OF AIDS PROGRESSION IS ASSOCIATED WITH PRE-EXISTING MICROBIAL
TRANSLOCATION IN PIGTAIL MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Klatt, Nichole R.; Canary, Lauren A.; Vinton, Carol L.; Pierce, Jordan; Brenchley, Jason M.] NIAID, Mol Microbiol Lab, Program Barrier Immun & Repair, NIH, Bethesda, MD 20892 USA.
[Morcock, David; Estes, Jacob D.] SAIC Frederick Inc, AIDS Canc & Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 20
BP 261
EP 261
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000026
ER
PT J
AU Breed, MW
Aye, PP
Lichtveld, CF
Midkiff, C
Schiro, F
Zelman, S
Jordan, APO
Sugimoto, C
Alvarez, X
Sandler, NG
Douek, DC
Kuroda, MJ
Pahar, B
Piatak, M
Lifson, JD
Keele, BF
Lackner, AA
Hoxie, JA
AF Breed, Matthew W.
Aye, Pyone P.
Lichtveld, Cornelis F.
Midkiff, Cecily
Schiro, Faith
Zelman, Samra
Jordan, Andrea P. O.
Sugimoto, Chie
Alvarez, Xavier
Sandler, Netanya G.
Douek, Daniel C.
Kuroda, Marcelo J.
Pahar, Bapi
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Keele, Brandon F.
Lackner, Andrew A.
Hoxie, James A.
TI ELITE CONTROL AND PROTECTION FROM A PATHOGENIC HETEROLOGOUS SIV
CHALLENGE IN PIGTAIL MACAQUES INFECTED WITH A CYTOPLASMIC TAIL MUTANT OF
SIVMAC239
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Breed, Matthew W.; Aye, Pyone P.; Lichtveld, Cornelis F.; Midkiff, Cecily; Schiro, Faith; Sugimoto, Chie; Alvarez, Xavier; Kuroda, Marcelo J.; Pahar, Bapi; Lackner, Andrew A.] Tulane Natl Primate Res Ctr, Covington, LA USA.
[Zelman, Samra; Jordan, Andrea P. O.; Hoxie, James A.] Univ Penn, Philadelphia, PA 19104 USA.
[Sandler, Netanya G.; Douek, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.; Keele, Brandon F.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 25
BP 263
EP 263
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000031
ER
PT J
AU Demberg, T
Brocca-Cofano, E
Xiao, P
Venzon, D
Vargas-Inchaustegui, D
Lee, EM
Kalisz, I
Kalyanaraman, VS
DiPasquale, J
McKinnon, K
Robert-Guroff, M
AF Demberg, Thorsten
Brocca-Cofano, Egidio
Xiao, Peng
Venzon, David
Vargas-Inchaustegui, Diego
Lee, Eun Mi
Kalisz, Irene
Kalyanaraman, V. S.
DiPasquale, Janet
McKinnon, Katherine
Robert-Guroff, Marjorie
TI MEMORY B-CELL POPULATIONS DURING ANTIRETROVIRAL THERAPY AND THERAPEUTIC
ENVELOPE BOOSTING IN SIVMAC251-INFECTED RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Demberg, Thorsten; Brocca-Cofano, Egidio; Xiao, Peng; Vargas-Inchaustegui, Diego; DiPasquale, Janet; McKinnon, Katherine; Robert-Guroff, Marjorie] NCI, Vaccine Branch, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Lee, Eun Mi; Kalisz, Irene; Kalyanaraman, V. S.] Adv BioSci Labs Inc, Rockville, MD 20850 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 32
BP 265
EP 265
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000038
ER
PT J
AU Shingai, M
Donau, OK
Schmidt, SD
Gautam, R
Plishka, RJ
Buckler-White, A
Sadjadpour, R
Lee, W
LaBranche, CC
Montefiori, D
Mascola, JR
Nishimura, Y
Martin, MA
AF Shingai, Masashi
Donau, Olivia K.
Schmidt, Stephen D.
Gautam, Rajeev
Plishka, Ronald J.
Buckler-White, Alicia
Sadjadpour, Reza
Lee, Wendy
LaBranche, Celia C.
Montefiori, David
Mascola, John R.
Nishimura, Yoshiaki
Martin, Malcolm A.
TI THE VAST MAJORITY OF RHESUS MACAQUES INFECTED WITH THE R5-TROPIC SHIVAD8
GENERATE CROSS-REACTIVE ANTIBODIES THAT NEUTRALIZE MULTIPLE HIV-1
STRAINS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Shingai, Masashi; Donau, Olivia K.; Gautam, Rajeev; Plishka, Ronald J.; Buckler-White, Alicia; Sadjadpour, Reza; Lee, Wendy; Nishimura, Yoshiaki; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD USA.
[Schmidt, Stephen D.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[LaBranche, Celia C.; Montefiori, David] Duke Univ, Dept Surg, Med Ctr, Durham, NC 27706 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 43
BP 269
EP 269
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000049
ER
PT J
AU Ayala, VI
Barsov, EV
Trivett, MT
Jain, S
Ott, DE
Ohlen, C
AF Ayala, Victor I.
Barsov, Eugene V.
Trivett, Matthew T.
Jain, Sumiti
Ott, David E.
Ohlen, Claes
TI TRANSDUCTION OF AN SIV SPECIFIC TCR INTO DIFFERENT RHESUS CD3+T CELL
POPULATIONS AND COMPARISON OF THEIR ABILITY TO SUPPRESS SIV INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Ayala, Victor I.; Barsov, Eugene V.; Trivett, Matthew T.; Jain, Sumiti; Ott, David E.; Ohlen, Claes] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 50
BP 271
EP 272
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000056
ER
PT J
AU Foulds, KE
Donaldson, MM
Kao, SF
Quinn, DS
Fischer, W
Korber, BT
Letvin, NL
Koup, RA
Rao, SS
Mascola, JR
Nabel, GJ
Roederer, M
AF Foulds, Kathryn E.
Donaldson, Mitzi M.
Kao, Shing-Fen
Quinn, David S.
Fischer, Will
Korber, Bette T.
Letvin, Norman L.
Koup, Richard A.
Rao, Srinivas S.
Mascola, John R.
Nabel, Gary J.
Roederer, Mario
TI IMMUNOGENICITY OF SIV ENV AND GAG MOSAIC CONSTRUCTS IN RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Foulds, Kathryn E.; Donaldson, Mitzi M.; Kao, Shing-Fen; Quinn, David S.; Koup, Richard A.; Rao, Srinivas S.; Mascola, John R.; Nabel, Gary J.; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Fischer, Will; Korber, Bette T.] Los Alamos Natl Lab, Los Alamos, NM USA.
[Letvin, Norman L.] Harvard Univ, Beth Israel Deaconess Med Ctr, Med School, Div Viral Pathogenesis,Dept Med, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 48
BP 271
EP 271
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000054
ER
PT J
AU Gautam, R
Nishimura, Y
Lee, WR
Donau, O
Buckler-White, A
Shingai, M
Sadjadpour, R
Schmidt, SD
LaBranche, CC
Keele, BF
Montefiori, D
Mascola, JR
Martin, MA
AF Gautam, Rajeev
Nishimura, Yoshiaki
Lee, Wendy R.
Donau, Olivia
Buckler-White, Alicia
Shingai, Masashi
Sadjadpour, Reza
Schmidt, Stephen D.
LaBranche, Celia C.
Keele, Brandon F.
Montefiori, David
Mascola, John R.
Martin, Malcolm A.
TI PATHOGENICITY AND MUCOSAL TRANSMISSIBILITY OF R5-TROPIC SIMIAN/HUMAN
IMMUNODEFICIENCY VIRUSES SHIVAD8 IN RHESUS MACAQUES: IMPLICATIONS FOR
THEIR USE IN VACCINE STUDIES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Gautam, Rajeev; Nishimura, Yoshiaki; Lee, Wendy R.; Donau, Olivia; Buckler-White, Alicia; Shingai, Masashi; Sadjadpour, Reza; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD USA.
[Schmidt, Stephen D.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Keele, Brandon F.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, AIDS & Canc Virus Program, Frederick, MD USA.
[LaBranche, Celia C.; Montefiori, David] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27706 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 59
BP 274
EP 274
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000065
ER
PT J
AU Jain, S
Ayala, VI
Trivett, MT
Barsov, EV
Ohlen, C
Ott, DE
AF Jain, Sumiti
Ayala, Victor I.
Trivett, Matthew T.
Barsov, Eugene V.
Ohlen, Claes
Ott, David E.
TI USING TRIM5 alpha TO PRODUCE DURABLE ANTI-VIRAL CD4+EFFECTOR T CELLS FOR
BOTH IN VITRO AND IN VIVO SIV SUPPRESSION STUDIES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Jain, Sumiti; Ayala, Victor I.; Trivett, Matthew T.; Barsov, Eugene V.; Ohlen, Claes; Ott, David E.] SAIC Frederick Inc, AIDS & Canc Vaccine Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 68
BP 277
EP 277
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000074
ER
PT J
AU Matsuda, K
Brown, CR
Foley, B
Goeken, R
Whitted, S
Dang, Q
Wu, F
Plishka, R
White, AB
Hirsch, VM
AF Matsuda, Kenta
Brown, Charles R.
Foley, Brian
Goeken, Robert
Whitted, Sonya
Dang, Que
Wu, Fan
Plishka, Ronald
White, Alicia-Buckler
Hirsch, Vanessa M.
TI LASER CAPTURE MICRODISSECTION STUDY OF VIRAL POPULATIONS IN THE CENTRAL
NERVOUS SYSTEM OF MACAQUES WITH SIV ENCEPHALITIS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Matsuda, Kenta; Brown, Charles R.; Goeken, Robert; Whitted, Sonya; Dang, Que; Wu, Fan; Plishka, Ronald; White, Alicia-Buckler; Hirsch, Vanessa M.] NIH, Bethesda, MD USA.
[Foley, Brian] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 73
BP 278
EP 279
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000079
ER
PT J
AU Patterson, J
McKinnon, K
Parish, S
Berzofsky, J
Robert-Guroff, M
Terabe, M
AF Patterson, Jean
McKinnon, Kathy
Parish, Stan
Berzofsky, Jay
Robert-Guroff, Marjorie
Terabe, Masaki
TI FUNCTIONAL NKT AND B CELLS IN THE BONE MARROW ARE ASSOCIATED WITH
CONTROL OF SIV INFECTION IN THE RHESUS MACAQUE MODEL OF AIDS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Patterson, Jean; McKinnon, Kathy; Robert-Guroff, Marjorie] NCI, Sect Immune Biol Retroviral Infect, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Parish, Stan; Berzofsky, Jay; Terabe, Masaki] NCI, Mol Genet & Vaccine Res Sect, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 75
BP 279
EP 279
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000081
ER
PT J
AU Warrier, R
Barouch, DH
Miller, CJ
Hahn, BH
Shaw, GM
Keele, BF
AF Warrier, Ranjit
Barouch, Dan H.
Miller, Christopher J.
Hahn, Beatrice H.
Shaw, George M.
Keele, Brandon F.
TI NO EVIDENCE OF UNIDENTIFIED TRANSMITTED/FOUNDER VARIANTS IN RHESUS
MACAQUES UP TO SIX MONTHS POST-INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Warrier, Ranjit; Hahn, Beatrice H.; Shaw, George M.] Univ Penn, Philadelphia, PA 19104 USA.
[Barouch, Dan H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Miller, Christopher J.] Univ Calif Davis, Davis, CA 95616 USA.
[Keele, Brandon F.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0047-2565
EI 1600-0684
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD OCT
PY 2013
VL 42
IS 5
MA 91
BP 284
EP 284
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 217BR
UT WOS:000324332000097
ER
PT J
AU Anderson, C
von Geldern, G
Johnson, T
Sacktor, N
McArthur, J
Nath, A
AF Anderson, Caroline
von Geldern, Gloria
Johnson, Tory
Sacktor, Ned
McArthur, Justin
Nath, Avindra
TI Accumulation of neurofilament heavy chain in neurons and CSF of HIV
patients on antiretroviral drugs with normal neurocognitive function
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Anderson, Caroline; von Geldern, Gloria; Johnson, Tory; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
[Sacktor, Ned; McArthur, Justin] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
EM caroline.anderson2@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P9
BP S4
EP S5
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200010
ER
PT J
AU Anderson, M
Enose-Akahata, Y
Massoud, R
Ngouth, N
Tanaka, Y
Oh, U
Jacobson, S
AF Anderson, Monique
Enose-Akahata, Yoshimi
Massoud, Raya
Ngouth, Nyater
Tanaka, Yuetsu
Oh, Unsong
Jacobson, Steven
TI HTLV-1 epigenetic modification of the FoxP3 TSDR in HAM/TSP decreases
the functional proliferative suppression of Tregs
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Anderson, Monique] NINDS, Neuroimmunol Branch, NIH, UVA, Bethesda, MD 20892 USA.
[Enose-Akahata, Yoshimi; Massoud, Raya; Ngouth, Nyater; Jacobson, Steven] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Oh, Unsong] Virginia Commonwealth Univ, Dept Neurol, Richmond, VA 23284 USA.
EM andersonmr2@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P10
BP S5
EP S5
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200011
ER
PT J
AU Bae, M
Bandaru, VVR
Lee, M
Nath, A
Chen, XS
Geiger, JD
Gorospe, MM
Mattson, MP
Haughey, N
AF Bae, Mihyun
Bandaru, Veera Venkata Ratnam
Lee, Myounghwa
Nath, Avindra
Chen, Xuesong
Geiger, Jonathan D.
Gorospe, Myriam M.
Mattson, Mark P.
Haughey, Norman
TI Activation of TRPML1 clears intraneuronal Abeta in pre-clinical models
of HIV infection
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Bae, Mihyun; Bandaru, Veera Venkata Ratnam; Haughey, Norman] Johns Hopkins Univ, Sch Med, Dept Neurol, Div Neuroimmunol & Neurol Infect, Baltimore, MD 21205 USA.
[Lee, Myounghwa; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
[Chen, Xuesong; Geiger, Jonathan D.] Univ N Dakota, Sch Med & Hlth Sci, Dept Pharmacol Physiol & Therapeut, Grand Forks, ND 58201 USA.
[Gorospe, Myriam M.] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Mattson, Mark P.] NIA, Lab Neurosci, NIH, Baltimore, MD 21224 USA.
EM mbae002@gmail.com
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P15
BP S7
EP S7
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200016
ER
PT J
AU Billioux, BJ
Leibovitch, E
Brunetto, G
Dustin, IM
Inati, S
Schreiber, J
Eze, C
Zaghloul, K
Jacobson, S
Theodore, WH
AF Billioux, Bridgette Jeanne
Leibovitch, Emily
Brunetto, Giovanna
Dustin, Irene M.
Inati, Sarah
Schreiber, John
Eze, Chigo
Zaghloul, Kareem
Jacobson, Steve
Theodore, William H.
TI Human Herpes Virus 6 in Human Epilepsy: Data from Surgical Resections
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Billioux, Bridgette Jeanne; Leibovitch, Emily; Brunetto, Giovanna; Jacobson, Steve] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Dustin, Irene M.; Schreiber, John; Eze, Chigo; Theodore, William H.] NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA.
[Inati, Sarah] NINDS, EEG Lab, NIH, Bethesda, MD 20892 USA.
[Zaghloul, Kareem] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
EM bridgette.billioux@nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P28
BP S14
EP S14
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200029
ER
PT J
AU Bora, A
Mohien, CU
Chaerkady, R
Chang, LD
Moxley, R
Sacktor, N
McArthur, JC
Haughey, N
Nath, A
Graham, DR
AF Bora, Adriana
Mohien, Ceereena Ubaida
Chaerkady, Raghothama
Chang, Linda
Moxley, Richard
Sacktor, Ned
McArthur, Justin C.
Haughey, Norm
Nath, Avindra
Graham, David R.
TI Proteomics evaluation of CSF patients with HIV-associated neurocognitive
impairment using iTRAQ labeling
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Bora, Adriana; Moxley, Richard; Sacktor, Ned; McArthur, Justin C.; Haughey, Norm] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
[Mohien, Ceereena Ubaida; Graham, David R.] Johns Hopkins Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD USA.
[Chaerkady, Raghothama] Johns Hopkins Sch Med, Prote Core Facil, Baltimore, MD USA.
[Chang, Linda] Univ Hawaii, John A Burns Sch Med, Dept Med, Honolulu, HI 96822 USA.
[Nath, Avindra] NINDS, NIH, Bethesda, MD 20892 USA.
EM abora1@jhmi.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P31
BP S15
EP S16
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200032
ER
PT J
AU Byrareddy, S
Thorat, S
Sharma, P
Hemashettar, GH
Matsuda, K
Hirsch, V
Girolami, U
Novembre, F
Villinger, F
Ruprecht, R
AF Byrareddy, Siddappa
Thorat, Swati
Sharma, Prachi
Hemashettar, Girish Hemashettar
Matsuda, Kenta
Hirsch, Vanessa
Girolami, Umberto
Novembre, Francis
Villinger, Francois
Ruprecht, Ruth
TI Macrophage/microglia lineage-related R5-tropic simian-human
immunodeficiency viruses as tools to induce and study HAND
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Byrareddy, Siddappa; Villinger, Francois] Emory Univ, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Byrareddy, Siddappa; Thorat, Swati; Hemashettar, Girish Hemashettar; Ruprecht, Ruth] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Byrareddy, Siddappa; Thorat, Swati; Hemashettar, Girish Hemashettar; Ruprecht, Ruth] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Sharma, Prachi; Novembre, Francis; Villinger, Francois] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Matsuda, Kenta; Hirsch, Vanessa] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD USA.
[Girolami, Umberto] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
EM siddappa.n.byrareddy@emory.edu
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P34
BP S17
EP S17
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200035
ER
PT J
AU Caruso, B
Brunetto, G
Massoud, R
Switzer, B
Jacobson, S
AF Caruso, Breanna
Brunetto, Giovanna
Massoud, Raya
Switzer, Bill
Jacobson, Steven
TI Digital Droplet PCR for Precise Quantification of Human T-Lymphotropic
Virus 1
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Caruso, Breanna; Brunetto, Giovanna; Massoud, Raya; Jacobson, Steven] NINDS, NIB, NIH, Bethesda, MD 20892 USA.
[Switzer, Bill] CDC, NCHHSTP, OID, Atlanta, GA 30333 USA.
EM breanna.caruso@nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P38
BP S19
EP S19
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200039
ER
PT J
AU Enose-Akahata, Y
Massoud, R
Virtanen, J
Jacobson, S
AF Enose-Akahata, Yoshimi
Massoud, Raya
Virtanen, Jussi
Jacobson, Steven
TI Correlation of increased CXCL13/IL-21 with intrathecal humoral immune
responses to HTLV-1 in CSF of patients with HAM/TSP
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Enose-Akahata, Yoshimi; Massoud, Raya; Virtanen, Jussi; Jacobson, Steven] NINDS, Viral Immunol Sect, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
EM akahatay@ninds.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P54
BP S26
EP S26
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200055
ER
PT J
AU Ferenczy, M
Johnson, K
Major, E
AF Ferenczy, Michael
Johnson, Kory
Major, Eugene
TI Cell culture and bioinformatic identification of putative progressive
multifocal leukoencephalopathy risk factors
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Ferenczy, Michael; Major, Eugene] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
[Johnson, Kory] NINDS, Bioinformat Sect, NIH, Bethesda, MD 20892 USA.
EM michael.ferenczy@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P59
BP S28
EP S29
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200060
ER
PT J
AU Gerena, Y
Menendez-Delmestre, R
Skolasky, R
Hechavarria, R
Perez, S
Hilera, C
Gonzalez, C
Nath, A
Wojna, V
AF Gerena, Yamil
Menendez-Delmestre, Raissa
Skolasky, Richard
Hechavarria, Rosa
Perez, Sebastian
Hilera, Claudia
Gonzalez, Claribel
Nath, Avindra
Wojna, Valerie
TI Higher Levels of Plasma Soluble Insulin-Like Growth Factor-1 Receptor
are Associated with Severity of HAND in HIV-seropositive Women
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Gerena, Yamil] Univ Puerto Rico Med Sci Campus, NeuroAIDS Res Program, Dept Pharmaceut Sci, San Juan, PR USA.
[Gerena, Yamil] Univ Puerto Rico Med Sci Campus, NeuroAIDS Res Program, Dept Pharmacol, San Juan, PR USA.
[Menendez-Delmestre, Raissa; Gonzalez, Claribel] Univ Puerto Rico Med Sci Campus, NeuroAIDS Res Program, San Juan, PR USA.
[Skolasky, Richard] Johns Hopkins Univ, Dept Orthopaed Surg, Baltimore, MD USA.
[Hechavarria, Rosa] Univ Puerto Rico Med Sci Campus, NeuroAIDS Res Program, Dept Phys Med & Rehabil, San Juan, PR USA.
[Perez, Sebastian] Univ Puerto Rico Med Sci Campus, Sch Med, San Juan, PR USA.
[Hilera, Claudia] Univ Puerto Rico Rio Piedras Campus, Dept Biol, San Juan, PR USA.
[Nath, Avindra] NINDS, NIH, Bethesda, MD 20892 USA.
[Wojna, Valerie] Univ Puerto Rico Med Sci Campus, NeuroAIDS Res Program, Div Neurol, Dept Internal Med, San Juan, PR USA.
EM yamil.gerena@upr.edu
NR 0
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P67
BP S32
EP S32
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200068
ER
PT J
AU Hategan, AP
Steiner, J
Dimitriadis, E
Nath, A
AF Hategan, Alina Popescu
Steiner, Joseph
Dimitriadis, Emilios
Nath, Avindra
TI HIV-Tat protein enhances amyloid beta aggregation
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Hategan, Alina Popescu; Steiner, Joseph; Nath, Avindra] NINDS, NIH, Sect Infect Nervous Syst, Bethesda, MD 20892 USA.
NIBIB, NIH, Scanning Probe Microscopy Unit, Bethesda, MD USA.
EM alina.popescu@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P140
BP S66
EP S66
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200141
ER
PT J
AU Herz, J
McGavern, D
AF Herz, Jasmin
McGavern, Dorian
TI Therapeutic Clearance of the Virally Infected Nervous System is Mediated
by Noncytopathic T cell interactions with Resident Microglia
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Herz, Jasmin; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
EM herzjn@mail.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P78
BP S37
EP S38
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200079
ER
PT J
AU Iordanskiy, S
Van Duyne, R
Sampey, G
Fry, K
Romerio, F
Kashanchi, F
AF Iordanskiy, Sergey
Van Duyne, Rachel
Sampey, Gavin
Fry, Kelsi
Romerio, Fabio
Kashanchi, Fatah
TI Irradiation-induced cellular stress activates virus replication and
apoptosis in HIV-1 infected macrophage model cells and in the brain of
infected humanized mice
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Iordanskiy, Sergey; Van Duyne, Rachel; Sampey, Gavin; Fry, Kelsi; Kashanchi, Fatah] George Mason Univ, Natl Ctr Biodef & Infect Dis, Dept Mol & Microbiol, Fairfax, VA 22030 USA.
[Van Duyne, Rachel] NCI, Virus Cell Interact Sect, HIV Drug Resistance Program, NIH, Bethesda, MD 20892 USA.
[Romerio, Fabio] Univ Maryland, Sch Med, Inst Human Virol, Baltimore, MD 21201 USA.
EM siord6@gmail.com
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P81
BP S39
EP S39
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200082
ER
PT J
AU Johnson, T
von Geldern, G
Tyagi, R
Sacktor, N
McArthur, J
Letendre, S
Hasbun, R
Petito, C
Roh, D
Verma, A
Nath, A
AF Johnson, Tory
von Geldern, Gloria
Tyagi, Richa
Sacktor, Ned
McArthur, Justin
Letendre, Scott
Hasbun, Rodrigo
Petito, Carol
Roh, David
Verma, Ashok
Nath, Avindra
TI Detection of HIV-Tat protein in brain and CSF of patients on
antiretroviral therapy
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Johnson, Tory; von Geldern, Gloria; Tyagi, Richa; Nath, Avindra] NINDS, NIH, Bethesda, MD 20892 USA.
[Sacktor, Ned; McArthur, Justin] Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA.
[Letendre, Scott] Univ Calif San Diego, San Diego, CA 92103 USA.
[Hasbun, Rodrigo] Univ Texas Houston, Houston, TX USA.
[Petito, Carol; Roh, David; Verma, Ashok] Univ Miami, Jackson Mem Hosp, Coral Gables, FL 33124 USA.
EM tory.johnson@nih.gov
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P84
BP S40
EP S41
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200085
ER
PT J
AU Leibovitch, E
Brunetto, G
Caruso, B
Fenton, K
Ohayon, J
Reich, D
Jacobson, S
AF Leibovitch, Emily
Brunetto, Giovanna
Caruso, Breanna
Fenton, Kaylan
Ohayon, Joan
Reich, Daniel
Jacobson, Steven
TI Coinfection of human herpesviruses 6A (HHV-6A) and HHV-6B demonstrated
by digital droplet PCR
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Leibovitch, Emily; Brunetto, Giovanna; Caruso, Breanna; Fenton, Kaylan; Ohayon, Joan; Reich, Daniel; Jacobson, Steven] NINDS, NIH, Bethesda, MD 20892 USA.
EM emily.leibovitch@nih.gov
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P101
BP S48
EP S49
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200102
ER
PT J
AU Li, WX
Tyagi, R
Henderson, L
Nath, A
AF Li, Wenxue
Tyagi, Richa
Henderson, Lisa
Nath, Avindra
TI Activation of HERV-K expression in the brain of ALS patients
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Li, Wenxue; Tyagi, Richa; Henderson, Lisa; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
EM liw8@mail.nih.gov
NR 0
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P103
BP S49
EP S50
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200104
ER
PT J
AU Liu, W
Massoud, R
Reich, D
Nair, G
Jacobson, S
AF Liu, Winston
Massoud, Raya
Reich, Daniel
Nair, Govind
Jacobson, Steve
TI Quantifying Spinal Cord Cross-sectional Area in HTLV-1 Associated
Myelopathy/Tropical Spastic Paraparesis and Multiple Sclerosis
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Liu, Winston; Massoud, Raya; Reich, Daniel; Nair, Govind; Jacobson, Steve] NINDS, Bethesda, MD 20892 USA.
EM winston.w.liu@gmail.com
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P104
BP S50
EP S50
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200105
ER
PT J
AU Massoud, R
Enose-Akahata, Y
Ohayon, J
Fenton, K
Cortese, I
Jacobson, S
Waldmann, T
AF Massoud, Raya
Enose-Akahata, Yoshimi
Ohayon, Joan
Fenton, Kaylan
Cortese, Irene
Jacobson, Steven
Waldmann, Thomas
TI Clinical trial of a humanized monoclonal anti-IL15Rbeta (CD122)
antibody, in HTLV-1 associated myelopathy/tropical spastic paraparesis
(HAM/TSP)
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Massoud, Raya; Enose-Akahata, Yoshimi; Ohayon, Joan; Fenton, Kaylan; Cortese, Irene; Jacobson, Steven] NINDS, NIH, Bethesda, MD 20892 USA.
[Waldmann, Thomas] NCI, NIH, Bethesda, MD 20892 USA.
EM raya.massoud@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P113
BP S54
EP S54
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200114
ER
PT J
AU Nayak, D
McGavern, D
AF Nayak, Debasis
McGavern, Dorian
TI Tetherin is critical for the resolution of a persistent viral infection
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Nayak, Debasis; McGavern, Dorian] NINDS, NIH, Bethesda, MD 20892 USA.
EM nayakdn@ninds.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P131
BP S62
EP S63
PG 2
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200132
ER
PT J
AU Park, M
Tran, T
El Baz, R
Cuconati, A
Arthos, J
Duffy, C
Chaiken, I
Schnur, D
Song, FB
Lam, P
Reynolds, C
Reitz, A
Khan, Z
Jain, P
AF Park, Michael
Thuong Tran
El Baz, Rasha
Cuconati, Andrea
Arthos, James
Duffy, Caitlin
Chaiken, Irwin
Schnur, Dora
Song, Fengbin
Lam, Patrick
Reynolds, Charles
Reitz, Allen
Khan, Zafar
Jain, Pooja
TI DC-SIGN as potential target for early intervention and transmission of
HIV-1
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Park, Michael; Thuong Tran; El Baz, Rasha; Khan, Zafar; Jain, Pooja] Drexel Univ, Coll Med, Drexel Inst Biotechnol & Virol Res, Philadelphia, PA USA.
[Park, Michael; Thuong Tran; El Baz, Rasha; Khan, Zafar; Jain, Pooja] Drexel Univ, Coll Med, Dept Microbiol & Immunol, Philadelphia, PA USA.
[Cuconati, Andrea; Song, Fengbin; Reynolds, Charles] Hepatitis B Fdn, Inst Hepatitis & Virus Res, Philadelphia, PA USA.
[Arthos, James] NIAID, Lab Immunoregulat, Boston, MA USA.
[Duffy, Caitlin; Chaiken, Irwin] Drexel Univ, Coll Med, Dept Biochem & Mol Biol, Philadelphia, PA USA.
EM zafar.khan@drexelmed.edu
NR 0
TC 0
Z9 0
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P135
BP S64
EP S64
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200136
ER
PT J
AU Sagar, D
Masih, S
Schell, T
Jacobson, S
Wigdahl, B
Jain, P
Khan, Z
AF Sagar, Divya
Masih, Shet
Schell, Todd
Jacobson, Steven
Wigdahl, Brian
Jain, Pooja
Khan, Zafar
TI In vivo immunogenicity of Tax 11-19 epitope in HLA-A2/DTR transgenic
mice: implication for dendritic cell-based anti-HTLV-1 vaccine
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Sagar, Divya; Masih, Shet; Jain, Pooja; Khan, Zafar] Drexel Univ, Coll Med, Dept Microbiol & Immunol, Philadelphia, PA USA.
[Schell, Todd] Penn State Univ, Coll Med, Dept Microbiol & Immunol, University Pk, PA 16802 USA.
[Jacobson, Steven] NIH, Viral Immunol Sect, Neuroimmunol Branch, Bethesda, MD USA.
[Wigdahl, Brian] Drexel Univ, Inst Mol Med & Infect Dis, Dept Microbiol & Immunol, Ctr Mol Virol & Translat Neurosci,Coll Med, Philadelphia, PA USA.
EM pooja.jain@drexelmed.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P149
BP S70
EP S70
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200150
ER
PT J
AU Taylor, K
Woods, T
Peterson, K
AF Taylor, Katherine
Woods, Tyson
Peterson, Karin
TI Innate immune induced neuronal death during bunyavirus infection is
mediated by SARM
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Taylor, Katherine; Woods, Tyson; Peterson, Karin] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Bethesda, MD 20892 USA.
EM petersonka@niaid.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P173
BP S81
EP S81
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200174
ER
PT J
AU Taylor, K
Woods, T
Winkler, C
Peterson, K
AF Taylor, Katherine
Woods, Tyson
Winkler, Clayton
Peterson, Karin
TI Age-dependent susceptibility to La Crosse Virus-induced neurological
disease mediated by TLR3/RLR signaling pathways
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Taylor, Katherine; Woods, Tyson; Winkler, Clayton; Peterson, Karin] NIH, Rocky Mt Lab, LPVD, Neuroimmunol Unity, Bethesda, MD 20892 USA.
EM katherine.taylor@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P172
BP S81
EP S81
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200173
ER
PT J
AU Tyagi, R
Li, WX
Parades, D
Nath, A
AF Tyagi, Richa
Li, Wenxue
Parades, Danelvis
Nath, Avindra
TI Recycling HIVAntiretrovirals for inhibition of Human Endogenous
Retrovirus-K
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Tyagi, Richa; Li, Wenxue; Parades, Danelvis; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
EM tyagi.richa@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P179
BP S84
EP S84
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200180
ER
PT J
AU Virtanen, JO
Enose-Akahata, Y
Massoud, R
Jacobson, S
AF Virtanen, Jussi Oskari
Enose-Akahata, Yoshimi
Massoud, Raya
Jacobson, Steven
TI Intrathecal immune response to HTLV-1 antigens in HAM/TSP
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Virtanen, Jussi Oskari; Enose-Akahata, Yoshimi; Massoud, Raya; Jacobson, Steven] NINDS, NIH, Bethesda, MD 20892 USA.
EM virtanenjo@ninds.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P185
BP S87
EP S87
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200186
ER
PT J
AU Virtanen, JO
Kowalak, J
Leibovitch, E
Lee, N
Enose-Akahata, Y
Jacobson, S
AF Virtanen, Jussi Oskari
Kowalak, Jeffrey
Leibovitch, Emily
Lee, Naomi
Enose-Akahata, Yoshimi
Jacobson, Steve
TI Virus-induced cellular targets for intrathecal autoimmunity in multiple
sclerosis
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Virtanen, Jussi Oskari; Kowalak, Jeffrey; Leibovitch, Emily; Lee, Naomi; Enose-Akahata, Yoshimi; Jacobson, Steve] NINDS, NIH, Bethesda, MD 20892 USA.
[Kowalak, Jeffrey] NIMH, Bethesda, MD USA.
EM virtanenjo@ninds.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P184
BP S86
EP S86
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200185
ER
PT J
AU Winkler, C
Woods, T
Peterson, KE
AF Winkler, Clayton
Woods, Tyson
Peterson, Karin E.
TI Leukocyte CNS infiltration precedes neurological disease following La
Crosse virus infection
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Meeting Abstract
CT 12th International Symposium on NeuroVirology
CY OCT 29-NOV 02, 2013
CL Washington, DC
C1 [Winkler, Clayton; Woods, Tyson; Peterson, Karin E.] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Bethesda, MD USA.
EM clayton.winkler@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
SU 1
MA P192
BP S90
EP S90
PG 1
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 236EM
UT WOS:000325777200193
ER
PT J
AU Benzo, R
Siemion, W
Novotny, P
Sternberg, A
Kaplan, RM
Ries, A
Wise, R
Martinez, F
Utz, J
Sciurba, F
AF Benzo, Roberto
Siemion, Wendy
Novotny, Paul
Sternberg, Alice
Kaplan, Robert M.
Ries, Andrew
Wise, Robert
Martinez, Fernando
Utz, James
Sciurba, Frank
CA Natl Emphysema Treatment Trial NET
TI Factors to Inform Clinicians About the End of Life in Severe Chronic
Obstructive Pulmonary Disease
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Chronic obstructive pulmonary disease; severe COPD; end-stage COPD;
palliative care; end-of-life care; gait speed; mortality; prediction
tools
ID AIR-FLOW OBSTRUCTION; OF-LIFE; PALLIATIVE CARE; SEVERE COPD;
PHYSICAL-ACTIVITY; SEVERE EMPHYSEMA; HEALTH-STATUS; GAIT SPEED;
MORTALITY; HOSPITALIZATION
AB Context. Palliative services have historically been offered to terminal patients with cancer, but much less so in other chronic illnesses such as chronic obstructive pulmonary disease (COPD) because of difficulties in predicting the trajectory to death.
Objectives. The goal of this study was to determine if the change over time of the key parameters (trajectory) in patients with severe COPD can independently predict short-term mortality.
Methods. We analyzed data from 1218 patients with severe COPD. Multivariate models for trajectory change were used to forecast mortality at 12 months.
Results. Changes in several variables by defined cutpoints increase significantly and independently the odds of dying in 12 months. The earliest and strongest predictors were the decrease in gait speed by 0.14 m/s or six-minute walk by 50 m (odds ratio [OR] 4.40, P < 0.0001). Alternatively, if six-minute walk or gait speed were not used, change toward perceiving a very sedentary state using a single question (OR 3.56, P=0.0007) and decrease in maximal inspiratory pressure greater than 11 cmH(2)O (OR 2.19, P=0.0217) were predictive, followed by change toward feeling upset or downhearted (OR 2.44, P=0.0250), decrease in room air resting partial pressure of oxygen greater than 5 mmHg (OR 2.46, P=0.0156), and increase in room air resting partial pressure of carbon dioxide greater than 3 mmHg (OR 2.8, P=0.0039). Change over time models were more discriminative (higher c-statistics) than change from baseline models.
Conclusion. The changes in defined variables and patient-reported outcomes by defined cutpoints were independently associated with increased 12-month mortality in patients with severe COPD. These results may inform clinicians when to initiate end-of-life communications and palliative care. (C) 2013 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.
C1 [Benzo, Roberto; Siemion, Wendy; Utz, James] Mayo Clin, Dept Med, Rochester, MN 55902 USA.
[Novotny, Paul] Mayo Clin, Ctr Canc, Rochester, MN 55902 USA.
[Sternberg, Alice] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Wise, Robert] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[Kaplan, Robert M.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Ries, Andrew] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Martinez, Fernando] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
[Sciurba, Frank] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
RP Benzo, R (reprint author), Mayo Clin, Dept Med, Div Pulm & Crit Care, Mindful Breathing Lab, 200 1st St SW, Rochester, MN 55902 USA.
EM benzo.roberto@mayo.edu
OI Wise, Robert/0000-0002-8353-2349
FU National Heart Lung and Blood Institute, National Institutes of Health
[1R01CA163293-01]; National Heart, Lung, and Blood Institute
[N01HR76101, N01HR76102, N01HR76103, N01HR76104, N01HR76105, N01HR76106,
N01HR76107, N01HR76108, N01HR76109, N01HR76110,, N01HR76111, N01HR76112,
N01HR76113, N01HR76114, N01HR76115, N01HR76116, N01HR76118, N01HR76119];
Centers for Medicare and Medicaid Services (formerly the Health Care
Financing Administration); Agency for Healthcare Research and Quality
FX Dr. Benzo is supportedby grant 1R01CA163293-01 from the National Heart
Lung and Blood Institute, National Institutes of Health. The National
Emphysema Treatment Trial (NETT) is supported by contracts with the
National Heart, Lung, and Blood Institute (N01HR76101, N01HR76102,
N01HR76103, N01HR76104, N01HR76105, N01HR76106, N01HR76107, N01HR76108,
N01HR76109, N01HR76110, N01HR76111, N01HR76112, N01HR76113, N01HR76114,
N01HR76115, N01HR76116, N01HR76118, and N01HR76119), the Centers for
Medicare and Medicaid Services (formerly the Health Care Financing
Administration), and the Agency for Healthcare Research and Quality. The
authors declare no conflicts of interest.
NR 30
TC 13
Z9 13
U1 2
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD OCT
PY 2013
VL 46
IS 4
BP 491
EP +
DI 10.1016/j.jpainsymman.2012.10.283
PG 13
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 232BL
UT WOS:000325463300008
PM 23522520
ER
PT J
AU Murnane, KS
Andersen, ML
Rice, KC
Howell, LL
AF Murnane, Kevin S.
Andersen, Monica L.
Rice, Kenner C.
Howell, Leonard L.
TI Selective serotonin 2A receptor antagonism attenuates the effects of
amphetamine on arousal and dopamine overflow in non-human primates
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Article
DE 5-HT2A; amphetamine; arousal; M100907; microdialysis; rhesus monkeys
ID RHESUS-MONKEYS; 3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA;
PARKINSONS-DISEASE; MONOAMINE CONTENT; SLEEP; WAKEFULNESS; NEURONS;
COCAINE; STEREOISOMERS; LESIONS
AB The objective of the present study was to further elucidate the mechanisms involved in the wake-promoting effects of psychomotor-stimulants. Many previous studies have tightly linked the effects of stimulants to dopamine neurotransmission, and some studies indicate that serotonin 2A receptors modulate these effects. However, the role of dopamine in arousal is controversial, most notably because dopamine neurons do not change firing rates across arousal states. In the present study, we examined the wake-promoting effects of the dopamine-releaser amphetamine using non-invasive telemetric monitoring. These effects were evaluated in rhesus monkeys as a laboratory animal model with high translational relevance for human disorders of sleep and arousal. To evaluate the role of dopamine in the wake-promoting effects of amphetamine, we used in vivo microdialysis targeting the caudate nucleus, as this approach provides clearly interpretable measures of presynaptic dopamine release. This is beneficial in the present context because some of the inconsistencies between previous studies examining the role of dopamine in arousal may be related to differences between postsynaptic dopamine receptors. We found that amphetamine significantly and dose-dependently increased arousal at doses that engendered higher extracellular dopamine levels. Moreover, antagonism of serotonin 2A receptors attenuated the effects of amphetamine on both wakefulness and dopamine overflow. These findings further elucidate the role of dopamine and serotonin 2A receptors in arousal, and they suggest that increased dopamine neurotransmission may be necessary for the wake-promoting effects of amphetamine, and possibly other stimulants.
C1 [Murnane, Kevin S.; Andersen, Monica L.; Howell, Leonard L.] Yerkes Natl Primate Res Ctr, Div Neuropharmacol & Neurol Dis, Atlanta, GA USA.
[Andersen, Monica L.] Univ Fed Sao Paulo UNIFESP, Dept Psicobiol, Sao Paulo, Brazil.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, NIH, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, NIH, Bethesda, MD USA.
[Howell, Leonard L.] Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA.
RP Howell, LL (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, 954 Gatewood Rd, Atlanta, GA 30322 USA.
EM lhowell@emory.edu
RI Andersen, Monica/C-7616-2012
OI Andersen, Monica/0000-0002-1894-6748
FU USPHS [DA010344, DA012514, RR000165]; National Institute on Drug Abuse;
National Institute on Alcohol Abuse and Alcoholism
FX The authors would like to thank both Juliet Brown and Lisa Neidert for
their expert technical assistance. These studies were supported by USPHS
grants (DA010344, DA012514 and RR000165). A portion of this work was
supported by the Intramural Research Programs of National Institute on
Drug Abuse and National Institute on Alcohol Abuse and Alcoholism.
NR 28
TC 5
Z9 5
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0962-1105
EI 1365-2869
J9 J SLEEP RES
JI J. Sleep Res.
PD OCT
PY 2013
VL 22
IS 5
BP 581
EP 588
DI 10.1111/jsr.12045
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 217CW
UT WOS:000324335300013
PM 23879373
ER
PT J
AU Heymann, JB
Winkler, DC
Yim, YI
Eisenberg, E
Greene, LE
Steven, AC
AF Heymann, J. Bernard
Winkler, Dennis C.
Yim, Yang-In
Eisenberg, Evan
Greene, Lois E.
Steven, Alasdair C.
TI Clathrin-coated vesicles from brain have small payloads: A cryo-electron
tomographic study
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE Clathrin-mediated endocytosis; Cryo-electron microscopy;
Three-dimensional image reconstruction; Adaptor proteins; Fullerenes
ID TRANSMISSION ELECTRON-MICROSCOPY; MEDIATED ENDOCYTOSIS; BINDING SUBUNIT;
PROTEIN COMPLEX; KIDNEY-CELL; MEMBRANE; AP-2; AUXILIN; VISUALIZATION;
RESOLUTION
AB Clathrin coats, which stabilize membrane curvature during endocytosis and vesicular trafficking, form highly polymorphic fullerene lattices. We used cryo-electron tomography to visualize coated particles in isolates from bovine brain. The particles range from similar to 66 to similar to 134 nm in diameter, and only 20% of them (all >= 80 nm) contain vesicles. The remaining 80% are clathrin "baskets", presumably artifactual assembly products. Polyhedral models were built for 54 distinct coat geometries. In true coated vesicles (CVs), most vesicles are offset to one side, leaving a crescent of interstitial space between the coat and the membrane for adaptor proteins and other components. The latter densities are fewer on the membrane-proximal side, which may represent the last part of the vesicle to bud off. A small number of densities - presumably cargo proteins - are associated with the interior surface of the vesicles. The clathrin coat, adaptor proteins, and vesicle membrane contribute almost all of the mass of a CV, with most cargoes accounting for only a few percent. The assembly of a CV therefore represents a massive biosynthetic effort to internalize a relatively diminutive payload. Such a high investment may be needed to overcome the resistance of membranes to high curvature. Published by Elsevier Inc.
C1 [Heymann, J. Bernard; Winkler, Dennis C.; Steven, Alasdair C.] NIAMSD, Struct Biol Res Lab, Bethesda, MD 20892 USA.
[Yim, Yang-In; Eisenberg, Evan; Greene, Lois E.] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Heymann, JB (reprint author), NIH, Bldg 50,Room 1515,50 South Dr MSC 8025, Bethesda, MD 20892 USA.
EM Bernard_Heymann@nih.gov
OI Heymann, Bernard/0000-0002-8872-5326
FU Intramural Research Program of NIAMS, NIH; Intramural Research Program
of NHLBI, NIH; [NIHP41RR-01081]
FX Molecular graphics images were produced using the UCSF Chimera package
from the Resource for Biocomputing, Visualization and Informatics at the
University of California, San Francisco (supported by NIHP41RR-01081).
This work was supported by the Intramural Research Programs of NIAMS and
NHLBI, NIH.
NR 73
TC 3
Z9 4
U1 0
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
EI 1095-8657
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD OCT
PY 2013
VL 184
IS 1
BP 43
EP 51
DI 10.1016/j.jsb.2013.05.006
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 234WM
UT WOS:000325675000006
PM 23688956
ER
PT J
AU Noinaj, N
Cornelissen, CN
Buchanan, SK
AF Noinaj, Nicholas
Cornelissen, Cynthia Nau
Buchanan, Susan K.
TI Structural insight into the lactoferrin receptors from pathogenic
Neisseria
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE Neisseria meningitidis; Gonorrhoeae; Lactoferrin; Transferrin; Iron
acquisition; TonB
ID HUMAN SERUM TRANSFERRIN; BINDING-PROTEIN B; N-LOBE; SWISS-MODEL;
CRYSTAL-STRUCTURE; PROVIDES INSIGHT; IRON; MENINGITIDIS; GONORRHOEAE;
IDENTIFICATION
AB Neisseria are pathogenic bacteria that cause gonorrhea, septicemia, and meningitis. Like other pathogenic bacteria, Neisseria must acquire iron for survival from their local environment within the human host. Instead of secreting siderophores to scavenge iron, Neisseria steal iron from human iron binding proteins such as hemoglobin, transferrin and lactoferrin for survival. Recently we reported the crystal structures of the Neisseria meningitidis transferrin receptors TbpA and TbpB, as well as the structures of apo and holo human transferrin. We also analyzed these proteins using small angle X-ray scattering and electron microscopy to provide the molecular details explaining how Neisseria are able to interact with and extract iron from transferrin. Here, we utilize the structural reports, as well as the recently reported structure of the N-lobe of LbpB from Moraxella bovis, to assemble improved 3D homology models for the neisserial lactoferrin import receptors LbpA and LbpB, both of which are important vaccine targets against N. meningitidis. We then analyzed these models to gain structural insights into the lactoferrin-iron import system and form a mechanistic model fashioned in parallel to the homologous transferrin-iron import system. Published by Elsevier Inc.
C1 [Noinaj, Nicholas; Buchanan, Susan K.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Cornelissen, Cynthia Nau] Virginia Commonwealth Univ, Med Ctr, Dept Microbiol & Immunol, Richmond, VA 23298 USA.
RP Buchanan, SK (reprint author), NIDDK, NIH, Bethesda, MD 20892 USA.
EM skbuchan@helix.nih.gov
FU Intramural Program of the National Institute of Diabetes and Digestive
and Kidney Diseases, National Institutes of Health; U.S. Public Health
Service from the National Institute of Allergy and Infectious Diseases
at the National Institutes of Health [AI065555, AI084400]; SE STI Center
from the National Institute of Allergy and Infectious Diseases [U19
AI31496]
FX N.N. and S.K.B. are supported by the Intramural Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health. Funding was provided to C.N.C. by U.S. Public
Health Service grant numbers AI065555 and AI084400 from the National
Institute of Allergy and Infectious Diseases at the National Institutes
of Health. C.N.C. is also supported by the SE STI Center grant (U19
AI31496) from the National Institute of Allergy and Infectious Diseases.
NR 43
TC 12
Z9 12
U1 3
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
EI 1095-8657
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD OCT
PY 2013
VL 184
IS 1
BP 83
EP 92
DI 10.1016/j.jsb.2013.02.009
PG 10
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 234WM
UT WOS:000325675000010
PM 23462098
ER
PT J
AU Vasunilashorn, S
Ferrucci, L
Crimmins, EM
Bandinelli, S
Guralnik, JM
Patel, KV
AF Vasunilashorn, Sarinnapha
Ferrucci, Luigi
Crimmins, Eileen M.
Bandinelli, Stefania
Guralnik, Jack M.
Patel, Kushang V.
TI Association of Inflammation with Loss of Ability to Walk 400 Meters:
Longitudinal Findings from the Invecchiare in Chianti Study
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE inflammation; mobility; 400-m walk; functional limitation; aging
ID C-REACTIVE PROTEIN; OLDER PERSONS; PHYSICAL FUNCTION;
CARDIOVASCULAR-DISEASE; MOBILITY LIMITATION; PERFORMANCE; MORTALITY;
INCHIANTI; MARKERS; DISABILITY
AB ObjectivesTo examine relationships between eight markers of inflammation (interleukin (IL)-6, IL-6 receptor (R), C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha, TNF receptor 1 (R1), TNFR2, IL-1 receptor antagonist, IL-18) and incident loss of ability to walk 400m.
DesignProspective cohort study.
SettingOlder adults enrolled in the Invecchiare in Chianti Study.
ParticipantsCommunity-dwelling participants aged 65 and older (N=1,006).
MeasurementsThe eight inflammatory markers were measured at baseline, and an inflammation score was calculated based on the number of inflammatory markers for which the participant was in the highest quartile. Incidence of mobility disability was determined in participants able to walk 400m at baseline. Logistic regression models were used to determine whether each of the inflammatory markers and the inflammation score predicted loss of the ability to walk 400m at 6-year follow-up.
ResultsAfter adjusting for covariates, individuals with a TNFR1 level in each of the highest three quartiles (Q2, 3, 4) were more likely to be unable to walk 400m at follow-up than those with TNFR1 levels in Q1. When adjusting for the same covariates, participants with an inflammation score of 3 or 4 were more likely to become unable to walk 400m at follow-up than participants with a score of 0.
ConclusionThese results provide additional evidence that inflammation is a factor in the mechanisms that cause incident mobility disability and suggest that a combined measure of inflammatory markers may improve prediction of functional prognosis.
C1 [Vasunilashorn, Sarinnapha] Princeton Univ, Off Populat Res, Princeton, NJ 08544 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Crimmins, Eileen M.] Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Los Angeles, CA 90089 USA.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Guralnik, Jack M.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[Patel, Kushang V.] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA.
RP Vasunilashorn, S (reprint author), Princeton Univ, Off Populat Res, 263 Wallace Hall, Princeton, NJ 08544 USA.
EM svasunil@princeton.edu
FU Italian Ministry of Health [ICS 110.1/RS97.71]; National Institutes of
Health (NIH), National Institute on Aging [N01-AG-1-2111]; NIH from the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development [R24HD047879]
FX The InCHIANTI Study was supported as a targeted project (ICS
110.1/RS97.71) by the Italian Ministry of Health and in part by the
Intramural Research Program of the National Institutes of Health (NIH),
National Institute on Aging (Contract N01-AG-1-2111). This research was
supported in part by NIH Grant R24HD047879 from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development.
NR 25
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD OCT
PY 2013
VL 61
IS 10
BP 1743
EP 1749
DI 10.1111/jgs.12446
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 233FG
UT WOS:000325551500014
PM 24083386
ER
PT J
AU Murphy, TP
Reynolds, MR
Cohen, DJ
Regensteiner, JG
Massaro, JM
Cutlip, DE
Mohler, ER
Cerezo, J
Oldenburg, NC
Thum, CC
Goldberg, S
Hirsch, AT
AF Murphy, Timothy P.
Reynolds, Matthew R.
Cohen, David J.
Regensteiner, Judith G.
Massaro, Joseph M.
Cutlip, Donald E.
Mohler, Emile R.
Cerezo, Joselyn
Oldenburg, Niki C.
Thum, Claudia C.
Goldberg, Suzanne
Hirsch, Alan T.
TI Correlation of Patient-reported Symptom Outcomes and Treadmill Test
Outcomes after Treatment for Aortoiliac Claudication
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; ENDOLUMINAL REVASCULARIZATION CLEVER; PERIPHERAL
ARTERIAL-DISEASE; PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY; SUPERVISED
EXERCISE PROGRAM; RANDOMIZED CONTROLLED-TRIAL; INTERMITTENT
CLAUDICATION; ENDOVASCULAR REVASCULARIZATION; FUNCTIONAL STATUS;
PERFORMANCE
AB Purpose: To examine the relationship between objective treadmill test outcomes and subjective symptom outcomes among patients. with claudication treated with stent revascularization (ST) compared with supervised exercise (SE).
Materials and Methods: Five scales of the Peripheral Artery Questionnaire and Walking Impairment Questionnaire were correlated with peak walking time and treadmill claudication onset time.
Results: The correlation between change in disease-specific quality of life (QOL) and change in peak walking time differed according to treatment group, With statistically significant correlations for all five scales for the ST group and weaker trends for the SE group, only one of which was statistically significant. In contrast, improvements in disease-specific QOL correlated well with increases in claudication onset time, with no significant interaction with treatment group for any of the five scales.
Conclusions: Disease-specific QOL results at 6 months in the Claudication: Exercise Vs. Endoluminal Revascularization (CLEVER) study show that improved maximal treadmill walking in patients with claudication treated with SE correlated poorly with self-reported symptom relief. Conversely, patients treated with ST showed good correlation between improved maximal treadmill walking and self-reported symptom improvement. The correlation between claudication onset time and self-reported symptom relief was good across treatment groups. This finding indicates that traditional objective treadmill test outcomes may not correlate well with symptom relief in patients with claudication. Future studies should investigate these data and improve understanding of patient relevance of traditional Objective treadmill-based treatment outcomes.
C1 [Murphy, Timothy P.; Cerezo, Joselyn] Rhode Isl Hosp, Vasc Dis Res Ctr, Dept Diagnost Imaging, Providence, RI 02903 USA.
[Reynolds, Matthew R.; Cutlip, Donald E.] Boston Univ, Dept Internal Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Thum, Claudia C.] Boston Univ, Harvard Clin Res Inst, Boston, MA 02215 USA.
[Massaro, Joseph M.] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
[Cohen, David J.] Univ Missouri, Dept Internal Med, Kansas City, MO 64110 USA.
[Regensteiner, Judith G.] Univ Colorado, Sch Med, Dept Exercise Physiol, Aurora, CO USA.
[Mohler, Emile R.] Univ Penn, Dept Internal Med, Philadelphia, PA 19104 USA.
[Oldenburg, Niki C.] Univ Minnesota, Sch Med, Dept Epidemiol, Minneapolis, MN 55455 USA.
[Hirsch, Alan T.] Univ Minnesota, Sch Med, Dept Internal Med, Minneapolis, MN 55455 USA.
[Goldberg, Suzanne] NHLBI, Bethesda, MD 20892 USA.
RP Murphy, TP (reprint author), Rhode Isl Hosp, Vasc Dis Res Ctr, Dept Diagnost Imaging, Gerry 337,593 Eddy St, Providence, RI 02903 USA.
EM tmurphy@lifespan.org
FU Medtronic; Boston Scientific; Abbott Vascular; Medrad; Medtronic, Inc.;
Amylin; American Diabetes Association; National Institutes of Health;
Aastrom Biosciences; Cytokinetics; VM Biopharma; Cordis/Johnson Johnson;
Otsuka Pharmaceuticals; National Heart, Lung and Blood Institute
[HL77221, HL081656]; Cordis/Johnson & Johnson (Warren, New Jersey); eV3
(Plymouth, Minnesota); Boston Scientific (Natick, Massachusetts)
FX T.P.M. received grant support from Abbott Vascular, Cordis/Johnson &
Johnson, and Otsuka Pharmaceuticals and is a consultant for
Microvention/Terumo, Inc. D.J.C. received research grant support from
Medtronic, Boston Scientific, Abbott Vascular, and Medrad and is a
consultant for Medtronic, Inc. M.R.R. is a paid consultant for
Medtronic, Inc. J.G.R. received research grant support from Amylin, the
American Diabetes Association, and the National Institutes of Health.
E.R.M. is a Data Safety Monitoring Board member for Viromed
BioPharma/Synteract. A.T.H. received research grants from Abbott
Vascular, Aastrom Biosciences, Cytokinetics, and VM Biopharma and is a
consultant for AstraZeneca, Merck, Novartis, Pozen, and Shire HGT. None
of the other authors have identified a conflict of interest.; The CLEVER
(Claudication: Exercise Vs. Endoluminal Revascularization) study was
sponsored mostly by the National Heart, Lung and Blood Institute (grants
HL77221 and HL081656) and also received financial support from
Cordis/Johnson & Johnson (Warren, New Jersey), eV3 (Plymouth,
Minnesota), and Boston Scientific (Natick, Massachusetts). Otsuka
America Inc (San Francisco, California) donated cilostazol for all study
participants throughout the study. Omron Healthcare Inc (Lake Forest
Illinois) donated pedometers. Krames Staywell (San Bruno, California)
donated pnnt materials for study participants on exercise and diet.
NR 26
TC 7
Z9 7
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD OCT
PY 2013
VL 24
IS 10
BP 1427
EP 1435
DI 10.1016/j.jvir.2013.05.057
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 231TW
UT WOS:000325442300001
PM 23906799
ER
PT J
AU Clark, C
AF Clark, Cindy
TI Copyright Questions and Answers for Information Professionals: From the
Columns of Against the Grain
SO LEARNED PUBLISHING
LA English
DT Book Review
C1 [Clark, Cindy] NIH, Natl Inst Hlth NIH Lib, Off Res Serv, Bethesda, MD 20892 USA.
RP Clark, C (reprint author), NIH, Natl Inst Hlth NIH Lib, Off Res Serv, Bethesda, MD 20892 USA.
EM clarkc@ors.od.nih.gov
NR 1
TC 0
Z9 0
U1 1
U2 5
PU ASSOC LEARNED PROFESSIONAL SOC PUBL
PI W SUSSEX
PA SOUTH HOUSE, THE STREET WORTHING, W SUSSEX BN13 3UU, ENGLAND
SN 0953-1513
EI 1741-4857
J9 LEARN PUBL
JI Learn. Publ.
PD OCT
PY 2013
VL 26
IS 4
BP 310
EP 310
DI 10.1087/201304011
PG 1
WC Information Science & Library Science
SC Information Science & Library Science
GA 231VA
UT WOS:000325445300011
ER
PT J
AU Bergsagel, PL
Kuehl, WM
AF Bergsagel, P. L.
Kuehl, W. M.
TI Degree of focal immunoglobulin heavy chain locus deletion as a measure
of B-cell tumor purity
SO LEUKEMIA
LA English
DT Letter
ID MYELOMA
C1 [Bergsagel, P. L.] Mayo Clin, Ctr Comprehens Canc, Scottsdale, AZ 85259 USA.
[Kuehl, W. M.] Natl Canc Inst, Ctr Canc Res, Genet Branch, Bethesda, MD USA.
RP Bergsagel, PL (reprint author), Mayo Clin, Ctr Comprehens Canc, Scottsdale, AZ 85259 USA.
EM Bergsagel.Leif@mayo.edu
FU NIA NIH HHS [R01 AG020686]
NR 4
TC 2
Z9 2
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
EI 1476-5551
J9 LEUKEMIA
JI Leukemia
PD OCT
PY 2013
VL 27
IS 10
BP 2067
EP 2068
DI 10.1038/leu.2013.139
PG 2
WC Oncology; Hematology
SC Oncology; Hematology
GA 234KN
UT WOS:000325642600015
PM 23644420
ER
PT J
AU Prasad, V
AF Prasad, Vinay
TI Why Randomized Controlled Trials Are Needed to Accept New Practices: 2
Medical Worldviews
SO MAYO CLINIC PROCEEDINGS
LA English
DT Editorial Material
ID CLINICAL-PRACTICE GUIDELINES; CONFLICTS-OF-INTEREST; CYP2C19 GENOTYPE;
CARDIOVASCULAR EVENTS; METAANALYSIS; REVERSAL; BENEFITS; EFFICACY;
APPENDECTOMY; TECHNOLOGIES
C1 NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Prasad, V (reprint author), NCI, Med Oncol Branch, NIH, 10 Ctr Dr,10-12N226, Bethesda, MD 20892 USA.
EM vinayak.prasad@nih.gov
NR 39
TC 5
Z9 5
U1 2
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-6196
EI 1942-5546
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD OCT
PY 2013
VL 88
IS 10
BP 1046
EP 1050
DI 10.1016/j.mayocp.2013.04.026
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 232DR
UT WOS:000325470800008
PM 24079676
ER
PT J
AU Prasad, V
Cifu, A
AF Prasad, Vinay
Cifu, Adam
TI In reply I-Reversal of Medical Practices
SO MAYO CLINIC PROCEEDINGS
LA English
DT Letter
C1 [Prasad, Vinay] NCI, Bethesda, MD 20892 USA.
[Cifu, Adam] Univ Chicago, Chicago, IL 60637 USA.
RP Prasad, V (reprint author), NCI, Bethesda, MD 20892 USA.
NR 6
TC 2
Z9 2
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-6196
EI 1942-5546
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD OCT
PY 2013
VL 88
IS 10
BP 1183
EP 1184
DI 10.1016/j.mayocp.2013.08.011
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 232DR
UT WOS:000325470800028
PM 24079692
ER
PT J
AU Willis, GB
Smith, T
Lee, HJ
AF Willis, Gordon B.
Smith, Tenbroeck
Lee, Hyunshik J.
TI Do Additional Recontacts to Increase Response Rate Improve Physician
Survey Data Quality?
SO MEDICAL CARE
LA English
DT Article
DE survey research; physician survey; response rate; data quality;
recontact
ID NONRESPONSE; ATTITUDES
AB Background:Although response rates for physician surveys have been decreasing, it is not clear whether this trend is associated with an increase in survey nonresponse bias. One means for assessing potential bias is to conduct a level-of-effort analysis that compares data estimates for respondents interviewed during the first recruitment contact to respondents interviewed at later recontact cycles.Methods:We compared early and later responders within the Survey of Physician Attitudes Regarding the Care of Cancer Survivors with respect to both demographic characteristics and aggregate survey responses to items on survivor care knowledge, attitudes, and practices.Results:Accumulating additional completions across each of 4 respondent contact attempts improved weighted response rates (35.0%, 46.9%, 52.3%, and 57.6%, respectively). However, the majority of estimates for analyzed variables remained relatively unchanged over additional cycles of recontact.Conclusions:We conclude that additional respondent recontact attempts, especially beyond a single recontact, had little influence on key data distributions, suggesting that these were ineffective in reducing nonresponse bias. Further, the conduct of additional recruitment recontacts was an inefficient means for increasing statistical power. For the conduct of physician surveys, a practice that may in some cases be cost-effective, while also controlling total survey error, is to establish a larger initial sample; to either eliminate nonresponse follow-up or to limit this to one recontact; and to accept a somewhat lower final overall survey response rate.
C1 [Willis, Gordon B.] NCI, Bethesda, MD 20892 USA.
[Smith, Tenbroeck] Amer Canc Soc Inc, Atlanta, GA USA.
[Lee, Hyunshik J.] WESTAT Corp, Rockville, MD 20850 USA.
RP Willis, GB (reprint author), NCI, 9609 Med Ctr Dr,Rm 3E358,MSC 9762, Bethesda, MD 20892 USA.
EM willisg@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 15
TC 16
Z9 16
U1 2
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD OCT
PY 2013
VL 51
IS 10
BP 945
EP 948
PG 4
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 222SI
UT WOS:000324751000014
PM 23969583
ER
PT J
AU Liu, YX
Liu, ST
Nacif, MS
Sibley, CT
Bluemke, DA
Summers, RM
Yao, JH
AF Liu, Yixun
Liu, Songtao
Nacif, Marcelo S.
Sibley, Christopher T.
Bluemke, David A.
Summers, Ronald M.
Yao, Jianhua
TI A framework to measure myocardial extracellular volume fraction using
dual-phase low dose CT images
SO MEDICAL PHYSICS
LA English
DT Article
DE extracellular volume fraction; low dose; cardiac CT; deformable model;
modeling
ID SEGMENTATION; HEART; FIBROSIS; T1; MR; ENHANCEMENT; RESOLUTION; MODEL
AB Purpose: Myocardial extracellular volume fraction (ECVF) is a surrogate imaging biomarker of diffuse myocardial fibrosis, a hallmark of pathologic ventricular remodeling. Low dose cardiac CT is emerging as a promising modality to detect diffuse interstitial myocardial fibrosis due to its fast acquisition and low radiation; however, the insufficient contrast in the low dose CT images poses great challenge to measure ECVF from the image.
Methods: To deal with this difficulty, the authors present a complete ECVF measurement framework including a point-guided myocardial modeling, a deformable model-based myocardium segmentation, nonrigid registration of pre- and post-CT, and ECVF calculation.
Results: The proposed method was evaluated on 20 patients by two observers. Compared to the manually delineated reference segmentations, the accuracy of our segmentation in terms of true positive volume fraction (TPVF), false positive volume fraction (FPVF), and average surface distance (ASD), were 92.18% +/- 3.52%, 0.31% +/- 0.10%, 0.69 +/- 0.14 mm, respectively. The interobserver variability measured by concordance correlation coefficient regarding TPVF, FPVF, and ASD were 0.95, 0.90, 0.94, respectively, demonstrating excellent agreement. Bland-Altman method showed 95% limits of agreement between ECVF at CT and ECVF at MR.
Conclusions: The proposed framework demonstrates its efficiency, accuracy, and noninvasiveness in ECVF measurement and dramatically advances the ECVF at cardiac CT toward its clinical use. (C) 2013 American Association of Physicists in Medicine.
C1 [Liu, Yixun; Summers, Ronald M.; Yao, Jianhua] NIH, Clin Image Proc Serv, Ctr Clin, Bethesda, MD 20892 USA.
[Liu, Songtao; Nacif, Marcelo S.; Sibley, Christopher T.; Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Liu, Songtao; Sibley, Christopher T.; Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, Mol Biomed Imaging Lab, NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Yao, JH (reprint author), NIH, Clin Image Proc Serv, Ctr Clin, Bethesda, MD 20892 USA.
EM JYao@cc.nih.gov
OI Bluemke, David/0000-0002-8323-8086
FU Intramural Research Program of the Clinical Center, National Institutes
of Health (NIH); NIH Intramural program
FX This research was supported in part by the Intramural Research Program
of the Clinical Center, National Institutes of Health (NIH). Funded by
the NIH Intramural program. The segmentation method of the proposed
framework was accepted at RSNA2012. The software system of the proposed
framework was accepted for demonstration in Quantitative Imaging Reading
Room (QIRR) at RSNA2012. The authors declare that they have no competing
interests.
NR 24
TC 0
Z9 0
U1 0
U2 3
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 OCT
PY 2013
VL 40
IS 10
AR 103501
DI 10.1118/1.4819936
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 231DT
UT WOS:000325394400048
PM 24089934
ER
PT J
AU Xie, TW
Bolch, WE
Lee, C
Zaidi, H
AF Xie, Tianwu
Bolch, Wesley E.
Lee, Choonsik
Zaidi, Habib
TI Pediatric radiation dosimetry for positron-emitting radionuclides using
anthropomorphic phantoms
SO MEDICAL PHYSICS
LA English
DT Article
DE radiation dosimetry; PET; Monte Carlo; computational models; pediatrics
ID INTERNAL DOSE ASSESSMENT; PERSONAL-COMPUTER SOFTWARE; NUCLEAR-MEDICINE;
COMPUTATIONAL PHANTOMS; S-VALUES; NEWBORN PATIENT; VOXEL PHANTOMS;
CAMERA IMAGES; HUMAN ANATOMY; UF SERIES
AB Purpose: Positron emission tomography (PET) plays an important role in the diagnosis, staging, treatment, and surveillance of clinically localized diseases. Combined PET/CT imaging exhibits significantly higher sensitivity, specificity, and accuracy than conventional imaging when it comes to detecting malignant tumors in children. However, the radiation dose from positron-emitting radionuclide to the pediatric population is a matter of concern since children are at a particularly high risk when exposed to ionizing radiation.
Methods: The authors evaluate the absorbed fractions and specific absorbed fractions (SAFs) of monoenergy photons/electrons as well as S-values of 9 positron-emitting radionuclides (C-11, N-13, O-15, F-18, Cu-64, Ga-68, Rb-82, Y-86, and I-124) in 48 source regions for 10 anthropomorphic pediatric hybrid models, including the reference newborn, 1-, 5-, 10-, and 15-yr-old male and female models, using the Monte Carlo N-Particle eXtended general purpose Monte Carlo transport code.
Results: The self-absorbed SAFs and S-values for most organs were inversely related to the age and body weight, whereas the cross-dose terms presented less correlation with body weight. For most source/target organ pairs, Rb-82 and Y-86 produce the highest self-absorbed and cross-absorbed S-values, respectively, while Cu-64 produces the lowest S-values because of the low-energy and high-frequency of electron emissions. Most of the total self-absorbed S-values are contributed from non-penetrating particles (electrons and positrons), which have a linear relationship with body weight. The dependence of self-absorbed S-values of the two annihilation photons varies to the reciprocal of 0.76 power of the mass, whereas the self-absorbed S-values of positrons vary according to the reciprocal mass.
Conclusions: The produced S-values for common positron-emitting radionuclides can be exploited for the assessment of radiation dose delivered to the pediatric population from various PET radiotracers used in clinical and research settings. The mass scaling method for positron-emitters can be used to derive patient-specific S-values from data of reference phantoms. (C) 2013 American Association of Physicists in Medicine.
C1 [Xie, Tianwu; Zaidi, Habib] Univ Hosp Geneva, Div Nucl Med & Mol Imaging, CH-1211 Geneva 4, Switzerland.
[Bolch, Wesley E.] Univ Florida, Dept Biomed Engn, Gainesville, FL 32611 USA.
[Lee, Choonsik] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
[Zaidi, Habib] Univ Geneva, Geneva Neurosci Ctr, CH-1205 Geneva, Switzerland.
[Zaidi, Habib] Univ Groningen, Univ Med Ctr Groningen, Dept Nucl Med & Mol Imaging, NL-9700 RB Groningen, Netherlands.
RP Zaidi, H (reprint author), Univ Hosp Geneva, Div Nucl Med & Mol Imaging, CH-1211 Geneva 4, Switzerland.
EM habib.zaidi@hcuge.ch
FU Swiss National Science Foundation [SNSF 31003A-135576]; Geneva Cancer
League
FX This work was supported by the Swiss National Science Foundation under
Grant No. SNSF 31003A-135576 and the Geneva Cancer League.
NR 62
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U1 0
U2 9
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 OCT
PY 2013
VL 40
IS 10
AR 102502
DI 10.1118/1.4819939
PG 14
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 231DT
UT WOS:000325394400037
PM 24089923
ER
PT J
AU Gherardini, FC
AF Gherardini, Frank C.
TI Borrelia burgdorferi HtrA may promote dissemination and irritation
SO MOLECULAR MICROBIOLOGY
LA English
DT Editorial Material
ID HIGH-TEMPERATURE REQUIREMENT; HUMAN ARTICULAR CHONDROCYTES; LYME-DISEASE
SPIROCHETE; MYCOBACTERIUM-TUBERCULOSIS; FIBRONECTIN FRAGMENTS;
STRESS-RESPONSE; E-CADHERIN; PROTEASE; BINDING; GLYCOSAMINOGLYCAN
C1 [Gherardini, Frank C.] NIAID, Lab Zoonot Pathogens, Div Intramural Res, Hamilton, MT 59840 USA.
[Gherardini, Frank C.] NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Gherardini, FC (reprint author), NIAID, Lab Zoonot Pathogens, Div Intramural Res, Hamilton, MT 59840 USA.
EM fgherardini@niaid.nih.gov
NR 32
TC 7
Z9 7
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0950-382X
EI 1365-2958
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 2013
VL 90
IS 2
BP 209
EP 213
DI 10.1111/mmi.12390
PG 5
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 232IG
UT WOS:000325486100001
PM 23998919
ER
PT J
AU Altschul, S
Demchak, B
Durbin, R
Gentleman, R
Krzywinski, M
Li, H
Nekrutenko, A
Robinson, J
Rasband, W
Taylor, J
Trapnell, C
AF Altschul, Stephen
Demchak, Barry
Durbin, Richard
Gentleman, Robert
Krzywinski, Martin
Li, Heng
Nekrutenko, Anton
Robinson, James
Rasband, Wayne
Taylor, James
Trapnell, Cole
TI The anatomy of successful computational biology software
SO NATURE BIOTECHNOLOGY
LA English
DT Editorial Material
AB Creators of software widely used in computational biology discuss the factors that contributed to their success
C1 [Altschul, Stephen] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Demchak, Barry] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Durbin, Richard] Wellcome Trust Sanger Inst, Hinxton, England.
[Gentleman, Robert] Genentech Inc, San Francisco, CA USA.
[Krzywinski, Martin] British Columbia Canc Res Ctr, Vancouver, BC V5Z 1L3, Canada.
[Li, Heng; Robinson, James] Broad Inst, Cambridge, MA USA.
[Nekrutenko, Anton] Penn State Univ, University Pk, PA 16802 USA.
[Rasband, Wayne] NIMH, Bethesda, MD 20892 USA.
[Taylor, James] Emory Univ, Atlanta, GA 30322 USA.
[Trapnell, Cole] Harvard Univ, Cambridge, MA 02138 USA.
RP Altschul, S (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RI Tang, Macy/B-9798-2014; Li, Heng/D-9344-2011; Taylor, James/F-1026-2011;
OI Li, Heng/0000-0003-4874-2874; Taylor, James/0000-0001-5079-840X; Durbin,
Richard/0000-0002-9130-1006; Demchak, Barry/0000-0001-7065-7786;
Nekrutenko, Anton/0000-0002-5987-8032
FU Intramural NIH HHS [ZIA LM000072-18]; NIGMS NIH HHS [R01 GM070743]
NR 0
TC 8
Z9 8
U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1087-0156
EI 1546-1696
J9 NAT BIOTECHNOL
JI Nat. Biotechnol.
PD OCT
PY 2013
VL 31
IS 10
BP 894
EP 897
DI 10.1038/nbt.2721
PG 4
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 233CA
UT WOS:000325541300017
PM 24104757
ER
PT J
AU Aguilar-Arnal, L
Hakim, O
Patel, VR
Baldi, P
Hager, GL
Sassone-Corsi, P
AF Aguilar-Arnal, Lorena
Hakim, Ofir
Patel, Vishal R.
Baldi, Pierre
Hager, Gordon L.
Sassone-Corsi, Paolo
TI Cycles in spatial and temporal chromosomal organization driven by the
circadian clock
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID REGULATORY MOTIF SITES; GENE-EXPRESSION; HUMAN GENOME; DBP
TRANSCRIPTION; 3 DIMENSIONS; E-BOX; CHROMATIN; METABOLISM; ARCHITECTURE;
MAMMALS
AB Dynamic transitions in the epigenome have been associated with regulated patterns of nuclear organization. The accumulating evidence that chromatin remodeling is implicated in circadian function prompted us to explore whether the clock may control nuclear architecture. We applied the chromosome conformation capture on chip technology in mouse embryonic fibroblasts (MEFs) to demonstrate the presence of circadian long-range interactions using the clock-controlled Dbp gene as bait. The circadian genomic interactions with Dbp were highly specific and were absent in MEFs whose clock was disrupted by ablation of the Bmal1 gene (also called Arntl). We establish that the Dbp circadian interactome contains a wide variety of genes and clock-related DNA elements. These findings reveal a previously unappreciated circadian and clock-dependent shaping of the nuclear landscape.
C1 [Aguilar-Arnal, Lorena; Sassone-Corsi, Paolo] Univ Calif Irvine, Dept Biol Chem, Ctr Epigenet & Metab, Irvine, CA 92717 USA.
[Hakim, Ofir; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
[Patel, Vishal R.; Baldi, Pierre] Univ Calif Irvine, Dept Comp Sci, Inst Genom & Bioinformat, Irvine, CA USA.
RP Sassone-Corsi, P (reprint author), Univ Calif Irvine, Dept Biol Chem, Ctr Epigenet & Metab, Irvine, CA 92717 USA.
EM pfbaldi@ics.uci.edu; psc@uci.edu
FU European Molecular Biology Organization (EMBO) [ALTF 411-2009]; NIH
[R01-GM081634, AG041504, AG033888, LM010235-01A1, 5T15LM007743]; Sirtris
Pharmaceuticals [SP-48984]; National Science Foundation [IIS-0513376]
FX We thank R. L. Schiltz and T. A. Johnson (NCI, NIH) for assisting with
cell culture; R. Orozco-Solis, K. Eckel-Mahan, S. Sahar (Center for
Epigenetics and Metabolism, University of California Irvine) and M.
Groudine (Fred Hutchinson Cancer Research Center) for critical reading
of the manuscript; S. Dilag (Center for Epigenetics and Metabolism,
University of California Irvine) for technical support; X. Kong
(Department of Biological Chemistry, University of California Irvine)
for sharing FISH expertise and reagents; and all the members of the P.
S.-C., G. L. H. and P. B. laboratories for discussions. This work was
supported in part by the following grants: European Molecular Biology
Organization (EMBO) long-term fellowship ALTF 411-2009 (to L. A.-A.),
NIH grants R01-GM081634, AG041504 and AG033888 (to P. S.-C.) and Sirtris
Pharmaceuticals grant SP-48984 (to P. S.-C.). The work of V. R. P. and
P. B. is supported by the following grants: National Science Foundation
grant IIS-0513376 and NIH grants LM010235-01A1 and 5T15LM007743 (to
P.B.).
NR 77
TC 31
Z9 31
U1 1
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
EI 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD OCT
PY 2013
VL 20
IS 10
BP 1206
EP +
DI 10.1038/nsmb.2667
PG 10
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 230UV
UT WOS:000325369500012
PM 24056944
ER
PT J
AU Vandevijvere, S
Monteiro, C
Krebs-Smith, SM
Lee, A
Swinburn, B
Kelly, B
Neal, B
Snowdon, W
Sacks, G
AF Vandevijvere, S.
Monteiro, C.
Krebs-Smith, S. M.
Lee, A.
Swinburn, B.
Kelly, B.
Neal, B.
Snowdon, W.
Sacks, G.
CA INFORMAS
TI Monitoring and benchmarking population diet quality globally: a
step-wise approach
SO OBESITY REVIEWS
LA English
DT Review
DE Diet quality; INFORMAS; monitoring; ultra-processed foods
ID HEALTHY EATING INDEX; EXPENDITURES SURVEYS HCES; CORONARY-HEART-DISEASE;
CARDIOVASCULAR RISK-FACTORS; FOOD BALANCE SHEETS; OUT-OF-HOME;
GESTATIONAL DIABETES-MELLITUS; N-3 FATTY-ACIDS; MEDITERRANEAN DIET;
NUTRITION TRANSITION
AB INFORMAS (International Network for Food and Obesity/non-communicable diseases Research, Monitoring and Action Support) aims to monitor and benchmark the healthiness of food environments globally. In order to assess the impact of food environments on population diets, it is necessary to monitor population diet quality between countries and over time. This paper reviews existing data sources suitable for monitoring population diet quality, and assesses their strengths and limitations. A step-wise framework is then proposed for monitoring population diet quality. Food balance sheets (FBaS), household budget and expenditure surveys (HBES) and food intake surveys are all suitable methods for assessing population diet quality. In the proposed minimal' approach, national trends of food and energy availability can be explored using FBaS. In the expanded' and optimal' approaches, the dietary share of ultra-processed products is measured as an indicator of energy-dense, nutrient-poor diets using HBES and food intake surveys, respectively. In addition, it is proposed that pre-defined diet quality indices are used to score diets, and some of those have been designed for application within all three monitoring approaches. However, in order to enhance the value of global efforts to monitor diet quality, data collection methods and diet quality indicators need further development work.
C1 [Vandevijvere, S.; Swinburn, B.] Univ Auckland, Sch Populat Hlth, Auckland 1142, New Zealand.
[Monteiro, C.] Univ Sao Paulo, Ctr Epidemiol Studies Hlth & Nutr, BR-05508 Sao Paulo, Brazil.
[Krebs-Smith, S. M.] NCI, Bethesda, MD 20892 USA.
[Lee, A.] Queensland Univ Technol, Sch Publ Hlth & Social Work, Brisbane, Qld 4001, Australia.
[Lee, A.] Queensland Univ Technol, Sch Exercise & Nutr Sci, Brisbane, Qld 4001, Australia.
[Swinburn, B.; Snowdon, W.; Sacks, G.] Deakin Univ, WHO Collaborating Ctr Obes Prevent, Burwood, Vic, Australia.
[Kelly, B.] Univ Wollongong, Sch Hlth & Soc, Wollongong, NSW, Australia.
[Neal, B.] Univ Sydney, George Inst Global Hlth, Sydney, NSW 2006, Australia.
[Snowdon, W.] Pacific Res Ctr Prevent Obes & Noncommunicable Di, Suva, Fiji.
RP Vandevijvere, S (reprint author), Univ Auckland, Sch Populat Hlth, Private Bag 92019, Auckland 1142, New Zealand.
EM s.vandevijvere@auckland.ac.nz
RI Monteiro, Carlos/F-9892-2012;
OI Lee, Amanda/0000-0001-6887-5426; Sacks, Gary/0000-0001-9736-1539
FU Rockefeller Foundation; International Obesity Taskforce (IOTF);
University of Auckland; Deakin University; George Institute, University
of Sydney; Queensland University of Technology; University of Oxford;
University of Pennsylvania Perelman School of Medicine; World Cancer
Research Fund International; University of Toronto; Australian National
University; Faculty of Health at Deakin University
FX The authors wish to thank Janice Albert and Piero Conforti from the Food
and Agricultural Organisation (FAO) for their helpful comments on this
paper. The Rockefeller Foundation kindly supported the work of INFORMAS
by hosting the first formal meeting of INFORMAS at the Rockefeller
Foundation Bellagio Centre, Italy, from 19 to 23 November 2012. The
following organizations provided funding support for the travel of
participants to Italy for this meeting and the preparation of background
research papers: The Rockefeller Foundation, International Obesity
Taskforce (IOTF), University of Auckland, Deakin University, The George
Institute, University of Sydney, Queensland University of Technology,
University of Oxford, University of Pennsylvania Perelman School of
Medicine, World Cancer Research Fund International, University of
Toronto, The Australian National University. The Faculty of Health at
Deakin University kindly supported the costs for open access
availability of this paper, and the Australian National Health and
Medical Research Council Centre for Research Excellence in Obesity
Policy and Food Systems (APP1041020) supported the coordination and
finalizing of INFORMAS manuscripts.
NR 203
TC 17
Z9 17
U1 0
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1467-7881
EI 1467-789X
J9 OBES REV
JI Obes. Rev.
PD OCT
PY 2013
VL 14
SU 1
SI SI
BP 135
EP 149
DI 10.1111/obr.12082
PG 15
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 226ZJ
UT WOS:000325076200012
PM 24074217
ER
PT J
AU Zinkel, SRJ
Moe, M
Stern, EA
Hubbard, VS
Yanovski, SZ
Yanovski, JA
Schoeller, DA
AF Zinkel, S. R. J.
Moe, M., III
Stern, E. A.
Hubbard, V. S.
Yanovski, S. Z.
Yanovski, J. A.
Schoeller, D. A.
TI Comparison of total energy expenditure between school and summer months
SO PEDIATRIC OBESITY
LA English
DT Article
DE Adolescents; obesity; overweight; seasonal variation; doubly labeled
water
ID BODY-MASS INDEX; PHYSICAL-ACTIVITY; SEASONAL-VARIATION; YOUNG-CHILDREN;
RISK-FACTORS; US CHILDREN; OBESITY; OVERWEIGHT; PREVALENCE; CHILDHOOD
AB ObjectiveRecent data report that the youth experience greater weight gain during summer than during school months. We tested the hypothesis that a difference in total energy expenditure (TEE) between school and summer months exists and may contribute to summer weight gain.
Subjects and methodsA secondary analysis was performed on cross-sectional TEE data from school-age, sedentary African-American and Caucasian youth based in or near the District of Columbia who were at-risk for adult obesity because they had body mass index (BMI)85th percentile or had overweight parents. TEE was estimated from 18-O and deuterium measurements during 1-week intervals using urine samples collected after ingestion of doubly labelled water. Differences in summer- and school-time TEE were assessed using analysis of covariance. The data were adjusted for fat-free mass (FFM) as determined by deuterium dilution to adjust for the effect of body size on TEE.
ResultsData were collected from 162 youth (average age 102 years, BMI 28 +/- 8kgm(-2) and BMIz-score 1.96+0.96). Of these, 96 youth had TEE measured during the school year (September-June); 66 different youths had TEE measured during summer months (June-August). After adjustment for FFM, average summertime TEE was 2450 +/- 270 kcald(-1) and average school-time TEE was 2510 +/- 350 kcald(-1) (P=0.26).
ConclusionNo difference in TEE was detected between the school year and the summer months. These data suggest that seasonal differences in youth weight gain are not necessarily due to differences in energy expenditures.
C1 [Zinkel, S. R. J.; Moe, M., III; Schoeller, D. A.] Univ Wisconsin, Dept Nutr Sci, Madison, WI 53706 USA.
[Stern, E. A.; Yanovski, S. Z.; Yanovski, J. A.] NICHD, Sect Growth & Obes, PREGEN, Hatfield Clin Res Ctr,NIH, Bethesda, MD USA.
[Hubbard, V. S.] NIDDK, Div Nutr Res Coordinat, NIH, Bethesda, MD USA.
[Yanovski, J. A.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
RP Schoeller, DA (reprint author), 1415 Linden Dr, Madison, WI 53706 USA.
EM dschoell@nutrisci.wisc.edu
OI Yanovski, Jack/0000-0001-8542-1637
FU NIH: NICHD; NIH: NIDDK; NIH: NIMHD; Eunice Kennedy Shriver National
Institute of Child Health and Human Development; National Center on
Minority Health and Health Disparities of the National Institutes of
Health; National Institutes of Diabetes and Digestive and Kidney
Diseases [T32DK007665]
FX This research was supported in part by the Intramural and Extramural
Research Programs of the NIH: NICHD, NIDDK, and NIMHD. Dr. J. Yanovski
is a Commissioned Officer in the United States Public Health Service and
is supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development and the
National Center on Minority Health and Health Disparities of the
National Institutes of Health. S. Zinkel was supported by training grant
T32DK007665 from the National Institutes of Diabetes and Digestive and
Kidney Diseases. The National Institute of Diabetes and Digestive and
Kidney Diseases had no role in the preparation, review or approval of
the manuscript.
NR 31
TC 7
Z9 7
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-6310
EI 2047-6302
J9 PEDIATR OBES
JI Pediatr. Obes.
PD OCT
PY 2013
VL 8
IS 5
BP 404
EP 410
DI 10.1111/j.2047-6310.2012.00120.x
PG 7
WC Pediatrics
SC Pediatrics
GA 218VY
UT WOS:000324461800012
PM 23637099
ER
PT J
AU Sherafat-Kazemzadeh, R
Ivey, L
Kahn, SR
Sapp, JC
Hicks, MD
Kim, RC
Krause, AJ
Shomaker, LB
Biesecker, LG
Han, JC
Yanovski, JA
AF Sherafat-Kazemzadeh, R.
Ivey, L.
Kahn, S. R.
Sapp, J. C.
Hicks, M. D.
Kim, R. C.
Krause, A. J.
Shomaker, L. B.
Biesecker, L. G.
Han, J. C.
Yanovski, J. A.
TI Hyperphagia among patients with Bardet-Biedl syndrome
SO PEDIATRIC OBESITY
LA English
DT Article
DE Bardet-Biedl syndrome; hyperphagia; obesity syndromes; polyphagia
ID PRADER-WILLI-SYNDROME; OBESITY; MUTATION
AB BackgroundThe importance of hyperphagia as a cause for energy imbalance in humans with Bardet-Biedl syndrome (BBS) has not been established. We therefore compared hyperphagic symptoms in patients with BBS vs. controls.
Methods:We studied 13 patients with BBS and 23 non-syndromic controls with similar age, sex and body mass index (BMI) z-score. A 13-item hyperphagia questionnaire was completed by patients' parents/guardians.
ResultsTotal hyperphagia questionnaire score was higher in BBS than controls (27.69.0 vs. 19.1 +/- 7.9, P=0.005). Behaviour and drive subscales were higher for BBS than controls (12.5 +/- 4.1 vs. 7.8 +/- 3.2, P=0.001, and 11.2 +/- 4.1 vs. 8.3 +/- 3.8, P=0.04, respectively); severity was not significantly different between groups (3.8 +/- 1.5 vs. 3.0 +/- 1.3, P=0.072). After adjustment for demographic variables and BMI z-score, total and behaviour subscale scores remained significantly different between groups, suggesting food-seeking activity, rather than preoccupation with food may be the main hyperphagic feature among patients with BBS.
ConclusionAppetite dysregulation may contribute to obesity in BBS.
C1 [Sherafat-Kazemzadeh, R.; Kahn, S. R.; Hicks, M. D.; Kim, R. C.; Krause, A. J.; Shomaker, L. B.; Han, J. C.; Yanovski, J. A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, SGO, Program Dev Endocrinol & Genet PDEGEN, NIH,DHHS, Bethesda, MD USA.
[Ivey, L.; Sapp, J. C.; Biesecker, L. G.] NHGRI, Human Dev Sect, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Hicks, M. D.; Kim, R. C.; Han, J. C.] NICHD, Unit Metab & Neuroendocrinol, SGO, PDEGEN,NIH,DHHS, Bethesda, MD 20892 USA.
RP Yanovski, JA (reprint author), NICHD, Sect Growth & Obes, Program Dev Endocrinol & Genet, NIH,Hatfield Clin Res Ctr, 10 Ctr Dr,Room 1E 3330,MSC 1103, Bethesda, MD 20892 USA.
EM jy15i@nih.gov
OI Yanovski, Jack/0000-0001-8542-1637
FU NICHD; NHGRI, NIH
FX This research was supported by the Intramural Research Programs of the
NICHD, and NHGRI, NIH. J.A.Y. is a Commissioned Officer in the U. S.
Public Health Service, Department of Health and Human Services. The
funding organizations played no role in the design and conduct of the
study; the collection, management, analysis, and interpretation of data;
or the preparation or review of the manuscript.
NR 20
TC 3
Z9 3
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-6310
EI 2047-6302
J9 PEDIATR OBES
JI Pediatr. Obes.
PD OCT
PY 2013
VL 8
IS 5
BP E64
EP E67
DI 10.1111/j.2047-6310.2013.00182.x
PG 4
WC Pediatrics
SC Pediatrics
GA 218VY
UT WOS:000324461800004
PM 23776152
ER
PT J
AU Bornstein, MH
Hahn, CS
Suwalsky, JTD
AF Bornstein, Marc H.
Hahn, Chun-Shin
Suwalsky, Joan T. D.
TI Physically Developed and Exploratory Young Infants Contribute to Their
Own Long-Term Academic Achievement
SO PSYCHOLOGICAL SCIENCE
LA English
DT Article
DE academic achievement; adolescent development; cognitive development;
infant development
ID FIT INDEXES; 3-MONTH-OLD INFANTS; PERCEPTION; MOTOR; CHILDHOOD;
ATTENTION; CASCADES; BEHAVIOR; SYSTEMS; SKILLS
AB A developmental cascade defines a longitudinal relation in which one psychological characteristic uniquely affects another psychological characteristic later in time, separately from other intrapersonal and extrapersonal factors. Here, we report results of a large-scale (N = 374), normative, prospective, 14-year longitudinal, multivariate, multisource, controlled study of a developmental cascade from infant motor-exploratory competence at 5 months to adolescent academic achievement at 14 years, through conceptually related and age-appropriate measures of psychometric intelligence at 4 and 10 years and academic achievement at 10 years. This developmental cascade applied equally to girls and boys and was independent of children's behavioral adjustment and social competence; mothers' supportive caregiving, verbal intelligence, education, and parenting knowledge; and the material home environment. Infants who were more motorically mature and who explored more actively at 5 months of age achieved higher academic levels as 14-year-olds.
RP Bornstein, MH (reprint author), NICHHD, 6705 Rockledge Dr,Suite 8030, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU Intramural NIH HHS [ZIA HD001119-26]
NR 47
TC 24
Z9 24
U1 1
U2 27
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0956-7976
EI 1467-9280
J9 PSYCHOL SCI
JI Psychol. Sci.
PD OCT
PY 2013
VL 24
IS 10
BP 1906
EP 1917
DI 10.1177/0956797613479974
PG 12
WC Psychology, Multidisciplinary
SC Psychology
GA 233GC
UT WOS:000325554800004
PM 23964000
ER
PT J
AU Lomax, GP
Hull, SC
Lowenthal, J
Rao, M
Isasi, R
AF Lomax, Geoffrey P.
Hull, Sara Chandros
Lowenthal, Justin
Rao, Mahendra
Isasi, Rosario
TI The DISCUSS Project: Induced Pluripotent Stem Cell Lines From Previously
Collected Research Biospecimens and Informed Consent: Points to Consider
SO STEM CELLS TRANSLATIONAL MEDICINE
LA English
DT Article
AB Human somatic cell reprogramming is a leading technology for accelerating disease modeling and drug discovery. Research organizations are sponsoring initiatives to create libraries of induced pluripotent stem cell (iPSC) lines for broad distribution and application. Donor informed consent plays a critical role in supporting the ethical conduct of iPSC research. To date, our organizations have focused on informed consent considerations for somatic cell collection intended specifically for iPSC derivation and distribution. This article considers how somatic cells obtained under general (biomedical) research protocols can be used for iPSC derivation. We present draft Points to Consider regarding the use of human somatic cells for iPSC research. Our goal is to initiate a process designed to develop consensus for the use of previously collected specimens for iPSC research. We anticipate publishing final considerations in early 2014.
C1 [Lomax, Geoffrey P.] Calif Inst Regenerat Med, San Francisco, CA USA.
[Hull, Sara Chandros] NHGRI, NIH, Off Clin Director, Bethesda, MD 20892 USA.
[Hull, Sara Chandros; Lowenthal, Justin] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
[Rao, Mahendra] NIH, Ctr Regenerat Med, Bethesda, MD 20892 USA.
[Rao, Mahendra] NIAMSD, NIH, Lab Stem Cell Biol, Bethesda, MD 20892 USA.
[Isasi, Rosario] McGill Univ, Fac Med, Ctr Genom & Policy, Dept Human Genet, Montreal, PQ, Canada.
RP Lomax, GP (reprint author), 210 King St, San Francisco, CA 94107 USA.
EM glomax@cirm.ca.gov
OI Lowenthal, Justin/0000-0001-5909-0520
NR 11
TC 8
Z9 8
U1 0
U2 7
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 2157-6564
EI 2157-6580
J9 STEM CELL TRANSL MED
JI Stem Cells Transl. Med.
PD OCT
PY 2013
VL 2
IS 10
BP 727
EP 730
DI 10.5966/sctm.2013-0099
PG 4
WC Cell & Tissue Engineering
SC Cell Biology
GA 231AE
UT WOS:000325384600007
PM 23990574
ER
PT J
AU Gutova, M
Frank, JA
D'Apuzzo, M
Khankaldyyan, V
Gilchrist, MM
Annala, AJ
Metz, MZ
Abramyants, Y
Herrmann, KA
Ghoda, LY
Najbauer, J
Brown, CE
Blanchard, MS
Lesniak, MS
Kim, SU
Barish, ME
Aboody, KS
Moats, RA
AF Gutova, Margarita
Frank, Joseph A.
D'Apuzzo, Massimo
Khankaldyyan, Vazgen
Gilchrist, Megan M.
Annala, Alexander J.
Metz, Marianne Z.
Abramyants, Yelena
Herrmann, Kelsey A.
Ghoda, Lucy Y.
Najbauer, Joseph
Brown, Christine E.
Blanchard, M. Suzette
Lesniak, Maciej S.
Kim, Seung U.
Barish, Michael E.
Aboody, Karen S.
Moats, Rex A.
TI Magnetic Resonance Imaging Tracking of Ferumoxytol-Labeled Human Neural
Stem Cells: Studies Leading to Clinical Use
SO STEM CELLS TRANSLATIONAL MEDICINE
LA English
DT Article
DE Cell transplantation; Cellular therapy; Clinical trials; In vivo
tracking; Neural stem cell; Stem cell; Stem cell transplantation
ID SUPERPARAMAGNETIC IRON-OXIDE; SOLID TUMORS; NANOPARTICLES; RECEPTOR;
BRAIN; MRI; PROTAMINE; TOXICITY; DELIVERY; THERAPY
AB Numerous stem cell-based therapies are currently under clinical investigation, including the use of neural stem cells (NSCs) as delivery vehicles to target therapeutic agents to invasive brain tumors. The ability to monitor the time course, migration, and distribution of stem cells following transplantation into patients would provide critical information for optimizing treatment regimens. No effective cell-tracking methodology has yet garnered clinical acceptance. A highly promising noninvasive method for monitoring NSCs and potentially other cell types in vivo involves preloading them with ultrasmall superparamagnetic iron oxide nanoparticles (USPIOs) to enable cell tracking using magnetic resonance imaging (MRI). We report here the preclinical studies that led to U.S. Food and Drug Administration approval for first-in-human investigational use of ferumoxytol to label NSCs prior to transplantation into brain tumor patients, followed by surveillance serial MRI. A combination of heparin, protamine sulfate, and ferumoxytol (HPF) was used to label the NSCs. HPF labeling did not affect cell viability, growth kinetics, or tumor tropism in vitro, and it enabled MRI visualization of NSC distribution within orthotopic glioma xenografts. MRI revealed dynamic in vivo NSC distribution at multiple time points following intracerebral or intravenous injection into glioma-bearing mice that correlated with histological analysis. Preclinical safety/toxicity studies of intracerebrally administered HPF-labeled NSCs in mice were also performed, and they showed no significant clinical or behavioral changes, no neuronal or systemic toxicities, and no abnormal accumulation of iron in the liver or spleen. These studies support the clinical use of ferumoxytol labeling of cells for post-transplant MRI visualization and tracking.
C1 [Gutova, Margarita; Gilchrist, Megan M.; Annala, Alexander J.; Metz, Marianne Z.; Abramyants, Yelena; Herrmann, Kelsey A.; Ghoda, Lucy Y.; Najbauer, Joseph; Barish, Michael E.; Aboody, Karen S.] City Hope Natl Med Ctr, Dept Neurosci, Duarte, CA 91010 USA.
[D'Apuzzo, Massimo] City Hope Natl Med Ctr, Dept Pathol, Duarte, CA 91010 USA.
[Brown, Christine E.] City Hope Natl Med Ctr, Dept Canc Immunotherapy & Tumor Immunol, Duarte, CA 91010 USA.
[Blanchard, M. Suzette] City Hope Natl Med Ctr, Dept Informat Sci, Duarte, CA 91010 USA.
[Aboody, Karen S.] City Hope Natl Med Ctr, Div Neurosurg, Duarte, CA 91010 USA.
City Hope Natl Med Ctr, Beckman Res Inst, Duarte, CA 91010 USA.
[Frank, Joseph A.] Ctr Clin, Frank Lab Radiol & Imaging Sci, Bethesda, MD USA.
[Frank, Joseph A.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Khankaldyyan, Vazgen; Moats, Rex A.] Univ So Calif, Keck Sch Med, CHLA, Dept Radiol, Los Angeles, CA 90033 USA.
[Khankaldyyan, Vazgen; Moats, Rex A.] Univ So Calif, Keck Sch Med, CHLA, Dept Pathol, Los Angeles, CA 90033 USA.
[Khankaldyyan, Vazgen; Moats, Rex A.] Univ So Calif, Keck Sch Med, CHLA, Dept Biomed Engn, Los Angeles, CA 90033 USA.
[Lesniak, Maciej S.] Univ Chicago, Pritzker Sch Med, Brain Tumor Ctr, Chicago, IL 60637 USA.
[Kim, Seung U.] Univ British Columbia, Dept Med, Div Neurol, UBC Hosp, Vancouver, BC, Canada.
RP Moats, RA (reprint author), Dept Radiol, 4650 Sunset Blvd, Los Angeles, CA 90027 USA.
EM kaboody@coh.org; RMoats@chla.usc.edu
RI Moats, Rex/F-5995-2015
FU Naval Research Grant [N00014-02-1 0958]; California Institute for
Regenerative Medicine [DR1-01421]; NIH/National Institute of
Neurological Disorders and Stroke [U01 NS069997]; NIH/National Cancer
Institute [P30-CA033572]; Rosalinde and Arthur Gilbert Foundation; STOP
Cancer
FX We acknowledge the technical support of Elizabeth Garcia, Soraya
Aramburo, and Valerie V. Valenzuela; the technical expertise and advice
of Sofia Loera of the Pathology Core and Drs. Marcia Miller and Zhuo Li
in the Electron Microscopy Core (supported by funding from Naval
Research Grant N00014-02-1 0958); and the editorial assistance of Dr.
Keely L. Walker (City of Hope). We thank Catherine Matsumoto and
Katherine Furness of the Office of IND Development and Research Affairs
(City of Hope) for their assistance with preparation of the IND
amendment to the FDA. We also thank the Imaging Group at CHLA especially
Gevorg Karapetyan, Ira Harutyunyan, Anahit Hovsepyan, and Seda
Mkhitaryan. This work was supported by funding from the California
Institute for Regenerative Medicine (DR1-01421), NIH/National Institute
of Neurological Disorders and Stroke (U01 NS069997), NIH/National Cancer
Institute (P30-CA033572), the Rosalinde and Arthur Gilbert Foundation,
and STOP Cancer.
NR 42
TC 34
Z9 37
U1 2
U2 36
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 2157-6564
EI 2157-6580
J9 STEM CELL TRANSL MED
JI Stem Cells Transl. Med.
PD OCT
PY 2013
VL 2
IS 10
BP 766
EP 775
DI 10.5966/sctm.2013-0049
PG 10
WC Cell & Tissue Engineering
SC Cell Biology
GA 231AE
UT WOS:000325384600011
PM 24014682
ER
PT J
AU Clore, GM
Venditti, V
AF Clore, G. Marius
Venditti, Vincenzo
TI Structure, dynamics and biophysics of the cytoplasmic protein-protein
complexes of the bacterial phosphoenolpyruvate: sugar phosphotransferase
system
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
DE signal transduction; protein-protein recognition; bacterial
phosphotransferase system; NMR spectroscopy; hybrid methods in structure
determination; residual dipolar couplings; solution X-ray scattering;
sparsely populated states; encounter complexes
ID PHOSPHORYL TRANSFER COMPLEX; RESIDUAL DIPOLAR COUPLINGS; PARAMAGNETIC
RELAXATION ENHANCEMENT; MANNITOL TRANSPORTER IIMANNITOL; N-TERMINAL
DOMAIN; X-RAY-SCATTERING; TRANSIENT ENCOUNTER COMPLEXES; RESTRAINED
MOLECULAR-DYNAMICS; HIGH-RESOLUTION STRUCTURE; COLI GLUCOSE-TRANSPORTER
AB The bacterial phosphotransferase system (PTS) couples phosphoryl transfer, via a series of bimolecular protein-protein interactions, to sugar transport across the membrane. The multitude of complexes in the PTS provides a paradigm for studying protein interactions, and for understanding how the same binding surface can specifically recognize a diverse array of targets. Fifteen years of work aimed at solving the solution structures of all soluble protein-protein complexes of the PTS has served as a test bed for developing NMR and integrated hybrid approaches to study larger complexes in solution and to probe transient, spectroscopically invisible states, including encounter complexes. We review these approaches, highlighting the problems that can be tackled with these methods, and summarize the current findings on protein interactions.
C1 [Clore, G. Marius; Venditti, Vincenzo] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Clore, GM (reprint author), NIDDK, Chem Phys Lab, NIH, Bldg 2, Bethesda, MD 20892 USA.
EM mariusc@mail.nih.gov
RI Clore, G. Marius/A-3511-2008
OI Clore, G. Marius/0000-0003-3809-1027
FU Intramural Program of the NIH, NIDDK; Intramural AIDS Targeted Antiviral
Program of the Office of the Director of the NIH
FX G.M.C. thanks members of his laboratory, past and present, and
colleagues who have made major contributions to the work on complexes of
the PTS, in particular, D. Garrett, M. Cai, G. Wang, G. Cornilescu, D.
Williams, J. Hu, K Hu, J-Y. Suh, Y-S. Jung, C. Tang, J. Iwahara, Y.
Takayama, A. Grishaev, and C. Schwieters. This work was supported by
funds from the Intramural Program of the NIH, NIDDK, and the Intramural
AIDS Targeted Antiviral Program of the Office of the Director of the NIH
(to G.M.C.).
NR 100
TC 13
Z9 13
U1 0
U2 27
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 OCT
PY 2013
VL 38
IS 10
BP 515
EP 530
DI 10.1016/j.tibs.2013.08.003
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 233VG
UT WOS:000325597000006
PM 24055245
ER
PT J
AU Yaniv, Y
Juhaszova, M
Sollott, SJ
AF Yaniv, Yael
Juhaszova, Magdalena
Sollott, Steven J.
TI Age-related changes of myocardial ATP supply and demand mechanisms
SO TRENDS IN ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
DE aging; cardiac work; bioenergetics; mitochondria; respiration
ID RAT-HEART MITOCHONDRIA; OXIDATIVE-PHOSPHORYLATION; SUBSTRATE METABOLISM;
CARDIAC MITOCHONDRIA; ESSENTIAL COMPONENT; DIASTOLIC FUNCTION;
RESPIRATORY-CHAIN; LIPID-COMPOSITION; SKELETAL-MUSCLE; LEFT-VENTRICLE
AB In advanced age, the resting myocardial oxygen consumption rate (MVO2) and cardiac work (CW) in the rat remain intact. However, MVO2, CW and cardiac efficiency achieved at high demand are decreased with age, compared to maximal values in the young. Whether this deterioration is due to decrease in myocardial ATP demand, ATP supply, or the control mechanisms that match them remains controversial Here we discuss evolving perspectives of age-related changes of myocardial ATP supply and demand mechanisms, and critique experimental models used to investigate aging. Specifically, we evaluate experimental data collected at the level of isolated mitochondria, tissue, or organism, and discuss how mitochondrial energetic mechanisms change in advanced age, both at basal and high energy-demand levels.
C1 [Yaniv, Yael; Juhaszova, Magdalena; Sollott, Steven J.] NIA, Cardiovasc Sci Lab, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Sollott, SJ (reprint author), NIA, Cardiovasc Sci Lab, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
EM sollotts@mail.nih.gov
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
FU Intramural Research Program of the National Institute on Aging, National
Institutes of Health
FX We thank Dr Edward G. Lakatta for useful discussions. This work was
supported entirely by the Intramural Research Program of the National
Institute on Aging, National Institutes of Health.
NR 93
TC 9
Z9 9
U1 1
U2 7
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1043-2760
J9 TRENDS ENDOCRIN MET
JI Trends Endocrinol. Metab.
PD OCT
PY 2013
VL 24
IS 10
BP 495
EP 505
DI 10.1016/j.tem.2013.06.001
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 233RY
UT WOS:000325588400003
PM 23845538
ER
PT J
AU Svatek, RS
Rosenberg, JE
Galsky, MD
Lee, CT
Latini, DM
Bochner, BH
Weizer, AZ
Apolo, AB
Sridhar, SS
Kamat, AM
Hansel, D
Flaig, TW
Smith, ND
Lotan, Y
AF Svatek, Robert S.
Rosenberg, Jonathan E.
Galsky, Matthew D.
Lee, Cheryl T.
Latini, David M.
Bochner, Bernard H.
Weizer, Alon Z.
Apolo, Andrea B.
Sridhar, Srikala S.
Kamat, Ashish M.
Hansel, Donna
Flaig, Thomas W.
Smith, Norm D.
Lotan, Yair
TI Summary of the 6th annual bladder cancer think tank: New directions in
urologic research
SO UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS
LA English
DT Review
AB The 6th Annual Bladder Cancer Think Tank brought together a multidisciplinary group of clinicians, researchers, and representatives from the National Cancer Institute and Industry in an effort to advance bladder cancer research efforts. This year's meeting comprised panel discussions and research involving 5 separate working groups, including the Survivorship, Clinical Trials, Standardization of Care, Data Mining, and Translational Science working groups. In this manuscript, the accomplishments and objectives of the working groups are summarized. Notable efforts include: (1) the development of a survivorship care plan for early and late-stage bladder cancer; (2) the development of consensus criteria for eligibility and endpoints for bladder cancer clinical trials; (3) an improved understanding of current practice patterns regarding the use of perioperative chemotherapy in an effort to standardize care; (4) creation of a comprehensive handbook to assist researchers with developing bladder cancer databases; and (5) identification of response to therapy of high-grade non muscle invasive disease through a collaborative exchange of expertise and resources. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Svatek, Robert S.] Univ Texas Hlth Sci Ctr San Antonio, Dept Urol, San Antonio, TX 78229 USA.
[Rosenberg, Jonathan E.] Harvard Univ, Sch Med, Lank Ctr Genitourinary Oncol, Boston, MA 02215 USA.
[Galsky, Matthew D.] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY 10029 USA.
[Lee, Cheryl T.; Weizer, Alon Z.] Univ Michigan, Dept Urol, Ann Arbor, MI 48109 USA.
[Latini, David M.] Baylor Coll Med, Scott Dept Urol, Houston, TX 77030 USA.
[Bochner, Bernard H.] Mem Sloan Kettering Canc Ctr, Dept Urol, New York, NY 10065 USA.
[Apolo, Andrea B.] NCI, Med Oncol Branch & Affiliates, Bethesda, MD 20892 USA.
[Sridhar, Srikala S.] Univ Toronto, Princess Margaret Hosp, Dept Med Oncol & Hematol, Toronto, ON M5G 2M9, Canada.
[Kamat, Ashish M.] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
[Hansel, Donna] Cleveland Clin, Dept Pathol, Cleveland, OH 44195 USA.
[Flaig, Thomas W.] Univ Colorado, Sch Med, Div Med Oncol, Aurora, CO 80045 USA.
[Smith, Norm D.] Univ Chicago, Dept Urol, Chicago, IL 60637 USA.
[Lotan, Yair] Univ Texas SW Med Ctr Dallas, Dept Urol, Dallas, TX 75390 USA.
RP Lotan, Y (reprint author), Univ Texas SW Med Ctr Dallas, Dept Urol, Dallas, TX 75390 USA.
EM yair.lotan@utsouthwestern.edu
OI Latini, David/0000-0002-6161-4861
NR 3
TC 3
Z9 3
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1078-1439
EI 1873-2496
J9 UROL ONCOL-SEMIN ORI
JI Urol. Oncol.-Semin. Orig. Investig.
PD OCT
PY 2013
VL 31
IS 7
BP 968
EP 973
DI 10.1016/j.urolonc.2011.12.017
PG 6
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA 234SJ
UT WOS:000325664300003
PM 22300756
ER
PT J
AU Lambert, PF
McBride, A
Bernard, HU
AF Lambert, Paul F.
McBride, Alison
Bernard, Hans Ulrich
TI Special issue: The Papillomavirus Episteme
SO VIROLOGY
LA English
DT Editorial Material
C1 [Lambert, Paul F.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[McBride, Alison] NIH, Bethesda, MD USA.
[Bernard, Hans Ulrich] Univ Calif Irvine, Irvine, CA USA.
RP Lambert, PF (reprint author), Univ Wisconsin, Sch Med & Publ Hlth, 1400 Univ Ave, Madison, WI 53706 USA.
EM plambert@wisc.edu
OI McBride, Alison/0000-0001-5607-5157
NR 0
TC 1
Z9 1
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 0042-6822
J9 VIROLOGY
JI Virology
PD OCT
PY 2013
VL 445
IS 1-2
BP 1
EP 1
DI 10.1016/j.virol.2013.07.017
PG 1
WC Virology
SC Virology
GA 229YY
UT WOS:000325305000001
ER
PT J
AU Van Doorslaer, K
AF Van Doorslaer, Koenraad
TI Evolution of the Papillomaviridae
SO VIROLOGY
LA English
DT Article
DE Papillomayiridae; Co-evolution; Evolution; Niche adaptation;
Recombination; Codon usage; Mutation rate
ID HUMAN ALPHA-PAPILLOMAVIRUS; CODON USAGE BIAS; HPV E6 PROTEINS;
PHYLOGENETIC ANALYSIS; DIVERSIFYING SELECTION; MOLECULAR EVOLUTION; DNA
VIRUSES; RISK CLASSIFICATION; TUMOR-SUPPRESSOR; P53 DEGRADATION
AB Viruses belonging to the Papillomaviridae family have been isolated from a variety of mammals, birds and non-avian reptiles. It is likely that most, if not all, amniotes carry a broad array of viral types. To date, the complete genomic sequence of more than 240 distinct viral types has been characterized at the nucleotide level. The analysis of this sequence information has begun to shed light on the evolutionary history of this important virus family. The available data suggests that many different evolutionary mechanisms have influenced the papillomavirus phylogenetic tree. Increasing evidence supports that the ancestral papillomavirus initially specialized to infect different ecological niches on the host. This episode of niche sorting was followed by extensive episodes of co-speciation with the host. This review attempts to summarize our current understanding of the papillomavirus evolution. Published by Elsevier Inc.
C1 NIAID, DNA Tumor Virus Sect, Viral Dis Lab, NIH, Bethesda, MD USA.
RP Van Doorslaer, K (reprint author), NIAID, DNA Tumor Virus Sect, Viral Dis Lab, NIH, Bethesda, MD USA.
EM Koenraad.vandoorslaer@nih.gov
OI Van Doorslaer, Koenraad/0000-0002-2985-0733
FU Intramural Research Program of the NIH, NIAID
FX I am grateful to Drs. McBride, Khan and Heslin for critical reading of
the manuscript. The author's research is supported by the Intramural
Research Program of the NIH, NIAID.
NR 100
TC 26
Z9 26
U1 3
U2 30
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 OCT
PY 2013
VL 445
IS 1-2
BP 11
EP 20
DI 10.1016/j.viro1.2013.05.012
PG 10
WC Virology
SC Virology
GA 229YY
UT WOS:000325305000003
PM 23769415
ER
PT J
AU McBride, AA
AF McBride, Alison A.
TI The Papillomavirus E2 proteins
SO VIROLOGY
LA English
DT Article
DE HPV; Papillomavirus; E2; Replication; Transcription; Tethering;
Genomics; Structure; Mutation
ID DNA-BINDING DOMAIN; CERVICAL-CARCINOMA CELLS; COTTONTAIL RABBIT
PAPILLOMAVIRUS; TRANSCRIPTIONAL ACTIVATION FUNCTION; HPV18 REGULATORY
REGION; CARBOXY-TERMINAL DOMAIN; E1 REPLICATION PROTEIN; TYPE-8 LATE
PROMOTER; HIGH-COPY-NUMBER; BOVINE PAPILLOMAVIRUS
AB The papillomavirus E2 proteins are pivotal to the viral life cycle and have well characterized functions in transcriptional regulation, initiation of DNA replication and partitioning the viral genome. The E2 proteins also function in vegetative DNA replication, post-transcriptional processes and possibly packaging. This review describes structural and functional aspects of the E2 proteins and their binding sites on the viral genome. It is intended to be a reference guide to this viral protein. Published by Elsevier Inc.
C1 [McBride, Alison A.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP McBride, AA (reprint author), Room 3W20B4,Bldg 33,33 North Dr, Bethesda, MD 20892 USA.
EM amcbride@nih.gov
OI McBride, Alison/0000-0001-5607-5157
FU Intramural Research Program of the NIAID, NIH.
FX I am grateful to Koenraad van Doorslaer for critical reading of the
manuscript. I apologize to authors whose work I have omitted because of
space constraints. This work was funded by the Intramural Research
Program of the NIAID, NIH.
NR 291
TC 63
Z9 64
U1 1
U2 27
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 OCT
PY 2013
VL 445
IS 1-2
BP 57
EP 79
DI 10.1016/j.viro1.2013.06.006
PG 23
WC Virology
SC Virology
GA 229YY
UT WOS:000325305000006
PM 23849793
ER
PT J
AU Buck, CB
Day, PM
Trus, BL
AF Buck, Christopher B.
Day, Patricia M.
Trus, Benes L.
TI The papillomavirus major capsid protein L1
SO VIROLOGY
LA English
DT Article
DE HPV; HPV16; Virion; Papillomaviridae; L2; Maturation
ID VIRUS-LIKE PARTICLES; SURFACE HEPARAN-SULFATE; NUCLEAR IMPORT; HPV16 L1;
MONOCLONAL-ANTIBODIES; HUMAN KERATINOCYTES; DNA-BINDING; IN-VIVO;
INFECTION; TYPE-16
AB The elegant icosahedral surface of the papillomavirus virion is formed by a single protein called Ll. Recombinant Ll proteins can spontaneously self-assemble into a highly immunogenic structure that closely mimics the natural surface of native papillomavirus virions. This has served as the basis for two highly successful vaccines against cancer-causing human papillomaviruses (HPVs). During the viral life cycle, the capsid must undergo a variety of conformational changes, allowing key functions including the encapsidation of the similar to 8 kb viral genomic DNA, maturation into a more stable state to survive transit between hosts, mediating attachment to new host cells, and finally releasing the viral DNA into the newly infected host cell. This brief review focuses on conserved sequence and structural features that underlie the functions of this remarkable protein. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Buck, Christopher B.; Day, Patricia M.] NCI, Cellular Oncol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Trus, Benes L.] NIH, Imaging Sci Lab, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Buck, CB (reprint author), NCI, Cellular Oncol Lab, Ctr Canc Res, Bldg 37,Room 4118,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM buckc@mail.nih.gov
RI Kim, Seongman/N-6910-2014;
OI Buck, Christopher/0000-0003-3165-8094
FU Intramural Research Program of the NIH; Center for Information
Technology (CIT); National Cancer Institute's Center for Cancer
Research; National Institute of Arthritis, Musculoskeletal and Skin
Diseases
FX This research was supported in part by the Intramural Research Program
of the NIH, the Center for Information Technology (CIT), the National
Cancer Institute's Center for Cancer Research, and the National
Institute of Arthritis, Musculoskeletal and Skin Diseases. The authors
are grateful to Alasdair Steven and Naiqian Cheng for their work on the
HPV16 capsid structure shown in Fig. 1 and to Tom Magaldi for assistance
in rendering the structures shown in Fig. 2.
NR 69
TC 30
Z9 30
U1 3
U2 19
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 OCT
PY 2013
VL 445
IS 1-2
BP 169
EP 174
DI 10.1016/j.virol.2013.05.038
PG 6
WC Virology
SC Virology
GA 229YY
UT WOS:000325305000011
PM 23800545
ER
PT J
AU Zajicek, A
Fossler, MJ
Barrett, JS
Worthington, JH
Ternik, R
Charkoftaki, G
Lum, S
Breitkreutz, J
Baltezor, M
Macheras, P
Khan, M
Agharkar, S
MacLaren, DD
AF Zajicek, Anne
Fossler, Michael J.
Barrett, Jeffrey S.
Worthington, Jeffrey H.
Ternik, Robert
Charkoftaki, Georgia
Lum, Susan
Breitkreutz, Joerg
Baltezor, Mike
Macheras, Panos
Khan, Mansoor
Agharkar, Shreeram
MacLaren, David Douglas
TI A Report from the Pediatric Formulations Task Force: Perspectives on the
State of Child-Friendly Oral Dosage Forms
SO AAPS JOURNAL
LA English
DT Editorial Material
DE children; drugs; formulations; manufacturing; palatability; pediatrics;
regulatory
ID BIOPHARMACEUTICS CLASSIFICATION-SYSTEM; ELECTRONIC TONGUE; DOSING
ACCURACY; YOUNG-CHILDREN; DRUGS; SUSPENSIONS; ADHERENCE; SELECTION;
DELIVERY; DEVICES
AB Despite the fact that a significant percentage of the population is unable to swallow tablets and capsules, these dosage forms continue to be the default standard. These oral formulations fail many patients, especially children, because of large tablet or capsule size, poor palatability, and lack of correct dosage strength. The clinical result is often lack of adherence and therapeutic failure. The American Association of Pharmaceutical Scientists formed a Pediatric Formulations Task Force, consisting of members with various areas of expertise including pediatrics, formulation development, clinical pharmacology, and regulatory science, in order to identify pediatric, manufacturing, and regulatory issues and areas of needed research and regulatory guidance. Dosage form and palatability standards for all pediatric ages, relative bioavailability requirements, and small batch manufacturing capabilities and creation of a viable economic model were identified as particular needs. This assessment is considered an important first step for a task force seeking creative approaches to providing more appropriate oral formulations for children.
C1 [Zajicek, Anne] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Fossler, Michael J.] GlaxoSmithKline, Clin Pharmacol Modeling & Simulat, King Of Prussia, PA USA.
[Barrett, Jeffrey S.] Childrens Hosp Philadelphia, Clin Pharmacol & Therapeut Div, Philadelphia, PA 19104 USA.
[Worthington, Jeffrey H.] Senopsys LLC, Woburn, MA USA.
[Ternik, Robert] Eli Lilly & Co, Small Mol Design & Dev, Indianapolis, IN 46285 USA.
[Charkoftaki, Georgia; Macheras, Panos] Univ Athens, Fac Pharm, Lab Biopharmaceut & Pharmacokinet, Athens 11528, Greece.
[Lum, Susan] Hlth Canada, Bur Pharmaceut Sci, Therapeut Prod Directorate, Ottawa, ON K1A 0L2, Canada.
[Breitkreutz, Joerg] Univ Dusseldorf, Inst Pharmaceut & Biopharmaceut, D-40225 Dusseldorf, Germany.
[Baltezor, Mike] Univ Kansas, Inst Adv Med Innovat, Biotechnol Innovat & Optimizat Ctr, Lawrence, KS 66045 USA.
[Khan, Mansoor] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Agharkar, Shreeram] Sanofi R&D, Global CMC Strategy & Sci Affairs, Lead Generat & Candidate Realizat, Bridgewater, NJ USA.
[MacLaren, David Douglas] Eli Lilly & Co, Drug Product Dev & CT Mfg, Indianapolis, IN 46285 USA.
RP Zajicek, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
EM zajiceka@mail.nih.gov
RI Breitkreutz, Joerg/B-9581-2017
OI Breitkreutz, Joerg/0000-0002-3982-9823
NR 49
TC 17
Z9 17
U1 1
U2 27
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1550-7416
J9 AAPS J
JI AAPS J.
PD OCT
PY 2013
VL 15
IS 4
BP 1072
EP 1081
DI 10.1208/s12248-013-9511-5
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 227PR
UT WOS:000325126300018
PM 23907486
ER
PT J
AU Gandhi, AS
Zhu, MS
Pang, SK
Wohlfarth, A
Scheidweiler, KB
Liu, HF
Huestis, MA
AF Gandhi, Adarsh S.
Zhu, Mingshe
Pang, Shaokun
Wohlfarth, Ariane
Scheidweiler, Karl B.
Liu, Hua-fen
Huestis, Marilyn A.
TI First Characterization of AKB-48 Metabolism, a Novel Synthetic
Cannabinoid, Using Human Hepatocytes and High-Resolution Mass
Spectrometry
SO AAPS JOURNAL
LA English
DT Article
DE AKB-48; cannabinoids; human hepatocytes; metabolism; time-of-flight mass
spectrometry
ID LC-MS/MS; HUMAN URINE; JWH-018
AB Since the federal authorities scheduled the first synthetic cannabinoids, JWH-018 and JWH-073, new synthetic cannabinoids were robustly marketed. N-(1-Adamantyl)-1-pentylindazole-3-carboxamide (AKB-48), also known as APINACA, was recently observed in Japanese herbal smoking blends. The National Forensic Laboratory Information System registered 443 reports of AKB-48 cases in the USA from March 2010 to January 2013. In May 2013, the Drug Enforcement Administration listed AKB-48 as a Schedule I drug. Recently, AKB-48 was shown to have twice the CB1 receptor binding affinity than CB2. These pharmacological effects and the difficulty in detecting the parent compound in urine highlight the importance of metabolite identification for developing analytical methods for clinical and forensic investigations. Using human hepatocytes and TripleTOF mass spectrometry, we identified 17 novel phase I and II AKB-48 metabolites, products of monohydroxylation, dihydroxylation, or trihydroxylation on the aliphatic adamantane ring or N-pentyl side chain. Glucuronide conjugation of some mono- and dihydroxylated metabolites also occurred. Oxidation and dihydroxylation on the adamantane ring and N-pentyl side chain formed a ketone. More metabolites were identified after 3 h of incubation than at 1 h. For the first time, we present a AKB-48 metabolic scheme obtained from human hepatocytes and high-resolution mass spectrometry. These data are needed to develop analytical methods to identify AKB-48 consumption in clinical and forensic testing.
C1 [Gandhi, Adarsh S.; Wohlfarth, Ariane; Scheidweiler, Karl B.; Huestis, Marilyn A.] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Zhu, Mingshe] Bristol Myers Squibb Res & Dev, Dept Biotransformat, Princeton, NJ 08543 USA.
[Pang, Shaokun; Liu, Hua-fen] AB SCIEX, Foster City, CA 94404 USA.
RP Huestis, MA (reprint author), NIDA, Intramural Res Program, NIH, 251 Bayview Blvd,Suite 200,Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institute on Drug Abuse, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute on Drug Abuse, National Institutes of Health.
NR 23
TC 37
Z9 37
U1 3
U2 22
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1550-7416
J9 AAPS J
JI AAPS J.
PD OCT
PY 2013
VL 15
IS 4
BP 1091
EP 1098
DI 10.1208/s12248-013-9516-0
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 227PR
UT WOS:000325126300020
PM 23913126
ER
PT J
AU Glaus, J
Vandeleur, C
Gholam-Rezaee, M
Castelao, E
Perrin, M
Rothen, S
Bovet, P
Marques-Vidal, P
von Kanel, R
Merikangas, K
Mooser, V
Waterworth, DM
Waeber, G
Vollenweider, P
Preisig, M
AF Glaus, J.
Vandeleur, C.
Gholam-Rezaee, M.
Castelao, E.
Perrin, M.
Rothen, S.
Bovet, P.
Marques-Vidal, P.
von Kaenel, R.
Merikangas, K.
Mooser, V.
Waterworth, D. M.
Waeber, G.
Vollenweider, P.
Preisig, M.
TI Atypical depression and alcohol misuse are related to the cardiovascular
risk in the general population
SO ACTA PSYCHIATRICA SCANDINAVICA
LA English
DT Article
DE depression; substance use disorders; weight gain; risk factors;
cardio-vascular diseases
ID CORONARY-HEART-DISEASE; TEST-RETEST RELIABILITY; GENETIC-STUDIES DIGS;
PSYCHIATRIC-DISORDERS; DIAGNOSTIC INTERVIEW; METABOLIC SYNDROME; ANXIETY
DISORDERS; MENTAL-HEALTH; UNITED-STATES; META-ANALYSIS
AB ObjectiveThe aims of the present study were to assess the associations between mood, anxiety and substance use disorders, including their subtypes, and the prevalence of cardiovascular risk factors (CVRFs).
MethodThorough physical investigations, biological measures and standardized interview techniques were used to assess 3716 subjects of an urban area, aged 35-66 years.
ResultsAtypical depression was associated with increased prevalence of overweight, diabetes and the metabolic syndrome (OR=1.5, 95% C.I. 1.1-2.0; OR=2.0, 95% C.I. 1.1-3.5, OR=1.6, 95% C.I. 1.0-2.4 respectively), whereas decreased prevalence of overweight was found in melancholic (OR=0.7, 95% C.I. 0.6-0.9) and unspecified depression (OR=0.8, 95% C.I. 0.7-1.0). Alcohol abuse was associated with diabetes (OR=1.8, 95% C.I. 1.1-2.9) and dyslipidemia (OR=1.3, 95% C.I. 1.0-1.8), alcohol dependence with dyslipidemia only (OR=1.4, 95% C.I. 1.0-2.0). Almost all mental disorders were associated with a lifetime history of regular cigarette smoking, and atypical depression, alcohol misuse and drug dependence were associated with inactivity.
ConclusionTo conclude results emphasize the need to subtype depression and to pay particular attention to the atypical subtype. Comorbid alcohol misuse may further increase the cardiovascular risk. Efforts to diminish smoking in subjects with mental disorders could be crucial measures to reduce their high incidence of cardiovascular disease.
C1 [Glaus, J.; Vandeleur, C.; Gholam-Rezaee, M.; Castelao, E.; Perrin, M.; Rothen, S.; Preisig, M.] Univ Lausanne Hosp, Dept Psychiat, Lausanne, Switzerland.
[Bovet, P.; Marques-Vidal, P.] Univ Lausanne Hosp, Inst Social & Prevent, Lausanne, Switzerland.
[von Kaenel, R.] Univ Hosp Bern, Dept Gen Internal Med, CH-3010 Bern, Switzerland.
[Merikangas, K.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
[Mooser, V.; Waterworth, D. M.] GlaxoSmithKline, Med Genet, Philadelphia, PA USA.
[Waeber, G.; Vollenweider, P.] Univ Lausanne Hosp, Dept Internal Med, Lausanne, Switzerland.
RP Glaus, J (reprint author), Univ Lausanne Hosp, Dept Psychiat, Ctr Res Psychiat Epidemiol & Psychopathol CEPP, Site Cery, CH-1008 Prilly, Switzerland.
EM jennifer.glaus@chuv.ch
RI Colaus, PsyColaus/K-6607-2013; Rothen, Stephane/E-8325-2014; Bovet,
Pascal/F-4477-2011; Glaus, Jennifer/C-7887-2017; Marques-Vidal,
Pedro/C-9449-2009
OI Rothen, Stephane/0000-0003-3891-277X; Bovet, Pascal/0000-0002-0242-4259;
Glaus, Jennifer/0000-0001-8883-9473; Marques-Vidal,
Pedro/0000-0002-4548-8500
FU Swiss National Science Foundation [32003B-105993, 32003B-118308,
33CSC0-122661]; GlaxoSmithKline Clinical Genetics
FX The authors express their gratitude to the Lausanne inhabitants who
volunteered to participate in the PsyCoLaus study and to the
collaborators who contributed to the coordination of the study and the
collection of data. They also thank all the investigators of the CoLaus
study, who made the psychiatric study possible, as well as many GSK
employees who contributed to the execution of this study. This research
was supported by three grants from the Swiss National Science Foundation
(#32003B-105993, #32003B-118308 and #33CSC0-122661 to M. Preisig) and
two grants from GlaxoSmithKline Clinical Genetics to G. Waeber, P.
Vollenweider and M. Preisig. The funding organization played no role in
the design or conduct of the study, the collection, management,
analysis, or interpretation of the data; or the preparation, review, or
approval of the manuscript.
NR 62
TC 13
Z9 13
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-690X
J9 ACTA PSYCHIAT SCAND
JI Acta Psychiatr. Scand.
PD OCT
PY 2013
VL 128
IS 4
BP 282
EP 293
DI 10.1111/acps.12057
PG 12
WC Psychiatry
SC Psychiatry
GA 224WQ
UT WOS:000324922700006
PM 23216242
ER
PT J
AU Sparta, DR
Hopf, FW
Gibb, SL
Cho, SL
Stuber, GD
Messing, RO
Ron, D
Bonci, A
AF Sparta, Dennis R.
Hopf, Frederic Woodward
Gibb, Stuart L.
Cho, Saemi L.
Stuber, Garret D.
Messing, Robert O.
Ron, Dorit
Bonci, Antonello
TI Binge Ethanol-Drinking Potentiates Corticotropin Releasing Factor R1
Receptor Activity in the Ventral Tegmental Area
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Corticotropin Releasing Factor; Ethanol; Binge Drinking; Ventral
Tegmental Area; NMDA
ID STRESS-INDUCED RELAPSE; CRF-BINDING-PROTEIN; ADULT MALE RATS; C57BL/6J
MICE; ALCOHOL-DRINKING; EXCITATORY TRANSMISSION; POSTNATAL-DEVELOPMENT;
DOPAMINE NEURONS; SEEKING BEHAVIOR; DARK PROCEDURES
AB BackgroundCorticotropin releasing factor (CRF) and urocortin play an important role in many stress responses and also can regulate ethanol (EtOH) intake. Adaptations in CRF signaling in the central amygdala promote EtOH consumption after long-term EtOH intake in dependent animals and also after brief periods of binge EtOH intake. Thus, even brief episodes of EtOH consumption can alter the function of the CRF system, allowing CRF to regulate EtOH intake. Here, we examined whether brief binge EtOH consumption leads to CRF receptor adaptations within the ventral tegmental area (VTA), a structure involved in signaling rewarding and aversive events and important in the development and expression of drug and alcohol addiction.
MethodsWe utilized a mouse model of binge drinking known as drinking in the dark (DID), where C57BL/6J mice drink approximately 6g/kg in 4 hours and achieve blood EtOH concentrations of approximately 100mg/dl, which is equivalent to binge drinking in humans. We used ex vivo whole-cell recordings from putative VTA dopamine (DA) neurons to examine CRF regulation of NMDA receptor (NMDAR) currents. We also examined the impact of CRF receptor antagonist injection in the VTA on binge EtOH intake.
ResultsEx vivo whole-cell recordings from putative VTA DA neurons showed enhanced CRF-mediated potentiation of NMDAR currents in juvenile mice that consumed EtOH in the DID procedure. CRF-induced potentiation of NMDAR currents in EtOH-drinking mice was blocked by administration of CP-154,526 (3M), a selective CRF1 receptor antagonist. Furthermore, intra-VTA infusion of CP-154,526 (1g) significantly reduced binge EtOH consumption in adult mice. These results were not due to alterations of VTA NMDAR number or function, suggesting that binge drinking may enhance signaling through VTA CRF1 receptors onto NMDARs.
ConclusionsAltered CRF1 receptor-mediated signaling in the VTA promotes binge-like EtOH consumption in mice, which supports the idea that CRF1 receptors may therefore be a promising pharmacological target for reducing binge drinking in humans.
C1 [Sparta, Dennis R.; Hopf, Frederic Woodward; Gibb, Stuart L.; Cho, Saemi L.; Stuber, Garret D.; Messing, Robert O.; Ron, Dorit] Univ Calif San Francisco, Dept Neurol, Ernest Gallo Clin & Res Ctr, San Francisco, CA USA.
[Bonci, Antonello] NIDA, Intramural Res Program, Baltimore, MD 21224 USA.
[Bonci, Antonello] Johns Hopkins Sch Med, Solomon H Snyder Neurosci Inst, Baltimore, MD USA.
RP Hopf, FW (reprint author), Gallo Res Ctr, 5858 Horton St,Suite 200, Emeryville, CA 94608 USA.
EM woody@gallo.ucsf.edu; antonello.bonci@nih.gov
RI Messing, Robert/D-3642-2015; Stuber, Garret/E-1160-2011
OI Messing, Robert/0000-0002-5345-4431;
FU NIH [7F32AA0 18610]; NIH/NIAAA [R01A/MH13438, DA016782-06]; State of
California for medical research on alcohol and substance abuse through
the University of California, San Francisco
FX We thank A. Koopmans, L. Wang, R. Kermarrec, and A. Kisch-Hancock for
assistance with behavioral experiments. This study was supported by NIH
through 7F32AA0 18610 (DRS), NIH/NIAAA R01A/MH13438 (DR), and
DA016782-06 (AB), and funds provided by the State of California for
medical research on alcohol and substance abuse through the University
of California, San Francisco (ROM, DR, AB).
NR 59
TC 18
Z9 18
U1 1
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2013
VL 37
IS 10
BP 1680
EP 1687
DI 10.1111/acer.12153
PG 8
WC Substance Abuse
SC Substance Abuse
GA 229KR
UT WOS:000325263500007
PM 23763790
ER
PT J
AU Khan, S
Okuda, M
Hasin, DS
Secades-Villa, R
Keyes, K
Lin, KH
Grant, B
Blanco, C
AF Khan, Sharaf
Okuda, Mayumi
Hasin, Deborah S.
Secades-Villa, Roberto
Keyes, Katherine
Lin, Keng-Han
Grant, Bridget
Blanco, Carlos
TI Gender Differences in Lifetime Alcohol Dependence: Results from the
National Epidemiologic Survey on Alcohol and Related Conditions
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE NESARC; Alcohol Dependence; Gender Differences; Epidemiology
ID GENERAL-POPULATION SAMPLE; PSYCHIATRIC DIAGNOSTIC MODULES;
SUBSTANCE-ABUSE TREATMENT; IV AUDADIS-IV; UNITED-STATES; FAMILY-HISTORY;
RISK-FACTORS; USE-DISORDER; ENVIRONMENTAL CONTRIBUTIONS; 12-MONTH
PREVALENCE
AB BackgroundAn extensive clinical literature has noted gender differences in the etiology and clinical characteristics of individuals with alcohol dependence (AD). Despite this knowledge, many important questions remain.
MethodsUsing the 2001 to 2002 National Epidemiologic Survey on Alcohol and Related Conditions (n=43,093), we examined differences in sociodemographic characteristics, psychiatric and medical comorbidities, clinical correlates, risk factors, and treatment-utilization patterns of men (N=2,974) and women (N=1,807) with lifetime AD.
ResultsMen with lifetime AD were more likely than women to be diagnosed with any substance use disorder and antisocial personality disorder, whereas women were more likely to have mood and anxiety disorders. After adjusting for sociodemographic characteristics and gender differences in psychiatric comorbidity in the general population, AD was associated with externalizing disorders and any mood disorder among women only. Men with AD met more criteria, had longer episodes, and were younger at the age of first drink. There were no gender differences in remission rates. Women with AD were more likely to have a family and a spouse with history of alcohol use disorders. Treatment rates were low for both genders, and women were more likely to report social stigmatization as a treatment barrier.
ConclusionsThere are important gender differences in the psychiatric comorbidities, risk factors, clinical characteristics, and treatment-utilization patterns among individuals with lifetime AD.
C1 [Khan, Sharaf; Okuda, Mayumi; Hasin, Deborah S.; Secades-Villa, Roberto; Keyes, Katherine; Lin, Keng-Han; Blanco, Carlos] Columbia Univ, New York State Psychiat Inst, Dept Psychiat, New York, NY USA.
[Secades-Villa, Roberto] Univ Oviedo, Dept Psychol, Oviedo 33003, Spain.
[Grant, Bridget] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, Dept Hlth & Human Serv,NIH, Bethesda, MD 90034 USA.
RP Secades-Villa, R (reprint author), Univ Oviedo, Fac Psicol, Plaza Feijoo S-N, Oviedo 33003, Spain.
EM secades@uniovi.es
RI Okuda, Mayumi/L-6210-2013;
OI Okuda, Mayumi/0000-0002-3479-5599; Secades-Villa,
Roberto/0000-0001-8106-6594
FU NIH [DA019606-S3, DA020783-S4, DA019606, DA020783, DA023200, DA023973,
MH076051, MH082773, CA133050, AA014223, AA018111]; American Foundation
for Suicide Prevention; New York State Psychiatric Institute; Spanish
Ministry of Education [PR2010-0501]
FX Work on this manuscript was supported by NIH grants DA019606-S3 and
DA020783-S4 (SK), DA019606, DA020783, DA023200, DA023973, MH076051,
MH082773, and CA133050 (CB) and AA014223 and AA018111 (DSH), a grant
from the American Foundation for Suicide Prevention (CB), the New York
State Psychiatric Institute (CB, DSH), and by Spanish Ministry of
Education grant PR2010-0501 (RS-V).
NR 50
TC 20
Z9 21
U1 4
U2 24
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2013
VL 37
IS 10
BP 1696
EP 1705
DI 10.1111/acer.12158
PG 10
WC Substance Abuse
SC Substance Abuse
GA 229KR
UT WOS:000325263500009
PM 23763329
ER
PT J
AU Xuan, ZM
Nelson, TF
Heeren, T
Blanchette, J
Nelson, DE
Gruenewald, P
Naimi, TS
AF Xuan, Ziming
Nelson, Toben F.
Heeren, Timothy
Blanchette, Jason
Nelson, David E.
Gruenewald, Paul
Naimi, Timothy S.
TI Tax Policy, Adult Binge Drinking, and Youth Alcohol Consumption in the
United States
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Youth Drinking; Adult Drinking; Binge Drinking; Tax; Alcohol Policy
ID RISK BEHAVIORS; HIGH-SCHOOL; DRUG-USE; STUDENTS; SMOKING; AGE; US
AB BackgroundPrior research attributed youth alcohol consumption to the attitudes and drinking patterns among adults. Yet at a population level, few have examined the relationship between state-level adult binge drinking prevalence and youth drinking behaviors, or whether tax policy plays a role in this relationship.
MethodsWe analyzed 6 biennial surveys (1999 to 2009) of individual-level youth alcohol use and related behaviors from state-based Youth Risk Behavior Surveys and corresponding years of state-level adult binge drinking prevalence from the Behavioral Risk Factor Surveillance System. We employed logistic regression with generalized estimating equations method to assess the extent to which state adult binge drinking predicted individual-level youth drinking outcomes and examined the role of alcohol taxes in that relationship.
ResultsPopulation-aggregate analyses based on 194 state-year strata showed a positive correlation between state adult binge drinking and youth binge drinking (Pearson r=0.40, p<0.01). For individual-level youth drinking outcomes, a 5 percentage point increase in binge drinking prevalence among adults was associated with a 12% relative increase in the odds of alcohol use (adjusted OR=1.12, 95% CI: 1.08, 1.16). Taxes were strongly inversely related with adult and youth drinking measures, and the effect of tax on youth drinking was attenuated after controlling for adult binge drinking.
ConclusionsBoth tax and adult binge drinking are strong predictors of youth drinking. Tax may affect youth drinking through its effect on adult alcohol consumption. Implementing effective alcohol policies to reduce excessive drinking in the general population is an important strategy to reduce youth drinking.
C1 [Xuan, Ziming] Boston Univ, Sch Publ Hlth, Dept Community Hlth Sci, Boston, MA 02118 USA.
[Nelson, Toben F.] Univ Minnesota Epidemiol & Community Hlth, Minneapolis, MN USA.
[Heeren, Timothy] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA.
[Blanchette, Jason; Naimi, Timothy S.] Boston Med Ctr, Boston, MA USA.
[Nelson, David E.] NCI, NIH, Bethesda, MD 20892 USA.
[Gruenewald, Paul] Pacific Inst Res & Evaluat, Prevent Res Ctr, Berkeley, CA USA.
RP Xuan, ZM (reprint author), Boston Univ, Sch Publ Hlth, Dept Community Hlth Sci, 801 Massachusetts Ave, Boston, MA 02118 USA.
EM zxuan@bu.edu
OI Nelson, Toben/0000-0001-9934-7546
FU U.S. National Institutes of Health [1R01AA018377-01A1]
FX This research was supported by a grant from the U.S. National Institutes
of Health grant no. 1R01AA018377-01A1 (PI: Timothy S. Naimi). The
authors would like to thank Ms. Lisa Whittle from the CDC for her
support in providing state-based YRBS data sets and related documents,
and Dr. Dafna Kanny from the CDC for her review and comments on this
manuscript.
NR 24
TC 14
Z9 14
U1 0
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2013
VL 37
IS 10
BP 1713
EP 1719
DI 10.1111/acer.12152
PG 7
WC Substance Abuse
SC Substance Abuse
GA 229KR
UT WOS:000325263500011
PM 23711219
ER
PT J
AU Hanlon, JT
Boudreau, RM
Perera, S
Strotmeyer, ES
Newman, AB
Simonsick, EM
Shorr, RI
Bauer, DC
Donohue, JM
AF Hanlon, Joseph T.
Boudreau, Robert M.
Perera, Subashan
Strotmeyer, Elsa S.
Newman, Anne B.
Simonsick, Eleanor M.
Shorr, Ronald I.
Bauer, Douglas C.
Donohue, Julie M.
TI Racial differences in antilipemic use and lipid control in high-risk
older adults: Post-Medicare Part D
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID HEALTH-CARE ACCESS; BODY-COMPOSITION; CARDIOVASCULAR-DISEASE;
ELDERLY-PATIENTS; HEART-DISEASE; CHOLESTEROL; DISPARITIES; SENIORS;
ASSOCIATION; QUALITY
AB Background Older blacks are less likely to receive guideline-recommended antilipemic therapy and achieve lipid control than older whites because, in part, of out-of-pocket costs. We sought to determine whether racial differences in antilipemic use and lipid control narrowed after Medicare Part D's implementation.
Methods This before-after study included 1,091 black and white adults 70 years or older with coronary heart disease and/or diabetes mellitus from the Health Aging and Body Composition Study. Primary outcomes were antilipemic use and low-density lipoprotein cholesterol control. Key independent variables were race, time (pre-Part D vs post-Part D), and their interaction.
Results Before Part D, fewer blacks than whites reported taking an antilipemic (32.70% vs 49.35%), and this difference was sustained after Part D (blacks 48.30% vs whites 64.57%). Multivariable generalized estimating equations confirmed no post-Part D change in racial differences in antilipemic use (adjusted ratio of the odds ratio 1.07, 95% CI 0.79-1.45). Compared with whites, more blacks had poor lipid control both before Part D (24.30% vs 12.36%, respectively) and after Part D (24.46% vs 13.72%, respectively), with no post-Part D change in racial differences in lipid control (adjusted ratio of the odds ratio 0.82, 95% CI 0.51-1.33).
Conclusion Although antilipemic use increased after Medicare Part D for both races, this policy change was associated with a change neither in lipid control for either racial group nor in the racial differences in antilipemic use or lipid control.
C1 [Hanlon, Joseph T.; Perera, Subashan] Univ Pittsburgh, Dept Med Geriatr, Pittsburgh, PA USA.
[Boudreau, Robert M.; Strotmeyer, Elsa S.; Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Simonsick, Eleanor M.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
[Shorr, Ronald I.] North Florida South Georgia Vet Hlth Syst GRECC, Gainesville, FL USA.
[Bauer, Douglas C.] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Donohue, Julie M.] Univ Pittsburgh, Dept Hlth Policy & Management, Pittsburgh, PA USA.
RP Hanlon, JT (reprint author), Kaufman Med Bldg,Suite 514,3471 5th Ave, Pittsburgh, PA 15213 USA.
EM jth14@pitt.edu
RI Perera, Subashan/D-7603-2014; Strotmeyer, Elsa/F-3015-2014; Newman,
Anne/C-6408-2013;
OI Newman, Anne/0000-0002-0106-1150; Strotmeyer, Elsa/0000-0002-4093-6036;
Boudreau, Robert/0000-0003-0162-5187; Donohue, Julie/0000-0003-2418-6017
FU AHRQ HHS [K12 HS019461, R01 HS017695, R01 HS018721]; NCATS NIH HHS [KL2
TR000146, UL1 TR000005]; NIA NIH HHS [K07 AG033174, P30 AG024827, R01
AG027017, R01 AG028050, R01 AG034056, T32 AG021885]; NINR NIH HHS [R01
NR010135, R01 NR012459]
NR 43
TC 3
Z9 3
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2013
VL 166
IS 4
BP 792
EP 797
DI 10.1016/j.ahj.2013.07.001
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 227EL
UT WOS:000325092300036
PM 24093862
ER
PT J
AU Chuang, SC
Rota, M
Gunter, MJ
Zeleniuch-Jacquotte, A
Eussen, SJPM
Vollset, SE
Ueland, PM
Norat, T
Ziegler, RG
Vineis, P
AF Chuang, Shu-Chun
Rota, Matteo
Gunter, Marc J.
Zeleniuch-Jacquotte, Anne
Eussen, Simone J. P. M.
Vollset, Stein Emil
Ueland, Per Magne
Norat, Teresa
Ziegler, Regina G.
Vineis, Paolo
TI Quantifying the Dose-Response Relationship Between Circulating Folate
Concentrations and Colorectal Cancer in Cohort Studies: A Meta-Analysis
Based on a Flexible Meta-Regression Model
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Review
DE circulating folate; colorectal cancer; dose-response relationship
ID NESTED CASE-CONTROL; METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM;
FOLIC-ACID FORTIFICATION; PLASMA FOLATE; SERUM FOLATE;
DEGRADATION-PRODUCTS; ANALYTICAL RECOVERY; US POPULATION; RISK; DIETARY
AB Most epidemiologic studies on folate intake suggest that folate may be protective against colorectal cancer, but the results on circulating (plasma or serum) folate are mostly inconclusive. We conducted a meta-analysis of case-control studies nested within prospective studies on circulating folate and colorectal cancer risk by using flexible meta-regression models to test the linear and nonlinear dose-response relationships. A total of 8 publications (10 cohorts, representing 3,477 cases and 7,039 controls) were included in the meta-analysis. The linear and nonlinear models corresponded to relative risks of 0.96 (95 confidence interval (CI): 0.91, 1.02) and 0.99 (95 CI: 0.96, 1.02), respectively, per 10 nmol/L of circulating folate in contrast to the reference value. The pooled relative risks when comparing the highest with the lowest category were 0.80 (95 CI: 0.61, 0.99) for radioimmunoassay and 1.03 (95 CI: 0.83, 1.22) for microbiological assay. Overall, our analyses suggest a null association between circulating folate and colorectal cancer risk. The stronger association for the radioimmunoassay-based studies could reflect differences in cohorts and study designs rather than assay performance. Further investigations need to integrate more accurate measurements and flexible modeling to explore the effects of folate in the presence of genetic, lifestyle, dietary, and hormone-related factors.
C1 [Chuang, Shu-Chun] Natl Hlth Res Inst, Inst Populat Hlth Sci, Div Hlth Policy Translat, Miaoli, Taiwan.
[Chuang, Shu-Chun; Gunter, Marc J.; Norat, Teresa; Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England.
[Rota, Matteo] Univ Milano Bicocca, Dept Hlth Sci, Ctr Biostat Clin Epidemiol, Monza, Italy.
[Zeleniuch-Jacquotte, Anne] NYU, Sch Med, Dept Populat Hlth, New York, NY USA.
[Eussen, Simone J. P. M.; Ueland, Per Magne] Univ Bergen, Inst Med, Pharmacol Sect, Bergen, Norway.
[Eussen, Simone J. P. M.; Vollset, Stein Emil] Univ Bergen, Dept Publ Hlth & Primary Hlth Care, Bergen, Norway.
[Eussen, Simone J. P. M.] Maastricht Univ, Med Ctr, Dept Epidemiol, Sch Publ Hlth & Primary Care, Maastricht, Netherlands.
[Vollset, Stein Emil] Norwegian Inst Publ Hlth, Div Epidemiol, Bergen, Norway.
[Ueland, Per Magne] Haukeland Hosp, Lab Clin Biochem, N-5021 Bergen, Norway.
[Ziegler, Regina G.] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Chuang, SC (reprint author), Natl Hlth Res Inst, Inst Populat Hlth Sci, Div Hlth Policy Translat, 35 Keyan Rd, Zhunan 35053, Miaoli County, Taiwan.
EM scchuang@nhri.org.tw
RI Chuang, Shu-Chun/N-3358-2013; Rota, Matteo/B-7488-2013; Ueland,
Per/C-7340-2013; eussen, simone/C-7851-2017;
OI Zeleniuch-Jacquotte, Anne/0000-0001-9350-1303
FU World Cancer Research Fund [2008/51]; European Commission
[ECNIS2-266198]; National Health Research Institutes, Taiwan
[PH-102-PP-29]
FX This paper was made possible by grant 2008/51 from the World Cancer
Research Fund, grant ECNIS2-266198 to P.V. from the European Commission,
and grant PH-102-PP-29 to S-C.C. from the National Health Research
Institutes, Taiwan.
NR 49
TC 4
Z9 4
U1 0
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 1
PY 2013
VL 178
IS 7
BP 1028
EP 1037
DI 10.1093/aje/kwt083
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 227YN
UT WOS:000325151700005
PM 23863758
ER
PT J
AU Richard, SA
Black, RE
Gilman, RH
Guerrant, RL
Kang, G
Lanata, CF
Molbak, K
Rasmussen, ZA
Sack, RB
Valentiner-Branth, P
Checkley, W
AF Richard, Stephanie A.
Black, Robert E.
Gilman, Robert H.
Guerrant, Richard L.
Kang, Gagandeep
Lanata, Claudio F.
Molbak, Kare
Rasmussen, Zeba A.
Sack, R. Bradley
Valentiner-Branth, Palle
Checkley, William
CA Childhood Malnutrition Infection N
TI Diarrhea in Early Childhood: Short-term Association With Weight and
Long-term Association With Length
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE child health; diarrhea; malnutrition; stunting; wasting
ID RURAL BANGLADESH; PERUVIAN CHILDREN; LINEAR GROWTH; RISK-FACTORS;
YOUNG-CHILDREN; MALNUTRITION; INFECTION; COMMUNITY; HEALTH; MORBIDITY
AB The short-term association between diarrhea and weight is well-accepted, but the long-term association between diarrhea and growth is less clear. Using data from 7 cohort studies (Peru, 19851987; Peru, 19891991; Peru, 19951998; Brazil, 19891998; Guinea-Bissau, 19871990; Guinea-Bissau, 19961997; and Bangladesh, 19931996), we evaluated the lagged relationship between diarrhea and growth in the first 2 years of life. Our analysis included 1,007 children with 597,638 child-days of diarrhea surveillance and 15,629 anthropometric measurements. We calculated the associations between varying diarrhea burdens during lagged 30-day periods and length at 24 months of age. The cumulative association between the average diarrhea burden and length at age 24 months was 0.38 cm (95 confidence interval: 0.59, 0.17). Diarrhea during the 30 days prior to anthropometric measurement was consistently associated with lower weight at most ages, but there was little indication of a short-term association with length. Diarrhea was associated with a small but measurable decrease in linear growth over the long term. These findings support a focus on prevention of diarrhea as part of an overall public health strategy for improving child health and nutrition; however, more research is needed to explore catch-up growth and potential confounders.
C1 [Richard, Stephanie A.; Black, Robert E.; Gilman, Robert H.; Sack, R. Bradley; Checkley, William] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD 21205 USA.
[Guerrant, Richard L.] Univ Virginia, Sch Med, Ctr Global Hlth, Charlottesville, VA 22908 USA.
[Kang, Gagandeep] Christian Med Coll & Hosp, Dept Gastrointestinal Sci, Vellore, Tamil Nadu, India.
[Lanata, Claudio F.] Inst Invest Nutr, Lima, Peru.
[Molbak, Kare; Valentiner-Branth, Palle] Statens Serum Inst, Dept Epidemiol,Statens, DK-2300 Copenhagen, Denmark.
[Richard, Stephanie A.; Rasmussen, Zeba A.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Checkley, W (reprint author), Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, 1800 Orleans Ave,Suite 9121, Baltimore, MD 21205 USA.
EM wcheckle@jhsph.edu
OI Kang, Gagandeep/0000-0002-3656-564X
FU Bill and Melinda Gates Foundation of the Etiology, Risk Factors and
Interactions of Enteric Infections and Malnutrition; Consequences for
Child Health and Development (MAL-ED) Project; National Heart, Lung, and
Blood Institute, National Institutes of Health [R00HL096955]
FX Drs. Stephanie A. Richard and William Checkley were supported in part by
a Bill and Melinda Gates Foundation Award as part of the Etiology, Risk
Factors and Interactions of Enteric Infections and Malnutrition and the
Consequences for Child Health and Development (MAL-ED) Project. Dr.
Stephanie A. Richard was a Sommer Scholar in the Department of
International Health, Johns Hopkins Bloomberg School of Public Health,
during the conduct of this work. Dr. William Checkley was supported by a
Pathway to Independence Award (R00HL096955) from the National Heart,
Lung, and Blood Institute, National Institutes of Health.
NR 45
TC 30
Z9 31
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 OCT 1
PY 2013
VL 178
IS 7
BP 1129
EP 1138
DI 10.1093/aje/kwt094
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 227YN
UT WOS:000325151700017
PM 23966558
ER
PT J
AU Gail, MH
Sheehy, T
Cosentino, M
Pee, D
Diaz-Mayoral, NA
Garcia-Closas, M
Caporaso, NE
Pitt, K
Ziegler, RG
AF Gail, Mitchell H.
Sheehy, Tim
Cosentino, Mark
Pee, David
Diaz-Mayoral, Norma A.
Garcia-Closas, Montserrat
Caporaso, Neil E.
Pitt, Karen
Ziegler, Regina G.
TI Maximizing DNA Yield for Epidemiologic Studies: No More Buffy Coats?
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE all-cell-pellet fraction; buffy coat; DNA extraction yield; residual
blood cells; whole blood
ID BLOOD; STORAGE
AB Some molecular analyses require microgram quantities of DNA, yet many epidemiologic studies preserve only the buffy coat. In Frederick, Maryland, in 2010, we estimated DNA yields from 5 mL of whole blood and from equivalent amounts of all-cell-pellet (ACP) fraction, buffy coat, and residual blood cells from fresh blood (n 10 volunteers) and from both fresh and frozen blood (n 10). We extracted DNA with the QIAamp DNA Blood Midi Kit (Qiagen Sciences, Germantown, Maryland) for silica spin column capture and measured double-stranded DNA. Yields from frozen blood fractions were not statistically significantly different from those obtained from fresh fractions. ACP fractions yielded 80.6 (95 confidence interval: 66, 97) of the yield of frozen whole blood and 99.3 (95 confidence interval: 86, 100) of the yield of fresh blood. Frozen buffy coat and residual blood cells each yielded only half as much DNA as frozen ACP, and the yields were more variable. Assuming that DNA yield and quality from frozen ACP are stable, we recommend freezing plasma and ACP. Not only does ACP yield twice as much DNA as buffy coat but it is easier to process, and its yield is less variable from person to person. Long-term stability studies are needed. If one wishes to separate buffy coat before freezing, one should also save the residual blood cell fraction, which contains just as much DNA.
C1 [Gail, Mitchell H.; Caporaso, Neil E.; Pitt, Karen; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Cosentino, Mark; Diaz-Mayoral, Norma A.] SAIC Frederick Inc, Lab Biospecimen & Biorepository Res, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Pee, David] Informat Management Serv Inc, Rockville, MD USA.
[Sheehy, Tim] Promega, Global Genom, Madison, WI USA.
[Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, Sutton, Surrey, England.
RP Gail, MH (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 7-E138, Bethesda, MD 20892 USA.
EM gailm@mail.nih.gov
RI Diaz-Mayoral, Norma/B-8416-2012; Garcia-Closas, Montserrat /F-3871-2015
OI Garcia-Closas, Montserrat /0000-0003-1033-2650
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Intramural Research Program of the Division of
Cancer Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health
FX This project was funded in whole or in part by the National Cancer
Institute, National Institutes of Health, under contract
HHSN261200800001E and by the Intramural Research Program of the Division
of Cancer Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health.
NR 7
TC 3
Z9 3
U1 0
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 OCT 1
PY 2013
VL 178
IS 7
BP 1170
EP 1176
DI 10.1093/aje/kwt079
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 227YN
UT WOS:000325151700022
PM 23857774
ER
PT J
AU Pantin, J
Tian, X
Shah, AA
Kurlander, R
Ramos, C
Cook, L
Khuu, H
Stroncek, D
Leitman, S
Barrett, J
Donohue, T
Young, NS
Geller, N
Childs, RW
AF Pantin, Jeremy
Tian, Xin
Shah, Avni A.
Kurlander, Roger
Ramos, Catalina
Cook, Lisa
Khuu, Hahn
Stroncek, David
Leitman, Susan
Barrett, John
Donohue, Theresa
Young, Neal S.
Geller, Nancy
Childs, Richard W.
TI Rapid donor T-cell engraftment increases the risk of chronic
graft-versus-host disease following salvage allogeneic peripheral blood
hematopoietic cell transplantation for bone marrow failure syndromes
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID SEVERE APLASTIC-ANEMIA; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA;
COLONY-STIMULATING FACTOR; IDENTICAL SIBLING TRANSPLANTATION;
ANTITHYMOCYTE GLOBULIN; IRON OVERLOAD; STEM-CELLS; IMMUNOSUPPRESSIVE
THERAPY; MYELODYSPLASTIC SYNDROME; UNRELATED DONORS
AB The risk of graft-rejection after allogeneic hematopoietic cell transplantation using conventional cyclophosphamide-based conditioning is increased in patients with bone marrow failure syndromes (BMFS) who are heavily transfused and often HLA-alloimmunized. Fifty-six patients with BMFS underwent fludarabine-based reduced-intensity conditioning and allogeneic peripheral blood progenitor cell (PBPC) transplantation at a single institution. The conditioning regimen consisted of intravenous cyclophosphamide, fludarabine, and equine antithymocyte globulin. Graft-versus-host disease (GVHD) prophylaxis included cyclosporine A alone or in combination with either mycophenolate mofetil or methotrexate. To reduce the risk of graft-rejection/failure, unmanipulated G-CSF mobilized PBPCs obtained from an HLA-identical or single HLA-antigen mismatched relative were transplanted rather than donor bone marrow. Despite a high prevalence of pretransplant HLA-alloimmunization (41%) and a heavy prior transfusion burden, graft-failure did not occur with all patients having sustained donor lympho-hematopoietic engraftment. The cumulative incidence of grade II-IV acute-GVHD and chronic-GVHD was 51.8% and 72%, respectively; with 87.1% surviving at a median follow-up of 4.5 years. A multivariate analysis showed pretransplant alloimmunization and rapid donor T-cell engraftment (95% donor by day 30) were both significantly (P < 0.05) associated with the development of chronic-GVHD (adjusted HR 2.13 and 2.99, respectively). These data show fludarabine-based PBPC transplantation overcomes the risk of graft-failure in patients with BMFS, although rapid donor T-cell engraftment associated with this approach appears to increase the risk of chronic-GVHD. (Clinicaltrials.gov identifier: NCT00003838). Am. J. Hematol. 88:874-882, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Pantin, Jeremy; Ramos, Catalina; Cook, Lisa; Barrett, John; Donohue, Theresa; Young, Neal S.; Childs, Richard W.] NHLBI, Hematol Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Pantin, Jeremy] Georgia Regents Univ, Div Hematol Med Oncol & BMT, Dept Med, Augusta, GA USA.
[Tian, Xin; Geller, Nancy] NHLBI, Off Biostat Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Shah, Avni A.] NCI, Med Oncol Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Kurlander, Roger] NIH, Dept Lab Med, Clin Res Ctr, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Khuu, Hahn; Stroncek, David; Leitman, Susan] NIH, Dept Transfus Med, Clin Res Ctr, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Childs, RW (reprint author), NHLBI, Hematol Branch, NIH, 10 Ctr Dr,Bldg 10 CRC Rm 3E-5330, Bethesda, MD 20892 USA.
EM childsr@nih.gov
OI Pantin, Jeremy/0000-0001-7536-0623
FU NIH, NHLBI
FX Contract grant sponsor: Intramural Research Program of the NIH, NHLBI.
NR 60
TC 3
Z9 3
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD OCT
PY 2013
VL 88
IS 10
BP 874
EP 882
DI 10.1002/ajh.23526
PG 9
WC Hematology
SC Hematology
GA 224UP
UT WOS:000324915600009
PM 23813900
ER
PT J
AU Lai, WS
Stumpo, DJ
Kennington, EA
Burkholder, AB
Ward, JM
Fargo, DL
Blackshear, PJ
AF Lai, Wi S.
Stumpo, Deborah J.
Kennington, Elizabeth A.
Burkholder, Adam B.
Ward, James M.
Fargo, David L.
Blackshear, Perry J.
TI Life without TTP: apparent absence of an important anti-inflammatory
protein in birds
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE tristetraprolin; zinc finger proteins; innate immunity; AU-rich
elements; mRNA turnover
ID TRISTETRAPROLIN-DEFICIENCY SYNDROME; MESSENGER-RNA DECAY; TNF-ALPHA;
CHICKEN; CELLS; SENSITIVITY; ZFP36L3; GENOME; FAMILY; MEMBER
AB Both innate and adaptive immunity in birds are different from their mammalian counterparts. Understanding bird immunity is important because of the enormous potential impact of avian infectious diseases, both in their role as food animals and as potential carriers of zoonotic diseases in man. The anti-inflammatory protein tristetraprolin (TTP) is an important component of the mammalian innate immune response, in that it binds to and destabilizes key cytokine mRNAs. TTP knockout mice exhibit a severe systemic inflammatory syndrome, and they are abnormally sensitive to innate immune stimuli such as LPS. TTP orthologs have been found in most vertebrates studied, including frogs. Here, we attempted to identify TTP orthologs in chicken and other birds, using database searches and deep mRNA sequencing. Although sequences encoding the two other widely expressed TTP family members, ZFP36L1 and ZFP36L2, were identified, we did not find sequences corresponding to TTP in any bird species. Sequences corresponding to TTP were identified in both lizards and alligators, close evolutionary relatives of birds. The induction kinetics of Zfp36l1 and Zfp36l2 mRNAs in LPS-stimulated chicken macrophages or serum-stimulated chick embryo fibroblasts did not resemble the normal mammalian TTP response to these stimuli, suggesting that the other two family members might not compensate for the TTP deficiency in regulating rapidly induced mRNA targets. Several mammalian TTP target transcripts have chicken counterparts that contain one or more potential TTP binding sites, raising the possibility that birds express other proteins that subsume TTP's function as a rapidly inducible regulator of AU-rich element (ARE)-dependent mRNA turnover.
C1 [Lai, Wi S.; Stumpo, Deborah J.; Kennington, Elizabeth A.; Blackshear, Perry J.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA.
[Burkholder, Adam B.; Ward, James M.; Fargo, David L.] NIEHS, Integrat Bioinformat Grp, Res Triangle Pk, NC 27709 USA.
[Blackshear, Perry J.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Blackshear, Perry J.] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA.
RP Blackshear, PJ (reprint author), NIEHS, Box F1-13,Bldg 101,111 Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM black009@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences
FX We are grateful to the members of the National Institutes of Health
(NIH) Intramural Sequencing Center for their help with mRNASeq. We thank
Drs. Jacqueline Smith and David Burt for helpful discussions, Dr. Uma
Babu of the FDA for the HD11 cells, and Dr. Tom Randall for help with
the phylogenetic analysis. We thank Drs. Dori Germolec and Bill Schrader
for critical review of the manuscript. This study was supported by the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences.
NR 32
TC 8
Z9 8
U1 0
U2 7
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD OCT
PY 2013
VL 305
IS 7
BP R689
EP R700
DI 10.1152/ajpregu.00310.2013
PG 12
WC Physiology
SC Physiology
GA 230PB
UT WOS:000325353000004
PM 23904106
ER
PT J
AU Deveney, CM
Connolly, ME
Haring, CT
Bones, BL
Reynolds, RC
Kim, P
Pine, DS
Leibenluft, E
AF Deveney, Christen M.
Connolly, Megan E.
Haring, Catherine T.
Bones, Brian L.
Reynolds, Richard C.
Kim, Pilyoung
Pine, Daniel S.
Leibenluft, Ellen
TI Neural Mechanisms of Frustration in Chronically Irritable Children
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID PEDIATRIC BIPOLAR DISORDER; SEVERE MOOD DYSREGULATION; EMOTION
REGULATION; BEHAVIORAL-RESPONSES; NEGATIVE AFFECT; REWARD; CORTEX;
ANGER; RISK
AB Objective: Irritability is common in children and adolescents and is the cardinal symptom of disruptive mood dysregulation disorder, a new DSM-5 disorder, yet its neural correlates remain largely unexplored. The authors conducted a functional MRI study to examine neural responses to frustration in children with severe mood dysregulation.
Method: The authors compared emotional responses, behavior, and neural activity between 19 severely irritable children (operationalized using criteria for severe mood dysregulation) and 23 healthy comparison children during a cued-attention task completed under nonfrustrating and frustrating conditions.
Results: Children in both the severe mood dysregulation and the healthy comparison groups reported increased frustration and exhibited decreased ability to shift spatial attention during the frustration condition relative to the nonfrustration condition. However, these effects of frustration were more marked in the severe. mood dysregulation group than in the comparison group.. During the frustration condition, participants in the severe mood dysregulation group exhibited deactivation of the left amygdala, the left and right striatum, the parietal cortex, and the posterior cingulate on negative feedback trials, relative to the comparison group (i.e., between-group effect) and to the severe mood dysregulation group's responses on positive feedback trials (i.e., within-group effect). In contrast, neural response to positive feedback during the frustration condition did not differ between groups.
Conclusions: In response to negative feedback received in the context of frustration, children with severe, chronic irritability showed abnormally reduced activation in regions implicated in emotion, attention, and reward processing. Frustration appears to reduce attention flexibility, particularly in severely irritable children, which may contribute to emotion regulation deficits in this population. Further research is needed to relate these findings to irritability specifically, rather than to other clinical features of severe mood dysregulation.
C1 [Deveney, Christen M.] NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
NIMH, Sci & Stat Comp Core, Bethesda, MD 20892 USA.
RP Deveney, CM (reprint author), NIMH, Emot & Dev Branch, Bethesda, MD 20892 USA.
EM deveneycm@mail.nih.gov
FU NIMH Intramural Research Program
FX Supported by the NIMH Intramural Research Program.
NR 26
TC 26
Z9 26
U1 1
U2 21
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2013
VL 170
IS 10
BP 1186
EP 1194
DI 10.1176/appi.ajp.2013.12070917
PG 9
WC Psychiatry
SC Psychiatry
GA 230ZV
UT WOS:000325383700020
PM 23732841
ER
PT J
AU Britton, JC
Grillon, C
Lissek, S
Norcross, MA
Szuhany, KL
Chen, G
Ernst, M
Nelson, EE
Leibenluft, E
Shechner, T
Pine, DS
AF Britton, Jennifer C.
Grillon, Christian
Lissek, Shmuel
Norcross, Maxine A.
Szuhany, Kristin L.
Chen, Gang
Ernst, Monique
Nelson, Eric E.
Leibenluft, Ellen
Shechner, Tomer
Pine, Daniel S.
TI Response to Learned Threat: An fMRI Study in Adolescent and Adult
Anxiety
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID CONDITIONED FEAR; CHILDHOOD ANXIETY; PREFRONTAL CORTEX; PANIC DISORDER;
EXTINCTION; HUMANS; MECHANISMS; CHILDREN; RISK; AMYGDALA
AB Objective: Poor threat-safety discrimination reflects prefrontal cortex dysfunction in adult anxiety disorder's. While adolescent anxiety disorders are impairing and predict high risk for adult anxiety disorders, the neural correlates of threat-safety discrimination have not been investigated in this population. The authors compared prefrontal cortex function in anxious and healthy adolescents and adults following conditioning and extinction, processes requiring threat-safety learning.
Method: Anxious and healthy adolescents and adults (N=114) completed fear conditioning and extinction in the clinic. The conditioned stimuli (CS+) were neutral faces, paired with an aversive scream. Physiological and subjective data were acquired. Three weeks later, 82 participants viewed the CS+ and morphed images resembling the CS+ in an MRI scanner. During scanning, participants made difficult threat-safety discriminations while appraising threat and explicit memory of the CS+.
Results: During conditioning and extinction, the anxious groups reported more fear than the healthy groups, but the anxious adolescent and adult groups did not differ on physiological measures. During imaging, both anxious adolescents and adults exhibited lower activation in the subgenual anterior cingulate cortex than their healthy counterparts, specifically when appraising threat. Compared with their age-matched counterpart groups, anxious adults exhibited reduced activation in the ventromedial prefrontal cortex when appraising threat, whereas anxious adolescents exhibited a U-shaped pattern of activation, with greater activation in response to the most extreme CS+ and CS-.
Conclusions: Two regions of the prefrontal cortex are involved in anxiety disorders. Reduced subgenual anterior cingulate cortex engagement is a shared feature in adult and adolescent anxiety disorders, but ventromedial prefrontal cortex dysfunction is age-specific. The unique U-shaped pattern of activation in the ventromedial prefrontal cortex in many anxious adolescents may reflect heightened sensitivity to threat and safety conditions. How variations in the pattern relate to later risk for adult illness remains to be determined.
C1 [Britton, Jennifer C.] Univ Miami, Dept Psychol, Coral Gables, FL 33124 USA.
NIMH, Bethesda, MD 20892 USA.
Univ Minnesota, Dept Psychol, Minneapolis, MN 55455 USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
Boston Univ, Dept Psychol, Boston, MA 02215 USA.
RP Britton, JC (reprint author), Univ Miami, Dept Psychol, POB 248185, Coral Gables, FL 33124 USA.
EM j.britton@miami.edu
OI Nelson, Eric/0000-0002-3376-2453
FU Intramural Research Program of NIMH/NIH [K99-MH-091183]
FX Supported in part by grant K99-MH-091183 from the Intramural Research
Program of NIMH/NIH (to Dr. Britton).
NR 35
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U1 3
U2 20
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2013
VL 170
IS 10
BP 1195
EP 1204
DI 10.1176/appi.ajp.2013.12050651
PG 10
WC Psychiatry
SC Psychiatry
GA 230ZV
UT WOS:000325383700021
PM 23929092
ER
PT J
AU Rajendran, K
Trampush, JW
Rindskopf, D
Marks, DJ
O'Neill, S
Halperin, JM
AF Rajendran, Khushmand
Trampush, Joey W.
Rindskopf, David
Marks, David J.
O'Neill, Sarah
Halperin, Jeffrey M.
TI Association Between Variation in Neuropsychological Development and
Trajectory of ADHD Severity in Early Childhood
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ADOLESCENTS/YOUNG ADULTS;
PREFRONTAL CORTEX; BRAIN-DEVELOPMENT; TEACHER RATINGS; DIAGNOSED ADHD;
CHILDREN; PRESCHOOL; SYMPTOMS; IMPACT
AB Objective: This longitudinal study examined if changes in neuropsychological functioning were associated with the trajectory of symptoms related to attention deficit hyperactivity disorder (ADHD) and impairment between preschool and school age.
Method: The sample consisted of 3- and 4-year-old children (N=138) who were identified as being at risk for ADHD based on parent and teacher reports. Neuropsychological functioning was measured annually using the NEPSY at four time points (mean ages, 4.19, 5.36, 6.35, and 7.35 years). ADHD symptoms and impairment were assessed with semiannual parent and teacher reports using the ADHD Rating Scale-IV and the Children's Problems Checklist at 10 time points (mean ages at baseline and final assessment, 4.19 and 8.81 years, respectively). Hierarchical linear modeling was used to assess the trajectories of change in neuropsychological functioning and ADHD severity as well as the association of change in neuropsychological functioning with change in ADHD severity over time.
Results: Baseline neuropsychological functioning was not significantly associated with the slope of change in ADHD severity. However, the magnitude of change in neuropsychological functioning was linearly associated with the trajectory of ADHD symptom severity and impairment, such that individuals with greater neuropsychological growth over time had a greater diminution of ADHD severity and impairment. Family socioeconomic status at baseline was significantly associated with initial ADHD severity and impairment, but not with change over time.
Conclusions: Interventions that enhance neuropsychological functioning at an early age may be beneficial in attenuating long-term ADHD severity and impairment.
C1 [Halperin, Jeffrey M.] CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
Zucker Hillside Hosp, Div Psychiat Res, Glen Oaks, NY USA.
Feinstein Inst Med Res, Ctr Psychiat Neurosci, Glen Oaks, NY USA.
NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA.
CUNY, Grad Ctr, New York, NY USA.
NYU, Langone Med Ctr, Ctr Child Study, New York, NY 10003 USA.
RP Halperin, JM (reprint author), CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
EM jeffrey.halperin@qc.cuny.edu
OI Marks, David/0000-0002-8133-2730
FU NIMH [R01MH068286]
FX Supported by NIMH grant R01MH068286 (principal investigator, J.M.H.).
NR 39
TC 17
Z9 17
U1 1
U2 20
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2013
VL 170
IS 10
BP 1205
EP 1211
DI 10.1176/appi.ajp.2012.12101360
PG 7
WC Psychiatry
SC Psychiatry
GA 230ZV
UT WOS:000325383700022
PM 23897408
ER
PT J
AU Sayers, BC
Taylor, AJ
Glista-Baker, EE
Shipley-Phillips, JK
Dackor, RT
Edin, ML
Lih, FB
Tomer, KB
Zeldin, DC
Langenbach, R
Bonner, JC
AF Sayers, Brian C.
Taylor, Alexia J.
Glista-Baker, Ellen E.
Shipley-Phillips, Jeanette K.
Dackor, Ryan T.
Edin, Matthew L.
Lih, Fred B.
Tomer, Kenneth B.
Zeldin, Darryl C.
Langenbach, Robert
Bonner, James C.
TI Role of Cyclooxygenase-2 in Exacerbation of Allergen-Induced Airway
Remodeling by Multiwalled Carbon Nanotubes
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE carbon nanotubes; nanoparticles; asthma; inflammation; COX-2
ID ULTRAFINE PARTICLES; PROSTAGLANDIN D-2; EPITHELIAL-CELLS; LUNG-DISEASES;
ASTHMA; MICE; INFLAMMATION; INTERLEUKIN-13; IL-13; HYPERRESPONSIVENESS
AB The emergence of nanotechnology has produced a multitude of engineered nanomaterials such as carbon nanotubes (CNTs), and concerns have been raised about their effects on human health, especially for susceptible populations such as individuals with asthma. Multiwalled CNTs (MWCNTs) have been shown to exacerbate ovalbumin (OVA)-induced airway remodeling in mice. Moreover, cyclooxygenase-2 (COX-2) has been described as a protective factor in asthma. We postulated that COX-2-deficient (COX-2(-/-)) mice would be susceptible to MWCNT-induced exacerbations of allergen-induced airway remodeling, including airway inflammation, fibrosis, and mucus-cell metaplasia (i.e., the formation of goblet cells). Wild-type (WT) or COX-2(-/-) mice were sensitized to OVA to induce allergic airway inflammation before a single dose of MWCNTs (4 mg/kg) delivered to the lungs by oropharyngeal aspiration. MWCNTs significantly increased OVA-induced lung inflammation and mucus-cell metaplasia in COX-2(-/-) mice compared with WT mice. However, airway fibrosis after exposure to allergen and MWCNTs was no different between WT and COX-2(-/-) mice. Concentrations of certain prostanoids (prostaglandinD2 and thromboxane B-2) were enhanced by OVA or MWCNTs in COX-2(-/-) mice. No differences in COX-1 mRNA concentrations were evident between WT and COX-2(-/-) mice treated with OVA and MWCNTs. Interestingly, MWCNTs significantly enhanced allergen-induced cytokines involved in Th2 (IL-13 and IL-5), Th1 (CXCL10), and Th17 (IL-17A) inflammatory responses in COX-2(-/-) mice, but not in WT mice. We conclude that exacerbations of allergen-induced airway inflammation and mucus-cell metaplasia by MWCNTs are enhanced by deficiencies in COX-2, and are associated with the activation of a mixed Th1/Th2/Th17 immune response.
C1 [Sayers, Brian C.; Taylor, Alexia J.; Glista-Baker, Ellen E.; Bonner, James C.] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA.
[Shipley-Phillips, Jeanette K.] N Carolina State Univ, Coll Vet Med, Dept Populat Hlth & Pathobiol, Lab Adv Elect & Light Opt Methods, Raleigh, NC USA.
[Dackor, Ryan T.; Edin, Matthew L.; Zeldin, Darryl C.] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Lih, Fred B.; Tomer, Kenneth B.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Langenbach, Robert] NIEHS, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
RP Bonner, JC (reprint author), N Carolina State Univ, Dept Environm & Mol Toxicol, Campus Box 7633, Raleigh, NC 27695 USA.
EM james_bonner@ncsu.edu
OI Edin, Matthew/0000-0002-7042-500X
FU National Institute of Environmental Health Sciences [RC2-ES018772,
R01-ES020897]; Intramural Research Program of the National Institutes of
Health; National Institutes of Environmental Health Sciences
[T32-ES007046-31]
FX This work was funded by National Institute of Environmental Health
Sciences grants RC2-ES018772 (J.C.B.) and R01-ES020897 (J.C.B.), and the
Intramural Research Program of the National Institutes of Health and the
National Institutes of Environmental Health Sciences (D. C. Z., R. L.,
R. T. D., M. L. E., F. B. L., and K. B. T.). E.E.G.-B. and B. C. S. are
supported by National Institute of Environmental Health Sciences
training grant T32-ES007046-31.
NR 51
TC 11
Z9 12
U1 0
U2 7
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD OCT
PY 2013
VL 49
IS 4
BP 525
EP 535
DI 10.1165/rcmb.2013-0019OC
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 230OQ
UT WOS:000325351700004
PM 23642096
ER
PT J
AU Hricik, DE
Nickerson, P
Formica, RN
Poggio, ED
Rush, D
Newell, KA
Goebel, J
Gibson, IW
Fairchild, RL
Riggs, M
Spain, K
Ikle, D
Bridges, ND
Heeger, PS
AF Hricik, D. E.
Nickerson, P.
Formica, R. N.
Poggio, E. D.
Rush, D.
Newell, K. A.
Goebel, J.
Gibson, I. W.
Fairchild, R. L.
Riggs, M.
Spain, K.
Ikle, D.
Bridges, N. D.
Heeger, P. S.
CA CTOT-01 Consortium
TI Multicenter Validation of Urinary CXCL9 as a Risk-Stratifying Biomarker
for Kidney Transplant Injury
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Acute rejection; biomarker; chemokines; kidney allograft; kidney graft
function
ID RENAL-ALLOGRAFT REJECTION; MESSENGER-RNA; T-CELLS; MODELS; CXCR3;
CLASSIFICATION; INFLAMMATION; EXPRESSION; PREDICTION; CHEMOKINES
AB Noninvasive biomarkers are needed to assess immune risk and ultimately guide therapeutic decision-making following kidney transplantation. A requisite step toward these goals is validation of markers that diagnose and/or predict relevant transplant endpoints. The Clinical Trials in Organ Transplantation-01 protocol is a multicenter observational study of biomarkers in 280 adult and pediatric first kidney transplant recipients. We compared and validated urinary mRNAs and proteins as biomarkers to diagnose biopsy-proven acute rejection (AR) and stratify patients into groups based on risk for developing AR or progressive renal dysfunction. Among markers tested for diagnosing AR, urinary CXCL9 mRNA (odds ratio [OR] 2.77, positive predictive value [PPV] 61.5%, negative predictive value [NPV] 83%) and CXCL9 protein (OR 3.40, PPV 67.6%, NPV 92%) were the most robust. Low urinary CXCL9 protein in 6-month posttransplant urines obtained from stable allograft recipients classified individuals least likely to develop future AR or a decrement in estimated glomerular filtration rate between 6 and 24 months (92.5-99.3% NPV). Our results support using urinary CXCL9 for clinical decision-making following kidney transplantation. In the context of acute dysfunction, low values can rule out infectious/immunological causes of injury. Absent urinary CXCL9 at 6 months posttransplant defines a subgroup at low risk for incipient immune injury.
C1 [Hricik, D. E.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Nickerson, P.; Rush, D.; Gibson, I. W.] Univ Manitoba, Winnipeg, MB, Canada.
[Formica, R. N.] Yale Univ, Sch Med, New Haven, CT USA.
[Poggio, E. D.; Fairchild, R. L.] Cleveland Clin, Cleveland, OH 44106 USA.
[Newell, K. A.] Emory Univ, Med Ctr, Atlanta, GA 30322 USA.
[Goebel, J.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Riggs, M.; Spain, K.; Ikle, D.] Rho, Chapel Hill, NC USA.
[Bridges, N. D.] NIAID, Transplantat Branch, NIH, Bethesda, MD 20892 USA.
[Heeger, P. S.] Mt Sinai, Icahn Sch Med, New York, NY 10029 USA.
RP Heeger, PS (reprint author), Mt Sinai, Icahn Sch Med, New York, NY 10029 USA.
EM peter.heeger@mssm.edu
OI Rush, David/0000-0002-3451-9447; Nickerson, Peter/0000-0002-7393-7799
FU National Institutes of Health [AI63594-06]
FX The study was supported by National Institutes of Health U01 grant
AI63594-06 awarded to P. Heeger. The CTOT-01 consortium members thank
the following personnel for the support of the work: Cincinnati
Children's Hospital, Cincinnati, OH: Barbara Logan; Cleveland Clinic,
Cleveland, OH: Jennifer Czerr and Leslie Iosue; Emory University Medical
Center, Atlanta, GA: Brandi Johnson, Margret Kamel and Amy S. Newell;
Icahn School of Medicine at Mount Sinai, New York, NY: Dean Firkus,
Brandy Haydel, Neha Karajgikhar, Sherif Mikhail, Katya Ostrow, Yasir
Qureshi, Jason Rothfeld, Jennifer Smar, Paulina Trzcinka, Rosie Wickham,
Tina Yao and Praeophayom Wauhop; University Hospitals Case Medical
Center, Cleveland, OH: Victoria Rodriguez, Maureen Tessman and Tracey
Lee; University of Manitoba, Winnipeg Manitoba, Canada: Jennifer
Bestland, Iga Dembinski, Shirley Frederickson, Susan McMurrich and Myrna
Ross.
NR 30
TC 52
Z9 53
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD OCT
PY 2013
VL 13
IS 10
BP 2634
EP 2644
DI 10.1111/ajt.12426
PG 11
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 224ZN
UT WOS:000324932200018
PM 23968332
ER
PT J
AU Kelly, RJ
Thomas, A
Rajan, A
Chun, G
Lopez-Chavez, A
Szabo, E
Spencer, S
Carter, CA
Guha, U
Khozin, S
Poondru, S
Van Sant, C
Keating, A
Steinberg, SM
Figg, W
Giaccone, G
AF Kelly, R. J.
Thomas, A.
Rajan, A.
Chun, G.
Lopez-Chavez, A.
Szabo, E.
Spencer, S.
Carter, C. A.
Guha, U.
Khozin, S.
Poondru, S.
Van Sant, C.
Keating, A.
Steinberg, S. M.
Figg, W.
Giaccone, G.
TI A phase I/II study of sepantronium bromide (YM155, survivin suppressor)
with paclitaxel and carboplatin in patients with advanced non-small-cell
lung cancer
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE survivin; non-small-cell lung cancer; apoptosis; sepantronium bromide
ID SOLID TUMORS; APOPTOSIS; PATHWAY
AB This phase I/II study examined the safety and efficacy of Sepantronium Bromide (S), a small-molecule selective survivin suppressant, administered in combination with carboplatin (C) and paclitaxel (P).
Forty-one patients were treated on study. Twenty-two patients received escalating doses of S (3.6-12 mg/m(2)) and 19 with untreated stage IV non-small-cell lung cancer (NSCLC) were treated with the maximum tolerated dose of 10 mg/m(2) in combination with standard doses of C (AUC6) and P (200 mg/m(2)) for six cycles. S was administered as a continuous intravenous infusion (CIVI) over 72 h in 21-day treatment cycles. Study end points included safety and toxic effect, response rate, progression-free and overall survival (PFS and OS), as well as exploratory pharmacodynamic correlates.
Treatment with S was well tolerated, and toxic effects were mostly hematological in the phase II study. Two (11%) partial responses were observed with a median PFS of 5.7 months and median OS 16.1 months. Pharmacodynamic analysis did not demonstrate an association with response.
The combination of S (10 mg/m(2)/day 72-h CIVI) administered with C and P every 3 weeks exhibited a favorable safety profile but failed to demonstrate an improvement in response rate in advanced NSCLC.
NCT01100931.
C1 [Kelly, R. J.] Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Thomas, A.; Rajan, A.; Chun, G.; Lopez-Chavez, A.; Spencer, S.; Guha, U.; Khozin, S.; Figg, W.; Giaccone, G.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Szabo, E.] NCI, Lung & Upper Aerodigest Canc Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
[Carter, C. A.] Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
[Poondru, S.; Van Sant, C.; Keating, A.] Astellas Pharma Global Dev, Northbrook, IL USA.
[Steinberg, S. M.] NCI, Biostat & Data Management Sect, Off Clin Director, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Giaccone, G (reprint author), NCI, Ctr Canc Res, 10 Ctr Dr,Room 12N226, Bethesda, MD 20892 USA.
EM giacconeg@mail.nih.gov
RI Figg Sr, William/M-2411-2016; Giaccone, Giuseppe/E-8297-2017;
OI Giaccone, Giuseppe/0000-0002-5023-7562; Thomas,
Anish/0000-0003-3293-3115
FU National Cancer Institute, National Institutes of Health; NIH, National
Cancer Institute, Center for Cancer Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health. This work
was supported by the Intramural Research Program of the NIH, National
Cancer Institute, Center for Cancer Research.
NR 22
TC 38
Z9 41
U1 1
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD OCT
PY 2013
VL 24
IS 10
BP 2601
EP 2606
DI 10.1093/annonc/mdt249
PG 6
WC Oncology
SC Oncology
GA 227ZI
UT WOS:000325153800023
PM 23857959
ER
PT J
AU Kroneman, A
Vega, E
Vennema, H
Vinje, J
White, PA
Hansman, G
Green, K
Martella, V
Katayama, K
Koopmans, M
AF Kroneman, Annelies
Vega, Everardo
Vennema, Harry
Vinje, Jan
White, Peter A.
Hansman, Grant
Green, Kim
Martella, Vito
Katayama, Kazuhiko
Koopmans, Marion
TI Proposal for a unified norovirus nomenclature and genotyping
SO ARCHIVES OF VIROLOGY
LA English
DT Article
ID NORWALK-LIKE VIRUSES; INFECTIOUS INTESTINAL DISEASE; UNITED-STATES;
ACUTE GASTROENTERITIS; MOLECULAR EPIDEMIOLOGY; ENTERIC CALICIVIRUSES;
MAXIMUM-LIKELIHOOD; OUTBREAKS; CLASSIFICATION; TAXONOMY
AB Noroviruses belong to a genus of genetically diverse viruses within the family Caliciviridae and cause acute gastroenteritis in humans and animals. They are subdivided into genogroups, each of which further segregates into genotypes. Until recently, a new genotype was based on a defined pairwise distance cutoff of complete VP1 sequences, but with the increasing number of available norovirus sequences, this cutoff is no longer accurate, and sequences in the public database have been misclassified. In this paper, we demonstrate that the pairwise distance cutoff method can no longer be used and outline a phylogenetic approach to classify noroviruses. Furthermore, we propose a dual nomenclature using both ORF1 and VP1 sequences, as recombination is common and recognizing recombinant viruses may be relevant. With the continuing emergence of new norovirus lineages, we propose to coordinate nomenclature of new norovirus genotypes through an international norovirus working group.
C1 [Kroneman, Annelies; Vennema, Harry; Koopmans, Marion] Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands.
[Vega, Everardo; Vinje, Jan] Ctr Dis Control & Prevent, Atlanta, GA USA.
[White, Peter A.] Univ New S Wales, Sch Biotechnol & Biomol Sci, Fac Sci, Sydney, NSW, Australia.
[Hansman, Grant] Heidelberg Univ, CHS Fdn, Heidelberg, Germany.
[Green, Kim] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Green, Kim] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Martella, Vito] Univ Bari Aldo Moro, Dept Vet Publ Hlth, Valenzano, Italy.
[Katayama, Kazuhiko] Natl Inst Infect Dis, Dept Virol 2, Tokyo, Japan.
[Koopmans, Marion] Erasmus MC, Dept Virol, Rotterdam, Netherlands.
RP Kroneman, A (reprint author), Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands.
EM annelies.kroneman@rivm.nl
RI White, Peter/C-6573-2012; Martella, Vito/K-3146-2016;
OI White, Peter/0000-0002-6046-9631; Martella, Vito/0000-0002-5740-6947;
Hansman, Grant/0000-0001-8735-4618; Vinje, Jan/0000-0002-1530-3675
NR 49
TC 173
Z9 183
U1 5
U2 61
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD OCT
PY 2013
VL 158
IS 10
BP 2059
EP 2068
DI 10.1007/s00705-013-1708-5
PG 10
WC Virology
SC Virology
GA 226BA
UT WOS:000325008000004
PM 23615870
ER
PT J
AU Kuhn, JH
Bekal, S
Cai, YY
Clawson, AN
Domier, LL
Herrel, M
Jahrling, PB
Kondo, H
Lambert, KN
Mihindukulasuriya, KA
Nowotny, N
Radoshitzky, SR
Schneider, U
Staeheli, P
Suzuki, N
Tesh, RB
Wang, D
Wang, LF
Dietzgen, RG
AF Kuhn, Jens H.
Bekal, Sadia
Cai, Yingyun
Clawson, Anna N.
Domier, Leslie L.
Herrel, Marieke
Jahrling, Peter B.
Kondo, Hideki
Lambert, Kris N.
Mihindukulasuriya, Kathie A.
Nowotny, Norbert
Radoshitzky, Sheli R.
Schneider, Urs
Staeheli, Peter
Suzuki, Nobuhiro
Tesh, Robert B.
Wang, David
Wang, Lin-Fa
Dietzgen, Ralf G.
TI Nyamiviridae: Proposal for a new family in the order Mononegavirales
SO ARCHIVES OF VIROLOGY
LA English
DT Article
ID ARGAS-PERSICARGAS-ARBOREUS; METAGENOMIC ANALYSIS; QUARANFIL CHENUDA;
NYAMANINI VIRUSES; MATRIX PROTEIN; VIRAL WORLD; RNA VIRUSES;
ARBOVIRUSES; TICKS; EGYPT
AB Nyamanini virus (NYMV) and Midway virus (MIDWV) are unclassified tick-borne agents that infect land birds and seabirds, respectively. The recent molecular characterization of both viruses confirmed their already known close serological relationship and revealed them to be nonsegmented, single- and negative-stranded RNA viruses that are clearly related to, but quite distinct from, members of the order Mononegavirales (bornaviruses, filoviruses, paramyxoviruses, and rhabdoviruses). A third agent, soybean cyst nematode virus 1 (SbCNV-1, previously named soybean cyst nematode nyavirus), was recently found to be an additional member of this new virus group. Here, we review the current knowledge about all three viruses and propose classifying them as members of a new mononegaviral family, Nyamiviridae.
C1 [Kuhn, Jens H.; Cai, Yingyun; Clawson, Anna N.; Jahrling, Peter B.] NIAID, Integrated Res Facil Ft Detrick IRF Frederick, Div Clin Res DCR, NIH, Frederick, MD 21702 USA.
[Bekal, Sadia] Univ Illinois, Dept Agr & Biol Engn, Chicago, IL 60680 USA.
[Domier, Leslie L.; Lambert, Kris N.] Univ Illinois, Dept Crop Sci, Chicago, IL 60680 USA.
[Herrel, Marieke; Schneider, Urs; Staeheli, Peter] Univ Freiburg, Dept Virol, D-79106 Freiburg, Germany.
[Kondo, Hideki; Suzuki, Nobuhiro] Okayama Univ, Inst Plant Sci & Resources, Kurashiki, Okayama, Japan.
[Mihindukulasuriya, Kathie A.] Washington Univ, Sch Med, Genome Inst, St Louis, MO USA.
[Nowotny, Norbert] Univ Vet Med, Vienna, Austria.
[Nowotny, Norbert] Sultan Qaboos Univ, Coll Med & Hlth Sci, Muscat, Oman.
[Radoshitzky, Sheli R.] US Army Med Res Inst Infect Dis, Frederick, MD USA.
[Tesh, Robert B.] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[Tesh, Robert B.] Univ Texas Med Branch, Ctr Biodef & Emerging Infect Dis, Galveston, TX 77555 USA.
[Wang, David] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
[Wang, David] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Wang, Lin-Fa] CSIRO, Australian Anim Hlth Lab, Geelong, Vic, Australia.
[Wang, Lin-Fa] Duke Natl Univ Singapore NUS, Grad Sch Med, Program Emerging Infect Dis, Singapore, Singapore.
[Dietzgen, Ralf G.] Univ Queensland, Queensland Alliance Agr & Food Innovat, St Lucia, Qld, Australia.
RP Kuhn, JH (reprint author), NIAID, Integrated Res Facil Ft Detrick IRF Frederick, Div Clin Res DCR, NIH, B-8200 Res Plaza, Frederick, MD 21702 USA.
EM kuhnjens@mail.nih.gov
RI Suzuki, Nobuhiro/B-2517-2011; Kuhn, Jens H./B-7615-2011;
OI Kuhn, Jens H./0000-0002-7800-6045; Mihindukulasuriya,
Kathie/0000-0001-9372-3758
FU Intramural NIH HHS [Z99 AI999999]
NR 69
TC 8
Z9 9
U1 1
U2 16
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
EI 1432-8798
J9 ARCH VIROL
JI Arch. Virol.
PD OCT
PY 2013
VL 158
IS 10
BP 2209
EP 2226
DI 10.1007/s00705-013-1674-y
PG 18
WC Virology
SC Virology
GA 226BA
UT WOS:000325008000028
PM 23636404
ER
PT J
AU Haroon, N
Inman, RD
Learch, TJ
Weisman, MH
Lee, M
Rahbar, MH
Ward, MM
Reveille, JD
Gensler, LS
AF Haroon, Nigil
Inman, Robert D.
Learch, Thomas J.
Weisman, Michael H.
Lee, MinJae
Rahbar, Mohammad H.
Ward, Michael M.
Reveille, John D.
Gensler, Lianne S.
TI The Impact of Tumor Necrosis Factor alpha Inhibitors on Radiographic
Progression in Ankylosing Spondylitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; AXIAL SPONDYLOARTHRITIS; SPINAL
MOBILITY; DOUBLE-BLIND; TRIAL; EFFICACY; SAFETY; COHORT; DAMAGE;
SEVERITY
AB ObjectiveTo study the effect of tumor necrosis factor (TNF) inhibitors on progressive spinal damage in patients with ankylosing spondylitis (AS).
MethodsAll AS patients meeting the modified New York criteria who had been monitored prospectively and had at least 2 sets of spinal radiographs a minimum of 1.5 years apart were included in the study (n = 334). The patients received standard therapy, which included nonsteroidal antiinflammatory drugs and TNF inhibitors. Radiographic severity was assessed by the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS). Patients with a rate of AS progression that was 1 mSASSS unit/year were considered progressors. Univariable and multivariable regression analyses were done. Propensity score matching and sensitivity analysis were performed. A zero-inflated negative binomial (ZINB) model was used to analyze the effect of TNF inhibitors on the change in the mSASSS with varying followup periods. Potential confounders, such as disease activity (as assessed by the Bath Ankylosing Spondylitis Disease Activity Index), the erythrocyte sedimentation rate, C-reactive protein level, HLA-B27 positivity, sex, age at onset, smoking burden (number of pack-years), and baseline damage, were included in the model.
ResultsTNF inhibitor treatment was associated with a 50% reduction in the odds of progression, with an odds ratio (OR) of 0.52 (95% confidence interval [95% CI] 0.30-0.88, P = 0.02). Patients with a delay of >10 years in starting therapy were more likely to experience progression as compared to those who started earlier (OR 2.4 [95% CI 1.09-5.3], P = 0.03). In the ZINB model, the use of TNF inhibitors significantly reduced disease progression when the gap between radiographs was >3.9 years. The protective effect of TNF inhibitors was stronger after propensity score matching.
ConclusionTreatment with TNF inhibitors appears to reduce radiographic progression in AS patients, especially with early initiation and with longer duration of followup.
C1 [Haroon, Nigil; Inman, Robert D.] Univ Hlth Network, Toronto, ON, Canada.
[Haroon, Nigil; Inman, Robert D.] Univ Toronto, Toronto, ON M5T 2S8, Canada.
[Learch, Thomas J.; Weisman, Michael H.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Lee, MinJae; Rahbar, Mohammad H.; Reveille, John D.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Ward, Michael M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Gensler, Lianne S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Haroon, N (reprint author), Univ Toronto, Div Rheumatol, 1E-425,399 Bathurst St, Toronto, ON M5T 2S8, Canada.
EM Nigil.Haroon@uhn.ca; Lianne.Gensler@ucsf.edu
FU NIH [UL1-TR-000124]; Arthritis Society, Canada; Arthritis Research
Foundation, Toronto (CIBC); Rosalind Russell Medical Research Center for
Arthritis; Spondylitis Association of America; NIH (National Institute
of Arthritis and Musculoskeletal and Skin Diseases)
[P01-AR-052915-06A1]; Janssen; AbbVie; Amgen; Pfizer; Amgen Canada;
Pfizer Canada; Janssen Canada; Abbott Canada; UCB; Abbott; AbbVie for
Advisory Board service
FX Supported by the NIH (initially by National Center for Research
Resources grant UL1-RR-033176 and currently by National Center for
Advancing Translational Sciences grant UL1-TR-000124). Dr. Haroon's work
was supported by The Arthritis Society, Canada and by the Arthritis
Research Foundation, Toronto (CIBC Young Investigator award). Dr.
Gensler's work was supported by the Rosalind Russell Medical Research
Center for Arthritis, the Spondylitis Association of America (Young
Investigator award), and the NIH (National Institute of Arthritis and
Musculoskeletal and Skin Diseases grant P01-AR-052915-06A1).
Administrative costs for the Spondyloarthritis Research Consortium of
Canada database, which includes the patients from Toronto, are supported
in part by The Arthritis Society, Canada and by unrestricted educational
grants from Janssen, AbbVie, Amgen, and Pfizer.; Dr. Haroon has received
consulting fees, speaking fees, and/or honoraria from Amgen Canada,
Pfizer Canada, AbbVie, and Janssen Canada (less than $10,000 each). Dr.
Inman has received consulting fees, speaking fees, and/or honoraria from
Pfizer Canada, Abbott Canada, Janssen Canada, and UCB (less than $10,000
each). Dr. Reveille has received consulting fees, speaking fees, and/or
honoraria from Abbott and UCB (less than $10,000 each). Dr. Gensler has
received consulting fees and/or honoraria from UCB and AbbVie for
Advisory Board service (less than $10,000 each).
NR 32
TC 115
Z9 125
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
IS 10
BP 2645
EP 2654
DI 10.1002/art.38070
PG 10
WC Rheumatology
SC Rheumatology
GA 227TE
UT WOS:000325136600019
ER
PT J
AU Wang, JH
New, JS
Xie, ST
Yang, PA
Wu, Q
Li, J
Luo, B
Ding, YN
Druey, KM
Hsu, HC
Mountz, JD
AF Wang, John H.
New, James S.
Xie, Shutao
Yang, PingAr
Wu, Qi
Li, Jun
Luo, Bao
Ding, Yanna
Druey, Kirk M.
Hsu, Hui-Chen
Mountz, John D.
TI Extension of the Germinal Center Stage of B Cell Development Promotes
Autoantibodies in BXD2 Mice
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; CYCLIC CITRULLINATED PEPTIDE; INDUCED
CYTIDINE DEAMINASE; FOLLICULAR DENDRITIC CELLS; ANTIBODY CLASS SWITCH;
RHEUMATOID-ARTHRITIS; PATHOGENIC AUTOANTIBODIES; PLASMA-CELLS; HAPTEN
NP; T-CELLS
AB ObjectiveRegulator of G protein signaling (RGS) proteins inhibit chemokine signaling by desensitizing G protein-coupled receptor signals. This study was undertaken to determine the mechanisms by which RGS13 promotes the generation of pathogenic autoantibodies in germinal centers (GCs), using BXD2-Rgs13(-/-) mice.
MethodsConfocal and light microscopy imaging techniques were used to determine the location of cells that express RGS13 and activation-induced cytidine deaminase (AID) in the mouse spleen, and the number of plasmablasts. The levels of GC and plasma cell program transcripts in GC B cells were determined by real-time quantitative polymerase chain reaction (qPCR). Differential interleukin-17 (IL-17)-mediated expression of RGS13 in GC versus non-GC B cells was analyzed using A20 and 70Z/3 B cells.
ResultsIn the spleens of BXD2 mice, RGS13 was mainly expressed by GC B cells and was stimulated by IL-17 but not IL-21. IL-17 up-regulated RGS13 in A20 GC cells but not 70Z/3 non-GC B cells. BXD2- Rgs13(-/-) mice exhibited smaller GCs and lower AID levels, suggesting lower somatic hypermutation and affinity maturation. However, GC B cells from BXD2- Rgs13(-/-) mice showed increased levels of IgM(bright) plasmablasts, up-regulation of the genes encoding plasma program, including interferon regulatory factor 4, B lymphocyte-induced maturation protein 1, and X-box binding protein 1 and the p-CREB target genes Fosb and Obf1, and down-regulation of the GC program genes Aid, Pax5, and Bach2 compared to BXD2 mice. BXD2-Rgs13(-/-) mice had lower titers of IgG autoantibodies and IgG deposits in the glomeruli, suggesting reduced autoantibody pathogenicity.
ConclusionRGS13 deficiency is associated with a reduction in GC program genes and the exit of fewer pathogenic IgM plasmablasts in BXD2 mice. Our findings indicate that prolonged GC program, mediated by up-regulation of RGS13, enhances AID expression and enables the generation of pathogenic autoantibodies in autoreactive GCs.
C1 [Wang, John H.; New, James S.; Xie, Shutao; Yang, PingAr; Wu, Qi; Li, Jun; Luo, Bao; Ding, Yanna; Hsu, Hui-Chen; Mountz, John D.] Univ Alabama Birmingham, Birmingham, AL 35294 USA.
[Druey, Kirk M.] NIAID, NIH, Bethesda, MD 20892 USA.
[Mountz, John D.] Birmingham VA Med Ctr, Birmingham, AL USA.
RP Mountz, JD (reprint author), Univ Alabama Birmingham, SHEL 307,1825 Univ Blvd, Birmingham, AL 35294 USA.
EM jdmountz@uab.edu
FU NIH (National Institute of Allergy and Infectious Diseases)
[1-AI-071110, ARRA 3R01-AI-71110-02S1, 1R01-AI-083705]; NIH (National
Institute of Arthritis and Musculoskeletal and Skin Diseases)
[P30-AR-048311, P30-AI-027767]; NIH (National Institute of Allergy and
Infectious Diseases Intramural Research Program); Department of Veterans
Affairs [1I01BX000600-01]; Rheumatology Research Foundation; Alliance
for Lupus Research; Arthritis Foundation; Lupus Research Institute; NIH
[P30-AR-048311, P30-A-I027767]
FX Supported by the NIH (National Institute of Allergy and Infectious
Diseases grants 1-AI-071110, ARRA 3R01-AI-71110-02S1, and
1R01-AI-083705, National Institute of Arthritis and Musculoskeletal and
Skin Diseases grants P30-AR-048311 and P30-AI-027767, and the National
Institute of Allergy and Infectious Diseases Intramural Research
Program), the Department of Veterans Affairs (Merit Review grant
1I01BX000600-01), the Rheumatology Research Foundation (Within Our Reach
grant), the Alliance for Lupus Research, the Arthritis Foundation, and
the Lupus Research Institute. Flow cytometry and confocal imaging data
acquisition were performed at the University of Alabama at Birmingham
Comprehensive Flow Cytometry Core (supported by NIH grants P30-AR-048311
and P30-A-I027767) and Analytic Imaging and Immunoreagents Core
(supported by NIH grant P30-AR-048311).
NR 48
TC 9
Z9 9
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2013
VL 65
IS 10
BP 2703
EP 2712
DI 10.1002/art.38059
PG 10
WC Rheumatology
SC Rheumatology
GA 227TE
UT WOS:000325136600026
PM 23818250
ER
PT J
AU Lunenfeld, B
Stratton, P
AF Lunenfeld, Bruno
Stratton, Pamela
TI The clinical consequences of an ageing world and preventive strategies
SO BEST PRACTICE & RESEARCH CLINICAL OBSTETRICS & GYNAECOLOGY
LA English
DT Article
DE ageing; life expectancy; health expectancy; preventive strategies;
fertility rate
ID HORMONE REPLACEMENT THERAPY; CORONARY-HEART-DISEASE; QUALITY-OF-LIFE;
CANCER-RISK; ORAL-CONTRACEPTIVES; OVARIAN-CANCER; POSTMENOPAUSAL WOMEN;
CARDIOVASCULAR RISK; HEALTH EXPECTANCY; COLORECTAL-CANCER
AB Over the past century, the world has seen unprecedented declines in mortality rates, leading to an accelerated increase in the world population. This century will realise falling fertility rates alongside ageing populations. The 20th century was the century of population growth; the 21st century will be remembered as the century of ageing. Increase in life expectancy is one of the highest achievements of humankind; however, ageing and age-related disease is a mounting challenge for individuals, families, and for social, economic, and healthcare systems. Since healthy life expectancy has lagged behind the increase in life expectancy, the rise in morbidity will increase the burden on healthcare systems. Implementation of preventive health strategies to decrease, delay or prevent frailty, lung, breast and colon cancer, cardiovascular disease, metabolic syndrome, osteoporosis and osteopaenia, may increase health expectancy, and permit women to age gracefully and maintain independent living, without disability, for as long as possible. Published by Elsevier Ltd.
C1 [Lunenfeld, Bruno] Bar Ilan Univ, Fac Life Sci, IL-52900 Ramat Gan, Israel.
[Stratton, Pamela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
RP Lunenfeld, B (reprint author), Bar Ilan Univ, Fac Life Sci, IL-52900 Ramat Gan, Israel.
EM blunenfeld@gmail.com
FU Intramural Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development; NIH Clinical Center
FX This work was supported in part by the Intramural Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
and the NIH Clinical Center. We thank Nancy Terry, MLS, informationist
at the NIH Clinical Center for her assistance in formatting the
references for publication.
NR 84
TC 10
Z9 10
U1 1
U2 13
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6934
J9 BEST PRACT RES CL OB
JI Best Pract. Res. Clin. Obstet. Gynaecol.
PD OCT
PY 2013
VL 27
IS 5
BP 643
EP 659
DI 10.1016/j.bpobgyn.2013.02.005
PG 17
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 227ML
UT WOS:000325117900002
PM 23541823
ER
PT J
AU Barao, I
Wright, PW
Sungur, CM
Anderson, SK
Redelman, D
Murphy, WJ
AF Barao, Isabel
Wright, Paul W.
Sungur, Can M.
Anderson, Stephen K.
Redelman, Doug
Murphy, William J.
TI Differential Expression of the Ly49G(B6), but Not the Ly49G(BALB),
Receptor Isoform during Natural Killer Cell Reconstitution after
Hematopoietic Stem Cell Transplantation
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Ly49G; Natural killer cell; Hematopoietic stem cell transplantation
ID CLASS-I MOLECULES; MHC CLASS-I; INHIBITORY RECEPTORS; NK CELLS;
SELF-TOLERANCE; MISSING SELF; REPERTOIRE; EDUCATION; RECOGNITION;
ACTIVATION
AB Inhibitory natural killer (NK) cell receptors specific for major histocompatibility complex class I (MHC-I) molecules include Ly49 receptors in mice and killer immunoglobulin-like receptors (KIR) in humans. The "licensing" or "arming" models imply that engagement of these receptors to self MHC-I molecules during NK cell development educates NK cells to be more responsive to cancer and viral infection. We recently reported that hematopoietic stem cell transplantation (HSCT) induced rapid and preferential expansion of functionally competent Ly49G(+), but not other Ly49 family, NK cells independent of NK cell licensing via Ly49 MHC-I interactions. We now extend these studies to evaluate expression of the two Ly49G receptor isoforms Ly49G(B6) and Ly49G(BALB), using mice with different MHC-I haplotypes that express one or both of the isoforms. NK cells from CB6F(1) (H-2(bxd)). j hybrid mice express two different alleles for Ly49G receptor, Ly49G(B6) and Ly49G(BALB). We found that CB6F(1) mice had more Ly49G(B6+) NK cells than Ly49(BALB+) NK cells, and that only Ly49G(B6+) NK cells increased in relative numbers and in Ly49G mean fluorescence intensity values after HSCT similar to the B6 parental strain. We further observed that Ly49G(+) NK cells in BALB/c (H-2(d)) and BALB.B (H-2(b)) mice, which have the same background genes, recover slowly after HSCT, in contrast to Ly49G(+) NK cells in B6 (H-2(b)) recipients. The difference in expression of Ly49G(B6) relative to Ly49G(BALB) was linked to differences in the activity of the Prol promoter between the two alleles. Thus, we conclude that the Ly49G(B6) receptor dominates Ly49G expression on NK cells after HSCT in strains in which that allele is expressed. The data suggest that Ly49 allelic polymorphism within a particular Ly49 family member can differentially affect NK cell recovery after HSCT depending on the background genes of the recipient, not on the MHC-I haplotype. (C) 2013 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
C1 [Barao, Isabel] Univ Nevada, Dept Microbiol & Immunol, Reno, NV 89557 USA.
[Wright, Paul W.; Anderson, Stephen K.] SAIC Frederick, Canc & Inflammat Program, Lab Expt Immunol, Frederick, MD USA.
[Wright, Paul W.; Anderson, Stephen K.] NCI, Frederick, MD 21701 USA.
[Redelman, Doug] Univ Nevada, Dept Physiol, Reno, NV 89557 USA.
[Sungur, Can M.; Murphy, William J.] Univ Calif Davis, Dept Dermatol, Sacramento, CA 95817 USA.
RP Murphy, WJ (reprint author), Univ Calif Davis, Sch Med, CTSC IRC, Dept Dermatol, Suite 1630,2921 Stockton Blvd, Sacramento, CA 95817 USA.
EM wmjmurphy@ucdavis.edu
RI Anderson, Stephen/B-1727-2012
OI Anderson, Stephen/0000-0002-7856-4266
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001 E]; NIH, National Cancer Institute, Center for Cancer
Research
FX This project was funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
HHSN261200800001 E. This research was supported by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research.
NR 29
TC 1
Z9 1
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2013
VL 19
IS 10
BP 1446
EP 1452
DI 10.1016/j.bbmt.2013.07.021
PG 7
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 225PO
UT WOS:000324975000007
PM 23911940
ER
PT J
AU Salit, RB
Fowler, DH
Dean, RM
Pavletic, SZ
Hakim, FT
Steinberg, SM
Hardy, NT
Sportes, C
Gress, RE
Bishop, MR
AF Salit, Rachel B.
Fowler, Daniel H.
Dean, Robert M.
Pavletic, Steven Z.
Hakim, Frances T.
Steinberg, Seth M.
Hardy, Nancy T.
Sportes, Claude
Gress, Ronald E.
Bishop, Michael R.
TI Host Lymphocyte Depletion as a Strategy to Facilitate Early Full Donor
Chimerism after Reduced-Intensity Allogeneic Stem Cell Transplantation
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Reduced-intensity transplantation; Engraftment; Lymphocyte depletion
ID BONE-MARROW-TRANSPLANTATION; MINIMAL RESIDUAL DISEASE; HEMATOLOGIC
MALIGNANCIES; CONDITIONING REGIMEN; MYELOGENOUS LEUKEMIA;
MULTIPLE-MYELOMA; T-CELLS; ENGRAFTMENT; IMPACT; CHEMOTHERAPY
AB Reduced-intensity conditioning (RIC) allogeneic hematopoietic stem cell transplantation (RIC-alloHSCT) is associated with lower toxicity but higher rates of prolonged mixed chimerism than myeloablative conditioning. Decreased pretransplantation host T cell numbers are associated with less graft rejection and early full donor chimerism. To compensate for variability in pretransplantation host lymphocyte numbers and facilitate the achievement of rapid full donor chimerism, we tested a strategy of targeted lymphocyte depletion (TLD) using chemotherapy at conventional doses to provide cytoreduction and lymphocyte depletion before RIC-alloHSCT. In our study, 111 patients with advanced hematologic malignancies received 1 to 3 cycles of conventional-dose chemotherapy to reduce circulating lymphocytes to a predetermined level. Patients then underwent RIC-alloHSCT from HLA-matched siblings. Patients received a median of 2 cycles of TLD chemotherapy, resulting in a median 71% decline in CD4(+) count. All patients engrafted; there were no late graft failures. By day +14, median CD3(+) chimerism was 99% donor and was significantly associated with lower post-TLD CD4(+) counts (P = .012). One- and 5-year treatment-related mortality were 15% and 21%, respectively. At 1-year follow-up, 66% of patients had achieved complete remission (CR) of which 92% were not in CR at the time of transplantation. Overall survival at 1 and 5 years post transplantation were 66% and 47%, respectively. (C) 2013 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
C1 [Salit, Rachel B.; Fowler, Daniel H.; Pavletic, Steven Z.; Hakim, Frances T.; Hardy, Nancy T.; Sportes, Claude; Gress, Ronald E.; Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Salit, Rachel B.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA.
[Dean, Robert M.] Cleveland Clin Fdn, Taussig Canc Ctr, Cleveland, OH 44195 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Bishop, Michael R.] Univ Chicago, Chicago, IL 60637 USA.
RP Salit, RB (reprint author), Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N,D2-100,POB 19024, Seattle, WA 98109 USA.
EM rsalit@fhcrc.org
NR 39
TC 2
Z9 2
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2013
VL 19
IS 10
BP 1509
EP 1513
DI 10.1016/j.bbmt.2013.08.001
PG 5
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 225PO
UT WOS:000324975000016
PM 23948062
ER
PT J
AU Rezvani, K
Brody, JD
Kohrt, HE
Logan, AC
Advani, R
Czerwinski, DK
Weng, WK
Negrin, RS
Carlton, V
Faham, M
Levy, R
Barrett, J
AF Rezvani, Katayoun
Brody, Joshua D.
Kohrt, Holbrook E.
Logan, Aaron C.
Advani, Ranjana
Czerwinski, Debra Katherine
Weng, Wen-Kai
Negrin, Robert S.
Carlton, Victoria
Faham, Malek
Levy, Ronald
Barrett, John
TI Cancer Vaccines and T Cell Therapy (vol 19, pg S97, 2013)
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Correction
C1 [Rezvani, Katayoun] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Brody, Joshua D.] Mt Sinai Sch Med, Lymphoma Immunotherapy Program, New York, NY USA.
[Kohrt, Holbrook E.; Logan, Aaron C.; Advani, Ranjana; Czerwinski, Debra Katherine; Weng, Wen-Kai; Negrin, Robert S.; Levy, Ronald] Stanford Univ, Med Ctr, Dept Med, Stanford, CA 94305 USA.
[Carlton, Victoria; Faham, Malek] Sequenta Inc, San Francisco, CA USA.
[Barrett, John] NHLBI, Stem Cell Transplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Rezvani, K (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2013
VL 19
IS 10
BP 1530
EP 1530
DI 10.1016/j.bbmt.2013.03.005
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 225PO
UT WOS:000324975000023
ER
PT J
AU Yaniv, Y
Stern, MD
Lakatta, EG
Maltsev, VA
AF Yaniv, Yael
Stern, Michael D.
Lakatta, Edward G.
Maltsev, Victor A.
TI Mechanisms of Beat-to-Beat Regulation of Cardiac Pacemaker Cell Function
by Ca2+ Cycling Dynamics
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID SINOATRIAL NODE CELLS; RYANODINE RECEPTOR; K+ CURRENT; CAFFEINE;
PHOSPHODIESTERASE; AUTOMATICITY; RELEASE; CALCIUM; RHYTHM; MODELS
AB Whether intracellular Ca2+ cycling dynamics regulate cardiac pacemaker cell function on a beat-to-beat basis remains unknown. Here we show that under physiological conditions, application of low concentrations of caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous action potential cycle length (CL) and increases Ca2+ transient amplitude for several cycles. Numerical simulations, using a modified Maltsev-Lakatta coupled-clock model, faithfully reproduced these effects, and also the effects of CL prolongation and dysrhythmic spontaneous beating (produced by cytosolic Ca2+ buffering) and an acute CL reduction (produced by flash-induced Ca2+ release from a caged Ca2+ buffer), which we had reported previously. Three contemporary numerical Models (including the original Maltsev-Lakatta model) failed to reproduce the experimental results. In our proposed new model, Ca2+ releases acutely change the CL via activation of the Na+/Ca2+ exchanger current. Time-dependent CL reductions after flash-induced Ca2+ releases (the memory effect) are linked to changes in Ca2+ available for pumping into sarcoplasmic reticulum which, in turn, changes the sarcoplasmic reticulum Ca2+ load, diastolic Ca2+ releases, and Na+/Ca2+ exchanger current. These results support the idea that Ca2+ regulates CL in cardiac pacemaker cells on a beat-to-beat basis, and suggest a more realistic numerical mechanism of this regulation.
C1 [Yaniv, Yael; Stern, Michael D.; Lakatta, Edward G.; Maltsev, Victor A.] NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Maltsev, VA (reprint author), NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM maltsevvi@grc.nia.nih.gov
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
FU Intramural Research Program of the National Institute on Aging, National
Institutes of Health
FX The work was supported by the Intramural Research Program of the
National Institute on Aging, National Institutes of Health.
NR 38
TC 15
Z9 15
U1 0
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD OCT 1
PY 2013
VL 105
IS 7
BP 1551
EP 1561
DI 10.1016/j.bpj.2013.08.024
PG 11
WC Biophysics
SC Biophysics
GA 230ZO
UT WOS:000325383000004
PM 24094396
ER
PT J
AU Cope, SM
Shinde, S
Best, RB
Ghirlanda, G
Vaiana, SM
AF Cope, Stephanie M.
Shinde, Sandip
Best, Robert B.
Ghirlanda, Giovanna
Vaiana, Sara M.
TI Cyclic N-Terminal Loop of Amylin Forms Non Amyloid Fibers
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID GENE-RELATED PEPTIDE; CIRCULAR-DICHROISM; DIABETES-MELLITUS; FIBRIL
FORMATION; ALPHA-HELICES; BETA-SHEETS; HUMAN IAPP; POLYPEPTIDE;
PROTEINS; CALCITONIN
AB We report for the first time, to our knowledge, that the N-terminal loop (N_loop) of amylin (islet amyloid polypeptide (IAPP) residues 1-8) forms extremely long and stable non-beta-sheet fibers in solution under the same conditions in which human amylin (hIAPP) forms amyloid fibers. This observation applies to the cyclic, oxidized form of the N_loop but not to the linear, reduced form, which does not form fibers. Our findings indicate a potential role of direct N_loop-N_loop interactions in hIAPP aggregation, which has not been previously explored, with important implications for the mechanism of hIAPP amyloid fiber formation, the inhibitory action of IAPP variants, and the competition between ordered and disordered aggregation in peptides of the calcitonin peptide family.
C1 [Cope, Stephanie M.; Vaiana, Sara M.] Arizona State Univ, Ctr Biol Phys, Tempe, AZ 85287 USA.
[Cope, Stephanie M.; Vaiana, Sara M.] Arizona State Univ, Dept Phys, Tempe, AZ 85287 USA.
[Shinde, Sandip; Ghirlanda, Giovanna] Arizona State Univ, Dept Chem & Biochem, Tempe, AZ USA.
[Best, Robert B.] Univ Cambridge, Dept Chem, Cambridge CB2 1EW, England.
[Best, Robert B.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Vaiana, SM (reprint author), Arizona State Univ, Ctr Biol Phys, Tempe, AZ 85287 USA.
EM sara.vaiana@asu.edu
RI Best, Robert/H-7588-2016
OI Best, Robert/0000-0002-7893-3543
FU ASU; National Science Foundation [0449842]; Royal Society University
Research Fellowship; Intramural research program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health (NIH)
FX This work was supported by ASU start-up funds to S.M.V. G.G. and S.S.
were supported in part by National Science Foundation CAREER award
0449842. R.B.B. was supported by a Royal Society University Research
Fellowship and by the Intramural research program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health (NIH).
NR 62
TC 4
Z9 4
U1 1
U2 32
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD OCT 1
PY 2013
VL 105
IS 7
BP 1661
EP 1669
DI 10.1016/j.bpj.2013.08.026
PG 9
WC Biophysics
SC Biophysics
GA 230ZO
UT WOS:000325383000015
PM 24094407
ER
PT J
AU Shi, ZM
Zhang, CL
Zhou, MH
Zhen, SQ
Taylor, AW
AF Shi, Zumin
Zhang, Cuilin
Zhou, Minghao
Zhen, Shiqi
Taylor, Anne W.
TI Exposure to the Chinese famine in early life and the risk of anaemia in
adulthood
SO BMC PUBLIC HEALTH
LA English
DT Article
DE Chinese famine; Anemia; Adults; Fetal exposure
ID LONG-TERM HEALTH; IRON-DEFICIENCY; METABOLIC SYNDROME; MATERNAL STRESS;
DUTCH FAMINE; GREAT LEAP; CONSEQUENCES; ASSOCIATION; OVERWEIGHT;
CHILDREN
AB Background: Famine exposure during the early stage of life is related to a number of adulthood diseases. The objective of this study was to examine the association of early life exposure to the famine in China (1959-1961) with the risk of anaemia in adulthood.
Methods: We used the data of 2007 adults born between 1954 and 1964 in Jiangsu province from the 2002 Chinese National Nutrition and Health Survey. Anaemia was defined as haemoglobin concentration <12 g/dl in women and <13 g/dl in men.
Results: Prevalence of anaemia in adulthood in nonexposed, fetal-exposed, early-childhood, mid-childhood, and late-childhood exposed to famine groups were 26.0%, 33.8%, 28.1%, 28.2% and 29.7%, respectively. Overall, fetal-exposed to famine was associated with 37% increased risk of anaemia as compared with those non-exposed after adjusting for income, education, place of residence, smoking, alcohol drinking, job, hypertension and BMI; relative risk (95% confidence interval) (RR (95% CI)) was 1.37 (1.09, 1.71). In general, this association appeared to be stronger among men, those who were currently overweight or obese, or those of lower educational levels. Corresponding RR (95% CI) was 1.87 (1.21-2.87), 1.75 (1.20-2.56), and 2.07 (1.37-3.12), respectively.
Conclusions: Fetal exposure to the Chinese famine was associated with an increased risk of anaemia in adulthood.
C1 [Shi, Zumin; Zhen, Shiqi] Jiangsu Prov Ctr Dis Control & Prevent, Dept Nutr & Foodborne Dis Prevent, Nanjing, Jiangsu, Peoples R China.
[Shi, Zumin; Taylor, Anne W.] Univ Adelaide, Discipline Med, Adelaide, SA 5000, Australia.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20852 USA.
[Zhou, Minghao] Jiangsu Prov Ctr Dis Control & Prevent, Nanjing 210009, Jiangsu, Peoples R China.
RP Shi, ZM (reprint author), Jiangsu Prov Ctr Dis Control & Prevent, Dept Nutr & Foodborne Dis Prevent, Nanjing, Jiangsu, Peoples R China.
EM zumin.shi@adelaide.edu.au
RI Shi, Zumin/A-1093-2009; Taylor, Anne/F-5708-2010
OI Shi, Zumin/0000-0002-3099-3299; Taylor, Anne/0000-0002-4422-7974
FU Jiangsu Provincial Natural Science Foundation [BK2008464]; Jiangsu
Provincial Health Bureau, China; Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health & Human
Development, National Institutes of Health
FX The study is supported by Jiangsu Provincial Natural Science Foundation
(BK2008464) and the Jiangsu Provincial Health Bureau, China.; Dr. Cuilin
Zhang were supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health & Human Development,
National Institutes of Health.
NR 33
TC 2
Z9 3
U1 2
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2458
J9 BMC PUBLIC HEALTH
JI BMC Public Health
PD OCT 1
PY 2013
VL 13
AR 904
DI 10.1186/1471-2458-13-904
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 227RJ
UT WOS:000325131100001
PM 24079608
ER
PT J
AU Chen, Y
Copeland, WK
Vedanthan, R
Grant, E
Lee, JE
Gu, DF
Gupta, PC
Ramadas, K
Inoue, M
Tsugane, S
Tamakoshi, A
Gao, YT
Yuan, JM
Shu, XO
Ozasa, K
Tsuji, I
Kakizaki, M
Tanaka, H
Nishino, Y
Chen, CJ
Wang, RW
Yoo, KY
Ahn, YO
Ahsan, H
Pan, WH
Chen, CS
Pednekar, MS
Sauvaget, C
Sasazuki, S
Yang, G
Koh, WP
Xiang, YB
Ohishi, W
Watanabe, T
Sugawara, Y
Matsuo, K
You, SL
Park, SK
Kim, DH
Parvez, F
Chuang, SY
Ge, WZ
Rolland, B
McLerran, D
Sinha, R
Thornquist, M
Kang, D
Feng, Z
Boffetta, P
Zheng, W
He, J
Potter, JD
AF Chen, Yu
Copeland, Wade K.
Vedanthan, Rajesh
Grant, Eric
Lee, Jung Eun
Gu, Dongfeng
Gupta, Prakash C.
Ramadas, Kunnambath
Inoue, Manami
Tsugane, Shoichiro
Tamakoshi, Akiko
Gao, Yu-Tang
Yuan, Jian-Min
Shu, Xiao-Ou
Ozasa, Kotaro
Tsuji, Ichiro
Kakizaki, Masako
Tanaka, Hideo
Nishino, Yoshikazu
Chen, Chien-Jen
Wang, Renwei
Yoo, Keun-Young
Ahn, Yoon-Ok
Ahsan, Habibul
Pan, Wen-Harn
Chen, Chung-Shiuan
Pednekar, Mangesh S.
Sauvaget, Catherine
Sasazuki, Shizuka
Yang, Gong
Koh, Woon-Puay
Xiang, Yong-Bing
Ohishi, Waka
Watanabe, Takashi
Sugawara, Yumi
Matsuo, Keitaro
You, San-Lin
Park, Sue K.
Kim, Dong-Hyun
Parvez, Faruque
Chuang, Shao-Yuan
Ge, Wenzhen
Rolland, Betsy
McLerran, Dale
Sinha, Rashmi
Thornquist, Mark
Kang, Daehee
Feng, Ziding
Boffetta, Paolo
Zheng, Wei
He, Jiang
Potter, John D.
TI Association between body mass index and cardiovascular disease mortality
in east Asians and south Asians: pooled analysis of prospective data
from the Asia Cohort Consortium
SO BMJ-BRITISH MEDICAL JOURNAL
LA English
DT Article
ID CORONARY-HEART-DISEASE; INDIVIDUAL PATIENT DATA; ALL-CAUSE MORTALITY;
MIDDLE-AGED MEN; FAT-FREE MASS; RISK-FACTORS; FOLLOW-UP; WEIGHT CHANGE;
HEMORRHAGIC STROKE; ISCHEMIC-STROKE
AB Objective To evaluate the association between body mass index and mortality from overall cardiovascular disease and specific subtypes of cardiovascular disease in east and south Asians.
Design Pooled analyses of 20 prospective cohorts in Asia, including data from 835 082 east Asians and 289 815 south Asians. Cohorts were identified through a systematic search of the literature in early 2008, followed by a survey that was sent to each cohort to assess data availability.
Setting General populations in east Asia (China, Taiwan, Singapore, Japan, and Korea) and south Asia (India and Bangladesh).
Participants 1 124 897 men and women (mean age 53.4 years at baseline).
Main outcome measures Risk of death from overall cardiovascular disease, coronary heart disease, stroke, and (in east Asians only) stroke subtypes.
Results 49 184 cardiovascular deaths (40 791 in east Asians and 8393 in south Asians) were identified during a mean follow-up of 9.7 years. East Asians with a body mass index of 25 or above had a raised risk of death from overall cardiovascular disease, compared with the reference range of body mass index (values 22.5-24.9; hazard ratio 1.09 (95% confidence interval 1.03 to 1.15), 1.27 (1.20 to 1.35), 1.59 (1.43 to 1.76), 1.74 (1.47 to 2.06), and 1.97 (1.44 to 2.71) for body mass index ranges 25.0-27.4, 27.5-29.9, 30.0-32.4, 32.5-34.9, and 35.0-50.0, respectively). This association was similar for risk of death from coronary heart disease and ischaemic stroke; for haemorrhagic stroke, the risk of death was higher at body mass index values of 27.5 and above. Elevated risk of death from cardiovascular disease was also observed at lower categories of body mass index (hazard ratio 1.19 (95% confidence interval 1.02 to 1.39) and 2.16 (1.37 to 3.40) for body mass index ranges 15.0-17.4 and <15.0, respectively), compared with the reference range. In south Asians, the association between body mass index and mortality from cardiovascular disease was less pronounced than that in east Asians. South Asians had an increased risk of death observed for coronary heart disease only in individuals with a body mass index greater than 35 (hazard ratio 1.90, 95% confidence interval 1.15 to 3.12).
Conclusions Body mass index shows a U shaped association with death from overall cardiovascular disease among east Asians: increased risk of death from cardiovascular disease is observed at lower and higher ranges of body mass index. A high body mass index is a risk factor for mortality from overall cardiovascular disease and for specific diseases, including coronary heart disease, ischaemic stroke, and haemorrhagic stroke in east Asians. Higher body mass index is a weak risk factor for mortality from cardiovascular disease in south Asians.
C1 [Chen, Yu; Ge, Wenzhen] NYU, Sch Med, Dept Populat Hlth, New York, NY USA.
[Copeland, Wade K.; Rolland, Betsy; McLerran, Dale; Thornquist, Mark; Potter, John D.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Vedanthan, Rajesh] Icahn Sch Med Mt Sinai, Zena & Michael Wiener Cardiovasc Inst, New York, NY USA.
[Grant, Eric; Ozasa, Kotaro] Radiat Effects Res Fdn, Dept Epidemiol, Hiroshima, Japan.
[Lee, Jung Eun] Sookmyung Womens Univ, Dept Food & Nutr, Seoul, South Korea.
[Gu, Dongfeng] Chinese Acad Med Sci, Dept Evidence Based Med, Beijing 100730, Peoples R China.
[Gu, Dongfeng] Chinese Acad Med Sci, Dept Populat Genet & Prevent, Fu Wai Hosp, Beijing 100730, Peoples R China.
[Gu, Dongfeng] Chinese Acad Med Sci, Cardiovasc Inst, Beijing 100730, Peoples R China.
[Gu, Dongfeng] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Gupta, Prakash C.; Pednekar, Mangesh S.] Healis Sekhsaria Inst Publ Hlth, Navi Mumbai, India.
[Ramadas, Kunnambath] Reg Canc Ctr, Div Radiat Oncol, Trivandrum 695011, Kerala, India.
[Inoue, Manami; Tsugane, Shoichiro; Sasazuki, Shizuka] Natl Canc Ctr, Res Ctr Canc Prevent & Screening, Epidemiol & Prevent Div, Tokyo 104, Japan.
[Tamakoshi, Akiko] Hokkaido Univ, Grad Sch Med, Dept Publ Hlth, Sapporo, Hokkaido, Japan.
[Inoue, Manami] Univ Tokyo, Grad Sch Med, AXA Dept Hlth & Human Secur, Tokyo, Japan.
[Gao, Yu-Tang; Xiang, Yong-Bing] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
[Yuan, Jian-Min; Wang, Renwei] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Yuan, Jian-Min] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Shu, Xiao-Ou; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Sch Med, Dept Med,Div Epidemiol, Vanderbilt Epidemiol Ctr,Vanderbilt Ingram Canc C, Nashville, TN 37212 USA.
[Tsuji, Ichiro; Kakizaki, Masako] Tohoku Univ, Grad Sch Med, Dept Publ Hlth & Forens Med, Div Epidemiol, Sendai, Miyagi 980, Japan.
[Tanaka, Hideo; Matsuo, Keitaro] Aichi Canc Ctr Res Inst, Div Epidemiol & Prevent, Nagoya, Aichi, Japan.
[Nishino, Yoshikazu] Miyagi Canc Ctr Res Inst, Div Canc Epidemiol & Prevent, Sendai, Miyagi, Japan.
[Chen, Chien-Jen; You, San-Lin] Acad Sinica, Genom Res Ctr, Taipei 115, Taiwan.
[Chen, Chien-Jen; Pan, Wen-Harn] Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol & Prevent Med, Taipei 10764, Taiwan.
[Yoo, Keun-Young; Ahn, Yoon-Ok; Park, Sue K.; Kang, Daehee] Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea.
[Ahsan, Habibul] Univ Chicago, Ctr Comprehens Canc, Dept Hlth Studies, Chicago, IL 60637 USA.
[Ahsan, Habibul] Univ Chicago, Ctr Comprehens Canc, Dept Med, Chicago, IL 60637 USA.
[Ahsan, Habibul] Univ Chicago, Ctr Comprehens Canc, Dept Human Genet, Chicago, IL 60637 USA.
[Pan, Wen-Harn; Chuang, Shao-Yuan] Natl Hlth Res Inst, Inst Populat Hlth Sci, Div Prevent Med & Hlth Serv Res, Miaoli, Taiwan.
[Pan, Wen-Harn] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
[Chen, Chung-Shiuan; He, Jiang] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA USA.
[Sauvaget, Catherine] Int Agcy Res Canc, Screening Grp, F-69372 Lyon, France.
[Koh, Woon-Puay] Natl Univ Singapore, Duke NUS Grad Med Sch Singapore, Singapore 117548, Singapore.
[Koh, Woon-Puay] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore.
[Ohishi, Waka] Radiat Effects Res Fdn, Dept Clin Studies, Hiroshima, Japan.
[Watanabe, Takashi; Sugawara, Yumi] Tohoku Univ, Grad Sch Med, Dept Publ Hlth & Forens Med, Div Epidemiol, Sendai, Miyagi 980, Japan.
[You, San-Lin] Fu Jen Catholic Univ, Dept Publ Hlth, Taipei, Taiwan.
[Park, Sue K.; Kang, Daehee] Seoul Natl Univ, Grad Sch, Dept Biomed Sci, Canc Res Inst, Seoul, South Korea.
[Kim, Dong-Hyun] Hallym Univ, Coll Med, Dept Social & Prevent Med, Seoul, South Korea.
[Parvez, Faruque] Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY USA.
[Sinha, Rashmi] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Boffetta, Paolo] Icahn Sch Med Mt Sinai, Tisch Canc Inst & Inst Translat Epidemiol, New York, NY USA.
[Boffetta, Paolo] Int Prevent Res Inst, Lyon, France.
[Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
[Feng, Ziding] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
[Matsuo, Keitaro] Kyushu Univ, Fac Med Sci, Dept Prevent Med, Fukuoka 812, Japan.
[Potter, John D.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
RP Potter, JD (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
EM yu.chen@nyumc.org
RI Chen, Chien-Jen/C-6976-2008; Chuang, Shao-Yuan/B-3478-2011; Tsugane,
Shocichiro/A-2424-2015; Sinha, Rashmi/G-7446-2015; Tanaka,
Hideo/A-8145-2016;
OI Sinha, Rashmi/0000-0002-2466-7462; Potter, John/0000-0001-5439-1500;
Kakizaki, Masako/0000-0001-6030-8953; Yuan,
Jian-Min/0000-0002-4620-3108; Sauvaget, Catherine/0000-0002-8053-4963;
Matsuo, Keitaro/0000-0003-1761-6314
FU US National Cancer Institute at the National Institutes of Health
[R03CA150038]; Fred Hutchinson Cancer Research Center; Ministry of
Health, Labour and Welfare, Japan; Radiation Effects Research Foundation
(RERF); Ministry of Education, Culture, Sports, Science and Technology,
Japan; China National Hypertension Survey Epidemiology Follow-up Study
(CHEFS); American Heart Association [9750612N]; National Heart, Lung,
and Blood Institute [U01 HL072507]; Chinese Academy of Medical Sciences
Shanghai Cohort Study (SCS); National Institutes for Health
[R01CA0403092, R01CA144034, R37CA70867, R01CA55069, R35CA53890,
R01CA80205, P42ES010349, R01CA102484, R01CA107431]; Shanghai Men's
Health Study (SMHS; National Institutes for Health [RO1 CA 82729];
Shanghai Women's Health Study (SWHS); Community-Based Cancer Screening
Project (CBCSP); National Science Council and Department of Health,
Taiwan; Disease risk FACtor Two-township Study (CVDFACTS); Department of
Health, Taiwan [DOH80-27, DOH81-021, DOH8202-1027, DOH83-TD-015,
DOH84-TD-006]; Korea Multi-center Cancer Cohort (KMCC); Ministry of
Education, Science and Technology, Korea [2009-0087452]; National
Research Foundation of Korea [2009-0087452]; Singapore Chinese Health
Study (SCHS); Health Effects of Arsenic Longitudinal Study (HEALS);
Trivandrum Oral Cancer Screening (TOCS) trial (Association for
International Cancer Research, Scotland, UK; and Cancer Research UK);
Mumbai Cohort Study (MCS); International Agency for Research on Cancer,
Lyon, France; Clinical Trials Service Unit, Oxford, UK; World Health
Organisation, Geneva, Switzerland
FX This work was supported by the US National Cancer Institute at the
National Institutes of Health (R03CA150038) and by the Fred Hutchinson
Cancer Research Center. The cohorts participating in the pooled analysis
were supported by the following grants: 3-Prefecture Aichi, Ibaraki,
Japan Collaborative Cohort Study (JACC), Japan Public Health
Center-Based Study 1 (JPHC1), Japan Public Health Center-Based Study 2
(JPHC2), and 3-Prefecture Miyagi, Miyagi, Ohsaki (National Cancer Center
Research and Development Fund, A Grant-in-Aid for Cancer Research; Grant
for Health Services and Grant for Comprehensive Research on
Cardiovascular and Life-Style Related Diseases from the Ministry of
Health, Labour and Welfare, Japan; Grant for the Scientific Research
from the Ministry of Education, Culture, Sports, Science and Technology,
Japan); Radiation Effects Research Foundation (RERF; Hiroshima and
Nagasaki, Japan is a private, non-profit foundation funded by the
Japanese Ministry of Health, Labour, and Welfare and the US Department
of Energy; grant for scientific research from the Ministry of Education,
Culture, Sports, Science and Technology, Japan); China National
Hypertension Survey Epidemiology Follow-up Study (CHEFS; American Heart
Association (9750612N); National Heart, Lung, and Blood Institute (U01
HL072507)); Chinese Academy of Medical Sciences Shanghai Cohort Study
(SCS; National Institutes for Health (R01CA0403092, R01CA144034));
Shanghai Men's Health Study (SMHS; National Institutes for Health (RO1
CA 82729)); Shanghai Women's Health Study (SWHS; National Institutes for
Health (R37CA70867)); Community-Based Cancer Screening Project (CBCSP;
National Science Council and Department of Health, Taiwan); Disease risk
FACtor Two-township Study (CVDFACTS; Department of Health, Taiwan
(DOH80-27, DOH81-021, DOH8202-1027, DOH83-TD-015, and DOH84-TD-006));
Korea Multi-center Cancer Cohort (KMCC; Ministry of Education, Science
and Technology, Korea (2009-0087452), National Research Foundation of
Korea (2009-0087452)); Singapore Chinese Health Study (SCHS; National
Institutes for Health (R01CA55069, R35CA53890, R01CA80205,
R01CA144034)); Health Effects of Arsenic Longitudinal Study (HEALS;
National Institutes for Health (P42ES010349, R01CA102484, R01CA107431));
Trivandrum Oral Cancer Screening (TOCS) trial (Association for
International Cancer Research, Scotland, UK; and Cancer Research UK);
Mumbai Cohort Study (MCS; International Agency for Research on Cancer,
Lyon, France; Clinical Trials Service Unit, Oxford, UK; World Health
Organisation, Geneva, Switzerland).
NR 91
TC 15
Z9 16
U1 5
U2 24
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BMJ-BRIT MED J
JI BMJ-British Medical Journal
PD OCT 1
PY 2013
VL 347
AR f5446
DI 10.1136/bmj.f5446
PG 19
WC Medicine, General & Internal
SC General & Internal Medicine
GA 231OK
UT WOS:000325426300001
PM 24473060
ER
PT J
AU Irani, SR
Stagg, CJ
Schott, JM
Rosenthal, CR
Schneider, SA
Pettingill, P
Pettingill, R
Waters, P
Thomas, A
Voets, NL
Cardoso, MJ
Cash, DM
Manning, EN
Lang, B
Smith, SJM
Vincent, A
Johnson, MR
AF Irani, Sarosh R.
Stagg, Charlotte J.
Schott, Jonathan M.
Rosenthal, Clive R.
Schneider, Susanne A.
Pettingill, Philippa
Pettingill, Rosemary
Waters, Patrick
Thomas, Adam
Voets, Natalie L.
Cardoso, Manuel J.
Cash, David M.
Manning, Emily N.
Lang, Bethan
Smith, Shelagh J. M.
Vincent, Angela
Johnson, Michael R.
TI Faciobrachial dystonic seizures: the influence of immunotherapy on
seizure control and prevention of cognitive impairment in a broadening
phenotype
SO BRAIN
LA English
DT Article
DE faciobrachial dystonic seizures; LGI1; limbic encephalitis; autoimmune;
epilepsy
ID POTASSIUM-CHANNEL ANTIBODY; CONTACTIN-ASSOCIATED PROTEIN-2;
CENTRAL-NERVOUS-SYSTEM; LIMBIC ENCEPHALITIS; MOVEMENT-DISORDER;
MORVANS-SYNDROME; LEUCINE-RICH; EPILEPSY; AUTOIMMUNITY; NEUROMYOTONIA
AB Voltage-gated potassium channel complex antibodies, particularly those directed against leucine-rich glioma inactivated 1, are associated with a common form of limbic encephalitis that presents with cognitive impairment and seizures. Faciobrachial dystonic seizures have recently been reported as immunotherapy-responsive, brief, frequent events that often predate the cognitive impairment associated with this limbic encephalitis. However, these observations were made from a retrospective study without serial cognitive assessments. Here, we undertook the first prospective study of faciobrachial dystonic seizures with serial assessments of seizure frequencies, cognition and antibodies in 10 cases identified over 20 months. We hypothesized that (i) faciobrachial dystonic seizures would show a differential response to anti-epileptic drugs and immunotherapy; and that (ii) effective treatment of faciobrachial dystonic seizures would accelerate recovery and prevent the development of cognitive impairment. The 10 cases expand both the known age at onset (28 to 92 years, median 68) and clinical features, with events of longer duration, simultaneously bilateral events, prominent automatisms, sensory aura, and post-ictal fear and speech arrest. Ictal epileptiform electroencephalographic changes were present in three cases. All 10 cases were positive for voltage-gated potassium channel-complex antibodies (346-4515 pM): nine showed specificity for leucine-rich glioma inactivated 1. Seven cases had normal clinical magnetic resonance imaging, and the cerebrospinal fluid examination was unremarkable in all seven tested. Faciobrachial dystonic seizures were controlled more effectively with immunotherapy than anti-epileptic drugs (P = 0.006). Strikingly, in the nine cases who remained anti-epileptic drug refractory for a median of 30 days (range 11-200), the addition of corticosteroids was associated with cessation of faciobrachial dystonic seizures within 1 week in three and within 2 months in six cases. Voltage-gated potassium channel-complex antibodies persisted in the four cases with relapses of faciobrachial dystonic seizures during corticosteroid withdrawal. Time to recovery of baseline function was positively correlated with time to immunotherapy (r = 0.74; P = 0.03) but not time to anti-epileptic drug administration (r = 0.55; P = 0.10). Of 10 cases, the eight cases who received anti-epileptic drugs (n = 3) or no treatment (n = 5) all developed cognitive impairment. By contrast, the two who did not develop cognitive impairment received immunotherapy to treat their faciobrachial dystonic seizures (P = 0.02). In eight cases without clinical magnetic resonance imaging evidence of hippocampal signal change, cross-sectional volumetric magnetic resonance imaging post-recovery, after accounting for age and head size, revealed cases (n = 8) had smaller brain volumes than healthy controls (n = 13) (P < 0.001). In conclusion, faciobrachial dystonic seizures can be prospectively identified as a form of epilepsy with an expanding phenotype. Immunotherapy is associated with excellent control of the frequently anti-epileptic drug refractory seizures, hastens time to recovery, and may prevent the subsequent development of cognitive impairment observed in this study.
C1 [Irani, Sarosh R.; Rosenthal, Clive R.; Pettingill, Philippa; Pettingill, Rosemary; Waters, Patrick; Lang, Bethan; Vincent, Angela] Univ Oxford, Nuffield Dept Clin Neurosci, Oxford OX3 9DS, England.
[Stagg, Charlotte J.; Thomas, Adam; Voets, Natalie L.] John Radcliffe Hosp, Oxford Ctr Funct MRI Brain, Nuffield Dept Clin Neurosci, Oxford OX3 9DU, England.
[Schott, Jonathan M.; Cardoso, Manuel J.; Cash, David M.; Manning, Emily N.] UCL, Inst Neurol, Dementia Res Ctr, London, England.
[Schneider, Susanne A.] Univ Kiel, Dept Neurol, D-24105 Kiel, Germany.
[Thomas, Adam] NIMH, Funct MRI Facil, NIH, Bethesda, MD 20892 USA.
[Cardoso, Manuel J.; Cash, David M.] UCL, Ctr Med Image Comp, London WC1E 6BT, England.
[Smith, Shelagh J. M.] Natl Hosp Neurol & Neurosurg, Dept Clin Neurophysiol, London WC1N 3BG, England.
[Johnson, Michael R.] Univ London Imperial Coll Sci Technol & Med, Div Brain Sci, London, England.
RP Irani, SR (reprint author), Univ Oxford, John Radcliffe Hosp, Nuffield Dept Clin Neurosci, Oxford OX3 9DS, England.
EM saroshirani@doctors.net.uk
RI Schott, Jonathan/A-9065-2011;
OI Schott, Jonathan/0000-0003-2059-024X; Stagg,
Charlotte/0000-0002-5542-5036; Thomas, Adam/0000-0002-2850-1419; Irani,
Sarosh/0000-0002-7667-9748
FU National Institute for Health Research, Department of Health, UK
[RDA/07/03/036]; US-UK Fulbright Commission; MS Society; Oxford NIHR
Biomedical Research Centre; Medical Research Council; Imperial College
Healthcare Trust Biomedical Research Centre; Epilepsy Research UK
FX This work was supported by the National Institute for Health Research,
Department of Health, UK (RDA/07/03/036 S.R.I.), 'US-UK Fulbright
Commission and the MS Society' (S.R.I.), the Oxford NIHR Biomedical
Research Centre (P.W., A.V.), Medical Research Council (P.P.), Imperial
College Healthcare Trust Biomedical Research Centre (M.R.J.), and
Epilepsy Research UK (S.R.I., B.L.).
NR 41
TC 87
Z9 91
U1 0
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD OCT
PY 2013
VL 136
BP 3151
EP 3162
DI 10.1093/brain/awt212
PN 10
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 228DU
UT WOS:000325166500029
PM 24014519
ER
PT J
AU Pesatori, AC
Carugno, M
Consonni, D
Hung, RJ
Papadoupolos, A
Landi, MT
Brenner, H
Muller, H
Harris, CC
Duell, EJ
Andrew, AS
McLaughlin, JR
Schwartz, AG
Wenzlaff, AS
Stucker, I
AF Pesatori, A. C.
Carugno, M.
Consonni, D.
Hung, R. J.
Papadoupolos, A.
Landi, M. T.
Brenner, H.
Mueller, H.
Harris, C. C.
Duell, E. J.
Andrew, A. S.
McLaughlin, J. R.
Schwartz, A. G.
Wenzlaff, A. S.
Stucker, I.
TI Hormone use and risk for lung cancer: a pooled analysis from the
International Lung Cancer Consortium (ILCCO)
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE lung cancer; exogenous hormones; oral contraceptives; hormone
replacement therapy; pooled analysis
ID PRACTITIONERS ORAL-CONTRACEPTION; REPLACEMENT THERAPY; REPRODUCTIVE
FACTORS; POSTMENOPAUSAL WOMEN; ESTROGEN-RECEPTOR; RANDOMIZED-TRIAL;
ROYAL-COLLEGE; COHORT; EXPRESSION; HEALTH
AB Background: The association between oral contraceptive (OC) use, hormone replacement therapy (HRT) and lung cancer risk in women is still debated.
Methods: We performed a pooled analysis of six case-control studies (1961 cases and 2609 controls) contributing to the International Lung Cancer Consortium. Potential associations were investigated with multivariable unconditional logistic regression and meta-analytic models. Multinomial logistic regressions were performed to investigate lung cancer risk across histologic types.
Results: A reduced lung cancer risk was found for OC (odds ratio (OR) = 0.81; 95% confidence interval (CI): 0.68-0.97) and HRT ever users (OR = 0.77; 95% CI: 0.66-0.90). Both oestrogen only and oestrogen vertical bar progestin HRT were associated with decreased risk (OR = 0.76; 95% CI: 0.61-0.94, and OR = 0.66; 95% CI: 0.49-0.88, respectively). No dose-response relationship was observed with years of OC/HRT use. The greatest risk reduction was seen for squamous cell carcinoma (OR = 0.53; 95% CI: 0.37-0.76) in OC users and in both adenocarcinoma (OR = 0.79; 95% CI: 0.66-0.95) and small cell carcinoma (OR = 0.37; 95% CI: 0.19-0.71) in HRT users. No interaction with smoking status or BMI was observed.
Conclusion: Our findings suggest that exogenous hormones can play a protective role in lung cancer aetiology. However, given inconsistencies with epidemiological evidence from cohort studies, further and larger investigations are needed for a more comprehensive view of lung cancer development in women.
C1 [Pesatori, A. C.; Carugno, M.] Univ Milan, Epidemiol Res Ctr, Dept Clin Sci & Community Hlth, EPOCA, I-20122 Milan, Italy.
[Pesatori, A. C.; Carugno, M.; Consonni, D.] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Epidemiol Unit, I-20122 Milan, Italy.
[Hung, R. J.; McLaughlin, J. R.] Univ Toronto, Div Epidemiol, Canc Care Ontario Res Chair Populat Studies, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Papadoupolos, A.; Stucker, I.] INSERM, Environm Epidemiol Canc Team, Ctr Res Epidemiol & Populat Hlth CESP, U108, F-94807 Villejuif, France.
[Papadoupolos, A.; Stucker, I.] Univ Paris Sud, UMRS 1018, F-94807 Villejuif, France.
[Landi, M. T.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Brenner, H.; Mueller, H.] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69120 Heidelberg, Germany.
[Harris, C. C.] NCI, Lab Human Carcinogenesis, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Duell, E. J.] Hosp Llobregat, Catalan Inst Oncol ICO IDIBELL, Canc Epidemiol Res Program, Unit Nutr Environm & Canc, Barcelona 08908, Spain.
[Andrew, A. S.] Geisel Sch Med Dartmouth, Dept Community & Family Med, Sect Biostat & Epidemiol, Lebanon, NH 03756 USA.
[McLaughlin, J. R.] Publ Hlth Ontario, Toronto, ON M5G 1V2, Canada.
[Schwartz, A. G.; Wenzlaff, A. S.] Wayne State Univ, Karmanos Canc Inst, Sch Med, Detroit, MI 48201 USA.
RP Pesatori, AC (reprint author), Univ Milan, Epidemiol Res Ctr, Dept Clin Sci & Community Hlth, EPOCA, Via San Barnaba 8, I-20122 Milan, Italy.
EM angela.pesatori@unimi.it
RI Hung, Rayjean/A-7439-2013; Consonni, Dario/K-7943-2016; Brenner,
Hermann/B-4627-2017;
OI Consonni, Dario/0000-0002-8935-3843; Brenner,
Hermann/0000-0002-6129-1572; Duell, Eric J/0000-0001-5256-0163;
pesatori, angela/0000-0002-0261-3252
FU Intramural Research Program of the National Institutes of Health
(National Cancer Institute, Division of Cancer Epidemiology and
Genetics); Lombardy Region (Environmental Epidemiology Program); CARIPLO
Foundation (Milan, Italy); National Cancer Institute Grant [R01CA87895]
FX This work was supported by Intramural Research Program of the National
Institutes of Health (National Cancer Institute, Division of Cancer
Epidemiology and Genetics), Lombardy Region (Environmental Epidemiology
Program), CARIPLO Foundation (Milan, Italy) and National Cancer
Institute Grant R01CA87895. We express our gratitude to all the study
participants and collaborators whose commitment made this pooled
analysis possible.
NR 50
TC 10
Z9 11
U1 1
U2 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD OCT 1
PY 2013
VL 109
IS 7
BP 1954
EP 1964
DI 10.1038/bjc.2013.506
PG 11
WC Oncology
SC Oncology
GA 228UM
UT WOS:000325216700032
PM 24002594
ER
PT J
AU Wang, JB
Abnet, CC
Chen, W
Dawsey, SM
Fan, JH
Yin, LY
Yin, J
Major, JM
Taylor, PR
Qiao, YL
Freedman, ND
AF Wang, J-B
Abnet, C. C.
Chen, W.
Dawsey, S. M.
Fan, J-H
Yin, L-Y
Yin, J.
Major, J. M.
Taylor, P. R.
Qiao, Y-L
Freedman, N. D.
TI Association between serum 25(OH) vitamin D, incident liver cancer and
chronic liver disease mortality in the Linxian Nutrition Intervention
Trials: a nested case-control study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE serum vitamin D; chronic liver disease; liver cancer; a nested
case-control study
ID CIRCULATING 25-HYDROXYVITAMIN D; METABOLIC BONE-DISEASE;
1,25-DIHYDROXYVITAMIN D-3; PARATHYROID-HORMONE; IN-VITRO; RISK;
ESOPHAGEAL; HEPATITIS; CIRRHOSIS; CHINA
AB Background: Although vitamin D deficiency has been noted in cross-sectional studies of chronic liver disease and laboratory studies suggest possible benefits of vitamin D in preventing liver cancer, little epidemiologic data are available.
Methods: We performed a nested case-control study in the Linxian Nutrition Intervention Trials on participants developing incident liver cancer or dying from chronic liver disease over 22 years of follow-up. Baseline serum 25(OH) vitamin D was measured for 226 incident liver cancer cases, 282 chronic liver disease deaths and 1063 age-, sex- and trial-matched controls. Unconditional logistical regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
Results: The median serum vitamin D level in controls was low (20 nmol l(-1)). Compared with the lowest quartile, subjects in the fourth quartile had lower risk of chronic liver disease death (OR = 0.34, 95% CI = 0.21-0.55). For liver cancer incidence, risk estimates were below one, but were not statistically significant. Associations, however, were significant among participants with higher serum calcium levels (Q4 vs Q1, OR = 0.43, 95% CI = 0.21-0.89). Results for chronic liver disease did not vary by serum calcium level.
Conclusion: In a low vitamin D population, higher serum 25(OH) vitamin D concentrations were associated with significantly lower risk of chronic liver disease deaths, and among those with higher serum calcium, incident liver cancer. Our results suggest a possible protective role for vitamin D in these diseases.
C1 [Wang, J-B; Chen, W.; Fan, J-H; Yin, J.; Qiao, Y-L] Chinese Acad Med Sci, Dept Canc Epidemiol, Canc Inst Hosp, Beijing 100021, Peoples R China.
[Wang, J-B; Chen, W.; Fan, J-H; Yin, J.; Qiao, Y-L] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Wang, J-B; Abnet, C. C.; Dawsey, S. M.; Major, J. M.; Freedman, N. D.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
[Yin, L-Y] Chongqing Med Univ, Dept Occupat & Environm Hlth, Sch Publ Hlth, Chongqing 400016, Peoples R China.
[Taylor, P. R.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20850 USA.
RP Qiao, YL (reprint author), Chinese Acad Med Sci, Dept Canc Epidemiol, Canc Inst Hosp, Beijing 100021, Peoples R China.
EM qiaoy@cicams.ac.cn; freedmanne@mail.nih.gov
RI Qiao, You-Lin/B-4139-2012; Abnet, Christian/C-4111-2015; Freedman,
Neal/B-9741-2015
OI Qiao, You-Lin/0000-0001-6380-0871; Abnet, Christian/0000-0002-3008-7843;
Freedman, Neal/0000-0003-0074-1098
FU National Cancer Institute [N01-SC-91030, N01-RC-47701]; Intramural
Research Program of the Division of Cancer Epidemiology and Genetics,
National Cancer Institute, National Institutes of Health; Cancer
Institute, Chinese Academy of Medical Sciences
FX This work was supported in part by National Cancer Institute contracts
(N01-SC-91030 and N01-RC-47701 to the Cancer Institute, Chinese Academy
of Medical Sciences); in part by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health; and in part by Cancer Institute, Chinese
Academy of Medical Sciences. This study was approved by the
Institutional Review Boards of US National Institutes of Health and the
Chinese Academy of Medical Science, and all NIT participants gave
informed consent for the use of their blood samples and all data.
NR 39
TC 10
Z9 10
U1 1
U2 13
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 OCT 1
PY 2013
VL 109
IS 7
BP 1997
EP 2004
DI 10.1038/bjc.2013.546
PG 8
WC Oncology
SC Oncology
GA 228UM
UT WOS:000325216700037
PM 24008664
ER
PT J
AU Enewold, L
McGlynn, KA
Zahm, SH
Jatoi, I
Anderson, WF
Gill, AA
Shriver, CD
Zhu, KM
AF Enewold, Lindsey
McGlynn, Katherine A.
Zahm, Shelia H.
Jatoi, Ismail
Anderson, William F.
Gill, Abegail A.
Shriver, Craig D.
Zhu, Kangmin
TI Surveillance Mammography Among Female Department of Defense
Beneficiaries A Study by Race and Ethnicity
SO CANCER
LA English
DT Article
DE breast cancer; mammography; surveillance; survivor; epidemiology; health
care access
ID BREAST-CANCER SURVIVORS; AMERICAN-SOCIETY; PATTERNS; WOMEN
AB BACKGROUNDAnnual surveillance mammography is recommended after a diagnosis of breast cancer. Previous studies have suggested that surveillance mammography varies by demographics and initial tumor characteristics, which are related to an individual's access to health care. The Military Health System of the Department of Defense provides beneficiaries with equal access health care and thus offers an excellent opportunity to assess whether racial differences in surveillance mammography persist when access to care is equal.
METHODSAmong female beneficiaries with a history of breast cancer, logistic regression was used to assess racial/ethnic variations in the use of surveillance mammography during 3 periods of 12 months each, beginning 1 year after diagnosis adjusting for demographic, tumor, and health characteristics.
RESULTSThe rate of overall surveillance mammography decreased from 70% during the first year to 59% during the third year (P<.01). Although there was an overall tendency for surveillance mammography to be higher among minority women compared with non-Hispanic white women, after adjusting for covariates, the difference was found to be significant only during the first year among black women (odds ratio [OR], 1.46; 95% confidence interval [95% CI], 1.10-1.95) and the second year among Asian/Pacific Islander (OR, 2.29; 95%CI, 1.52-3.44) and Hispanic (OR, 1.92; 95%CI, 1.17-3.18) women. When stratified by age at diagnosis and type of breast cancer surgery performed, significant racial differences tended to be observed among younger women (aged <50 years) and only among women who had undergone mastectomies.
CONCLUSIONSMinority women were equally or more likely than non-Hispanic white women to receive surveillance mammography within the Military Health System. The racial disparities in surveillance mammography reported in other studies were not observed in a system with equal access to health care. Cancer 2013;119:3531-3538.. (c) 2013 American Cancer Society.
Although minority women are often less likely than non-Hispanic white women to receive surveillance mammography, this finding was not observed within an equal access health care system. The racial disparities in surveillance mammography reported in other studies may be due to racial/ethnic variations in health care access.
C1 [Enewold, Lindsey; Gill, Abegail A.; Zhu, Kangmin] Walter Reed Natl Mil Med Ctr, John P Murtha Canc Ctr, Div Mil Epidemiol & Populat Sci, Rockville, MD USA.
[Enewold, Lindsey; McGlynn, Katherine A.; Zahm, Shelia H.; Anderson, William F.] NCI, NIH, Bethesda, MD 20892 USA.
[Jatoi, Ismail] Univ Texas Hlth Sci Ctr San Antonio, Dept Surg, San Antonio, TX 78229 USA.
[Shriver, Craig D.] Walter Reed Natl Mil Med Ctr, John P Murtha Canc Ctr, Bethesda, MD USA.
[Shriver, Craig D.] Walter Reed Natl Mil Med Ctr, Breast Ctr, Bethesda, MD USA.
[Shriver, Craig D.] Walter Reed Natl Mil Med Ctr, Gen Surg Serv, Bethesda, MD USA.
[Shriver, Craig D.; Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
RP Enewold, L (reprint author), NCI Shady Grove, DCCPS, ARP, Hlth Serv Econ Branch, 9609 Med Ctr Dr,Room 3E506, Bethesda, MD 20892 USA.
EM enewoldlr@mail.nih.gov
RI Zahm, Shelia/B-5025-2015
FU John P. Murtha Cancer Center; Walter Reed National Military Cancer
Center via the Uniformed Services University of the Health Sciences
under the Henry M. Jackson Foundation for the Advancement of Military
Medicine.
FX Supported by the John P. Murtha Cancer Center, Walter Reed National
Military Cancer Center via the Uniformed Services University of the
Health Sciences under the auspices of the Henry M. Jackson Foundation
for the Advancement of Military Medicine.
NR 26
TC 4
Z9 4
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD OCT 1
PY 2013
VL 119
IS 19
BP 3531
EP 3538
DI 10.1002/cncr.28242
PG 8
WC Oncology
SC Oncology
GA 224XK
UT WOS:000324925500017
PM 23913448
ER
PT J
AU Driver, DI
Gogtay, N
Rapoport, JL
AF Driver, David I.
Gogtay, Nitin
Rapoport, Judith L.
TI Childhood Onset Schizophrenia and Early Onset Schizophrenia Spectrum
Disorders
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Schizophrenia; Childhood onset schizophrenia; Childhood psychosis
ID COMPLEX DEVELOPMENTAL DISORDER; CORTICAL BRAIN-DEVELOPMENT; TREATMENT
DELAY; 1ST-EPISODE PSYCHOSIS; UNTREATED PSYCHOSIS; GRAY-MATTER;
NONPSYCHOTIC CHILDREN; PSYCHIATRIC-DISORDERS; PREMORBID ADJUSTMENT;
EMOTIONAL DISORDERS
AB The clinical severity, impact on development, and poor prognosis of childhood onset schizophrenia may represent a more homogeneous group. Positive symptoms in children are necessary for the diagnosis and hallucinations are more often multimodal. In healthy children and children with a variety of other psychiatric illnesses, hallucinations are not uncommon and diagnosis should not be based on these alone. Childhood onset schizophrenia is an extraordinarily rare illness that is poorly understood but seems continuous with the adult onset disorder. Once a diagnosis is affirmed, aggressive medication treatment combined with family education and individual counseling may defer further deterioration.
C1 [Driver, David I.; Gogtay, Nitin; Rapoport, Judith L.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
RP Rapoport, JL (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10,Room 3N202,10 Ctr Dr,MSC 1600, Bethesda, MD 20892 USA.
EM rapoporj@mail.nih.gov
RI Gogtay, Nitin/A-3035-2008
FU Intramural NIH HHS [Z01 MH002581-17]
NR 102
TC 13
Z9 14
U1 1
U2 32
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD OCT
PY 2013
VL 22
IS 4
BP 539
EP +
DI 10.1016/j.chc.2013.04.001
PG 18
WC Psychiatry
SC Psychiatry
GA 228MP
UT WOS:000325191200002
PM 24012072
ER
PT J
AU Kwong, MLM
Neyns, B
Yang, JC
AF Kwong, Mei Li M.
Neyns, Bart
Yang, James C.
TI Adoptive T-cell Transfer Therapy and Oncogene-Targeted Therapy for
Melanoma: The Search for Synergy
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID METASTATIC MELANOMA; BRAF INHIBITION; TUMOR INFILTRATION;
ANTIGEN-EXPRESSION; ANTITUMOR-ACTIVITY; PHASE-II; VEMURAFENIB;
IMMUNOTHERAPY; SURVIVAL; MEK
AB The clinical strengths of immunotherapy and small-molecule inhibitors targeting the mitogen-activated protein kinase (MAPK) pathway appear to be largely complementary for the treatment of advanced melanoma. In current practice, most patients with BRAF V600 mutant melanomas will see both modalities. Several in vitro and in vivo studies suggest that combining immunotherapy with MAPK inhibition may have synergistic effects. First, mouse models show that adoptive cell therapy (ACT) can be enhanced by vaccination. Rapid tumor destruction by vemurafenib could provide a vaccine-like stimulus to adoptively transferred T cells. Second, both in mice and in early clinical trials, melanoma metastases treated with MAPK inhibitors seem to display increased T-cell infiltrates. Third, MAPK inhibition upregulates the expression of some melanoma antigens and, therefore, may enhance T-cell recognition of vemurafenib-treated melanomas. Fourth, vemurafenib may sensitize tumor cells to immune destruction. Finally, some investigators have found that an optimal antitumor effect from MAPK inhibition is dependent on an intact host immune response. Currently, the Surgery Branch of the National Cancer Institute has initiated a phase II trial combining the BRAF inhibitor vemurafenib with ACT using tumor-infiltrating lymphocytes in patients with BRAF-mutant tumors to investigate the safety and efficacy of this combination. The proposed mechanisms for synergy between these two modalities can be complex, and their optimal combination may require testing a variety of sequences and schedules. (C) 2013 AACR.
C1 [Kwong, Mei Li M.; Yang, James C.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Neyns, Bart] Univ Ziekenhuis Brussel, Dept Med Oncol, Brussels, Belgium.
RP Yang, JC (reprint author), NCI, 10 Ctr Dr,Rm 3-5952, Bethesda, MD 20892 USA.
EM JamesYang@mail.nih.gov
OI Yang, James Chih-Hsin/0000-0002-5586-5138
FU Intramural NIH HHS [Z99 CA999999]
NR 30
TC 9
Z9 9
U1 0
U2 2
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 OCT 1
PY 2013
VL 19
IS 19
BP 5292
EP 5299
DI 10.1158/1078-0432.CCR-13-0261
PG 8
WC Oncology
SC Oncology
GA 228RA
UT WOS:000325203700006
PM 24089442
ER
PT J
AU Harford, TC
Yi, HY
Grant, BF
AF Harford, Thomas C.
Yi, Hsiao-ye
Grant, Bridget F.
TI Other- and self-directed forms of violence and their relationships to
DSM-IV substance use and other psychiatric disorders in a national
survey of adults
SO COMPREHENSIVE PSYCHIATRY
LA English
DT Article
ID ENVIRONMENTAL RISK-FACTORS; COMMON MENTAL-DISORDERS; EPIDEMIOLOGIC
SURVEY; UNITED-STATES; SUICIDE ATTEMPTS; EXTERNALIZING PSYCHOPATHOLOGY;
PERSONALITY-DISORDERS; ALCOHOL; BEHAVIOR; POPULATION
AB Objective: To examine associations between DSM-IV psychiatric disorders and other- and self-directed violence in the general population.
Methods: Data were obtained from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Waves 1 & 2 (n = 34,653). Four violence categories were derived from a latent class analysis (LCA) of 5 other-directed and 4 self-directed violent behavior indicators. Multinomial logistic regression examined class associations for gender, race ethnicity, age and DSM-IV substance use, mood, anxiety, and personality disorders.
Results: Approximately 16% of adults reported some form of violent behavior distributed as follows: other-directed only, 4.6%; self-directed only, 9.3%; combined self- and other-directed, 2.0%; and no violence, 84.1%. The majority of the DSM-IV disorders included in this study were significantly and independently related to each form of violence. Generally, other-directed violence was more strongly associated with any substance use disorders (81%) and any personality disorders (42%), while self-directed violence was more strongly associated with mood (41%) and anxiety disorders (57%). Compared with these two forms of violence, the smaller group with combined self- and other-directed violence was more strongly associated with any substance use disorders (88%), mood disorders (63%), and personality disorders (76%).
Conclusion: Findings from this study are consistent with recent conceptualizations of disorders as reflecting externalizing disorders and internalizing disorders. The identification of the small category with combined forms of violence further extends numerous clinical studies which established associations between self- and other-directed violent behaviors. The extent to which the combined violence category represents a meaningful and reliable category of violence requires further detailed studies. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Harford, Thomas C.; Yi, Hsiao-ye] CSR Inc, Alcohol Epidemiol Data Syst, Arlington, VA 22201 USA.
[Grant, Bridget F.] NIAAA, NIH, Bethesda, MD USA.
RP Yi, HY (reprint author), NIAAA, Alcohol Epidemiol Data Syst, NIH, CSR Inc, Arlington, VA 22201 USA.
EM hyi@csrincorporated.com
FU Intramural Research Program of the National Institute on Alcohol Abuse
and Alcoholism (NIAAA), National Institutes of Health (NIH); Alcohol
Epidemiologic Data System; NIAAA [HHSN267200800023C]
FX This research was supported in part by the Intramural Research Program
of the National Institute on Alcohol Abuse and Alcoholism (NIAAA),
National Institutes of Health (NIH), and by the Alcohol Epidemiologic
Data System funded by NIAAA Contract No. HHSN267200800023C to CSR,
Incorporated. The views and opinions expressed in this report are those
of the authors and should not be construed to represent the views of the
sponsoring agency or the Federal Government.
NR 44
TC 10
Z9 10
U1 3
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0010-440X
EI 1532-8384
J9 COMPR PSYCHIAT
JI Compr. Psychiat.
PD OCT
PY 2013
VL 54
IS 7
BP 731
EP 739
DI 10.1016/j.comppsych.2013.02.003
PG 9
WC Psychiatry
SC Psychiatry
GA 226ME
UT WOS:000325039600001
PM 23587529
ER
PT J
AU Okano, T
Kelley, MW
AF Okano, Takayuki
Kelley, Matthew W.
TI Expression of Insulin-Like Growth Factor Binding Proteins During Mouse
Cochlear Development
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE differentiation; cellular patterning; gradient
ID MAMMALIAN INNER-EAR; GENE-EXPRESSION; CELL-PROLIFERATION; MESSENGER-RNA;
FACTOR SYSTEM; FACTOR IGF; DIFFERENTIATION; ORGAN; CORTI; MICE
AB Background: Insulin-like growth factor (IGF) signaling plays important roles in growth and cellular differentiation in the cochlear sensory epithelium. However, the roles of IGF binding proteins (IGFBPs), a family of IGF modulators, remain to be elucidated in this system. To begin to examine the role of IGFBPs, we used reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization to determine the temporal and spatial patterns of expression for Igfbps within the developing mouse cochlea. Results: RT-PCR analysis indicates that Igfpb2-5 are expressed in the cochlea between embryonic day (E) 13.5 and postnatal day (P) 0. In addition, the expression of each Igfbp significantly increased between E13.5 and P0. In situ hybridization indicates that Igfbp2, 3, 4, and 5 have distinct and complementary expression patterns in the developing cochlea. Moreover, expression patterns of Igfbp3 and 5 demonstrate contrasting gradients along the basal-to-apical axis of the cochlea. Conclusions:Igfbp2-5 are expressed in distinct and complementary patterns during cochlear development. These data suggest that IGFBPs may act to precisely regulate activation of IGF signaling in the developing cochlea in a cell type-specific manner, contributing to cellular patterning and differentiation in the cochlea. Developmental Dynamics 242:1210-1221, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Okano, Takayuki; Kelley, Matthew W.] Natl Inst Deafness & Other Commun Disorders, Lab Cochlear Dev, NIH, Bethesda, MD USA.
RP Kelley, MW (reprint author), Porter Neurosci Res Ctr, 35 Convent Dr,Bldg 35,2A-100, Bethesda, MD USA.
EM kelleymt@nidcd.nih.gov
FU NIH; Intramural Program
FX Grant sponsors: NIH; Intramural Program.
NR 43
TC 3
Z9 3
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD OCT
PY 2013
VL 242
IS 10
BP 1210
EP 1221
DI 10.1002/dvdy.24005
PG 12
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 227IV
UT WOS:000325107000009
PM 23813480
ER
PT J
AU Fiori, JL
Shin, YK
Kim, W
Krzysik-Walker, SM
Gonzalez-Mariscal, I
Carlson, OD
Sanghvi, M
Moaddel, R
Farhang, K
Gadkaree, SK
Doyle, ME
Pearson, KJ
Mattison, JA
de Cabo, R
Egan, JM
AF Fiori, Jennifer L.
Shin, Yu-Kyong
Kim, Wook
Krzysik-Walker, Susan M.
Gonzalez-Mariscal, Isabel
Carlson, Olga D.
Sanghvi, Mitesh
Moaddel, Ruin
Farhang, Kathleen
Gadkaree, Shekhar K.
Doyle, Maire E.
Pearson, Kevin J.
Mattison, Julie A.
de Cabo, Rafael
Egan, Josephine M.
TI Resveratrol Prevents beta-Cell Dedifferentiation in Nonhuman Primates
Given a High-Fat/High-Sugar Diet
SO DIABETES
LA English
DT Article
ID GLUCAGON-LIKE PEPTIDE-1; PROTEIN-KINASE-C; INSULIN SENSITIVITY;
GLUCOSE-TOLERANCE; SUPPLEMENTATION; ACTIVATION; APOPTOSIS; RECEPTOR;
PROLIFERATION; DETERMINANTS
AB Eating a Westernized diet high in fat and sugar leads to weight gain and numerous health problems, including the development of type 2 diabetes mellitus (T2DM). Rodent studies have shown that resveratrol supplementation reduces blood glucose levels, preserves -cells in islets of Langerhans, and improves insulin action. Although rodent models are helpful for understanding -cell biology and certain aspects of T2DM pathology, they fail to reproduce the complexity of the human disease as well as that of nonhuman primates. Rhesus monkeys were fed a standard diet (SD), or a high-fat/high-sugar diet in combination with either placebo (HFS) or resveratrol (HFS+Resv) for 24 months, and pancreata were examined before overt dysglycemia occurred. Increased glucose-stimulated insulin secretion and insulin resistance occurred in both HFS and HFS+Resv diets compared with SD. Although islet size was unaffected, there was a significant decrease in -cells and an increase in -cells containing glucagon and glucagon-like peptide 1 with HFS diets. Islets from HFS+Resv monkeys were morphologically similar to SD. HFS diets also resulted in decreased expression of essential -cell transcription factors forkhead box O1 (FOXO1), NKX6-1, NKX2-2, and PDX1, which did not occur with resveratrol supplementation. Similar changes were observed in human islets where the effects of resveratrol were mediated through Sirtuin 1. These findings have implications for the management of humans with insulin resistance, prediabetes, and diabetes.
C1 [Fiori, Jennifer L.; Shin, Yu-Kyong; Kim, Wook; Krzysik-Walker, Susan M.; Gonzalez-Mariscal, Isabel; Carlson, Olga D.; Sanghvi, Mitesh; Moaddel, Ruin; Farhang, Kathleen; Gadkaree, Shekhar K.; Egan, Josephine M.] NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA.
[Shin, Yu-Kyong] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA.
[Kim, Wook] Ajou Univ, Dept Mol Sci & Technol, Suwon 441749, South Korea.
[Doyle, Maire E.] Johns Hopkins Bayview Med Ctr, Div Endocrinol, Baltimore, MD USA.
[Pearson, Kevin J.; Mattison, Julie A.; de Cabo, Rafael] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Pearson, Kevin J.] Univ Kentucky, Coll Med, Grad Ctr Nutr Sci, Lexington, KY USA.
RP Egan, JM (reprint author), NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA.
EM eganj@grc.nia.nih.gov
RI de Cabo, Rafael/J-5230-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; Gonzalez Mariscal,
Isabel/0000-0003-1186-1212
FU Intramural Research Program of the National Institute on Aging; Office
of Dietary Supplements; Basic Science Research Program through the
National Research Foundation of Korea (NRF); Ministry of Science, ICT,
and Future Planning [2012R1A1A1041352]; JDRF; Sanford Project, Sioux
Falls, SD
FX This work was supported by the Intramural Research Program of the
National Institute on Aging and by a grant from the Office of Dietary
Supplements awarded to K.J.P. W. K. was supported by the Basic Science
Research Program through the National Research Foundation of Korea (NRF)
and funded by the Ministry of Science, ICT, and Future Planning
(2012R1A1A1041352). M. E. D. was supported by the JDRF and The Sanford
Project, Sioux Falls, SD.
NR 54
TC 48
Z9 48
U1 3
U2 15
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2013
VL 62
IS 10
BP 3500
EP 3513
DI 10.2337/db13-0266
PG 14
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RG
UT WOS:000324748200033
PM 23884882
ER
PT J
AU Genuth, SM
Backlund, JYC
Bayless, M
Bluemke, DA
Cleary, PA
Crandall, J
Lachin, JM
Lima, JAC
Miao, CL
Turkbey, EB
AF Genuth, Saul M.
Backlund, Jye-Yu C.
Bayless, Margaret
Bluemke, David A.
Cleary, Patricia A.
Crandall, Jill
Lachin, John M.
Lima, Joao A. C.
Miao, Culian
Turkbey, Evrim B.
CA DCCT EDIC Res Grp
TI Effects of Prior Intensive Versus Conventional Therapy and History of
Glycemia on Cardiac Function in Type 1 Diabetes in the DCCT/EDIC
SO DIABETES
LA English
DT Article
ID CORONARY-HEART-DISEASE; COMPLICATIONS TRIAL COHORT; INTIMA-MEDIA
THICKNESS; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; RISK-FACTORS;
PULSE PRESSURE; MAGNETIC-RESONANCE; FOLLOW-UP; MELLITUS
AB Intensive diabetes therapy reduces the prevalence of coronary calcification and progression of atherosclerosis and the risk of cardiovascular disease (CVD) events in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study. The effects of intensive therapy on measures of cardiac function and structure and their association with glycemia have not been explored in type 1 diabetes (T1DM). We assess whether intensive treatment compared with conventional treatment during the DCCT led to differences in these parameters during EDIC. After 6.5 years of intensive versus conventional therapy in the DCCT, and 15 years of additional follow-up in EDIC, left ventricular (LV) indices were measured by cardiac magnetic resonance (CMR) imaging in 1,017 of the 1,371 members of the DCCT cohort. There were no differences between the DCCT intensive versus conventional treatment in end diastolic volume (EDV), end systolic volume, stroke volume (SV), cardiac output (CO), LV mass, ejection fraction, LV mass/EDV, or aortic distensibility (AD). Mean DCCT/EDIC HbA(1c) over time was associated with EDV, SV, CO, LV mass, LV mass/EDV, and AD. These associations persisted after adjustment for CVD risk factors. Cardiac function and remodeling in T1DM assessed by CMR in the EDIC cohort was associated with prior glycemic exposure, but there was no effect of intensive versus conventional treatment during the DCCT on cardiac parameters.
C1 [Genuth, Saul M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Backlund, Jye-Yu C.; Cleary, Patricia A.; Lachin, John M.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Bayless, Margaret] Univ Iowa, Iowa City, IA USA.
[Bluemke, David A.; Turkbey, Evrim B.] NIH, Bethesda, MD 20892 USA.
[Crandall, Jill] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Lima, Joao A. C.; Miao, Culian] Johns Hopkins Univ, Baltimore, MD USA.
RP Genuth, SM (reprint author), Case Western Reserve Univ, Cleveland, OH 44106 USA.
EM smg15@case.edu
OI Lachin, John/0000-0001-9838-2841; Bluemke, David/0000-0002-8323-8086
FU Division of Diabetes, Endocrinology, and Metabolic Diseases of the
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK); National Eye Institute; National Institute of Neurological
Disorders and Stroke; General Clinical Research Centers Program,
National Center for Research Resources; Clinical and Translation Science
Centers Program, National Center for Research Resources; Genentech;
NIDDK
FX The DCCT/EDIC project is supported by contracts with the Division of
Diabetes, Endocrinology, and Metabolic Diseases of the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the
National Eye Institute, the National Institute of Neurological Disorders
and Stroke, the General Clinical Research Centers Program and the
Clinical and Translation Science Centers Program, the National Center
for Research Resources, and Genentech through a Cooperative Research and
Development Agreement with the NIDDK.
NR 56
TC 12
Z9 12
U1 0
U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
EI 1939-327X
J9 DIABETES
JI Diabetes
PD OCT
PY 2013
VL 62
IS 10
BP 3561
EP 3569
DI 10.2337/db12-0546
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RG
UT WOS:000324748200040
PM 23520132
ER
PT J
AU Yaghootkar, H
Lamina, C
Scott, RA
Dastani, Z
Hivert, MF
Warren, LL
Stancakova, A
Buxbaum, SG
Lyytikaeinen, LP
Henneman, P
Wu, Y
Cheung, CYY
Pankow, JS
Jackson, AU
Gustafsson, S
Zhao, JH
Ballantyne, CM
Xie, WJ
Bergman, RN
Boehnke, M
el Bouazzaoui, F
Collins, FS
Dunn, SH
Dupuis, J
Forouhi, NG
Gillson, C
Hattersley, AT
Hong, JY
Kaehoenen, M
Kuusisto, J
Kedenko, L
Kronenberg, F
Doria, A
Assimes, TL
Ferrannini, E
Hansen, T
Hao, K
Haering, H
Knowles, JW
Lindgren, CM
Nolan, JJ
Paananen, J
Pedersen, O
Quertermous, T
Smith, U
Lehtimaeki, T
Liu, CT
Loos, RJF
McCarthy, MI
Morris, AD
Vasan, RS
Spector, TD
Teslovich, TM
Tuomilehto, J
van Dijk, KW
Viikari, JS
Zhu, N
Langenberg, C
Ingelsson, E
Semple, RK
Sinaiko, AR
Palmer, CNA
Walker, M
Lam, KSL
Paulweber, B
Mohlke, KL
van Duijn, C
Raitakari, OT
Bidulescu, A
Wareham, NJ
Laakso, M
Waterworth, DM
Lawlor, DA
Meigs, JB
Richards, JB
Frayling, TM
AF Yaghootkar, Hanieh
Lamina, Claudia
Scott, Robert A.
Dastani, Zari
Hivert, Marie-France
Warren, Liling L.
Stancakova, Alena
Buxbaum, Sarah G.
Lyytikaeinen, Leo-Pekka
Henneman, Peter
Wu, Ying
Cheung, Chloe Y. Y.
Pankow, James S.
Jackson, Anne U.
Gustafsson, Stefan
Zhao, Jing Hua
Ballantyne, Christie M.
Xie, Weijia
Bergman, Richard N.
Boehnke, Michael
el Bouazzaoui, Fatiha
Collins, Francis S.
Dunn, Sandra H.
Dupuis, Josee
Forouhi, Nita G.
Gillson, Christopher
Hattersley, Andrew T.
Hong, Jaeyoung
Kaehoenen, Mika
Kuusisto, Johanna
Kedenko, Lyudmyla
Kronenberg, Florian
Doria, Alessandro
Assimes, Themistocles L.
Ferrannini, Ele
Hansen, Torben
Hao, Ke
Haering, Hans
Knowles, Joshua W.
Lindgren, Cecilia M.
Nolan, John J.
Paananen, Jussi
Pedersen, Oluf
Quertermous, Thomas
Smith, Ulf
Lehtimaeki, Terho
Liu, Ching-Ti
Loos, Ruth J. F.
McCarthy, Mark I.
Morris, Andrew D.
Vasan, Ramachandran S.
Spector, Tim D.
Teslovich, Tanya M.
Tuomilehto, Jaakko
van Dijk, Ko Willems
Viikari, Jorma S.
Zhu, Na
Langenberg, Claudia
Ingelsson, Erik
Semple, Robert K.
Sinaiko, Alan R.
Palmer, Colin N. A.
Walker, Mark
Lam, Karen S. L.
Paulweber, Bernhard
Mohlke, Karen L.
van Duijn, Cornelia
Raitakari, Olli T.
Bidulescu, Aurelian
Wareham, Nick J.
Laakso, Markku
Waterworth, Dawn M.
Lawlor, Debbie A.
Meigs, James B.
Richards, J. Brent
Frayling, Timothy M.
CA GENESIS Consortium
RISC Consortium
TI Mendelian Randomization Studies Do Not Support a Causal Role for Reduced
Circulating Adiponectin Levels in Insulin Resistance and Type 2 Diabetes
SO DIABETES
LA English
DT Article
ID MOLECULAR-WEIGHT ADIPONECTIN; GREATER-THAN-G; PLASMA ADIPONECTIN;
ADIPOSE-TISSUE; ASSOCIATION ANALYSES; METABOLIC PROFILE;
GENETIC-VARIANTS; SUPPRESSION TEST; GLYCEMIC TRAITS; OBESE WOMEN
AB Adiponectin is strongly inversely associated with insulin resistance and type 2 diabetes, but its causal role remains controversial. We used a Mendelian randomization approach to test the hypothesis that adiponectin causally influences insulin resistance and type 2 diabetes. We used genetic variants at the ADIPOQ gene as instruments to calculate a regression slope between adiponectin levels and metabolic traits (up to 31,000 individuals) and a combination of instrumental variables and summary statistics-based genetic risk scores to test the associations with gold-standard measures of insulin sensitivity (2,969 individuals) and type 2 diabetes (15,960 case subjects and 64,731 control subjects). In conventional regression analyses, a 1-SD decrease in adiponectin levels was correlated with a 0.31-SD (95% CI 0.26-0.35) increase in fasting insulin, a 0.34-SD (0.30-0.38) decrease in insulin sensitivity, and a type 2 diabetes odds ratio (OR) of 1.75 (1.47-2.13). The instrumental variable analysis revealed no evidence of a causal association between genetically lower circulating adiponectin and higher fasting insulin (0.02 SD; 95% CI -0.07 to 0.11; N = 29,771), nominal evidence of a causal relationship with lower insulin sensitivity (-0.20 SD; 95% CI -0.38 to -0.02; N = 1,860), and no evidence of a relationship with type 2 diabetes (OR 0.94; 95% CI 0.75-1.19; N = 2,777 case subjects and 13,011 control subjects). Using the ADIPOQ summary statistics genetic risk scores, we found no evidence of an association between adiponectin-lowering alleles and insulin sensitivity (effect per weighted adiponectin-lowering allele: -0.03 SD; 95% CI -0.07 to 0.01; N = 2,969) or type 2 diabetes (OR per weighted adiponectin-lowering allele: 0.99; 95% CI 0.95-1.04; 15,960 case subjects vs. 64,731 control subjects). These results do not provide any consistent evidence that interventions aimed at increasing adiponectin levels will improve insulin sensitivity or risk of type 2 diabetes.
C1 [Yaghootkar, Hanieh; Xie, Weijia; Hattersley, Andrew T.; Frayling, Timothy M.] Univ Exeter, Sch Med, Exeter, Devon, England.
[Lamina, Claudia; Kronenberg, Florian] Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, A-6020 Innsbruck, Austria.
[Scott, Robert A.; Zhao, Jing Hua; Forouhi, Nita G.; Gillson, Christopher; Loos, Ruth J. F.; Langenberg, Claudia; Wareham, Nick J.] Inst Met Sci, MRC Epidemiol Unit, Cambridge, England.
[Dastani, Zari] McGill Univ, Jewish Gen Hosp, Lady Davis Inst, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3T 1E2, Canada.
[Hivert, Marie-France] Univ Sherbrooke, Dept Med, Sherbrooke, PQ J1K 2R1, Canada.
[Hivert, Marie-France; Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Warren, Liling L.] GlaxoSmithKline, Res Triangle Pk, NC USA.
[Stancakova, Alena; Kuusisto, Johanna; Hao, Ke; Paananen, Jussi; Laakso, Markku] Univ Eastern Finland, Kuopio, Finland.
[Buxbaum, Sarah G.] Jackson State Univ, Sch Hlth Sci, Jackson, MS USA.
[Lyytikaeinen, Leo-Pekka; Lehtimaeki, Terho] Fimlab Labs, Dept Clin Chem, Tampere, Finland.
[Lyytikaeinen, Leo-Pekka; Lehtimaeki, Terho] Univ Tampere, Sch Med, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Henneman, Peter; el Bouazzaoui, Fatiha; van Dijk, Ko Willems] Leiden Univ, Dept Human Genet, Med Ctr, NL-2300 RA Leiden, Netherlands.
[Wu, Ying; Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Cheung, Chloe Y. Y.; Lam, Karen S. L.] Univ Hong Kong, Li Ka Shing Fac Med, Dept Med, Hong Kong, Hong Kong, Peoples R China.
[Pankow, James S.; Zhu, Na] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Jackson, Anne U.; Boehnke, Michael; Teslovich, Tanya M.] Univ Michigan, Dept Biostat & Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Gustafsson, Stefan; Ingelsson, Erik] Uppsala Univ, Mol Epidemiol & Sci Life Lab, Dept Med Sci, Uppsala, Sweden.
[Ballantyne, Christie M.] Baylor Coll Med, Houston, TX USA.
[Ballantyne, Christie M.] Methodist DeBakey Heart & Vasc Ctr, Houston, TX USA.
[Bergman, Richard N.] Cedars Sinai Med Ctr, Diabetes & Obes Res Inst, Los Angeles, CA 90048 USA.
[Collins, Francis S.] Natl Inst Hlth, Natl Human Genome Res Inst, Genome Technol Branch, Bethesda, MD USA.
[Dunn, Sandra H.] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
[Dupuis, Josee; Hong, Jaeyoung; Liu, Ching-Ti] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Kaehoenen, Mika] Tampere Univ Hosp, Dept Clin Psychol, Tampere, Finland.
[Kaehoenen, Mika] Univ Tampere, Sch Med, FIN-33101 Tampere, Finland.
[Kedenko, Lyudmyla; Paulweber, Bernhard] Paracelsus Private Med Univ Salzburg, St Johann Spital, Dept Internal Med 1, Salzburg, Austria.
[Doria, Alessandro] Joslin Diabet Ctr, Sect Genet & Epidemiol, Boston, MA 02215 USA.
[Assimes, Themistocles L.; Knowles, Joshua W.; Quertermous, Thomas] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA.
[Assimes, Themistocles L.; Knowles, Joshua W.; Quertermous, Thomas] Stanford Univ, Sch Med, Cardiovasc Inst, Stanford, CA 94305 USA.
Univ Pisa, Dept Internal Med, Pisa, Italy.
[Haering, Hans; Pedersen, Oluf] Univ Copenhagen, Fac Hlth Sci, Novo Nordisk Fdn Ctr Basic Metab Res, Copenhagen, Denmark.
Univ Southern Denmark, Fac Hlth Sci, Odense, Denmark.
Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
Univ Tubingen, Dept Internal Med, Div Endocrinol Diabetol Nephrol Vasc Med & Clin C, Tubingen, Germany.
[Ferrannini, Ele; Lindgren, Cecilia M.; McCarthy, Mark I.; Ingelsson, Erik] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Hansen, Torben; Nolan, John J.] Steno Diabet Ctr, DK-2820 Gentofte, Denmark.
[Haering, Hans] Hagedorn Res Inst, Copenhagen, Denmark.
[Haering, Hans] Univ Copenhagen, Fac Hlth Sci, Inst Biomed Sci, Copenhagen, Denmark.
[Haering, Hans] Univ Aarhus, Fac Hlth Sci, Aarhus, Denmark.
[Smith, Ulf] Sahlgrens Acad, Lundberg Lab Diabet Res, Dept Mol & Clin Med, Gothenburg, Sweden.
[Loos, Ruth J. F.] Inst Child Hlth & Dev, Charles Bronfman Inst Personalized Med, Mt Sinai Sch Med, Dept Prevent Med, New York, NY USA.
[McCarthy, Mark I.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[McCarthy, Mark I.] Churchill Hosp, Oxford Natl Inst Hlth Res Biomed Res Ctr, Oxford OX3 7LJ, England.
[Morris, Andrew D.; Palmer, Colin N. A.] Univ Dundee, Ninewells Hosp & Med Sch, Med Res Inst, Dundee DD1 9SY, Scotland.
[Vasan, Ramachandran S.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Vasan, Ramachandran S.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Spector, Tim D.; Richards, J. Brent] Kings Coll London, Twin Res & Genet Epidemiol, London WC2R 2LS, England.
[Tuomilehto, Jaakko] Natl Inst Hlth & Welf, Diabetes Prevent Unit, Helsinki, Finland.
[Tuomilehto, Jaakko] King Abdulaziz Univ, Jeddah 21413, Saudi Arabia.
[Tuomilehto, Jaakko] Hosp Univ La Paz, Red RECAVA Grp RD06 0014 0015, Madrid, Spain.
[Tuomilehto, Jaakko] Danube Univ Krems, Ctr Vasc Prevent, Krems, Austria.
[Viikari, Jorma S.] Turku Univ Hosp, Dept Med, FIN-20520 Turku, Finland.
[Viikari, Jorma S.] Univ Turku, Dept Med, Turku, Finland.
[Semple, Robert K.] Natl Inst Hlth Res Cambridge Biomed Res Ctr, Cambridge, England.
[Semple, Robert K.] Univ Cambridge, Metab Res Labs, Inst Metab Sci, Cambridge, England.
[Sinaiko, Alan R.] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
[Walker, Mark] Newcastle Univ, Sch Med, Inst Cellular Med, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Lam, Karen S. L.] Univ Hong Kong, Li Ka Shing Fac Med, Res Ctr Heart Brain Hormone & Hlth Aging, Hong Kong, Hong Kong, Peoples R China.
[van Duijn, Cornelia] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Raitakari, Olli T.] Turku Univ Hosp, Dept Clin Physiol & Nucl Med, FIN-20520 Turku, Finland.
[Raitakari, Olli T.] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Bidulescu, Aurelian] Inst Cardiovasc Res, Morehouse Sch Med, Atlanta, GA USA.
[Bidulescu, Aurelian] Morehouse Sch Med, Dept Community Hlth & Prevent Med, Atlanta, GA 30310 USA.
[Waterworth, Dawn M.] GlaxoSmithKline, Upper Merion, PA USA.
[Lawlor, Debbie A.] Univ Bristol, Dept Social Med, Bristol, Avon, England.
[Richards, J. Brent] McGill Univ, Dept Med Human Genet Epidemiol & Biostat, Montreal, PQ, Canada.
RP Frayling, TM (reprint author), Univ Exeter, Sch Med, Exeter, Devon, England.
EM tim.frayling@pms.ac.uk
RI Colaus, PsyColaus/K-6607-2013; Palmer, Colin/C-7053-2008; Willems van
Dijk, Ko/A-1798-2008; Bidulescu, Aurelian/N-2617-2014; Kronenberg,
Florian/B-1736-2008; Lyytikainen, Leo-Pekka/C-8544-2016; Study,
GoDARTS/K-9448-2016; Buxbaum, Sarah/E-1970-2013;
OI Palmer, Colin/0000-0002-6415-6560; Willems van Dijk,
Ko/0000-0002-2172-7394; Ramachandran, Vasan/0000-0001-7357-5970; Semple,
Robert/0000-0001-6539-3069; Bidulescu, Aurelian/0000-0001-8211-8309;
Kronenberg, Florian/0000-0003-2229-1120; Lyytikainen,
Leo-Pekka/0000-0002-7200-5455; Paananen, Jussi/0000-0001-5100-4907;
Buxbaum, Sarah/0000-0002-4886-3564; Forouhi, Nita/0000-0002-5041-248X;
Lawlor, Debbie A/0000-0002-6793-2262; Pankow, James/0000-0001-7076-483X;
Hattersley, Andrew/0000-0001-5620-473X
FU Biotechnology and Biological Sciences Research Council [G20234];
Canadian Institutes of Health Research; Diabetes UK [12/0004470]; FIC
NIH HHS [TW05596]; Intramural NIH HHS; Medical Research Council
[G0500070, G0600705, MC_U106179471, MC_U106188470, MC_UP_A100_1003,
MC_UU_12013/5]; NCATS NIH HHS [UL1 TR000454]; NCRR NIH HHS
[MO1-RR-00400, RR20649, UL1 RR025008, UL1RR025005]; NHGRI NIH HHS [1Z01
HG000024, N01-HG-65403, U01HG004402]; NHLBI NIH HHS [HL52851, HL085144,
N01-HC-25195, N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019,
N01-HC-55020, N01-HC-55021, N01-HC-55022, N01-HC-95170, N01-HC-95171,
N01-HC-95172, R01 HL105756, R01HL086694, R01HL087641, R01HL59367, RC2
HL102419, UH1 HL073461]; NIDDK NIH HHS [DK062370, DK072193, DK078150,
DK36836-25, DK56350, K24 DK080140, P30 DK020572, R01 DK072193, R01
DK078616, R01 DK093757, R01DK056918]; NIEHS NIH HHS [ES10126]; NIMHD NIH
HHS [P20 MD006899]; NINR NIH HHS [T32 NR009759]; Wellcome Trust [,
090532, 098498, 100574]
NR 58
TC 42
Z9 42
U1 0
U2 26
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2013
VL 62
IS 10
BP 3589
EP 3598
DI 10.2337/db13-0128
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RG
UT WOS:000324748200043
PM 23835345
ER
PT J
AU Mahendran, Y
Vangipurapu, J
Cederberg, H
Stancakova, A
Pihlajamaki, J
Soininen, P
Kangas, AJ
Paananen, J
Civelek, M
Saleem, NK
Pajukanta, P
Lusis, AJ
Bonnycastle, LL
Morken, MA
Collins, FS
Mohlke, KL
Boehnke, M
Ala-Korpela, M
Kuusisto, J
Laakso, M
AF Mahendran, Yuvaraj
Vangipurapu, Jagadish
Cederberg, Henna
Stancakova, Alena
Pihlajamaki, Jussi
Soininen, Pasi
Kangas, Antti J.
Paananen, Jussi
Civelek, Mete
Saleem, Niyas K.
Pajukanta, Paeivi
Lusis, Aldons J.
Bonnycastle, Lori L.
Morken, Mario A.
Collins, Francis S.
Mohlke, Karen L.
Boehnke, Michael
Ala-Korpela, Mika
Kuusisto, Johanna
Laakso, Markku
TI Association of Ketone Body Levels With Hyperglycemia and Type 2 Diabetes
in 9,398 Finnish Men
SO DIABETES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PANCREATIC BETA-CELLS; FREE-FATTY-ACID;
GLUCOSE-TOLERANCE; INSULIN SENSITIVITY; CHRONIC EXPOSURE; BLOOD KETONE;
LOCI; HYDROXYBUTYRATE; BODIES
AB We investigated the association of the levels of ketone bodies (KBs) with hyperglycemia and with 62 genetic risk variants regulating glucose levels or type 2 diabetes in the population-based Metabolic Syndrome in Men (METSIM) study, including 9,398 Finnish men without diabetes or newly diagnosed type 2 diabetes. Increasing fasting and 2-h plasma glucose levels were associated with elevated levels of acetoacetate (AcAc) and -hydroxybutyrate (BHB). AcAc and BHB predicted an increase in the glucose area under the curve in an oral glucose tolerance test, and AcAc predicted the conversion to type 2 diabetes in a 5-year follow-up of the METSIM cohort. Impaired insulin secretion, but not insulin resistance, explained these findings. Of the 62 single nucleotide polymorphisms associated with the risk of type 2 diabetes or hyperglycemia, the glucose-increasing C allele of GCKR significantly associated with elevated levels of fasting BHB levels. Adipose tissue mRNA expression levels of genes involved in ketolysis were significantly associated with insulin sensitivity (Matsuda index). In conclusion, high levels of KBs predicted subsequent worsening of hyperglycemia, and a common variant of GCKR was significantly associated with BHB levels.
C1 [Mahendran, Yuvaraj; Vangipurapu, Jagadish; Cederberg, Henna; Stancakova, Alena; Pihlajamaki, Jussi; Paananen, Jussi; Saleem, Niyas K.; Kuusisto, Johanna; Laakso, Markku] Univ Eastern Finland, Dept Med, Kuopio, Finland.
[Cederberg, Henna; Pihlajamaki, Jussi; Kuusisto, Johanna; Laakso, Markku] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
[Pihlajamaki, Jussi] Univ Eastern Finland, Dept Clin Nutr, Kuopio, Finland.
[Soininen, Pasi; Kangas, Antti J.; Ala-Korpela, Mika] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
[Soininen, Pasi; Ala-Korpela, Mika] Univ Eastern Finland, Sch Pharm, Nucl Magnet Resonance Metabol Lab, Kuopio, Finland.
[Civelek, Mete; Lusis, Aldons J.] Univ Calif Los Angeles, Dept Human Genet, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA.
[Civelek, Mete; Lusis, Aldons J.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Pajukanta, Paeivi] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
[Bonnycastle, Lori L.; Morken, Mario A.; Collins, Francis S.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Ala-Korpela, Mika] Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
[Ala-Korpela, Mika] Oulu Univ Hosp, Unit Gen Practice, Oulu, Finland.
RP Laakso, M (reprint author), Univ Eastern Finland, Dept Med, Kuopio, Finland.
EM markku.laakso@kuh.fi
OI Paananen, Jussi/0000-0001-5100-4907; Civelek, Mete/0000-0002-8141-0284
FU Academy of Finland; Finnish Diabetes Research Foundation; Finnish
Cardiovascular Research Foundation; Jenny and Antti Wihuri Foundation;
University of Oulu; University of Eastern Finland; EVO from the Kuopio
University Hospital [5263]; National Institutes of Health (NIH)
[HL-095056, HL-28481, DK-093757, DK-072193]; [DK-062370];
[1Z01-HG-000024]
FX This work was supported by the Academy of Finland (A. S. and M. L.;
Responding to Public Health Challenges Research Programme to M.A.-K.),
the Finnish Diabetes Research Foundation (M. L.), the Finnish
Cardiovascular Research Foundation (M.A.-K. and M. L.), the Jenny and
Antti Wihuri Foundation (A.J.K.), Strategic Research Funding from the
University of Oulu (M.A.-K.), Strategic Research Funding from the
University of Eastern Finland (M. L.), EVO Grant 5263 from the Kuopio
University Hospital (M. L.), DK-062370 (M. B.), 1Z01-HG-000024 (F. S.
C.), National Institutes of Health (NIH) Grant HL-095056 (P. P.), NIH
Grant HL-28481 (P. P. and A.J.L.), and NIH grants DK-093757 and
DK-072193 (K.L.M.).
NR 40
TC 26
Z9 27
U1 2
U2 12
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
EI 1939-327X
J9 DIABETES
JI Diabetes
PD OCT
PY 2013
VL 62
IS 10
BP 3618
EP 3626
DI 10.2337/db12-1363
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RG
UT WOS:000324748200046
PM 23557707
ER
PT J
AU Chakkera, HA
Chang, YH
Ayub, A
Gonwa, TA
Weil, EJ
Knowler, WC
AF Chakkera, Harini A.
Chang, Yu-Hui
Ayub, Asad
Gonwa, Thomas A.
Weil, E. Jennifer
Knowler, William C.
TI Validation of a Pretransplant Risk Score for New-Onset Diabetes After
Kidney Transplantation
SO DIABETES CARE
LA English
DT Article
ID INTERNAL VALIDATION; PREDICTION MODELS; MELLITUS; RECIPIENTS;
HYPERGLYCEMIA; IMPACT
AB OBJECTIVEIdentification of patients at high risk for new-onset diabetes after kidney transplantation (NODAT) will facilitate clinical trials for its prevention.RESEARCH DESIGN AND METHODSWe previously described a pretransplant predictive risk model for NODAT using seven pretransplant variables (age, planned use of maintenance corticosteroids, prescription for gout medicine, BMI, fasting glucose, fasting triglycerides, and family history of diabetes). We have now applied the initial model to a cohort of 474 transplant recipients from another center for validation. We performed two analyses in the validation cohort. The first was a standard model with variables derived from the original study. The second was a summary score model, in which the sum of dichotomized variables (all the variables dichotomized at clinically relevant cut points) was used to categorize, individuals into low (0-1), intermediate (2, 3), or high (4-7) risk groups. We also conducted a combined database analyses, merging the initial and validation cohorts (n = 792) to obtain better estimates for a prediction equation.RESULTSAlthough the frequency of several risk factors differed significantly between the two cohorts, the models performed similarly in each cohort. Using the summary score model, incidences of NODAT in low-risk, medium-risk, and high-risk groups in the initial cohort were 12, 29, and 56%, and in the validation cohort incidences were 11, 29, and 51%.CONCLUSIONSA pretransplant model for NODAT, including many type 2 diabetes risk factors, predicted NODAT in the validation cohort.
C1 [Chakkera, Harini A.] Mayo Clin, Div Nephrol, Scottsdale, AZ USA.
[Chakkera, Harini A.] Mayo Clin, Div Transplantat, Scottsdale, AZ USA.
[Chang, Yu-Hui] Mayo Clin, Div Hlth Sci Res, Scottsdale, AZ USA.
[Ayub, Asad; Gonwa, Thomas A.] Mayo Clin, Div Nephrol, Jacksonville, FL 32224 USA.
[Ayub, Asad; Gonwa, Thomas A.] Mayo Clin, Div Transplantat, Jacksonville, FL 32224 USA.
[Weil, E. Jennifer; Knowler, William C.] Natl Inst Diabet & Digest & Kidney Dis, NIH, Phoenix, AZ USA.
RP Chakkera, HA (reprint author), Mayo Clin, Div Nephrol, Scottsdale, AZ USA.
EM chakkera.harini@mayo.edu
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases; Mayo Clinic Foundation
FX This research was supported in part by the Intramural Research Program
of the National Institute of Diabetes and Digestive and Kidney Diseases
and a Mayo Clinic Foundation Career Development Grant.
NR 25
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PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2013
VL 36
IS 10
BP 2881
EP 2886
DI 10.2337/dc13-0428
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RT
UT WOS:000324749500017
PM 24009296
ER
PT J
AU Jensen, MK
Bartz, TM
Djousse, L
Kizer, JR
Zieman, SJ
Rimm, EB
Siscovick, DS
Psaty, BM
Ix, JH
Mukamal, KJ
AF Jensen, Majken K.
Bartz, Traci M.
Djousse, Luc
Kizer, Jorge R.
Zieman, Susan J.
Rimm, Eric B.
Siscovick, David S.
Psaty, Bruce M.
Ix, Joachim H.
Mukamal, Kenneth J.
TI Genetically Elevated Fetuin-A Levels, Fasting Glucose Levels, and Risk
of Type 2 Diabetes The Cardiovascular Health Study
SO DIABETES CARE
LA English
DT Article
ID RECEPTOR TYROSINE KINASE; INSULIN-RECEPTOR; FATTY LIVER; GLYCOPROTEIN
GENE; ASSOCIATION; POLYMORPHISM; INHIBITOR; AHSG; MELLITUS; DESIGN
AB OBJECTIVEFetuin-A levels are associated with higher risk of type 2 diabetes, but it is unknown if the association is causal. We investigated common (>5%) genetic variants in the fetuin-A gene (AHSG) fetuin-A levels, fasting glucose, and risk of type 2 diabetes.RESEARCH DESIGN AND METHODSGenetic variation, fetuin-A levels, and fasting glucose were assessed in 2,893 Caucasian and 542 African American community-living individuals 65 years of age or older in 1992-1993.RESULTSCommon AHSG variants (rs4917 and rs2248690) were strongly associated with fetuin-A concentrations (P < 0.0001). In analyses of 259 incident cases of type 2 diabetes, the single nucleotide polymorphisms (SNPs) were not associated with diabetes risk during follow-up and similar null associations were observed when 579 prevalent cases were included. As expected, higher fetuin-A levels were associated with higher fasting glucose concentrations (1.9 mg/dL [95% CI, 1.2-2.7] higher per SD in Caucasians), but Mendelian randomization analyses using both SNPs as unbiased proxies for measured fetuin-A did not support an association between genetically predicted fetuin-A levels and fasting glucose (-0.3 mg/dL [95% CI, -1.9 to 1.3] lower per SD in Caucasians). The difference between the associations of fasting glucose with actual and genetically predicted fetuin-A level was statistically significant (P = 0.001). Results among the smaller sample of African Americans trended in similar directions but were statistically insignificant.CONCLUSIONSCommon variants in the AHSG gene are strongly associated with plasma fetuin-A concentrations, but not with risk of type 2 diabetes or glucose concentrations, raising the possibility that the association between fetuin-A and type 2 diabetes may not be causal.
C1 [Jensen, Majken K.; Rimm, Eric B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Bartz, Traci M.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Djousse, Luc] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
[Djousse, Luc] Boston Vet Affairs Healthcare Syst, Boston, MA USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
[Kizer, Jorge R.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Zieman, Susan J.] NIA, NIH, Bethesda, MD 20892 USA.
[Rimm, Eric B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med,Dept Med, Boston, MA 02115 USA.
[Siscovick, David S.; Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Siscovick, David S.; Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Siscovick, David S.; Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Siscovick, David S.; Psaty, Bruce M.] Grp Hlth Res Inst, Grp Hlth Cooperat, Seattle, WA USA.
[Ix, Joachim H.] Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Nephrol, San Diego, CA 92103 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Prevent Med, San Diego, CA 92103 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
RP Jensen, MK (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
EM mkjensen@hsph.harvard.edu
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute (NHLBI) [R01 HL094555]; NHLBI
CARe project (Broad Institute of Massachusetts Institute of Technology
and Harvard) [N01HC65226]; NHLBI [HHSN268201200036C, HHSN268200800007C,
N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083,
N01HC85086, HL080295]; National Institute on Aging [AG023629]
FX This study was supported by a grant from the National Heart, Lung, and
Blood Institute (NHLBI) (R01 HL094555 to L.D., J.R.K., S.J.Z., J.H.I.,
and K.J.M.), and genotyping was funded by the NHLBI CARe project (Broad
Institute of Massachusetts Institute of Technology and Harvard,
N01HC65226). The CHS was supported by contracts HHSN268201200036C,
HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081,
N01HC85082, N01HC85083, and N01HC85086 and by grant HL080295 from the
NHLBI, with additional contribution from the National Institute of
Neurological Disorders and Stroke. Additional support was provided by
AG023629 from the National Institute on Aging.
NR 26
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2013
VL 36
IS 10
BP 3121
EP 3127
DI 10.2337/dc12-2323
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RT
UT WOS:000324749500051
PM 23801724
ER
PT J
AU Orchard, TJ
Lyons, TJ
Cleary, PA
Braffett, BH
Maynard, J
Cowie, C
Gubitosi-Klug, RA
Way, J
Anderson, K
Barnie, A
Villavicencio, S
AF Orchard, Trevor J.
Lyons, Timothy J.
Cleary, Patricia A.
Braffett, Barbara H.
Maynard, John
Cowie, Catherine
Gubitosi-Klug, Rose A.
Way, Jeff
Anderson, Karen
Barnie, Annette
Villavicencio, Stephan
CA DCCT EDIC Res Grp
TI The Association of Skin Intrinsic Fluorescence With Type 1 Diabetes
Complications in the DCCT/EDIC Study
SO DIABETES CARE
LA English
DT Article
ID ADVANCED GLYCATION ENDPRODUCTS; CORONARY-ARTERY CALCIFICATION;
GLOMERULAR-FILTRATION-RATE; END-PRODUCTS; COLLAGEN GLYCATION; TRIAL
COHORT; INTERVENTIONS; MELLITUS; TRIAL/EPIDEMIOLOGY; EPIDEMIOLOGY
AB OBJECTIVETo determine whether skin intrinsic fluorescence (SIF) is associated with long-term complications of type 1 diabetes (T1D) and, if so, whether it is independent of chronic glycemic exposure and previous intensive therapy.RESEARCH DESIGN AND METHODSWe studied 1,185 (92%) of 1,289 active Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) participants from 2010 to 2011. SIF was determined using a fluorescence spectrometer and related cross-sectionally to recently determined measures of retinopathy (stereo fundus photography), cardiac autonomic neuropathy (CAN; R-R interval), confirmed clinical neuropathy, nephropathy (albumin excretion rate [AER]), and coronary artery calcification (CAC).RESULTSOverall, moderately strong associations were seen with all complications, before adjustment for mean HbA(1c) over time, which rendered these associations nonsignificant with the exception of sustained AER >30 mg/24 h and CAC, which were largely unaffected by adjustment. However, when examined within the former DCCT treatment group, associations were generally weaker in the intensive group and nonsignificant after adjustment, while in the conventional group, associations remained significant for CAN, sustained AER >30 mg/24 h, and CAC even after mean HbA(1c) adjustment.CONCLUSIONSSIF is associated with T1D complications in DCCT\EDIC. Much of this association appears to be related to historical glycemic exposure, particularly in the previously intensively treated participants, in whom adjustment for HbA(1c) eliminates statistical significance.
C1 [Orchard, Trevor J.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Lyons, Timothy J.] Univ Oklahoma, Oklahoma City, OK USA.
[Cleary, Patricia A.; Braffett, Barbara H.; Anderson, Karen; Villavicencio, Stephan] George Washington Univ, Rockville, MD USA.
[Maynard, John; Way, Jeff] VeraLight Inc, Albuquerque, NM USA.
[Cowie, Catherine] NIDDK, Bethesda, MD USA.
[Gubitosi-Klug, Rose A.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Barnie, Annette] Univ Toronto, Toronto, ON, Canada.
RP Orchard, TJ (reprint author), Univ Pittsburgh, Pittsburgh, PA 15260 USA.
EM tjo@pitt.edu
OI orchard, trevor/0000-0001-9552-3215
FU Division of Diabetes, Endocrinology and Metabolic Diseases of the
National Institute of Diabetes and Digestive and Kidney Diseases;
National Eye Institute; National Institute of Neurological Disorders and
Stroke; General Clinical Research Centers Program; Clinical and
Translational Science Awards Program; National Center for Research
Resources; VeraLight; Genentech; National Institute of Diabetes and
Digestive and Kidney Diseases; VeraLight, Inc.
FX Abbott, Animas, Aventis, Becton Dickinson, Bayer, Can Am, Eli Lilly,
LifeScan, Medtronic MiniMed, Omron, and Roche contributed free or
discounted supplies and/or equipment. The DCCT/EDIC project is supported
by contracts with the Division of Diabetes, Endocrinology and Metabolic
Diseases of the National Institute of Diabetes and Digestive and Kidney
Diseases, National Eye Institute, National Institute of Neurological
Disorders and Stroke, the General Clinical Research Centers Program and
the Clinical and Translational Science Awards Program, National Center
for Research Resources, VeraLight, and Genentech through a Cooperative
Research and Development Agreement with the National Institute of
Diabetes and Digestive and Kidney Diseases. T.J.O. and T.J.L. have
received grant support from VeraLight, Inc. J.M. is an employee and
stock option holder of VeraLight, Inc. J.W. is an employee and stock
option holder of VeraLight, Inc. A. B. is an independent insulin pump
trainer who receives payment from Medtronic, Animas, Spirit, and OmniPod
pumps. No other potential conflicts of interest relevant to this article
were reported.
NR 39
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2013
VL 36
IS 10
BP 3146
EP 3153
DI 10.2337/dc12-2661
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RT
UT WOS:000324749500055
PM 23813757
ER
PT J
AU Pop-Busui, R
Lu, J
Brooks, MM
Albert, S
Althouse, AD
Escobedo, J
Green, J
Palumbo, P
Perkins, BA
Whitehouse, F
Jones, TLZ
AF Pop-Busui, Rodica
Lu, Jiang
Brooks, Maria Mori
Albert, Stewart
Althouse, Andrew D.
Escobedo, Jorge
Green, Jenifer
Palumbo, Pasquale
Perkins, Bruce A.
Whitehouse, Fred
Jones, Teresa L. Z.
CA BARI 2D Study Grp
TI Impact of Glycemic Control Strategies on the Progression of Diabetic
Peripheral Neuropathy in the Bypass Angioplasty Revascularization
Investigation 2 Diabetes (BARI 2D) Cohort
SO DIABETES CARE
LA English
DT Article
ID FACTOR-KAPPA-B; COMPLICATIONS TRIAL; ROSIGLITAZONE TREATMENT;
INSULIN-RESISTANCE; GAMMA-LIGAND; CELL-DEATH; PIOGLITAZONE; METFORMIN;
INTERVENTIONS; NEPHROPATHY
AB OBJECTIVEThe Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial demonstrated similar long-term clinical effectiveness of insulin-sensitizing (IS) versus insulin-providing (IP) treatments for type 2 diabetes on cardiovascular outcomes in a cohort with documented coronary artery disease. We evaluated the effects of randomized glycemic control strategy (IS vs. IP) on the prevalence and incidence of diabetic peripheral neuropathy (DPN).RESEARCH DESIGN AND METHODSDPN (defined as Michigan Neuropathy Screening Instrument [MNSI] clinical examination score >2) was assessed at baseline and yearly for 4 years. DPN prevalence and incidence were compared by intention-to-treat modeling by logistic generalized estimating equation models for prevalence and Kaplan-Meier estimates and Cox regression models for incidence rates.RESULTSResults are reported for 2,159 BARI 2D participants (70% males) with valid baseline and at least one follow-up MNSI score (mean age 62 9 years, mean HbA(1c) 7.7 +/- 1.6%, diabetes duration 10 +/- 9 years). There were no differences in the prevalence of DPN between the IS and the IP groups throughout the 4 years of follow-up. In 1,075 BARI 2D participants with no DPN at baseline, the 4-year cumulative incidence rate of DPN was significantly lower in the IS (66%) than in the IP (72%) strategy group (P = 0.02), which remained significant after adjusting for the in-trial HbA(1c) (P = 0.04). In subgroup analyses, IS strategy had a greater benefit in men (hazard ratio 0.75 [99% CI 0.58-0.99], P < 0.01).CONCLUSIONSAmong patients with type 2 diabetes followed for up to 4 years during BARI 2D, a glycemic control therapy with IS significantly reduced the incidence of DPN compared with IP therapy and may add further benefit for men.
C1 [Pop-Busui, Rodica] Univ Michigan, Dept Internal Med, Div Metab Endocrinol & Diabet, Ann Arbor, MI 48109 USA.
[Lu, Jiang; Brooks, Maria Mori; Althouse, Andrew D.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Albert, Stewart] St Louis Univ, Sch Med, Dept Internal Med, Div Endocrinol, St Louis, MO USA.
[Escobedo, Jorge] Reg Hosp 1, Mexican Inst Social Secur, Unidad Invest Epidemiol Clin, Mexico City, DF, Mexico.
[Green, Jenifer] Duke Univ, Med Ctr, Dept Med, Div Endocrinol, Durham, NC 27710 USA.
[Palumbo, Pasquale] Mayo Clin, Div Prevent Med, Dept Internal Med, Scottsdale, AZ USA.
[Perkins, Bruce A.] Univ Toronto, Dept Med, Div Endocrinol, Toronto, ON, Canada.
[Whitehouse, Fred] Henry Ford Hlth Syst, Henry Ford Med Grp, Div Endocrinol & Diabet, Detroit, MI USA.
[Jones, Teresa L. Z.] NIDDK, NIH, Bethesda, MD USA.
RP Pop-Busui, R (reprint author), Univ Michigan, Dept Internal Med, Div Metab Endocrinol & Diabet, Ann Arbor, MI 48109 USA.
EM rpbusui@umich.edu
OI Brooks, Maria/0000-0002-2030-7873
FU National Heart, Lung, and Blood Institute; National Institute of
Diabetes and Digestive and Kidney Diseases [U01-HL-061744,
U01-HL-061746, U01-HL-061748, U01-HL-063804]; GlaxoSmithKline;
Bristol-Myers Squibb; Merck; Medtronic; Boehringer Ingelheim
FX The trial was sponsored by the National Heart, Lung, and Blood Institute
and the National Institute of Diabetes and Digestive and Kidney Diseases
(U01-HL-061744, U01-HL-061746, U01-HL-061748, U01-HL-063804), with
additional support from multiple industry sponsors, including the
manufacturer of rosiglitazone GlaxoSmithKline (a detailed list is
provided in Supplementary Funding Sources).; R.P.-B. received a research
grant from Amylin Pharmaceuticals (now Bristol-Myers Squibb) unrelated
to the manuscript. J.G. received a research grant from Amylin
Pharmaceuticals (now Bristol-Myers Squibb) and Merck unrelated to this
manuscript and is a member of the Merck speakers' bureau. B. A. P.
received speaker honoraria from Medtronic Inc., Johnson and Johnson,
Roche, GlaxoSmithKline Canada, Novo Nordisk, Eli Lilly, and
sanofi-aventis; has received research grant support from Medtronic and
Boehringer Ingelheim; and serves on an advisory board for Neurometrix,
Inc. No other potential conflicts of interest relevant to this article
were reported.
NR 37
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2013
VL 36
IS 10
BP 3208
EP 3215
DI 10.2337/dc13-0012
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RT
UT WOS:000324749500063
PM 23757426
ER
PT J
AU Chakkera, HA
Pham, PT
Pomeroy, J
Weil, EJ
Knowler, WC
AF Chakkera, Harini A.
Phuong-Thu Pham
Pomeroy, Jeremy
Weil, E. Jennifer
Knowler, William C.
TI Response to Comment on: Chakkera et al. Can New-Onset Diabetes After
Kidney Transplant Be Prevented? Diabetes Care 2013;36:1406-1412
SO DIABETES CARE
LA English
DT Letter
ID INSULIN
C1 [Chakkera, Harini A.] Mayo Clin, Div Nephrol & Transplantat, Phoenix, AZ USA.
[Phuong-Thu Pham] UCLA Hlth Syst, Internal Med Nephrol, Los Angeles, CA USA.
[Pomeroy, Jeremy; Weil, E. Jennifer; Knowler, William C.] Natl Inst Diabet & Digest & Kidney Dis, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ USA.
RP Chakkera, HA (reprint author), Mayo Clin, Div Nephrol & Transplantat, Phoenix, AZ USA.
EM chakkera.harini@mayo.edu
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PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2013
VL 36
IS 10
BP E183
EP E183
DI 10.2337/dc13-1656
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222RT
UT WOS:000324749500010
PM 24065856
ER
PT J
AU Vehik, K
Fiske, SW
Logan, CA
Agardh, D
Cilio, CM
Hagopian, W
Simell, O
Roivainen, M
She, JX
Briese, T
Oikarinen, S
Hyoty, H
Ziegler, AG
Rewers, M
Lernmark, A
Akolkar, B
Krischer, JP
Burkhardt, BR
AF Vehik, Kendra
Fiske, Steven W.
Logan, Chad A.
Agardh, Daniel
Cilio, Corrado M.
Hagopian, William
Simell, Olli
Roivainen, Merja
She, Jin-Xiong
Briese, Thomas
Oikarinen, Sami
Hyoty, Heikki
Ziegler, Anette-G.
Rewers, Marian
Lernmark, Ake
Akolkar, Beena
Krischer, Jeffrey P.
Burkhardt, Brant R.
CA TEDDY Study Grp
TI Methods, quality control and specimen management in an international
multicentre investigation of type 1 diabetes: TEDDY
SO DIABETES-METABOLISM RESEARCH AND REVIEWS
LA English
DT Article
DE quality control; data integrity; stool sample preservation; RNA;
biomarker stability; metabolic biomarkers; T-cell viability
ID ENVIRONMENTAL DETERMINANTS; YOUNG; WORKSHOP; SYSTEM; BLOOD; RISK
AB BackgroundThe vast array and quantity of longitudinal samples collected in The Environmental Determinants of Diabetes in the Young study present a series of challenges in terms of quality control procedures and data validity. To address this, pilot studies have been conducted to standardize and enhance both biospecimen collection and sample obtainment in terms of autoantibody collection, stool sample preservation, RNA, biomarker stability, metabolic biomarkers and T-cell viability.
Research Design and MethodsThe Environmental Determinants of Diabetes in the Young is a multicentre, international prospective study (n=8677) designed to identify environmental triggers of type 1 diabetes (T1D) in genetically at-risk children from ages 3months until 15years. The study is conducted through six primary clinical centres located in four countries.
ResultsAs of May 2012, over three million biological samples and 250 million total data points have been collected, which will be analysed to assess autoimmunity status, presence of inflammatory biomarkers, genetic factors, exposure to infectious agents, dietary biomarkers and other potentially important environmental exposures in relation to autoimmunity and progression to T1D.
ConclusionsDetailed procedures were utilized to standardize both data harmonization and management when handling a large quantity of longitudinal samples obtained from multiple locations. In addition, a description of the available specimens is provided that serve as an invaluable repository for the elucidation of determinants in T1D focusing on autoantibody concordance and harmonization, transglutaminase autoantibody, inflammatory biomarkers (T-cells), genetic proficiency testing, RNA lab internal quality control testing, infectious agents (monitoring cross-contamination, virus preservation and nasal swab collection validity) and HbA(1c) testing. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Vehik, Kendra; Fiske, Steven W.; Logan, Chad A.; Krischer, Jeffrey P.; Burkhardt, Brant R.] Univ S Florida, Morsani Coll Med, Pediat Epidemiol Ctr, Tampa, FL 33612 USA.
[Agardh, Daniel; Cilio, Corrado M.; Lernmark, Ake] Lund Univ, Malmo Univ Hosp, Dept Clin Sci, Malmo, Sweden.
[Hagopian, William] Pacific Northwest Diabet Res Inst, Seattle, WA USA.
[Simell, Olli] Univ Turku, Dept Pediat, Turku, Finland.
[Roivainen, Merja] Natl Inst Hlth & Welf, Helsinki, Finland.
[She, Jin-Xiong] Med Coll Georgia, Augusta, GA 30912 USA.
[Briese, Thomas] Columbia Univ, Mailman Sch Publ Hlth, Ctr Infect & Immun, New York, NY USA.
[Oikarinen, Sami; Hyoty, Heikki] Univ Tampere, Sch Med, Dept Virol, FIN-33101 Tampere, Finland.
[Hyoty, Heikki] Tampere Univ Hosp, Dept Clin Microbiol, Ctr Lab Med, Tampere, Finland.
[Ziegler, Anette-G.] Helmholtz Zentrum Munchen, Inst Diabet Res, Neuherberg, Germany.
[Ziegler, Anette-G.] Forschergrp Diabet eV, Neuherberg, Germany.
[Rewers, Marian] Univ Colorado Denver, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
[Akolkar, Beena] NIDDK, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD USA.
[Burkhardt, Brant R.] Univ S Florida, Dept Cell Biol Microbiol & Mol Biol, Tampa, FL 33612 USA.
RP Vehik, K (reprint author), Univ S Florida, Morsani Coll Med, Pediat Epidemiol Ctr, 3650 Spectrum Blvd,STE 100, Tampa, FL 33612 USA.
EM kendra.vehik@epi.usf.edu
RI Ziegler, Anette-Gabriele/M-4614-2014; oikarinen, sami/E-3611-2015
OI Ziegler, Anette-Gabriele/0000-0002-6290-5548;
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[U01 DK63829, U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01
DK63836, U01 DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4
DK63865, UC4 DK63863, UC4 DK63836, UC4 DK63790, UC4DK095300,
HHSN267200700014C]; National Institute of Allergy and Infectious
Diseases (NIAID); National Institute of Child Health and Human
Development (NICHD); National Institute of Environmental Health Sciences
(NIEHS); Juvenile Diabetes Research Foundation (JDRF); Centers for
Disease Control and Prevention (CDC)
FX The TEDDY Study Group (see online appendix) is funded by U01 DK63829,
U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01 DK63836, U01
DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4 DK63865, UC4
DK63863, UC4 DK63836, UC4 DK63790 and UC4DK095300 and contract no.
HHSN267200700014C from the National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK), National Institute of Allergy and
Infectious Diseases (NIAID), National Institute of Child Health and
Human Development (NICHD), National Institute of Environmental Health
Sciences (NIEHS), Juvenile Diabetes Research Foundation (JDRF) and
Centers for Disease Control and Prevention (CDC).
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PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1520-7560
J9 DIABETES-METAB RES
JI Diabetes-Metab. Res. Rev.
PD OCT
PY 2013
VL 29
IS 7
BP 557
EP 567
DI 10.1002/dmrr.2427
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 226KW
UT WOS:000325035600006
PM 23674484
ER
PT J
AU Erdag, G
Chowdhuri, SR
Fetsch, P
Erickson, D
Hughes, MS
Filie, AC
AF Erdag, Gulsun
Chowdhuri, Sinchita Roy
Fetsch, Patricia
Erickson, Dana
Hughes, Marybeth S.
Filie, Armando C.
TI KBA.62 and S100 Protein Expression in Cytologic Samples of Metastatic
Malignant Melanoma
SO DIAGNOSTIC CYTOPATHOLOGY
LA English
DT Article
DE KBA.62; S100 protein; immunocytochemistry/immunohistochemistry;
cytology; melanoma
ID FINE-NEEDLE-ASPIRATION; T-CELLS MART-1; IMMUNOCYTOCHEMICAL ANALYSIS;
AMELANOTIC MELANOMAS; MONOCLONAL-ANTIBODY; S-100 PROTEIN; DIAGNOSIS;
BIOPSY; TYROSINASE; EFFUSIONS
AB The diagnosis of melanoma can be challenging, especially in metastatic lesions, due to the ability of melanoma cells to morphologically mimic carcinoma, sarcoma and even lymphoma cells. Moreover, melanomas can exhibit negative immunostaining for the melanoma markers HMB-45 and MART-1/Melan-A, often used in the diagnosis of this tumor. KBA.62 is a recently described antibody that reacts with benign and malignant melanocytic proliferations. In this study, we report our experience with KBA.62 and S100 protein immunostaining in the diagnosis of metastatic melanoma on fine-needle aspiration and effusion samples. We reviewed 60 cytology samples from 58 patients with metastatic melanoma. Our results showed that KBA.62 stained 75% of the cases and S100 protein 87% of the cases. KBA.62 and S100 protein stained the majority of metastatic melanomas that were negative for HMB-45 and MART-1; KBA.62 stained 73% of the cases and S100 protein 73% of the cases. The majority (85%) of the cases negative for HMB-45 and MART-1 were positive for KBA.62 and/or S100 protein. Additionally, we also observed that KBA.62 staining was positive in the majority of epithelioid and spindle cell type melanoma cells. In conclusion, the performances of KBA.62 and S100 protein were similar and both markers are useful in the diagnosis of metastatic melanoma in cytology material, especially when the tumor cells lack expression of HMB-45 and MART-1. Diagn. Cytopathol. 2013;41:847-851. (c) 2013 Wiley Periodicals, Inc.
C1 [Erdag, Gulsun; Chowdhuri, Sinchita Roy; Fetsch, Patricia; Erickson, Dana; Filie, Armando C.] NCI, Cytopathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Hughes, Marybeth S.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Filie, AC (reprint author), NCI, Cytopathol Sect, Pathol Lab, Ctr Canc Res, 10 Ctr Dr Bldg 10 Room 2A19, Bethesda, MD 20892 USA.
EM afilie@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute
FX Contract grant sponsors: Intramural Research Program of the NIH,
National Cancer Institute.
NR 26
TC 0
Z9 0
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 8755-1039
J9 DIAGN CYTOPATHOL
JI Diagn. Cytopathol.
PD OCT
PY 2013
VL 41
IS 10
BP 847
EP 851
DI 10.1002/dc.22948
PG 5
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA 224WS
UT WOS:000324923000001
PM 23554410
ER
PT J
AU Horner-Johnson, W
Dobbertin, K
Lee, JC
Andresen, EM
AF Horner-Johnson, Willi
Dobbertin, Konrad
Lee, Jae Chul
Andresen, Elena M.
CA Expert Panel Disability Hlth
TI Disparities in chronic conditions and health status by type of
disability
SO DISABILITY AND HEALTH JOURNAL
LA English
DT Article
DE People with disabilities; Health status disparities; Chronic conditions;
Adult; Population surveillance
ID QUALITY-OF-LIFE; GENDER-DIFFERENCES; POPULATION; CARE; OBESITY; ADULTS;
WOMEN
AB Background: Prior research has established health disparities between people with and without disabilities. However, disparities within the disability population, such as those related to type of disability, have been much less studied.
Objective: To examine differences in chronic conditions and health status between subgroups of people with different types of disability.
Methods: We analyzed Medical Expenditure Panel Survey annual data files from 2002 to 2008. Logistic regression analyses considered disparity from three perspectives: 1) basic differences, unadjusted for other factors; 2) controlling for key demographic and health covariates; and 3) controlling for a larger set of demographic variables and socioeconomic status as well as health and access to healthcare.
Results: Individuals with vision, physical, cognitive, or multiple disability types fared worse than people with hearing impairment on most health outcomes. This was most consistently true for people with multiple disabilities. Even when all covariates were accounted for, people with multiple types of disability were significantly more likely (p < 0.05) than those with hearing impairment (reference group) to report every poor health outcome with the exception of BMI >= 25 and lung disease.
Conclusions: While many of the differences between disability types were reduced when controlling for other factors, some differences remained significant. This argues for a more individualized approach to understanding and preventing chronic conditions and poor health in specific disability groups. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Horner-Johnson, Willi; Dobbertin, Konrad; Andresen, Elena M.] Oregon Hlth & Sci Univ, Inst Dev & Disabil, Portland, OR 97239 USA.
[Lee, Jae Chul] NIH, Dept Rehabil Med, Clin Res Ctr, Bethesda, MD 20892 USA.
RP Horner-Johnson, W (reprint author), Oregon Hlth & Sci Univ, Inst Dev & Disabil, 707 SW Gaines St, Portland, OR 97239 USA.
EM hornerjo@ohsu.edu
OI Horner-Johnson, Willi/0000-0003-3568-1400
FU National Institute on Disability and Rehabilitation Research/DOE
[H133A080031]
FX This work was supported by grant # H133A080031 from the National
Institute on Disability and Rehabilitation Research/DOE. However, the
contents do not necessarily represent the policy of the Department of
Education, and you should not assume endorsement by the Federal
Government.
NR 27
TC 12
Z9 13
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-6574
J9 DISABIL HEALTH J
JI Disabil. Health J.
PD OCT
PY 2013
VL 6
IS 4
BP 280
EP 286
DI 10.1016/j.dhjo.2013.04.006
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health; Rehabilitation
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Rehabilitation
GA 224CJ
UT WOS:000324858900003
PM 24060250
ER
PT J
AU Cannons, JL
Zhao, F
Schwartzberg, PL
AF Cannons, Jennifer L.
Zhao, Fang
Schwartzberg, Pamela L.
TI Ncking BCR-mediated PI3K activation
SO EMBO REPORTS
LA English
DT Editorial Material
ID RECRUITMENT; REGULATORS; FAMILY
C1 [Cannons, Jennifer L.; Zhao, Fang; Schwartzberg, Pamela L.] NHGRI, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Zhao, Fang] Univ Chicago, Pritzker Sch Med, Chicago, IL 60637 USA.
RP Cannons, JL (reprint author), NHGRI, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM pams@mail.nih.gov
NR 10
TC 1
Z9 1
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD OCT
PY 2013
VL 14
IS 10
BP 852
EP 853
DI 10.1038/embor.2013.133
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 229HL
UT WOS:000325253100005
PM 23969954
ER
PT J
AU Matzat, LH
Dale, RK
Lei, EP
AF Matzat, Leah H.
Dale, Ryan K.
Lei, Elissa P.
TI Messenger RNA is a functional component of a chromatin insulator complex
SO EMBO REPORTS
LA English
DT Article
DE RNA; chromatin; insulator; Drosophila; nuclear organization
ID NUCLEAR-ORGANIZATION; DROSOPHILA; ACCESSIBILITY; REPRESSION; BINDING;
LOCUS; DNA
AB Chromatin insulators are DNA protein complexes situated throughout the genome capable of demarcating independent transcriptional domains. Previous studies point to an important role for RNA in gypsy chromatin insulator function in Drosophila; however, the identity of these putative insulator-associated RNAs is not currently known. Here we utilize RNA-immunoprecipitation and high throughput sequencing (RIP-seq) to isolate RNAs stably associated with gypsy insulator complexes. Strikingly, these RNAs correspond to specific sense-strand, spliced and polyadenylated mRNAs, including two insulator protein transcripts. In order to assess the functional significance of these associated mRNAs independent of their coding function, we expressed untranslatable versions of these transcripts in developing flies and observed both alteration of insulator complex nuclear localization as well as improvement of enhancer-blocking activity. Together, these data suggest a novel, noncoding mechanism by which certain mRNAs contribute to chromatin insulator function.
C1 [Matzat, Leah H.; Dale, Ryan K.; Lei, Elissa P.] NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
RP Lei, EP (reprint author), NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM leielissa@niddk.nih.gov
OI Dale, Ryan/0000-0003-2664-3744
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX We thank W. Bender and V. Corces for fly strains, M. Levine for alpha-Dl
antisera and N. Perrimon for the pCa4B plasmid. We thank members of the
Lei laboratory, J. Birchler, E. Clough, C. Kaplan, J. Kassis and V.
Sartorelli for critical reading of the manuscript. This work was funded
by the Intramural Research Program of the National Institute of Diabetes
and Digestive and Kidney Diseases.
NR 22
TC 11
Z9 11
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD OCT
PY 2013
VL 14
IS 10
BP 916
EP 922
DI 10.1038/embor.2013.118
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 229HL
UT WOS:000325253100016
PM 23917615
ER
PT J
AU Kleinau, G
Neumann, S
Gruters, A
Krude, H
Biebermann, H
AF Kleinau, Gunnar
Neumann, Susanne
Grueters, Annette
Krude, Heiko
Biebermann, Heike
TI Novel Insights on Thyroid-Stimulating Hormone Receptor Signal
Transduction
SO ENDOCRINE REVIEWS
LA English
DT Review
ID PROTEIN-COUPLED-RECEPTORS; HUMAN THYROTROPIN RECEPTOR; HUMAN
CHORIONIC-GONADOTROPIN; SITE-DIRECTED MUTAGENESIS; ADENYLATE-CYCLASE
ACTIVATION; FREE ALPHA-SUBUNIT; HUMAN TSH RECEPTOR; TERMINAL
EXTRACELLULAR DOMAIN; BETA(2) ADRENERGIC-RECEPTOR; RESONANCE
ENERGY-TRANSFER
AB The TSH receptor (TSHR) is a member of the glycoprotein hormone receptors, a subfamily of family A G protein-coupled receptors. The TSHR is of great importance for the growth and function of the thyroid gland. The TSHR and its endogenous ligand TSH are pivotal proteins with respect to a variety of physiological functions and malfunctions. The molecular events of TSHR regulation can be summarized as a process of signal transduction, including signal reception, conversion, and amplification. The steps during signal transduction from the extra-to the intracellular sites of the cell are not yet comprehensively understood. However, essential new insights have been achieved in recent years on the interrelated mechanisms at the extracellular region, the transmembrane domain, and intracellular components. This review contains a critical summary of available knowledge of the molecular mechanisms of signal transduction at the TSHR, for example, the key amino acids involved in hormone binding or in the structural conformational changes that lead to G protein activation or signaling regulation. Aspects of TSHR oligomerization, signaling promiscuity, signaling selectivity, phenotypes of genetic variations, and potential extrathyroidal receptor activity are also considered, because these are relevant to an understanding of the overall function of the TSHR, including physiological, pathophysiological, and pharmacological perspectives. Directions for future research are discussed.
C1 [Kleinau, Gunnar; Grueters, Annette; Krude, Heiko; Biebermann, Heike] Charite, Inst Expt Pediat Endocrinol, D-13353 Berlin, Germany.
[Neumann, Susanne] NIDDK, NIH, Lab Endocrinol & Receptor Biol, Bethesda, MD 20892 USA.
RP Biebermann, H (reprint author), Charite, Inst Expt Pediat Endocrinol, Ostring 3,Augustenburger Pl 1, D-13353 Berlin, Germany.
EM Gunnar.Kleinau@charite.de; Heike.Biebermann@charite.de
FU Deutsche Forschungsgemeinschaft (DFG) [BI 893/6-2, BI893/5-1, KL
2334/21, KL 2334/21-2]; Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health [Z01DK011006]
FX This work was supported by the Deutsche Forschungsgemeinschaft (DFG),
projects BI 893/6-2, BI893/5-1, and KL 2334/21, -2, and by the
Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health
(Z01DK011006).
NR 413
TC 30
Z9 33
U1 2
U2 31
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD OCT
PY 2013
VL 34
IS 5
BP 691
EP 724
DI 10.1210/er.2012-1072
PG 34
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 229OQ
UT WOS:000325277200004
PM 23645907
ER
PT J
AU Clark, ML
Peel, JL
Balakrishnan, K
Breysse, PN
Chillrud, SN
Naeher, LP
Rodes, CE
Vette, AF
Balbus, JM
AF Clark, Maggie L.
Peel, Jennifer L.
Balakrishnan, Kalpana
Breysse, Patrick N.
Chillrud, Steven N.
Naeher, Luke P.
Rodes, Charles E.
Vette, Alan F.
Balbus, John M.
TI Health and Household Air Pollution from Solid Fuel Use: The Need for
Improved Exposure Assessment
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Review
ID PARTICULATE MATTER CONCENTRATIONS; ACUTE RESPIRATORY-INFECTIONS;
WOOD-SMOKE EXPOSURE; CARBON-MONOXIDE; BIOMASS FUELS; PARTICLE
DEPOSITION; PULMONARY-DISEASE; LUNG-CANCER; COOK STOVES; INDOOR
AB Background: Nearly 3 billion people worldwide rely on solid fuel combustion to meet basic -household energy needs. The resulting exposure to air pollution causes an estimated 4.5% of the global burden of disease. Large variability and a lack of resources for research and development have resulted in highly uncertain exposure estimates.
Objective: We sought to identify research priorities for exposure assessment that will more accurately and precisely define exposure-response relationships of household air pollution necessary to inform future cleaner-burning cookstove dissemination programs.
Data Sources: As part of an international workshop in May 2011, an expert group characterized the state of the science and developed recommendations for exposure assessment of household air pollution.
Synthesis: The following priority research areas were identified to explain variability and reduce uncertainty of household air pollution exposure measurements: improved characterization of spatial and temporal variability for studies examining both short-and long-term health effects; development and validation of measurement technology and approaches to conduct complex exposure assessments in resource-limited settings with a large range of pollutant concentrations; and development and validation of biomarkers for estimating dose. Addressing these priority research areas, which will inherently require an increased allocation of resources for cookstove research, will lead to better characterization of exposure-response relationships.
Conclusions: Although the type and extent of exposure assessment will necessarily depend on the goal and design of the cookstove study, without improved understanding of exposure-response relationships, the level of air pollution reduction necessary to meet the health targets of cookstove interventions will remain uncertain.
C1 [Clark, Maggie L.; Peel, Jennifer L.] Colorado State Univ, Dept Environm & Radiol Hlth Sci, Ft Collins, CO 80523 USA.
[Balakrishnan, Kalpana] Sri Ramachandra Univ, Dept Environm Hlth Engn, Madras, Tamil Nadu, India.
[Breysse, Patrick N.] Johns Hopkins Univ, Baltimore, MD USA.
[Chillrud, Steven N.] Columbia Univ, Lamont Doherty Earth Observ, Palisades, NY USA.
[Naeher, Luke P.] Univ Georgia, Dept Environm Hlth Sci, Athens, GA 30602 USA.
[Rodes, Charles E.] Res Triangle Inst, Res Triangle Pk, NC 27709 USA.
[Vette, Alan F.] US EPA, Res Triangle Pk, NC 27711 USA.
[Balbus, John M.] NIEHS, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
RP Clark, ML (reprint author), Colorado State Univ, 1681 Campus Delivery, Ft Collins, CO 80523 USA.
EM Maggie.Clark@ColoState.edu
RI Balakrishnan, Kalpana/B-6653-2015
OI Balakrishnan, Kalpana/0000-0002-5905-1801
FU U.S. Department of State; U.S. Department of Health and Human Services;
National Institutes of Health (NIH); National Cancer Institute; National
Eye Institute; National Heart, Lung, and Blood Institute; National
Institute of Environmental Health Sciences (NIEHS); U.S. Environmental
Protection Agency (EPA); Centers for Disease Control and Prevention;
U.S. Agency for International Development, and the World Health
Organization
FX Support for the workshop was provided by the U.S. Department of State,
the U.S. Department of Health and Human Services, the National
Institutes of Health (NIH) [Eunice Kennedy Shriver National Institute of
Child Health and Human Development; National Cancer Institute; National
Eye Institute; National Heart, Lung, and Blood Institute; National
Institute of Environmental Health Sciences (NIEHS); John E. Fogarty
International Center; and Office of Behavioral and Social Sciences
Research], the U.S. Environmental Protection Agency (EPA), the Centers
for Disease Control and Prevention, the U.S. Agency for International
Development, and the World Health Organization.
NR 72
TC 39
Z9 39
U1 8
U2 75
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2013
VL 121
IS 10
BP 1120
EP 1128
DI 10.1289/ehp.1206429
PG 9
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 227YU
UT WOS:000325152400012
PM 23872398
ER
PT J
AU Hoppin, JA
Jaramillo, R
London, SJ
Bertelsen, RJ
Salo, PM
Sandler, DP
Zeldin, DC
AF Hoppin, Jane A.
Jaramillo, Renee
London, Stephanie J.
Bertelsen, Randi J.
Salo, Paeivi M.
Sandler, Dale P.
Zeldin, Darryl C.
TI Phthalate Exposure and Allergy in the US Population: Results from NHANES
2005-2006
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; IN-HOUSE DUST; METABOLITE CONCENTRATIONS;
REPRODUCTIVE AGE; NATIONAL-HEALTH; URINARY LEVELS; URBAN COHORT; ASTHMA;
CHILDREN; MICE
AB Background: Environmental exposures to phthalates, particularly high-molecular-weight (HMW) phthalates, are suspected to contribute to allergy.
Objective: We assessed whether phthalate metabolites are associated with allergic symptoms and sensitization in a large nationally representative sample.
Methods: We used data on urinary phthalate metabolites and allergic symptoms (hay fever, rhinitis, allergy, wheeze, asthma) and sensitization from participants >= 6 years of age in the National Health and Nutrition Examination Survey (NHANES) 2005-2006. Allergen sensitization was defined as a positive response to at least one of 19 specific IgE antigens (>= 0.35 kU/L). Odds ratios (ORs) per one log(10) unit change in phthalate concentration were estimated using logistic regression adjusting for age, race, body mass index, gender, creatinine, and cotinine. Separate analyses were conducted for children (6-17 years of age) and adults.
Results: The HMW phthalate metabolite mono-benzyl phthalate (MBzP) was the only metabolite positively associated with current allergic symptoms in adults (wheeze, asthma, hay fever, and rhinitis). Mono-(3-carboxypropyl) phthalate and the sum of diethylhexyl phthalate metabolites (both representing HMW phthalate exposures) were positively associated with allergic sensitization in adults. Conversely, in children, HMW phthalate metabolites were inversely associated with asthma and hay fever. Of the low-molecular-weight phthalate metabolites, mono-ethyl phthalate was inversely associated with allergic sensitization in adults (OR = 0.79; 95% CI: 0.70, 0.90).
Conclusion: In this cross-sectional analysis of a nationally representative sample, HMW phthalate metabolites, particularly MBzP, were positively associated with allergic symptoms and sensitization in adults, but there was no strong evidence for associations between phthalates and allergy in children 6-17 years of age.
C1 [Hoppin, Jane A.; London, Stephanie J.; Bertelsen, Randi J.; Sandler, Dale P.] NIEHS, Epidemiol Branch, NIH, Dept Heath & Human Serv, Res Triangle Pk, NC 27709 USA.
[Jaramillo, Renee] SRA Int, Durham, NC USA.
[Bertelsen, Randi J.] Norwegian Inst Publ Hlth, Div Environm Med, Oslo, Norway.
[Salo, Paeivi M.; Zeldin, Darryl C.] NIEHS, Biol Res Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Hoppin, JA (reprint author), NIEHS, Epidemiol Branch, MD A3-05,POB 12233, Res Triangle Pk, NC 27709 USA.
EM hoppin1@niehs.nih.gov
OI Sandler, Dale/0000-0002-6776-0018; London, Stephanie/0000-0003-4911-5290
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01-ES025041]
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences (Z01-ES025041).
NR 45
TC 29
Z9 29
U1 7
U2 41
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2013
VL 121
IS 10
BP 1129
EP 1134
DI 10.1289/ehp.1206211
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 227YU
UT WOS:000325152400013
PM 23799650
ER
PT J
AU Gosavi, RA
Knudsen, GA
Birnbaum, LS
Pedersen, LC
AF Gosavi, Rajendrakumar A.
Knudsen, Gabriel A.
Birnbaum, Linda S.
Pedersen, Lars C.
TI Mimicking of Estradiol Binding by Flame Retardants and Their
Metabolites: A Crystallographic Analysis
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID HUMAN ESTROGEN SULFOTRANSFERASE; POLYBROMINATED DIPHENYL ETHERS;
TETRABROMOBISPHENOL-A; CYTOSOLIC SULFOTRANSFERASES; POTENT INHIBITION;
SULFURYL TRANSFER; CRYSTAL-STRUCTURE; THYROID-HORMONE; HOUSE-DUST;
IN-VITRO
AB Background: Brominated flame retardants (BFRs), used in many types of consumer goods, are being studied because of concerns about possible health effects related to endocrine disruption, immunotoxicity, reproductive toxicity, and neurotoxicity. Tetrabromobisphenol A (TBBPA), the most widely used BFR, and human metabolites of certain congeners of polybrominated diphenyl ether (e.g., 3-OH-BDE-47) have been suggested to inhibit estrogen sulfo-transferase, potentially affecting estrogen metabolism.
Objectives: Our primary goal was to understand the structural mechanism for inhibition of the hormone-metabolizing enzyme estrogen sulfo-transferase by certain BFRs. We also sought to understand various factors that facilitate the binding of flame retardants in the enzyme binding pocket.
Methods: We used X-ray crystallography to obtain atomic detail of the binding modes of TBBPA and 3-OH-BDE-47 to estrogen sulfo-transferase for comparison with binding of the endogenous substrate estradiol.
Results: The crystal structures reveal how BFRs mimic estradiol binding as well as the various inter-actions between the compounds and protein residues that facilitate its binding. In addition, the structures provide insights into the ability of the sulfo-transferase substrate binding pocket to accommodate a range of halogenated compounds that satisfy minimal structural criteria.
Conclusions: Our results show how BFRs or their metabolites can bind to and inhibit a key hormone-metabolizing enzyme, potentially causing endocrine disruption.
C1 [Gosavi, Rajendrakumar A.; Pedersen, Lars C.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Knudsen, Gabriel A.; Birnbaum, Linda S.] NCI, Lab Toxicol & Toxicokinet, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
RP Pedersen, LC (reprint author), F3-09,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM pederse2@niehs.nih.gov
RI Knudsen, Gabriel/G-3706-2013
OI Knudsen, Gabriel/0000-0002-7208-6451
FU National Institute of Environmental Health Sciences; National Institutes
of Health (NIH) [ZIAES102645]; National Cancer Institute, NIH
[ZIABC011476]
FX This research was supported in part by the Intramural Research Program
of the National Institute of Environmental Health Sciences, National
Institutes of Health (NIH) (project ZIAES102645 to L.C.P.) and in part
by the Intramural Research Program of the National Cancer Institute, NIH
(project ZIABC011476 to L.S.B.).
NR 51
TC 35
Z9 35
U1 1
U2 27
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2013
VL 121
IS 10
BP 1194
EP 1199
DI 10.1289/ehp.1306902
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 227YU
UT WOS:000325152400023
PM 23959441
ER
PT J
AU Golding, J
Steer, CD
Hibbeln, JR
Emmett, PM
Lowery, T
Jones, R
AF Golding, Jean
Steer, Colin D.
Hibbeln, Joseph R.
Emmett, Pauline M.
Lowery, Tony
Jones, Robert
TI Dietary Predictors of Maternal Prenatal Blood Mercury Levels in the
ALSPAC Birth Cohort Study
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID UK TOTAL DIET; METHYLMERCURY EXPOSURE; CHILD-DEVELOPMENT; FISH
CONSUMPTION; REACTION CELL; ICP-MS; POPULATION; CADMIUM; FOOD; AGE
AB BACKGROUND: Very high levels of prenatal maternal mercury have adverse effects on the developing fetal brain. It has been suggested that all possible sources of mercury should be avoided. However, although seafood is a known source of mercury, little is known about other dietary components that contribute to the overall levels of blood mercury.
OBJECTIVE: Our goal was to quantify the contribution of components of maternal diet to prenatal blood mercury level.
METHODS: Whole blood samples and information on diet and sociodemographic factors were collected from pregnant women (n = 4,484) enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC). The blood samples were assayed for total mercury using inductively coupled plasma dynamic reaction cell mass spectrometry. Linear regression was used to estimate the relative contributions of 103 dietary variables and 6 sociodemographic characteristics to whole blood total mercury levels (TBM; untransformed and log-transformed) based on R-2 values.
RESULTS: We estimated that maternal diet accounted for 19.8% of the total variation in ln-TBM, with 44% of diet-associated variability (8.75% of the total variation) associated with seafood consumption (white fish, oily fish, and shellfish). Other dietary components positively associated with TBM included wine and herbal teas, and components with significant negative associations included white bread, meat pies or pasties, and french fries.
CONCLUSIONS: Although seafood is a source of dietary mercury, seafood appeared to explain a relatively small proportion of the variation in TBM in our UK study population. Our findings require confirmation, but suggest that limiting seafood intake during pregnancy may have a limited impact on prenatal blood mercury levels.
C1 [Golding, Jean; Steer, Colin D.; Emmett, Pauline M.] Univ Bristol, Ctr Child & Adolescent Hlth, Bristol, Avon, England.
[Hibbeln, Joseph R.] NIAAA, NIH, US Dept HHS, Bethesda, MD USA.
[Lowery, Tony] NOAA, Natl Marine Fisheries Serv, Natl Seafood Inspect Lab, Pascagoula, MS USA.
[Jones, Robert] Ctr Dis Control & Prevent, Inorgan & Radiat Analyt Toxicol Branch, Atlanta, GA USA.
RP Golding, J (reprint author), Sch Social & Community Med, Ctr Child & Adolescent Hlth, Oakfield House,Oakfield Rd, Bristol BS8 2BN, Avon, England.
EM jean.golding@bristol.ac.uk
OI Emmett, Pauline/0000-0003-1076-4779; Golding, Jean/0000-0003-2826-3307
FU National Oceanic and Atmospheric Administration (NOAA); Intramural
Research Program of the National Institute on Alcohol Abuse and
Alcoholism, National Institutes of Health (NIH)
FX The UK Medical Research Council (MRC), the Wellcome Trust, and the
University of Bristol currently provide core support for ALSPAC. The
assays of the maternal blood samples were carried out at the Centers for
Disease Control and Prevention with funding from the National Oceanic
and Atmospheric Administration (NOAA), and the statistical analyses were
carried out in Bristol with funding from NOAA and support from the
Intramural Research Program of the National Institute on Alcohol Abuse
and Alcoholism, National Institutes of Health (NIH).
NR 45
TC 26
Z9 28
U1 3
U2 35
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2013
VL 121
IS 10
BP 1214
EP 1218
DI 10.1289/ehp.1206115
PG 5
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 227YU
UT WOS:000325152400026
PM 23811414
ER
PT J
AU Verner, MA
McDougall, R
Glynn, A
Andersen, ME
Clewell, HJ
Longnecker, MP
AF Verner, Marc-Andre
McDougall, Robin
Glynn, Anders
Andersen, Melvin E.
Clewell, Harvey J., III
Longnecker, Matthew P.
TI Is the Relationship between Prenatal Exposure to PCB-153 and Decreased
Birth Weight Attributable to Pharmacokinetics?
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID POLYCHLORINATED-BIPHENYLS; SERUM-LIPIDS; PREGNANCY; HUMANS;
LIPOPROTEINS; AGE
AB BACKGROUND: A recent meta-analysis based on data from > 7,000 pregnancies reported an -association between prenatal polychlorinated biphenyl (PCB)-153 exposure and reduced birth weight. Gestational weight gain, which is associated negatively with PCB levels in maternal and cord blood, and positively with birth weight, could substantially confound this association.
OBJECTIVE: We sought to estimate the influence of gestational weight gain on the association between PCB-153 exposure and birth weight using a pharmacokinetic model.
METHODS: We modified a recently published pharmacokinetic model and ran Monte Carlo simulations accounting for variability in physiologic parameters and their correlations. We evaluated the pharmacokinetic model by comparing simulated plasma PCB-153 levels during pregnancy to serial measurements in 10 pregnant women from another study population. We estimated the association between simulated plasma PCB-153 levels and birth weight using linear regression models.
RESULTS: The plasma PCB-153 level profiles generated with the pharmacokinetic model were comparable to measured levels in 10 pregnant women. We estimated a 118-g decrease in birth weight (95% CI: -129, -106 g) for each 1-mu g/L increase in simulated cord plasma PCB-153, compared with the 150-g decrease estimated based on the previous meta-analysis. The estimated decrease in birth weight was reduced to -6 g (95% CI: -18, 6 g) when adjusted for simulated gestational weight gain.
CONCLUSION: Our findings suggest that associations previously noted between PCB levels and birth weight may be attributable to confounding by maternal weight gain during pregnancy.
C1 [Verner, Marc-Andre] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med, Boston, MA 02115 USA.
[Verner, Marc-Andre] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[McDougall, Robin] Univ Ontario Inst Technol, Oshawa, ON, Canada.
[Glynn, Anders] Swedish Natl Food Agcy, Uppsala, Sweden.
[Glynn, Anders] Uppsala Univ, Evolutionary Biol Ctr, Dept Environm Toxicol, Uppsala, Sweden.
[Andersen, Melvin E.; Clewell, Harvey J., III] Hamner Inst Hlth Sci, Res Triangle Pk, NC USA.
[Longnecker, Matthew P.] NIEHS, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
RP Verner, MA (reprint author), Brigham & Womens Hosp, Channing Div Network Med, 181 Longwood Ave, Boston, MA 02115 USA.
EM marcandre.verner@channing.harvard.edu
OI Verner, Marc-Andre/0000-0002-1935-8913; Andersen,
Melvin/0000-0002-3894-4811; Longnecker, Matthew/0000-0001-6073-5322
FU American Chemistry Council (ACC) Long-Range Research Initiative;
Intramural Research Program of the National Institute of Environmental
Health Sciences, National Institutes of Health
FX This study was supported by the American Chemistry Council (ACC)
Long-Range Research Initiative and the Intramural Research Program of
the National Institute of Environmental Health Sciences, National
Institutes of Health. M.-A. V. conducted this study as a consultant for
the Hamner Institutes for Health Sciences, an independent nonprofit
organization. M.P.L. received no compensation from the ACC.
NR 26
TC 21
Z9 21
U1 1
U2 14
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2013
VL 121
IS 10
BP 1219
EP 1224
DI 10.1289/ehp.1206457
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 227YU
UT WOS:000325152400027
PM 23934733
ER
PT J
AU Ardeljan, D
Meyerle, CB
Agron, E
Wang, JJ
Mitchell, P
Chew, EY
Zhao, J
Maminishkis, A
Chan, CC
Tuo, JS
AF Ardeljan, Daniel
Meyerle, Catherine B.
Agron, Elvira
Wang, Jie Jin
Mitchell, Paul
Chew, Emily Y.
Zhao, Jing
Maminishkis, Arvydas
Chan, Chi-Chao
Tuo, Jingsheng
TI Influence of TIMP3/SYN3 polymorphisms on the phenotypic presentation of
age-related macular degeneration
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE age-related macular degeneration; TIMP3; phenotype; single-nucleotide
polymorphism; Blue Mountains Eye Study; Age-Related Eye Diseases Study
ID SORSBYS FUNDUS DYSTROPHY; BLUE MOUNTAINS EYE; TISSUE INHIBITOR;
METALLOPROTEINASES-3 TIMP3; BRUCHS MEMBRANE; RISK-FACTORS; VISUAL-LOSS;
MUTATION; DISEASE; AREDS
AB Age-related macular degeneration (AMD) is a leading cause of irreversible central visual loss in the elderly. A recent genome-wide association studies (GWAS) reported that rs9621532 near the tissue inhibitor of metalloproteinase 3 (TIMP3)/synapsin III (SYN3) region of 22q12.3 is associated with AMD. In this study, we characterize its phenotypic influence on AMD using three independent study cohorts: case-control studies from the National Eye Institute Clinical Center (NEI, n = 397) and the Age-Related Eye Disease Study (n = 523) as well as a nested case-control study from Blue Mountains Eye Study (BMES, n = 852). Comparisons between cases and controls show no association between rs9621532 and AMD in the three sample sets. However, stratifying NEI cases uncovers a moderate protective role of rs9621532 in neovascular AMD (nAMD) and the association adhered to a dominant model (odds ratios = 0.32; 95% CI: 0.11-0.89; P = 0.02). The BMES data followed the same pattern of association with nAMD as that seen in the NEI sample but did not reach statistical significance. Polychotomous logistic regression showed a trend that rs9621532 correlates with less severe disease, for example, with the majority of carriers having intermediate AMD rather than nAMD/geographic atrophy AMD. Functionally, rs9621532 influences TIMP3 mRNA expression in cultured primary human fetal retinal pigment epithelium (hfRPE) cells. In hfRPE donors carrying the protective rs9625132 allele, we measured a reduction in TIMP3 mRNA by quantitative RT-PCR. Our data suggest that rs9621532 carriers have a lower risk of developing nAMD, potentially because of decreased transcription of TIMP3.
C1 [Ardeljan, Daniel; Chan, Chi-Chao; Tuo, Jingsheng] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Meyerle, Catherine B.; Agron, Elvira; Chew, Emily Y.] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Wang, Jie Jin; Mitchell, Paul] Univ Sydney, Dept Ophthalmol, Ctr Vis Res, Westmead, NSW 2145, Australia.
[Wang, Jie Jin; Mitchell, Paul] Univ Sydney, Westmead Millennium Inst, Westmead, NSW 2145, Australia.
[Zhao, Jing; Maminishkis, Arvydas] NEI, Sect Epithelial & Retinal Physiol & Dis, NIH, Bethesda, MD 20892 USA.
RP Tuo, JS (reprint author), NEI, Immunol Lab, NIH, 10-10N103,10 Ctr Dr, Bethesda, MD 20892 USA.
EM tuoj@nei.nih.gov
RI Wang, Jie Jin/P-1499-2014; Mitchell, Paul/P-1498-2014;
OI Wang, Jie Jin/0000-0001-9491-4898; Tuo, Jingsheng/0000-0002-1372-7810
FU Intramural Research Program of National Eye Institute, NIH; Australian
National Health and Medical Research Council
FX We thank Angel Garced, Katherine Shimel, and Sun-min Ro, for their
assistance in contacting study participants and collecting blood
samples. We also thank the study participants and their families for
enrolling in this study. This research was supported by the Intramural
Research Program of National Eye Institute, NIH and the Australian
National Health and Medical Research Council.
NR 31
TC 11
Z9 11
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD OCT
PY 2013
VL 21
IS 10
BP 1152
EP 1157
DI 10.1038/ejhg.2013.14
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 222JO
UT WOS:000324727200026
PM 23422939
ER
PT J
AU Zanotti-Fregonara, P
Lammertsma, AA
Innis, RB
AF Zanotti-Fregonara, Paolo
Lammertsma, Adriaan A.
Innis, Robert B.
TI Suggested pathway to assess radiation safety of F-18-labeled PET tracers
for first-in-human studies
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Letter
ID DOSIMETRY; BIODISTRIBUTION; CANCER; HUMANS; PROBE
C1 [Zanotti-Fregonara, Paolo; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Lammertsma, Adriaan A.] Vrije Univ Amsterdam Med Ctr, Dept Radiol & Nucl Med, Amsterdam, Netherlands.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 20
TC 10
Z9 10
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2013
VL 40
IS 11
BP 1781
EP 1783
DI 10.1007/s00259-013-2512-x
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 227QO
UT WOS:000325128800016
PM 23868334
ER
PT J
AU Slezak, JM
Katz, JL
AF Slezak, Jonathan M.
Katz, Jonathan L.
TI An Influence of Delayed Reinforcement on the Effectiveness of
Psychostimulants to Enhance Indices of Attention Under a Five-Choice
Serial Reaction Time Procedure in Male Rats
SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE five-choice serial reaction time procedure; d-amphetamine;
methylphenidate; ADHD; delayed reinforcement
ID DEFICIT/HYPERACTIVITY DISORDER ADHD; DEFICIT HYPERACTIVITY DISORDER;
D-AMPHETAMINE; STIMULANT-DRUGS; TASK; PERFORMANCE; METHYLPHENIDATE;
SENSITIVITY; ATOMOXETINE; FRUSTRATION
AB The five-choice serial reaction time (5-CSRT) procedure has been considered a translational tool for assessments of the psychopharmacology of attention in preclinical research. Because greater sensitivity to delayed reinforcement may promote the development of attention-deficit/hyperactivity disorder (ADHD) symptoms, effects of reinforcer delay and psychostimulants on performances under a 5-CSRT procedure were determined. Male rats were trained to respond under a 5-CSRT procedure with different delay-of-reinforcement conditions (0, 2, 4, 8, 16 s), and effects of d-amphetamine, methylphenidate, and morphine (as a negative control) were assessed at 0- and 16-s delays. Under nondrug conditions, as the delay increased both response latency and the number of trials in which a response did not occur (omissions) increased, and the percent correct on trials when responses were emitted decreased. Only modest increases in the percent correct were found with psychostimulants during the 0-s delay condition; however, more substantial enhancements were found with a 16-s delay. Consistent effects of both psychostimulants at either delay on omissions and response latency were not observed. Morphine increased omissions and response latency at both delays and decreased the percent correct (16-s delay). Generally, responses during the intertrial interval were not systematically affected under any condition. The current results demonstrate that measures of attention in a 5-CSRT procedure are sensitive to changes in the delay to reinforcer delivery. More important, psychostimulants significantly enhanced a measure of attention only when reinforcers were delayed, which may be reflective of the psychopharmacological mechanisms involved with clinical treatment of ADHD symptoms.
C1 [Slezak, Jonathan M.; Katz, Jonathan L.] NIDA, Psychobiol Sect, Mol Targets & Medicat Discovery Res Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
[Slezak, Jonathan M.] Johns Hopkins Univ, Dept Neurol, Sch Med, Baltimore, MD 21218 USA.
RP Katz, JL (reprint author), NIDA, Psychobiol Sect, Intramural Res Program, NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM jkatz@intra.nida.nih.gov
OI Katz, Jonathan/0000-0002-1068-1159
FU National Institute on Drug Abuse
FX Financial support for this project was provided by the National
Institute on Drug Abuse Intramural Research Program. The authors would
like to acknowledge the expert technical assistance of Bettye Campbell.
All authors have contributed in a significant way to the manuscript, and
all authors have read and approved the final manuscript. No authors have
conflicts of interest.
NR 32
TC 1
Z9 1
U1 0
U2 5
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1064-1297
J9 EXP CLIN PSYCHOPHARM
JI Exp. Clin. Psychopharmacol.
PD OCT
PY 2013
VL 21
IS 5
SI SI
BP 355
EP 362
DI 10.1037/a0033726
PG 8
WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy;
Psychiatry
SC Psychology; Pharmacology & Pharmacy; Psychiatry
GA 229DK
UT WOS:000325241800003
PM 24099356
ER
PT J
AU Mishra, PK
Ottmann, AR
Basrai, MA
AF Mishra, Prashant K.
Ottmann, Alicia R.
Basrai, Munira A.
TI Structural Integrity of Centromeric Chromatin and Faithful Chromosome
Segregation Requires Pat1
SO GENETICS
LA English
DT Article
ID H3 VARIANT CSE4; SACCHAROMYCES-CEREVISIAE; BUDDING YEAST; HISTONE H3;
TRANSMISSION FIDELITY; KINETOCHORE FUNCTION; TOPOISOMERASE-II; DNA;
PROTEIN; GENE
AB The kinetochore (centromeric DNA and associated protein complex) is essential for faithful chromosome segregation and maintenance of genome stability. Here we report that an evolutionarily conserved protein Pat1 is a structural component of Saccharomyces cerevisiae kinetochore and associates with centromeres in a NDC10-dependent manner. Consistent with a role for Pat1 in kinetochore structure and function, a deletion of PAT1 results in delay in sister chromatid separation, errors in chromosome segregation, and defects in structural integrity of centromeric chromatin. Pat1 is involved in topological regulation of minichromosomes as altered patterns of DNA supercoiling were observed in pat1 Delta cells. Studies with pat1 alleles uncovered an evolutionarily conserved region within the central domain of Pat1 that is required for its association with centromeres, sister chromatid separation, and faithful chromosome segregation. Taken together, our data have uncovered a novel role for Pat1 in maintaining the structural integrity of centromeric chromatin to facilitate faithful chromosome segregation and proper kinetochore function.
C1 [Mishra, Prashant K.; Ottmann, Alicia R.; Basrai, Munira A.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Basrai, MA (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, 41 Medlars Dr,Room B624, Bethesda, MD 20892 USA.
EM basraim@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
FX We thank Roy Parker, Duncan Clarke, Sue Biggins, Jennifer Gerton, Jeff
Bachant, and Richard Baker for reagents, Kathy McKinnon of the NCI
Vaccine branch FACS Core, Thomas Johnson for help with Southern
hybridization, Suresh Ambudkar, Suneet Shukla, and Eduardo Chufan for
assistance with phospho-imaging, and members of the Basrai lab for
discussions. Support for this research was provided by the Intramural
Research Program of the National Cancer Institute, National Institutes
of Health.
NR 62
TC 10
Z9 10
U1 0
U2 2
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 1943-2631
J9 GENETICS
JI Genetics
PD OCT
PY 2013
VL 195
IS 2
BP 369
EP +
DI 10.1534/genetics.113.155291
PG 16
WC Genetics & Heredity
SC Genetics & Heredity
GA 229RY
UT WOS:000325286200008
PM 23893485
ER
PT J
AU Wesolowska, N
Amariei, FL
Rong, YKS
AF Wesolowska, Natalia
Amariei, Flavia L.
Rong, Yikang S.
TI Clustering and Protein Dynamics of Drosophila melanogaster Telomeres
SO GENETICS
LA English
DT Article
ID NUCLEAR-ENVELOPE; DNA-SEQUENCES; INTERPHASE NUCLEI; SIR4 PROTEINS;
CHROMOSOME; YEAST; CELLS; LOCALIZATION; CENTROMERES; KLARSICHT
AB Telomeres are obligatory chromosomal landmarks that demarcate the ends of linear chromosomes to distinguish them from broken ends and can also serve to organize the genome. In both budding and fission yeast, they cluster at the periphery of the nucleus, potentially to establish a compartment of silent chromatin. To gain insight into telomere organization in higher organisms, we investigated their distribution in interphase nuclei of Drosophila melanogaster. We focused on the syncytial blastoderm, an excellent developmental stage for live imaging due to the synchronous division of the nuclei at this time. We followed the EGFP-labeled telomeric protein HOAP in vivo and found that the 16 telomeres yield four to six foci per nucleus, indicative of clustering. Furthermore, we confirmed clustering in other somatic tissues. Importantly, we observed that HOAP signal intensity in the clusters increases in interphase, potentially due to loading of HOAP to newly replicated telomeres. To determine the rules governing clustering, we used in vivo imaging and fluorescence in situ hybridization to test several predictions. First, we inspected mutant embryos that develop as haploids and found that clustering is not mediated by associations between homologs. Second, we probed specifically for a telomere of novel sequence and found strong evidence against DNA sequence identity and homology as critical factors. Third, we ruled out predominance of intrachromosomal interactions by marking both ends of a chromosome. Based on these results, we propose that clustering is independent of sequence and is likely maintained by an as yet undetermined factor.
C1 [Wesolowska, Natalia; Amariei, Flavia L.; Rong, Yikang S.] NCI, Lab Biochem & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Wesolowska, Natalia] NIH, Bethesda, MD 20892 USA.
[Wesolowska, Natalia] Johns Hopkins Univ, Grad Partnership Program, Bethesda, MD 20892 USA.
RP Wesolowska, N (reprint author), NIH, Lab Biochem & Mol Biol, 37 Convent Dr,Room 6056, Bethesda, MD 20892 USA.
EM wesolown@mail.nih.gov; rongy@mail.nih.gov
NR 49
TC 7
Z9 7
U1 2
U2 8
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 1943-2631
J9 GENETICS
JI Genetics
PD OCT
PY 2013
VL 195
IS 2
BP 381
EP +
DI 10.1534/genetics.113.155408
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 229RY
UT WOS:000325286200009
PM 23893488
ER
PT J
AU Brown, JL
Kassis, JA
AF Brown, J. Lesley
Kassis, Judith A.
TI Architectural and Functional Diversity of Polycomb Group Response
Elements in Drosophila
SO GENETICS
LA English
DT Article
ID GROUP PROTEIN COMPLEXES; DNA-BINDING PROTEIN; ENGRAILED GENE; HOMEOTIC
GENE; METHYLTRANSFERASE ACTIVITY; CHROMATIN BINDING; BITHORAX COMPLEX;
REGULATORY DNA; TARGET GENES; GAGA FACTOR
AB Polycomb group response elements (PREs) play an essential role in gene regulation by the Polycomb group (PcG) repressor proteins in Drosophila. PREs are required for the recruitment and maintenance of repression by the PcG proteins. PREs are made up of binding sites for multiple DNA-binding proteins, but it is still unclear what combination(s) of binding sites is required for PRE activity. Here we compare the binding sites and activities of two closely linked yet separable PREs of the Drosophila engrailed (en) gene, PRE1 and PRE2. Both PRE1 and PRE2 contain binding sites for multiple PRE-DNA-binding proteins, but the number, arrangement, and spacing of the sites differs between the two PREs. These differences have functional consequences. Both PRE1 and PRE2 mediate pairing-sensitive silencing of mini-white, a functional assay for PcG repression; however, PRE1 requires two binding sites for Pleiohomeotic (Pho), whereas PRE2 requires only one Pho-binding site for this activity. Furthermore, for full pairing-sensitive silencing activity, PRE1 requires an AT-rich region not found in PRE2. These two PREs behave differently in a PRE embryonic and larval reporter construct inserted at an identical location in the genome. Our data illustrate the diversity of architecture and function of PREs.
C1 [Brown, J. Lesley; Kassis, Judith A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Kassis, JA (reprint author), 6 Ctr Dr MSC 2785,Bldg 6B,Rm 3B-331, Bethesda, MD 20892 USA.
EM jkassis@mail.nih.gov
OI Kassis, Judith/0000-0001-9268-3213
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health
FX We thank Miki Fujioka for the bxd-Ubx-lacZ RCME vector and for
transgenic lines; Bill McGinnis for the generous gift of Grh antibodies;
and Emma Hornick for construction of the bxd-Ubx-lacZ reporter
constructs. We also thank Yuzhong Cheng, Payal Ray, and Sandip De for
critical reading of this manuscript. This work was supported by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health.
NR 77
TC 12
Z9 12
U1 0
U2 8
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 1943-2631
J9 GENETICS
JI Genetics
PD OCT
PY 2013
VL 195
IS 2
BP 407
EP 419
DI 10.1534/genetics.113.153247
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 229RY
UT WOS:000325286200011
PM 23934890
ER
PT J
AU Guo, YB
Park, JM
Cui, BW
Humes, E
Gangadharan, S
Hung, S
FitzGerald, PC
Hoe, KL
Grewal, SIS
Craig, NL
Levin, HL
AF Guo, Yabin
Park, Jung Min
Cui, Bowen
Humes, Elizabeth
Gangadharan, Sunil
Hung, Stevephen
FitzGerald, Peter C.
Hoe, Kwang-Lae
Grewal, Shiv I. S.
Craig, Nancy L.
Levin, Henry L.
TI Integration Profiling of Gene Function With Dense Maps of Transposon
Integration
SO GENETICS
LA English
DT Article
ID YEAST SCHIZOSACCHAROMYCES-POMBE; SACCHAROMYCES-CEREVISIAE; FISSION
YEAST; GENOME; DNA; SCREEN; HIV-1
AB Understanding how complex networks of genes integrate to produce dividing cells is an important goal that is limited by the difficulty in defining the function of individual genes. Current resources for the systematic identification of gene function such as siRNA libraries and collections of deletion strains are costly and organism specific. We describe here integration profiling, a novel approach to identify the function of eukaryotic genes based upon dense maps of transposon integration. As a proof of concept, we used the transposon Hermes to generate a library of 360,513 insertions in the genome of Schizosaccharomyces pombe. On average, we obtained one insertion for every 29 bp of the genome. Hermes integrated more often into nucleosome free sites and 33% of the insertions occurred in ORFs. We found that ORFs with low integration densities successfully identified the genes that are essential for cell division. Importantly, the nonessential ORFs with intermediate levels of insertion correlated with the nonessential genes that have functions required for colonies to reach full size. This finding indicates that integration profiles can measure the contribution of nonessential genes to cell division. While integration profiling succeeded in identifying genes necessary for propagation, it also has the potential to identify genes important for many other functions such as DNA repair, stress response, and meiosis.
C1 [Guo, Yabin; Park, Jung Min; Humes, Elizabeth; Hung, Stevephen; Levin, Henry L.] NCI, Sect Eukaryot Transposable Elements, Program Cellular Regulat & Metab,NIH, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Cui, Bowen; Grewal, Shiv I. S.] NCI, Lab Biochem & Mol Biol, NIH, Bethesda, MD 20892 USA.
[FitzGerald, Peter C.] NCI, Genome Anal Unit, NIH, Bethesda, MD 20892 USA.
[Gangadharan, Sunil; Craig, Nancy L.] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA.
[Gangadharan, Sunil; Craig, Nancy L.] Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA.
[Hoe, Kwang-Lae] Chungnam Natl Univ, Dept New Drug Discovery & Dev, Taejon 305764, South Korea.
RP Levin, HL (reprint author), NIH, 18 Lib Dr,Room 106, Bethesda, MD 20892 USA.
EM henry_levin@nih.gov
OI , Guo/0000-0001-8316-8527
FU National Institutes of Health (NIH) from the Eunice Kennedy Shriver
National Institute of Child Health and Human Development; National
Cancer Institute; NIH [RO1GM076425]
FX We thank Jacqueline Hayles for kindly sharing data on the colony size of
the strains with gene deletions. This research was supported by the
Intramural Research Program of the National Institutes of Health (NIH)
from the Eunice Kennedy Shriver National Institute of Child Health and
Human Development and by the Intramural Program of the National Cancer
Institute. The work by S. G. and N.L.C. was supported by NIH grant
RO1GM076425.
NR 27
TC 8
Z9 8
U1 2
U2 12
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
EI 1943-2631
J9 GENETICS
JI Genetics
PD OCT
PY 2013
VL 195
IS 2
BP 599
EP +
DI 10.1534/genetics.113.152744
PG 29
WC Genetics & Heredity
SC Genetics & Heredity
GA 229RY
UT WOS:000325286200026
PM 23893486
ER
PT J
AU Neyret-Kahn, H
Benhamed, M
Ye, T
Le Gras, S
Cossec, JC
Lapaquette, P
Bischof, O
Ouspenskaia, M
Dasso, M
Seeler, J
Davidson, I
Dejean, A
AF Neyret-Kahn, Helene
Benhamed, Moussa
Ye, Tao
Le Gras, Stephanie
Cossec, Jack-Christophe
Lapaquette, Pierre
Bischof, Oliver
Ouspenskaia, Maia
Dasso, Mary
Seeler, Jacob
Davidson, Irwin
Dejean, Anne
TI Sumoylation at chromatin governs coordinated repression of a
transcriptional program essential for cell growth and proliferation
SO GENOME RESEARCH
LA English
DT Article
ID RNA-POLYMERASE-III; SUMO MODIFICATION; HETEROCHROMATIN FORMATION;
SUBSTRATE PROTEINS; DNA-REPAIR; SENESCENCE; GENES; EXPRESSION; YEAST;
CTCF
AB Despite numerous studies on specific sumoylated transcriptional regulators, the global role of SUMO on chromatin in relation to transcription regulation remains largely unknown. Here, we determined the genome-wide localization of SUMO1 and SUMO2/3, as well as of UBC9 (encoded by UBE2I) and PIASY (encoded by PIAS4), two markers for active sumoylation, along with Pol II and histone marks in proliferating versus senescent human fibroblasts together with gene expression profiling. We found that, whereas SUMO alone is widely distributed over the genome with strong association at active promoters, active sumoylation occurs most prominently at promoters of histone and protein biogenesis genes, as well as Pol I rRNAs and Pol III tRNAs. Remarkably, these four classes of genes are up-regulated by inhibition of sumoylation, indicating that SUMO normally acts to restrain their expression. In line with this finding, sumoylation-deficient cells show an increase in both cell size and global protein levels. Strikingly, we found that in senescent cells, the SUMO machinery is selectively retained at histone and tRNA gene clusters, whereas it is massively released from all other unique chromatin regions. These data, which reveal the highly dynamic nature of the SUMO landscape, suggest that maintenance of a repressive environment at histone and tRNA loci is a hallmark of the senescent state. The approach taken in our study thus permitted the identification of a common biological output and uncovered hitherto unknown functions for active sumoylation at chromatin as a key mechanism that, in dynamically marking chromatin by a simple modifier, orchestrates concerted transcriptional regulation of a network of genes essential for cell growth and proliferation.
C1 [Neyret-Kahn, Helene; Benhamed, Moussa; Cossec, Jack-Christophe; Lapaquette, Pierre; Bischof, Oliver; Seeler, Jacob; Dejean, Anne] Inst Pasteur, Dept Cell Biol & Infect, Lab Nucl Org & Oncogenesis, F-75015 Paris, France.
[Neyret-Kahn, Helene; Benhamed, Moussa; Cossec, Jack-Christophe; Lapaquette, Pierre; Bischof, Oliver; Seeler, Jacob; Dejean, Anne] INSERM, U993, F-75015 Paris, France.
[Neyret-Kahn, Helene; Benhamed, Moussa; Cossec, Jack-Christophe; Lapaquette, Pierre; Bischof, Oliver; Seeler, Jacob; Davidson, Irwin; Dejean, Anne] Equipe Labellisee Ligue Canc, F-75013 Paris, France.
[Ye, Tao; Le Gras, Stephanie; Davidson, Irwin] CNRS INSERM UDS, Inst Genet & Biol Mol & Cellulaire, Dept Funct Genom & Canc, F-67404 Illkirch Graffenstaden, France.
[Ouspenskaia, Maia; Dasso, Mary] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Davidson, I (reprint author), Equipe Labellisee Ligue Canc, F-75013 Paris, France.
EM irwin@igbmc.fr; anne.dejean@pasteur.fr
OI Seeler, Jacob/0000-0001-8209-8555; Dasso, Mary/0000-0002-5410-1371;
Davidson, Irwin/0000-0001-5533-1171
FU LNCC; Odyssey-RE; INCa; Universite de Strasbourg; ANR; ERC; EEC
(EuTRACC); MRT; ARC
FX We thank R. Santoro and M. Werner for rRNA/tRNA reagents and advice. We
acknowledge A. Andrieux for technical assistance. This work was
supported by grants from LNCC, Odyssey-RE, INCa, Universite de
Strasbourg, ANR, ERC, and EEC (EuTRACC). The IGBMC high-throughput
sequencing facility is a member of the "France Genomique" consortium
(ANR10-INBS-09-08). H.N.-K. was supported by the MRT and ARC.
NR 55
TC 32
Z9 32
U1 0
U2 19
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
J9 GENOME RES
JI Genome Res.
PD OCT
PY 2013
VL 23
IS 10
BP 1563
EP 1579
DI 10.1101/gr.154872.113
PG 17
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 228QQ
UT WOS:000325202100001
PM 23893515
ER
PT J
AU Mandyam, MC
Soliman, EZ
Alonso, A
Dewland, TA
Heckbert, SR
Vittinghoff, E
Cummings, SR
Ellinor, PT
Chaitman, BR
Stocke, K
Applegate, WB
Arking, DE
Butler, J
Loehr, LR
Magnani, JW
Murphy, RA
Satterfield, S
Newman, AB
Marcus, GM
AF Mandyam, Mala C.
Soliman, Elsayed Z.
Alonso, Alvaro
Dewland, Thomas A.
Heckbert, Susan R.
Vittinghoff, Eric
Cummings, Steven R.
Ellinor, Patrick T.
Chaitman, Bernard R.
Stocke, Karen
Applegate, William B.
Arking, Dan E.
Butler, Javed
Loehr, Laura R.
Magnani, Jared W.
Murphy, Rachel A.
Satterfield, Suzanne
Newman, Anne B.
Marcus, Gregory M.
TI The QT interval and risk of incident atrial fibrillation
SO HEART RHYTHM
LA English
DT Article
DE Atrial fibrillation; Epidemiology; Risk; QT interval; Electrocardiogram;
ECG
ID CARDIOVASCULAR HEALTH; REFRACTORY PERIOD; DELAYED AFTERDEPOLARIZATIONS;
ATHEROSCLEROSIS RISK; ASSOCIATION; HEART; PREVALENCE; ECG; CONTRIBUTES;
ARRHYTHMIAS
AB BACKGROUND Abnormal atrial repolarization is important in the development of atrial fibrillation (AF), but no direct measurement is available in clinical medicine.
OBJECTIVE To determine whether the QT interval, a marker of ventricular repolarization, could be used to predict incident AF.
METHODS We examined a prolonged QT interval corrected by using the Framingham formula (QTFram) as a predictor of incident AF in the Atherosclerosis Risk in Communities (ARIC) study. The Cardiovascular Health Study (CHS) and Health, Aging, and Body Composition (ABC) study were used for validation. Secondary predictors included QT duration as a continuous variable, a short QT interval, and QT intervals corrected by using other formulas.
RESULTS Among 14,538 ARIC study participants, a prolonged QTFram predicted a roughly 2-fold increased risk of AF (hazard ratio [HR] 2.05; 95% confidence interval [CI] 1.42-2.96; P < .001). No substantive attenuation was observed after adjustment for age, race, sex, study center, body mass index, hypertension, diabetes, coronary disease, and heart failure. The findings were validated in Cardiovascular Health Study and Health, Aging, and Body Composition study and were similar across various QT correction methods. Also in the ARIC study, each 10-ms increase in QTFram was associated with an increased unadjusted (HR 1.14; 95% CI 1.10-1.17; P < .001) and adjusted (HR 1.11; 95% CI 1.07-1.14; P < .001) risk of AF. Findings regarding a short QT interval were inconsistent across cohorts. CONCLUSION A prolonged QT interval is associated with an increased risk of incident AF.
C1 [Mandyam, Mala C.; Dewland, Thomas A.; Marcus, Gregory M.] Univ Calif San Francisco, Div Cardiol, Electrophysiol Sect, San Francisco, CA 94143 USA.
[Soliman, Elsayed Z.] Wake Forest Univ, Sch Med, Epidemiol Cardiol Res Ctr, Dept Epidemiol & Prevent, Winston Salem, NC 27109 USA.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Vittinghoff, Eric] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Cummings, Steven R.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
[Chaitman, Bernard R.] St Louis Univ, Sch Med, ECG Core Lab, St Louis, MO USA.
[Stocke, Karen] St Louis Univ, Sch Med, ECG Core Lab, St Louis, MO USA.
[Applegate, William B.] Wake Forest Univ, Sch Med, Div Gerontol & Geriatr Med, Winston Salem, NC 27109 USA.
[Arking, Dan E.] Johns Hopkins Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Butler, Javed] Emory Univ, Dept Med, Div Cardiol, Atlanta, GA 30322 USA.
[Loehr, Laura R.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Magnani, Jared W.] Boston Univ, Cardiovasc Med Sect, Dept Med, Boston, MA 02215 USA.
[Murphy, Rachel A.] Natl Inst Aging, Intramural Res Program, Lab Populat Sci, Bethesda, MD USA.
[Satterfield, Suzanne] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[Newman, Anne B.] Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
RP Marcus, GM (reprint author), Univ Calif San Francisco, Div Cardiol, Electrophysiol Sect, 505 Parnassus Ave,M-1180B,Box 0124, San Francisco, CA 94143 USA.
EM marcusg@medicine.ucsf.edu
RI Newman, Anne/C-6408-2013; Alonso, Alvaro/A-4917-2010
OI Newman, Anne/0000-0002-0106-1150; Alonso, Alvaro/0000-0002-2225-8323
FU University of California San Franciscos Clinical & Translational Science
Institute (UCSF CTSI); National Center for Research Resources; National
Center for Advancing Translational Sciences; Office of the Director,
National Institutes of Health (NIH) [TL1 RR024129]; National Heart,
Lung, and Blood Institute (NHLBI) [HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C, HHSN268201100012C]; NHLBI
[HHSN268201200036C, N01HC85239, N01 HC55222, N01HC85079, N01HC85080,
N01HC85081, N01HC85082, N01HC85083, N01HC85086, HL080295, HL068986];
National Institute on Aging (NIA) [AG023629]; NIA [N01-AG-6-2101,
N01-AG-6-2103, N01-AG-6-2106, R01-AG028050]; National Institute of
Nursing Research grant [R01-NR012459]; Intramural Research Program of
the NIH, NIA
FX This research was supported by the following: For the University of
California San Franciscos Clinical & Translational Science Institute
(UCSF CTSI): the National Center for Research Resources, the National
Center for Advancing Translational Sciences, and the Office of the
Director, National Institutes of Health (NIH), through UCSF-CTSI grant
number TL1 RR024129; for the Atherosclerosis Risk in Communities (ARIC)
study: a collaborative support from National Heart, Lung, and Blood
Institute (NHLBI) contracts HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C; for the
Cardiovascular Health Study (CHS): a support from NHLBI contracts
HHSN268201200036C, N01HC85239, N01 HC55222, N01HC85079, N01HC85080,
N01HC85081, N01HC85082, N01HC85083, and N01HC85086 and grants HL080295
and HL068986, with additional contribution from the National Institute
of Neurological Disorders and Stroke. Additional support was provided by
AG023629 from the National Institute on Aging (NIA). A full list of
principal CHS investigators and institutions can be found at
http://www.chs-nhlbi.org/PI.htm; for the Health, Aging, and Body
Composition (Health ABC) study: a support from NIA contracts
N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106 and grant R01-AG028050,
as well as the National Institute of Nursing Research grant
R01-NR012459. This research was supported in part by the Intramural
Research Program of the NIH, NIA. The contents of this publication are
solely the responsibility of the authors and do not necessarily
represent the official views of any of the supporting agencies or
sources.
NR 34
TC 15
Z9 16
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1547-5271
J9 HEART RHYTHM
JI Heart Rhythm
PD OCT
PY 2013
VL 10
IS 10
BP 1562
EP 1568
DI 10.1016/j.hrthm.2013.07.023
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 227XZ
UT WOS:000325150300030
PM 23872693
ER
PT J
AU Wang, H
Feng, DC
Park, O
Yin, S
Gao, B
AF Wang, Hua
Feng, Dechun
Park, Ogyi
Yin, Shi
Gao, Bin
TI Invariant NKT Cell Activation Induces Neutrophil Accumulation and
Hepatitis: Opposite Regulation by IL-4 and IFN-gamma
SO HEPATOLOGY
LA English
DT Article
ID KILLER T-CELLS; LIVER NATURAL-KILLER; PHASE I/II TRIAL;
ALPHA-GALACTOSYLCERAMIDE; INTERFERON-GAMMA; MEDIATED HEPATITIS;
CONCANAVALIN-A; IN-VIVO; INJURY; MICE
AB Alpha-Galactosylceramide (-Galcer), a specific agonist for invariant natural killer T (iNKT) cells, is being evaluated in clinical trials for the treatment of viral hepatitis and liver cancer. However, the results from -Galcer treatment are mixed, partially because of the variety of cytokines produced by activated iNKT cells that have an unknown synergistic effect on the progression of liver disease. It is well documented that injection of -Galcer induces mild hepatitis with a rapid elevation in the levels of interleukin (IL)-4 and a delayed elevation in the levels of interferon-gamma (IFN-), and both of these cytokines are thought to mediate many functions of iNKT cells. Surprisingly, genetic deletion of both IL-4 and IFN- aggravated, rather than abolished, -Galcer-induced iNKT hepatitis. Moreover, genetic ablation of IL-4, the IL-4 receptor, or its downstream signaling molecule signal transducer and activator of transcription (STAT)6 ameliorated -Galcer-induced neutrophil infiltration, liver injury, and hepatitis. In contrast, genetic deletion of IFN-, the IFN- receptor, or its downstream signaling molecule STAT1 enhanced liver neutrophil accumulation, thereby exacerbating liver injury and hepatitis. Moreover, depletion of neutrophils eradicated -Galcer-induced liver injury in wild-type, STAT1 knockout, and IFN- knockout mice. Conclusion: Our results propose a model in which activated iNKT cells rapidly release IL-4, which promotes neutrophil survival and hepatitis but also sequentially produce IFN-, which acts in a negative feedback loop to ameliorate iNKT hepatitis by inducing neutrophil apoptosis. Thus, modification of iNKT production of IL-4 and IFN- may have the potential to improve the efficacy of -Galcer in the treatment of liver disease. (Hepatology 2013;58:1474-1485)
C1 [Wang, Hua; Feng, Dechun; Park, Ogyi; Yin, Shi; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD 20892 USA.
RP Gao, B (reprint author), NIAAA, Lab Liver Dis, NIH, Bethesda, MD 20892 USA.
EM bgao@mail.nih.gov
RI Feng, Dechun/Q-5962-2016
FU NIAAA, NIH
FX This work was supported by the intramural program of NIAAA, NIH (to
B.G.).
NR 39
TC 19
Z9 20
U1 1
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2013
VL 58
IS 4
BP 1474
EP 1485
DI 10.1002/hep.26471
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 227XX
UT WOS:000325150100032
PM 23686838
ER
PT J
AU Hernandez-Hernandez, V
Pravincumar, P
Diaz-Font, A
May-Simera, H
Jenkins, D
Knight, M
Beales, PL
AF Hernandez-Hernandez, Victor
Pravincumar, Priyanka
Diaz-Font, Anna
May-Simera, Helen
Jenkins, Dagan
Knight, Martin
Beales, Philip L.
TI Bardet-Biedl syndrome proteins control the cilia length through
regulation of actin polymerization
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID PLANAR CELL POLARITY; MEDIATES CILIOGENESIS; FOCAL ADHESIONS; BBSOME;
RHO; DYNAMICS; COMPLEX; MECHANOTRANSDUCTION; CHONDROCYTES; CYTOSKELETON
AB Primary cilia are cellular appendages important for signal transduction and sensing the environment. Bardet-Biedl syndrome proteins form a complex that is important for several cytoskeleton-related processes such as ciliogenesis, cell migration and division. However, the mechanisms by which BBS proteins may regulate the cytoskeleton remain unclear. We discovered that Bbs4- and Bbs6-deficient renal medullary cells display a characteristic behaviour comprising poor migration, adhesion and division with an inability to form lamellipodial and filopodial extensions. Moreover, fewer mutant cells were ciliated [48% +/- 6 for wild-type (WT) cells versus 23% +/- 7 for Bbs4 null cells; P < 0.0001] and their cilia were shorter (2.55 mu m +/- 0.41 for WT cells versus 2.16 mu m +/- 0.23 for Bbs4 null cells; P < 0.0001). While the microtubular cytoskeleton and cortical actin were intact, actin stress fibre formation was severely disrupted, forming abnormal apical stress fibre aggregates. Furthermore, we observed over-abundant focal adhesions (FAs) in Bbs4-, Bbs6- and Bbs8-deficient cells. In view of these findings and the role of RhoA in regulation of actin filament polymerization, we showed that RhoA-GTP levels were highly upregulated in the absence of Bbs proteins. Upon treatment of Bbs4- deficient cells with chemical inhibitors of RhoA, we were able to restore the cilia length and number as well as the integrity of the actin cytoskeleton. Together these findings indicate that Bbs proteins play a central role in the regulation of the actin cytoskeleton and control the cilia length through alteration of RhoA levels.
C1 [Hernandez-Hernandez, Victor; Diaz-Font, Anna; Jenkins, Dagan; Beales, Philip L.] UCL Inst Child Hlth London, Mol Med Unit, London, England.
[Pravincumar, Priyanka; Knight, Martin] Queen Mary Univ London, Sch Engn & Mat Sci, London, England.
[May-Simera, Helen] Natl Inst Deafness & Commun Disorders, NIH, Bethesda, MD USA.
RP Beales, PL (reprint author), UCL Inst Child Hlth London, Mol Med Unit, London, England.
EM p.beales@ucl.ac.uk
OI Knight, Martin/0000-0003-3755-1597
FU NEWLIFE; WELLCOME TRUST ViP Award; SYSCILIA [EU-FP7 241955]; WELLCOME
TRUST; EPSRC
FX This work was funded by grants from NEWLIFE, a WELLCOME TRUST ViP Award
to D.J., SYSCILIA (EU-FP7 241955), and WELLCOME TRUST. P.L.B. is a
Wellcome Trust Senior Research Fellow. Priyanka Pravincumar is funded by
an EPSRC PhD Studentship. Funding to pay the Open Access publication
charges for this article was provided by Wellcome Trust.
NR 48
TC 20
Z9 20
U1 1
U2 12
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 OCT 1
PY 2013
VL 22
IS 19
BP 3858
EP 3868
DI 10.1093/hmg/ddt241
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 228CX
UT WOS:000325163900004
PM 23716571
ER
PT J
AU Parrow, NL
Fleming, RE
Minnick, MF
AF Parrow, Nermi L.
Fleming, Robert E.
Minnick, Michael F.
TI Sequestration and Scavenging of Iron in Infection
SO INFECTION AND IMMUNITY
LA English
DT Review
ID OUTER-MEMBRANE PROTEIN; INTRACELLULAR HEME-TRAFFICKING; PATHOGENIC
ESCHERICHIA-COLI; REGULATORY PEPTIDE HEPCIDIN; STAPHYLOCOCCUS-AUREUS
ISDG; ACUTE-PHASE PROTEINS; BINDING PROTEIN; VIBRIO-CHOLERAE;
HAEMOPHILUS-INFLUENZAE; DIETARY IRON
AB The proliferative capability of many invasive pathogens is limited by the bioavailability of iron. Pathogens have thus developed strategies to obtain iron from their host organisms. In turn, host defense strategies have evolved to sequester iron from invasive pathogens. This review explores the mechanisms employed by bacterial pathogens to gain access to host iron sources, the role of iron in bacterial virulence, and iron-related genes required for the establishment or maintenance of infection. Host defenses to limit iron availability for bacterial growth during the acute-phase response and the consequences of iron overload conditions on susceptibility to bacterial infection are also examined. The evidence summarized herein demonstrates the importance of iron bioavailability in influencing the risk of infection and the ability of the host to clear the pathogen.
C1 [Parrow, Nermi L.] NIDDK, Div Mol & Clin Nutr, NIH, Bethesda, MD USA.
[Fleming, Robert E.] St Louis Univ, Sch Med, Dept Pediat, St Louis, MO 63104 USA.
[Minnick, Michael F.] Univ Montana, Div Biol Sci, Missoula, MT 59812 USA.
RP Minnick, MF (reprint author), Univ Montana, Div Biol Sci, Missoula, MT 59812 USA.
EM mike.minnick@mso.umt.edu
FU Intramural Research Program of the National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases
FX N.L.P. is supported by the Intramural Research Program of the National
Institutes of Health, National Institute of Diabetes and Digestive and
Kidney Diseases.
NR 178
TC 25
Z9 25
U1 3
U2 18
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD OCT
PY 2013
VL 81
IS 10
BP 3503
EP 3514
DI 10.1128/IAI.00602-13
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 219SF
UT WOS:000324528700002
PM 23836822
ER
PT J
AU Alaro, JR
Partridge, A
Miura, K
Diouf, A
Lopez, AM
Angov, E
Long, CA
Burns, JM
AF Alaro, James R.
Partridge, Andrea
Miura, Kazutoyo
Diouf, Ababacar
Lopez, Ana M.
Angov, Evelina
Long, Carole A.
Burns, James M., Jr.
TI A Chimeric Plasmodium falciparum Merozoite Surface Protein Vaccine
Induces High Titers of Parasite Growth Inhibitory Antibodies
SO INFECTION AND IMMUNITY
LA English
DT Article
ID CARBOXYL-TERMINAL FRAGMENT; STAGE MALARIA VACCINE; PROTECTIVE
IMMUNE-RESPONSES; FACTOR-LIKE DOMAINS; B-CELL EPITOPES; T-CELL; CPG
OLIGODEOXYNUCLEOTIDE; RECOMBINANT PROTEIN; CHALLENGE INFECTION;
ESCHERICHIA-COLI
AB The C-terminal 19-kDa domain of Plasmodium falciparum merozoite surface protein 1 (PfMSP1(19)) is an established target of protective antibodies. However, clinical trials of PfMSP1(42), a leading blood-stage vaccine candidate which contains the protective epitopes of PfMSP1(19), revealed suboptimal immunogenicity and efficacy. Based on proof-of-concept studies in the Plasmodium yoelii murine model, we produced a chimeric vaccine antigen containing recombinant PfMSP1(19) (rPfMSP1(19)) fused to the N terminus of P. falciparum merozoite surface protein 8 that lacked its low-complexity Asn/Asp-rich domain, rPfMSP8 (Delta Asn/Asp). Immunization of mice with the chimeric rPfMSP1/8 vaccine elicited strong T cell responses to conserved epitopes associated with the rPfMSP8 (Delta Asn/Asp) fusion partner. While specific for PfMSP8, this T cell response was adequate to provide help for the production of high titers of antibodies to both PfMSP1(19) and rPfMSP8 (Delta Asn/Asp) components. This occurred with formulations adjuvanted with either Quil A or with Montanide ISA 720 plus CpG oligodeoxynucleotide (ODN) and was observed in both inbred and outbred strains of mice. PfMSP1/8-induced antibodies were highly reactive with two major alleles of PfMSP1(19) (FVO and 3D7). Of particular interest, immunization with PfMSP1/8 elicited higher titers of PfMSP1(19)-specific antibodies than a combined formulation of rPfMSP1(42) and rPfMSP8 (Delta Asn/Asp). As a measure of functionality, PfMSP1/8-specific rabbit IgG was shown to potently inhibit the in vitro growth of blood-stage parasites of the FVO and 3D7 strains of P. falciparum. These data support the further testing and evaluation of this chimeric PfMSP1/8 antigen as a component of a multivalent vaccine for P. falciparum malaria.
C1 [Alaro, James R.; Partridge, Andrea; Lopez, Ana M.; Long, Carole A.; Burns, James M., Jr.] Drexel Univ, Coll Med, Ctr Mol Parasitol, Dept Microbiol & Immunol, Philadelphia, PA 19104 USA.
[Alaro, James R.; Miura, Kazutoyo; Diouf, Ababacar; Long, Carole A.] NIAID, Malaria Immunol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Angov, Evelina] Walter Reed Army Inst Res, US Mil Malaria Res Program, Malaria Vaccine Branch, Silver Spring, MD USA.
RP Burns, JM (reprint author), Drexel Univ, Coll Med, Ctr Mol Parasitol, Dept Microbiol & Immunol, Philadelphia, PA 19104 USA.
EM jburns@drexelmed.edu
FU NIH-NIAID [AI035661]; PATH Malaria Vaccine Initiative
FX This work was supported by NIH-NIAID grant AI035661 (J.M.B.) and the
Intramural Program of NIH-NIAID (C.A.L.). The GIA Reference Center where
the GIA assay was performed is supported by the PATH Malaria Vaccine
Initiative.
NR 73
TC 6
Z9 6
U1 0
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD OCT
PY 2013
VL 81
IS 10
BP 3843
EP 3854
DI 10.1128/IAI.00522-13
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 219SF
UT WOS:000324528700035
PM 23897613
ER
PT J
AU Sullivan, MD
Katon, WJ
Lovato, LC
Miller, ME
Murray, AM
Horowitz, KR
Bryan, RN
Gerstein, HC
Marcovina, S
Akpunonu, BE
Johnson, J
Yale, JF
Williamson, J
Launer, LJ
AF Sullivan, Mark D.
Katon, Wayne J.
Lovato, Laura C.
Miller, Michael E.
Murray, Anne M.
Horowitz, Karen R.
Bryan, R. Nick
Gerstein, Hertzel C.
Marcovina, Santica
Akpunonu, Basil E.
Johnson, Janice
Yale, Jean Francois
Williamson, Jeff
Launer, Lenore J.
TI Association of Depression With Accelerated Cognitive Decline Among
Patients With Type 2 Diabetes in the ACCORD-MIND Trial
SO JAMA PSYCHIATRY
LA English
DT Article
ID CONTROL CARDIOVASCULAR RISK; 3 DECADES LATER; MAJOR DEPRESSION;
HIPPOCAMPAL VOLUME; INSULIN-RESISTANCE; DEMENTIA; SYMPTOMS;
METAANALYSIS; DISEASE; IMPAIRMENT
AB IMPORTANCE Depression has been identified as a risk factor for dementia among patients with type 2 diabetes mellitus but the cognitive domains and patient groups most affected have not been identified.
OBJECTIVE To determine whether comorbid depression in patients with type 2 diabetes accelerates cognitive decline.
DESIGN A 40-month cohort study of participants in the Action to Control Cardiovascular Risk in Diabetes-Memory in Diabetes (ACCORD-MIND) trial.
SETTING Fifty-two clinics organized into 6 clinical networks across the United States and Canada.
PARTICIPANTS Two thousand nine hundred seventy-seven participants with type 2 diabetes at high risk for cardiovascular events.
INTERVENTION The Digit Symbol Substitution Test, Rey Auditory Verbal Learning Test, and the modified Stroop test were used to assess cognition. The 9-item Patient Health Questionnaire was used to assess depression.
MAIN OUTCOMES AND MEASURES Mixed-effects statistical models were used to analyze cognitive test outcomes incorporating depression as a time-dependent covariate.
RESULTS Participants with scores indicative of depression (9-item Patient Health Questionnaire, >= 10) showed greater cognitive decline during 40-month follow-up on all tests, with the following differences in estimated least squares means: Digit Symbol Substitution Test, 0.72 (95% CI, 0.25 to 1.19; P = .003), Rey Auditory Verbal Learning Test, 0.18 (95% CI, 0.07 to 0.29; P = .001), and Stroop interference, -1.06 (95% CI, -1.93 to -0.18; P = .02). This effect of depression on risk of cognitive decline did not differ according to previous cardiovascular disease; baseline cognition or age; or intensive vs standard glucose-lowering treatment, blood pressure treatment, lipid treatment, or insulin treatment. Addition of demographic and clinical covariates to models did not significantly change the cognitive decline associated with depression.
CONCLUSIONS AND RELEVANCE Depression in patients with type 2 diabetes was associated with greater cognitive decline in all domains, across all treatment arms, and in all participant subgroups assessed. Future randomized trials will be necessary to determine if depression treatment can lower the risk of cognitive decline in patients with diabetes.
C1 [Sullivan, Mark D.; Katon, Wayne J.; Marcovina, Santica; Johnson, Janice] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Lovato, Laura C.; Miller, Michael E.; Williamson, Jeff] Wake Forest Univ, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA.
[Murray, Anne M.] Univ Minnesota, Dept Internal Med, Minneapolis, MN USA.
[Horowitz, Karen R.] Case Western Univ, Dept Internal Med, Cleveland, OH USA.
[Bryan, R. Nick] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Gerstein, Hertzel C.] McMaster Univ, Dept Internal Med, Hamilton, ON, Canada.
[Akpunonu, Basil E.] Univ Toledo, Dept Med, Toledo, OH 43606 USA.
[Yale, Jean Francois] McGill Univ, Dept Internal Med, Montreal, PQ, Canada.
[Launer, Lenore J.] NIA, Bethesda, MD 20892 USA.
RP Sullivan, MD (reprint author), Univ Washington, POB 356560, Seattle, WA 98195 USA.
EM sullimar@uw.edu
FU National Institute on Aging [AG-0002]; National Heart, Lung, and Blood
Institute [AG-0002, N01-HC-95178, N01-HC-95179, N01-HC-95180,
N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184]; National
Institute on Aging Intramural Research Program
FX ACCORD-MIND was funded through an intra-agency agreement between the
National Institute on Aging and National Heart, Lung, and Blood
Institute (grant AG-0002) and the National Institute on Aging Intramural
Research Program. ACCORD was funded by National Heart, Lung, and Blood
Institute grants N01-HC-95178; N01-HC-95179; N01-HC-95180; N01-HC-95181;
N01-HC-95182; N01-HC-95183; and N01-HC-95184.
NR 48
TC 36
Z9 39
U1 5
U2 23
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-622X
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD OCT
PY 2013
VL 70
IS 10
BP 1041
EP 1047
DI 10.1001/jamapsychiatry.2013.1965
PG 7
WC Psychiatry
SC Psychiatry
GA 228KE
UT WOS:000325184100008
PM 23945905
ER
PT J
AU Kumar, R
Nguyen, EA
Roth, LA
Oh, SS
Gignoux, CR
Huntsman, S
Eng, C
Moreno-Estrada, A
Sandoval, K
Penaloza-Espinosa, RI
Lopez-Lopez, M
Avila, PC
Farber, HJ
Tcheurekdjian, H
Rodriguez-Cintron, W
Rodriguez-Santana, JR
Serebrisky, D
Thyne, SM
Williams, LK
Winkler, C
Bustamante, CD
Perez-Stable, EJ
Borrell, LN
Burchard, EG
AF Kumar, Rajesh
Nguyen, Elizabeth A.
Roth, Lindsey A.
Oh, Sam S.
Gignoux, Christopher R.
Huntsman, Scott
Eng, Celeste
Moreno-Estrada, Andres
Sandoval, Karla
Penaloza-Espinosa, Rosenda I.
Lopez-Lopez, Marisol
Avila, Pedro C.
Farber, Harold J.
Tcheurekdjian, Haig
Rodriguez-Cintron, William
Rodriguez-Santana, Jose R.
Serebrisky, Denise
Thyne, Shannon M.
Williams, L. Keoki
Winkler, Cheryl
Bustamante, Carlos D.
Perez-Stable, Eliseo J.
Borrell, Luisa N.
Burchard, Esteban G.
TI Factors associated with degree of atopy in Latino children in a
nationwide pediatric sample: The Genes-environments and Admixture in
Latino Asthmatics (GALA II) study
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Latino; atopy; region of origin; genetic ancestry; immigration; kin
test; aeroallergen
ID DAY-CARE ATTENDANCE; DUST-MITE ALLERGEN; BLOOD IGE LEVELS; BIRTH COHORT;
SOCIOECONOMIC-STATUS; CHILDHOOD ASTHMA; PUERTO-RICAN; 1ST YEAR;
COCKROACH ALLERGEN; MEXICAN-AMERICANS
AB Background: Atopy varies by ethnicity, even within Latino groups. This variation might be due to environmental, sociocultural, or genetic factors.
Objective: We sought to examine risk factors for atopy within a nationwide study of US Latino children with and without asthma.
Methods: Aeroallergen skin test responses were analyzed in 1830 US Latino subjects. Key determinants of atopy included country/region of origin, generation in the United States, acculturation, genetic ancestry, and site to which subjects migrated. Serial multivariate zero-inflated negative binomial regressions stratified by asthma status examined the association of each key determinant variable with the number of positive skin test responses. In addition, the independent effect of each key variable was determined by including all key variables in the final models.
Results: In baseline analyses African ancestry was associated with 3 times (95% CI, 1.62-5.57) as many positive skin test responses in asthmatic participants and 3.26 times (95% CI, 1.02-10.39) as many positive skin test responses in control participants. Generation and recruitment site were also associated with atopy in crude models. In final models adjusted for key variables, asthmatic patients of Puerto Rican (exp[beta] [95% CI], 1.31 [1.021.69]) and mixed (exp[beta] [95% CI], 1.27 [1.03-1.56]) ethnicity had a greater probability of positive skin test responses compared with Mexican asthmatic patients. Ancestry associations were abrogated by recruitment site but not region of origin.
Conclusions: Puerto Rican ethnicity and mixed origin were associated with degree of atopy within US Latino children with asthma. African ancestry was not associated with degree of atopy after adjusting for recruitment site. Local environment variation, represented by site, was associated with degree of sensitization.
C1 [Kumar, Rajesh] Northwestern Univ, Childrens Mem Hosp, Div Allergy & Immunol, Chicago, IL 60614 USA.
[Kumar, Rajesh] Northwestern Univ, Dept Pediat, Feinberg Sch Med, Chicago, IL 60611 USA.
[Nguyen, Elizabeth A.; Roth, Lindsey A.; Oh, Sam S.; Gignoux, Christopher R.; Huntsman, Scott; Eng, Celeste; Perez-Stable, Eliseo J.; Burchard, Esteban G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Moreno-Estrada, Andres; Sandoval, Karla; Bustamante, Carlos D.] Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA.
[Penaloza-Espinosa, Rosenda I.; Lopez-Lopez, Marisol] Univ Autonoma Metropolitana Xochimilco, Div Biol & Hlth Sci, Dept Syst Biol, Mexico City, DF, Mexico.
[Avila, Pedro C.] Northwestern Univ, Div Allergy Immunol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Farber, Harold J.] Texas Childrens Hosp, Baylor Coll Med, Dept Pediat, Sect Pulmonol, Houston, TX 77030 USA.
[Tcheurekdjian, Haig] Case Western Reserve Univ, Allergy Immunol Associates, Cleveland, OH 44106 USA.
[Tcheurekdjian, Haig] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
[Tcheurekdjian, Haig] Case Western Reserve Univ, Dept Pediat, Cleveland, OH 44106 USA.
[Rodriguez-Cintron, William] Vet Caribbean Hlth Care Syst, San Juan, PR USA.
[Rodriguez-Santana, Jose R.] CSP, Ctr Neumol Pediatr, San Juan, PR USA.
[Serebrisky, Denise] Jacobi Med Ctr, Pediat Pulm Div, Bronx, NY USA.
[Thyne, Shannon M.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
[Williams, L. Keoki] Henry Ford Hlth Syst, Dept Internal Med, Detroit, MI USA.
[Winkler, Cheryl] NCI, Ctr Canc Res, Basic Res Lab, SAIC Frederick, Frederick, MD 21701 USA.
[Borrell, Luisa N.] CUNY, Dept Hlth Sci, Grad Program Publ Hlth, Lehman Coll, Bronx, NY USA.
[Burchard, Esteban G.] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, San Francisco, CA 94143 USA.
RP Kumar, R (reprint author), Childrens Mem Hosp, Div Allergy & Clin Immunol, 2300 Childrens Plaza,Box 60, Chicago, IL 60614 USA.
EM rkumar@childrensmemorial.org
OI Nguyen, Elizabeth/0000-0002-8070-6382
FU National Institutes of Health [ES015794, AI077439, HL088133, HL078885,
CA113710, AI079139, HL004464, HL104608, AI061774, HL079055, DK064695,
M01-RR00188, HHSN26120080001E, MD006902]; Flight Attendant Medical
Research Institute (FAMRI); RWJF Amos Medical Faculty; Sandler
Foundation; American Asthma Foundation; Ernest S. Bazley Grant; National
Heart, Lung, and Blood Institute K23 [K23HL093023]; National Institute
on Minority Health and Health Disparities of the National Institutes of
Health [P60MD006902]; National Institutes of Health, National Cancer
Institute, Center for Cancer Research; National Heart, Lung, and Blood
Institute (NHLBI); National Institutes of Health (NIH); NHLBI/National
Institute of Allergy and Infectious Diseases (NIAID); EMD China;
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK); NIAID; Merck
FX Supported in part by the National Institutes of Health grants (ES015794,
AI077439, HL088133, HL078885, CA113710, AI079139, HL004464, HL104608,
AI061774, HL079055, DK064695, and M01-RR00188; HHSN26120080001E; and
MD006902); the Flight Attendant Medical Research Institute (FAMRI); an
RWJF Amos Medical Faculty Development Award (to E. G. B.); the Sandler
Foundation; the American Asthma Foundation (to E. G. B); an Ernest S.
Bazley Grant (to P.C.A.); National Heart, Lung, and Blood Institute K23
(K23HL093023, to R.K.). In addition, the research reported in this
publication was also supported by the National Institute on Minority
Health and Health Disparities of the National Institutes of Health under
award no. P60MD006902. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health. Furthermore, 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. This research was supported in part by the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, Center for Cancer Research.; Disclosure of potential conflict
of interest: R. Kumar, E. A. Nguyen, S. S. Oh, S. Huntsman, C. Eng, A.
Moreno-Estrada, K. Sandoval, R. I. Penaloza- Espinosa, M. Lopez-Lopez,
P. C. Avila, W. Rodriguez-Cintron, J. R. Rodriguez-Santana, D.
Serebrisky, S. M. Thyne, C. Winkler, C. D. Bustamante, E. J.
Perez-Stable, L. N. Borrell, and E. G. Burchard received research
support from the National Heart, Lung, and Blood Institute (NHLBI) and
the National Institutes of Health (NIH). C. R. Gignoux has received
research support from the NHLBI and NIH and owns stock in 23 and Me. L.
A. Roth, S. Huntsman, C. Eng, D. Serebrisky, and C. D. Bustamante have
received research support from the NHLBI. P. C. Avila has received
research support from the NHLBI/National Institute of Allergy and
Infectious Diseases (NIAID). H. J. Farber has received grants from the
NIH and NHLBI and has received honoraria for talks on asthma from EMD
China. L. K. Williams has received research support from the NHLBI,
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), and NIAID and has received research support from Merck. The
rest of the authors declare that they have no relevant conflicts of
interest.
NR 66
TC 9
Z9 10
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2013
VL 132
IS 4
BP 896
EP +
DI 10.1016/j.jaci.2013.02.046
PG 11
WC Allergy; Immunology
SC Allergy; Immunology
GA 227FR
UT WOS:000325096500017
PM 23684070
ER
PT J
AU Vernon, R
Shen, Y
Baker, D
Lange, OF
AF Vernon, Robert
Shen, Yang
Baker, David
Lange, Oliver F.
TI Improved chemical shift based fragment selection for CS-Rosetta using
Rosetta3 fragment picker
SO JOURNAL OF BIOMOLECULAR NMR
LA English
DT Article
DE Protein structure; NMR; Sparse data; Chemical shifts
ID PROTEIN-STRUCTURE DETERMINATION; NMR STRUCTURE DETERMINATION; STRUCTURE
PREDICTION; STRUCTURE GENERATION; SECONDARY STRUCTURE; DIPOLAR
COUPLINGS; RECOGNITION; REPLACEMENT; FEATURES; PLUS
AB A new fragment picker has been developed for CS-Rosetta that combines beneficial features of the original fragment picker, MFR, used with CS-Rosetta, and the fragment picker, NNMake, that was used for purely sequence based fragment selection in the context of ROSETTA de-novo structure prediction. Additionally, the new fragment picker has reduced sensitivity to outliers and other difficult to match data points rendering the protocol more robust and less likely to introduce bias towards wrong conformations in cases where data is bad, missing or inconclusive. The fragment picker protocol gives significant improvements on 6 of 23 CS-Rosetta targets. An independent benchmark on 39 protein targets, whose NMR data sets were published only after protocol optimization had been finished, also show significantly improved performance for the new fragment picker (van der Schot et al. in J Biomol NMR, 2013).
C1 [Vernon, Robert; Lange, Oliver F.] Tech Univ Munich, Dept Chem, Biomol NMR, D-85747 Garching, Germany.
[Vernon, Robert; Lange, Oliver F.] Tech Univ Munich, Munich Ctr Integrated Prot Sci, D-85747 Garching, Germany.
[Vernon, Robert; Baker, David] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Shen, Yang] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Baker, David] Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA.
[Lange, Oliver F.] Helmholtz Zentrum Munchen, Inst Biol Struct, D-85764 Neuherberg, Germany.
RP Lange, OF (reprint author), Tech Univ Munich, Dept Chem, Biomol NMR, Lichtenbergstr 4, D-85747 Garching, Germany.
EM oliver.lange@tum.de
RI Shen, Yang/C-3064-2008; Baker, David/K-8941-2012
OI Shen, Yang/0000-0003-1408-8034; Baker, David/0000-0001-7896-6217
NR 30
TC 14
Z9 14
U1 0
U2 16
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0925-2738
J9 J BIOMOL NMR
JI J. Biomol. NMR
PD OCT
PY 2013
VL 57
IS 2
BP 117
EP 127
DI 10.1007/s10858-013-9772-4
PG 11
WC Biochemistry & Molecular Biology; Spectroscopy
SC Biochemistry & Molecular Biology; Spectroscopy
GA 228BP
UT WOS:000325160400004
PM 23975356
ER
PT J
AU Ali, MS
Starke, RM
Jabbour, PM
Tjoumakaris, SI
Gonzalez, LF
Rosenwasser, RH
Owens, GK
Koch, WJ
Greig, NH
Dumont, AS
AF Ali, Muhammad S.
Starke, Robert M.
Jabbour, Pascal M.
Tjoumakaris, Stavropoula I.
Gonzalez, L. Fernando
Rosenwasser, Robert H.
Owens, Gary K.
Koch, Walter J.
Greig, Nigel H.
Dumont, Aaron S.
TI TNF-alpha induces phenotypic modulation in cerebral vascular smooth
muscle cells: implications for cerebral aneurysm pathology
SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
LA English
DT Article
DE Cerebral aneurysm; Cerebral vascular smooth muscle cells; Smooth muscle
cell phenotypic modulation; TNF-alpha
ID NECROSIS-FACTOR-ALPHA; INTRACRANIAL ANEURYSMS; GENE-EXPRESSION; IN-VIVO;
ATHEROSCLEROSIS; DIFFERENTIATION; INFLAMMATION; DISEASE; RATS;
NEUROINFLAMMATION
AB Little is known about vascular smooth muscle cell (SMC) phenotypic modulation in the cerebral circulation or pathogenesis of intracranial aneurysms. Tumor necrosis factor-alpha (TNF-alpha) has been associated with aneurysms, but potential mechanisms are unclear. Cultured rat cerebral SMCs overexpressing myocardin induced expression of key SMC contractile genes (SM-alpha-actin, SM-22 alpha, smooth muscle myosin heavy chain), while dominant-negative cells suppressed expression. Tumor necrosis factor-alpha treatment inhibited this contractile phenotype and induced pro-inflammatory/matrix-remodeling genes (monocyte chemoattractant protein-1, matrix metalloproteinase-3, matrix metalloproteinase-9, vascular cell adhesion molecule-1, interleukin-1 beta). Tumor necrosis factor-alpha increased expression of KLF4, a known regulator of SMC differentiation. Kruppel-like transcription factor 4 (KLF4) small interfering RNA abrogated TNF-alpha activation of inflammatory genes and suppression of contractile genes. These mechanisms were confirmed in vivo after exposure of rat carotid arteries to TNF-alpha and early on in a model of cerebral aneurysm formation. Treatment with the synthesized TNF-alpha inhibitor 3,6-dithiothalidomide reversed pathologic vessel wall alterations after induced hypertension and hemodynamic stress. Chromatin immunoprecipitation assays in vivo and in vitro demonstrated that TNF-alpha promotes epigenetic changes through KLF4-dependent alterations in promoter regions of myocardin, SMCs, and inflammatory genes. In conclusion, TNF-alpha induces phenotypic modulation of cerebral SMCs through myocardin and KLF4-regulated pathways. These results demonstrate a novel role for TNF-alpha in promoting a pro-inflammatory/matrix-remodeling phenotype, which has important implications for the mechanisms behind intracranial aneurysm formation.
C1 [Ali, Muhammad S.; Starke, Robert M.; Jabbour, Pascal M.; Tjoumakaris, Stavropoula I.; Gonzalez, L. Fernando; Rosenwasser, Robert H.; Dumont, Aaron S.] Thomas Jefferson Univ, Joseph & Marie Field Cerebrovasc Res Lab, Div Neurovasc & Endovasc Surg, Dept Neurol Surg, Philadelphia, PA 19107 USA.
[Starke, Robert M.] Univ Virginia, Dept Neurol Surg, Charlottesville, VA USA.
[Owens, Gary K.] Robert M Berne Cardiovasc Res Ctr, Dept Mol Physiol & Biophys, Charlottesville, VA USA.
[Koch, Walter J.] Temple Univ, Ctr Translat Med, Philadelphia, PA 19122 USA.
[Koch, Walter J.] Temple Univ, Dept Pharmacol, Philadelphia, PA 19122 USA.
[Greig, Nigel H.] NIA, NIH, Translat Gerontol Branch, Intramural Res Program, Baltimore, MD 21224 USA.
RP Dumont, AS (reprint author), Thomas Jefferson Univ, Joseph & Marie Field Cerebrovasc Res Lab, Div Neurovasc & Endovasc Surg, Dept Neurol Surg, 909 Walnut St,2nd Floor, Philadelphia, PA 19107 USA.
EM aaron.dumont@jefferson.edu
FU NIH [K08NS067072, R01 HL57353, R01 HL098538, R01 HL087867, P01 HL091799,
P01 HL07544]; Intramural Research Program of NIH
FX This work was supported by NIH grants K08NS067072 to ASD, NIH grants R01
HL57353 (GKO), R01 HL098538 (GKO), and R01 HL087867 to GKO, and NIH P01
HL091799 and P01 HL07544 Project 2 to WJK. NHG is supported by the
Intramural Research Program of NIH.
NR 42
TC 34
Z9 36
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0271-678X
J9 J CEREBR BLOOD F MET
JI J. Cereb. Blood Flow Metab.
PD OCT
PY 2013
VL 33
IS 10
BP 1564
EP 1573
DI 10.1038/jcbfm.2013.109
PG 10
WC Endocrinology & Metabolism; Hematology; Neurosciences
SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology
GA 228PV
UT WOS:000325199600011
PM 23860374
ER
PT J
AU Galeano, ME
Martinez, M
Amarilla, AA
Russomando, G
Miagostovich, MP
Parra, GI
Leite, JP
AF Galeano, Maria Eugenia
Martinez, Magaly
Amarilla, Alberto A.
Russomando, Graciela
Miagostovich, Marize Pereira
Parra, Gabriel I.
Leite, Jose Paulo
TI Molecular epidemiology of norovirus strains in Paraguayan children
during 2004-2005: Description of a possible new GII.4 cluster
SO JOURNAL OF CLINICAL VIROLOGY
LA English
DT Article
DE Norovirus; Acute gastroenteritis; Paraguayan children; GII.4 norovirus
ID NORWALK-LIKE VIRUSES; A ROTAVIRUS STRAINS; RIO-DE-JANEIRO;
UNITED-STATES; GENOGROUP-II; HOSPITALIZED CHILDREN; ACUTE
GASTROENTERITIS; BRAZIL; ARGENTINA; OUTBREAKS
AB Background: Noroviruses (NoV) have been shown to be an important cause of morbidity and mortality in children worldwide, only second after Group A rotaviruses (RVA). In Paraguay, acute gastroenteritis (AGE) is the third cause of mortality in children <= 5 years old.
Objectives: To analyze the presence and diversity of NoV in Paraguayan children <5 years old presenting AGE.
Study design: Three hundred seventy eight fecal samples, negative for pathogenic bacteria and RVA, were collected from children admitted as ambulatory and hospitalized patients in a large private hospital from Asuncion, Paraguay from 2004 to 2005. The presence and diversity of NoV was determined by two different RT-PCR strategies and nucleotide sequencing.
Results: One hundred and sixty one samples were positive for NoV by partial amplification of the viral polymerase gene (RdRp). No seasonality or differences in the viral prevalence for the different age-groups were detected. Gil and GI NoVs were associated to 58% and 42% of the infections, respectively. The genotype was determined in 18% (291161) NoV-positive samples. The genotypes detected were: GII.4 (18%), GII.17 (18%), GII.6 (14%), GII.7 (14%), GII.3 (10%), GII.5 (3%), GII.8 (3%), GII.16 (3%), GI.3 (14%) and GI.8 (3%). Amplification of the ORF2 from the GII.4 strains showed the presence of a new GII.4 variant.
Conclusions: The results showed a continuous circulation of NoV in children throughout the two years of study and an extensive diversity of genotypes co-circulating, highlighting the need for better surveillance of NoV in Paraguayan children. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Galeano, Maria Eugenia; Miagostovich, Marize Pereira; Leite, Jose Paulo] Minist Hlth, Oswaldo Cruz Fdn, Inst Oswaldo Cruz, Lab Comparat & Environm Virol, Rio De Janeiro, Brazil.
[Galeano, Maria Eugenia; Martinez, Magaly; Amarilla, Alberto A.; Russomando, Graciela; Parra, Gabriel I.] Natl Univ Asuncion, Hlth Sci Res Inst, Dept Mol Biol & Genet, Asuncion, Paraguay.
RP Parra, GI (reprint author), NIAID, NIH, Infect Dis Lab, Caliciviruses Sect, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gabriel.parra@hotmail.com
RI Amarilla, Alberto/C-3112-2012; Leite, Joao/B-9070-2012;
OI Amarilla, Alberto/0000-0002-4151-2024; Leite, Joao/0000-0003-0558-3519;
Parra, Gabriel/0000-0002-1102-4740
FU National Council for Scientific and Technological Development (CNPq);
Brazilian Federal Agency for Support and Evaluation of Graduate
Education (CAPES), through the Exchange Student Post-graduation Program
(PEC-PG); National University of Asuncion; Oswaldo Cruz
Institute/Fiocruz; PROEP/CNPq; Carlos Chagas Filho Foundation for
Research Support of the State of Rio de Janeiro (FAPERJ); CAPES; CNPq
FX MEG was a scholarship recipient from the National Council for Scientific
and Technological Development (CNPq), and the Brazilian Federal Agency
for Support and Evaluation of Graduate Education (CAPES), through the
Exchange Student Post-graduation Program (PEC-PG). This study was
partially supported by the National University of Asuncion, Oswaldo Cruz
Institute/Fiocruz, PROEP/CNPq, Carlos Chagas Filho Foundation for
Research Support of the State of Rio de Janeiro (FAPERJ), CAPES and
CNPq.
NR 51
TC 9
Z9 9
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1386-6532
J9 J CLIN VIROL
JI J. Clin. Virol.
PD OCT
PY 2013
VL 58
IS 2
BP 378
EP 384
DI 10.1016/j.jcv.2013.07.008
PG 7
WC Virology
SC Virology
GA 222RY
UT WOS:000324750000011
PM 23932334
ER
PT J
AU Mattson, MP
AF Mattson, Mark P.
TI Exercise and the brain: a slap on the HAND
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Editorial Material
ID NEUROTROPHIC FACTOR; HIV; NEUROTOXICITY; NEUROGENESIS; SENSITIVITY;
DEPRESSION; PLASTICITY; NEURONS; DISEASE; HEALTH
C1 NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
FU Intramural NIH HHS [Z01 AG000312-08, Z01 AG000317-08, ZIA AG000317-12]
NR 22
TC 0
Z9 0
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
IS 5
BP 407
EP 409
DI 10.1007/s13365-013-0208-4
PG 3
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 228YM
UT WOS:000325228100001
PM 24072548
ER
PT J
AU Lee, MH
Amin, ND
Venkatesan, A
Wang, TG
Tyagi, R
Pant, HC
Nath, A
AF Lee, Myoung-Hwa
Amin, Niranjana D.
Venkatesan, Arun
Wang, Tongguang
Tyagi, Richa
Pant, Harish C.
Nath, Avindra
TI Impaired neurogenesis and neurite outgrowth in an HIV-gp120 transgenic
model is reversed by exercise via BDNF production and Cdk5 regulation
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
DE HIV-gp120; Exercise; Adult neurogenesis; Dendritic arborization; BDNF;
Cdk5
ID CYCLIN-DEPENDENT KINASE-5; COAT PROTEIN GP120; OBJECT RECOGNITION
MEMORY; GENERATED GRANULE CELLS; ADULT BRAIN; HIPPOCAMPAL NEUROGENESIS;
PHYSICAL-EXERCISE; NERVOUS-SYSTEM; DENTATE GYRUS; MOUSE MODEL
AB Human immunodeficiency virus (HIV) infection-associated neurocognitive disorders is accompanied with brain atrophy. In these patients, impairment of adult neurogenesis and neurite outgrowth in the hippocampus may contribute to cognitive dysfunction. Although running exercises can enhance neurogenesis and normalize neurite outgrowth, the underlying molecular mechanisms are not well understood. The HIV envelope protein, gp120, has been shown to impair neurogenesis. Using a gp120 transgenic mouse model, we demonstrate that exercise stimulated neural progenitor cell (NPC) proliferation in the hippocampal dentate gyrus and increased the survival rate and generation of newborn cells. However, sustained exercise activity was necessary as the effects were reversed by detraining. Exercise also normalized dendritic outgrowth of neurons. Furthermore, it increased the expression of hippocampal brain-derived neurotrophic factor (BDNF) and normalized hyperactivation of cyclin-dependent kinase 5 (Cdk5). Hyperactivated Cdk5 or gp120 treatment led to aberrant neurite outgrowth and BDNF treatment normalized the neurite outgrowth in NPC cultures. These results suggest that sustained exercise has trophic activity on the neuronal lineage which is mediated by Cdk5 modulation of the BDNF pathway.
C1 [Lee, Myoung-Hwa; Wang, Tongguang; Tyagi, Richa; Nath, Avindra] NIH, Sect Infect Nervous Syst, Bethesda, MD 20892 USA.
[Amin, Niranjana D.; Pant, Harish C.] NINDS, Neuronal Cytoskeletal Prot Regulatory Sect, NIH, Bethesda, MD 20892 USA.
[Venkatesan, Arun] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA.
RP Nath, A (reprint author), NIH, Sect Infect Nervous Syst, MD Bldg 10,Room 7C-103,10 Ctr Dr, Bethesda, MD 20892 USA.
EM natha@mail.nih.gov
FU NIH [R01-DA024593, R01-NS039253]; NINDS intramural funds
FX We thank Dr. Valerie Toodle for technical assistance. This work was
supported by grants from the NIH (R01-DA024593; R01-NS039253) and NINDS
intramural funds.
NR 61
TC 18
Z9 18
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
IS 5
BP 418
EP 431
DI 10.1007/s13365-013-0194-6
PG 14
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 228YM
UT WOS:000325228100003
PM 23982957
ER
PT J
AU Kranick, SM
Zerbe, CS
AF Kranick, Sarah M.
Zerbe, Christa S.
TI Case report from the NIH Clinical Center: CNS nocardiosis
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
ID BRAIN-ABSCESS; TRANSVALENSIS; INFECTIONS
C1 [Kranick, Sarah M.] NINDS, Sect Infect Nervous Syst, NINDS Consult Serv, Bethesda, MD 20892 USA.
[Zerbe, Christa S.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Kranick, SM (reprint author), NINDS, Sect Infect Nervous Syst, NINDS Consult Serv, Bldg 10 Rm 6-5700,10 Ctr Dr, Bethesda, MD 20892 USA.
EM sarah.kranick@nih.gov
FU NIH Intramural Program
FX This research was supported by the NIH Intramural Program
NR 9
TC 2
Z9 2
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
J9 J NEUROVIROL
JI J. Neurovirol.
PD OCT
PY 2013
VL 19
IS 5
BP 505
EP 507
DI 10.1007/s13365-013-0193-7
PG 3
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 228YM
UT WOS:000325228100012
PM 23996690
ER
PT J
AU Erba, PA
Minichilli, F
Giona, F
Linari, S
Dambrosia, J
Pierini, A
Filocamo, M
Di Rocco, M
Buffoni, F
Brady, RO
Mariani, G
AF Erba, Paola A.
Minichilli, Fabrizio
Giona, Fiorina
Linari, Silvia
Dambrosia, James
Pierini, Anna
Filocamo, Mirella
Di Rocco, Maja
Buffoni, Ferdinando
Brady, Roscoe O.
Mariani, Giuliano
TI Tc-99m-Sestamibi Scintigraphy to Monitor the Long-Term Efficacy of
Enzyme Replacement Therapy on Bone Marrow Infiltration in Patients with
Gaucher Disease
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE Tc-99m-sestamibi; Gaucher disease; bone marrow disease; scintigraphic
score; enzyme replacement therapy
ID TYPE-1; INVOLVEMENT; GLUCOCEREBROSIDASE; IMIGLUCERASE; DEFICIENCY;
CHILDREN; OUTCOMES; SCORE; MRI
AB Assessing the skeletal response to enzyme replacement therapy (ERT) in Gaucher disease (GD) is problematic. We investigated the reliability of Tc-99m-sestamibi scintigraphy in monitoring changes in bone marrow involvement induced by ERT. Methods: In 52 GD patients, the efficacy of ERT on bone marrow disease was monitored using at least 2 sequential Tc-99m-sestamibi scans; 17 patients were receiving ERT at enrollment, and 35 were ERT-naive. We elaborated a dose-response model by statistical analysis based on linear mixed models. Results: Patients whose marrow disease improved had received a significantly higher ERT dose per month than patients who did not improve. Significantly more patients reached near-disappearance of marrow disease if their disease burden at enrollment had been lower and the duration of clinical signs shorter. The response of the marrow scintigraphic score was more pronounced in ERT-naive patients. No relevant effect of ERT on marrow disease was observed until platelet count and splenomegaly had improved. Conclusion: Although based on localized evaluation, changes in the Tc-99m-sestamibi score closely correlated with the main determinants of ERT, with a definite dose-response relationship. The threshold at which ERT induced any improvement in bone marrow disease was 35-36 U/kg/mo; in ERT-naive patients, the scintigraphic score declined by 1 unit after ERT at 28 U/kg/mo.
C1 [Erba, Paola A.; Mariani, Giuliano] Univ Pisa, Reg Ctr Nucl Med, I-56126 Pisa, Italy.
[Minichilli, Fabrizio; Pierini, Anna] CNR, Inst Clin Physiol, I-56100 Pisa, Italy.
[Giona, Fiorina] Univ Roma La Sapienza, Dept Cell Biotechnol & Hematol, I-00185 Rome, Italy.
[Linari, Silvia] Careggi Univ Hosp, Agcy Hemophilia, Florence, Italy.
[Linari, Silvia] Careggi Univ Hosp, Reg Reference Ctr Inherited Bleeding Disorders, Florence, Italy.
[Dambrosia, James] NINDS, Biostat Branch, NIH, Bethesda, MD 20892 USA.
[Filocamo, Mirella; Di Rocco, Maja] G Gaslini Childrens Hosp, Genoa, Italy.
[Buffoni, Ferdinando] Town Hosp, Nucl Med Serv, Massa, Italy.
[Brady, Roscoe O.] NINDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Mariani, G (reprint author), Univ Pisa, Reg Ctr Nucl Med, Via Roma 67, I-56126 Pisa, Italy.
EM giuliano.mariani@med.unipi.it
FU Italian Association of Gaucher Disease
FX We thank all patients who participated in this investigation and the
Italian Association of Gaucher Disease for its support. Thanks are also
due to the following colleagues who either referred patients for the
study or performed some of the 99mTc-sestamibi scans: Rosanna
Gatti (Genoa, Italy), Angela Amendola (formerly in Rome, now in Potenza,
Italy), Assuero Giorgetti, Marzio Perri, Isabella Raugei (Pisa, Italy),
Isabella Raugei, Giuseppe Villa (Genoa, Italy), Massimo Morfini
(Florence, Italy), and Maria D. Cappellini (Milan, Italy).
NR 40
TC 1
Z9 1
U1 0
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT 1
PY 2013
VL 54
IS 10
BP 1717
EP 1724
DI 10.2967/jnumed.113.121871
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 230LP
UT WOS:000325341300010
PM 23990684
ER
PT J
AU Gumuscu, B
Thompson, EI
Grovas, AC
Zach, TL
Warkentin, PI
Coccia, PF
AF Gumuscu, Burak
Thompson, Elizabeth I.
Grovas, Alfred C.
Zach, Terrence L.
Warkentin, Phyllis I.
Coccia, Peter F.
TI Successful Unrelated Cord Blood Transplantation For Homozygous
alpha-Thalassemia
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE homozygous -thalassemia; stem cell transplantation for
hemoglobinopathies; cord blood transplantation; hydrops fetalis
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; INTRAUTERINE
TRANSFUSIONS; BETA-THALASSEMIA; HYDROPS-FETALIS; IRON OVERLOAD; BARTS
HYDROPS; DISEASE; CHILDREN
AB A now 10-year-old Laotian female was delivered at 30-week gestation by cesarean section because of severe hydrops. Fetal blood sampling revealed homozygous -thalassemia. After immediate resuscitation, the infant was supported with frequent red cell transfusions. At 44 months of age, she received a 5 of 6 human leukocyte antigen-matched unrelated cord blood transplantation. She was treated with phlebotomy and chelation therapy with Deferasirox for correction of hemosiderosis and has been transfusion-independent since 41 days after transplant. She is currently 6 years after transplantation with stable, 100% donor engraftment, resolved iron overload, and normal growth and development.
C1 [Gumuscu, Burak] NCI, NIH, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Gumuscu, Burak] Childrens Natl Med Ctr, Dept Pediat Hematol Oncol, Washington, DC 20010 USA.
[Thompson, Elizabeth I.; Grovas, Alfred C.; Warkentin, Phyllis I.; Coccia, Peter F.] Univ Nebraska, Med Ctr, Dept Pediat, Div Hematol Oncol, Omaha, NE USA.
[Warkentin, Phyllis I.] Univ Nebraska, Med Ctr, Dept Pathol Microbiol, Omaha, NE USA.
[Zach, Terrence L.] Creighton Univ, Sch Med, Dept Pediat, Omaha, NE 68178 USA.
RP Coccia, PF (reprint author), Univ Nebraska, Med Ctr, Dept Pediat, 982168 Nebraska Med Ctr, Omaha, NE 68198 USA.
EM pcoccia@unmc.edu
NR 20
TC 3
Z9 3
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1077-4114
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD OCT
PY 2013
VL 35
IS 7
BP 570
EP 572
DI 10.1097/MPH.0b013e31827e7f6a
PG 3
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 228VS
UT WOS:000325220400031
PM 23337553
ER
PT J
AU Rajan, A
Kotlyar, D
Giaccone, G
AF Rajan, Arun
Kotlyar, David
Giaccone, Giuseppe
TI Acute Autoimmune Hepatitis, Myositis, and Myasthenic Crisis in a Patient
with Thymoma
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
ID GRAVIS
C1 [Rajan, Arun; Kotlyar, David; Giaccone, Giuseppe] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Giaccone, G (reprint author), NCI, Med Oncol Branch, 12N-226,10 Ctr Dr, Bethesda, MD 20892 USA.
EM giacconeg@mail.nih.gov
RI Giaccone, Giuseppe/E-8297-2017
OI Giaccone, Giuseppe/0000-0002-5023-7562
FU Intramural NIH HHS [Z01 BC010854-01]
NR 4
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD OCT
PY 2013
VL 8
IS 10
BP E87
EP E88
DI 10.1097/JTO.0b013e318298832b
PG 2
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 222SL
UT WOS:000324751300001
PM 24457247
ER
PT J
AU Izumi, T
Burdick, R
Shigemi, M
Plisov, S
Hu, WS
Pathak, VK
AF Izumi, Taisuke
Burdick, Ryan
Shigemi, Mayu
Plisov, Sergey
Hu, Wei-Shau
Pathak, Vinay K.
TI Mov10 and APOBEC3G Localization to Processing Bodies Is Not Required for
Virion Incorporation and Antiviral Activity
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIV-1 GENOMIC RNA; P-BODIES; 7SL RNA;
REVERSE TRANSCRIPTION; ANTIRETROVIRAL FACTOR; CYTIDINE DEAMINASES;
STRESS GRANULES; MESSENGER-RNAS; REPLICATION
AB Mov10 and APOBEC3G (A3G) localize to cytoplasmic granules called processing bodies (P bodies), incorporate into human immunodeficiency virus type 1 (HIV-1) virions, and inhibit viral replication. The functional relevance of Mov10/A3G P-body localization to virion incorporation and antiviral activity has not been fully explored. We found that a helicase V mutant of Mov10 exhibits significantly reduced localization to P bodies but still efficiently inhibits viral infectivity via virion incorporation. Disruption of the P bodies by DDX6 knockdown also confirmed Mov10 antiviral activity without P-body localization. In addition, overexpression of SRP19, which binds to 7SL RNA, depleted A3G from P bodies but did not affect its virion incorporation. Sucrose gradient sedimentation assays revealed that the majority of Mov10, A3G, HIV-1 RNA, and Gag formed high-molecular-mass (HMM) complexes that are converted to low-molecular-mass (LMM) complexes after RNase A treatment. In contrast, the P-body markers DCP2, LSM1, eIF4e, DDX6, and AGO1 were in LMM complexes, whereas AGO2, an effector protein of the RNA-induced silencing complex that localizes to P bodies, was present in both LMM and HMM complexes. Depletion of AGO2 indicated that RNA-induced silencing function is required for Mov10's ability to reduce Gag expression upon overexpression, but not its virion incorporation or effect on virus infectivity. We conclude that the majority of Mov10 and A3G are in HMM complexes, whereas most of the P-body markers are in LMM complexes, and that virion incorporation and the antiviral activities of Mov10 and A3G do not require their localization to P bodies.
C1 [Izumi, Taisuke; Burdick, Ryan; Shigemi, Mayu; Pathak, Vinay K.] NCI, Ctr Canc Res, HIV Drug Resistance Program, Viral Mutat Sect, Frederick, MD 21701 USA.
[Plisov, Sergey; Hu, Wei-Shau] NCI, Ctr Canc Res, HIV Drug Resistance Program, Viral Recombinat Sect, Frederick, MD 21701 USA.
RP Pathak, VK (reprint author), NCI, Ctr Canc Res, HIV Drug Resistance Program, Viral Mutat Sect, Frederick, MD 21701 USA.
EM vinay.pathak@nih.gov
RI Izumi, Taisuke/J-5607-2014
OI Izumi, Taisuke/0000-0002-9694-1459
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; JSPS Research Fellowship for Japanese
Biomedical and Behavioral Researchers at NIH
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research. T. I.
was supported by a JSPS Research Fellowship for Japanese Biomedical and
Behavioral Researchers at NIH.
NR 68
TC 14
Z9 14
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 OCT
PY 2013
VL 87
IS 20
BP 11047
EP 11062
DI 10.1128/JVI.02070-13
PG 16
WC Virology
SC Virology
GA 229OF
UT WOS:000325275800011
PM 23926332
ER
PT J
AU Sloan, EA
Kearney, MF
Gray, LR
Anastos, K
Daar, ES
Margolick, J
Maldarelli, F
Hammarskjold, ML
Rekosh, D
AF Sloan, Emily A.
Kearney, Mary F.
Gray, Laurie R.
Anastos, Kathryn
Daar, Eric S.
Margolick, Joseph
Maldarelli, Frank
Hammarskjold, Marie-Louise
Rekosh, David
TI Limited Nucleotide Changes in the Rev Response Element (RRE) during
HIV-1 Infection Alter Overall Rev-RRE Activity and Rev Multimerization
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; CTL ESCAPE VIRUS; HIV-1-INFECTED
INDIVIDUALS; PERIPHERAL-BLOOD; RAPID SELECTION; NUCLEAR-EXPORT; T-CELLS;
IN-VIVO; RNA; TRANSMISSION
AB HIV-1 Rev and the Rev response element (RRE) enable a critical step in the viral replication cycle by facilitating the nuclear export of intron-containing mRNAs, yet their activities have rarely been analyzed in natural infections. This study characterized their genetic and functional variation in a small cohort of HIV-infected individuals. Multiple Rev and RRE sequences were obtained using single-genome sequencing (SGS) of plasma samples collected within 6 months after seroconversion and at a later time. This allowed the identification of cognate sequences that were linked in vivo in the same viral genome and acted together as a functional unit. Phylogenetic analyses of these sequences indicated that 4/5 infections were founded by a single transmission event. Rev and RRE variants from each time point were subjected to functional analysis as both cognate pairs and as individual components. While a range of Rev-RRE activities were seen, the activity of cognate pairs from a single time point clustered to a discrete level, which was termed the set point. In 3/5 patients, this set point changed significantly over the time period studied. In all patients, RRE activity was more sensitive to sequence variation than Rev activity and acted as the primary driver of the cognate set point. Selected patient RREs were also shown to have differences in Rev multimerization using gel shift binding assays. Thus, rather than acting as a simple on-off switch or maintaining a constant level of activity throughout infection, the Rev-RRE system can fluctuate, presumably to control replication.
C1 [Sloan, Emily A.; Gray, Laurie R.; Hammarskjold, Marie-Louise; Rekosh, David] Univ Virginia, Dept Microbiol Immunol & Canc Biol, Charlottesville, VA 22903 USA.
[Sloan, Emily A.; Gray, Laurie R.; Hammarskjold, Marie-Louise; Rekosh, David] Univ Virginia, Myles H Thaler Ctr AIDS & Human Retrovirus Res, Charlottesville, VA USA.
[Kearney, Mary F.; Maldarelli, Frank] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA.
[Anastos, Kathryn] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Anastos, Kathryn] Montefiore Med Ctr, Dept Med, Bronx, NY 10467 USA.
[Daar, Eric S.] Univ Calif Los Angeles, Med Ctr, Angeles Biomed Res Inst Harbor, Torrance, CA 90509 USA.
[Margolick, Joseph] Johns Hopkins Bloomberg Sch Publ, Baltimore, MD USA.
RP Rekosh, D (reprint author), Univ Virginia, Dept Microbiol Immunol & Canc Biol, Charlottesville, VA 22903 USA.
EM dr4u@virginia.edu
FU National Institutes of Health [AI087505, AI068501, UO1-AI-35004];
University of Virginia
FX This work was supported by grants AI087505 and AI068501 as well as ARRA
supplements or other supplements to WIHS grant UO1-AI-35004 from the
National Institutes of Health. Salary support for M.-L.H. and D. R. was
provided by the Charles H. Ross, Jr., and Myles H. Thaler Endowments at
the University of Virginia.
NR 54
TC 9
Z9 10
U1 0
U2 8
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 OCT
PY 2013
VL 87
IS 20
BP 11173
EP 11186
DI 10.1128/JVI.01392-13
PG 14
WC Virology
SC Virology
GA 229OF
UT WOS:000325275800022
PM 23926352
ER
PT J
AU Govindasamy, L
DiMattia, MA
Gurda, BL
Halder, S
McKenna, R
Chiorini, JA
Muzyczka, N
Zolotukhin, S
Agbandje-McKenna, M
AF Govindasamy, Lakshmanan
DiMattia, Michael A.
Gurda, Brittney L.
Halder, Sujata
McKenna, Robert
Chiorini, John A.
Muzyczka, Nicholas
Zolotukhin, Sergei
Agbandje-McKenna, Mavis
TI Structural Insights into Adeno-Associated Virus Serotype 5
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ADENO-ASSOCIATED VIRUS; HEPARAN-SULFATE PROTEOGLYCAN; PHOTOREALISTIC
MOLECULAR GRAPHICS; LEBER CONGENITAL AMAUROSIS; MEDIATED GENE-THERAPY;
ELECTRON-DENSITY MAPS; AAV2 CAPSID GENE; EFFICIENT TRANSDUCTION;
SIALIC-ACID; TYPE-2 CAPSIDS
AB The adeno-associated viruses (AAVs) display differential cell binding, transduction, and antigenic characteristics specified by their capsid viral protein (VP) composition. Toward structure-function annotation, the crystal structure of AAV5, one of the most sequence diverse AAV serotypes, was determined to 3.45-angstrom resolution. The AAV5 VP and capsid conserve topological features previously described for other AAVs but uniquely differ in the surface-exposed HI loop between beta H and beta I of the core beta-barrel motif and have pronounced conformational differences in two of the AAV surface variable regions (VRs), VR-IV and VR-VII. The HI loop is structurally conserved in other AAVs despite amino acid differences but is smaller in AAV5 due to an amino acid deletion. This HI loop is adjacent to VR-VII, which is largest in AAV5. The VR-IV, which forms the larger outermost finger-like loop contributing to the protrusions surrounding the icosahedral 3-fold axes of the AAVs, is shorter in AAV5, creating a smoother capsid surface topology. The HI loop plays a role in AAV capsid assembly and genome packaging, and VR-IV and VR-VII are associated with transduction and antigenic differences, respectively, between the AAVs. A comparison of interior capsid surface charge and volume of AAV5 to AAV2 and AAV4 showed a higher propensity of acidic residues but similar volumes, consistent with comparable DNA packaging capacities. This structure provided a three-dimensional (3D) template for functional annotation of the AAV5 capsid with respect to regions that confer assembly efficiency, dictate cellular transduction phenotypes, and control antigenicity.
C1 [Govindasamy, Lakshmanan; DiMattia, Michael A.; Gurda, Brittney L.; Halder, Sujata; McKenna, Robert; Agbandje-McKenna, Mavis] Univ Florida, Coll Med, Dept Biochem & Mol Biol, Ctr Struct Biol,McKnight Brain Inst, Gainesville, FL 32610 USA.
[Chiorini, John A.] NIDCR, NIH, MPTB, Bethesda, MD USA.
[Muzyczka, Nicholas] Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Gainesville, FL USA.
[Muzyczka, Nicholas] Univ Florida, Coll Med, Powell Gene Therapy Ctr, Gainesville, FL USA.
[Zolotukhin, Sergei] Univ Florida, Coll Med, Dept Pediat, Div Cell & Mol Therapy, Gainesville, FL USA.
RP Agbandje-McKenna, M (reprint author), Univ Florida, Coll Med, Dept Biochem & Mol Biol, Ctr Struct Biol,McKnight Brain Inst, Gainesville, FL 32610 USA.
EM mckenna@ufl.edu
OI Gurda, Brittney /0000-0002-0174-9385
FU U.S. Department of Energy, Office of Science, Office of Basic Energy
Sciences [DE-AC02-98CH10886]; U.S. Department of Energy, Basic Energy
Sciences, Office of Science [W-31-109-Eng-38]; National Science
Foundation; National Institutes of Health/National Institute of General
Medical Sciences under NSF [DMR-0936384]; National Institute of General
Medical Sciences, National Institutes of Health [GM-103485]; Intramural
Research Program of the NIH; NIDCR; NIH [R01 GM082946, P01 HL51811]
FX The NSLS is supported by the U.S. Department of Energy, Office of
Science, Office of Basic Energy Sciences, under contract number
DE-AC02-98CH10886. Use of the Advanced Photon Source was supported by
the U.S. Department of Energy, Basic Energy Sciences, Office of Science,
under contract number W-31-109-Eng-38. CHESS is supported by the
National Science Foundation and the National Institutes of
Health/National Institute of General Medical Sciences under NSF award
DMR-0936384 and the MacCHESS facility through award GM-103485 from the
National Institute of General Medical Sciences, National Institutes of
Health. This research was supported by the Intramural Research Program
of the NIH and NIDCR to J.A.C. and NIH R01 GM082946 (M.A.-M., R. M.,
N.M., and S.Z.) and P01 HL51811 (M.A.-M., R. M., and N.M.).
NR 122
TC 18
Z9 18
U1 0
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 OCT
PY 2013
VL 87
IS 20
BP 11187
EP 11199
DI 10.1128/JVI.00867-13
PG 13
WC Virology
SC Virology
GA 229OF
UT WOS:000325275800023
PM 23926356
ER
PT J
AU Frey, S
Pircher, H
Follo, M
Collins, P
Krempl, C
Ehl, S
AF Frey, Stefanie
Pircher, Hanspeter
Follo, Marie
Collins, Peter
Krempl, Christine
Ehl, Stephan
TI In Situ Evolution of Virus-Specific Cytotoxic T Cell Responses in the
Lung
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; PNEUMONIA VIRUS; INFLUENZA-VIRUS; MICE;
INFECTION; DISEASE; PATHOGENESIS; EXPRESSION; IMMUNITY; MEMORY
AB Cytotoxic T cells (CTL) play a critical role in the clearance of respiratory viral infections, but they also contribute to disease manifestations. In this study, we infected mice with a genetically modified pneumonia virus of mice (PVM) that allowed visualization of virus-specific CTL and infected cells in situ. The first virus-specific T cells entered the lung via blood vessels in the scattered foci of PVM-infected cells, which densely clustered around the bronchi at day 7 after infection. At this time, overall pulmonary virus load was maximal, but the mice showed no overt signs of disease. On days 8 to 9, T cells gained access to the infected bronchial epithelium and to the lung interstitium, which was associated with a reduction in the number of virus-infected cells within the initial clusters but could not prevent further virus spread throughout the lung tissue. Interestingly, recruitment of virus-specific CTL throughout the parenchyma was still ongoing on day 10, when the virus infection was already largely controlled. This also represented the peak of clinical disease. Thus, disease was associated with an exuberant T cell infiltration late in the course of the infection, which may be required to completely eliminate virus at residual foci of infection. PVM-induced immunopathology may thus result from the need to generate widespread T cell infiltrates to complete the elimination of virus-infected cells in a large organ like the lung. This experimental model provides the first insights into the spatiotemporal evolution of pulmonary antiviral T cell immunity in vivo.
C1 [Frey, Stefanie; Ehl, Stephan] Univ Med Ctr Freiburg, Ctr Chron Immunodeficiency, Freiburg, Germany.
[Pircher, Hanspeter] Univ Freiburg, Inst Med Microbiol & Hyg, D-79106 Freiburg, Germany.
[Follo, Marie] Univ Med Ctr Freiburg, Dept Internal Med 1, Freiburg, Germany.
[Collins, Peter] NIAID, Bethesda, MD 20892 USA.
[Krempl, Christine] Julius Maximilian Univ, Inst Virol & Immunobiol, Wurzburg, Germany.
[Ehl, Stephan] Univ Med Ctr Freiburg, Ctr Pediat & Adolescent Med, Freiburg, Germany.
RP Ehl, S (reprint author), Univ Med Ctr Freiburg, Ctr Chron Immunodeficiency, Freiburg, Germany.
EM stephan.ehl@uniklinik-freiburg.de
RI Krempl, Christine/O-2081-2015
FU Bundesministerium fur Bildung und Forschung [BMBF 01 EO 0803]; Deutsche
Forschungsgemeinschaft [DFG EH145/4-2, KR2964/1-2]; Intramural Research
Program of NIAID, NIH
FX This work was supported by the Bundesministerium fur Bildung und
Forschung (BMBF 01 EO 0803) and the Deutsche Forschungsgemeinschaft (DFG
EH145/4-2 and KR2964/1-2). P. C. was supported by the Intramural
Research Program of NIAID, NIH.
NR 33
TC 1
Z9 1
U1 1
U2 12
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 OCT
PY 2013
VL 87
IS 20
BP 11267
EP 11275
DI 10.1128/JVI.00255-13
PG 9
WC Virology
SC Virology
GA 229OF
UT WOS:000325275800030
PM 23946463
ER
PT J
AU Bakkum-Gamez, JN
Wentzensen, N
Maurer, M
Podratz, K
Sherman, M
Shridhar, V
AF Bakkum-Gamez, Jamie N.
Wentzensen, Nicolas
Maurer, Matt
Podratz, Karl
Sherman, Mark
Shridhar, Viji
TI Detecting Endometrial Cancer Using the Common Tampon
SO JOURNAL OF WOMENS HEALTH
LA English
DT Meeting Abstract
C1 [Wentzensen, Nicolas; Sherman, Mark] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 OCT 1
PY 2013
VL 22
IS 10
BP 882
EP 882
PG 1
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 227TD
UT WOS:000325136500017
ER
PT J
AU Lai, C
Grant, C
Dunleavy, K
AF Lai, Catherine
Grant, Cliona
Dunleavy, Kieron
TI Interpreting MYC and BCL2 in diffuse large B-cell lymphoma
SO LEUKEMIA & LYMPHOMA
LA English
DT Editorial Material
ID RITUXIMAB PLUS CYCLOPHOSPHAMIDE; POOR-PROGNOSIS; C-MYC; VINCRISTINE;
DOXORUBICIN; PREDNISONE; EXPRESSION
C1 [Lai, Catherine; Grant, Cliona; Dunleavy, Kieron] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Dunleavy, K (reprint author), NCI, Metab Branch, Bldg 10,Room 4N-115,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM dunleavk@mail.nih.gov
NR 10
TC 3
Z9 3
U1 0
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD OCT
PY 2013
VL 54
IS 10
BP 2091
EP 2092
DI 10.3109/10428194.2013.806803
PG 2
WC Oncology; Hematology
SC Oncology; Hematology
GA 220MX
UT WOS:000324589800002
PM 24041377
ER
PT J
AU Cherry, BM
Korde, N
Kwok, M
Manasanch, EE
Bhutani, M
Mulquin, M
Zuchlinski, D
Yancey, MA
Maric, I
Calvo, KR
Braylan, R
Stetler-Stevenson, M
Yuan, C
Tembhare, P
Zingone, A
Costello, R
Roschewski, MJ
Landgren, O
AF Cherry, Benjamin M.
Korde, Neha
Kwok, Mary
Manasanch, Elisabet E.
Bhutani, Manisha
Mulquin, Marcia
Zuchlinski, Diamond
Yancey, Mary Ann
Maric, Irina
Calvo, Katherine R.
Braylan, Raul
Stetler-Stevenson, Maryalice
Yuan, Constance
Tembhare, Prashant
Zingone, Adriana
Costello, Rene
Roschewski, Mark J.
Landgren, Ola
TI Modeling progression risk for smoldering multiple myeloma: results from
a prospective clinical study
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Multiple myeloma; smoldering myeloma; disease classification
ID UNDETERMINED SIGNIFICANCE MGUS; EARLY TREATMENT STRATEGIES; LIGHT-CHAIN
RATIO; MONOCLONAL GAMMOPATHY; PRECURSOR DISEASE; FUTURE
AB The risk of progression to multiple myeloma (MM) from the precursor condition smoldering MM (SMM) varies considerably among individual patients. Reliable markers for progression to MM are vital to advance the understanding of myeloma precursor disease and for the development of intervention trials designed to delay/prevent MM. The Mayo Clinic and Spanish PETHEMA have proposed models to stratify patient risk based on clinical parameters. The aim of our study was to define the degree of concordance between these two models by comparing the distribution of patients with SMM classified as low, medium and high risk for progression. A total of 77 patients with SMM were enrolled in our prospective natural history study. Per study protocol, each patient was assigned risk scores based on both the Mayo and the Spanish models. The Mayo Clinic model identified 38, 35 and four patients as low, medium and high risk, respectively. The Spanish PETHEMA model classified 17, 22 and 38 patients as low, medium and high risk, respectively. There was significant discordance in overall patient risk classification (28.6% concordance) and in classifying patients as low versus high (p < 0.0001), low versus non-low (p = 0.0007) and high versus non-high (p < 0.0001) risk. There is a need for prospectively validated models to characterize individual patient risk of transformation to MM.
C1 [Cherry, Benjamin M.; Korde, Neha; Kwok, Mary; Manasanch, Elisabet E.; Bhutani, Manisha; Mulquin, Marcia; Zuchlinski, Diamond; Yancey, Mary Ann; Zingone, Adriana; Costello, Rene; Roschewski, Mark J.; Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Bethesda, MD 20892 USA.
[Kwok, Mary] Walter Reed Natl Mil Med Ctr, Bethesda, MD USA.
[Maric, Irina; Calvo, Katherine R.; Braylan, Raul] NIH, Hematol Serv, Dept Lab Med, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice; Yuan, Constance; Tembhare, Prashant] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Landgren, O (reprint author), NCI, Multiple Myeloma Sect, Metab Branch, NIH, 9000 Rockville Pike,Bldg 10 Room 13N240, Bethesda, MD 20892 USA.
EM landgreo@mail.nih.gov
OI Roschewski, Mark/0000-0003-0278-2635; Calvo,
Katherine/0000-0002-0771-4191
FU Intramural Research Program of the NCI of the National Institutes of
Health (NIH)
FX This work was supported by the Intramural Research Program of the NCI of
the National Institutes of Health (NIH).
NR 11
TC 30
Z9 30
U1 0
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD OCT
PY 2013
VL 54
IS 10
BP 2215
EP 2218
DI 10.3109/10428194.2013.764419
PG 4
WC Oncology; Hematology
SC Oncology; Hematology
GA 220MX
UT WOS:000324589800023
PM 23311294
ER
PT J
AU Jang, H
Subramanian, S
Devasahayam, N
Saito, K
Matsumoto, S
Krishna, MC
McMillan, AB
AF Jang, Hyungseok
Subramanian, Sankaran
Devasahayam, Nallathamby
Saito, Keita
Matsumoto, Shingo
Krishna, Murali C.
McMillan, Alan B.
TI Single Acquisition Quantitative Single-Point Electron Paramagnetic
Resonance Imaging
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE EPR imaging; quantitative imaging; single point imaging; gridding;
tissue oxygenation; hypoxia
ID DATA EXTRAPOLATION METHOD; TIME-DOMAIN EPR; TRUNCATION ARTIFACTS;
CYCLING HYPOXIA; TUMOR HYPOXIA; RESOLUTION; OXYGENATION; REMOVAL;
RECONSTRUCTION; TRANSFORM
AB PurposeElectron paramagnetic resonance imaging has emerged as a promising noninvasive technology to dynamically image tissue oxygenation. Owing to its extremely short spin-spin relaxation times, electron paramagnetic resonance imaging benefits from a single-point imaging scheme where the entire free induction decay signal is captured using pure phase encoding. However, direct T-2(*)/pO(2) quantification is inhibited owing to constant magnitude gradients which result in time-decreasing field of view. Therefore, conventional acquisition techniques require repeated imaging experiments with differing gradient amplitudes (typically 3), which results in long acquisition time.
MethodsIn this study, gridding was evaluated as a method to reconstruct images with equal field of view to enable direct T-2(*)/pO(2) quantification within a single imaging experiment. Additionally, an enhanced reconstruction technique that shares high spatial k-space regions throughout different phase-encoding time delays was investigated (k-space extrapolation).
ResultsThe combined application of gridding and k-space extrapolation enables pixelwise quantification of T-2(*) from a single acquisition with improved image quality across a wide range of phase-encoding time delays. The calculated T-2(*)/pO(2) does not vary across this time range.
ConclusionsBy utilizing gridding and k-space extrapolation, accurate T-2(*)/pO(2) quantification can be achieved within a single data set to allow enhanced temporal resolution (by a factor of 3). Magn Reson Med, 70:1173-1181, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Jang, Hyungseok; McMillan, Alan B.] Univ Wisconsin, Dept Radiol, Wisconsin Inst Med Res, Madison, WI 53706 USA.
[Subramanian, Sankaran; Devasahayam, Nallathamby; Saito, Keita; Matsumoto, Shingo; Krishna, Murali C.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP McMillan, AB (reprint author), Univ Wisconsin, Dept Radiol, Wisconsin Inst Med Res, Rm 1305,1111 Highland Ave, Madison, WI 53706 USA.
EM abmcmillan@wisc.edu
FU National Institute of Biomedical Imaging and Bioengineering of the
National Institutes of Health [1R21EB013770]
FX Grant sponsor: The National Institute of Biomedical Imaging and
Bioengineering of the National Institutes of Health under Award Number
1R21EB013770.
NR 33
TC 3
Z9 3
U1 0
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD OCT
PY 2013
VL 70
IS 4
BP 1173
EP 1181
DI 10.1002/mrm.24886
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 227TB
UT WOS:000325136300030
PM 23913515
ER
PT J
AU Valera, A
Colomo, L
Martinez, A
de Jong, D
Balague, O
Matheu, G
Martinez, M
Taddesse-Heath, L
Jaffe, ES
Bacchi, CE
Campo, E
AF Valera, Alexandra
Colomo, Lluis
Martinez, Antonio
de Jong, Daphne
Balague, Olga
Matheu, Gabriel
Martinez, Monica
Taddesse-Heath, Lekidelu
Jaffe, Elaine S.
Bacchi, Carlos E.
Campo, Elias
TI ALK-positive large B-cell lymphomas express a terminal B-cell
differentiation program and activated STAT3 but lack MYC rearrangements
SO MODERN PATHOLOGY
LA English
DT Article
DE ALK-positive large B-cell lymphoma; ALK; MYC; plasmablastic lymphoma;
STAT3
ID T(2/5)(P23,Q35) CHROMOSOME-TRANSLOCATION; OF-THE-LITERATURE; C-MYC;
CLINICOPATHOLOGICAL ENTITY; PLASMABLASTIC LYMPHOMA; COMPLEX KARYOTYPE;
KINASE; FUSION; TRANSCRIPTION; PROGNOSIS
AB ALK-positive large B-cell lymphoma is an aggressive lymphoid neoplasm characterized by a monomorphic proliferation of immunoblast-like cells expressing a plasmablastic phenotype and carrying ALK rearrangements. MYC rearrangements are frequent in plasmablastic lymphomas, advanced plasma cell myelomas and a subgroup of diffuse large B-cell lymphomas, but their presence in ALK-positive large B-cell lymphomas is unknown. MYC expression is downregulated by BLIMP1, a master modulator of plasma cell differentiation. BLIMP1 and MYC are upregulated by STAT3, a signal transducer activated by ALK. To determine the role of BLIMP1, MYC and STAT3 in the pathogenesis of ALK-positive large B-cell lymphomas, we investigated MYC rearrangement and the expression of MYC, phosphorylated STAT3, BLIMP1, PAX5 and XBP1 in 12 ALK-positive large B-cell lymphomas. All cases expressed ALK with a granular cytoplasmic pattern. Nine cases had a split signal consistent with an ALK rearrangement. Three additional cases showed a deletion of the 50 or 30 end of the ALK probe consistent with cryptic translocation. PAX5 was virtually negative in all cases tested, whereas BLIMP1 was expressed in all tumors and XBP1 in 11 of 12. Phosphorylated STAT3 was observed in all cases with a strong and diffuse nuclear pattern. MYC rearrangements were not identified in any tumor, but MYC gains and amplification were detected in six cases and one case, respectively. MYC protein was expressed in all tumors independently of MYC gene alterations. These results indicate that ALK-positive large B-cell lymphomas express a complete plasmablastic differentiation program but, contrary to plasmablastic lymphomas, do not have MYC rearrangements. STAT3 is constantly activated and may be an alternative mechanism to promote MYC expression in these tumors. The relevance of the ALK/STAT3 pathway in the pathogenesis of ALK-positive large B-cell lymphomas may offer an attractive target for new therapies.
C1 [Valera, Alexandra; Colomo, Lluis; Martinez, Antonio; Campo, Elias] Univ Barcelona, Hematopathol Sect, Pathol Lab, Hosp Clin Barcelona,Inst Invest Biomed August Pi, E-08036 Barcelona, Spain.
[de Jong, Daphne; Balague, Olga] Antoni Leeuwenhoek Hosp, Netherlands Canc Inst, Dept Pathol, Amsterdam, Netherlands.
[Matheu, Gabriel] Hosp Manacor, Dept Pathol, Mallorca, Spain.
[Martinez, Monica] Lab Hematopatol, Mendoza, Argentina.
[Taddesse-Heath, Lekidelu] Howard Univ Hosp, Dept Pathol, Washington, DC USA.
[Jaffe, Elaine S.] NCI, Dept Pathol, NIH, Bethesda, MD USA.
[Bacchi, Carlos E.] Consultoria Patol, Botucatu, SP, Brazil.
RP Campo, E (reprint author), Univ Barcelona, Hematopathol Sect, Pathol Lab, Hosp Clin Barcelona,Inst Invest Biomed August Pi, Villarroel 170, E-08036 Barcelona, Spain.
EM ecampo@clinic.ub.es
RI Jaffe, Elaine/G-8984-2014; Colomo, Luis/A-2259-2016;
OI Jaffe, Elaine/0000-0003-4632-0301; Colomo, Luis/0000-0001-5236-5085;
Campo, elias/0000-0001-9850-9793
FU 'Comision Interministerial de Ciencia y Tecnologia Espanola' (CICYT)
[SAF 12/38432]; Red Tematica de Investigacion Cooperativa del Cancer
(RTICC) [RD12/0036/0086]; Conveni Programa de Feno/Genotipatge per al
diagnostic i tractament individualitzat del pacient oncologic, La Caixa
FX We thank Elena Gonzalvo, Laura Gelabert and Monica Marin for their
excellent technical assistance. This study was funded by 'Comision
Interministerial de Ciencia y Tecnologia Espanola' (CICYT) SAF 12/38432,
Red Tematica de Investigacion Cooperativa del Cancer (RTICC)
(RD12/0036/0086) and 'Conveni Programa de Feno/Genotipatge per al
diagnostic i tractament individualitzat del pacient oncologic, La
Caixa'. Figure 3 was produced using Servier Medical Art
(http://www.servier.com/).
NR 57
TC 9
Z9 10
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD OCT
PY 2013
VL 26
IS 10
BP 1329
EP 1337
DI 10.1038/modpathol.2013.73
PG 9
WC Pathology
SC Pathology
GA 228TR
UT WOS:000325214000006
PM 23599149
ER
PT J
AU Li, SL
Park, H
Trempus, CS
Gordon, D
Liu, YP
Cotsarelis, G
Morris, RJ
AF Li, Shulan
Park, Heuijoon
Trempus, Carol S.
Gordon, Derek
Liu, Yaping
Cotsarelis, George
Morris, Rebecca J.
TI A Keratin 15 Containing Stem Cell Population From the Hair Follicle
Contributes to Squamous Papilloma Development in the Mouse
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE skin carcinogenesis; stem cells; hair follicles; papillomas
ID SKIN-CANCER; EPIDERMAL TUMORS; CARCINOGENESIS; EXPRESSION; BULGE; RAS;
CARCINOMAS; INITIATION; PROMOTION; TARGETS
AB The multistage model of nonmelanoma skin carcinogenesis has contributed significantly to our understanding of epithelial cancer in general. We used the Krt1-15CrePR1;R26R transgenic mouse to determine the contribution of keratin 15+ cells from the hair follicle to skin tumor development by following the labeled progeny of the keratin 15 expressing cells into papillomas. We present three novel observations. First, we found that keratin 15 expressing cells contribute to most of the papillomas by 20 weeks of promotion. Second, in contrast to the transient behavior of labeled keratin 15-derived progeny in skin wound healing, keratin 15 progeny persist in papillomas, and some malignancies for many months following transient induction of the reporter gene. Third, papillomas have surprising heterogeneity not only in their cellular composition, but also in their expression of the codon 61 signature Ha-ras mutation with approximately 30% of keratin 15-derived regions expressing the mutation. Together, these results demonstrate that keratin 15 expressing cells of the hair follicle contribute to cutaneous papillomas with long term persistence and a subset of which express the Ha-ras signature mutation characteristic of initiated cells. (c) 2012 Wiley Periodicals, Inc.
C1 [Li, Shulan; Park, Heuijoon; Morris, Rebecca J.] Columbia Univ, Dept Dermatol, Med Ctr, New York, NY 10027 USA.
[Trempus, Carol S.] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Gordon, Derek] Rutgers State Univ, Dept Genet, Piscataway, NJ USA.
[Liu, Yaping; Cotsarelis, George] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
[Morris, Rebecca J.] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
RP Morris, RJ (reprint author), Univ Minnesota, Hormel Inst, 801 16th Ave NE, Austin, MN 55912 USA.
FU NIH [CA097957]
FX This work was supported by NIH grant CA097957 to R.J.M. and G. C. This
work was conducted (in part) in the Intramural Research Program of the
NIH and National Institute of Environmental Health Sciences (NIEHS). We
thank Leon C. King from the National Health and Environmental Effects
Research Laboratory, United States Environmental Protection Agency,
Research Triangle Park, NC for performing the adduct analysis. We thank
Xiao-Jing Wang of the Department of Dermatology, OHSU for providing the
CrePr1 construct. We also thank Ann Bode and Ashok Singh of The Hormel
Institute for critically reading the manuscript and for their helpful
suggestions, and Ashok Singh for assistance with submission of the
manuscript.
NR 31
TC 8
Z9 8
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0899-1987
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD OCT
PY 2013
VL 52
IS 10
BP 751
EP 759
DI 10.1002/mc.21896
PG 9
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA 227JL
UT WOS:000325108800001
PM 22431489
ER
PT J
AU Jefferson, WN
Chevalier, DM
Phelps, JY
Cantor, AM
Padilla-Banks, E
Newbold, RR
Archer, TK
Kinyamu, HK
Williams, CJ
AF Jefferson, Wendy N.
Chevalier, Dominique M.
Phelps, Jazma Y.
Cantor, Amy M.
Padilla-Banks, Elizabeth
Newbold, Retha R.
Archer, Trevor K.
Kinyamu, H. Karimi
Williams, Carmen J.
TI Persistently Altered Epigenetic Marks in the Mouse Uterus After Neonatal
Estrogen Exposure
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID ENDOCRINE-DISRUPTING CHEMICALS; POLYCOMB GROUP PROTEINS; EMBRYONIC
STEM-CELLS; DIETHYLSTILBESTROL EXPOSURE; REPRODUCTIVE-TRACT;
DEVELOPMENTAL EXPOSURE; LACTOFERRIN GENE; HISTONE H3; EXPRESSION;
RECEPTOR
AB Neonatal exposure to diethylstilbestrol (DES) causes permanent alterations in female reproductive tract gene expression, infertility, and uterine cancer in mice. To determine whether epigenetic mechanisms could explain these phenotypes, we first tested whether DES altered uterine expression of chromatin-modifying proteins. DES treatment significantly reduced expression of methylcytosine dioxygenase TET oncogene family, member 1 (TET1) on postnatal day 5; this decrease was correlated with a subtle decrease in DNA 5-hydroxymethylcytosine in adults. There were also significant reductions in histone methyltransferase enhancer of zeste homolog 2 (EZH2), histone lysine acetyltransferase 2A (KAT2A), and histone deacetylases HDAC1, HDAC2, and HDAC3. Uterine chromatin immunoprecipitation was used to analyze the locus-specific association of modified histones with 2 genes, lactoferrin (Ltf) and sine oculis homeobox 1 (Six1), which are permanently upregulated in adults after neonatal DES treatment. Three histone modifications associated with active transcription, histone H3 lysine 9 acetylation (H3K9ac), H3 lysine 4 trimethylation (H3K4me3), and H4 lysine 5 acetylation (H4K5ac) were enriched at specific Ltf promoter regions after DES treatment, but this enrichment was not maintained in adults. H3K9ac, H4K5ac, and H3K4me3 were enriched at Six1 exon 1 immediately after neonatal DES treatment. As adults, DES-treated mice had greater differences in H4K5ac and H3K4me3 occupancy at Six1 exon 1 and new differences in these histone marks at an upstream region. These findings indicate that neonatal DES exposure temporarily alters expression of multiple chromatin-modifying proteins and persistently alters epigenetic marks in the adult uterus at the Six1 locus, suggesting a mechanism for developmental exposures leading to altered reproductive function and increased cancer risk.
C1 [Jefferson, Wendy N.; Chevalier, Dominique M.; Phelps, Jazma Y.; Cantor, Amy M.; Padilla-Banks, Elizabeth; Williams, Carmen J.] NIEHS, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Archer, Trevor K.; Kinyamu, H. Karimi] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Newbold, Retha R.] NIEHS, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
RP Williams, CJ (reprint author), NIEHS, NIH, US Dept Hlth & Human Serv, POB 12233,MD E4-05, Res Triangle Pk, NC 27709 USA.
EM williamsc5@niehs.nih.gov
RI Williams, Carmen/E-2170-2013
OI Williams, Carmen/0000-0001-6440-7086
FU Intramural Research Program of the National Institutes of Health,
National Institutes of Environmental Health Sciences [ES102405,
ES071006]
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institutes of Environmental
Health Sciences, ES102405 (to C.J.W.) and ES071006 (to T.K.A.).
NR 51
TC 14
Z9 14
U1 0
U2 8
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 OCT
PY 2013
VL 27
IS 10
BP 1666
EP 1677
DI 10.1210/me.2013-1211
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 226YA
UT WOS:000325071600009
PM 24002655
ER
PT J
AU ZeRuth, GT
Takeda, Y
Jetten, AM
AF ZeRuth, Gary T.
Takeda, Yukimasa
Jetten, Anton M.
TI The Kruppel-Like Protein Gli-Similar 3 (Glis3) Functions as a Key
Regulator of Insulin Transcription
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID NEONATAL DIABETES-MELLITUS; LOOP-HELIX PROTEIN; BETA-CELL FUNCTION;
GENE-TRANSCRIPTION; ZINC-FINGER; ACETYLTRANSFERASE ACTIVITY;
PHYSIOLOGICAL FUNCTIONS; P300; ACTIVATION; ASSOCIATION
AB Transcriptional regulation of insulin in pancreatic beta-cells is mediated primarily through enhancer elements located within the 5' upstream regulatory region of the preproinsulin gene. Recently, the Kruppel-like transcription factor, Gli-similar 3 (Glis3), was shown to bind the insulin (INS) promoter and positively influence insulin transcription. In this report, we examined in detail the synergistic activation of insulin transcription by Glis3 with coregulators, CREB-binding protein (CBP)/p300, pancreatic and duodenal homeobox 1 (Pdx1), neuronal differentiation 1 (NeuroD1), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA). Our data show that Glis3 expression, the binding of Glis3 to GlisBS, and its recruitment of CBP are required for optimal activation of the insulin promoter in pancreatic beta-cells not only by Glis3, but also by Pdx1, MafA, and NeuroD1. Mutations in the GlisBS or small interfering RNA-directed knockdown of GLIS3 diminished insulin promoter activation by Pdx1, NeuroD1, and MafA, and neither Pdx1 nor MafA was able to stably associate with the insulin promoter when the GlisBS were mutated. In addition, a GlisBS mutation in the INS promoter implicated in the development of neonatal diabetes similarly abated activation by Pdx1, NeuroD1, and MafA that could be reversed by increased expression of exogenous Glis3. We therefore propose that recruitment of CBP/p300 by Glis3 provides a scaffold for the formation of a larger transcriptional regulatory complex that stabilizes the binding of Pdx1, NeuroD1, and MafA complexes to their respective binding sites within the insulin promoter. Taken together, these results indicate that Glis3 plays a pivotal role in the transcriptional regulation of insulin and may serve as an important therapeutic target for the treatment of diabetes.
C1 [ZeRuth, Gary T.; Takeda, Yukimasa; Jetten, Anton M.] NIEHS, Cell Biol Sect, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
RP Jetten, AM (reprint author), NIEHS, 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 Intramural Research Program of the National Institute of Environmental
Health Sciences, National Institutes of Health [Z01-ES-100485]
FX This work was supported by the Intramural Research Program of the
National Institute of Environmental Health Sciences, National Institutes
of Health (Z01-ES-100485).
NR 45
TC 13
Z9 13
U1 0
U2 4
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 OCT
PY 2013
VL 27
IS 10
BP 1692
EP 1705
DI 10.1210/me.2013-1117
PG 14
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 226YA
UT WOS:000325071600011
PM 23927931
ER
PT J
AU Ikonomidou, VN
Richert, ND
Vortmeyer, A
Tovar-Moll, F
Bielekova, B
Cook, NE
Duyn, JH
Bagnato, F
AF Ikonomidou, Vasiliki N.
Richert, Nancy D.
Vortmeyer, Alexander
Tovar-Moll, Fernanda
Bielekova, Bibiana
Cook, Natalie E.
Duyn, Jeff H.
Bagnato, Francesca
TI Evolution of tumefactive lesions in multiple sclerosis: A 12-year study
with serial imaging in a single patient
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Article
DE Multiple sclerosis; tumefactive lesion; magnetic resonance imaging;
recovery; magnetization transfer imaging; tissue-specific imaging
AB We describe the acute presentation and the long-term evolution of recurrent tumefactive lesions (TLs) in a patient with relapsing-remitting multiple sclerosis. Five TLs occurred on three different occasions over a period of 12 years and these were followed by 73 serial magnetic resonance images (MRI). TL evolution was described by means of magnetization transfer imaging (MTI) and cerebrospinal fluid tissue specific imaging (TSI) over the follow-up period. During the study period, the patient had three clinical relapses with only minimal disability progression. MTI demonstrated that only the peripheral portion of each TL reverted to pre-lesional MT ratios within six months' post-enhancement. Recurring TLs may present a similar pattern of evolution that may be associated with a long-term favourable clinical outcome.
C1 [Ikonomidou, Vasiliki N.] George Mason Univ, Volgenau Sch Engn, Dept Bioengn, Fairfax, VA 22030 USA.
[Ikonomidou, Vasiliki N.; Richert, Nancy D.; Tovar-Moll, Fernanda; Bielekova, Bibiana; Cook, Natalie E.; Bagnato, Francesca] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Vortmeyer, Alexander] NINDS, Neurosurg Branch, NIH, Bethesda, MD 20892 USA.
[Duyn, Jeff H.] NINDS, Adv MRI Sect, LFMI, NIH, Bethesda, MD 20892 USA.
[Bagnato, Francesca] Univ Maryland, Dept Neurol, Baltimore, MD 21201 USA.
RP Bagnato, F (reprint author), Univ Maryland, Dept Neurol, 110 Paca St, Baltimore, MD 21201 USA.
EM fbagnato@umm.edu
FU Intramural Research Program of the NINDS-NIH
FX This research was supported by the Intramural Research Program of the
NINDS-NIH.
NR 9
TC 1
Z9 2
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER J
JI Mult. Scler. J.
PD OCT
PY 2013
VL 19
IS 11
BP 1539
EP 1543
DI 10.1177/1352458513498124
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 222QE
UT WOS:000324745400016
PM 24062416
ER
PT J
AU Hyde, RK
Liu, PP
AF Hyde, R. Katherine
Liu, P. Paul
TI Germline PAX5 mutations and B cell leukemia
SO NATURE GENETICS
LA English
DT Editorial Material
ID ACUTE MYELOID-LEUKEMIA; GATA2
C1 [Hyde, R. Katherine; Liu, P. Paul] US Natl Inst Hlth, Natl Human Genome Res Inst, Genet & Mol Biol Branch, Bethesda, MD USA.
RP Hyde, RK (reprint author), US Natl Inst Hlth, Natl Human Genome Res Inst, Genet & Mol Biol Branch, Bethesda, MD USA.
EM pliu@nhgri.nih.gov
OI Hyde, R. Katherine/0000-0003-2808-1749
NR 11
TC 1
Z9 1
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2013
VL 45
IS 10
SI SI
BP 1104
EP 1105
DI 10.1038/ng.2778
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA 225UQ
UT WOS:000324989600002
PM 24071841
ER
PT J
AU Weinstein, JN
Collisson, EA
Mills, GB
Shaw, KRM
Ozenberger, BA
Ellrott, K
Shmulevich, I
Sander, C
Stuart, JM
AF Weinstein, John N.
Collisson, Eric A.
Mills, Gordon B.
Shaw, Kenna R. Mills
Ozenberger, Brad A.
Ellrott, Kyle
Shmulevich, Ilya
Sander, Chris
Stuart, Joshua M.
CA Canc Genome Atlas Res Network
TI The Cancer Genome Atlas Pan-Cancer analysis project
SO NATURE GENETICS
LA English
DT Editorial Material
ID SQUAMOUS-CELL CARCINOMA; HUMAN BREAST-TUMORS; LUNG-CANCER; MOLECULAR
PORTRAITS; DRUG-SENSITIVITY; PROSTATE-CANCER; MUTATIONS; GENE;
IDENTIFICATION; HALLMARKS
AB The Cancer Genome Atlas (TCGA) Research Network has profiled and analyzed large numbers of human tumors to discover molecular aberrations at the DNA, RNA, protein and epigenetic levels. The resulting rich data provide a major opportunity to develop an integrated picture of commonalities, differences and emergent themes across tumor lineages. The Pan-Cancer initiative compares the first 12 tumor types profiled by TCGA. Analysis of the molecular aberrations and their functional roles across tumor types will teach us how to extend therapies effective in one cancer type to others with a similar genomic profile.
C1 [Weinstein, John N.] Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.
[Weinstein, John N.; Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
[Collisson, Eric A.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Shaw, Kenna R. Mills] NCI, Ctr Canc Genom, The Canc Genome Atlas Program Off, Bethesda, MD 20892 USA.
[Shaw, Kenna R. Mills] Univ Texas MD Anderson Canc Ctr, Inst Personalized Canc Therapy, Houston, TX 77030 USA.
[Ozenberger, Brad A.] US Natl Inst Hlth, Natl Human Genome Res Inst, Bethesda, MD USA.
[Ellrott, Kyle; Stuart, Joshua M.] Univ Calif Santa Cruz, Dept Biomol Engn, Santa Cruz, CA 95064 USA.
[Ellrott, Kyle; Stuart, Joshua M.] Univ Calif Santa Cruz, Ctr Biomol Sci & Engn, Santa Cruz, CA 95064 USA.
[Shmulevich, Ilya] Inst Syst Biol, Seattle, WA USA.
[Sander, Chris] Mem Sloan Kettering Canc Ctr, Computat Biol Ctr, New York, NY 10021 USA.
RP Stuart, JM (reprint author), Univ Calif Santa Cruz, Dept Biomol Engn, Santa Cruz, CA 95064 USA.
EM jstuart@ucsc.edu
RI Reva, Boris/B-6436-2014; Tang, Macy/B-9798-2014; Vaske,
Charles/D-6018-2013; Senbabaoglu, Yasin/I-4922-2013; Li,
Jun/O-9911-2014; Yuan, Yuan/H-4007-2013; Jacobsen, Anders/K-1081-2013;
tamborero, david/M-5283-2015; Gao, Jianjiong/B-5673-2016; Hirst,
Martin/B-7684-2016; Lee, Semin/S-2629-2016; Marra, Marco/B-5987-2008;
OI Sinha, Rileen/0000-0001-5497-5055; Herbrich,
Shelley/0000-0002-3825-6752; Ellrott, Kyle/0000-0002-6573-5900; Yang,
Da/0000-0002-8336-9457; Xia, Zheng/0000-0003-3364-8324; Perou,
Charles/0000-0001-9827-2247; Gehlenborg, Nils/0000-0003-0327-8297;
Miller, Martin L/0000-0003-3161-8690; Reva, Boris/0000-0002-8805-389X;
Schultz, Nikolaus/0000-0002-0131-4904; Kandoth,
Cyriac/0000-0002-1345-3573; Benz, Stephen/0000-0002-4067-0602; Seth,
Sahil/0000-0003-4579-3959; Lopez-Bigas, Nuria/0000-0003-4925-8988; Pot,
David/0000-0002-1480-9826; Gonzalez-Perez, Abel/0000-0002-8582-4660;
Vaske, Charles/0000-0001-8151-6612; Senbabaoglu,
Yasin/0000-0003-0958-958X; Li, Jun/0000-0002-1171-7141; Yuan,
Yuan/0000-0003-4706-7897; Jacobsen, Anders/0000-0001-6847-4980;
tamborero, david/0000-0002-7218-2806; Gao,
Jianjiong/0000-0002-5739-1781; Lee, Semin/0000-0002-9015-6046; Ojesina,
Akinyemi/0000-0003-0755-3639; Nelander, Sven/0000-0003-1758-1262
NR 43
TC 484
Z9 497
U1 23
U2 81
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2013
VL 45
IS 10
SI SI
BP 1113
EP 1120
DI 10.1038/ng.2764
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 225UQ
UT WOS:000324989600005
ER
PT J
AU Westra, HJ
Peters, MJ
Esko, T
Yaghootkar, H
Schurmann, C
Kettunen, J
Christiansen, MW
Fairfax, BP
Schramm, K
Powell, JE
Zhernakova, A
Zhernakova, DV
Veldink, JH
Van den Berg, LH
Karjalainen, J
Withoff, S
Uitterlinden, AG
Hofman, A
Rivadeneira, F
't Hoen, PAC
Reinmaa, E
Fischer, K
Nelis, M
Milani, L
Melzer, D
Ferrucci, L
Singleton, AB
Hernandez, DG
Nalls, MA
Homuth, G
Nauck, M
Radke, D
Volker, U
Perola, M
Salomaa, V
Brody, J
Suchy-Dicey, A
Gharib, SA
Enquobahrie, DA
Lumley, T
Montgomery, GW
Makino, S
Prokisch, H
Herder, C
Roden, M
Grallert, H
Meitinger, T
Strauch, K
Li, Y
Jansen, RC
Visscher, PM
Knight, JC
Psaty, BM
Ripatti, S
Teumer, A
Frayling, TM
Metspalu, A
van Meurs, JBJ
Franke, L
AF Westra, Harm-Jan
Peters, Marjolein J.
Esko, Tonu
Yaghootkar, Hanieh
Schurmann, Claudia
Kettunen, Johannes
Christiansen, Mark W.
Fairfax, Benjamin P.
Schramm, Katharina
Powell, Joseph E.
Zhernakova, Alexandra
Zhernakova, Daria V.
Veldink, Jan H.
Van den Berg, Leonard H.
Karjalainen, Juha
Withoff, Sebo
Uitterlinden, Andre G.
Hofman, Albert
Rivadeneira, Fernando
't Hoen, Peter A. C.
Reinmaa, Eva
Fischer, Krista
Nelis, Mari
Milani, Lili
Melzer, David
Ferrucci, Luigi
Singleton, Andrew B.
Hernandez, Dena G.
Nalls, Michael A.
Homuth, Georg
Nauck, Matthias
Radke, Doerte
Voelker, Uwe
Perola, Markus
Salomaa, Veikko
Brody, Jennifer
Suchy-Dicey, Astrid
Gharib, Sina A.
Enquobahrie, Daniel A.
Lumley, Thomas
Montgomery, Grant W.
Makino, Seiko
Prokisch, Holger
Herder, Christian
Roden, Michael
Grallert, Harald
Meitinger, Thomas
Strauch, Konstantin
Li, Yang
Jansen, Ritsert C.
Visscher, Peter M.
Knight, Julian C.
Psaty, Bruce M.
Ripatti, Samuli
Teumer, Alexander
Frayling, Timothy M.
Metspalu, Andres
van Meurs, Joyce B. J.
Franke, Lude
TI Systematic identification of trans eQTLs as putative drivers of known
disease associations
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GENE-EXPRESSION; LUPUS-ERYTHEMATOSUS;
MYOCARDIAL-INFARCTION; SUSCEPTIBILITY LOCI; RISK; POPULATION; BLOOD;
INTERFERON; VARIANTS
AB Identifying the downstream effects of disease-associated SNPs is challenging. To help overcome this problem, we performed expression quantitative trait locus (eQTL) meta-analysis in non-transformed peripheral blood samples from 5,311 individuals with replication in 2,775 individuals. We identified and replicated trans eQTLs for 233 SNPs (reflecting 103 independent loci) that were previously associated with complex traits at genome-wide significance. Some of these SNPs affect multiple genes in trans that are known to be altered in individuals with disease: rs4917014, previously associated with systemic lupus erythematosus (SLE)(1), altered gene expression of C1QB and five type I interferon response genes, both hallmarks of SLE2-4. DeepSAGE RNA sequencing showed that rs4917014 strongly alters the 3' UTR levels of IKZF1 in cis, and chromatin immunoprecipitation and sequencing analysis of the trans-regulated genes implicated IKZF1 as the causal gene. Variants associated with cholesterol metabolism and type 1 diabetes showed similar phenomena, indicating that large-scale eQTL mapping provides insight into the downstream effects of many trait-associated variants.
C1 [Westra, Harm-Jan; Zhernakova, Alexandra; Zhernakova, Daria V.; Karjalainen, Juha; Withoff, Sebo; Franke, Lude] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Peters, Marjolein J.; Uitterlinden, Andre G.; Rivadeneira, Fernando; van Meurs, Joyce B. J.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Peters, Marjolein J.; Uitterlinden, Andre G.; Hofman, Albert; Rivadeneira, Fernando; van Meurs, Joyce B. J.] Netherlands Genom Initiat Sponsored Netherlands C, Leiden, Netherlands.
[Peters, Marjolein J.; Uitterlinden, Andre G.; Hofman, Albert; Rivadeneira, Fernando; van Meurs, Joyce B. J.] Netherlands Genom Initiat Sponsored Netherlands C, Rotterdam, Netherlands.
[Esko, Tonu; Reinmaa, Eva; Fischer, Krista; Nelis, Mari; Milani, Lili; Perola, Markus; Metspalu, Andres] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
[Yaghootkar, Hanieh; Frayling, Timothy M.] Univ Exeter, Sch Med, Exeter, Devon, England.
[Schurmann, Claudia; Homuth, Georg; Voelker, Uwe; Teumer, Alexander] Univ Med Greifswald, Interfac Inst Genet & Funct Genom, Dept Funct Genom, Greifswald, Germany.
[Kettunen, Johannes; Ripatti, Samuli] Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki, Finland.
[Kettunen, Johannes; Perola, Markus; Salomaa, Veikko; Ripatti, Samuli] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Christiansen, Mark W.; Brody, Jennifer; Psaty, Bruce M.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Fairfax, Benjamin P.; Makino, Seiko; Knight, Julian C.] Wellcome Trust Ctr Human Genet, Oxford, England.
[Fairfax, Benjamin P.] Churchill Hosp, Canc & Haematol Ctr, Dept Oncol, Oxford OX3 7LJ, England.
[Schramm, Katharina; Prokisch, Holger; Meitinger, Thomas] Helmholz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Human Genet, Neuherberg, Germany.
[Schramm, Katharina; Prokisch, Holger; Meitinger, Thomas] Tech Univ Munich, Inst Human Genet, D-80290 Munich, Germany.
[Powell, Joseph E.; Visscher, Peter M.] Univ Queensland, Princess Alexandra Hosp, Diamantina Inst, Brisbane, Qld, Australia.
[Powell, Joseph E.; Visscher, Peter M.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
[Veldink, Jan H.; Van den Berg, Leonard H.] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Neurol, Utrecht, Netherlands.
[Uitterlinden, Andre G.; Hofman, Albert; Rivadeneira, Fernando] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
['t Hoen, Peter A. C.] Leiden Univ Med Ctr, Ctr Human & Clin Genet, Leiden, Netherlands.
[Melzer, David] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Exeter, Devon, England.
[Ferrucci, Luigi] NIA, Clin Res Branch, Adv Studies Translat Res Aging ASTRA Unit, Harbor Hosp, Baltimore, MD 21224 USA.
[Singleton, Andrew B.; Hernandez, Dena G.; Nalls, Michael A.] NIA, Neurogenet Lab, US NIH, Bethesda, MD 20892 USA.
[Hernandez, Dena G.] UCL, Inst Neurol, Reta Lila Labs, Dept Mol Neurosci, London, England.
[Nauck, Matthias] Univ Med Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
[Radke, Doerte] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
[Suchy-Dicey, Astrid; Enquobahrie, Daniel A.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Gharib, Sina A.] Univ Washington, Ctr Lung Biol, Dept Med, Div Pulm & Crit Care Med,Computat Med Core, Seattle, WA 98195 USA.
[Lumley, Thomas] Univ Auckland, Dept Stat, Auckland 1, New Zealand.
[Montgomery, Grant W.] Queensland Inst Med Res, Herston, Qld 4006, Australia.
[Herder, Christian; Roden, Michael] Univ Dusseldorf, Leibniz Ctr Diabet Res, German Diabet Ctr, Inst Clin Diabetol, D-40225 Dusseldorf, Germany.
[Roden, Michael] Univ Dusseldorf, Univ Hosp Dusseldorf, Dept Endocrinol & Diabetol, D-40225 Dusseldorf, Germany.
[Roden, Michael] Univ Dusseldorf, Univ Hosp Dusseldorf, Dept Metab Dis, D-40225 Dusseldorf, Germany.
[Grallert, Harald] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Res Unit Mol Epidemiol, Neuherberg, Germany.
[Meitinger, Thomas] German Ctr Cardiovasc Res DZHK, Gottingen, Germany.
[Meitinger, Thomas] Munich Heart Alliance, Munich, Germany.
[Strauch, Konstantin] Univ Munich, Inst Med Informat Biometry & Epidemiol, Neuherberg, Germany.
[Strauch, Konstantin] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Genet Epidemiol, Neuherberg, Germany.
[Li, Yang; Jansen, Ritsert C.] Univ Groningen, Groningen Bioinformat Ctr, Groningen, Netherlands.
[Psaty, Bruce M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Ripatti, Samuli] Wellcome Trust Res Labs, Sanger Inst, Cambridge, England.
RP Franke, L (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
EM lude@ludesign.nl
RI Knight, Julian/C-7242-2009; Grallert, Harald/B-3424-2013; Milani,
Lili/C-8759-2011; Ripatti, Samuli/H-9446-2014; Montgomery,
Grant/B-7148-2008; Meitinger, Thomas/O-1318-2015; Rivadeneira,
Fernando/O-5385-2015; Schurmann, Claudia/L-1204-2016; Zhernakova,
Daria/M-5619-2016; Franke, Lude/P-7036-2016; Prokisch,
Holger/N-8964-2013; Singleton, Andrew/C-3010-2009; Powell,
Joseph/G-3027-2014; Karjalainen, Juha/P-8624-2016
OI Visscher, Peter/0000-0002-2143-8760; Esko, Tonu/0000-0003-1982-6569;
Zhernakova, Alexandra/0000-0002-4574-0841; Peters,
Marjolein/0000-0003-3167-9063; Melzer, David/0000-0002-0170-3838;
Knight, Julian/0000-0002-0377-5536; Milani, Lili/0000-0002-5323-3102;
Ripatti, Samuli/0000-0002-0504-1202; Montgomery,
Grant/0000-0002-4140-8139; Rivadeneira, Fernando/0000-0001-9435-9441;
Schurmann, Claudia/0000-0003-4158-9192; Zhernakova,
Daria/0000-0001-6531-3890; Franke, Lude/0000-0002-5159-8802; Powell,
Joseph/0000-0001-9031-6356;
FU Intramural NIH HHS [Z99 AG999999]; Medical Research Council [G0500070];
NHLBI NIH HHS [R01 HL073410, R01 HL085251]; Wellcome Trust [090532]
NR 59
TC 393
Z9 397
U1 7
U2 60
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2013
VL 45
IS 10
SI SI
BP 1238
EP U195
DI 10.1038/ng.2756
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 225UQ
UT WOS:000324989600022
PM 24013639
ER
PT J
AU Torisu, T
Torisu, K
Lee, IH
Liu, J
Malide, D
Combs, CA
Wu, XFS
Rovira, II
Fergusson, MM
Weigert, R
Connelly, PS
Daniels, MP
Komatsu, M
Cao, L
Finkel, T
AF Torisu, Takehiro
Torisu, Kumiko
Lee, In Hye
Liu, Jie
Malide, Daniela
Combs, Christian A.
Wu, Xufeng S.
Rovira, Ilsa I.
Fergusson, Maria M.
Weigert, Roberto
Connelly, Patricia S.
Daniels, Mathew P.
Komatsu, Masaaki
Cao, Liu
Finkel, Toren
TI Autophagy regulates endothelial cell processing, maturation and
secretion of von Willebrand factor
SO NATURE MEDICINE
LA English
DT Article
ID WEIBEL-PALADE BODIES; UNCONVENTIONAL SECRETION; VONWILLEBRAND-FACTOR;
GENE ATG16L1; MICE; DISEASE; PROTEIN; MOUSE; ANGIOGENESIS; BIOGENESIS
AB Endothelial secretion of von Willebrand factor (VWF) from intracellular organelles known as Weibel-Palade bodies (WPBs) is required for platelet adhesion to the injured vessel wall. Here we demonstrate that WPBs are often found near or within autophagosomes and that endothelial autophagosomes contain abundant VWF protein. Pharmacological inhibitors of autophagy or knockdown of the essential autophagy genes Atg5 or Atg7 inhibits the in vitro secretion of VWF. Furthermore, although mice with endothelial-specific deletion of Atg7 have normal vessel architecture and capillary density, they exhibit impaired epinephrine-stimulated VWF release, reduced levels of high-molecular weight VWF multimers and a corresponding prolongation of bleeding times. Endothelial-specific deletion of Atg5 or pharmacological inhibition of autophagic flux results in a similar in vivo alteration of hemostasis. Thus, autophagy regulates endothelial VWF secretion, and transient pharmacological inhibition of autophagic flux may be a useful strategy to prevent thrombotic events.
C1 [Torisu, Takehiro; Torisu, Kumiko; Lee, In Hye; Liu, Jie; Rovira, Ilsa I.; Fergusson, Maria M.; Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Malide, Daniela; Combs, Christian A.] NHLBI, Light Microscopy Core, NIH, Bethesda, MD 20892 USA.
[Wu, Xufeng S.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Weigert, Roberto] Natl Inst Dent & Craniofacial Res, Intracellular Membrane Trafficking Unit, NIH, Bethesda, MD USA.
[Connelly, Patricia S.; Daniels, Mathew P.] NHLBI, Electron Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
[Komatsu, Masaaki] Tokyo Metropolitan Inst Med Sci, Lab Frontier Sci, Tokyo 113, Japan.
[Cao, Liu] China Med Univ, Key Lab Med Cell Biol, Shenyang, Peoples R China.
RP Finkel, T (reprint author), NHLBI, Ctr Mol Med, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
FU NIH Intramural Funds; Japan Society for the Promotion of Science
Research Fellowship in Biomedical and Behavioral Research at the NIH
FX We are grateful to S. Gutkind (NIH) for help with primary endothelial
cell isolation, T. Carter for the gift of the VWF monomeric GFP plasmid
(VWF-mGFP), J. Lippincott-Schwartz (NIH) for the LC3-mCherry plasmid and
Y. Fitz (NIH) for help with coagulation measurements. We thank B.
Zinselmeyer (NIH) for assistance with the spot cluster analysis and C.
A. Brantner (NIH) for help performing cryo-immunogold electron
microscopy. This work was supported by NIH Intramural Funds. T.T. is a
recipient of a Japan Society for the Promotion of Science Research
Fellowship in Biomedical and Behavioral Research at the NIH.
NR 57
TC 53
Z9 55
U1 2
U2 22
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 OCT
PY 2013
VL 19
IS 10
BP 1281
EP +
DI 10.1038/nm.3288
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 232YW
UT WOS:000325531700027
PM 24056772
ER
PT J
AU Falzarano, D
de Wit, E
Rasmussen, AL
Feldmann, F
Okumura, A
Scott, DP
Brining, D
Bushmaker, T
Martellaro, C
Baseler, L
Benecke, AG
Katze, MG
Munster, VJ
Feldmann, H
AF Falzarano, Darryl
de Wit, Emmie
Rasmussen, Angela L.
Feldmann, Friederike
Okumura, Atsushi
Scott, Dana P.
Brining, Doug
Bushmaker, Trenton
Martellaro, Cynthia
Baseler, Laura
Benecke, Arndt G.
Katze, Michael G.
Munster, Vincent J.
Feldmann, Heinz
TI Treatment with interferon-alpha 2b and ribavirin improves outcome in
MERS-CoV-infected rhesus macaques
SO NATURE MEDICINE
LA English
DT Article
ID ACUTE RESPIRATORY SYNDROME; SONIC HEDGEHOG; CONVALESCENT PLASMA; HUMAN
CORONAVIRUS; SARS PATIENTS; HEPATITIS-C; TGF-BETA; LUNG; PNEUMONIA;
GROWTH
AB The emergence of Middle East respiratory syndrome coronavirus (MERS-CoV) is of global concern: the virus has caused severe respiratory illness, with 111 confirmed cases and 52 deaths1 at the time of this article's publication. Therapeutic interventions have not been evaluated in vivo; thus, patient management relies exclusively on supportive care, which, given the high case-fatality rate, is not highly effective. The rhesus macaque is the only known model organism for MERS-CoV infection, developing an acute localized to widespread pneumonia with transient clinical disease(2,3) that recapitulates mild to moderate human MERSCoV cases(4,5). The combination of interferon-alpha 2b and ribavirin was effective in reducing MERS-CoV replication in vitro(6); therefore, we initiated this treatment 8 h after inoculation of rhesus macaques. In contrast to untreated, infected macaques, treated animals did not develop breathing abnormalities and showed no or very mild radiographic evidence of pneumonia. Moreover, treated animals showed lower levels of systemic (serum) and local (lung) proinflammatory markers, in addition to fewer viral genome copies, distinct gene expression and less severe histopathological changes in the lungs. Taken together, these data suggest that treatment of MERS-CoV infected rhesus macaques with IFN-alpha 2b and ribavirin reduces virus replication, moderates the host response and improves clinical outcome. As these two drugs are already used in combination in the clinic for other infections, IFN-alpha 2b and ribavirin should be considered for the management of MERS-CoV cases.
C1 [Falzarano, Darryl; de Wit, Emmie; Martellaro, Cynthia; Baseler, Laura; Feldmann, Heinz] NIAID, Dis Modeling & Transmiss Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
[Rasmussen, Angela L.; Okumura, Atsushi; Benecke, Arndt G.; Katze, Michael G.] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Feldmann, Friederike; Scott, Dana P.; Brining, Doug] NIAID, Rocky Mt Vet Branch, Div Intramural Res, NIH,Rocky Mt Labs, Hamilton, MT USA.
[Bushmaker, Trenton; Munster, Vincent J.] NIAID, Virus Ecol Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
[Baseler, Laura] Purdue Univ, Dept Comparat Pathobiol, W Lafayette, IN 47907 USA.
[Benecke, Arndt G.] Univ Paris 06, CNRS, UMR7224, Paris, France.
[Katze, Michael G.] Univ Washington, Washington Natl Primate Res Ctr, Seattle, WA 98195 USA.
[Feldmann, Heinz] Univ Manitoba, Dept Med Microbiol, Winnipeg, MB, Canada.
RP Feldmann, H (reprint author), NIAID, Dis Modeling & Transmiss Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
EM feldmannh@niaid.nih.gov
RI Okumura, Atsushi/E-8012-2015
OI Okumura, Atsushi/0000-0002-7779-3059
FU Intramural Research Program, NIAID, NIH; NIAID Regional Centers of
Excellence [U54 AI081680]; Systems Virology (NIH/ NIAID)
[HHSN272200800060C]; Washington National Primate Research Center
[P51OD010425]
FX D.F., E.d.W., V.J.M. and H.F. conceived of and designed the study. D.F.,
E.d.W., A.L.R., F.F., A.O., D.P.S., T.B., C.M. and D.B. performed the
experiments. D.F., E.d.W., A.L.R., A.O., D.P.S., L.B., A.G.B., V.J.M.,
M.G.K. and H.F. analyzed the data. D.F., A.L.R., M.G.K. and H.F. wrote
the manuscript. This work was supported in part by the Intramural
Research Program, NIAID, NIH, in addition to the NIAID Regional Centers
of Excellence (U54 AI081680), Systems Virology (NIH/ NIAID contract
number HHSN272200800060C) and Washington National Primate Research
Center (P51OD010425) to M.G.K.
NR 37
TC 100
Z9 112
U1 0
U2 19
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 OCT
PY 2013
VL 19
IS 10
BP 1313
EP +
DI 10.1038/nm.3362
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 232YW
UT WOS:000325531700031
PM 24013700
ER
PT J
AU Pandey, GS
Yanover, C
Miller-Jenkins, LM
Garfield, S
Cole, SA
Curran, JE
Moses, EK
Rydz, N
Simhadri, V
Kimchi-Sarfaty, C
Lillicrap, D
Viel, KR
Przytycka, TM
Pierce, GF
Howard, TE
Sauna, ZE
AF Pandey, Gouri Shankar
Yanover, Chen
Miller-Jenkins, Lisa M.
Garfield, Susan
Cole, Shelley A.
Curran, Joanne E.
Moses, Eric K.
Rydz, Natalia
Simhadri, Vijaya
Kimchi-Sarfaty, Chava
Lillicrap, David
Viel, Kevin R.
Przytycka, Teresa M.
Pierce, Glenn F.
Howard, Tom E.
Sauna, Zuben E.
CA PATH Personalized Alternative
TI Endogenous factor VIII synthesis from the intron 22-inverted F8 locus
may modulate the immunogenicity of replacement therapy for hemophilia A
SO NATURE MEDICINE
LA English
DT Article
ID COAGULATION-FACTOR VIII; MONOCLONAL-ANTIBODIES; HUMAN-LIVER; INHIBITOR;
ANTIGEN; HISTORY; GENE
AB Neutralizing antibodies (inhibitors) to replacement factor VIII (FVIII, either plasma derived or recombinant) impair the effective management of hemophilia A1. Individuals with hemophilia A due to major deletions of the FVIII gene (F8) lack antigenically cross-reactive material in their plasma ("CRM-negative"), and the prevalence of inhibitors in these individuals may be as high as 90%. Conversely, individuals with hemophilia A caused by F8 missense mutations are CRM-positive, and their overall prevalence of inhibitors is < 10% (ref. 2). Individuals with the F8 intron 22 inversion (found in similar to 50% of individuals with severe hemophilia A) have been grouped with the former on the basis of their genetic defect and CRM-negative status. However, only similar to 20% of these individuals develop inhibitors3. Here we demonstrate that the levels of F8 mRNA and intracellular FVIII protein in B lymphoblastoid cells and liver biopsies from individuals with the intron 22 inversion are comparable to those in healthy controls. These results support the hypothesis that most individuals with the intron 22 inversion are tolerized to FVIII and thus do not develop inhibitors. Furthermore, we developed a new pharmacogenetic algorithm that permits the stratification of inhibitor risk for individuals and subpopulations by predicting the immunogenicity of replacement FVIII using, as input, the number of putative T cell epitopes in the infused protein and the competence of major histocompatibility complex class II molecules to present such epitopes. This algorithm showed statistically significant accuracy in predicting the presence of inhibitors in 25 unrelated individuals with the intron 22 inversion.
C1 [Pandey, Gouri Shankar; Simhadri, Vijaya; Kimchi-Sarfaty, Chava; Sauna, Zuben E.] US FDA, Ctr Biol Evaluat & Res, Div Hematol, Lab Hemostasis, Bethesda, MD 20892 USA.
[Yanover, Chen] Fred Hutchinson Canc Res Ctr, Program Computat Biol, Seattle, WA 98104 USA.
[Miller-Jenkins, Lisa M.] NCI, Lab Cell Biol, Expt Carcinogenesis Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Garfield, Susan] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Cole, Shelley A.; Curran, Joanne E.; Moses, Eric K.] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Rydz, Natalia; Lillicrap, David] Queens Univ, Dept Pathol & Mol Med, Kingston, ON, Canada.
[Viel, Kevin R.] Histonis, Atlanta, GA USA.
[Przytycka, Teresa M.] Natl Ctr Biotechnol Informat, Natl Lib Med, NIH, Bethesda, MD USA.
[Pierce, Glenn F.] Biogen Idec Hemophilia, Waltham, MA USA.
[Howard, Tom E.] Vet Affairs Greater Los Angeles Healthcare Syst, Dept Pathol & Lab Med, Los Angeles, CA USA.
[Howard, Tom E.] Univ So Calif, Keck Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90033 USA.
[Howard, Tom E.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
RP Sauna, ZE (reprint author), US FDA, Ctr Biol Evaluat & Res, Div Hematol, Lab Hemostasis, Bethesda, MD 20892 USA.
EM tom.howard@va.gov; zuben.sauna@fda.hhs.gov
RI Yanover, Chen/A-3754-2012
OI Yanover, Chen/0000-0003-3663-4286
FU US National Institute of Allergy and Infectious Diseases Committee on
Human Research [10-01178]; modernization of science program of the
Center for Biologics Evaluation and Research, US Food and Drug
Administration; National Heart, Lung and Blood Institute, National
Institutes of Health [1RC2-HL101851, HL-71130, HL-72533)]; Bayer
Healthcare Corporation; Bayer Hemophilia Awards Program; Baxter
Healthcare Corporation; Clinical Translational Science Institute at the
University of Southern California; Intramural Program of the US National
Library of Medicine, NIH
FX We would like to thank P. Matzinger, B. Golding, J. Lozier, D. Levin, M.
Carcao, V. Blanchette, G. Rivard and V. La Terza for helpful comments
and J. Sauna for help with the graphics. We thank S. V. Ambudkar (US
National Cancer Institute) for the use of facilities, M. J. Lenardo and
K. Shafer-Weaver (US National Institute of Allergy and Infectious
Diseases) for the gift of the purified C2 domain of FVIII and P. Stock
(University of California, San Francisco) for liver tissue samples.
These samples were obtained under the University of California
University-Wide AIDS Research Program (TP-99-SF-001) Committee on Human
Research (H802423454) and the Solid Organ Transplantation in HIV:
Multi-Site Study (AI052748) funded by the US National Institute of
Allergy and Infectious Diseases Committee on Human Research (10-01178).
Research conducted in the laboratory of Z. E. S. is funded by the
modernization of science program of the Center for Biologics Evaluation
and Research, US Food and Drug Administration. Research conducted in the
laboratory of T. E. H. is funded by grants from the National Heart, Lung
and Blood Institute, National Institutes of Health (1RC2-HL101851,
HL-71130 and HL-72533), the Bayer Healthcare Corporation, Bayer
Hemophilia Awards Program, Baxter Healthcare Corporation and the
Clinical Translational Science Institute at the University of Southern
California. The work of T. M. P. is fully supported by the Intramural
Program of the US National Library of Medicine, NIH.
NR 22
TC 27
Z9 27
U1 2
U2 19
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 OCT
PY 2013
VL 19
IS 10
BP 1318
EP +
DI 10.1038/nm.3270
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 232YW
UT WOS:000325531700032
PM 24037092
ER
PT J
AU Fridlyand, J
Simon, RM
Walrath, JC
Roach, N
Buller, R
Schenkein, DP
Flaherty, KT
Allen, JD
Sigal, EV
Scher, HI
AF Fridlyand, Jane
Simon, Richard M.
Walrath, Jessica C.
Roach, Nancy
Buller, Richard
Schenkein, David P.
Flaherty, Keith T.
Allen, Jeff D.
Sigal, Ellen V.
Scher, Howard I.
TI Considerations for the successful co-development of targeted cancer
therapies and companion diagnostics
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Article
ID CLINICAL-TRIAL DESIGNS; ADAPTIVE SIGNATURE DESIGN; GROWTH-FACTOR
RECEPTOR; PREDICTIVE BIOMARKERS; MONOCLONAL-ANTIBODY; IMATINIB MESYLATE;
WORKING GROUP; TUMOR-CELLS; ONCOLOGY; EXPRESSION
AB As diagnostic tests become increasingly important for optimizing the use of drugs to treat cancers, the co-development of a targeted therapy and its companion diagnostic test is becoming more prevalent and necessary. In July 2011, the US Food and Drug Administration released a draft guidance that gave the agency's formal definition of companion diagnostics and introduced a drug-diagnostic co-development process for gaining regulatory approval. Here, we identify areas of drug-diagnostic co-development that were either not covered by the guidance or that would benefit from increased granularity, including how to determine when clinical studies should be limited to biomarker-positive patients, defining the diagnostically selected patient population in which to use a companion diagnostic, and defining and clinically validating a biomarker signature for assays that use more than one biomarker. We propose potential approaches that sponsors could use to deal with these challenges and provide strategies to help guide the future co-development of drugs and diagnostics.
C1 [Fridlyand, Jane] Genentech Inc, San Francisco, CA 94080 USA.
[Simon, Richard M.] US Natl Canc Inst, Bethesda, MD 20892 USA.
[Walrath, Jessica C.; Allen, Jeff D.; Sigal, Ellen V.] Friends Canc Res, South Washington, DC 20036 USA.
[Roach, Nancy] Fight Colorectal Canc, Alexandria, VA 22314 USA.
[Buller, Richard] Pfizer, San Diego, CA 92121 USA.
[Schenkein, David P.] Agios Pharmaceut, Cambridge, MA 02139 USA.
[Flaherty, Keith T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Scher, Howard I.] Mem Sloan Kettering Canc Ctr, New York, NY 10065 USA.
RP Walrath, JC (reprint author), Friends Canc Res, 1800 M St NW,Suite 1050, South Washington, DC 20036 USA.
EM jwalrath@focr.org
NR 47
TC 24
Z9 25
U1 3
U2 22
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD OCT
PY 2013
VL 12
IS 10
BP 743
EP 755
DI 10.1038/nrd4101
PG 13
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 227XT
UT WOS:000325149700013
PM 24008432
ER
PT J
AU Bersani, FS
Girardi, N
Sanna, L
Mazzarini, L
Santucci, C
Kotzalidis, GD
Sani, G
De Rossi, P
Raccah, RN
Caltagirone, SS
Battipaglia, M
Capezzuto, S
Bersani, G
Girardi, P
AF Bersani, Francesco Saverio
Girardi, Nicoletta
Sanna, Livia
Mazzarini, Lorenzo
Santucci, Chiara
Kotzalidis, Giorgio D.
Sani, Gabriele
De Rossi, Pietro
Raccah, Ruggero N.
Caltagirone, Saverio Simone
Battipaglia, Mariella
Capezzuto, Silvia
Bersani, Giuseppe
Girardi, Paolo
TI Deep Transcranial Magnetic Stimulation for treatment-resistant bipolar
depression: A case report of acute and maintenance efficacy
SO NEUROCASE
LA English
DT Article
DE Deep Transcranial Magnetic Stimulation; Treatment-resistant bipolar
disorder; Bipolar depression; Prefrontal cortex; Maintenance treatment
of bipolar disorder
ID BRAIN-REGIONS; RATING-SCALE; H-COIL; ADD-ON; DISORDER; FEASIBILITY; ECT;
DEFINITION; IMPAIRMENT; SYMPTOMS
AB Deep Transcranial Magnetic Stimulation (dTMS) is currently being evaluated as a possible treatment for several neuropsychiatric disorders and has been demonstrated as a safe and effective procedure. This case presents a patient with bipolar depression that has been treated with 20 daily consecutive dTMS sessions and with one dTMS session every 2 weeks for the following 3 months. Depressive symptoms improved rapidly and response was maintained during the next 6 months; cognitive performances also improved. This report suggests that add-on dTMS may help overcoming drug-resistance in bipolar depression and protect from subsequent bipolar episodes of any polarity.
C1 [Bersani, Francesco Saverio; Girardi, Nicoletta] Univ Roma La Sapienza, Dept Neurol & Psychiat, I-00185 Rome, Italy.
[Sanna, Livia; Mazzarini, Lorenzo; Santucci, Chiara; Kotzalidis, Giorgio D.; Sani, Gabriele; De Rossi, Pietro; Caltagirone, Saverio Simone; Battipaglia, Mariella; Girardi, Paolo] Univ Roma La Sapienza, NESMOS Dept Neurosci Mental Hlth & Sensory Organs, Sch Med & Psychol, St Andrea Hosp, I-00185 Rome, Italy.
[Mazzarini, Lorenzo; Capezzuto, Silvia; Girardi, Paolo] Suore Hosp Sacred Heart Jesus, Dept Neuropsychiat, Viterbo, Italy.
[Raccah, Ruggero N.] ATID Ltd Adv Technol Innovat Distribut, Rome, Italy.
[Bersani, Giuseppe] Sapienza Univ Rome, Dept Med Surg Sci & Biotechnol, Latina, Italy.
[De Rossi, Pietro] NIMH, Bethesda, MD 20892 USA.
RP Bersani, FS (reprint author), Univ Roma La Sapienza, Dept Neurol & Psychiat, Viale Univ 30, I-00185 Rome, Italy.
EM bersani.fs@tiscali.it
OI Bersani, Francesco Saverio/0000-0002-7555-8020
NR 48
TC 19
Z9 19
U1 1
U2 9
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1355-4794
EI 1465-3656
J9 NEUROCASE
JI Neurocase
PD OCT 1
PY 2013
VL 19
IS 5
BP 451
EP 457
DI 10.1080/13554794.2012.690429
PG 7
WC Clinical Neurology; Psychiatry; Psychology
SC Neurosciences & Neurology; Psychiatry; Psychology
GA 225QO
UT WOS:000324977600006
PM 22827578
ER
PT J
AU Yeatts, SD
Palesch, YY
Moy, CS
Selim, M
AF Yeatts, Sharon D.
Palesch, Yuko Y.
Moy, Claudia S.
Selim, Magdy
TI High Dose Deferoxamine in Intracerebral Hemorrhage (Hi-Def) Trial:
Rationale, Design, and Methods
SO NEUROCRITICAL CARE
LA English
DT Article
DE Intracerebral hemorrhage; Deferoxamine; Clinical trial; Futility design
ID ACTIVATED FACTOR-VII; PERIHEMATOMAL EDEMA; IRON CHELATOR; STROKE TRIALS;
BRAIN-INJURY; RAT MODEL; HEMATOMA; SAFETY; TOLERABILITY; EXPRESSION
AB Hemoglobin degradation products, in particular iron, have been implicated in secondary neuronal injury following intracerebral hemorrhage (ICH). The iron chelator Deferoxamine Mesylate (DFO) exerts diverse neuroprotective effects, reduces perihematoma edema (PHE) and neuronal damage, and improves functional recovery after experimental ICH. We hypothesize that treatment with DFO could minimize neuronal injury and improve outcome in ICH patients. As a prelude to test this hypothesis, we conducted a Phase I, open-label study to determine the tolerability, safety, and maximum tolerated dose (MTD) of DFO in patients with ICH. Intravenous infusions of DFO in doses up to 62 mg/kg/day (up to a maximum of 6000 mg/day) were well-tolerated and did not seem to increase serious adverse events (SAEs) or mortality. We have initiated a multi-center, double-blind, randomized, placebo-controlled, Phase II clinical trial (High Dose Deferoxamine [HI-DEF] in Intracerebral Hemorrhage) to determine if it is futile to move DFO forward to Phase III efficacy evaluation.
We will randomize 324 subjects with spontaneous ICH to either DFO at 62 mg/kg/day (up to a maximum daily dose of 6000 mg/day) or saline placebo, given by intravenous infusion for 5 consecutive days. Treatment will be initiated within 24 hours after ICH symptom onset. All subjects will be followed for 3 months and will receive standard of care therapy while participating in the study. At 3 months, the proportion of DFO-treated subjects with a good clinical outcome, assessed by modified Rankin Scale, will be compared to the placebo proportion in a futility analysis.
The Hi-Def trial is expected to advance our understanding of the pathopgysiology of secondary neuronal injury in ICH and will provide a crucial "Go/No Go" signal as to whether a Phase III trial to investigate the efficacy of DFO is warranted.
C1 [Yeatts, Sharon D.; Palesch, Yuko Y.] Med Univ S Carolina, Coll Med, Dept Publ Hlth Sci, Data Coordinat Unit, Charleston, SC 29425 USA.
[Moy, Claudia S.] NINDS, NIH, Bethesda, MD 20892 USA.
[Selim, Magdy] Beth Israel Deaconess Med Ctr, Dept Neurol, Stroke Div, Boston, MA 02215 USA.
RP Selim, M (reprint author), Beth Israel Deaconess Med Ctr, Dept Neurol, Stroke Div, 330 Brookline Ave,Palmer 127, Boston, MA 02215 USA.
EM mselim@bidmc.harvard.edu
FU National Institute of Health [U01 NS074425]
FX The study was supported by the National Institute of Health (Grant # U01
NS074425).
NR 33
TC 24
Z9 24
U1 0
U2 8
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1541-6933
J9 NEUROCRIT CARE
JI Neurocrit. Care
PD OCT
PY 2013
VL 19
IS 2
BP 257
EP 266
DI 10.1007/s12028-013-9861-y
PG 10
WC Critical Care Medicine; Clinical Neurology
SC General & Internal Medicine; Neurosciences & Neurology
GA 221GB
UT WOS:000324644800017
PM 23943316
ER
PT J
AU Cotch, MF
Freeman, EE
AF Cotch, Mary Frances
Freeman, Ellen E.
TI Health Care Services: Addressing the Global Challenge of Universal Eye
Health
SO OPHTHALMIC EPIDEMIOLOGY
LA English
DT Editorial Material
C1 [Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Freeman, Ellen E.] Univ Montreal, Dept Ophtalmol, Montreal, PQ, Canada.
RP Cotch, MF (reprint author), NEI, Div Epidemiol & Clin Applicat, NIH, 10 Ctr Dr Clin Res Ctr,Room 3-2531,MSC 1204, Bethesda, MD 20892 USA.
EM mfc@nei.nih.gov
OI Cotch, Mary Frances/0000-0002-2046-4350; Freeman,
Ellen/0000-0002-1403-8427
FU Intramural NIH HHS [Z99 EY999999]
NR 11
TC 0
Z9 0
U1 1
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0928-6586
J9 OPHTHAL EPIDEMIOL
JI Ophthalmic Epidemiol.
PD OCT
PY 2013
VL 20
IS 5
BP 255
EP 257
DI 10.3109/09286586.2013.823217
PG 3
WC Ophthalmology
SC Ophthalmology
GA 226BC
UT WOS:000325008200001
PM 24007494
ER
PT J
AU Ramasamy, D
Joseph, S
Valaguru, V
Mitta, VP
Ravilla, TD
Cotch, MF
AF Ramasamy, Dhivya
Joseph, Sanil
Valaguru, Vijayakumar
Mitta, Vinod P.
Ravilla, Thulasiraj D.
Cotch, Mary Frances
TI Cluster Randomized Trial to Compare Spectacle Delivery Systems at
Outreach Eye Camps in South India
SO OPHTHALMIC EPIDEMIOLOGY
LA English
DT Article
DE Eye camp; India; outreach; refractive error; spectacle dispensing;
spectacles
ID CATARACT-SURGERY; BLINDNESS; BARRIERS
AB Purpose: To study the optimal method for delivery of spectacles at eye camps to maximize procurement and use.
Methods: A cluster randomized controlled trial, undertaken in the catchment districts of Aravind Eye Hospital - Theni, in the state of Tamil Nadu, India. Community eye camps (n = 21) were allocated to offer one of three types of service for purchase of spectacles to correct refractive error: (1) Issuance of a prescription only; (2) booking orders for spectacles with subsequent delivery; (3) on-the-spot fitting and dispensing of spectacles. Follow-up questionnaires were administered 6 weeks after interventions to assess patient outcomes. The primary outcome measured was spectacle procurement at follow-up 6 weeks post-screening. Secondary outcomes included use of and satisfaction with spectacles. Reasons for purchase/non-purchase were also assessed.
Results: Compared to those who were issued only a prescription and adjusting for distance from base hospital, spectacle procurement was significantly higher for those allowed to book spectacles for subsequent delivery (odds ratio, OR, 8.79, 95% confidence interval, CI, 4.61-16.78) and for those receiving spectacles on the spot (OR 13.97, 95% CI 8.12-24.05). Among those with spectacles at 6 weeks, spectacle use was nearly universal and satisfaction with spectacles varied between 92 and 94% among the three different dispensing modalities.
Conclusion: Making spectacles available on the spot is important to ensure procurement in a context where availability and access to dispensing opticians is poor.
C1 [Ramasamy, Dhivya; Joseph, Sanil; Valaguru, Vijayakumar; Ravilla, Thulasiraj D.] Aravind Eye Care Syst, LAICO, Madurai 625020, Tamil Nadu, India.
[Mitta, Vinod P.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Cotch, Mary Frances] NEI, NIH, Bethesda, MD 20892 USA.
RP Ramasamy, D (reprint author), Aravind Eye Care Syst, LAICO, 72 Kuruvikaran Salai, Madurai 625020, Tamil Nadu, India.
EM dhivya@aravind.org
OI Cotch, Mary Frances/0000-0002-2046-4350
FU Aravind Eye Care System
FX This study was internally funded by Aravind Eye Care System
NR 15
TC 1
Z9 1
U1 0
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0928-6586
J9 OPHTHAL EPIDEMIOL
JI Ophthalmic Epidemiol.
PD OCT
PY 2013
VL 20
IS 5
BP 308
EP 314
DI 10.3109/09286586.2013.822897
PG 7
WC Ophthalmology
SC Ophthalmology
GA 226BC
UT WOS:000325008200010
PM 24070102
ER
PT J
AU Arana, Y
Verastegui, M
Tuero, I
Grandjean, L
Garcia, HH
Gilman, RH
AF Arana, Yanina
Verastegui, Manuela
Tuero, Iskra
Grandjean, Louis
Garcia, Hector H.
Gilman, Robert H.
TI Characterization of the carbohydrate components of Taenia solium
oncosphere proteins and their role in the antigenicity
SO PARASITOLOGY RESEARCH
LA English
DT Article
ID ENTAMOEBA-HISTOLYTICA; PORCINE CYSTICERCOSIS; GLYCOPROTEIN ANTIGENS;
TRICHINELLA-SPIRALIS; CELL-SURFACE; PIGS; VACCINATION; PARASITES;
EPITOPES; LECTIN
AB This study examines the carbohydrate composition of Taenia solium whole oncosphere antigens (WOAs), in order to improve the understanding of the antigenicity of the T. solium. Better knowledge of oncosphere antigens is crucial to accurately diagnose previous exposure to T. solium eggs and thus predict the development of neurocysticercosis. A set of seven lectins conjugates with wide carbohydrate specificity were used on parasite fixations and somatic extracts. Lectin fluorescence revealed that d-mannose, d-glucose, d-galactose and N-acetyl-d-galactosamine residues were the most abundant constituents of carbohydrate chains on the surface of T. solium oncosphere. Lectin blotting showed that posttranslational modification with N-glycosylation was abundant while little evidence of O-linked carbohydrates was observed. Chemical oxidation and enzymatic deglycosylation in situ were performed to investigate the immunoreactivity of the carbohydrate moieties. Linearizing or removing the carbohydrate moieties from the protein backbones did not diminish the immunoreactivity of these antigens, suggesting that a substantial part of the host immune response against T. solium oncosphere is directed against the peptide epitopes on the parasite antigens. Finally, using carbohydrate probes, we demonstrated for the first time that the presence of several lectins on the surface of the oncosphere was specific to carbohydrates found in intestinal mucus, suggesting a possible role in initial attachment of the parasite to host cells.
C1 [Arana, Yanina; Verastegui, Manuela; Grandjean, Louis; Garcia, Hector H.; Gilman, Robert H.] Univ Peruana Cayetano Heredia, Fac Sci & Philosophy, Dept Cellular & Mol Sci, Lima, Peru.
[Tuero, Iskra] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Grandjean, Louis] Univ London Imperial Coll Sci Technol & Med, Wellcome Ctr Clin Trop Med, London W2 1PG, England.
[Garcia, Hector H.] Inst Ciencias Neurol, Cysticercosis Unit, Lima, Peru.
[Gilman, Robert H.] Johns Hopkins Univ, Dept Int Hlth, Bloomberg Sch Hyg & Publ Hlth, Baltimore, MD 21205 USA.
[Gilman, Robert H.] AB PRISMA, Lima 32, Peru.
RP Verastegui, M (reprint author), Univ Peruana Cayetano Heredia, Fac Sci & Philosophy, Dept Cellular & Mol Sci, POB 5045, Lima, Peru.
EM mveraste@jhsph.edu
FU Gates project [23981]; International Foundation for Science (IFS)
[B/4103-1]; RG-ER anonymous fund for Tropical Research
FX Funding for this project came from the Gates project 23981,
International Foundation for Science (IFS) grant B/4103-1 and the RG-ER
anonymous fund for Tropical Research. We thank Dr. Eric Cossio, Dr.
Carlos Carmona, Cecilia Casaravilla, and Dr. Holger Mayta and the
administrative help of Ms. Marjory Meza and the technical assistance of
MSc. Milagros Zavaleta.
NR 40
TC 2
Z9 2
U1 0
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0932-0113
EI 1432-1955
J9 PARASITOL RES
JI Parasitol. Res.
PD OCT
PY 2013
VL 112
IS 10
BP 3569
EP 3578
DI 10.1007/s00436-013-3542-9
PG 10
WC Parasitology
SC Parasitology
GA 216ZR
UT WOS:000324326500024
PM 23982308
ER
PT J
AU Blanch-Hartigan, D
AF Blanch-Hartigan, Danielle
TI Patient satisfaction with physician errors in detecting and identifying
patient emotion cues
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Article
DE Emotion recognition; Emotion cue; Physician-patient relationship;
Patient-centered care
ID MEDICAL CONSULTATIONS; CARE; METAANALYSIS; RESPONSES; ACCURACY;
STUDENTS; SYSTEM; SKILLS
AB Objective: Previous research has examined physicians' ability to respond to or identify the type of emotion cues. Yet in physician-patient interactions, identification and response are preceded by the ability to detect whether an emotion cue has occurred. This research assesses consequences of emotion detection errors for patient satisfaction.
Methods: Participants responding to an online survey read one of six randomly assigned descriptions of a physician-patient interaction varying on: whether the patient presented an emotion cue; whether the physician detected an emotion cue; and whether the physician correctly identified the cue. Participants then rated satisfaction with the physician.
Results: Satisfaction was highest when the physician correctly detected the patient's emotion cue and lowest when the physician failed to detect the patient's emotion. Failing to detect the emotion cue had lower satisfaction than other emotion processing errors, including falsely detecting an emotion cue that was not there or incorrectly identifying the type of emotion.
Conclusions: Emotion cue detection has implications for patient satisfaction distinct from emotion identification.
Practice implications: Results suggest it may be better for physicians to incorrectly identify than miss an emotion. Training for healthcare providers should consider incorporating emotion detection. Published by Elsevier Ireland Ltd.
C1 [Blanch-Hartigan, Danielle] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Blanch-Hartigan, D (reprint author), NCI, Off Canc Survivorship, 6116 Execut Blvd,Suite 404,MSC 8336, Bethesda, MD 20892 USA.
EM danielleblanch@gmail.com
NR 31
TC 5
Z9 6
U1 1
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0738-3991
J9 PATIENT EDUC COUNS
JI Patient Educ. Couns.
PD OCT
PY 2013
VL 93
IS 1
BP 56
EP 62
DI 10.1016/j.pec.2013.04.010
PG 7
WC Public, Environmental & Occupational Health; Social Sciences,
Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
Topics
GA 226TE
UT WOS:000325058100008
PM 23669151
ER
PT J
AU Nesheim, SR
Hardnett, F
Wheeling, JT
Siberry, GK
Paul, ME
Emmanuel, P
Bohannon, B
Dominguez, K
AF Nesheim, Steven R.
Hardnett, Felicia
Wheeling, John T.
Siberry, George K.
Paul, Mary E.
Emmanuel, Patricia
Bohannon, Beverly
Dominguez, Kenneth
CA LEGACY Consortium
TI Incidence of Opportunistic Illness Before and After Initiation of Highly
Active Antiretroviral Therapy in Children
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE HIV infection; pediatric; immune reconstitution inflammatory syndrome;
opportunistic infection; highly active antiretroviral therapy
ID IMMUNE RECONSTITUTION SYNDROME; HIV-INFECTED CHILDREN;
BACILLE-CALMETTE-GUERIN; INFLAMMATORY-SYNDROME; BCG; LYMPHADENITIS;
MANIFESTATION; TUBERCULOSIS; DISEASE; ZOSTER
AB Background: Little is known about immune reconstitution inflammatory syndrome in children in the United States.
Methods: LEGACY is a longitudinal cohort study of HIV-infected participants 0-24 years at enrollment during 2005 to 2007 from 22 US clinics. For this analysis, we included participants with complete medical record abstraction from birth or time of HIV diagnosis through 2006. Opportunistic illness (OI) included AIDS-defining conditions and selected HIV-related diagnoses. We calculated the incidence (#/100 patient-years) of OI diagnosed in the months pre- and postinitiation of the first highly active antiretroviral therapy (HAART) regimen which was followed by 1 log reduction in HIV viral load. We defined OI as immune reconstitution inflammatory syndrome if an OI incidence increased after HAART initiation. Responders were defined as experiencing 1 log decline in viral load within 6 months after HAART initiation.
Results: Among 575 patients with complete chart abstraction, 524 received HAART. Of these 524 patients, 343 were responders, 181 were nonresponders and 86 experienced OI. Responders accounted for 98 of 124 (79%) of OI. Pre-HAART and post-HAART OI incidences were 43.7 and 24.4 (P = 0.003), respectively, among responders and 15.9 and 9.1 (P = 0.2), respectively, among nonresponders. Overall, OI incidences among responders and nonresponders were 33.8 and 12.3, respectively (P = 0.002). Responders were more likely than nonresponders to experience herpes simplex and herpes zoster before HAART initiation (all, P < 0.002).
Conclusions: The lack of immune reconstitution inflammatory syndrome in participants initiating HAART may be due to low overall OI rates. The unexpectedly higher OI prevalence comprised mainly of herpes simplex and zoster, before HAART initiation among responders, may have motivated them to better adhere to HAART.
C1 [Nesheim, Steven R.] Emory Univ, Sch Med, Atlanta, GA USA.
[Nesheim, Steven R.; Bohannon, Beverly; Dominguez, Kenneth] Ctr Dis Control & Prevent, Epidemiol Branch, Atlanta, GA 30333 USA.
[Hardnett, Felicia] Ctr Dis Control & Prevent, Quantitat Sci & Informat Branch, Div HIV AIDS Prevent, Natl Ctr HIV Viral Hepatitis STD & TB Prevent, Atlanta, GA 30333 USA.
[Wheeling, John T.] Northrop Grumman Inc, Atlanta, GA USA.
[Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent Maternal AIDS Branch, NIH, Rockville, MD USA.
[Paul, Mary E.] Baylor Coll Med, Houston, TX 77030 USA.
[Emmanuel, Patricia] Univ S Florida, Sch Med, Tampa, FL 33620 USA.
RP Nesheim, SR (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd, Atlanta, GA 30333 USA.
EM sxn9@cdc.gov
FU Centers for Disease Control and Prevention, Atlanta, GA [200-2004-09976]
FX The LEGACY project was funded by the Centers for Disease Control and
Prevention, Atlanta, GA, contract number 200-2004-09976.
NR 30
TC 2
Z9 2
U1 0
U2 4
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 OCT
PY 2013
VL 32
IS 10
BP 1089
EP 1095
DI 10.1097/INF.0b013e31829ee893
PG 7
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 224ML
UT WOS:000324890500016
PM 24067552
ER
PT J
AU Rice, ML
Zeldow, B
Siberry, GK
Purswani, M
Malee, K
Hoffman, HJ
Frederick, T
Buchanan, A
Sirois, PA
Allison, SM
Williams, PL
AF Rice, Mabel L.
Zeldow, Bret
Siberry, George K.
Purswani, Murli
Malee, Kathleen
Hoffman, Howard J.
Frederick, Toni
Buchanan, Ashley
Sirois, Patricia A.
Allison, Susannah M.
Williams, Paige L.
CA PHACS
TI Evaluation of Risk for Late Language Emergence After In Utero
Antiretroviral Drug Exposure in HIV-exposed Uninfected Infants
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE pregnancy; HIV-exposed infants; antiretroviral; cohort study; language
delay
ID BILIRUBIN INDUCES APOPTOSIS; INFECTED WOMEN; NEONATAL
HYPERBILIRUBINEMIA; CHILDREN; PREGNANCY; OUTCOMES; BORN; DELIVERY;
PROTEASE; NEURONS
AB Background: Combination antiretroviral (cARV) regimens are recommended for pregnant women with HIV to prevent perinatal HIV transmission. Safety is a concern for infants who were HIV-exposed but uninfected, particularly for neurodevelopmental problems, such as language delays.
Methods: We studied late language emergence (LLE) in HIV-exposed but uninfected children enrolled in a US-based prospective cohort study. LLE was defined as a caregiver-reported score 10th percentile in any of 4 domains of the MacArthur-Bates Communicative Development Inventory for 1-year olds and as 1 standard deviation below age-specific norms for the Ages and Stages Questionnaire for 2-year olds. Logistic regression models were used to evaluate associations of in utero cARV exposure with LLE, adjusting for infant, maternal and environmental characteristics.
Results: 1129 language assessments were conducted among 792 1- and 2-year-old children (50% male, 62% black and 37% Hispanic). Overall, 86% had in utero exposure to cARV and 83% to protease inhibitors. LLE was identified in 26% of 1-year olds and 23% of 2-year olds, with higher rates among boys. In adjusted models, LLE was not associated with maternal cARV or ARV drug classes in either age group. Among cARV-exposed 1-year olds, increased odds of LLE was observed for those exposed to atazanavir (adjusted odds ratio = 1.83, 95% confidence interval: 1.10-3.04), particularly after the first trimester (adjusted odds ratio = 3.56, P = 0.001), compared with atazanavir-unexposed infants. No associations of individual ARV drugs with LLE were observed among 2-year olds.
Conclusions: In utero cARV exposure showed little association with LLE, except for a higher risk of language delay observed in 1-year-old infants with atazanavir exposure.
C1 [Rice, Mabel L.] Univ Kansas, Hearing Dept, Lawrence, KS 66045 USA.
[Zeldow, Bret; Buchanan, Ashley; Williams, Paige L.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, NIH, Bethesda, MD USA.
[Purswani, Murli] Albert Einstein Coll Med, Bronx Lebanon Hosp Ctr, Bronx, NY 10467 USA.
[Malee, Kathleen] Northwestern Univ, Feinberg Sch Med Psychiat & Behav Sci, Chicago, IL 60611 USA.
[Hoffman, Howard J.] Natl Inst Deafness & Other Commun Disorders, Epidemiol & Stat Program, Div Sci Programs, NIH, Bethesda, MD USA.
[Frederick, Toni] USC, Keck Sch Med, Dept Res Pediat, Maternal Child & Adolescent Program Infect Dis &, Los Angeles, CA USA.
[Sirois, Patricia A.] Tulane Univ, Sch Med, Dept Pediat, New Orleans, LA 70112 USA.
[Allison, Susannah M.] NIMH, NIH, Bethesda, MD 20892 USA.
RP Rice, ML (reprint author), Univ Kansas, Dole Human Dev Ctr 3031, 1000 Sunnyside Ave, Lawrence, KS 66045 USA.
EM mabel@ku.edu
OI Rice, Mabel/0000-0002-8150-5523
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institute on Drug Abuse; National Institute of
Allergy and Infectious Diseases; Office of AIDS Research; National
Institute of Mental Health; National Institute of Neurological Disorders
and Stroke; National Institute on Deafness and Other Communication
Disorders; National Heart Lung and Blood Institute; National Institute
of Dental and Craniofacial Research; National Institute on Alcohol Abuse
and Alcoholism through Harvard University School of Public Health
[HD052102, 3 U01 HD052102-05S1, 3 U01 HD052102-06S3]; Tulane University
School of Medicine [HD052104, 3U01HD052104-06S1]
FX The Pediatric HIV/AIDS Cohort Study was supported by the Eunice Kennedy
Shriver National Institute of Child Health and Human Development with
cofunding from the National Institute on Drug Abuse, the National
Institute of Allergy and Infectious Diseases, the Office of AIDS
Research, the National Institute of Mental Health, the National
Institute of Neurological Disorders and Stroke, the National Institute
on Deafness and Other Communication Disorders, the National Heart Lung
and Blood Institute, the National Institute of Dental and Craniofacial
Research and the National Institute on Alcohol Abuse and Alcoholism,
through cooperative agreements with the Harvard University School of
Public Health (HD052102, 3 U01 HD052102-05S1, 3 U01 HD052102-06S3) and
the Tulane University School of Medicine (HD052104, 3U01HD052104-06S1).
The authors have no other funding or conflicts of interest to disclose.
NR 27
TC 14
Z9 14
U1 2
U2 6
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 OCT
PY 2013
VL 32
IS 10
BP E406
EP E413
DI 10.1097/INF.0b013e31829b80ee
PG 8
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 224ML
UT WOS:000324890500005
PM 24067563
ER
PT J
AU Jacobson, O
Chen, XY
AF Jacobson, Orit
Chen, Xiaoyuan
TI Interrogating Tumor Metabolism and Tumor Microenvironments Using
Molecular Positron Emission Tomography Imaging. Theranostic Approaches
to Improve Therapeutics
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; INTEGRIN ALPHA(V)BETA(3)
EXPRESSION; UROKINASE PLASMINOGEN-ACTIVATOR; METASTATIC BREAST-CANCER;
PROLIFERATION IN-VIVO; MET-BINDING PEPTIDE; PROSTATE-CANCER;
NEUROENDOCRINE TUMORS; TYROSINE KINASE
AB Positron emission tomography (PET) is a noninvasive molecular imaging technology that is becoming increasingly important for the measurement of physiologic, biochemical, and pharmacological functions at cellular and molecular levels in patients with cancer. Formation, development, and aggressiveness of tumor involve a number of molecular pathways, including intrinsic tumor cell mutations and extrinsic interaction between tumor cells and the microenvironment. Currently, evaluation of these processes is mainly through biopsy, which is invasive and limited to the site of biopsy. Ongoing research on specific target molecules of the tumor and its microenvironment for PET imaging is showing great potential. To date, the use of PET for diagnosing local recurrence and metastatic sites of various cancers and evaluation of treatment response is mainly based on [F-18]fluorodeoxyglucose ([F-18]FDG), which measures glucose metabolism. However, [F-18]FDG is not a target-specific PET tracer and does not give enough insight into tumor biology and/or its vulnerability to potential treatments. Hence, there is an increasing need for the development of selective biologic radiotracers that will yield specific biochemical information and allow for noninvasive molecular imaging. The possibility of cancer-associated targets for imaging will provide the opportunity to use PET for diagnosis and therapy response monitoring (theranostics) and thus personalized medicine. This article will focus on the review of non-[F-18]FDG PET tracers for specific tumor biology processes and their preclinical and clinical applications.
C1 [Jacobson, Orit; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD USA.
RP Chen, XY (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD USA.
EM shawn.chen@nih.gov
FU Intramural Research Program of the National Institutes of Health
[National Institute of Biomedical Imaging and Bioengineering]
FX This work is supported by the Intramural Research Program of the
National Institutes of Health [National Institute of Biomedical Imaging
and Bioengineering].
NR 362
TC 8
Z9 8
U1 2
U2 23
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD OCT
PY 2013
VL 65
IS 4
BP 1214
EP 1256
DI 10.1124/pr.113.007625
PG 43
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 227BU
UT WOS:000325083600005
PM 24064460
ER
PT J
AU Zhang, LW
Simpson, DA
Innes, CL
Chou, J
Bushel, PR
Paules, RS
Kaufmann, WK
Zhou, T
AF Zhang, Liwen
Simpson, Dennis A.
Innes, Cynthia L.
Chou, Jeff
Bushel, Pierre R.
Paules, Richard S.
Kaufmann, William K.
Zhou, Tong
TI Gene expression signatures but not cell cycle checkpoint functions
distinguish AT carriers from normal individuals
SO PHYSIOLOGICAL GENOMICS
LA English
DT Article
DE ataxia telangiectasia-mutated; ionizing radiation; gene expression
signature
ID ATAXIA-TELANGIECTASIA HETEROZYGOTES; BREAST-CANCER SUSCEPTIBILITY;
DNA-DAMAGE; ATM MUTATIONS; IONIZING-RADIATION; CHROMOSOMAL
RADIOSENSITIVITY; INCREASED SENSITIVITY; GAMMA-IRRADIATION; SEQUENCE
VARIANTS; HUMAN FIBROBLASTS
AB Ataxia telangiectasia (AT) is a rare autosomal recessive disease caused by mutations in the ataxia telangiectasia-mutated gene (ATM). AT carriers with one mutant ATM allele are usually not severely affected although they carry an increased risk of developing cancer. There has not been an easy and reliable diagnostic method to identify AT carriers. Cell cycle checkpoint functions upon ionizing radiation (IR)-induced DNA damage and gene expression signatures were analyzed in the current study to test for differential responses in human lymphoblastoid cell lines with different ATM genotypes. While both dose- and time-dependent G1 and G2 checkpoint functions were highly attenuated in ATM-/- cell lines, these functions were preserved in ATM+/- cell lines equivalent to ATM+/+ cell lines. However, gene expression signatures at both baseline (consisting of 203 probes) and post-IR treatment (consisting of 126 probes) were able to distinguish ATM+/- cell lines from ATM+/+ and ATM-/- cell lines. Gene ontology (GO) and pathway analysis of the genes in the baseline signature indicate that ATM function-related categories, DNA metabolism, cell cycle, cell death control, and the p53 signaling pathway, were overrepresented. The same analyses of the genes in the IR-responsive signature revealed that biological categories including response to DNA damage stimulus, p53 signaling, and cell cycle pathways were overrepresented, which again confirmed involvement of ATM functions. The results indicate that AT carriers who have unaffected G1 and G2 checkpoint functions can be distinguished from normal individuals and AT patients by expression signatures of genes related to ATM functions.
C1 [Zhang, Liwen] Fudan Univ, Peoples Hosp Shanghai 5, Dept Obstet & Gynecol, Shanghai 200433, Peoples R China.
[Simpson, Dennis A.; Kaufmann, William K.; Zhou, Tong] Univ N Carolina, Ctr Environm Hlth & Susceptibil, Dept Pathol & Lab Med, Chapel Hill, NC USA.
[Simpson, Dennis A.; Kaufmann, William K.; Zhou, Tong] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Innes, Cynthia L.; Paules, Richard S.] NIEHS, Environm Stress & Canc Grp, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
[Chou, Jeff] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
[Bushel, Pierre R.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Zhou, Tong] Gentris Corp, Morrisville, NC 27560 USA.
RP Zhou, T (reprint author), Gentris Corp, 133 Southctr Ct, Morrisville, NC 27560 USA.
EM Tong.Zhou@gentris.com
FU Public Health Service [ES-10126, ES-11391]; Intramural Research Program
of the National Institutes of Health, National Institute of
Environmental Health Sciences Grant [Z01 ES102345-04]
FX This work was supported in part by Public Health Service Grants ES-10126
and ES-11391 and in part by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences Grant Z01 ES102345-04.
NR 59
TC 0
Z9 0
U1 0
U2 5
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1094-8341
J9 PHYSIOL GENOMICS
JI Physiol. Genomics
PD OCT
PY 2013
VL 45
IS 19
BP 907
EP 916
DI 10.1152/physiolgenomics.00064.2013
PG 10
WC Cell Biology; Genetics & Heredity; Physiology
SC Cell Biology; Genetics & Heredity; Physiology
GA 227PM
UT WOS:000325125800004
PM 23943852
ER
PT J
AU Khattar, SK
Samal, S
LaBranche, CC
Montefiori, DC
Collins, PL
Samal, SK
AF Khattar, Sunil K.
Samal, Sweety
LaBranche, Celia C.
Montefiori, David C.
Collins, Peter L.
Samal, Siba K.
TI Comparative Immunogenicity of HIV-1 gp160, gp140 and gp120 Expressed by
Live Attenuated Newcastle Disease Virus Vector
SO PLOS ONE
LA English
DT Article
ID TYPE-1 ENVELOPE GLYCOPROTEIN; NEUTRALIZING ANTIBODY-RESPONSE; VACCINE
DEVELOPMENT; MONOMERIC GP120; FOREIGN GENE; IMMUNODEFICIENCY;
IMMUNIZATION; PROTEIN; ELICITS; TRIMERS
AB The development of a vaccine against human immunodeficiency virus-1 (HIV-1) capable of inducing broad humoral and cellular responses at both the systemic and mucosal levels will be critical for combating the global AIDS epidemic. We previously demonstrated the ability of Newcastle disease virus (NDV) as a vaccine vector to express oligomeric Env protein gp160 and induce potent humoral and mucosal immune responses. In the present study, we used NDV vaccine strain LaSota as a vector to compare the biochemical and immunogenic properties of vector-expressed gp160, gp120, and two versions of gp140 (a derivative of gp160 made by deleting the transmembrane and cytoplasmic domains), namely: gp140L, which contained the complete membrane-proximal external region (MPER), and gp140S, which lacks the distal half of MPER. We show that, similar to gp160, NDV-expressed gp140S and gp120, but not gp140L, formed higher-order oligomers that retained recognition by conformationally sensitive monoclonal antibodies. Immunization of guinea pigs by the intranasal route with rLaSota/gp140S resulted in significantly greater systemic and mucosal antibody responses compared to the other recombinants. Immunization with rLaSota/140S, rLaSota/140L rLaSota/120 resulted in mixed Th1/Th2 immune responses as compared to Th1-biased immune responses induced by rLaSota/160. Importantly, rLaSota/gp140S induced neutralizing antibody responses to homologous HIV-1 strain BaL.26 and laboratory adapted HIV-1 strain MN.3 that were stronger than those elicited by the other NDV recombinants. Additionally, rLaSota/gp140S induced greater CD4+ and CD8+ T-cell responses in mice. These studies illustrate that rLaSota/gp140S is a promising vaccine candidate to elicit potent mucosal, humoral and cellular immune responses to the HIV-1 Env protein.
C1 [Khattar, Sunil K.; Samal, Sweety; Samal, Siba K.] Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
[LaBranche, Celia C.; Montefiori, David C.] Duke Univ, Div Surg Sci, Durham, NC USA.
[Collins, Peter L.] NIAID, Infect Dis Lab, Bethesda, MD 20892 USA.
RP Samal, SK (reprint author), Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
EM ssamal@umd.edu
FU NIH [AI-093198]; NIAID Primate Central Immunology Laboratory
[HHSN27201100016C]; NIAID, NIH Intramural Research Program
FX This research was supported by NIH R21 grant AI-093198 awarded to S.K.S
and by the NIAID Primate Central Immunology Laboratory Contract
HHSN27201100016C awarded to D.C.M. P.L.C. was supported by the NIAID,
NIH Intramural Research Program. The views expressed herein neither
necessarily reflect the official policies of the Department of Health
and Human Services; nor does mention of trade names, commercial
practices, or organizations imply endorsement by the U.S. Government.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 57
TC 7
Z9 7
U1 0
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 1
PY 2013
VL 8
IS 10
AR e78521
DI 10.1371/journal.pone.0078521
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 231OR
UT WOS:000325427100089
PM 24098600
ER
PT J
AU Likhtarov, I
Thomas, G
Kovgan, L
Masiuk, S
Chepurny, M
Ivanova, O
Gerasymenko, V
Tronko, M
Bogdanova, T
Bouville, A
AF Likhtarov, I.
Thomas, G.
Kovgan, L.
Masiuk, S.
Chepurny, M.
Ivanova, O.
Gerasymenko, V.
Tronko, M.
Bogdanova, T.
Bouville, A.
TI Reconstruction of individual thyroid doses to the Ukrainian subjects
enrolled in the Chernobyl Tissue Bank
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Article
ID SHORT-LIVED RADIOIODINES; EXPOSED IN-UTERO; RADIOACTIVE CONTAMINATION;
REGION UKRAINE; ACCIDENT; CANCER; I-131; CHILDREN; DISEASES; COHORT
AB The Chernobyl Tissue Bank (CTB) is an organisation that collects and stores samples of tumoral thyroid tissue obtained from Ukrainian and Russian subjects who were treated surgically for a thyroid cancer and had been exposed to I-131 from the Chernobyl accident. By 2012, the CTB had collected specimens of thyroid tissue from 2267 residents of Ukraine for the purpose of radiation research. Arithmetic mean thyroid doses and uncertainties have been estimated for all but 24 subjects for whom residence at the time of exposure was not found. The subjects have been classified into six groups or sub-groups according to the type of dosimetry-related information that is available for each of them. Excluding the 325 subjects with negligible radiation exposure, the arithmetic mean of the thyroid dose over all subjects is estimated as 0.4 Gy, with individual values ranging from 1 mGy to 13 Gy. The uncertainties in the individual thyroid dose estimates, characterised by the geometric standard deviations of their probability distributions, range from 1.3 to 8.7, with an arithmetic mean of 3.2.
C1 [Likhtarov, I.; Kovgan, L.; Masiuk, S.; Chepurny, M.; Ivanova, O.; Gerasymenko, V.] Natl Acad Med Sci Ukraine, Natl Res Ctr Radiat Med, State Inst, UA-04050 Kiev, Ukraine.
[Likhtarov, I.; Kovgan, L.; Masiuk, S.; Chepurny, M.; Ivanova, O.; Gerasymenko, V.] Ukrainian Radiat Protect Inst, UA-04050 Kiev, Ukraine.
[Thomas, G.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Tronko, M.; Bogdanova, T.] Natl Acad Med Sci Ukraine, VP Komisarenko Inst Endocrinol & Metab, State Inst, UA-04114 Kiev, Ukraine.
[Bouville, A.] US Natl Canc Inst, Bethesda, MD 20892 USA.
RP Masiuk, S (reprint author), Natl Acad Med Sci Ukraine, Natl Res Ctr Radiat Med, State Inst, 53 Melnykova St, UA-04050 Kiev, Ukraine.
EM masja1979@gmail.com
FU European Union
FX This research was funded by the European Union through the contract
between Imperial College London and Ukrainian Radiation Protection
Institute.
NR 54
TC 3
Z9 4
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0144-8420
EI 1742-3406
J9 RADIAT PROT DOSIM
JI Radiat. Prot. Dosim.
PD OCT
PY 2013
VL 156
IS 4
BP 407
EP 423
DI 10.1093/rpd/nct096
PG 17
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 228KO
UT WOS:000325185200003
PM 23595409
ER
PT J
AU Hao, M
Cheng, TJ
Wang, YL
Bryant, HS
AF Hao Ming
Cheng Tiejun
Wang Yanli
Bryant, H. Stephen
TI Web search and data mining of natural products and their bioactivities
in PubChem
SO SCIENCE CHINA-CHEMISTRY
LA English
DT Article
DE natural products; drug discovery; PubChem; public database; data mining
ID SMALL MOLECULES; MEDICINAL CHEMISTRY; DRUG DISCOVERY; INFORMATION;
STRATEGIES; INHIBITORS; DATABASES
AB Natural products, as major resources for drug discovery historically, are gaining more attentions recently due to the advancement in genomic sequencing and other technologies, which makes them attractive and amenable to drug candidate screening. Collecting and mining the bioactivity information of natural products are extremely important for accelerating drug development process by reducing cost. Lately, a number of publicly accessible databases have been established to facilitate the access to the chemical biology data for small molecules including natural products. Thus, it is imperative for scientists in related fields to exploit these resources in order to expedite their researches on natural products as drug leads/candidates for disease treatment. PubChem, as a public database, contains large amounts of natural products associated with bioactivity data. In this review, we introduce the information system provided at PubChem, and systematically describe the applications for a set of PubChem web services for rapid data retrieval, analysis, and downloading of natural products. We hope this work can serve as a starting point for the researchers to perform data mining on natural products using PubChem.
C1 [Hao Ming; Cheng Tiejun; Wang Yanli; Bryant, H. Stephen] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Wang, YL (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM ywang@ncbi.nlm.nih.gov; bryant@ncbi.nlm.nih.gov
RI Cheng, Tiejun/A-5344-2010
OI Cheng, Tiejun/0000-0002-4486-3356
FU Intramural Research Program of the National Institutes of Health,
National Library of Medicine
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Library of Medicine.
NR 26
TC 2
Z9 2
U1 3
U2 30
PU SCIENCE PRESS
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, BEIJING 100717, PEOPLES R CHINA
SN 1674-7291
J9 SCI CHINA CHEM
JI Sci. China-Chem.
PD OCT
PY 2013
VL 56
IS 10
BP 1424
EP 1435
DI 10.1007/s11426-013-4910-0
PG 12
WC Chemistry, Multidisciplinary
SC Chemistry
GA 230VT
UT WOS:000325372100011
ER
PT J
AU Meschia, JF
Arnett, DK
Ay, H
Brown, RD
Benavente, OR
Cole, JW
de Bakker, PIW
Dichgans, M
Doheny, KF
Fornage, M
Grewal, RP
Gwinn, K
Jern, C
Conde, JJ
Johnson, JA
Jood, K
Laurie, CC
Lee, JM
Lindgren, A
Markus, HS
McArdle, PF
McClure, LA
Mitchell, BD
Schmidt, R
Rexrode, KM
Rich, SS
Rosand, J
Rothwell, PM
Rundek, T
Sacco, RL
Sharma, P
Shuldiner, AR
Slowik, A
Wassertheil-Smoller, S
Sudlow, C
Thijs, VNS
Woo, D
Worrall, BB
Wu, O
Kittner, SJ
AF Meschia, James F.
Arnett, Donna K.
Ay, Hakan
Brown, Robert D.
Benavente, Oscar R.
Cole, John W.
de Bakker, Paul I. W.
Dichgans, Martin
Doheny, Kimberly F.
Fornage, Myriam
Grewal, Raji P.
Gwinn, Katrina
Jern, Christina
Conde, Jordi Jimenez
Johnson, Julie A.
Jood, Katarina
Laurie, Cathy C.
Lee, Jin-Moo
Lindgren, Arne
Markus, Hugh S.
McArdle, Patrick F.
McClure, Leslie A.
Mitchell, Braxton D.
Schmidt, Reinhold
Rexrode, Kathryn M.
Rich, Stephen S.
Rosand, Jonathan
Rothwell, Peter M.
Rundek, Tatjana
Sacco, Ralph L.
Sharma, Pankaj
Shuldiner, Alan R.
Slowik, Agnieszka
Wassertheil-Smoller, Sylvia
Sudlow, Cathie
Thijs, Vincent N. S.
Woo, Daniel
Worrall, Bradford B.
Wu, Ona
Kittner, Steven J.
CA NINDS SiGN Study
TI Stroke Genetics Network (SiGN) Study Design and Rationale for a
Genome-Wide Association Study of Ischemic Stroke Subtypes
SO STROKE
LA English
DT Article
DE cerebral infarct; genetics; genomics
ID CAUSATIVE CLASSIFICATION; ATHEROSCLEROTIC STROKE; RISK; VARIANTS;
SYSTEM; HEALTH
AB Background and Purpose Meta-analyses of extant genome-wide data illustrate the need to focus on subtypes of ischemic stroke for gene discovery. The National Institute of Neurological Disorders and Stroke SiGN (Stroke Genetics Network) contributes substantially to meta-analyses that focus on specific subtypes of stroke.
Methods The National Institute of Neurological Disorders and Stroke SiGN includes ischemic stroke cases from 24 genetic research centers: 13 from the United States and 11 from Europe. Investigators harmonize ischemic stroke phenotyping using the Web-based causative classification of stroke system, with data entered by trained and certified adjudicators at participating genetic research centers. Through the Center for Inherited Diseases Research, the Network plans to genotype 10 296 carefully phenotyped stroke cases using genome-wide single nucleotide polymorphism arrays and adds to these another 4253 previously genotyped cases, for a total of 14 549 cases. To maximize power for subtype analyses, the study allocates genotyping resources almost exclusively to cases. Publicly available studies provide most of the control genotypes. Center for Inherited Diseases Research-generated genotypes and corresponding phenotypes will be shared with the scientific community through the US National Center for Biotechnology Information database of Genotypes and Phenotypes, and brain MRI studies will be centrally archived.
Conclusions The Stroke Genetics Network, with its emphasis on careful and standardized phenotyping of ischemic stroke and stroke subtypes, provides an unprecedented opportunity to uncover genetic determinants of ischemic stroke.
C1 [Meschia, James F.] Mayo Clin Jacksonville, Jacksonville, FL USA.
[Arnett, Donna K.; McClure, Leslie A.] Univ Alabama Birmingham, Birmingham, AL USA.
[Brown, Robert D.] Mayo Clin Rochester, Rochester, MN USA.
[Ay, Hakan; Rosand, Jonathan; Wu, Ona] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Benavente, Oscar R.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Cole, John W.; McArdle, Patrick F.; Mitchell, Braxton D.; Shuldiner, Alan R.; Kittner, Steven J.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Cole, John W.; McArdle, Patrick F.; Mitchell, Braxton D.; Shuldiner, Alan R.; Kittner, Steven J.] Vet Adm Med Ctr, Baltimore, MD 21218 USA.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[de Bakker, Paul I. W.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA USA.
[de Bakker, Paul I. W.] MIT, Broad Inst Harvard, Cambridge, MA USA.
[Dichgans, Martin] Univ Munich, Klinikum Univ Munchen, Munich, Germany.
[Doheny, Kimberly F.] Johns Hopkins Univ, Baltimore, MD USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Grewal, Raji P.] St Francis Med Ctr, Lynwood, CA USA.
[Gwinn, Katrina] NINDS Neurogenet Cluster, Bethesda, MD USA.
[Conde, Jordi Jimenez] Univ Mar, IMIM Hosp, Barcelona, Spain.
[Johnson, Julie A.] Univ Florida, Coll Pharm, Gainesville, FL USA.
[Jern, Christina; Jood, Katarina] Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Gothenburg, Sweden.
[Laurie, Cathy C.] Univ Washington, Seattle, WA 98195 USA.
[Lee, Jin-Moo] Washington Univ, Sch Med, St Louis, MO USA.
[Lindgren, Arne] Lund Univ, Lund, Sweden.
[Markus, Hugh S.] St Georges Univ London, London, England.
[Schmidt, Reinhold] Med Univ Graz, Graz, Austria.
[Rexrode, Kathryn M.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Rich, Stephen S.; Worrall, Bradford B.] Univ Virginia, Charlottesville, VA USA.
[Rothwell, Peter M.] Radcliffe Infirm, Oxford OX2 6HE, England.
[Rundek, Tatjana; Sacco, Ralph L.] Univ Miami, Coral Gables, FL 33124 USA.
[Sharma, Pankaj] Imperial Coll London, London, England.
[Slowik, Agnieszka] Jagiellonian Univ, Krakow, Poland.
[Wassertheil-Smoller, Sylvia] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Sudlow, Cathie] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Thijs, Vincent N. S.] Univ Ziekenhuizen Leuven, Louvain, Belgium.
[Woo, Daniel] Univ Cincinnati, Cincinnati, OH USA.
RP Kittner, SJ (reprint author), Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
EM skittner@umaryland.edu
RI de Bakker, Paul/B-8730-2009; Lee, Jin-Moo/K-2024-2015; McClure,
Leslie/P-2929-2015; JIMENEZ-CONDE, JORDI/C-1941-2012;
OI de Bakker, Paul/0000-0001-7735-7858; Lee, Jin-Moo/0000-0002-3979-0906;
Thijs, Vincent/0000-0002-6614-8417; Rexrode,
Kathryn/0000-0003-3387-8429; Bevan, Steve/0000-0003-0490-6830; Mitchell,
Braxton/0000-0003-4920-4744; Anderson, Christopher/0000-0002-0053-2002;
Gwinn, Katrina/0000-0002-8277-651X
FU National Institute of Neurological Disorders and Stroke (NINDS) [U01
NS069208]; Ministerio de Sanidad y Consumo de Espana; Instituto de Salud
Carlos III (ISC III) [PI051737]; GWA study of LeukoAraiosis (GWALA)
Bases geneticas de la leucoaraiosis; Fondos de Investigacion Sanitaria
ISC III [PI10/02064]; Fondos FEDER/EDRF Red de Investigacion
Cardiovascular [RD12/0042/0020]; Fundacio la Marato TV3 [76/C/2011];
British Council (UKIERI); Henry Smith Charity; Department of Health
(UK); Department of Health; National Institutes of Health
[HHSN268200782096C, NS 030678]; Wellcome Trust Clinical Research
Facility, Western General Hospital, Edinburgh; Binks Trust; Council
Brain Imaging Research Centre; Division of Clinical Neurosciences,
University of Edinburgh, a core area of the Wellcome Trust Clinical
Research Facility; Scottish Imaging Network - A Platform for Scientific
Excellence (SINAPSE) collaboration; Scottish Funding Council; Chief
Scientist Office; Wellcome Trust as part of the Wellcome Trust Case
Control Consortium [085475/B/08/Z, 085475/Z/08/Z, WT084724MA]; National
Institutes of Health Genes Affecting Stroke Risks and Outcomes Study
(GASROS) [K23 NS042720]; American Heart Association/Bugher Foundation
Centers for Stroke Prevention Research [0775010N]; NINDS [K23NS042695,
R01NS059727, R01 NS42733, R01 NS39987, R37 NS029993, R01 NS27517]; Deane
Institute for Integrative Research in Atrial Fibrillation and Stroke;
Keane Stroke Genetics Fund; National Center for Research Resources
[U54RR020278]; National Institutes of Health Genes, Environment and
Health Initiative (GEI)as part of the Gene Environment Association
Studies (GENEVA) consortium under GEI [U01 HG004436]; Mid-Atlantic
Nutrition and Obesity Research Center [P30 DK072488]; Office of Research
and Development, Medical Research Service; Baltimore Geriatrics
Research, Education, and Clinical Center of the Department of Veterans
Affairs; National Institutes of Health (NIH) Office of Research on
Women's Health [R01 NS45012, U01 NS069208-01]; Austrian Science Fund
(FWF) [P20545-P05, P13180, I904-B13]; National Institute on Aging [Z01
AG000954-06, Z01 AG000015-50]; Polish Ministry of Science and Higher
Education for Leading National Research Centers (KNOW); Medical College,
Jagiellonian University in Krakow, Poland [K/ZDS/002848]; Department of
Neurology of the University Hospitals Leuven; Fundamental Clinical
Research grant from FWO Flanders [1.8.009.08.N.00, 1800913N]; Swedish
Research Council, Region Skane [K2010-61X-20378-04-3]; Freemasons Lodge
of Instruction EOS in Lund; King Gustaf V's and Queen Victoria's
Foundation; Lund University; Swedish Stroke Association; New Jersey
Neuroscience Institute/JFK Medical Center, Edison, NJ; Neurogenetics
Foundation, Cranbury, NJ; Department of Neurology at University of Miami
Miller School of Medicine; Evelyn McKnight Brain Institute; National
Institutes of Health from the National Heart Lung and Blood Institute
[HL088521, HL34594]; National Cancer Institute [CA87969, CA49449];
Stroke Association; Medical Research Council; Wellcome Trust; Dunhill
Medical Trust; National Institutes of Health Research (NIHR); NIHR
Oxford Biomedical Research Centre based at Oxford University Hospitals
NHS Trust; University of Oxford; NIHR; NINDS, National Institutes of
Health, and Department of Health and Human Service [U01 NS041588];
Swedish Research Council [K2011-65X-14605-09-6]; Swedish Heart and Lung
Foundation [20100256]; Swedish state/Sahlgrenska University Hospital
[ALFGBG-148861]; Swedish Society of Medicine; Rune and Ulla Amlov
Foundation; US National Institute of Health and Neurological Disorders
and Stroke [U01NS38529-04A1]; Wellcome Trust, as part of the Wellcome
Trust Case Control Consortium [085475/B/08/Z, 085475/Z/08/Z,
WT084724MA]; National Heart, Lung, and Blood Institute, National
Institutes of Health, US Department of Health and Human Services
[N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118,
32119, 32122, 42107-26, 42129-32, 44221]; National Institutes of
Neurological Disorders and Stroke [R01NS042618]; Washington University
SPOTRIAS Center [P50 NS055977]; Barnes-Jewish Hospital Foundation; [R01
NS073346]
FX SiGN: The study was funded by a cooperative agreement grant from the
National Institute of Neurological Disorders and Stroke (NINDS) U01
NS069208.; BASICMAR: The BASICMAR Genetic Study was supported by the
Ministerio de Sanidad y Consumo de Espana, Instituto de Salud Carlos III
(ISC III) with the grants: "Registro BASICMAR" Funding for Research in
Health (PI051737); GWA study of LeukoAraiosis (GWALA) Bases geneticas de
la leucoaraiosis. Estudio de Genome Wide Association en poblacion
espanola. Consorcio Espanol de Genetica del Ictus (Genestroke). "GWALA
project" from Fondos de Investigacion Sanitaria ISC III (PI10/02064);
and Fondos FEDER/EDRF Red de Investigacion Cardiovascular
(RD12/0042/0020). Additional support provided by the Fundacio la Marato
TV3 with the grant "Genetic contribution to functional Outcome and
Disability after Stroke (GOD's) project" (76/C/2011). Assistance with
data cleaning was provided by the Research in Cardiovascular and
Inflammatory Diseases Program of Institute of Medical Investigations
Mar, Hospital del Mar, and the Barcelona Biomedical Research Park.;
BRAINS: BRAINS was supported by the British Council (UKIERI), Henry
Smith Charity, and Department of Health (UK). Dr Sharma was supported by
a Department of Health Senior Fellowship. CIDR: Genotyping services were
provided by the Johns Hopkins University Center for Inherited Disease
Research (CIDR), which is fully funded through a federal contract from
the National Institutes of Health to the Johns Hopkins University
(contract number HHSN268200782096C).; EDINBURGH: The Edinburgh Stroke
Study was supported by the Wellcome Trust (clinician scientist award to
Dr Sudlow) and the Binks Trust. Sample processing occurred in the
Genetics Core Laboratory of the Wellcome Trust Clinical Research
Facility, Western General Hospital, Edinburgh. Much of the neuroimaging
occurred in the Scottish Funding Council Brain Imaging Research Centre
(www.sbirc.ed.ac.uk), Division of Clinical Neurosciences, University of
Edinburgh, a core area of the Wellcome Trust Clinical Research Facility
and part of the Scottish Imaging Network - A Platform for Scientific
Excellence (SINAPSE) collaboration (www.sinapse.ac.uk), funded by the
Scottish Funding Council and the Chief Scientist Office. Genotyping was
performed at the Wellcome Trust Sanger Institute in the UK and funded by
the Wellcome Trust as part of the Wellcome Trust Case Control Consortium
2 project (085475/B/08/Z and 085475/Z/08/Z and WT084724MA).; GASROS: The
Massachusetts General Hospital Stroke Genetics Group was supported by
the National Institutes of Health Genes Affecting Stroke Risks and
Outcomes Study (GASROS) grant K23 NS042720, the American Heart
Association/Bugher Foundation Centers for Stroke Prevention Research
0775010N, and NINDS K23NS042695, R01NS059727, the Deane Institute for
Integrative Research in Atrial Fibrillation and Stroke, and by the Keane
Stroke Genetics Fund. Genotyping services were provided by the Broad
Institute Center for Genotyping and Analysis, supported by grant
U54RR020278 from the National Center for Research Resources.; GCNKSS:
The Greater Cincinnati/Northern Kentucky Stroke Study was supported by
the National Institutes of Health (NS 030678).; GEOS: The GEOS Study was
supported by the National Institutes of Health Genes, Environment and
Health Initiative (GEI) grant U01 HG004436, as part of the Gene
Environment Association Studies (GENEVA) consortium under GEI, with
additional support provided by the Mid-Atlantic Nutrition and Obesity
Research Center (P30 DK072488) and the Office of Research and
Development, Medical Research Service, and the Baltimore Geriatrics
Research, Education, and Clinical Center of the Department of Veterans
Affairs. Genotyping services were provided by the Johns Hopkins
University CIDR, which is fully funded through a federal contract from
the National Institutes of Health to the Johns Hopkins University
(contract number HHSN268200782096C). Assistance with data cleaning was
provided by the GENEVA Coordinating Center (U01 HG 004446; PI Bruce S
Weir). Study recruitment and assembly of data sets were supported by a
Cooperative Agreement with the Division of Adult and Community Health,
Centers for Disease Control and by grants from the NINDS and the
National Institutes of Health (NIH) Office of Research on Women's Health
(R01 NS45012, U01 NS069208-01).; GRAZ: The Austrian Stroke Prevention
Study was supported by the Austrian Science Fund (FWF) grant numbers
P20545-P05 and P13180 and I904-B13 (Era-Net). The Medical University of
Graz supports the databases of the Graz Stroke Study and the Austrian
Stroke Prevention Study.; ISGS and SWISS: The Ischemic Stroke Genetics
Study (ISGS) was supported by the NINDS (R01 NS42733; PI Dr Meschia).
The Sibling with Ischemic Stroke Study (SWISS) was supported by the
NINDS (R01 NS39987; PI Dr Meschia). Both SWISS and ISGS received
additional support, in part, from the Intramural Research Program of the
National Institute on Aging (Z01 AG000954-06; PI Andrew Singleton).
SWISS and ISGS used samples and clinical data from the NIH-NINDS Human
Genetics Resource Center DNA and Cell Line Repository
(http://ccr.coriell.org/ninds), human subjects protocol numbers 2003-081
and 2004-147. SWISS and ISGS used stroke-free participants from the
Baltimore Longitudinal Study of Aging (BLSA) as controls with the
permission of Dr Luigi Ferrucci. The inclusion of BLSA samples was
supported, in part, by the Intramural Research Program of the National
Institute on Aging (Z01 AG000015-50), human subjects protocol number
2003-078. This study used the high-performance computational
capabilities of the Biowulf Linux cluster at the NIH
(http://biowulf.nih.gov).; KRAKOW: Phenotypic data and genetic specimens
collection were funded by the grant from the Polish Ministry of Science
and Higher Education for Leading National Research Centers (KNOW) and by
the grant from the Medical College, Jagiellonian University in Krakow,
Poland: K/ZDS/002848.; LEUVEN: The Leuven Stroke genetics study was
supported by personal research funds from the Department of Neurology of
the University Hospitals Leuven. Vincent Thijs is supported by a
Fundamental Clinical Research grant from FWO Flanders (numbers
1.8.009.08.N.00 and 1800913N).; LUND: The Lund Stroke Register was
supported by the Swedish Research Council (K2010-61X-20378-04-3), Region
Skane, the Freemasons Lodge of Instruction EOS in Lund, King Gustaf V's
and Queen Victoria's Foundation, Lund University, and the Swedish Stroke
Association. Biobank services were provided by Region Skane Competence
Centre (RSKC Malmo), Skane University Hospital, Malmo, Sweden, and
Biobank, LabmedicinSkane, University and Regional Laboratories Region
Skane, Sweden.; MCISS: The Middlesex County Ischemic Stroke Study
(MCISS) was supported by intramural funding from the New Jersey
Neuroscience Institute/JFK Medical Center, Edison, NJ, and The
Neurogenetics Foundation, Cranbury, NJ. We acknowledge Dr Souvik Sen for
his advice and encouragement in the initiation and design of this
study.; MIAMISR and NOMAS(S): The Northern Manhattan Study (NOMAS) was
supported by grants from the NINDS (R37 NS029993, R01 NS27517). The
Cerebrovascular Biorepository at University of Miami/Jackson Memorial
Hospital (The Miami Stroke Registry, Institutional Review Board No.
20070386) was supported by the Department of Neurology at University of
Miami Miller School of Medicine and Evelyn McKnight Brain Institute.
Biorepository and DNA extraction services were provided by the Hussmann
Institute for Human Genomics at the Miller School of Medicine.; MUNICH:
The MUNICH study was supported by the Vascular Dementia Research
Foundation and the Jackstaedt Stiftung.; NHS: The Nurses' Health Study
work on stroke is supported by grants from the National Institutes of
Health, including HL088521 and HL34594 from the National Heart Lung and
Blood Institute, as well as grants from the National Cancer Institute
funding the questionnaire follow-up and blood collection: CA87969 and
CA49449.; OXVASC: The Oxford Vascular Study was supported by the Stroke
Association, Medical Research Council, Wellcome Trust, Dunhill Medical
Trust, National Institutes of Health Research (NIHR), and NIHR Oxford
Biomedical Research Centre based at Oxford University Hospitals NHS
Trust and University of Oxford. Rothwell is in receipt of Senior
Investigator Awards from the Wellcome Trust and the NIHR.; REGARDS: The
Reasons for Geographic and Racial Differences in Stroke Study was
supported by a cooperative agreement U01 NS041588 from the NINDS,
National Institutes of Health, and Department of Health and Human
Service. A full list of participating REGARDS investigators and
institutions can be found at http://www.regardsstudy.org.; SAHLSIS:
SAHLSIS was supported by the Swedish Research Council
(K2011-65X-14605-09-6), the Swedish Heart and Lung Foundation
(20100256), the Swedish state/Sahlgrenska University Hospital
(ALFGBG-148861), the Swedish Stroke Association, the Swedish Society of
Medicine, and the Rune and Ulla Amlov Foundation.; SPS3: The Secondary
Prevention of Small Subcortical Strokes trial was funded by the US
National Institute of Health and Neurological Disorders and Stroke grant
No. U01NS38529-04A1 (principal investigator, O.R.B.; co-principal
investigator, R. G. H.). The SPS3 Genetic Substudy (SPS3-GENES) was
funded by R01 NS073346 (co-principal investigators, J.A.J, O.R.B, A. R.
S.).; ST. GEORGE'S: The principal funding for this study was provided by
the Wellcome Trust, as part of the Wellcome Trust Case Control
Consortium 2 project (085475/B/08/Z and 085475/Z/08/Z and WT084724MA).
Collection of some of the St George's stroke cohort was supported by
project grant support from the Stroke Association.; WHI: The Women's
Health Initiatives (WHI) program was funded by the National Heart, Lung,
and Blood Institute, National Institutes of Health, US Department of
Health and Human Services through contracts N01WH22110, 24152, 32100-2,
32105-6, 32108-9, 32111-13, 32115, 32118 to 32119, 32122, 42107-26,
42129-32, and 44221. The Hormones and Biomarkers Predicting Stroke
(HaBPS) was supported by a grant from the National Institutes of
Neurological Disorders and Stroke (R01NS042618).; WUSTL: The collection,
extraction of DNA from blood, and storage of specimens were supported by
the Washington University SPOTRIAS Center grant (P50 NS055977, NINDS,
NIH). Basic demographic and clinical characterization of stroke
phenotype was prospectively collected in the Cognitive Rehabilitation
and Recovery Group (CRRG) registry. The Recovery Genomics after Ischemic
Stroke (ReGenesIS) study was supported by a grant from the Barnes-Jewish
Hospital Foundation.
NR 15
TC 19
Z9 19
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD OCT
PY 2013
VL 44
IS 10
BP 2694
EP 2702
DI 10.1161/STROKEAHA.113.001857
PG 9
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 223TC
UT WOS:000324831900020
PM 24021684
ER
PT J
AU Yadav, S
Cotlarciuc, I
Munroe, PB
Khan, MS
Nalls, MA
Bevan, S
Cheng, YC
Chen, WM
Malik, R
McCarthy, NS
Holliday, EG
Speed, D
Hasan, N
Pucek, M
Rinne, PE
Sever, P
Stanton, A
Shields, DC
Maguire, JM
McEvoy, M
Scott, RJ
Ferrucci, L
Macleod, MJ
Attia, J
Markus, HS
Sale, MM
Worrall, BB
Mitchell, BD
Dichgans, M
Sudlow, C
Meschia, JF
Rothwell, PM
Caulfield, M
Sharma, P
AF Yadav, Sunaina
Cotlarciuc, Ioana
Munroe, Patricia B.
Khan, Muhammad S.
Nalls, Michael A.
Bevan, Steve
Cheng, Yu-Ching
Chen, Wei-Min
Malik, Rainer
McCarthy, Nina S.
Holliday, Elizabeth G.
Speed, Douglas
Hasan, Nazeeha
Pucek, Mateusz
Rinne, Paul E.
Sever, Peter
Stanton, Alice
Shields, Denis C.
Maguire, Jane M.
McEvoy, Mark
Scott, Rodney J.
Ferrucci, Luigi
Macleod, Mary J.
Attia, John
Markus, Hugh S.
Sale, Michele M.
Worrall, Bradford B.
Mitchell, Braxton D.
Dichgans, Martin
Sudlow, Cathy
Meschia, James F.
Rothwell, Peter M.
Caulfield, Mark
Sharma, Pankaj
CA Int Stroke Genetics Consortium
TI Genome-Wide Analysis of Blood Pressure Variability and Ischemic Stroke
SO STROKE
LA English
DT Article
DE blood pressure variability; genes; GWAS; polymorphism; stroke
ID EPISODIC HYPERTENSION; POPULATION-STRUCTURE; COMMON VARIANTS;
RISK-FACTORS; ASSOCIATION; METAANALYSIS; TRIAL; PREVENTION; INFARCTION;
RATIONALE
AB Background and Purpose Visit-to-visit variability in blood pressure (vBP) is associated with ischemic stroke. We sought to determine whether such variability has genetic causes and whether genetic variants associated with BP variability are also associated with ischemic stroke.
Methods A Genome Wide Association Study (GWAS) for loci influencing BP variability was undertaken in 3802 individuals from the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT) study, in which long-term visit-to-visit and within-visit BP measures were available. Because BP variability is strongly associated with ischemic stroke, we genotyped the sentinel single nucleotide polymorphism in an independent ischemic stroke population comprising 8624 cases and 12 722 controls and in 3900 additional (Scandinavian) participants from the ASCOT study to replicate our findings.
Results The ASCOT discovery GWAS identified a cluster of 17 correlated single nucleotide polymorphisms within the NLGN1 gene (3q26.31) associated with BP variability. The strongest association was with rs976683 (P=1.4x10(-8)). Conditional analysis of rs976683 provided no evidence of additional independent associations at the locus. Analysis of rs976683 in patients with ischemic stroke found no association for overall stroke (odds ratio, 1.02; 95% CI, 0.97-1.07; P=0.52) or its subtypes: cardioembolic (odds ratio, 1.07; 95% CI, 0.97-1.16; P=0.17), large vessel disease (odds ratio, 0.98; 95% CI, 0.89-1.07; P=0.60), and small vessel disease (odds ratio, 1.07; 95% CI, 0.97-1.17; P=0.19). No evidence for association was found between rs976683 and BP variability in the additional (Scandinavian) ASCOT participants (P=0.18).
Conclusions We identified a cluster of single nucleotide polymorphisms at the NLGN1 locus showing significant association with BP variability. Follow-up analyses did not support an association with risk of ischemic stroke and its subtypes.
C1 [Yadav, Sunaina; Cotlarciuc, Ioana; Khan, Muhammad S.; Hasan, Nazeeha; Pucek, Mateusz; Rinne, Paul E.; Sever, Peter] Imperial Coll London, Imperial Coll Cerebrovascular Res Unit, London, England.
[Sever, Peter] Imperial Coll Cerebrovasc Res Unit, London, England.
Imperial Coll London, London, England.
[Holliday, Elizabeth G.; McEvoy, Mark; Attia, John] Univ Newcastle, Ctr Clin Epidemiol & Biostat, Sch Med & Publ Hlth, Newcastle, NSW 2300, Australia.
[Maguire, Jane M.] Univ Newcastle, Sch Nursing & Midwifery, Newcastle, NSW 2300, Australia.
[Scott, Rodney J.] Univ Newcastle, Sch Biomed Sci & Pharm, Newcastle, NSW 2300, Australia.
[Holliday, Elizabeth G.; Maguire, Jane M.; McEvoy, Mark; Scott, Rodney J.; Attia, John] Hunter Med Res Inst, Newcastle, NSW, Australia.
[Malik, Rainer; Dichgans, Martin] Univ Munich, Inst Stroke & Dementia Res ISD, Med Ctr, Klinikum Univ Munchen, Munich, Germany.
[Malik, Rainer; Dichgans, Martin] Munich Cluster Syst Neurol SyNergy, Munich, Germany.
[Bevan, Steve; Markus, Hugh S.] St Georges Univ London, Stroke & Dementia Res Ctr, London, England.
[Meschia, James F.] Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA.
[Cheng, Yu-Ching] Baltimore Vet Affairs Med Ctr, Baltimore, MD USA.
[Nalls, Michael A.] US Natl Inst Hlth, Natl Inst Aging, Neurogenet Lab, Bethesda, MD USA.
[Worrall, Bradford B.] Univ Virginia, Dept Neurol & Publ Hlth Sci, Charlottesville, VA USA.
[Sale, Michele M.] Univ Virginia, Div Cardiovasc Med, Dept Internal Med, Charlottesville, VA USA.
[Chen, Wei-Min; Sale, Michele M.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Chen, Wei-Min] Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA USA.
[Sudlow, Cathy] Univ Edinburgh, Inst Genet & Mol Med, Div Clin Neurosci, Edinburgh, Midlothian, Scotland.
[Rothwell, Peter M.] John Radcliffe Hosp, Dept Clin Neurol, Oxford OX3 9DU, England.
[Speed, Douglas] UCL, UCL Genet Inst, London, England.
[Macleod, Mary J.] Univ Aberdeen, Div Appl Med, Aberdeen, Scotland.
[McCarthy, Nina S.] Univ Western Australia, Ctr Genet Origins Hlth & Dis, Crawley, WA, Australia.
[McCarthy, Nina S.; Stanton, Alice] Royal Coll Surgeons Ireland, Dublin 2, Ireland.
[Shields, Denis C.] Univ Coll Dublin, Conway Inst Biomol & Biomed Res, Dublin 4, Ireland.
[Munroe, Patricia B.; Caulfield, Mark] Barts & London Med Sch, William Harvey Res Inst, Ctr Clin Pharmacol, London, England.
[Maguire, Jane M.] Gosford Hosp, Dept Neurosci, Gosford, NSW, Australia.
[Scott, Rodney J.] Hunter Area Pathol Serv, Div Genet, Newcastle, NSW, Australia.
[Cheng, Yu-Ching; Mitchell, Braxton D.] Univ Maryland, Dept Med, Baltimore, MD 21201 USA.
[Ferrucci, Luigi] NIH, Natl Inst Aging, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD USA.
RP Sharma, P (reprint author), Imperial Coll London, London SW7 2AZ, England.
EM pankaj.sharma@imperial.ac.uk
RI Stanton, Alice/F-4697-2012; Attia, John/F-5376-2013;
OI Macleod, Mary Joan/0000-0003-2115-8184; Attia, John/0000-0001-9800-1308;
Speed, Doug/0000-0002-0096-9765; Stanton, Alice/0000-0002-4961-165X;
Bevan, Steve/0000-0003-0490-6830; Mitchell, Braxton/0000-0003-4920-4744
FU Pfizer (NY, Servier Research Group, Paris, France); Leo Laboratories
(Copenhagen, Denmark); Hunter Medical Research Institute; National
health, Medical Research Council, University of Newcastle; Vincent
Fairfax Family Foundation; Department of Health (United Kingdom); Henry
Smith Charity; British Council; United Kingdom-India Education and
Research Institute (UKIERI); Qatar National Research Foundation;
National Institutes of Health (NIH) Genes, Environment, and Health
Initiative (GEI) [U01 HG004436]; NIH [HHSN268200782096C]; GENEVA
Coordinating Center [U01 HG 004446]; Office of Research and Development,
Medical Research Service, Baltimore Geriatrics Research, Education, and
Clinical Centre of the Department of Veterans Affairs; National
Institute of Neurological Disorders and Stroke (NINDS), NIH Office of
Research on Women's Health [R01 NS45012, U01 NS069208-01]; Department of
Veterans Affairs BLR&D Career Development Award (CDA-2); National
Institute on Aging [Z01 AG-000954-06, Z01 AG-000015-50]; NIH-NINDS [R01
NS-42733, R01 NS-39987]; NINDS/NIH [R01 NS34447]; National Human Genome
Research Institute [U01 HG005160]; Wellcome Trust [085475/B/08/Z,
085475/Z/08/Z, WT084724MA]
FX Anglo-Scandinavian Cardiac Outcome Trial was supported by Pfizer (NY,
Servier Research Group, Paris, France) and Leo Laboratories (Copenhagen,
Denmark). Australian Stroke Genetics Collaborative was funded through
grants from the Hunter Medical Research Institute and the National
health, Medical Research Council, University of Newcastle, and the
Vincent Fairfax Family Foundation. Bio-Repository of DNA in Stroke
received support from Department of Health (United Kingdom), Henry Smith
Charity, British Council, United Kingdom-India Education and Research
Institute (UKIERI), and the Qatar National Research Foundation
(www.BrainsGenetics.com). Genetics of Early Onset Stroke was supported
by the following grants: National Institutes of Health (NIH) Genes,
Environment, and Health Initiative (GEI) Grant U01 HG004436; NIH grant
HHSN268200782096C; GENEVA Coordinating Center grant U01 HG 004446;
Office of Research and Development, Medical Research Service, Baltimore
Geriatrics Research, Education, and Clinical Centre of the Department of
Veterans Affairs; National Institute of Neurological Disorders and
Stroke (NINDS), NIH Office of Research on Women's Health (R01 NS45012,
U01 NS069208-01); and Department of Veterans Affairs BLR&D Career
Development Award (CDA-2). Ischemic Stroke Genetics Study and Siblings
with Ischemic Stroke Study was supported in part by the Intramural
Research Program of the National Institute on Aging (NIH project Z01
AG-000954-06 and NIH project Z01 AG-000015-50), NIH-NINDS grant R01
NS-42733 (ISGS, Dr Meschia), and NIH-NINDS grant R01 NS-39987 (SWISS, Dr
Meschia). Vitamin Intervention for Stroke Prevention was funded by the
NINDS/NIH (R01 NS34447) and National Human Genome Research Institute
(grant U01 HG005160). Welcome Trust Case Control Consortium-Germany
(WTCCC) and WTCCC-UK were funded by the Wellcome Trust as part of the
WTCCC2 project (085475/B/08/Z, 085475/Z/08/Z, and WT084724MA). The other
authors report no conflicts.
NR 41
TC 7
Z9 9
U1 0
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD OCT
PY 2013
VL 44
IS 10
BP 2703
EP 2709
DI 10.1161/STROKEAHA.113.002186
PG 7
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 223TC
UT WOS:000324831900021
PM 23929743
ER
PT J
AU Pahigiannis, K
Waddy, SP
Koroshetz, W
AF Pahigiannis, Katherine
Waddy, Salina P.
Koroshetz, Walter
TI Toward Solutions for Minimizing Disparities in Stroke National Institute
of Neurological Disorders and Stroke Update
SO STROKE
LA English
DT Article
DE epidemiology; health behavior; primary prevention; secondary prevention;
stroke
C1 [Pahigiannis, Katherine; Koroshetz, Walter] NINDS, Off Director, NIH, Bethesda, MD 20892 USA.
[Waddy, Salina P.] NINDS, Off Clin Res, NIH, Bethesda, MD 20892 USA.
RP Koroshetz, W (reprint author), NINDS, NIH, Bldg 31,Room 8A52,31 Ctr Dr,MSC 2540, Bethesda, MD 20892 USA.
EM koroshetzw@mail.nih.gov
FU Intramural NIH HHS [Z99 NS999999]
NR 0
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD OCT
PY 2013
VL 44
IS 10
BP E129
EP E130
DI 10.1161/STROKEAHA.113.001418
PG 2
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 223TC
UT WOS:000324831900004
PM 24021681
ER
PT J
AU Woo, D
Rosand, J
Kidwell, C
McCauley, JL
Osborne, J
Brown, MW
West, SE
Rademacher, EW
Waddy, S
Roberts, JN
Koch, S
Gonzales, NR
Sung, G
Kittner, SJ
Birnbaum, L
Frankel, M
Testai, FD
Hall, CE
Elkind, MS
Flaherty, M
Coull, B
Chong, JY
Warwick, T
Malkoff, M
James, ML
Ali, LK
Worrall, BB
Jones, F
Watson, T
Leonard, A
Martinez, R
Sacco, RI
Langefeld, CD
AF Woo, Daniel
Rosand, Jonathan
Kidwell, Chelsea
McCauley, Jacob L.
Osborne, Jennifer
Brown, Mark W.
West, Sandra E.
Rademacher, Eric W.
Waddy, Salina
Roberts, Jamie N.
Koch, Sebastian
Gonzales, Nicole R.
Sung, Gene
Kittner, Steven J.
Birnbaum, Lee
Frankel, Michael
Testai, Fernando Daniel
Hall, Christiana E.
Elkind, Mitchell S. V.
Flaherty, Matthew
Coull, Bruce
Chong, Ji Y.
Warwick, Tanya
Malkoff, Marc
James, Michael L.
Ali, Latisha K.
Worrall, Bradford B.
Jones, Floyd
Watson, Tiffany
Leonard, Anne
Martinez, Rebecca
Sacco, Ralph I.
Langefeld, Carl D.
TI The Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) Study
Protocol
SO STROKE
LA English
DT Article
DE cerebral hemorrhage; genetics; genomics; hypertension; minority groups;
risk factors; stroke
ID QUALITY-OF-LIFE; COGNITIVE STATUS; STROKE; ADMIXTURE; BLACKS; WHITES;
RISK; EUROQOL; PANEL
AB Background and Purpose Epidemiological studies of intracerebral hemorrhage (ICH) have consistently demonstrated variation in incidence, location, age at presentation, and outcomes among non-Hispanic white, black, and Hispanic populations. We report here the design and methods for this large, prospective, multi-center case-control study of ICH.
Methods The Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study is a multi-center, prospective case-control study of ICH. Cases are identified by hot-pursuit and enrolled using standard phenotype and risk factor information and include neuroimaging and blood sample collection. Controls are centrally identified by random digit dialing to match cases by age (5 years), race, ethnicity, sex, and metropolitan region.
Results As of March 22, 2013, 1655 cases of ICH had been recruited into the study, which is 101.5% of the target for that date, and 851 controls had been recruited, which is 67.2% of the target for that date (1267 controls) for a total of 2506 subjects, which is 86.5% of the target for that date (2897 subjects). Of the 1655 cases enrolled, 1640 cases had the case interview entered into the database, of which 628 (38%) were non-Hispanic black, 458 (28%) were non-Hispanic white, and 554 (34%) were Hispanic. Of the 1197 cases with imaging submitted, 876 (73.2%) had a 24 hour follow-up CT available. In addition to CT imaging, 607 cases have had MRI evaluation.
Conclusions The ERICH study is a large, case-control study of ICH with particular emphasis on recruitment of minority populations for the identification of genetic and epidemiological risk factors for ICH and outcomes after ICH.
C1 [Woo, Daniel; Osborne, Jennifer; Frankel, Michael] Univ Cincinnati, Coll Med, Cincinnati, OH 45267 USA.
[Rosand, Jonathan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Kidwell, Chelsea] Georgetown Univ, Med Ctr, Dept Neurol, Washington, DC 20007 USA.
[McCauley, Jacob L.; West, Sandra E.] Univ Miami, John P Hussman Inst Human Genom, Coral Gables, FL 33124 USA.
[Brown, Mark W.; Langefeld, Carl D.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
[Rademacher, Eric W.] Univ Cincinnati, Inst Policy Res, Cincinnati, OH 45267 USA.
[Waddy, Salina; Roberts, Jamie N.] NINDS, Bethesda, MD 20892 USA.
[Koch, Sebastian; Sacco, Ralph I.] Univ Miami, Miller Sch Med, Coral Gables, FL 33124 USA.
[Gonzales, Nicole R.; Martinez, Rebecca] Univ Texas Med Sch Houston, Houston, TX USA.
[Sung, Gene] Univ So Calif, Neurocrit Care & Stroke Div, Los Angeles, CA USA.
[Koch, Sebastian] Univ Maryland, Baltimore Vet Adm Med Ctr, Baltimore, MD 21201 USA.
[Birnbaum, Lee; Jones, Floyd; Leonard, Anne] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Flaherty, Matthew] Emory Univ, Grady Mem Hosp, Atlanta, GA 30322 USA.
[Testai, Fernando Daniel] Univ Illinois, Chicago Med Ctr, Chicago, IL 60680 USA.
[Hall, Christiana E.] Univ Texas SW Med Ctr Dallas, Dept Neurol & Neurotherapeut, Dallas, TX 75390 USA.
[Elkind, Mitchell S. V.] Columbia Univ, New York, NY USA.
[Coull, Bruce] Univ Arizona, Tucson, AZ USA.
[Chong, Ji Y.] St Lukes Roosevelt Hosp, New York, NY USA.
[Warwick, Tanya] Univ Calif San Francisco, Fresno, CA USA.
[Malkoff, Marc] Univ New Mexico, Albuquerque, NM 87131 USA.
[James, Michael L.] Duke Univ, Dept Anesthesiol, Durham, NC USA.
[Ali, Latisha K.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Worrall, Bradford B.] Univ Virginia, Dept Neurol & Publ Hlth Sci, Charlottesville, VA USA.
[Watson, Tiffany] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
RP Woo, D (reprint author), Univ Cincinnati, Coll Med, Dept Neurol, 260 Stetson St ML 0525, Cincinnati, OH 45267 USA.
EM Daniel.woo@uc.edu
FU National Institute of Neurological Disorders and Stroke [NINDS:
U-01-NS069763]
FX This study was supported by a grant from the National Institute of
Neurological Disorders and Stroke (NINDS: U-01-NS069763). This report
does not represent the official view of NINDS, the National Institutes
of Health (NIH), or any part of the US Federal Government. No official
support or endorsement of this article by NINDS or NIH is intended or
should be inferred.
NR 23
TC 16
Z9 16
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD OCT
PY 2013
VL 44
IS 10
BP E120
EP E125
DI 10.1161/STROKEAHA.113.002332
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 223TC
UT WOS:000324831900001
PM 24021679
ER
PT J
AU Scheidweiler, KB
Himes, SK
Chen, X
Liu, HF
Huestis, MA
AF Scheidweiler, K. B.
Himes, S. K.
Chen, X.
Liu, H. F.
Huestis, M. A.
TI 11-Nor-9-Carboxy-Delta 9-Tetrahydrocannabinol Quantification in Human
Oral Fluid by Liquid Chromatography-Tandem Mass Spectrometry
SO THERAPEUTIC DRUG MONITORING
LA English
DT Meeting Abstract
CT 13th International Congress of Therapeutic Drug Monitoring and Clinical
Toxicology
CY SEP 22-26, 2013
CL Salt Lake City, UT
DE cannabinoids; carboxy THC; oral fluid; metabolites; analytical method;
LCMSMS
C1 [Scheidweiler, K. B.; Himes, S. K.; Huestis, M. A.] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Chen, X.; Liu, H. F.] ABSciex, Foster City, CA 94404 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0163-4356
EI 1536-3694
J9 THER DRUG MONIT
JI Ther. Drug Monit.
PD OCT
PY 2013
VL 35
IS 5
BP 687
EP 687
PG 1
WC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
SC Medical Laboratory Technology; Pharmacology & Pharmacy; Toxicology
GA 224LP
UT WOS:000324887600097
ER
PT J
AU Rao, M
AF Rao, Mahendra
TI Stem Cells for Therapy
SO TISSUE ENGINEERING AND REGENERATIVE MEDICINE
LA English
DT Article
DE regenerative medicine; stem cells; policy; regulations
ID REGENERATIVE MEDICINE; TRANSPLANTATION; IMMUNOTHERAPY; CHALLENGES;
INDUCTION; PRODUCTS
AB The regenerative medicine field is large, diverse and active on the Asian continent. Many different models have been successful and creative pioneers have shown what can work and equally importantly what does not. The field, however, remains in flux as regulations evolve, new funding mechanisms are developed and new technological breakthroughs are adopted.
C1 NIH, Ctr Regenerat Med, Bethesda, MD 20892 USA.
RP Rao, M (reprint author), NIH, Ctr Regenerat Med, Suite 1140,50 South Dr, Bethesda, MD 20892 USA.
EM mahendra.rao@nih.gov
NR 28
TC 7
Z9 7
U1 0
U2 6
PU KOREAN TISSUE ENGINEERING REGENERATIVE MEDICINE SOC
PI JONGRO-GU
PA 199-1, DONGSUNG-DONG,, JONGRO-GU, SEOUL 110-810, SOUTH KOREA
SN 1738-2696
J9 TISSUE ENG REGEN MED
JI Tissue Eng. Regen. Med.
PD OCT
PY 2013
VL 10
IS 5
BP 223
EP 229
DI 10.1007/s13770-013-1081-1
PG 7
WC Cell & Tissue Engineering; Engineering, Biomedical
SC Cell Biology; Engineering
GA 229CO
UT WOS:000325239600001
ER
PT J
AU Bornstein, MH
AF Bornstein, Marc H.
TI Parenting and child mental health: a cross-cultural perspective
SO WORLD PSYCHIATRY
LA English
DT Article
DE Culture; parenting; beliefs; behaviors; methodology; psychiatry; social
policy
ID MATERNAL EXPECTATIONS; DEVELOPING-COUNTRIES; REARING PRACTICES; CHINESE
CHILDREN; UNITED-STATES; AMERICAN; BEHAVIOR; MOTHERS; SELF;
SOCIALIZATION
AB In its most general instrumental sense, parenting consists of care of the young in preparing them to manage the tasks of life. Parents provide childhood experiences and populate the environments that guide children's development and so contribute to child mental health. Parenting is expressed in cognitions and practices. However, parents do not parent, and children do not grow up, in isolation, but in multiple contexts, and one notable context of parenting and child mental health is culture. Every culture is characterized, and distinguished from other cultures, by deep-rooted and widely acknowledged ideas about how one needs to feel, think, and act as an adequately functioning member of the culture. Insofar as parents subscribe to particular conventions of a culture, they likely follow prevailing cultural scripts in childrearing. Broadening our definition, it is therefore the continuing task of parents also to enculturate children by preparing them for the physical, psychosocial, and educational situations that are characteristic of their specific culture. Cross-cultural comparisons show that virtually all aspects of parenting children are informed by culture: culture influences when and how parents care for children, what parents expect of children, and which behaviors parents appreciate, emphasize and reward or discourage and punish. Thus, cultural norms become manifest in the mental health of children through parenting. Furthermore, variations in what is normative in different cultures challenge our assumptions about what is universal and inform our understanding of how parent-child relationships unfold in ways both culturally universal and specific. This essay concerns the contributions of culture to parenting and child mental health. No study of a single society can address this broad issue. It is possible, however, to learn lessons about parenting and child mental health from the study of different societies.
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 6705 Rockledge Dr, Bethesda, MD USA.
NR 81
TC 11
Z9 11
U1 8
U2 60
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1723-8617
J9 WORLD PSYCHIATRY
JI World Psychiatry
PD OCT
PY 2013
VL 12
IS 3
BP 258
EP 265
DI 10.1002/wps.20071
PG 8
WC Psychiatry
SC Psychiatry
GA 229KU
UT WOS:000325264000019
PM 24096792
ER
PT J
AU Krishna, MC
Matsumoto, S
Saito, K
Matsuo, M
Mitchell, JB
Ardenkjaer-Larsen, JH
AF Krishna, Murali C.
Matsumoto, Shingo
Saito, Keita
Matsuo, Masayuki
Mitchell, James B.
Ardenkjaer-Larsen, Jan H.
TI Magnetic resonance imaging of tumor oxygenation and metabolic profile
SO ACTA ONCOLOGICA
LA English
DT Review
ID CANCER-THERAPY; HYPOXIA; RADIOTHERAPY; BIOLOGY; CELL; CARCINOMA; HEAD;
NECK
AB The tumor microenvironment is distinct from normal tissue as a result of abnormal vascular network characterized by hypoxia, low pH, high interstitial fluid pressure and elevated glycolytic activity. This poses a barrier to treatments including radiation therapy and chemotherapy. Imaging methods which can characterize such features non-invasively and repeatedly will be of significant value in planning treatment as well as monitoring response to treatment. The three techniques based on magnetic resonance imaging (MRI) are reviewed here. Tumor pO(2) can be measured by two MRI methods requiring an exogenous contrast agent: electron paramagnetic resonance imaging (EPRI) and Overhauser magnetic resonance imaging (OMRI). Tumor metabolic profi le can be assessed by a third method, hyperpolarized metabolic MR, based on injection of hyperpolarized biological molecules labeled with C-13 or N-15 and MR spectroscopic imaging. Imaging pO(2) in tumors is now a robust pre-clinical imaging modality with potential for implementation clinically. Pre-clinical studies and an initial clinical study with hyperpolarized metabolic MR have been successful and suggest that the method may be part of image-guided radiotherapy to select patients for tailored individual treatment regimens.
C1 [Krishna, Murali C.; Matsumoto, Shingo; Saito, Keita; Matsuo, Masayuki; Mitchell, James B.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ardenkjaer-Larsen, Jan H.] GE Healthcare, Brondby, Denmark.
[Ardenkjaer-Larsen, Jan H.] Tech Univ Denmark, DK-2800 Lyngby, Denmark.
RP Ardenkjaer-Larsen, JH (reprint author), GE Healthcare, Pk Alle 295, DK-2605 Brondby, Denmark.
EM Jan.henrik.ardenkjaer-larsen@ge.com
RI Ardenkjar-Larsen, Jan Henrik/B-5765-2017
OI Ardenkjar-Larsen, Jan Henrik/0000-0001-6167-6926
NR 25
TC 10
Z9 10
U1 0
U2 19
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0284-186X
J9 ACTA ONCOL
JI Acta Oncol.
PD OCT
PY 2013
VL 52
IS 7
BP 1248
EP 1256
DI 10.3109/0284186X.2013.819118
PG 9
WC Oncology
SC Oncology
GA 223AU
UT WOS:000324776100002
PM 23957619
ER
PT J
AU Guha, S
Cao, M
Kane, RM
Savino, AM
Zou, SG
Dong, YQ
AF Guha, Sujay
Cao, Min
Kane, Ryan M.
Savino, Anthony M.
Zou, Sige
Dong, Yuqing
TI The longevity effect of cranberry extract in Caenorhabditis elegans is
modulated by daf-16 and osr-1
SO AGE
LA English
DT Article
DE Cranberry; Longevity; Aging intervention; daf-16; osr-1; Caenorhabditis
elegans
ID URINARY-TRACT-INFECTIONS; LIFE-SPAN; C. ELEGANS;
DROSOPHILA-MELANOGASTER; STRESS RESISTANCE; INHIBITION; PHYTOCHEMICALS;
EXPRESSION; BLUEBERRY; MECHANISM
AB Nutraceuticals are known to have numerous health and disease preventing properties. Recent studies suggest that extracts containing cranberry may have anti-aging benefits. However, little is known about whether and how cranberry by itself promotes longevity and healthspan in any organism. Here we examined the effect of a cranberry only extract on lifespan and healthspan in Caenorhabditis elegans. Supplementation of the diet with cranberry extract (CBE) increased the lifespan in C. elegans in a concentration-dependent manner. Cranberry also increased tolerance of C. elegans to heat shock, but not to oxidative stress or ultraviolet irradiation. In addition, we tested the effect of cranberry on brood size and motility and found that cranberry did not influence these behaviors. Our mechanistic studies indicated that lifespan extension induced by CBE requires the insulin/IGF signaling pathway and DAF-16. We also found that cranberry promotes longevity through osmotic stress resistant-1 (OSR-1) and one of its downstream effectors, UNC-43, but not through SEK-1, a component of the p38 MAP kinase pathway. However, SIR-2.1 and JNK signaling pathways are not required for cranberry to promote longevity. Our findings suggest that cranberry supplementation confers increased longevity and stress resistance in C. elegans through pathways modulated by daf-16 and osr-1. This study reveals the anti-aging property of widely consumed cranberry and elucidates the underpinning mechanisms.
C1 [Guha, Sujay; Cao, Min; Kane, Ryan M.; Savino, Anthony M.; Dong, Yuqing] Clemson Univ, Dept Biol Sci, Clemson, SC 29634 USA.
[Cao, Min; Dong, Yuqing] Clemson Univ, Inst Engaged Aging, Clemson, SC 29634 USA.
[Zou, Sige] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
[Dong, Yuqing] Clemson Univ, Clemson, SC 29634 USA.
RP Zou, SG (reprint author), NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
EM zous@grc.nia.nih.gov; ydong@clemson.edu
FU NIH National Center for Research Resources (NCRR); Clemson University;
National Institute on Aging, NIH
FX Caenorhabditis elegans strains used in this work were provided by the
Caenorhabditis Genetics Center, which is funded by the NIH National
Center for Research Resources (NCRR). We are grateful to members of the
Dong laboratory for the helpful discussions. We thank H. Knap for the
assistance with qPCR, Y. Wei and A. Tietje for the help with the
fluoremeter, T. Bruce for the assistance with microscopy. We especially
thank S. Smith and M. Bonaccorsi for the help with worm maintenance and
reagents preparation, and R. Ghaedian for providing cranberry extract.
We thank E. Spangler and A. Brown for editing this paper. This work was
supported by the Creative Inquiry fund at Clemson University to Y. D.
and M. C and the Intramural Research Program at the National Institute
on Aging, NIH to S.Z.
NR 79
TC 21
Z9 27
U1 2
U2 31
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
J9 AGE
JI Age
PD OCT
PY 2013
VL 35
IS 5
BP 1559
EP 1574
DI 10.1007/s11357-012-9459-x
PG 16
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 219XO
UT WOS:000324545200004
PM 22864793
ER
PT J
AU Rachmany, L
Tweedie, D
Li, YZ
Rubovitch, V
Holloway, HW
Miller, J
Hoffer, BJ
Greig, NH
Pick, CG
AF Rachmany, Lital
Tweedie, David
Li, Yazhou
Rubovitch, Vardit
Holloway, Harold W.
Miller, Jonathan
Hoffer, Barry J.
Greig, Nigel H.
Pick, Chaim G.
TI Exendin-4 induced glucagon-like peptide-1 receptor activation reverses
behavioral impairments of mild traumatic brain injury in mice
SO AGE
LA English
DT Article
DE Mild traumatic brain injury; Glucagon-like peptide-1; Exendin-4;
Liraglutide; Neuroprotection; Brain trauma; Incretin; Alzheimer's
disease; Glutamate toxicity; Oxidative stress
ID TYPE-2 DIABETES-MELLITUS; CLOSED-HEAD-INJURY; CLINICAL-PRACTICE
GUIDELINES; ANXIETY-LIKE BEHAVIOR; ALZHEIMERS-DISEASE; NEURODEGENERATIVE
DISEASES; PARKINSONS-DISEASE; LOCOMOTOR-ACTIVITY; COGNITIVE FUNCTION;
SOCIAL RECOVERY
AB Mild traumatic brain injury (mTBI) represents a major and increasing public health concern and is both the most frequent cause of mortality and disability in young adults and a chief cause of morbidity in the elderly. Albeit mTBI patients do not show clear structural brain defects and, generally, do not require hospitalization, they frequently suffer from long-lasting cognitive, behavioral, and emotional problems. No effective pharmaceutical therapy is available, and existing treatment chiefly involves intensive care management after injury. The diffuse neural cell death evident after mTBI is considered mediated by oxidative stress and glutamate-induced excitotoxicity. Prior studies of the long-acting GLP-1 receptor agonist, exendin-4 (Ex-4), an incretin mimetic approved for type 2 diabetes mellitus treatment, demonstrated its neurotrophic/protective activity in cellular and animal models of stroke, Alzheimer's and Parkinson's diseases, and, consequent to commonalities in mechanisms underpinning these disorders, Ex-4 was assessed in a mouse mTBI model. In neuronal cultures in this study, Ex-4 ameliorated H2O2-induced oxidative stress and glutamate toxicity. To evaluate in vivo translation, we administered steady-state Ex-4 (3.5 pM/kg/min) or saline to control and mTBI mice over 7 days starting 48 h prior to or 1 h post-sham or mTBI (30 g weight drop under anesthesia). Ex-4 proved well-tolerated and fully ameliorated mTBI-induced deficits in novel object recognition 7 and 30 days post-trauma. Less mTBI-induced impairment was evident in Y-maze, elevated plus maze, and passive avoidance paradigms, but when impairment was apparent Ex-4 induced amelioration. Together, these results suggest that Ex-4 may act as a neurotrophic/neuroprotective drug to minimize mTBI impairment.
C1 [Rachmany, Lital; Rubovitch, Vardit; Pick, Chaim G.] Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
[Rachmany, Lital; Rubovitch, Vardit; Pick, Chaim G.] Tel Aviv Univ, Sagol Sch Neurosci, IL-69978 Tel Aviv, Israel.
[Tweedie, David; Li, Yazhou; Holloway, Harold W.; Greig, Nigel H.] NIA, Lab Neurosci, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Miller, Jonathan; Hoffer, Barry J.] Case Western Reserve Univ, Sch Med, Dept Neurosurg, Cleveland, OH 44106 USA.
[Greig, Nigel H.] NIA, Drug Design & Dev Sect, Lab Neurosci, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Greig, NH (reprint author), NIA, Drug Design & Dev Sect, Lab Neurosci, Intramural Res Program,NIH, BRC Room 05 C220,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM Greign@grc.nia.nih.gov
FU National Institute on Aging, National Institutes of Health; Sackler
School of Medicine, Tel-Aviv University
FX This research was supported in part by the Intramural Research Program
of both the National Institute on Aging, National Institutes of Health,
and the Sackler School of Medicine, Tel-Aviv University.
NR 89
TC 25
Z9 25
U1 5
U2 33
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0161-9152
J9 AGE
JI Age
PD OCT
PY 2013
VL 35
IS 5
BP 1621
EP 1636
DI 10.1007/s11357-012-9464-0
PG 16
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 219XO
UT WOS:000324545200008
PM 22892942
ER
PT J
AU Shah, SK
Hull, SC
Spinner, MA
Berkman, BE
Sanchez, LA
Abdul-Karim, R
Hsu, AP
Claypool, R
Holland, SM
AF Shah, Seema K.
Hull, Sara Chandros
Spinner, Michael A.
Berkman, Benjamin E.
Sanchez, Lauren A.
Abdul-Karim, Ruquyyah
Hsu, Amy P.
Claypool, Reginald
Holland, Steven M.
TI What Does the Duty to Warn Require?
SO AMERICAN JOURNAL OF BIOETHICS
LA English
DT Editorial Material
ID GENETIC INFORMATION; SOCIETY
C1 [Shah, Seema K.; Hull, Sara Chandros; Spinner, Michael A.; Berkman, Benjamin E.; Abdul-Karim, Ruquyyah; Hsu, Amy P.; Claypool, Reginald; Holland, Steven M.] NIH, Bethesda, MD 20892 USA.
[Sanchez, Lauren A.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA.
RP Shah, SK (reprint author), NIH, Dept Bioeth, 10 Ctr Dr,10-1C118, Bethesda, MD 20892 USA.
EM shahse@cc.nih.gov
FU National Institutes of Health (NIH)
FX This article is not subject to U.S. Copyright Law. This research was
supported by the Intramural Research Program of the National Institutes
of Health (NIH) in the Warren G. Magnuson Clinical Center. The opinions
expressed are the view of the authors. They do not represent any
position or policy of the U.S. National Institutes of Health, the Public
Health Service, or the Department of Health and Human Services.
NR 9
TC 7
Z9 7
U1 2
U2 5
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1526-5161
EI 1536-0075
J9 AM J BIOETHICS
JI Am. J. Bioeth.
PD OCT 1
PY 2013
VL 13
IS 10
BP 62
EP 63
DI 10.1080/15265161.2013.828528
PG 2
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 217FV
UT WOS:000324345300023
PM 24024817
ER
PT J
AU Lee, JE
McLerran, DF
Rolland, B
Chen, Y
Grant, EJ
Vedanthan, R
Inoue, M
Tsugane, S
Gao, YT
Tsuji, I
Kakizaki, M
Ahsan, H
Ahn, YO
Pan, WH
Ozasa, K
Yoo, KY
Sasazuki, S
Yang, G
Watanabe, T
Sugawara, Y
Parvez, F
Kim, DH
Chuang, SY
Ohishi, W
Park, SK
Feng, ZD
Thornquist, M
Boffetta, P
Zheng, W
Kang, DH
Potter, J
Sinha, R
AF Lee, Jung Eun
McLerran, Dale F.
Rolland, Betsy
Chen, Yu
Grant, Eric J.
Vedanthan, Rajesh
Inoue, Manami
Tsugane, Shoichiro
Gao, Yu-Tang
Tsuji, Ichiro
Kakizaki, Masako
Ahsan, Habibul
Ahn, Yoon-Ok
Pan, Wen-Harn
Ozasa, Kotaro
Yoo, Keun-Young
Sasazuki, Shizuka
Yang, Gong
Watanabe, Takashi
Sugawara, Yumi
Parvez, Faruque
Kim, Dong-Hyun
Chuang, Shao-Yuan
Ohishi, Waka
Park, Sue K.
Feng, Ziding
Thornquist, Mark
Boffetta, Paolo
Zheng, Wei
Kang, Daehee
Potter, John
Sinha, Rashmi
TI Meat intake and cause-specific mortality: a pooled analysis of Asian
prospective cohort studies
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID FOOD-FREQUENCY QUESTIONNAIRE; SHANGHAI WOMENS HEALTH; COLORECTAL-CANCER
RISK; CARDIOVASCULAR-DISEASE; NUTRITION TRANSITION; HEART-DISEASE;
CONSUMPTION; VALIDITY; REPRODUCIBILITY; JAPAN
AB Background: Total or red meat intake has been shown to be associated with a higher risk of mortality in Western populations, but little is known of the risks in Asian populations.
Objective: We examined temporal trends in meat consumption and associations between meat intake and all-cause and cause-specific mortality in Asia.
Design: We used ecological data from the United Nations to compare country-specific meat consumption. Separately, 8 Asian prospective cohort studies in Bangladesh, China, Japan, Korea, and Taiwan consisting of 112,310 men and 184,411 women were followed for 6.6 to 15.6 y with 24,283 all-cause, 9558 cancer, and 6373 cardiovascular disease (CVD) deaths. We estimated the study-specific HRs and 95% CIs by using a Cox regression model and pooled them by using a random-effects model.
Results: Red meat consumption was substantially lower in the Asian countries than in the United States. Fish and seafood consumption was higher in Japan and Korea than in the United States. Our pooled analysis found no association between intake of total meat (red meat, poultry, and fish/seafood) and risks of all-cause, CVD, or cancer mortality among men and women; HRs (95% CIs) for all-cause mortality from a comparison of the highest with the lowest quartile were 1.02 (0.91, 1.15) in men and 0.93 (0.86, 1.01) in women.
Conclusions: Ecological data indicate an increase in meat intake in Asian countries; however, our pooled analysis did not provide evidence of a higher risk of mortality for total meat intake and provided evidence of an inverse association with red meat, poultry, and fish/seafood. Red meat intake was inversely associated with CVD mortality in men and with cancer mortality in women in Asian countries.
C1 [Lee, Jung Eun] Sookmyung Womens Univ, Dept Food & Nutr, Seoul, South Korea.
[McLerran, Dale F.; Rolland, Betsy; Vedanthan, Rajesh; Thornquist, Mark; Potter, John] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Chen, Yu] NYU, Sch Med, Dept Environm Med, New York, NY USA.
[Grant, Eric J.; Ozasa, Kotaro] Radiat Effects Res Fdn, Dept Epidemiol, Hiroshima, Japan.
[Inoue, Manami; Tsugane, Shoichiro; Sasazuki, Shizuka] Natl Canc Ctr, Ctr Canc Prevent & Screening, Epidemiol & Prevent Div, Tokyo 104, Japan.
[Gao, Yu-Tang] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
[Tsuji, Ichiro; Kakizaki, Masako; Watanabe, Takashi; Sugawara, Yumi] Tohoku Univ, Grad Sch Med, Dept Publ Hlth & Forens Med, Div Epidemiol, Sendai, Miyagi 980, Japan.
[Ahsan, Habibul] Univ Chicago, Ctr Comprehens Canc, Dept Hlth Studies, Dept Med, Chicago, IL 60637 USA.
[Ahsan, Habibul] Univ Chicago, Ctr Comprehens Canc, Dept Human Genet, Chicago, IL 60637 USA.
[Ahn, Yoon-Ok; Yoo, Keun-Young; Park, Sue K.; Kang, Daehee] Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea.
[Pan, Wen-Harn; Chuang, Shao-Yuan] Natl Hlth Res Inst, Inst Populat Hlth Sci, Div Prevent Med & Hlth Serv Res, Miaoli, Taiwan.
[Pan, Wen-Harn] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
[Pan, Wen-Harn] Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol & Prevent Med, Taipei 10764, Taiwan.
[Yang, Gong; Zheng, Wei] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr,Div Epidemiol, Vanderbilt Epidemiol Ctr,Dept Med, Nashville, TN 37212 USA.
[Parvez, Faruque] Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY USA.
[Kim, Dong-Hyun] Hallym Univ, Coll Med, Dept Social & Prevent Med, Chunchon, South Korea.
[Ohishi, Waka] Radiat Effects Res Fdn, Dept Clin Studies, Hiroshima, Japan.
[Feng, Ziding] Univ Texas MD Anderson Canc Ctr, Sect Early Canc Detect & Biomarkers, Houston, TX 77030 USA.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Boffetta, Paolo] Mt Sinai Sch Med, Inst Translat Epidemiol, New York, NY USA.
RP Sinha, R (reprint author), Natl Canc Inst, NIH, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,RM 6E336,MSC 9768, Bethesda, MD 20892 USA.
EM sinhar@mail.nih.gov
RI Chuang, Shao-Yuan/B-3478-2011; Tsugane, Shocichiro/A-2424-2015; Sinha,
Rashmi/G-7446-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Potter, John/0000-0001-5439-1500;
Lee, Jung Eun/0000-0003-1141-878X; Kakizaki, Masako/0000-0001-6030-8953
FU National Cancer Institute, NIH; Fred Hutchinson Cancer Research Center;
Japan Public Health Center-Based Study 1; Japan Public Health
Center-Based Study 2: National Cancer Center Research and Development
Fund; Ministry of Health, Labour and Welfare, Japan; Ministry of
Education, Culture, Sports, Science and Technology, Japan; Japanese
Ministry of Health, Labour and Welfare; US Department of Energy; RERF
Research Protocol [RP-A3-11]; Shanghai Women's Health Study: NIH
[R37CA70867]; CardioVascular Disease risk FACtor Two-township Study:
Department of Health, Taiwan [DOH80-27, DOH81-021, DOH8202-1027,
DOH83-TD-015, DOH84-TD-006]; Korea Multi-Center Cancer Cohort: Ministry
of Education, Science and Technology, Korea [2009-0087452]; National
Research Foundation of Korea [2009-0087452]; Health Effects of Arsenic
Longitudinal Study: NIH [P42ES010349, R01CA102484, R01CA107431]; Seoul
Male Cohort: National Research Grant for Basic Medical Sciences, Korea;
National Research Foundation of Korea
FX Supported by the National Cancer Institute, NIH (intramural funding),
and by the Fred Hutchinson Cancer Research Center. The cohorts
participating in the pooled analysis were supported by the following
grants: Japan Public Health Center-Based Study 1 and Japan Public Health
Center-Based Study 2: National Cancer Center Research and Development
Fund; Grant-in-Aid for Cancer Research; Grant for Health Services and
Grant for Comprehensive Research on Cardiovascular and Life-Style
Related Diseases from the Ministry of Health, Labour and Welfare, Japan;
and Grant for the Scientific Research from the Ministry of Education,
Culture, Sports, Science and Technology, Japan. The Radiation Effects
Research Foundation, Hiroshima and Nagasaki, Japan, is a private,
nonprofit foundation funded by the Japanese Ministry of Health, Labour
and Welfare and the US Department of Energy. This publication was
supported by RERF Research Protocol RP-A3-11; Shanghai Women's Health
Study: NIH (R37CA70867); CardioVascular Disease risk FACtor Two-township
Study: Department of Health, Taiwan (DOH80-27, DOH81-021, DOH8202-1027,
DOH83-TD-015, and DOH84-TD-006); The Korea Multi-Center Cancer Cohort:
Ministry of Education, Science and Technology, Korea (2009-0087452);
National Research Foundation of Korea (2009-0087452); Health Effects of
Arsenic Longitudinal Study: NIH (P42ES010349, R01CA102484, and
R01CA107431); Seoul Male Cohort: National Research Grant for Basic
Medical Sciences, Korea and National Research Foundation of Korea,
1992-2011.
NR 42
TC 25
Z9 26
U1 1
U2 29
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT
PY 2013
VL 98
IS 4
BP 1032
EP 1041
DI 10.3945/ajcn.113.062638
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 221YF
UT WOS:000324696100021
PM 23902788
ER
PT J
AU Stolzenberg-Solomon, RZ
Schairer, C
Moore, S
Hollenbeck, A
Silverman, DT
AF Stolzenberg-Solomon, Rachael Z.
Schairer, Catherine
Moore, Steve
Hollenbeck, Albert
Silverman, Debra T.
TI Lifetime adiposity and risk of pancreatic cancer in the NIH-AARP Diet
and Health Study cohort
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID BODY-MASS INDEX; PHYSICAL-ACTIVITY; ANTHROPOMETRIC FACTORS;
NATIONAL-INSTITUTES; EXOGENOUS INSULIN; POOLED-ANALYSIS; EPIC COHORT; US
ADULTS; WEIGHT; OBESITY
AB Background: The association of excess body weight across a life-time with pancreatic cancer has not been examined extensively.
Objective: We determined the association for body mass index (BMI) at different ages and adiposity duration and gain with incident pancreatic adenocarcinoma in the NIH-AARP Diet and Health Study cohort.
Design: Participants aged 50-71 y completed questionnaires at baseline (1995-1996) and 6 months later that queried height and weight history. We calculated HRs and 95% CIs by using Cox proportional hazards models adjusted for age, smoking, sex, and intakes of energy and total fat.
Results: Over an average follow-up of 10.5 y, 1206 and 2122 pancreatic cancer cases were identified in the subcohort who completed the second questionnaire (n = 273,975) and the baseline cohort (n = 501,698), respectively. Compared with normal weight, overweight or obesity at ages 18, 35, 50, or >50 y (baseline BMI) was significantly associated with pancreatic cancer, with HRs ranging from 1.15 to 1.53. A longer duration of BMI (in kg/m(2)) >25.0 was significantly associated with pancreatic cancer (overall HR per 10-y increment of duration: 1.06; 95% CI: 1.02, 1.09), with individuals who reported diabetes having the greatest risk (HR per 10-y increment of duration: 1.18; 95% CI: 1.05, 1.32; P-interaction = 0.01) and rates. A substantial gain in adiposity (>10 kg/m(2)) after age 50 y was significantly associated with increased pancreatic cancer risk. The etiologic fraction of pancreatic cancer explained by adiposity at any age was 14% overall and 21% in never smokers.
Conclusion: Overweight and obesity at any age are associated with increased pancreatic cancer.
C1 [Stolzenberg-Solomon, Rachael Z.; Moore, Steve] NCI, NIH, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet,Branch Nutr Epidemiol, Rockville, MD USA.
[Schairer, Catherine] NCI, NIH, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet,Branch Biostat, Rockville, MD USA.
[Silverman, Debra T.] NCI, NIH, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet,Branch Occupat & Envir, Rockville, MD USA.
[Hollenbeck, Albert] AARP, Environm Anal Dept, Washington, DC USA.
RP Stolzenberg-Solomon, RZ (reprint author), 6120 Executive Blvd,Suite 320, Rockville, MD 20852 USA.
EM rs221z@nih.gov
RI Moore, Steven/D-8760-2016
OI Moore, Steven/0000-0002-8169-1661
FU NIH, Division of Cancer Epidemiology and Genetics, National Cancer
Institute, Department of Health and Human Services
FX Supported by the Intramural Research Program of the NIH, Division of
Cancer Epidemiology and Genetics, National Cancer Institute, Department
of Health and Human Services.
NR 50
TC 22
Z9 23
U1 1
U2 7
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT
PY 2013
VL 98
IS 4
BP 1057
EP 1065
DI 10.3945/ajcn.113.058123
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 221YF
UT WOS:000324696100024
PM 23985810
ER
PT J
AU Kim, JK
Rho, J
Prasad, V
AF Kim, Julie K.
Rho, Jason
Prasad, Vinay
TI Handheld Ultrasounds: Pocket Sized, but Pocket Ready?
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID PHYSICAL-EXAMINATION; CARRIED ULTRASOUND; EMERGENCY; GUIDANCE
C1 [Kim, Julie K.; Rho, Jason] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Prasad, Vinay] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Kim, JK (reprint author), Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
NR 12
TC 5
Z9 5
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9343
J9 AM J MED
JI Am. J. Med.
PD OCT
PY 2013
VL 126
IS 10
BP 845
EP 846
DI 10.1016/j.amjmed.2013.03.029
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 218YV
UT WOS:000324469800012
PM 23910521
ER
PT J
AU Grobman, WA
Lai, YL
Rouse, DJ
Spong, CY
Varner, MW
Mercer, BM
Leveno, KJ
Iams, JD
Wapner, RJ
Sorokin, Y
Thorp, JM
Ramin, SM
Malone, FD
O'Sullivan, MJ
Hankins, GDV
Caritis, SN
AF Grobman, William A.
Lai, Yinglei
Rouse, Dwight J.
Spong, Catherine Y.
Varner, Michael W.
Mercer, Brian M.
Leveno, Kenneth J.
Iams, Jay D.
Wapner, Ronald J.
Sorokin, Yoram
Thorp, John M.
Ramin, Susan M.
Malone, Fergal D.
O'Sullivan, Mary J.
Hankins, Gary D. V.
Caritis, Steve N.
CA Eunice Kennedy Shriver Natl Inst
TI The association of cerebral palsy and death with
small-for-gestational-age birthweight in preterm neonates by
individualized and population-based percentiles
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE cerebral palsy; death; small for gestational age
ID FETAL-GROWTH; PREGNANCIES; STANDARDS
AB OBJECTIVE: The objective of the study was to determine whether an individualized growth standard (IS) improves the identification of preterm small-for-gestational-age (SGA) neonates at risk of developing moderate/severe cerebral palsy (CP) or death.
STUDY DESIGN: This study was a secondary analysis of data from a randomized trial of MgSO4 for the prevention of CP or death among anticipated preterm births. Singleton nonanomalous liveborns delivered before 34 weeks' were classified as SGA (less than the 10th percentile for their gestational age) by a population standard (PS) or an IS (incorporating maternal age, height, weight, parity, race/ethnicity, and neonatal sex). The primary outcome was the prediction of moderate or severe CP or death by age 2 years.
RESULTS: Of 1588 eligible newborns, 143 (9.4%) experienced CP (n = 33) or death (n = 110). Forty-four (2.8%) were SGA by the PS and 364 (22.9%) by the IS. All PS-SGA newborns also were identified as IS-SGA. SGA newborns by either standard had a similarly increased risk of CP or death (PS: relative risk [RR], 2.4, 95% confidence interval [CI], 1.3-4.3 vs IS: RR, 1.8, 95% CI, 1.3-2.5, respectively). The similarity of RRs remained after stratification by the MgSO4 treatment group. The IS was more sensitive (36% vs 6%, P < .001) but less specific (78% vs 98%, P < .001) for CP or death. The receiver operating characteristic curve analysis revealed a statistically lower area under the curve for the PS, although the ability of either method to predict which neonates would subsequently develop CP or death was poor (PS: 0.55, 95% CI, 0.49-0.60 vs IS: 0.59, 95% CI, 0.54-0.64, P < .001).
CONCLUSION: An individualized SGA growth standard does not improve the association with, or prediction of, CP or death by age 2 years.
C1 [Grobman, William A.] Northwestern Univ, Dept Obstet & Gynecol, Chicago, IL 60611 USA.
[Rouse, Dwight J.] Brown Univ, Providence, RI 02912 USA.
[Varner, Michael W.] Univ Utah, Hlth Sci Ctr, Salt Lake City, UT USA.
[Mercer, Brian M.] Case Western Reserve Univ, MetroHlth Med Ctr, Cleveland, OH 44106 USA.
[Leveno, Kenneth J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Iams, Jay D.] Ohio State Univ, Columbus, OH 43210 USA.
[Wapner, Ronald J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Wapner, Ronald J.] Drexel Univ, Philadelphia, PA 19104 USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Thorp, John M.] Univ N Carolina, Chapel Hill, NC USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Childrens Mem Hermann Hosp, Houston, TX 77030 USA.
[Malone, Fergal D.] Columbia Univ, New York, NY USA.
[O'Sullivan, Mary J.] Univ Miami, Miami, FL USA.
[Hankins, Gary D. V.] Univ Texas Med Branch, Galveston, TX 77555 USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Lai, Yinglei] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Grobman, WA (reprint author), Northwestern Univ, Dept Obstet & Gynecol, Chicago, IL 60611 USA.
RI Varner, Michael/K-9890-2013
OI caritis, steve/0000-0002-2169-0712; Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HD27869, HD34208, HD34116, HD40544, HD27915, HD34136,
HD21414, HD27917, HD27860, HD40560, HD40545, HD40485, HD40500, HD27905,
HD27861, HD34122, HD40512, HD53907, HD34210, HD21410, HD36801, HD19897];
National Center for Research Resources [M01-RR-000080]; National
Institutes of Health; Department of Health and Human Services; National
Institute of Neurological Disorders and Stroke
FX Supported by grants HD27869, HD34208, HD34116, HD40544, HD27915,
HD34136, HD21414, HD27917, HD27860, HD40560, HD40545, HD40485, HD40500,
HD27905, HD27861, HD34122, HD40512, HD53907, HD34210, HD21410, HD36801,
and HD19897 from the Eunice Kennedy Shriver National Institute of Child
Health and Human Development; and grant M01-RR-000080 from the National
Center for Research Resources, National Institutes of Health, Department
of Health and Human Services, and the National Institute of Neurological
Disorders and Stroke.
NR 15
TC 1
Z9 1
U1 0
U2 13
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD OCT
PY 2013
VL 209
IS 4
AR 340.e1
DI 10.1016/j.ajog.2013.06.007
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 221YY
UT WOS:000324698200015
PM 23770470
ER
PT J
AU Thorp, JM
Rice, MM
Harper, M
Klebanoff, M
Sorokin, Y
Varner, MW
Wapner, RJ
Caritis, SN
Iams, JD
Peaceman, AM
Mercer, BM
Sciscione, A
Rouse, DJ
Ramin, SM
Anderson, GB
AF Thorp, John M., Jr.
Rice, Madeline Murguia
Harper, Margaret
Klebanoff, Mark
Sorokin, Yoram
Varner, Michael W.
Wapner, Ronald J.
Caritis, Steve N.
Iams, Jay D.
Peaceman, Alan M.
Mercer, Brian M.
Sciscione, Anthony
Rouse, Dwight J.
Ramin, Susan M.
Anderson, Garland B.
CA Natl Inst Child Hlth Human Dev Mat
TI Advanced lipoprotein measures and recurrent preterm birth
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE birth; lipids; nutrition
ID LOW-DENSITY-LIPOPROTEIN; OF-THE-LITERATURE; RISK; ATHEROSCLEROSIS;
PREGNANCY; PREECLAMPSIA
AB OBJECTIVE: Lipoproteins are associated with atherogenic and inflammatory processes, and these processes may be related to adverse pregnancy outcomes. We therefore examined whether variations in lipoprotein particle size and concentration are associated with preterm birth (PTB) <35 weeks' gestation.
STUDY DESIGN: This is a case-control ancillary study to a randomized trial of omega-3 fatty acid supplementation to prevent recurrent PTB. We measured standard lipids and used nuclear magnetic resonance (NMR) spectroscopy to characterize 17 lipoprotein particles from plasma collected at the baseline randomization visit (16-21 weeks' gestation) in 128 cases (PTB <35 weeks' gestation) and 132 term controls. Logistic regression models controlled for study center, race/ethnicity, number of prior PTB, smoking, and treatment group, as well as total low-density lipoprotein (LDL), high-density lipoprotein, and triglyceride concentrations when examining LDLNMR, high-density lipoprotein(NMR), and very LDL (VLDL)(NMR), respectively.
RESULTS: Only 1 of the 17 NMR lipoproteins was associated with recurrent PTB. We observed an increased odds of recurrent PTB of 1.04 (95% confidence interval, 1.01-1.08; P = .02) per nanometer increase in VLDLNMR particle size and an odds ratio of 3.00 (confidence interval, 1.40-6.43; P = .005) for the third tertile of VLDLNMR particle size compared with the first tertile.
CONCLUSION: In women with prior PTB, variations in midpregnancy lipoproteins were not associated with recurrent PTB overall, however the association observed with VLDLNMR particle size is suggestive that PTB may be amenable to lifestyle, nutritional, or pharmacologic interventions.
C1 Univ N Carolina, Dept Obstet, Chapel Hill, NC 27599 USA.
[Thorp, John M., Jr.] Univ N Carolina, Dept Gynecol, Chapel Hill, NC 27599 USA.
[Harper, Margaret] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Varner, Michael W.] Univ Utah, Hlth Sci Ctr, Salt Lake City, UT USA.
[Wapner, Ronald J.] Columbia Univ, New York, NY USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Iams, Jay D.] Ohio State Univ, Columbus, OH 43210 USA.
[Mercer, Brian M.] Case Western Reserve Univ, MetrolHlth Med Ctr, Cleveland, OH 44106 USA.
[Peaceman, Alan M.] Northwestern Univ, Chicago, IL 60611 USA.
[Sciscione, Anthony] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
[Rouse, Dwight J.] Univ Alabama Birmingham, Birmingham, AL USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Anderson, Garland B.] Univ Texas Med Ctr, Galveston, TX USA.
[Rice, Madeline Murguia] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Klebanoff, Mark] NICHHD, Bethesda, MD 20892 USA.
RP Thorp, JM (reprint author), Univ N Carolina, Dept Obstet & Gynecol, 3025 Old Clin Bldg,CB 7570, Chapel Hill, NC 27599 USA.
EM john_thorp@med.unc.edu
RI Varner, Michael/K-9890-2013
OI caritis, steve/0000-0002-2169-0712; Peaceman, Alan/0000-0002-4515-4850;
Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [HD27860, HD27917, HD40560, HD34208, HD40485,
HD21410, HD27915, HD40500, HD40512, HD40544, MO1-RR-000080, HD34136,
HD27869, HD40545, HD36801, HD19897]
FX The project described was supported by grants from the Eunice Kennedy
Shriver National Institute of Child Health and Human Development (NICHD)
(HD27860, HD27917, HD40560, HD34208, HD40485, HD21410, HD27915, HD40500,
HD40512, HD40544, MO1-RR-000080, HD34136, HD27869, HD40545, HD36801,
HD19897) and does not necessarily represent the official views of the
NICHD or National Institutes of Health.
NR 19
TC 0
Z9 0
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD OCT
PY 2013
VL 209
IS 4
AR 342.e1
DI 10.1016/j.ajog.2013.06.005
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 221YY
UT WOS:000324698200016
PM 23770464
ER
PT J
AU Marino, N
Woditschka, S
Reed, LT
Nakayama, J
Mayer, M
Wetzel, M
Steeg, PS
AF Marino, Natascia
Woditschka, Stephan
Reed, L. Tiffany
Nakayama, Joji
Mayer, Musa
Wetzel, Maria
Steeg, Patricia S.
TI Breast Cancer Metastasis Issues for the Personalization of Its
Prevention and Treatment
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Review
ID CIRCULATING TUMOR-CELLS; FACTOR RECEPTOR 2; CLINICAL-IMPLICATIONS;
THERAPEUTIC TARGET; MOLECULAR-BIOLOGY; BONE METASTASES; HIGH-FREQUENCY;
GROWTH; BRAIN; PROGRESSION
AB Despite important progress in adjuvant and neoadjuvant therapies, metastatic disease often develops in breast cancer patients and remains the leading cause of their deaths. For patients with established metastatic disease, therapy is palliative, with few breaks and with mounting adverse effects. Many have hypothesized that a personalized or precision approach (the terms are used interchangeably) to cancer therapy, in which treatment is based on the individual characteristics of each patient, will provide better outcomes. Here, we discuss the molecular basis of breast cancer metastasis and the challenges in personalization of treatment. The instability of metastatic tumors remains a leading obstacle to personalization, because information from a patient's primary tumor may not accurately reflect the metastasis, and one metastasis may vary from another. Furthermore, the variable presence of tumor subpopulations, such as stem cells and dormant cells, may increase the complexity of the targeted treatments needed. Although molecular signatures and circulating biomarkers have been identified in breast cancer, there is lack of validated predictive molecular markers to optimize treatment choices for either prevention or treatment of metastatic disease. Finally, to maximize the information that can be obtained, increased attention to clinical trial design in the metastasis preventive setting is needed.
C1 [Marino, Natascia; Woditschka, Stephan; Reed, L. Tiffany; Nakayama, Joji; Steeg, Patricia S.] NCI, Womens Canc Sect, Lab Mol Pharmacol, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Mayer, Musa] AdvancedBC Org, New York, NY USA.
[Wetzel, Maria] Michigan Breast Canc Coalit, Baldwin, MI USA.
RP Marino, N (reprint author), NCI, Womens Canc Sect, Lab Mol Pharmacol, Ctr Canc Res, Bldg 37,Room 1126,37 Convent Dr, Bethesda, MD 20892 USA.
EM marinon@mail.nih.gov
FU Intramural Program of the National Cancer Institute
FX Supported by the Intramural Program of the National Cancer Institute.
NR 108
TC 19
Z9 19
U1 2
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD OCT
PY 2013
VL 183
IS 4
BP 1084
EP 1095
DI 10.1016/j.ajpath.2013.06.012
PG 12
WC Pathology
SC Pathology
GA 227MU
UT WOS:000325118800006
PM 23895915
ER
PT J
AU Li, HZ
Rodriguez-Canales, J
Liu, WL
Zhu, JQ
Hanson, JC
Pack, S
Zhuang, ZP
Emmert-Buck, MR
Rodgers, GP
AF Li, Hongzhen
Rodriguez-Canales, Jaime
Liu, Wenli
Zhu, Jianqiong
Hanson, Jeffrey C.
Pack, Svetlana
Zhuang, Zhengping
Emmert-Buck, Michael R.
Rodgers, Griffin P.
TI Deletion of the Olfactomedin 4 Gene Is Associated with Progression of
Human Prostate Cancer
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; CATHEPSIN-D; ASPARTIC PROTEASE; EPITHELIAL-CELLS;
CHROMOSOME 13Q; ALLELIC LOSS; HIGH-GRADE; CARCINOMA; HGC-1;
IDENTIFICATION
AB The olfactomedin 4 (OLFM4) gene is Located on chromosome 13q14.3, which frequently is deleted in human prostate cancer. However, direct genetic evidence of OLFM4 gene alteration in human prostate cancer has not yet been obtained. In this study, we investigated the genetics, protein expression, and functions of the OLFM4 gene in human prostate cancer. We found overall 25% deletions within the OLFM4 gene in cancerous epithelial cells compared with adjacent normal epithelial cells that were microdissected from 31 prostate cancer specimens using laser-capture microdissection and genomic DNA sequencing. We found 28% to 45% hemizygous and 15% to 57% homozygous deletions of the OLFM4 gene via fluorescence in situ hybridization analysis from 44 different prostate cancer patient samples. Moreover, homozygous deletion of the OLFM4 gene significantly correlated with advanced prostate cancer. By using immunohistochemical analysis of 162 prostate cancer tissue array samples representing a range of Gleason scores, we found that OLFM4 protein expression correlated inversely with advanced prostate cancer, consistent with the genetic results. We also showed that a truncated mutant of OLFM4 that lacks the olfactomedin domain eliminated suppression of PC-3 prostate cancer cell growth. Together, our findings indicate that OLFM4 is a novel candidate tumor-suppressor gene for chromosome 13q and may shed new light on strategies that could be used for the diagnosis, prognosis, and treatment of prostate cancer patients.
C1 [Li, Hongzhen; Liu, Wenli; Zhu, Jianqiong; Rodgers, Griffin P.] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Rodriguez-Canales, Jaime; Hanson, Jeffrey C.; Emmert-Buck, Michael R.] NINDS, Pathogenet Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Pack, Svetlana] NINDS, Chromosome Unit, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Zhuang, Zhengping] NINDS, Neurosurg Biol & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
[Rodriguez-Canales, Jaime] Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.
RP Rodgers, GP (reprint author), NHLBI, Mol & Clin Hematol Branch, NIH, Bldg 10,Room 9N119,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gr5n@nih.gov
RI Pack, Svetlana/C-2020-2014
FU NIH/National Institute of Diabetes and Digestive and Kidney Diseases
FX Supported by the Intramural Research Program, NIH/National Institute of
Diabetes and Digestive and Kidney Diseases.
NR 38
TC 8
Z9 9
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD OCT
PY 2013
VL 183
IS 4
BP 1329
EP 1338
DI 10.1016/j.ajpath.2013.06.028
PG 10
WC Pathology
SC Pathology
GA 227MU
UT WOS:000325118800027
PM 24070418
ER
PT J
AU Ren, JH
Sherman, A
Bertram, R
Goforth, PB
Nunemaker, CS
Waters, CD
Satin, LS
AF Ren, Jianhua
Sherman, Arthur
Bertram, Richard
Goforth, Paulette B.
Nunemaker, Craig S.
Waters, Christopher D.
Satin, Leslie S.
TI Slow oscillations of K-ATP conductance in mouse pancreatic islets
provide support for electrical bursting driven by metabolic oscillations
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE oscillations; ATP-sensitive potassium channels; islets; insulin
ID PULSATILE INSULIN-SECRETION; CYTOSOLIC CA2+ CONCENTRATION; BETA-CELLS;
PORTAL-VEIN; PLASMA-MEMBRANE; CALCIUM; MODEL; GLUCOSE; CURRENTS;
ELECTROPHYSIOLOGY
AB We used the patch clamp technique in situ to test the hypothesis that slow oscillations in metabolism mediate slow electrical oscillations in mouse pancreatic islets by causing oscillations in K-ATP channel activity. Total conductance was measured over the course of slow bursting oscillations in surface beta-cells of islets exposed to 11.1 mM glucose by either switching from current clamp to voltage clamp at different phases of the bursting cycle or by clamping the cells to -60 mV and running two-second voltage ramps from -120 to -50 mV every 20 s. The membrane conductance, calculated from the slopes of the ramp current-voltage curves, oscillated and was larger during the silent phase than during the active phase of the burst. The ramp conductance was sensitive to diazoxide, and the oscillatory component was reduced by sulfonylureas or by lowering extracellular glucose to 2.8 mM, suggesting that the oscillatory total conductance is due to oscillatory KATP channel conductance. We demonstrate that these results are consistent with the Dual Oscillator model, in which glycolytic oscillations drive slow electrical bursting, but not with other models in which metabolic oscillations are secondary to calcium oscillations. The simulations also confirm that oscillations in membrane conductance can be well estimated from measurements of slope conductance and distinguished from gap junction conductance. Furthermore, the oscillatory conductance was blocked by tolbutamide in isolated beta-cells. The data, combined with insights from mathematical models, support a mechanism of slow (similar to 5 min) bursting driven by oscillations in metabolism, rather than by oscillations in the intracellular free calcium concentration.
C1 [Ren, Jianhua; Goforth, Paulette B.; Satin, Leslie S.] Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA.
[Ren, Jianhua; Goforth, Paulette B.; Satin, Leslie S.] Univ Michigan, Sch Med, Brehm Diabet Ctr, Ann Arbor, MI 48109 USA.
[Sherman, Arthur] NIDDK, NIH, Lab Biol Modeling, Bethesda, MD USA.
[Bertram, Richard] Florida State Univ, Dept Math, Tallahassee, FL 32306 USA.
[Bertram, Richard] Florida State Univ, Program Mol Biophys, Tallahassee, FL 32306 USA.
[Bertram, Richard] Florida State Univ, Program Neurosci, Tallahassee, FL 32306 USA.
[Nunemaker, Craig S.; Waters, Christopher D.] Univ Virginia, Div Endocrinol & Metab, Charlottesville, VA USA.
RP Satin, LS (reprint author), Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA.
EM lsatin@umich.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases [RO1
DK-46409, R01 DK-080714, RO1 DK-089182]; Intramural Research Program of
the NIDDK
FX Work in the Satin laboratory was supported by National Institute of
Diabetes and Digestive and Kidney Diseases grant RO1 DK-46409. A.
Sherman was supported by the Intramural Research Program of the NIDDK.
R. Bertram was supported by National Institute of Diabetes and Digestive
and Kidney Diseases grant R01 DK-080714 and C. S. Nunemaker by RO1
DK-089182.
NR 47
TC 17
Z9 17
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD OCT
PY 2013
VL 305
IS 7
BP E805
EP E817
DI 10.1152/ajpendo.00046.2013
PG 13
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 230MO
UT WOS:000325344800005
PM 23921138
ER
PT J
AU Binder, AM
Adjemian, J
Olivier, KN
Prevots, DR
AF Binder, Alison M.
Adjemian, Jennifer
Olivier, Kenneth N.
Prevots, D. Rebecca
TI Epidemiology of Nontuberculous Mycobacterial Infections and Associated
Chronic Macrolide Use among Persons with Cystic Fibrosis
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE macrolides; cystic fibrosis; nontuberculous mycobacteria
ID AZITHROMYCIN; ABSCESSUS; PREVALENCE; RESISTANCE; DIAGNOSIS; CHILDREN
AB Rationale: Persons with cystic fibrosis (CF) are at high risk of nontuberculous mycobacterial (NTM) infection, with treatment requiring prolonged multidrug regimens that include macrolides. Although macrolides, specifically azithromycin, are used in the management of patients with CF with chronic Pseudomonas, macrolide-resistant NTM infections are of growing concern.
Objectives: To evaluate the relationship between chronic macrolide use and NTM infection among patients with CF included in the 2011 CF Patient Registry (CFPR).
Methods: We performed a nested case-control study: incident NTM cases were persons aged more than 5 years with at least one positive culture for NTM in 2011. Controls were persons with negative cultures in 2010 and 2011.
Measurements and Main Results: The 2011 CFPR included 27,112 patients; 5,403 (20%) were cultured for mycobacteria in 2010-2011 and met all inclusion criteria. Of these, 191 (4%) were NTM-positive in 2011 only (cases); 5,212 (96%) were NTM-negative in 2010 and 2011 (control subjects). Among the cases, 122 (64%) were culture-positive for Mycobacterium avium complex (MAC) and 69 (36%) for M. abscessus. Azithromycin use in 2010 was less frequently reported among MAC cases (57%; odds ratio = 0.7, P < 0.05) and M. abscessus cases (51%; odds ratio = 0.5, P < 0.01) than in control subjects (66%). Among adolescents and adults, patients with the greatest number of years on chronic macrolides were the least likely to develop incident NTM in 2011 (P < 0.01).
Conclusions: Patients with incident NTM infections from either MAC or M. abscessus were less likely to have had chronic azithromycin treatment in the past year. However, because macrolide monotherapy may lead to macrolide resistance, routine screening for NTM should be considered for persons with CF.
C1 [Binder, Alison M.; Adjemian, Jennifer; Prevots, D. Rebecca] NIAID, Epidemiol Unit, NIH, Bethesda, MD 20892 USA.
[Olivier, Kenneth N.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Adjemian, J (reprint author), Qrts 15 B-1,8 West Dr,MSC 2665, Bethesda, MD 20892 USA.
EM jennifer.adjemian@nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases
FX Supported by the Division of Intramural Research, National Institute of
Allergy and Infectious Diseases.
NR 23
TC 41
Z9 41
U1 0
U2 5
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD OCT 1
PY 2013
VL 188
IS 7
BP 807
EP 812
DI 10.1164/rccm.201307-1200OC
PG 6
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 230OG
UT WOS:000325350600011
PM 23927602
ER
PT J
AU Shi, YY
Gochuico, BR
Yu, GY
Tang, XM
Osorio, JC
Fernandez, IE
Risquez, CF
Patel, AS
Shi, Y
Wathelet, MG
Goodwin, AJ
Haspel, JA
Ryter, SW
Billings, EM
Kaminski, N
Morse, D
Rosas, IO
AF Shi, Yuanyuan
Gochuico, Bernadette R.
Yu, Guoying
Tang, Xiaomeng
Osorio, Juan C.
Fernandez, Isis E.
Risquez, Cristobal F.
Patel, Avignat S.
Shi, Ying
Wathelet, Marc G.
Goodwin, Andrew J.
Haspel, Jeffrey A.
Ryter, Stefan W.
Billings, Eric M.
Kaminski, Naftali
Morse, Danielle
Rosas, Ivan O.
TI Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1-mediated
Transforming Growth Factor-beta Receptor I Internalization and
Inhibiting Transforming Growth Factor-beta 1 Signaling
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE idiopathic pulmonary fibrosis; TGF-beta 1 signaling; syndecan-2;
alveolar macrophage
ID IDIOPATHIC PULMONARY-FIBROSIS; TGF-BETA; LUNG FIBROSIS;
EPITHELIAL-CELLS; TRANSGENIC MICE; DISEASE; MACROPHAGES; EXPRESSION;
BLEOMYCIN; PATHWAYS
AB Rationale: Alveolar transforming growth factor (TGF)-beta 1 signaling and expression of TGF-beta 1 target genes are increased in patients with idiopathic pulmonary fibrosis (IPF) and in animal models of pulmonary fibrosis. Internalization and degradation of TGF-beta receptor TbRI inhibits TGF-beta signaling and could attenuate development of experimental lung fibrosis.
Objectives: To demonstrate that after experimental lung injury, human syndecan-2 confers antifibrotic effects by inhibiting TGF-beta 1 signaling in alveolar epithelial cells.
Methods: Microarray assays were performed to identify genes differentially expressed in alveolar macrophages of patients with IPF versus control subjects. Transgenic mice that constitutively overexpress human syndecan-2 in macrophages were developed to test the antifibrotic properties of syndecan-2. In vitro assays were performed to determine syndecan-2-dependent changes in epithelial cell TGF-beta 1 signaling, TGF-beta 1, and TbRI internalization and apoptosis. Wildtype mice were treated with recombinant human syndecan-2 during the fibrotic phase of bleomycin-induced lung injury.
Measurements and Main Results: We observed significant increases in alveolar macrophage syndecan-2 levels in patients with IPF. Macrophage-specific overexpression of human syndecan-2 in transgenic mice conferred antifibrotic effects after lung injury by inhibiting TGF-beta 1 signaling and downstream expression of TGF-beta 1 target genes, reducing extracellular matrix production and alveolar epithelial cell apoptosis. In vitro, syndecan-2 promoted caveolin-1-dependent internalization of TGF-beta 1 and TbRI in alveolar epithelial cells, which inhibited TGF-beta 1 signaling and epithelial cell apoptosis. Therapeutic administration of human syndecan-2 abrogated lung fibrosis in mice.
Conclusions: Alveolar macrophage syndecan-2 exerts antifibrotic effects by promoting caveolin-1-dependent TGF-beta 1 and TbRI internalization and inhibiting TGF-beta 1 signaling in alveolar epithelial cells. Hence, molecules that facilitate TbRI degradation via endocytosis represent potential therapies for pulmonary fibrosis.
C1 [Shi, Yuanyuan; Osorio, Juan C.; Fernandez, Isis E.; Risquez, Cristobal F.; Patel, Avignat S.; Shi, Ying; Goodwin, Andrew J.; Haspel, Jeffrey A.; Ryter, Stefan W.; Morse, Danielle; Rosas, Ivan O.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Shi, Yuanyuan; Tang, Xiaomeng; Wathelet, Marc G.; Rosas, Ivan O.] Lovelace Resp Res Inst, Albuquerque, NM USA.
[Gochuico, Bernadette R.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Billings, Eric M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Yu, Guoying; Kaminski, Naftali] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
RP Rosas, IO (reprint author), Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM irosas@rics.bwh.harvard.edu
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX The authors thank Sandra MacDonald, Hai Ping Wu, Ping Ren, and Gustavo
Pacheco for their contributions. They also thank Dr. Jeanine D'Armiento
(University of Columbia) for kindly providing the alveolar
macrophage-specific SREP promoter construct and Dr. Steven D. Nathan
(INOVA Fair-fax Hospital) for enabling the procurement of human IPF
tissue samples. Finally, the authors thank Drs. Augustine M. K. Choi,
Joel Moss, and William A. Gahl for scientific guidance and critical
review of the manuscript. This research was supported in part by the
Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health.
NR 52
TC 10
Z9 10
U1 1
U2 4
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD OCT 1
PY 2013
VL 188
IS 7
BP 831
EP 841
DI 10.1164/rccm.201303-0434OC
PG 11
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 230OG
UT WOS:000325350600014
PM 23924348
ER
PT J
AU Gokhale, NA
AF Gokhale, Nikhil A.
TI Membrane phosphoinositides and protein-membrane interactions
SO AMINO ACIDS
LA English
DT Review
DE Proteins; Phosphoinositides; Lipids; Protein-membrane interactions;
Biochemistry; Signal transduction
ID PLASMA-MEMBRANE; PHOSPHORYLATION; SPECIFICITY; ENDOCYTOSIS; PI(4,5)P-2;
MUTATION; RECEPTOR; AKT/PKB; DOMAINS; COMPLEX
AB Proteins with polybasic clusters bind to negatively charged phosphoinositides at the cell membrane. In this review, I have briefly discussed the types of phosphoinositides naturally found on membrane surfaces and how they recruit protein complexes for carrying out the process of signal transduction. A large number of researchers from around the world are now focusing their attention on protein-membrane binding, as these interactions have started to offer us a much better insight into the process of cell signaling. The main areas discussed in this brief review article include the phosphoinositide binding specificities of proteins and the role of their lipid binding in signaling processes downstream of membrane recruitment.
C1 NIEHS, Inositol Signaling Grp, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Gokhale, NA (reprint author), NIEHS, Inositol Signaling Grp, Lab Signal Transduct, NIH, 111 TW Alexander Dr,Bldg 101 Room F-247, Res Triangle Pk, NC 27709 USA.
EM Nikhil.Gokhale@umassmed.edu
NR 35
TC 2
Z9 2
U1 0
U2 22
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0939-4451
J9 AMINO ACIDS
JI Amino Acids
PD OCT
PY 2013
VL 45
IS 4
BP 751
EP 754
DI 10.1007/s00726-013-1512-2
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 220HV
UT WOS:000324574500005
PM 23824360
ER
PT J
AU Anizan, S
Milman, G
Desrosiers, N
Barnes, AJ
Gorelick, DA
Huestis, MA
AF Anizan, Sebastien
Milman, Garry
Desrosiers, Nathalie
Barnes, Allan J.
Gorelick, David A.
Huestis, Marilyn A.
TI Oral fluid cannabinoid concentrations following controlled smoked
cannabis in chronic frequent and occasional smokers
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Tetrahydrocannabinol; Cannabinoids;
11-Nor-9-carboxy-tetrahydrocannabinol; Oral fluid; Statsure Saliva
Sampler; Drug testing
ID TANDEM MASS-SPECTROMETRY; METABOLITE
11-NOR-DELTA(9)-TETRAHYDROCANNABINOL-9-CARBOXYLIC ACID; 2-DIMENSIONAL
GAS-CHROMATOGRAPHY; LIQUID-CHROMATOGRAPHY; SIMULTANEOUS QUANTIFICATION;
PHARMACOKINETIC PROPERTIES; CYTOCHROME-P450 EXPRESSION; HEAVY USERS;
DELTA(9)-TETRAHYDROCANNABINOL; MARIJUANA
AB Oral fluid (OF) is an alternative biological matrix for monitoring cannabis intake in drug testing, and drugged driving (DUID) programs, but OF cannabinoid test interpretation is challenging. Controlled cannabinoid administration studies provide a scientific database for interpreting cannabinoid OF tests. We compared differences in OF cannabinoid concentrations from 19 h before to 30 h after smoking a 6.8 % THC cigarette in chronic frequent and occasional cannabis smokers. OF was collected with the Statsure Saliva Sampler (TM) OF device. 2D-GC-MS was used to quantify cannabinoids in 357 OF specimens; 65 had inadequate OF volume within 3 h after smoking. All OF specimens were THC-positive for up to 13.5 h after smoking, without significant differences between frequent and occasional smokers over 30 h. Cannabidiol (CBD) and cannabinol (CBN) had short median last detection times (2.5-4 h for CBD and 6-8 h for CBN) in both groups. THCCOOH was detected in 25 and 212 occasional and frequent smokers' OF samples, respectively. THCCOOH provided longer detection windows than THC in all frequent smokers. As THCCOOH is not present in cannabis smoke, its presence in OF minimizes the potential for false positive results from passive environmental smoke exposure, and can identify oral THC ingestion, while OF THC cannot. THC a parts per thousand yenaEuro parts per thousand 1 mu g/L, in addition to CBD a parts per thousand yenaEuro parts per thousand 1 mu g/L or CBN a parts per thousand yenaEuro parts per thousand 1 mu g/L suggested recent cannabis intake (a parts per thousand currency sign13.5 h), important for DUID cases, whereas THC a parts per thousand yenaEuro parts per thousand 1 mu g/L or THC a parts per thousand yenaEuro parts per thousand 2 mu g/L cutoffs had longer detection windows (a parts per thousand yen30 h), important for workplace testing. THCCOOH windows of detection for chronic, frequent cannabis smokers extended beyond 30 h, while they were shorter (0-24 h) for occasional cannabis smokers.
C1 [Anizan, Sebastien; Milman, Garry; Desrosiers, Nathalie; Barnes, Allan J.; Gorelick, David A.; Huestis, Marilyn A.] NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Desrosiers, Nathalie] Univ Maryland, Toxicol Program, Baltimore, MD 21224 USA.
[Huestis, Marilyn A.] NIDA, Intramural Res Program, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, Intramural Res Program, Biomed Res Ctr, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institutes of Health, Intramural Research Program, National
Institute on Drug Abuse
FX The authors would like to thank Dr D. M. Schwope for his contribution to
the study design. This research was funded by the National Institutes of
Health, Intramural Research Program, National Institute on Drug Abuse.
NR 47
TC 16
Z9 16
U1 2
U2 38
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD OCT
PY 2013
VL 405
IS 26
BP 8451
EP 8461
DI 10.1007/s00216-013-7291-5
PG 11
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 227LQ
UT WOS:000325114900007
PM 23954944
ER
PT J
AU Hamilton, JG
Hutson, SP
Moser, RP
Kobrin, SC
Frohnmayer, AE
Alter, BP
Han, PKJ
AF Hamilton, Jada G.
Hutson, Sadie P.
Moser, Richard P.
Kobrin, Sarah C.
Frohnmayer, Amy E.
Alter, Blanche P.
Han, Paul K. J.
TI Sources of Uncertainty and Their Association with Medical Decision
Making: Exploring Mechanisms in Fanconi Anemia
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Ambiguity; Uncertainty; Medical decision making; Fanconi anemia;
Hematopoietic stem cell transplantation
ID BONE-MARROW-TRANSPLANTATION; BREAST-CANCER; CELL TRANSPLANTATION;
RECEIVE TRANSPLANTS; PERCEIVED AMBIGUITY; HEALTH-CARE; RISK;
COMMUNICATION; INFORMATION; PERCEPTIONS
AB Effects of different sources of medical uncertainty on people's health-related cognitions, emotions, and decision making have yet to be systematically examined.
The aim of this study is to examine how uncertainties arising from different sources are associated with decision making regarding stem cell transplantation in Fanconi anemia, a rare, inherited bone marrow failure syndrome that typically presents during childhood.
Data were collected through a cross-sectional survey of 178 parents of 126 Fanconi anemia patients.
Two distinct sources of uncertainty were associated with decision outcomes: probability was associated with a lower likelihood of choosing stem cell transplantation, and ambiguity due to conflicting expert opinions was associated with greater decision-making difficulty. Concern about transplantation may mediate these associations.
Different sources of uncertainty have different effects on Fanconi anemia treatment decisions, which may be mediated by parents' emotional reactions. Further research is needed to elucidate these effects and help Fanconi anemia families cope with uncertainty.
C1 [Hamilton, Jada G.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH, Rockville, MD 20850 USA.
[Hamilton, Jada G.; Kobrin, Sarah C.] NCI, Proc Care Res Branch, Div Canc Control & Populat Sci, NIH, Rockville, MD 20850 USA.
[Hutson, Sadie P.] Univ Tennessee, Coll Nursing, Knoxville, TN USA.
[Hutson, Sadie P.; Alter, Blanche P.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA.
[Moser, Richard P.; Kobrin, Sarah C.] NCI, Sci Res & Technol Branch, Div Canc Control & Populat Sci, NIH, Rockville, MD 20850 USA.
[Frohnmayer, Amy E.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Han, Paul K. J.] Maine Med Ctr Res Inst, Ctr Outcomes Res & Evaluat, Scarborough, ME USA.
RP Hamilton, JG (reprint author), NCI, Canc Prevent Fellowship Program, Canc Prevent Div, NIH, 9609 Med Ctr Dr,Room 3E632, Rockville, MD 20850 USA.
EM jada.hamilton@nih.gov
OI Han, Paul/0000-0003-0165-1940
FU Intramural NIH HHS
NR 54
TC 12
Z9 12
U1 2
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD OCT
PY 2013
VL 46
IS 2
BP 204
EP 216
DI 10.1007/s12160-013-9507-5
PG 13
WC Psychology, Multidisciplinary
SC Psychology
GA 219GI
UT WOS:000324493900011
PM 23637072
ER
PT J
AU Tanaka, TQ
Deu, E
Molina-Cruz, A
Ashburne, MJ
Ali, O
Suri, A
Kortagere, S
Bogyo, M
Williamsona, KC
AF Tanaka, Takeshi Q.
Deu, Edgar
Molina-Cruz, Alvaro
Ashburne, Michael J.
Ali, Omar
Suri, Amreena
Kortagere, Sandhya
Bogyo, Matthew
Williamsona, Kim C.
TI Plasmodium Dipeptidyl Aminopeptidases as Malaria Transmission-Blocking
Drug Targets
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID FALCIPARUM GAMETOCYTES; HEMOGLOBIN DEGRADATION; LIFE-CYCLE; PARASITE;
MOSQUITO; BERGHEI; IDENTIFICATION; INFECTIVITY; MATURATION; PROTEASES
AB The Plasmodium falciparum and P. berghei genomes each contain three dipeptidyl aminopeptidase (dpap) homologs. dpap1 and -3 are critical for asexual growth, but the role of dpap2, the gametocyte-specific homolog, has not been tested. If DPAPs are essential for transmission as well as asexual growth, then a DPAP inhibitor could be used for treatment and to block transmission. To directly analyze the role of DPAP2, a dpap2-minus P. berghei (Pbdpap2 Delta) line was generated. The Pbdpap2 Delta parasites grew normally, differentiated into gametocytes, and generated sporozoites that were infectious to mice when fed to a mosquito. However, Pbdpap1 transcription was >2-fold upregulated in the Pbdpap2 Delta clonal lines, possibly compensating for the loss of Pbdpap2. The role of DPAP1 and -3 in the dpap2 Delta parasites was then evaluated using a DPAP inhibitor, ML4118S. When ML4118S was added to the Pbdpap2 Delta parasites just before a mosquito membrane feed, mosquito infectivity was not affected. To assess longer exposures to ML4118S and further evaluate the role of DPAPs during gametocyte development in a parasite that causes human malaria, the dpap2 deletion was repeated in P. falciparum. Viable P. falciparum dpap2 (Pfdpap2)-minus parasites were obtained that produced morphologically normal gametocytes. Both wild-type and Pfdpap2-negative parasites were sensitive to ML4118S, indicating that, unlike many antimalarials, ML4118S has activity against parasites at both the asexual and sexual stages and that DPAP1 and -3 may be targets for a dual-stage drug that can treat patients and block malaria transmission.
C1 [Tanaka, Takeshi Q.; Molina-Cruz, Alvaro; Williamsona, Kim C.] NIAID, Lab Malaria & Vector Res, Natl Inst Hlth, Rockville, MD USA.
[Deu, Edgar; Bogyo, Matthew] Stanford Sch Med, Dept Pathol, Stanford, CA USA.
[Ashburne, Michael J.; Ali, Omar; Suri, Amreena; Williamsona, Kim C.] Loyola Univ, Dept Biol, Chicago, IL 60611 USA.
[Kortagere, Sandhya] Drexel Univ, Coll Med, Dept Microbiol & Immunol, Philadelphia, PA 19104 USA.
RP Williamsona, KC (reprint author), NIAID, Lab Malaria & Vector Res, Natl Inst Hlth, Rockville, MD USA.
EM kwilli4@luc.edu
FU Divisions of Intramural Research at the National Institute of Allergy
and Infectious Diseases, National Institutes of Health; National
Institute of Allergy and Infectious Diseases, National Institutes of
Health [AI40592, AI48826]
FX This work was supported by the Divisions of Intramural Research at the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, and by Public Health Service grants AI40592 and
AI48826 from the National Institute of Allergy and Infectious Diseases,
National Institutes of Health.
NR 37
TC 3
Z9 3
U1 1
U2 14
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
EI 1098-6596
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2013
VL 57
IS 10
BP 4645
EP 4652
DI 10.1128/AAC.02495-12
PG 8
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 219BU
UT WOS:000324480300007
PM 23836185
ER
PT J
AU Safronetz, D
Falzarano, D
Scott, DP
Furuta, Y
Feldmann, H
Gowen, BB
AF Safronetz, David
Falzarano, Darryl
Scott, Dana P.
Furuta, Yousuke
Feldmann, Heinz
Gowen, Brian B.
TI Antiviral Efficacy of Favipiravir against Two Prominent Etiological
Agents of Hantavirus Pulmonary Syndrome
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID ORALLY-ADMINISTERED T-705; SIN NOMBRE VIRUS; INTRAVENOUS RIBAVIRIN;
ANDES VIRUS; HEMORRHAGIC-FEVER; DOUBLE-BLIND; IN-VITRO; INFECTION;
MODEL; DISEASE
AB Hantavirus pulmonary syndrome (HPS) is caused by infection with several Sigmodontinae- and Neotominae-borne hantaviruses and has a case fatality rate of 30 to 50%. Humans often become infected by inhalation of materials contaminated with virus-laden rodent urine or saliva, although human-to-human transmission has also been documented for Andes virus (ANDV). The ability to transmit via aerosolization, coupled with the high mortality rates and lack of therapeutic options, makes the development of medical countermeasures against HPS imperative. In the present study, we evaluated the efficacy of the broad-spectrum antiviral agent favipiravir (T-705) against Sin Nombre virus (SNV) and ANDV, the predominant causes of HPS in North and South America, respectively. In vitro, T-705 potently inhibited SNV and ANDV, as evidenced by decreased detection of viral RNA and reduced infectious titers. For both viruses, the 90% effective concentration was estimated at <= 5 mu g/ml (<= 31.8 mu M). In the lethal ANDV hamster model, daily administration of oral T-705 at 50 or 100 mg/kg of body weight diminished the detection of viral RNA and antigen in tissue specimens and significantly improved survival rates. Oral T-705 therapy remained protective against HPS when treatment was initiated prior to the onset of viremia. No disease model for SNV exists; however, using a hamster-adapted SNV, we found that daily administration of oral T-705 significantly reduced the detection of SNV RNA and antigen in tissue specimens, suggesting that the compound would also be effective against HPS in North America. Combined, these results suggest that T-705 treatment is beneficial for postexposure prophylaxis against HPS-causing viruses and should be considered for probable exposures.
C1 [Safronetz, David; Falzarano, Darryl; Feldmann, Heinz] NIAID, Virol Lab, Hamilton, MT USA.
[Scott, Dana P.] NIAID, Rocky Mt Vet Branch, Div Intramural Res, NIH, Hamilton, MT USA.
[Furuta, Yousuke] Toyama Chem Co Ltd, Project T 705, Tokyo, Japan.
[Gowen, Brian B.] Utah State Univ, Dept Anim Dairy & Vet Sci, Logan, UT 84322 USA.
RP Safronetz, D (reprint author), NIAID, Virol Lab, Hamilton, MT USA.
EM safronetzd@niaid.nih.gov; brian.gowen@usu.edu
FU Division of Intramural Research (DIR) of the National Institutes of
Allergy and Infectious Diseases (NIAID), National Institutes of Health
(NIH); NIH [U54 AI-065357]
FX This work was supported in part by the Division of Intramural Research
(DIR) of the National Institutes of Allergy and Infectious Diseases
(NIAID), National Institutes of Health (NIH). B. B. G. was supported by
NIH grant U54 AI-065357 (Rocky Mountain Regional Center of Excellence
for Biodefense and Emerging Infectious Disease Research).
NR 35
TC 21
Z9 21
U1 0
U2 11
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2013
VL 57
IS 10
BP 4673
EP 4680
DI 10.1128/AAC.00886-13
PG 8
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 219BU
UT WOS:000324480300011
PM 23856782
ER
PT J
AU Yedidi, RS
Maeda, K
Fyvie, WS
Steffey, M
Davis, DA
Palmer, I
Aoki, M
Kaufman, JD
Stahl, SJ
Garimella, H
Das, D
Wingfield, PT
Ghosh, AK
Mitsuya, H
AF Yedidi, Ravikiran S.
Maeda, Kenji
Fyvie, W. Sean
Steffey, Melinda
Davis, David A.
Palmer, Ira
Aoki, Manabu
Kaufman, Joshua D.
Stahl, Stephen J.
Garimella, Harisha
Das, Debananda
Wingfield, Paul T.
Ghosh, Arun K.
Mitsuya, Hiroaki
TI P2' Benzene Carboxylic Acid Moiety Is Associated with Decrease in
Cellular Uptake: Evaluation of Novel Nonpeptidic HIV-1 Protease
Inhibitors Containing P2 bis-Tetrahydrofuran Moiety
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS PROTEASE; ANTIRETROVIRAL THERAPY; BIOLOGICAL
EVALUATION; VIRAL INFECTIVITY; ESCHERICHIA-COLI; DIFFRACTION DATA;
IN-VITRO; DARUNAVIR; RESISTANT; POTENT
AB GRL007 and GRL008, two structurally related nonpeptidic human immunodeficiency virus type 1 (HIV-1) protease inhibitors (PIs) containing 3(R), 3a(S), 6a(R)-bis-tetrahydrofuranylurethane (bis-THF) as the P2 moiety and a sulfonamide isostere consisting of benzene carboxylic acid and benzene carboxamide as the P2 ' moiety, respectively, were evaluated for their antiviral activity and interactions with wild-type protease (PRWT). Both GRL007 (K-i of 12.7 pM with PRWT) and GRL008 (K-i of 8.9 pM) inhibited PRWT with high potency in vitro. X-ray crystallographic analysis of PRWT in complex with GRL007 or GRL008 showed that the bis-THF moiety of both compounds has three direct polar contacts with the backbone amide nitrogen atoms of Asp29 and Asp30 of PRWT. The P2' moiety of both compounds showed one direct contact with the backbone of Asp30' and a bridging polar contact with Gly48' through a water molecule. Cell-based antiviral assays showed that GRL007 was inactive (50% effective concentration [EC50] of >1 mu M) while GRL008 was highly active (EC50 of 0.04 mu M) against wild-type HIV-1. High-performance liquid chromatography (HPLC)/mass spectrometry-based cellular uptake assays showed 8.1- and 84-fold higher intracellular concentrations of GRL008 than GRL007 in human MT-2 and MT-4 cell extracts, respectively. Thus, GRL007, in spite of its favorable enzyme-inhibitory activity and protease binding profile, exhibited a lack of antiviral activity in cell-based assays, most likely due to its compromised cellular uptake associated with its P2' benzene carboxylic acid moiety. The anti-HIV-1 potency, favorable toxicity, and binding profile of GRL008 suggest that further optimization of the P2' moiety may improve its antiretroviral features.
C1 [Yedidi, Ravikiran S.; Maeda, Kenji; Garimella, Harisha; Das, Debananda; Mitsuya, Hiroaki] NCI, Expt Retrovirol Sect, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
[Yedidi, Ravikiran S.; Maeda, Kenji; Garimella, Harisha; Das, Debananda; Mitsuya, Hiroaki] NCI, Retroviral Dis Sect, NIH, Bethesda, MD 20892 USA.
[Fyvie, W. Sean; Steffey, Melinda; Ghosh, Arun K.] Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
[Fyvie, W. Sean; Steffey, Melinda; Ghosh, Arun K.] Purdue Univ, Dept Med Chem, W Lafayette, IN 47907 USA.
[Palmer, Ira; Kaufman, Joshua D.; Stahl, Stephen J.; Wingfield, Paul T.] NIAMSD, Prot Express Lab, NIH, Bethesda, MD 20892 USA.
[Aoki, Manabu; Mitsuya, Hiroaki] Kumamoto Univ, Grad Sch Biomed Sci, Dept Hematol, Kumamoto, Japan.
[Aoki, Manabu; Mitsuya, Hiroaki] Kumamoto Univ, Dept Infect Dis, Grad Sch Biomed Sci, Kumamoto, Japan.
[Aoki, Manabu] Kumamoto Hlth Sci Univ, Dept Med Technol, Kumamoto, Japan.
RP Mitsuya, H (reprint author), NCI, Expt Retrovirol Sect, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
EM hmitsuya@helix.nih.gov
OI Yedidi, Ravikiran/0000-0003-2755-1307
FU Intramural Research Program of Center for Cancer Research, National
Cancer Institute, National Institutes of Health; global education and
research center aiming at the control of AIDS; Monbu-Kagakusho;
Promotion of AIDS Research from the Ministry of Health, Welfare, and
Labor of Japan; National Institutes of Health [GM53386]; U.S. Department
of Energy, Office of Science, Office of Basic Energy Sciences
[DE-AC02-06CH11357]; Southeast Regional Collaborative Access Team
[SER-CAT] [W-31-109-Eng-38]; Michigan Economic Development Corporation;
Michigan Technology Tri-Corridor [085P1000817]
FX This study was supported in part by the Intramural Research Program of
Center for Cancer Research, National Cancer Institute, National
Institutes of Health (H. M.), in part by a grant from a global education
and research center aiming at the control of AIDS (Global Center of
Excellence supported by Monbu-Kagakusho), Promotion of AIDS Research
from the Ministry of Health, Welfare, and Labor of Japan, by a grant to
the Cooperative Research Project on Clinical and Epidemiological Studies
of Emerging and Re-emerging Infectious Diseases (Renkei Jigyo: number
78, Kumamoto University) of Monbu-Kagakusho (H. M.), and by a grant from
the National Institutes of Health (GM53386 to A. K. G.). 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
number DE-AC02-06CH11357 (Life Sciences Collaborative Access Team
[LS-CAT]) and contract number W-31-109-Eng-38 (Southeast Regional
Collaborative Access Team [SER-CAT]). Use of LS-CAT Sector 21 was
supported by the Michigan Economic Development Corporation and the
Michigan Technology Tri-Corridor for the support of this research
program (grant 085P1000817). Supporting institutions for SER-CAT may be
found at www.ser-cat.org/members.html.
NR 44
TC 8
Z9 9
U1 0
U2 11
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2013
VL 57
IS 10
BP 4920
EP 4927
DI 10.1128/AAC.00868-13
PG 8
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 219BU
UT WOS:000324480300040
PM 23877703
ER
PT J
AU Sionov, E
Chang, YC
Kwon-Chung, KJ
AF Sionov, Edward
Chang, Yun C.
Kwon-Chung, Kyung J.
TI Azole Heteroresistance in Cryptococcus neoformans: Emergence of
Resistant Clones with Chromosomal Disomy in the Mouse Brain during
Fluconazole Treatment
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID DRUG-RESISTANCE; ERG11
AB We have previously reported that Cryptococcus neoformans strains are innately heteroresistant to fluconazole in vitro, producing minor, highly resistant subpopulations due to adaptive formation of disomic chromosomes. Using a mouse model, we assessed the emergence of heteroresistant clones in the brain during fluconazole treatment and found that the occurrence of heteroresistant clones in vivo with chromosomal disomy is strain dependent. Interestingly, emergence of heteroresistant clones in vivo was unrelated to the strain's MIC to fluconazole.
C1 [Sionov, Edward; Chang, Yun C.; Kwon-Chung, Kyung J.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Kwon-Chung, KJ (reprint author), NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM June_Kwon-Chung@nih.gov
FU Intramural Program of the National Institute of Allergy and Infectious
Diseases, NIH
FX This study was supported by funds from the Intramural Program of the
National Institute of Allergy and Infectious Diseases, NIH.
NR 11
TC 14
Z9 15
U1 1
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2013
VL 57
IS 10
BP 5127
EP 5130
DI 10.1128/AAC.00694-13
PG 4
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 219BU
UT WOS:000324480300067
PM 23836187
ER
PT J
AU Laek, B
Szklo, M
McClelland, RL
Ding, JZ
Tsai, MY
Bluemke, DA
Tracy, R
Matsushita, K
AF Laek, Babray
Szklo, Moyses
McClelland, Robyn L.
Ding, Jingzhong
Tsai, Michael Y.
Bluemke, David A.
Tracy, Russell
Matsushita, Kunihiro
TI The prospective association of Chlamydia pneumoniae and four other
pathogens with development of coronary artery calcium: The Multi-Ethnic
Study of Atherosclerosis (MESA)
SO ATHEROSCLEROSIS
LA English
DT Article
DE Coronary calcium; Atherosclerosis; Pathogens; Infection
ID AORTIC-STENOSIS; SUBCLINICAL ATHEROSCLEROSIS; CARDIOVASCULAR-DISEASE;
RISK DEVELOPMENT; YOUNG-ADULTS; CALCIFICATION; PROGRESSION; ANTIBODIES;
HEAT-SHOCK-PROTEIN-60; QUANTIFICATION
AB Objective: Previous basic and cross-sectional studies obtained conflicting results regarding the association of pathogens with coronary artery calcium (CAC). The aim of this study is to prospectively evaluate this association in a population-based cohort.
Methods: We examined 5744 individuals aged 45-84 years at baseline (2000-02) who underwent repeated CAC assessment on average 2.4 years later (a half at visit 2 [2002-04] and the other half at visit 3 [2004-05]). CAC incidence was defined as newly detectable CAC at follow-up (475 cases of 2942 participants). CAC progression was defined as annualized change in CAC Agatston score >= 10 units/year if baseline CAC score >0 to <100 or >= 10%/year if baseline score >= 100 (1537 cases of 2802 participants). Seropositivity was assessed in the entire cohort for Chlamydia pneumoniae and in a random sample (n = 873) for Helicobacter pylori, cytomegalovirus, herpes simplex virus, and hepatitis A virus.
Results: Seropositivity to C. pneumoniae was not significantly associated with CAC incidence (odds ratio [OR] 1.11 [95% CI, 0.88-1.39], P = 0.371) or progression (1.14 [0.96-1.36], P = 0.135) even in unadjusted models. When CAC incidence and progression were combined, we observed significant association with C. pneumoniae seropositivity before adjustment (OR 1.17 [1.03-1.33], P = 0.016) but not in a model adjusting for traditional risk factors (1.04 [0.90-1.19], P = 0.611). The results were consistent across subgroups according to age, sex, and race/ethnicity. None of five pathogens or their accrual was associated with CAC incidence and progression in the subsample.
Conclusion: Our prospective study does not support the pathophysiological involvement of these pathogens in CAC development. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Laek, Babray; Szklo, Moyses; Matsushita, Kunihiro] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD 21205 USA.
[Laek, Babray] Erasmus Univ, Netherlands Inst Hlth Sci, NL-3015 GJ Rotterdam, Netherlands.
[McClelland, Robyn L.] Univ Washington, Dept Biostat, Seattle, WA 98115 USA.
[Ding, Jingzhong] Wake Forest Univ, Sch Med, Sticht Ctr Aging, Winston Salem, NC 27157 USA.
[Tsai, Michael Y.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Tracy, Russell] Univ Vermont, Dept Pathol, Colchester, VT 05446 USA.
RP Matsushita, K (reprint author), Johns Hopkins Univ, Dept Epidemiol, 615 N Wolfe St, Baltimore, MD 21205 USA.
EM babraylaek@gmail.com; mszklo@jhsph.edu; rmcclell@u.washington.edu;
jding@wfubmc.edu; tsaix001@tc.umn.edu; bluemked@nih.gov;
russell.tracy@uvm.edu; kmatsush@jhsph.edu
OI Bluemke, David/0000-0002-8323-8086
FU NIH [RO1-HL66075-01, RO1-HL-65580-01, R01-HL086719, K23-HL103844,
T32-HL007287-33]; MESA [NO1-HC-95159, NO1-HC-95169]
FX This study was supported by the NIH grants (RO1-HL66075-01,
RO1-HL-65580-01, R01-HL086719, K23-HL103844, T32-HL007287-33) and the
MESA study contracts (NO1-HC-95159 through NO1-HC-95169).
NR 29
TC 5
Z9 5
U1 0
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2013
VL 230
IS 2
BP 268
EP 274
DI 10.1016/j.atherosclerosis.2013.07.053
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 222RC
UT WOS:000324747800016
PM 24075755
ER
PT J
AU Folsom, AR
Pankow, JS
Li, XH
Duprez, DA
Jacobs, DR
Klein, R
Klein, B
Tang, WH
Wong, TY
Cotch, MF
Taylor, KD
Rich, SS
Hall, JL
Post, WS
Rotter, JI
AF Folsom, Aaron R.
Pankow, James S.
Li, Xiaohui
Duprez, Daniel A.
Jacobs, David R., Jr.
Klein, Ronald
Klein, Barbara
Tang, Weihong
Wong, Tien Yin
Cotch, Mary Frances
Taylor, Kent D.
Rich, Stephen S.
Hall, Jennifer L.
Post, Wendy S.
Rotter, Jerome I.
TI No association of 9p21 with arterial elasticity and retinal
microvascular findings
SO ATHEROSCLEROSIS
LA English
DT Article
DE Prospective study; 9p21 SNP; Retinal microvascular abnormalities;
Arterial elasticity
ID CORONARY-HEART-DISEASE; ATHEROSCLEROSIS MESA; CARDIOVASCULAR-DISEASE;
VESSEL DIAMETERS; VENULAR CALIBER; RISK; LOCUS; METAANALYSIS;
COMMUNITIES; POPULATIONS
AB Objective: How 9p21 variation affects risk of cardiovascular disease is unclear, so we assessed whether 9p21 variants are associated with arterial elasticity or retinal microvascular findings.
Methods: In the prospective Multi-Ethnic Study of Atherosclerosis (MESA) we assessed 378 SNPs in the 9p21 locus. Within four ethnic groups, we used an additive genetic model to relate the 9p21 SNPs to five vascular phenotypes: small and large elasticity derived from radial diastolic pulse contour analysis; Young's elastic modulus from carotid artery ultrasound measurements; and the diameter of the central retinal arteries and veins.
Results: In neither ethnic-specific nor pooled data was there any statistically significant association between any of the 9p21 SNPs and any of the five vascular phenotypes.
Conclusion: Our study does not support an association of 9p21 variation with arterial elasticity or retinal microvascular abnormalities. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Folsom, Aaron R.; Pankow, James S.; Jacobs, David R., Jr.; Tang, Weihong] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
[Li, Xiaohui; Taylor, Kent D.; Rotter, Jerome I.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Ctr, Inst Translat Genom & Populat Sci, Torrance, CA 90502 USA.
[Duprez, Daniel A.; Hall, Jennifer L.] Univ Minnesota, Dept Med, Div Cardiovasc, Minneapolis, MN 55455 USA.
[Klein, Ronald; Klein, Barbara] Univ Wisconsin, Dept Ophthalmol & Visual Sci, Madison, WI 53726 USA.
[Wong, Tien Yin] Natl Univ Singapore, Singapore Eye Res Inst, Singapore 177577, Singapore.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
[Post, Wendy S.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Div Cardiol, Dept Med, Baltimore, MD 21205 USA.
[Post, Wendy S.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
RP Folsom, AR (reprint author), Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, 1300 South 2nd St,Suite 300, Minneapolis, MN 55454 USA.
EM folso001@umn.edu
OI Cotch, Mary Frances/0000-0002-2046-4350; Klein,
Ronald/0000-0002-4428-6237; Pankow, James/0000-0001-7076-483X
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95169,
N01-HC-65226, N02-HL-64278]; National Center for Research Resources
[UL1-RR-024156, UL1-RR-025005]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95169, N01-HC-65226, and N02-HL-64278 from the National Heart,
Lung, and Blood Institute and by grants UL1-RR-024156 and UL1-RR-025005
from the National Center for Research Resources. The authors thank the
other investigators, the staff, and the participants of the MESA study
for their valuable contributions. A full list of participating MESA
investigators and institutions can be found at
http://www.mesa-nhlbi.org.
NR 26
TC 1
Z9 1
U1 0
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2013
VL 230
IS 2
BP 301
EP 303
DI 10.1016/j.atherosclerosis.2013.07.049
PG 3
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 222RC
UT WOS:000324747800022
PM 24075760
ER
PT J
AU Wu, CP
Hsiao, SH
Sim, HM
Luo, SY
Tuo, WC
Cheng, HW
Li, YQ
Huang, YH
Ambudkar, SV
AF Wu, Chung-Pu
Hsiao, Sung-Han
Sim, Hong-May
Luo, Shi-Yu
Tuo, Wei-Cherng
Cheng, Hsing-Wen
Li, Yan-Qing
Huang, Yang-Hui
Ambudkar, Suresh V.
TI Human ABCB1 (P-glycoprotein) and ABCG2 mediate resistance to BI 2536, a
potent and selective inhibitor of Polo-like kinase 1
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE ABC transporter; Multidrug resistance; Polo-like kinase 1; BI 2536
ID ACUTE MYELOID-LEUKEMIA; MULTIDRUG-RESISTANCE; PLK1 INHIBITION;
BREAST-CANCER; IN-VITRO; PHASE-I; DRUG TRANSPORTERS; SOLID TUMORS;
CELL-GROWTH; CHEMOTHERAPY
AB The overexpression of the serine/threonine specific Polo-like kinase 1 (Plk1) has been detected in various types of cancer, and thus has fast become an attractive therapeutic target for cancer therapy. BI 2536 is the first selective inhibitor of Plk1 that inhibits cancer cell proliferation by promoting G2/M cell cycle arrest at nanomolar concentrations. Unfortunately, alike most chemotherapeutic agents, the development of acquired resistance to BI 2536 is prone to present a significant therapeutic challenge. One of the most common mechanisms for acquired resistance in cancer chemotherapy is associated with the overexpression of ATP-binding cassette (ABC) transporters ABCB1, ABCC1 and ABCG2. Here, we discovered that overexpressing of either ABCB1 or ABCG2 is a novel mechanism of acquired resistance to BI 2536 in human cancer cells. Moreover, BI 2536 stimulates the ATPase activity of both ABCB1 and ABCG2 in a concentration-dependent manner, and inhibits the drug substrate transport mediated by these transporters. More significantly, the reduced chemosensitivity and BI 2536-mediated G2/M cell cycle arrest in cancer cells overexpressing either ABCB1 or ABCG2 can be significantly restored in the presence of selective inhibitor or other chemotherapeutic agents that also interact with ABCB1 and ABCG2, such as tyrosine kinase inhibitors nilotinib and lapatinib. Taken together, our findings indicate that in order to circumvent ABCB1 or ABCG2-mediated acquired resistance to BI 2536, a combined regimen of BI 2536 and inhibitors or clinically active drugs that potently inhibit the function of ABC drug transporters, should be considered as a potential treatment strategy in the clinic. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Wu, Chung-Pu; Li, Yan-Qing] Chang Gung Univ, Coll Med, Dept Physiol & Pharmacol, Tao Yuan 333, Taiwan.
[Wu, Chung-Pu; Hsiao, Sung-Han; Luo, Shi-Yu; Tuo, Wei-Cherng; Cheng, Hsing-Wen] Chang Gung Univ, Grad Inst Biomed Sci, Coll Med, Tao Yuan 333, Taiwan.
[Wu, Chung-Pu; Huang, Yang-Hui] Chang Gung Univ, Coll Med, Mol Med Res Ctr, Tao Yuan 333, Taiwan.
[Sim, Hong-May; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Wu, CP (reprint author), 259 Wen Hwa 1st Rd, Tao Yuan 333, Taiwan.
EM wuchung@mail.cgu.edu.tw
RI Ruan, YL/B-9813-2009
FU Chang Gung Medical Research Program [CMRPD190653]; Ministry of Education
[EMRPD1B0271]; Intramural Research Program of the National Cancer
Institute, NIH, Center for Cancer Research
FX The authors thank Dr Susan Bates (National Cancer Institute, NIH), for
providing FTC and tariquidar. This work was supported by funds from the
Chang Gung Medical Research Program (CMRPD190653) and grant to Chang
Gung University from the Ministry of Education EMRPD1B0271. Drs H.-M.
Sim and S.V. Ambudkar were supported by the Intramural Research Program
of the National Cancer Institute, NIH, Center for Cancer Research.
NR 47
TC 12
Z9 12
U1 0
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD OCT 1
PY 2013
VL 86
IS 7
BP 904
EP 913
DI 10.1016/j.bcp.2013.08.004
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 225QH
UT WOS:000324976900007
PM 23962445
ER
PT J
AU Chittori, S
Simanshu, DK
Banerjee, S
Murthy, AMV
Mathivanan, S
Savithri, HS
Murthy, MRN
AF Chittori, Sagar
Simanshu, Dhirendra Kumar
Banerjee, Sanchari
Murthy, Ambika Mosale Venkatesh
Mathivanan, Subashini
Savithri, Handanahal Subbarao
Murthy, Mathur Ramabhadrashastry Narasimha
TI Mechanistic features of Salmonella typhimurium propionate kinase (TdcD):
Insights from kinetic and crystallographic studies
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Article
DE Salmonella typhimurium; Short-chain fatty acid metabolism; Enzyme assay;
X-ray crystallography; Protein dynamics
ID BACTERIAL PHOSPHOTRANSFERASE SYSTEM; COMPLETE GENOME SEQUENCE; CHAIN
FATTY-ACIDS; ACETATE KINASE; ESCHERICHIA-COLI; L-THREONINE;
METHANOSARCINA-THERMOPHILA; ANAEROBIC DEGRADATION; CRYSTAL-STRUCTURES;
SUGAR-TRANSPORT
AB Short-chain fatty acids (SCFAs) play a major role in carbon cycle and can be utilized as a source of carbon and energy by bacteria. Salmonella typhimurium propionate kinase (StTdcD) catalyzes reversible transfer of the gamma-phosphate of ATP to propionate during L-threonine degradation to propionate. Kinetic analysis revealed that StTdcD possesses broad ligand specificity and could be activated by various SCFAs (propionate > acetate approximate to butyrate), nucleotides (ATP approximate to GTP > CTP approximate to TTP; dATP > dGTP > dCTP) and metal ions (Mg2+ approximate to Mn2+ > Co2+). Inhibition of StTdcD by tricarboxylic acid (TCA) cycle intermediates such as citrate, succinate, alpha-ketoglutarate and malate suggests that the enzyme could be under plausible feedback regulation. Crystal structures of StTdcD bound to PO4 (phosphate), AMP, ATP, Ap4 (adenosine tetraphosphate), GMP, GDP, GTP, CMP and CTP revealed that binding of nucleotide mainly involves hydrophobic interactions with the base moiety and could account for the broad biochemical specificity observed between the enzyme and nucleotides. Modeling and site-directed mutagenesis studies suggest Ala88 to be an important residue involved in determining the rate of catalysis with SCFA substrates. Molecular dynamics simulations on monomeric and dimeric forms of StTdcD revealed plausible open and closed states, and also suggested role for dimerization in stabilizing segment 235-290 involved in interfacial interactions and ligand binding. Observation of an ethylene glycol molecule bound sufficiently close to the gamma-phosphate in StTdcD complexes with triphosphate nucleotides supports direct in-line phosphoryl transfer. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Chittori, Sagar; Simanshu, Dhirendra Kumar; Banerjee, Sanchari; Mathivanan, Subashini; Murthy, Mathur Ramabhadrashastry Narasimha] Indian Inst Sci, Mol Biophys Unit, Bangalore 560012, Karnataka, India.
[Murthy, Ambika Mosale Venkatesh; Savithri, Handanahal Subbarao] Indian Inst Sci, Dept Biochem, Bangalore 560012, Karnataka, India.
RP Chittori, S (reprint author), NICHD, Lab Cellular & Mol Neurophysiol, Porter Neurosci Res Ctr, NIH,DHHS, Bethesda, MD 20892 USA.
EM sagar@mbu.iisc.ernet.in
OI Chittori, Sagar/0000-0003-1417-6552; Simanshu,
Dhirendra/0000-0002-9717-4618
FU Department of Science and Technology (DST); Department of Biotechnology
(DBT), Government of India; Council for Scientific and Industrial
Research (CSIR), Government of India; IISc
FX Financial assistance from the Department of Science and Technology (DST)
and the Department of Biotechnology (DBT), Government of India is
acknowledged. SC thanks the Council for Scientific and Industrial
Research (CSIR), Government of India for Senior Research Fellowship and
IISc for Research Associate fellowship. We thank James and Babu of X-ray
facility at the Molecular Biophysics Unit (MBU); Shankar Prasad Kanaujia
for the help in MD simulations; and Chhavi Mathur and Yuvaraj
Ranganathan for critical reading of the manuscript.
NR 46
TC 2
Z9 2
U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD OCT
PY 2013
VL 1834
IS 10
BP 2036
EP 2044
DI 10.1016/j.bbapap.2013.05.020
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 229BL
UT WOS:000325236700009
PM 23747922
ER
PT J
AU Locatelli-Hoops, SC
Gorshkova, I
Gawrisch, K
Yeliseev, AA
AF Locatelli-Hoops, Silvia C.
Gorshkova, Inna
Gawrisch, Klaus
Yeliseev, Alexei A.
TI Expression, surface immobilization, and characterization of functional
recombinant cannabinoid receptor CB2
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Article
DE Cannabinoid receptor CB2; Surface plasmon resonance (SPR); Rho-tag;
Functional immobilization
ID PROTEIN-COUPLED RECEPTOR; PLASMON RESONANCE; PARAMAGNETIC
PROTEOLIPOSOMES; MONOCLONAL-ANTIBODIES; BIOSENSOR TECHNOLOGY; CHEMOKINE
RECEPTORS; PURIFICATION; RHODOPSIN; BINDING; LIGAND
AB Human peripheral cannabinoid receptor CB2, a G protein-coupled receptor (GPCR) involved in regulation of immune response has become an important target for pharmaceutical drug development. Structural and functional studies on CB2 may benefit from immobilization of the purified and functional receptor onto a suitable surface at a controlled density and, preferably in a uniform orientation. The goal of this project was to develop a generic strategy for preparation of functional recombinant CB2 and immobilization at solid interfaces. Expression of CB2 as a fusion with Rho-tag (peptide composed of the last nine amino acids of rhodopsin) in E. coli was evaluated in terms of protein levels, accessibility of the tag, and activity of the receptor. The structural integrity of CB2 was tested by ligand binding to the receptor solubilized in detergent micelles, captured on tag-specific monoclonal 104 antibody-coated resin. Highly pure and functional CB2 was obtained by sequential chromatography on a 1D4- and Ni-NTA-resin and its affinity to the 1D4 antibody characterized by surface plasmon resonance (SPR). Either the purified receptor or fusion CB2 from the crude cell extract was captured onto a 1D4-coated CM4 chip (Biacore) in a quantitative fashion at uniform orientation as demonstrated by the SPR signal. Furthermore, the accessibility of the extracellular surface of immobilized CB2 and the affinity of interaction with a novel monoclonal antibody NAA-1 was studied by SPR. In summary, we present an integral strategy for purification, surface immobilization, ligand-and antibody binding studies of functional cannabinoid receptor CB2. Published by Elsevier B.V.
C1 [Locatelli-Hoops, Silvia C.; Gawrisch, Klaus; Yeliseev, Alexei A.] NIAAA, NIH, Bethesda, MD 20892 USA.
[Gorshkova, Inna] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
RP Yeliseev, AA (reprint author), NIAAA, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA.
EM yeliseeva@mail.nih.gov
FU NIAAA; NIBIB, NIH
FX This work was supported by the Intramural program of the NIAAA and
NIBIB, NIH. The authors thank Mrs. Lioudmila Zoubak for assistance with
expression and purification of CB2, Dr. Grzegorz Pizczek
(NHLBI) for making the Biacore 3000 SPR instrument available, and Dr.
John Northup for assistance with expression of G protein subunits.
NR 32
TC 1
Z9 1
U1 0
U2 27
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
EI 0006-3002
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD OCT
PY 2013
VL 1834
IS 10
BP 2045
EP 2056
DI 10.1016/j.bbapap.2013.06.003
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 229BL
UT WOS:000325236700010
PM 23777860
ER
PT J
AU Furumoto, Y
Gadina, M
AF Furumoto, Yasuko
Gadina, Massimo
TI The Arrival of JAK Inhibitors: Advancing the Treatment of Immune and
Hematologic Disorders
SO BIODRUGS
LA English
DT Article
ID PLACEBO-CONTROLLED TRIAL; JANUS KINASE INHIBITOR; CP-690,550
TOFACITINIB; RHEUMATOID-ARTHRITIS; CYTOKINE; MYELOFIBROSIS; RUXOLITINIB;
RESPONSES; ROLES; DEFICIENCY
AB Altered production of cytokines can result in pathologies ranging from autoimmune diseases to malignancies. The Janus kinase family is a small group of receptor-associated signaling molecules that is essential to the signal cascade originating from type I and type II cytokine receptors. Inhibition of tyrosine kinase enzymatic activity using small molecules has recently become a powerful tool for treatment of several malignancies. Twenty years after the discovery of these enzymes, two inhibitors for this class of kinases have been approved for clinical use and others are currently in the final stage of development. Here we review the principles of cytokines signaling, summarize our current knowledge of the approved inhibitors, and briefly introduce some of the inhibitors that are currently under development.
C1 [Furumoto, Yasuko; Gadina, Massimo] NIAMSD, Translat Immunol Sect, Off Sci & Technol, NIH, Bethesda, MD 20895 USA.
RP Gadina, M (reprint author), Bldg 10,Room 6D47-A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM gadinama@mail.nih.gov
FU Intramural NIH HHS [ZIC AR041181-04]
NR 41
TC 5
Z9 5
U1 0
U2 6
PU ADIS INT LTD
PI AUCKLAND
PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW
ZEALAND
SN 1173-8804
J9 BIODRUGS
JI Biodrugs
PD OCT
PY 2013
VL 27
IS 5
BP 431
EP 438
DI 10.1007/s40259-013-0040-7
PG 8
WC Oncology; Immunology; Pharmacology & Pharmacy
SC Oncology; Immunology; Pharmacology & Pharmacy
GA 219FG
UT WOS:000324490900002
PM 23743669
ER
PT J
AU Shneyderman, Y
Kiely, M
AF Shneyderman, Y.
Kiely, M.
TI Intimate partner violence during pregnancy: victim or perpetrator? Does
it make a difference?
SO BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY
LA English
DT Article
DE Intimate partner violence; pregnancy outcomes; risk factors
ID 18 US STATES/TERRITORIES; DOMESTIC VIOLENCE; BIRTH OUTCOMES; SUBSTANCE
USE; ADULT WOMEN; ALCOHOL-USE; HEALTH; PREVALENCE; WEIGHT; RISK
AB ObjectivesTo differentiate between forms of intimate partner violence (IPV) (victim only, perpetrator only, or participating in reciprocal violence) and examine risk profiles and pregnancy outcomes.
DesignProspective.
SettingWashington, DC, July 2001 to October 2003.
SampleA total of 1044 high-risk African-American pregnant women who participated in a randomised controlled trial to address IPV, depression, smoking and environmental tobacco smoke exposure.
MethodsMultivariable linear and logistic regression.
Main outcome measuresLow and very low birthweight, preterm and very preterm birth.
ResultsFive percent of women were victims only, 12% were perpetrators only, 27% participated in reciprocal violence and 55% reported no IPV. Women reporting reciprocal violence in the past year were more likely to drink, use illicit drugs and experience environmental tobacco smoke exposure and were less likely to be very happy about their pregnancies. Women reporting any type of IPV were more likely to be depressed than those reporting no IPV. Women experiencing reciprocal violence reported the highest levels of depression. Women who were victims of IPV were more likely to give birth prematurely and deliver low-birthweight and very-low-birthweight infants.
ConclusionsWe conclude that women were at highest risk for pregnancy risk factors when they participated in reciprocal violence and so might be at higher risk for long-term consequences, but women who were victims of IPV were more likely to show proximal negative outcomes like preterm birth and low birthweight infants. Different types of interventions may be needed for these two forms of IPV.
C1 [Shneyderman, Y.] CUNY, Borough Manhattan Community Coll, New York, NY 10021 USA.
[Kiely, M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, DHHS, Rockville, MD USA.
RP Kiely, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd, Rockville, MD USA.
EM kielym@nih.gov
OI Shneyderman, Yuliya/0000-0002-2242-0298
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Center on Minority Health and Health Disparities;
[3U18HD030445]; [3U18HD030447]; [5U18HD31206]; [3U18HD031919];
[5U18HD036104]
FX This study was supported by grants no. 3U18HD030445; 3U18HD030447;
5U18HD31206; 3U18HD031919 and 5U18HD036104, Eunice Kennedy Shriver
National Institute of Child Health and Human Development and the
National Center on Minority Health and Health Disparities. This research
was supported, in part, by the intramural programme of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development.
NR 58
TC 5
Z9 5
U1 2
U2 25
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1470-0328
J9 BJOG-INT J OBSTET GY
JI BJOG
PD OCT
PY 2013
VL 120
IS 11
BP 1375
EP 1385
DI 10.1111/1471-0528.12357
PG 11
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 216RU
UT WOS:000324302500009
PM 23786367
ER
PT J
AU Kiely, M
Gantz, MG
El-Khorazaty, MN
El-Mohandes, AAE
AF Kiely, M.
Gantz, M. G.
El-Khorazaty, M. N.
El-Mohandes, A. A. E.
TI Sequential screening for psychosocial and behavioural risk during
pregnancy in a population of urban African Americans
SO BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY
LA English
DT Article
DE African American; pregnancy; psychosocial risk
ID INTIMATE PARTNER VIOLENCE; LOW-BIRTH-WEIGHT; ENVIRONMENTAL
TOBACCO-SMOKE; RANDOMIZED-CONTROLLED-TRIAL; DEPRESSIVE SYMPTOMS;
MATERNAL SMOKING; MINORITY WOMEN; PRETERM BIRTH; SUBSTANCE USE;
LIFE-STYLE
AB ObjectiveScreening for psychosocial and behavioural risks, such as depression, intimate partner violence, and smoking, during pregnancy is considered to be state of the art in prenatal care. This prospective longitudinal analysis examines the added benefit of repeated screening, compared with a single screening, in identifying such risks during pregnancy.
DesignData were collected as part of a randomised controlled trial to address intimate partner violence, depression, smoking, and environmental tobacco smoke exposure in African American women.
SettingPrenatal care sites in the District of Columbia serving mainly women of minority background.
PopulationA cohort of 1044 African American pregnant women in the District of Columbia.
MethodsMothers were classified by their initial response (acknowledgement of risks), and these data were updated during pregnancy. Risks were considered new if they were not previously reported. Standard hypothesis tests and logistic regression were used to predict the acknowledgment of any new risk(s) during pregnancy.
Main outcome measuresNew risks: psychosocial variables to understand what factors might help identify the acknowledgement of additional risk(s).
ResultsRepeated screening identified more mothers acknowledging risk over time. Reported smoking increased by 11%, environmental tobacco smoke exposure increased by 19%, intimate partner violence increased by 9%, and depression increased by 20%. The psychosocial variables collected at the baseline that were entered into the logistic regression model included relationship status, education, Medicaid, illicit drug use, and alcohol use during pregnancy. Among these, only education less than high school was associated with the acknowledgement of new risk in the bivariate analyses, and significantly predicted the identification of new risks (OR 1.39, 95% CI 1.01-1.90).
ConclusionsIt is difficult to predict early on who will acknowledge new risks over the course of pregnancy, and thus all women should be screened repeatedly to allow for the identification of risks and intervention during prenatal care.
C1 [Kiely, M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
[Gantz, M. G.; El-Khorazaty, M. N.] RTI Int, Stat & Epidemiol Unit, Rockville, MD USA.
[El-Mohandes, A. A. E.] Univ Nebraska Med Ctr, Coll Publ Hlth, Omaha, NE USA.
RP Kiely, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd, Rockville, MD 20852 USA.
EM kielym@nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Center on Minority Health and Health Disparities;
[3U18HD030445]; [3U18HD030447]; [5U18HD31206]; [3U18HD031919];
[5U18HD036104]
FX This study was supported by grant nos 3U18HD030445, 3U18HD030447,
5U18HD31206, 3U18HD031919, and 5U18HD036104, and by the Eunice Kennedy
Shriver National Institute of Child Health and Human Development and the
National Center on Minority Health and Health Disparities. This research
was supported, in part, by the intramural program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development.
NR 46
TC 6
Z9 6
U1 2
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1470-0328
J9 BJOG-INT J OBSTET GY
JI BJOG
PD OCT
PY 2013
VL 120
IS 11
BP 1395
EP 1402
DI 10.1111/1471-0528.12202
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 216RU
UT WOS:000324302500011
PM 23906260
ER
PT J
AU Ganz, PA
Yip, CH
Gralow, JR
Distelhorst, SR
Albain, KS
Andersen, BL
Bevilacqua, JLB
de Azambuja, E
El Saghir, NS
Kaur, R
McTiernan, A
Partridge, AH
Rowland, JH
Singh-Carlson, S
Vargo, MM
Thompson, B
Anderson, BO
AF Ganz, Patricia A.
Yip, Cheng Har
Gralow, Julie R.
Distelhorst, Sandra R.
Albain, Kathy S.
Andersen, Barbara L.
Bevilacqua, Jose Luiz B.
de Azambuja, Evandro
El Saghir, Nagi S.
Kaur, Ranjit
McTiernan, Anne
Partridge, Ann H.
Rowland, Julia H.
Singh-Carlson, Savitri
Vargo, Mary M.
Thompson, Beti
Anderson, Benjamin O.
TI Supportive care after curative treatment for breast cancer (survivorship
care): Resource allocations in low- and middle-income countries. A
Breast Health Global Initiative 2013 consensus statement
SO BREAST
LA English
DT Review
DE Breast cancer; Supportive care; Survivorship; Low- and middle-income
countries; Resource allocations
ID QUALITY-OF-LIFE; FOLLOW-UP CARE; BODY-IMAGE; GUIDELINE IMPLEMENTATION;
CULTURAL COMPETENCE; SEXUAL DYSFUNCTION; MEDICAL-EDUCATION;
AMERICAN-SOCIETY; CONTROLLED-TRIAL; ARM LYMPHEDEMA
AB Breast cancer survivors may experience long-term treatment complications, must live with the risk of cancer recurrence, and often experience psychosocial complications that require supportive care services. In low- and middle-income settings, supportive care services are frequently limited, and program development for survivorship care and long-term follow-up has not been well addressed.
As part of the 5th Breast Health Global Initiative (BHGI) Global Summit, an expert panel identified nine key resources recommended for appropriate survivorship care, and developed resource-stratified recommendations to illustrate how health systems can provide supportive care services for breast cancer survivors after curative treatment, using available resources.
Key recommendations include health professional education that focuses on the management of physical and psychosocial long-term treatment complications. Patient education can help survivors transition from a provider-intense cancer treatment program to a post-treatment provider partnership and self-management program, and should include: education on recognizing disease recurrence or metastases; management of treatment-related sequelae, and psychosocial complications; and the importance of maintaining a healthy lifestyle. Increasing community awareness of survivorship issues was also identified as an important part of supportive care programs. Other recommendations include screening and management of psychosocial distress; management of long-term treatment-related complications including lymphedema, fatigue, insomnia, pain, and women's health issues; and monitoring survivors for recurrences or development of second primary malignancies. Where possible, breast cancer survivors should implement healthy lifestyle modifications, including physical activity, and maintain a healthy weight. Health professionals should provide well-documented patient care records that can follow a patient as they transition from active treatment to follow-up care. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
C1 [Ganz, Patricia A.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Yip, Cheng Har] Univ Malaya, Med Ctr, Kuala Lumpur, Malaysia.
[Gralow, Julie R.; Anderson, Benjamin O.] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
[Gralow, Julie R.; Distelhorst, Sandra R.; McTiernan, Anne; Thompson, Beti; Anderson, Benjamin O.] Fred Hutchinson Canc Ctr, Seattle, WA USA.
[Albain, Kathy S.] Loyola Univ Chicago, Stritch Sch Med, Maywood, IL USA.
[Andersen, Barbara L.] Ohio State Univ, Columbus, OH 43210 USA.
[Bevilacqua, Jose Luiz B.] Hosp Sirio Libanes, Sao Paulo, Brazil.
[de Azambuja, Evandro] Inst Jules Bordet, B-1000 Brussels, Belgium.
[El Saghir, Nagi S.] Amer Univ Beirut, Med Ctr, Beirut, Lebanon.
[Partridge, Ann H.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rowland, Julia H.] NCI, Bethesda, MD 20892 USA.
[Singh-Carlson, Savitri] Calif State Univ Long Beach, Sch Nursing, Long Beach, CA 90840 USA.
[Vargo, Mary M.] Case Western Reserve Univ, MetroHlth Rehabil Inst Ohio, Cleveland, OH 44106 USA.
RP Anderson, BO (reprint author), Univ Washington, Dept Surg, 1959 NE Pacific St,BB437A Bx 356410, Seattle, WA 98195 USA.
EM banderso@fhcrc.org
RI Yip, Cheng-Har/B-1909-2010; Bevilacqua, Jose Luiz/J-7739-2012
FU Fred Hutchinson Cancer Research Center; Susan G Komen for the Cure(R)
[INT-3063.0/Tracking, 221664]; International Atomic Energy Agency
Programme of Action for Cancer Therapy; National Cancer Institute;
Lancet Oncology; Elsevier; American Society of Clinical Oncology; Sheikh
Mohammed Hussein Al-Amoudi Center of Excellence in Breast Cancer; Pan
American Health Organization; European Society of Medical Oncology;
European School of Oncology; Open Society Foundations; LIVE-STRONG;
Sanofi
FX BHGI received (2012 Global Summit) grants and contributions from Fred
Hutchinson Cancer Research Center, Susan G Komen for the Cure (R)
(Contract ID: INT-3063.0/Tracking No: 221664), International Atomic
Energy Agency Programme of Action for Cancer Therapy, National Cancer
Institute, The Lancet Oncology, Elsevier, American Society of Clinical
Oncology, Sheikh Mohammed Hussein Al-Amoudi Center of Excellence in
Breast Cancer, Pan American Health Organization, European Society of
Medical Oncology, European School of Oncology, Open Society Foundations,
LIVE-STRONG, and an unrestricted educational grant from Sanofi.
NR 115
TC 25
Z9 26
U1 2
U2 39
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
J9 BREAST
JI Breast
PD OCT
PY 2013
VL 22
IS 5
BP 606
EP 615
DI 10.1016/j.breast.2013.07.049
PG 10
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 219OO
UT WOS:000324516800006
PM 24007941
ER
PT J
AU Cleary, J
Ddungu, H
Distelhorst, SR
Ripamonti, C
Rodin, GM
Bushnaq, MA
Clegg-Lamptey, JN
Connor, SR
Diwani, MB
Eniu, A
Harford, JB
Kumar, S
Rajagopal, MR
Thompson, B
Gralow, JR
Anderson, BO
AF Cleary, James
Ddungu, Henry
Distelhorst, Sandra R.
Ripamonti, Carla
Rodin, Gary M.
Bushnaq, Mohammad A.
Clegg-Lamptey, Joe N.
Connor, Stephen R.
Diwani, Msemo B.
Eniu, Alexandru
Harford, Joe B.
Kumar, Suresh
Rajagopal, M. R.
Thompson, Beti
Gralow, Julie R.
Anderson, Benjamin O.
TI Supportive and palliative care for metastatic breast cancer: Resource
allocations in low- and middle-income countries. A Breast Health Global
Initiative 2013 consensus statement
SO BREAST
LA English
DT Review
DE Metastatic breast cancer; Supportive care; Palliative care;
Site-specific metastasis; Low- and middle-income countries; Resource
allocations
ID MALIGNANT BOWEL OBSTRUCTION; CLINICAL-PRACTICE GUIDELINES; MCGILL PAIN
QUESTIONNAIRE; SCALE FACIT-SP; OF-LIFE CARE; REFERRAL PATTERNS; LUNG
METASTASES; PRACTICE RECOMMENDATIONS; FUNCTIONAL ASSESSMENT;
PROGNOSTIC-FACTORS
AB Many women diagnosed with breast cancer in low- and middle-income countries (LMICs) present with advanced-stage disease. While cure is not a realistic outcome, site-specific interventions, supportive care, and palliative care can achieve meaningful outcomes and improve quality of life.
As part of the 5th Breast Health Global Initiative (BHGI) Global Summit, an expert international panel identified thirteen key resource recommendations for supportive and palliative care for metastatic breast cancer. The recommendations are presented in three resource-stratified tables: health system resource allocations, resource allocations for organ-based metastatic breast cancer, and resource allocations for palliative care. These tables illustrate how health systems can provide supportive and palliative care services for patients at a basic level of available resources, and incrementally add services as more resources become available.
The health systems table includes health professional education, patient and family education, palliative care models, and diagnostic testing. The metastatic disease management table provides recommendations for supportive care for bone, brain, liver, lung, and skin metastases as well as bowel obstruction. The third table includes the palliative care recommendations: pain management, and psychosocial and spiritual aspects of care.
The panel considered pain management a priority at a basic level of resource allocation and emphasized the need for morphine to be easily available in LMICs. Regular pain assessments and the proper use of pharmacologic and non-pharmacologic interventions are recommended. Basic-level resources for psychosocial and spiritual aspects of care include health professional and patient and family education, as well as patient support, including community-based peer support. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
C1 [Cleary, James] Univ Wisconsin, Ctr Comprehens Canc, Madison, WI USA.
[Ddungu, Henry] Uganda Canc Inst, Kampala, Uganda.
[Ddungu, Henry; Distelhorst, Sandra R.; Thompson, Beti; Gralow, Julie R.; Anderson, Benjamin O.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Ripamonti, Carla] Fdn IRCCS, Ist Nazl Tumori Milano, Milan, Italy.
[Rodin, Gary M.] Princess Margaret Canc Ctr, Univ Hlth Network, Toronto, ON, Canada.
[Bushnaq, Mohammad A.] Jordan Palliat Care Soc, Amman, Jordan.
[Clegg-Lamptey, Joe N.] Univ Ghana, Sch Med, Accra, Ghana.
[Connor, Stephen R.] Worldwide Palliat Care Alliance & London, London, England.
[Connor, Stephen R.] Open Soc Fdn, New York, NY USA.
[Diwani, Msemo B.] Ocean Rd Canc Inst, Dar Es Salaam, Tanzania.
[Eniu, Alexandru] Canc Inst Ion Chiricuta, Cluj Napoca, Romania.
[Harford, Joe B.] NCI, Bethesda, MD 20892 USA.
[Gralow, Julie R.; Anderson, Benjamin O.] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
RP Anderson, BO (reprint author), Univ Washington, Dept Surg, 1959 NE Pacific St,BB437A Bx 356410, Seattle, WA 98195 USA.
EM banderso@fhcrc.org
RI Ripamonti, Carla/C-4557-2017;
OI Ripamonti, Carla/0000-0001-5495-5054; Connor,
Stephen/0000-0003-0332-2067
FU Fred Hutchinson Cancer Research Center; Susan G. Komen for the Cure(R)
[INT-3063.0/Tracking, 221664]; International Atomic Energy Agency
Programme of Action for Cancer Therapy; National Cancer Institute;
Lancet Oncology; Elsevier; American Society of Clinical Oncology; Sheikh
Mohammed Hussein Al-Amoudi Center of Excellence in Breast Cancer; Pan
American Health Organization; European Society of Medical Oncology;
European School of Oncology; Open Society Foundations; LIVE-STRONG;
Sanofi
FX BHGI received (2012 Global Summit) grants and contributions from Fred
Hutchinson Cancer Research Center, Susan G. Komen for the Cure (R)
(Contract ID: INT-3063.0/Tracking No: 221664); International Atomic
Energy Agency Programme of Action for Cancer Therapy, National Cancer
Institute, The Lancet Oncology, Elsevier, American Society of Clinical
Oncology, Sheikh Mohammed Hussein Al-Amoudi Center of Excellence in
Breast Cancer, Pan American Health Organization, European Society of
Medical Oncology, European School of Oncology, Open Society Foundations,
LIVE-STRONG, and an unrestricted educational grant from Sanofi.
NR 146
TC 20
Z9 20
U1 3
U2 30
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD OCT
PY 2013
VL 22
IS 5
BP 616
EP 627
DI 10.1016/j.breast.2013.07.052
PG 12
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 219OO
UT WOS:000324516800007
PM 23972474
ER
PT J
AU Kummar, S
Gutierrez, ME
Anderson, LW
Klecker, RW
Chen, A
Murgo, AJ
Doroshow, JH
Collins, JM
AF Kummar, Shivaani
Gutierrez, Martin E.
Anderson, Lawrence W.
Klecker, Raymond W., Jr.
Chen, Alice
Murgo, Anthony J.
Doroshow, James H.
Collins, Jerry M.
TI Pharmacogenetically driven patient selection for a first-in-human phase
I trial of batracylin in patients with advanced solid tumors and
lymphomas
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Pharmacogenetics; N-acetyl-batracylin; NAT2
ID POLYMORPHISM; NSC-320846; PHENOTYPE
AB Batracylin (daniquidone), an ATP-insensitive topoisomerase I/II inhibitor, demonstrated wide interspecies variation in preclinical models consistent with formation of a toxic metabolite, N-acetyl-batracylin, following metabolism by N-acetyl-transferase 2 (NAT2). To minimize exposure to this toxic metabolite, this first-in-human study was conducted in patients with advanced refractory solid tumors or lymphomas demonstrated to have a slow NAT2 acetylator genotype. The objectives were to determine the safety, maximum tolerated dose (MTD), and pharmacokinetics of batracylin and its metabolites.
Based on the MTD for rats, the most sensitive species, the starting dose was 5 mg/day for 7 days in 28-day cycles. Dose escalation followed accelerated titration design 4B, with restaging performed every 2 cycles.
Thirty-one patients were enrolled. Treatment was well tolerated; one patient experienced grade 3 toxicity (lymphopenia). Dose escalation was stopped at 400 mg/day due to grade 1 and 2 hemorrhagic cystitis. No objective responses were observed, but prolonged disease stabilization was observed in 2 patients, one with peritoneal mesothelioma (8 cycles) and another with adrenocortical cancer (18 cycles). Across an 80-fold range of doses, the ratios of systemic exposures for batracylin and N-acetyl batracylin were near 1.
Pharmacogenetically selected patients reached a dose that was 20-fold higher than the MTD in rats and 70 % of the MTD in mice. This genotype-guided strategy was successful in safely delivering batracylin to patients. However, due to unexpected cystitis, not preventable by hydration, and in the absence of a stronger signal for antitumor activity, further development of batracylin has been stopped.
C1 [Kummar, Shivaani; Gutierrez, Martin E.; Doroshow, James H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Kummar, Shivaani; Anderson, Lawrence W.; Chen, Alice; Murgo, Anthony J.; Doroshow, James H.; Collins, Jerry M.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Klecker, Raymond W., Jr.] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
RP Collins, JM (reprint author), NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
EM collinsje@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Developmental Therapeutics Program in the Division
of Cancer Treatment and Diagnosis of the National Cancer Institute
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 No. HHSN261200800001E. 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. This
research was supported [in part] by the Developmental Therapeutics
Program in the Division of Cancer Treatment and Diagnosis of the
National Cancer Institute.
NR 15
TC 4
Z9 4
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD OCT
PY 2013
VL 72
IS 4
BP 917
EP 923
DI 10.1007/s00280-013-2244-4
PG 7
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 224JB
UT WOS:000324879100022
PM 23912694
ER
PT J
AU Casati, A
Varghaei-Nahvi, A
Feldman, SA
Assenmacher, M
Rosenberg, SA
Dudley, ME
Scheffold, A
AF Casati, Anna
Varghaei-Nahvi, Azam
Feldman, Steven Alexander
Assenmacher, Mario
Rosenberg, Steven Aaron
Dudley, Mark Edward
Scheffold, Alexander
TI Clinical-scale selection and viral transduction of human na < ve and
central memory CD8(+) T cells for adoptive cell therapy of cancer
patients
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Immunotherapy; Adoptive cell therapy; T cell subsets; Naive and central
memory enrichment
ID TUMOR-INFILTRATING LYMPHOCYTES; SUPERIOR ANTITUMOR IMMUNITY; METASTATIC
MELANOMA; GENE-THERAPY; TRANSFER IMMUNOTHERAPY; NAIVE RATHER;
REGRESSION; ANTIGEN; DIFFERENTIATION; PERSISTENCE
AB The adoptive transfer of lymphocytes genetically engineered to express tumor-specific antigen receptors is a potent strategy to treat cancer patients. T lymphocyte subsets, such as na < ve or central memory T cells, selected in vitro prior to genetic engineering have been extensively investigated in preclinical mouse models, where they demonstrated improved therapeutic efficacy. However, so far, this is challenging to realize in the clinical setting, since good manufacturing practices (GMP) procedures for complex cell sorting and genetic manipulation are limited. To be able to directly compare the immunological attributes and therapeutic efficacy of na < ve (T-N) and central memory (T-CM) CD8(+) T cells, we investigated clinical-scale procedures for their parallel selection and in vitro manipulation. We also evaluated currently available GMP-grade reagents for stimulation of T cell subsets, including a new type of anti-CD3/anti-CD28 nanomatrix. An optimized protocol was established for the isolation of both CD8(+) T-N cells (CD4(-)CD62L(+)CD45RA(+)) and CD8(+) T-CM (CD4(-)CD62L(+)CD45RA(-)) from a single patient. The highly enriched T cell subsets can be efficiently transduced and expanded to large cell numbers, sufficient for clinical applications and equivalent to or better than current cell and gene therapy approaches with unselected lymphocyte populations. The GMP protocols for selection of T-N and T-CM we reported here will be the basis for clinical trials analyzing safety, in vivo persistence and clinical efficacy in cancer patients and will help to generate a more reliable and efficacious cellular product.
C1 [Casati, Anna; Assenmacher, Mario] Miltenyi Biotec GmbH, Res & Dev, Bergisch Gladbach, Germany.
[Varghaei-Nahvi, Azam; Feldman, Steven Alexander; Rosenberg, Steven Aaron; Dudley, Mark Edward] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Scheffold, Alexander] Charite, Dept Rheumatol & Clin Immunol, Charite, D-10117 Berlin, Germany.
[Scheffold, Alexander] Leibniz Assoc, German Rheumatism Res Ctr DRFZ Berlin, Berlin, Germany.
RP Scheffold, A (reprint author), Charite, Dept Rheumatol & Clin Immunol, Charite, Charitepl 1, D-10117 Berlin, Germany.
EM alexander.scheffold@charite.de
FU ATTRACT European Consortium [238778]; Marie Curie fellowship
FX This work was supported by grants from ATTRACT European Consortium
(FP7-PEOPLE-ITN-2008, Grant Agreement Number 238778); Anna Casati was
recipient of a Marie Curie fellowship.
NR 45
TC 17
Z9 17
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD OCT
PY 2013
VL 62
IS 10
BP 1563
EP 1573
DI 10.1007/s00262-013-1459-x
PG 11
WC Oncology; Immunology
SC Oncology; Immunology
GA 226BI
UT WOS:000325008800003
PM 23903715
ER
PT J
AU Marino, N
Marshall, JC
Collins, JW
Zhou, M
Qian, YZ
Veenstra, T
Steeg, PS
AF Marino, Natascia
Marshall, Jean-Claude
Collins, Joshua W.
Zhou, Ming
Qian, Yongzhen
Veenstra, Timothy
Steeg, Patricia S.
TI Nm23-H1 Binds to Gelsolin and Inactivates Its Actin-Severing Capacity to
Promote Tumor Cell Motility and Metastasis
SO CANCER RESEARCH
LA English
DT Article
ID LYSOPHOSPHATIDIC ACID; BREAST-CANCER; SUPPRESSOR EXPRESSION; DIPHOSPHATE
KINASE; DOWN-REGULATION; IN-VITRO; PROTEIN; MODULATION; INHIBITION;
APOPTOSIS
AB Nm23-H1 has been identified as a metastasis suppressor gene, but its protein interactions have yet to be understood with any mechanistic clarity. In this study, we evaluated the proteomic spectrum of interactions made by Nm23-H1 in 4T1 murine breast cancer cells derived from tissue culture, primary mammary tumors, and pulmonary metastases. By this approach, we identified the actin-severing protein Gelsolin as binding partner for Nm23-H1, verifying their interaction by coimmunoprecipitation in 4T1 cells as well as in human MCF7, MDA-MB-231T, and MDA-MB-435 breast cancer cells. In Gelsolin-transfected cells, coexpression of Nm23-H1 abrogated the actin-severing activity of Gelsolin. Conversely, actin severing by Gelsolin was abrogated by RNA interference-mediated silencing of endogenous Nm23-H1. Tumor cell motility was negatively affected in parallel with Gelsolin activity, suggesting that Nm23-H1 binding inactivated the actin-depolymerizing function of Gelsolin to inhibit cell motility. Using indirect immunoflourescence to monitor complexes formed by Gelsolin and Nm23-H1 in living cells, we observed their colocalization in a perinuclear cytoplasmic compartment that was associated with the presence of disrupted actin stress fibers. In vivo analyses revealed that Gelsolin overexpression increased the metastasis of orthotopically implanted 4T1 or tail vein-injected MDA-MB-231T cells (P = 0.001 and 0.04, respectively), along with the proportion of mice with diffuse liver metastases, an effect ablated by coexpression of Nm23-H1. We observed no variation in proliferation among lung metastases. Our findings suggest a new actin-based mechanism that can suppress tumor metastasis. (C) 2013 AACR.
C1 [Marino, Natascia; Marshall, Jean-Claude; Collins, Joshua W.; Qian, Yongzhen; Steeg, Patricia S.] NCI, Womens Canc Sect, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Zhou, Ming; Veenstra, Timothy] Sci Applicat Int Corp Frederick Inc, Frederick Natl Lab Canc Res, Lab Prote & Analyt Technol, Frederick, MD USA.
RP Marino, N (reprint author), NCI, NIH, 37 Convent Dr,Bldg 37,Room 1126, Bethesda, MD 20892 USA.
EM marinon@mail.nih.gov
FU National Cancer Institute, NIH [HHSN261200800001E]
FX This project has been funded with federal funds from the National Cancer
Institute, NIH, under contract number HHSN261200800001E.
NR 50
TC 12
Z9 12
U1 1
U2 12
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 OCT 1
PY 2013
VL 73
IS 19
BP 5949
EP 5962
DI 10.1158/0008-5472.CAN-13-0368
PG 14
WC Oncology
SC Oncology
GA 229NJ
UT WOS:000325273000011
PM 23940300
ER
PT J
AU Chai, Q
Wang, XL
Zeldin, DC
Lee, HC
AF Chai, Qiang
Wang, Xiao-Li
Zeldin, Darryl C.
Lee, Hon-Chi
TI Role of caveolae in shear stress-mediated endothelium-dependent dilation
in coronary arteries
SO CARDIOVASCULAR RESEARCH
LA English
DT Article
DE Caveolae; Shear stress; Coronary artery; Soluble epoxide hydrolase;
Calcium
ID SOLUBLE EPOXIDE HYDROLASE; NITRIC-OXIDE SYNTHASE; FLOW-INDUCED DILATION;
EPOXYEICOSATRIENOIC ACIDS; SIGNAL-TRANSDUCTION; OXIDATIVE STRESS;
SMOOTH-MUSCLE; CELLS; ACTIVATION; KINASE
AB Caveolae are membrane microdomains where important signalling pathways are assembled and molecular effects transduced. In this study, we hypothesized that shear stress-mediated vasodilation (SSD) of mouse small coronary arteries (MCA) is caveolae-dependent.
MCA (80150 m) isolated from wild-type (WT) and caveolin-1 null (Cav-1(/)) mice were subjected to physiological levels of shear stress (125 dynes/cm(2)) with and without pre-incubation of inhibitors of nitric oxide synthase (L-NAME), cyclooxygenase (indomethacin, INDO), or cytochrome P450 epoxygenase (SKF 525A). SSD was endothelium-dependent in WT and Cav-1(/) coronaries but that in Cav-1(/) was significantly diminished compared with WT. Pre-incubation with L-NAME, INDO, or SKF 525A significantly reduced SSD in WT but not in Cav-1(/) mice. Vessels from the soluble epoxide hydrolase null (Ephx2(/)) mice showed enhanced SSD, which was further augmented by the presence of arachidonic acid. In donordetector-coupled vessel experiments, Cav-1(/) donor vessels produced diminished dilation in WT endothelium-denuded detector vessels compared with WT donor vessels. Shear stress elicited a robust intracellular Ca-2 increase in vascular endothelial cells isolated from WT but not those from Cav-1(/) mice.
Integrity of caveolae is critical for endothelium-dependent SSD in MCA. Cav-1(/) endothelium is deficient in shear stress-mediated generation of vasodilators including NO, prostaglandins, and epoxyeicosatrienoic acids. Caveolae plays a critical role in endothelial signal transduction from shear stress to vasodilator production and release.
C1 [Chai, Qiang; Wang, Xiao-Li; Lee, Hon-Chi] Mayo Clin, Dept Internal Med, Div Cardiovasc Dis, Rochester, MN 55905 USA.
[Chai, Qiang] Shandong Acad Med Sci, Inst Basic Med, Dept Physiol, Jinan 250062, Peoples R China.
[Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Durham, NC 27709 USA.
RP Lee, HC (reprint author), Mayo Clin, Dept Internal Med, Div Cardiovasc Dis, Rochester, MN 55905 USA.
EM lee.honchi@mayo.edu
FU National Institute of Health, National Institute of Heart Lung and Blood
Institute [HL080118, HL74180]; Intramural Research program of the
National Institute of Environmental Health Sciences [Z01 ES025034]
FX This study was supported by funding from the National Institute of
Health, National Institute of Heart Lung and Blood Institute (HL080118
and HL74180), and the Intramural Research program of the National
Institute of Environmental Health Sciences (Z01 ES025034).
NR 42
TC 10
Z9 10
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD OCT 1
PY 2013
VL 100
IS 1
BP 151
EP 159
DI 10.1093/cvr/cvt157
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 223BP
UT WOS:000324779000018
PM 23787000
ER
PT J
AU Crane, DD
Ireland, R
Alinger, JB
Small, P
Bosio, CM
AF Crane, Deborah D.
Ireland, Robin
Alinger, Joshua B.
Small, Pamela
Bosio, Catharine M.
TI Lipids Derived from Virulent Francisella tularensis Broadly Inhibit
Pulmonary Inflammation via Toll-Like Receptor 2 and Peroxisome
Proliferator-Activated Receptor alpha
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID HUMAN DENDRITIC CELLS; FATTY-ACIDS; MYCOBACTERIAL LIPOMANNANS;
LIPOTEICHOIC ACID; TLR4-MD-2 COMPLEX; NUCLEAR RECEPTORS; SCHU S4;
INFECTION; GAMMA; METABOLISM
AB Francisella tularensis is a Gram-negative facultative intracellular pathogen that causes an acute lethal respiratory disease in humans. The heightened virulence of the pathogen is linked to its unique ability to inhibit Toll-like receptor (TLR)-mediated inflammatory responses. The bacterial component and mechanism of this inhibition are unknown. Here we show that lipids isolated from virulent but not attenuated strains of F. tularensis are not detected by host cells, inhibit production of proinflammatory cytokines by primary macrophages in response to known TLR ligands, and suppress neutrophil recruitment in vivo. We further show that lipid-mediated inhibition of inflammation is dependent on TLR2, MyD88, and the nuclear hormone and fatty acid receptor peroxisome proliferator-activated receptor alpha (PPAR alpha). Pathogen lipid-mediated interference with inflammatory responses through the engagement of TLR2 and PPAR alpha represents a novel manipulation of host signaling pathways consistent with the ability of highly virulent F. tularensis to efficiently evade host immune responses.
C1 [Crane, Deborah D.; Ireland, Robin; Alinger, Joshua B.; Bosio, Catharine M.] NIAID, Immun Pulm Pathogens Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT USA.
[Small, Pamela] Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA.
RP Bosio, CM (reprint author), NIAID, Immun Pulm Pathogens Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT USA.
EM bosioc@niaid.nih.gov
RI Bosio, Catharine/D-7456-2015
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 46
TC 15
Z9 15
U1 1
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD OCT
PY 2013
VL 20
IS 10
BP 1531
EP 1540
DI 10.1128/CVI.00319-13
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 224TG
UT WOS:000324911700007
PM 23925884
ER
PT J
AU Zarate, CA
AF Zarate, Carlos A., Jr.
TI New insights into the neurobiology, diagnosis, and treatment of mood
disorders
SO CNS SPECTRUMS
LA English
DT Editorial Material
C1 [Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH,Sect Neurobiol & Treatment Mood Disorders, Bethesda, MD 20891 USA.
RP Zarate, CA (reprint author), NIMH, Expt Therapeut & Pathophysiol Branch, Div Intramural Res Program, CRC, 10 Ctr Dr,Unit 7 SE,Rm 7-5342, Bethesda, MD 20891 USA.
EM zaratec@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 3
TC 0
Z9 0
U1 0
U2 4
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD OCT
PY 2013
VL 18
IS 5
BP 228
EP 230
DI 10.1017/S1092852913000254
PG 3
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 222EG
UT WOS:000324712200002
PM 23692663
ER
PT J
AU Niciu, MJ
Ionescu, DF
Mathews, DC
Richards, E
Zarate, CA
AF Niciu, Mark J.
Ionescu, Dawn F.
Mathews, Daniel C.
Richards, EricaM.
Zarate, Carlos A., Jr.
TI Second messenger/signal transduction pathways in major mood disorders:
moving from membrane to mechanism of action, part I: major depressive
disorder
SO CNS SPECTRUMS
LA English
DT Review
DE depression; major depressive disorder; signal transduction; second
messenger; intracellular cascades; antidepressants
ID GROWTH-FACTOR-I; CHRONIC ANTIDEPRESSANT TREATMENT; ELEMENT-BINDING
PROTEIN; NEUROTROPHIC FACTOR; FACTOR VEGF; RAT HIPPOCAMPUS; DELTA-FOSB;
IGF-I; ELECTROCONVULSIVE SEIZURE; TREATMENT RESPONSE
AB The etiopathogenesis and treatment of major mood disorders have historically focused on modulation of monoaminergic (serotonin, norepinephrine, dopamine) and amino acid [gamma-aminobutyric acid (GABA), glutamate] receptors at the plasma membrane. Although the activation and inhibition of these receptors acutely alter local neurotransmitter levels, their neuropsychiatric effects are not immediately observed. This time lag implicates intracellular neuroplasticity as primary in the mechanism of action of antidepressants and mood stabilizers. The modulation of intracellular second messenger/signal transduction cascades affects neurotrophic pathways that are both necessary and sufficient for monoaminergic and amino acid-based treatments. In this review, we will discuss the evidence in support of intracellular mediators in the pathophysiology and treatment of preclinical models of despair and major depressive disorder (MDD). More specifically, we will focus on the following pathways: cAMP/PKA/CREB, neurotrophin-mediated (MAPK and others), p11, Wnt/Fz/Dvl/GSK3b, and NF kappa B/Delta FosB. We will also discuss recent discoveries with rapidly acting antidepressants, which activate the mammalian target of rapamycin (mTOR) and release of inhibition on local translation via elongation factor stimulation. Throughout this discourse, we will highlight potential intracellular targets for therapeutic intervention. Finally, future clinical implications are discussed.
C1 [Niciu, Mark J.; Ionescu, Dawn F.; Mathews, Daniel C.; Richards, EricaM.; Zarate, Carlos A., Jr.] NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, Bethesda, MD 20814 USA.
[Zarate, Carlos A., Jr.] George Washington Univ, Washington, DC 20052 USA.
RP Niciu, MJ (reprint author), NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program,CRC, 10 Ctr Dr,Bldg 10,Room 7-5545, Bethesda, MD 20814 USA.
EM mark.niciu@nih.gov
RI Niciu, Mark/J-1766-2014; Ionescu, Dawn/K-5675-2015
OI Niciu, Mark/0000-0002-5612-3021;
FU National Institute of Mental Health, National Institutes of Health
(IRP-NIMH/NIH, Bethesda, MD, USA); 7SE Inpatient Mood and Anxiety
Disorders Research Unit of the NIMH/NIH
FX The authors gratefully acknowledge the support of the Intramural
Research Program of the National Institute of Mental Health, National
Institutes of Health (IRP-NIMH/NIH, Bethesda, MD, USA), and thank the
7SE Inpatient Mood and Anxiety Disorders Research Unit of the NIMH/NIH
for their support. The NIMH/NIH had no further role in the writing of
this review, or in the decision to submit the paper for publication.
NR 81
TC 14
Z9 14
U1 1
U2 26
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD OCT
PY 2013
VL 18
IS 5
BP 231
EP 241
DI 10.1017/S1092852913000059
PG 11
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 222EG
UT WOS:000324712200003
PM 23462230
ER
PT J
AU Niciu, MJ
Ionescu, DF
Mathews, DC
Richards, E
Zarate, CA
AF Niciu, Mark J.
Ionescu, Dawn F.
Mathews, Daniel C.
Richards, EricaM.
Zarate, Carlos A., Jr.
TI Second messenger/signal transduction pathways in major mood disorders:
moving from membrane to mechanism of action, part II: bipolar disorder
SO CNS SPECTRUMS
LA English
DT Review
DE Bipolar disorder; signal transduction; second messenger; intracellular
cascades; mood stabilizers; lithium
ID PROTEIN-KINASE-C; GLYCOGEN-SYNTHASE KINASE-3; RETICULUM STRESS-RESPONSE;
GENE-EXPRESSION; RAT-BRAIN; POSTMORTEM BRAIN; SODIUM VALPROATE;
DOWN-REGULATION; ADENYLYL-CYCLASE; CEREBRAL-CORTEX
AB In this second of two articles on second messenger/signal transduction cascades in major mood disorders, we will review the evidence in support of intracellular dysfunction and its rectification in the etiopathogenesis and treatment of bipolar disorder (BD). The importance of these cascades is highlighted by lithium's (the gold standard in BD psychopharmacology) ability to inhibit multiple critical loci in second messenger/signal transduction cascades including protein kinase C (involved in the IP3/PIP2 pathway) and GSK-3 beta (canonically identified in the Wnt/Fz/Dvl/GSK-3 beta cascade). As a result, and like major depressive disorder (MDD), more recent pathophysiological studies and rational therapeutic targets have been directed at these and other intracellular mediators. Even in the past decade, intracellular dysfunction in numerous neuroprotective/apoptotic cascades appears important in the pathophysiology and may be a future target for pharmacological interventions of BD.
C1 [Niciu, Mark J.; Ionescu, Dawn F.; Mathews, Daniel C.; Richards, EricaM.; Zarate, Carlos A., Jr.] NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, Bethesda, MD 20814 USA.
[Zarate, Carlos A., Jr.] George Washington Univ, Washington, DC USA.
RP Niciu, MJ (reprint author), NIMH, NIH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program,CRC, 10 Ctr Dr,Bldg 10,Room 7-5545, Bethesda, MD 20814 USA.
EM mark.niciu@nih.gov
RI Niciu, Mark/J-1766-2014; Ionescu, Dawn/K-5675-2015
OI Niciu, Mark/0000-0002-5612-3021;
FU NIMH/NIH (IRP-NIMH/NIH; Bethesda, MD, USA); 7SE Inpatient Mood and
Anxiety Disorders Research Unit of the NIMH/NIH; IRP-NIMH-NIH by NARSAD;
Brain & Behavior Mood Disorders Research Award
FX The authors gratefully acknowledge the support of the Intramural
Research Program of the NIMH/NIH (IRP-NIMH/NIH; Bethesda, MD, USA), and
thank the 7SE Inpatient Mood and Anxiety Disorders Research Unit of the
NIMH/NIH for their support. Funding for this work was supported by the
IRP-NIMH-NIH by a NARSAD Independent Investigator to C.A.Z., and by the
Brain & Behavior Mood Disorders Research Award to C.A.Z.
NR 76
TC 2
Z9 2
U1 0
U2 16
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD OCT
PY 2013
VL 18
IS 5
BP 242
EP 251
DI 10.1017/S1092852913000138
PG 10
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 222EG
UT WOS:000324712200004
PM 23472710
ER
PT J
AU Ionescu, DF
Niciu, M
Henter, ID
Zarate, CA
AF Ionescu, Dawn F.
Niciu, Markj.
Henter, Ioline D.
Zarate, Carlos A., Jr.
TI Defining anxious depression: a review of the literature
SO CNS SPECTRUMS
LA English
DT Review
DE Anxiety; anxious depression; depression; diagnosis; DSM-5; mixed anxiety
depressive disorder
ID MIXED ANXIETY-DEPRESSION; STAR-ASTERISK-D; NONANXIOUS DEPRESSION;
PRIMARY-CARE; MAJOR DEPRESSION; FOLLOW-UP; DISORDER; COMORBIDITY;
OUTPATIENTS; PREVALENCE
AB The diagnosis of anxious depression is presently inconsistent. The many different definitions of anxious depression have complicated its diagnosis, leading to clinical confusion and inconsistencies in the literature. This article reviewed the extant literature in order to identify the varying definitions of anxious depression, which were then compared using Feighner's diagnostic criteria. Notably, these suggest a different clinical picture of patients with anxious depression. For instance, relying on The International Classification of Diseases (ICD) or Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnoses yields a clinical picture of a comparatively mild or transient disorder; in contrast, using dimensional criteria such as DSM criteria combined with additional rating scales-most commonly the anxiety somatization factor score from the Hamilton Depression Rating Scale (HAM-D)-yields a more serious clinical picture. The evidence reviewed here suggests that defining anxious depression in a dimensional manner may be the most useful and clinically relevant way of differentiating it from other types of mood and anxiety disorders, and of highlighting the most clinically significant differences between patients with anxious depression versus depression or anxiety alone.
C1 [Ionescu, Dawn F.; Niciu, Markj.; Henter, Ioline D.; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Ionescu, DF (reprint author), NIMH, NIH, 10 Ctr Dr,MSC 1282,Bldg 10,Room 7-5545, Bethesda, MD 20892 USA.
EM dawn.ionescu@nih.gov
RI Niciu, Mark/J-1766-2014; Ionescu, Dawn/K-5675-2015
OI Niciu, Mark/0000-0002-5612-3021;
FU Intramural Research Program at the National Institute of Mental Health,
National Institutes of Health (IRP-NIMH-NIH)
FX The authors gratefully acknowledge the support of the Intramural
Research Program at the National Institute of Mental Health, National
Institutes of Health (IRP-NIMH-NIH).
NR 38
TC 12
Z9 13
U1 0
U2 17
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD OCT
PY 2013
VL 18
IS 5
BP 252
EP 260
DI 10.1017/S1092852913000114
PG 9
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 222EG
UT WOS:000324712200005
PM 23507190
ER
PT J
AU Richards, EM
Payne, JL
AF Richards, Erica M.
Payne, Jennifer L.
TI The management of mood disorders in pregnancy: alternatives to
antidepressants
SO CNS SPECTRUMS
LA English
DT Review
DE Peripartum; depression; mood disorder; persistent pulmonary
hypertension; holistic; poor neonatal adaptation
ID SEROTONIN-REUPTAKE INHIBITORS; TRANSCRANIAL MAGNETIC STIMULATION; MAJOR
DEPRESSIVE DISORDER; PERSISTENT PULMONARY-HYPERTENSION;
RANDOMIZED-CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; BRIGHT LIGHT
THERAPY; MAINTENANCE ELECTROCONVULSIVE-THERAPY; SEASONAL
AFFECTIVE-DISORDER; ST-JOHNS-WORT
AB The management of mood disorders during pregnancy is complex due to risks associated with medication use and risks associated with untreated depression. Antidepressant use during pregnancy is an exposure for the unborn child, and it currently remains unclear what long-term repercussions there might be from this exposure, though available data are reassuring. On the other hand, there are risks for both the mother and child of untreated depression during pregnancy. There is a real need for research into nonpharmacological strategies for the prevention of relapse of mood disorders in pregnant women who are off medications. We have reviewed a number of potential candidate interventions including psychotherapies, exercise, light box therapy (LBT), repetitive transcranial magnetic stimulation (rTMS), electroconvulsive therapy (ECT), holistic strategies, and nutritional and herbal supplements. Currently there is a lack of evidence supporting the use of such strategies in the prevention of depressive relapse during pregnancy, though most of these strategies have at least some support for their use in the treatment of a major depressive episode. Carefully conducted research using one or more of these strategies in women who want to discontinue antidepressants for pregnancy is sorely needed.
C1 [Richards, Erica M.] NIMH, Expt Therapeut & Pathophysiol Branch, Bethesda, MD 20892 USA.
[Payne, Jennifer L.] Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD 21205 USA.
[Payne, Jennifer L.] Johns Hopkins Sch Med, Womens Mood Disorders Ctr, Baltimore, MD 21205 USA.
RP Payne, JL (reprint author), Johns Hopkins Sch Med, Dept Psychiat, 550 N Broadway,Suite 305, Baltimore, MD 21205 USA.
EM jpayne5@jhmi.edu
FU Pfizer; Astra Zeneca
FX Jennifer Payne has the following disclosure information: Pfizer,
consultant, consulting fees; Astra Zeneca, consultant, consulting fees.
Erica Richards does not have anything to disclose.
NR 108
TC 4
Z9 4
U1 7
U2 39
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD OCT
PY 2013
VL 18
IS 5
BP 261
EP 271
DI 10.1017/S1092852913000151
PG 11
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 222EG
UT WOS:000324712200006
PM 23570692
ER
PT J
AU Guo, H
Bazuine, M
Jin, DZ
Huang, MM
Cushman, SW
Chen, XL
AF Guo, Hong
Bazuine, Merlijn
Jin, Daozhong
Huang, Merry M.
Cushman, Samuel W.
Chen, Xiaoli
TI Evidence for the Regulatory Role of Lipocalin 2 in High-Fat Diet-Induced
Adipose Tissue Remodeling in Male Mice
SO ENDOCRINOLOGY
LA English
DT Article
ID INSULIN-RESISTANCE; IN-VIVO; ADIPOCYTE DIFFERENTIATION; MATRIX
METALLOPROTEINASES; REGIONAL DIFFERENCES; LIPID-METABOLISM; GAMMA
AGONIST; TGF-BETA; OBESITY; INFLAMMATION
AB Lipocalin 2 (Lcn2) has previously been characterized as an adipokine/cytokine playing a role in glucose and lipid homeostasis. In this study, we investigate the role of Lcn2 in adipose tissue remodeling during high-fat diet (HFD)-induced obesity. We find that Lcn2 protein is highly abundant selectively in inguinal adipose tissue. During 16 weeks of HFD feeding, the inguinal fat depot expanded continuously, whereas the expansion of the epididymal fat depot was reduced in both wild-type (WT) and Lcn2(-/-) mice. Interestingly, the depot-specific effect of HFD on fat mass was exacerbated and appeared more pronounced and faster in Lcn2(-/-) mice than in WT mice. In Lcn2(-/-) mice, adipocyte hypertrophy in both inguinal and epididymal adipose tissue was more profoundly induced by age and HFD when compared with WT mice. The expression of peroxisome proliferator-activated receptor-gamma protein was significantly down-regulated, whereas the gene expression of extracellular matrix proteins was up-regulated selectively in epididymal adipocytes of Lcn2(-/-) mice. Consistent with these observations, collagen deposition was selectively higher in the epididymal, but not in the inguinal adipose depot of Lcn2(-/-) mice. Administration of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone (Rosi) restored adipogenic gene expression. However, Lcn2 deficiency did not alter the responsiveness of adipose tissue to Rosi effects on the extracellular matrix expression. Rosi treatment led to the further enlargement of adipocytes with improved metabolic activity in Lcn2(-/-) mice, which may be associated with a more pronounced effect of Rosi treatment in reducing TGF-beta in Lcn2(-/-) adipose tissue. Consistent with these in vivo observations, Lcn2 deficiency reduces the adipocyte differentiation capacity of stromal-vascular cells isolated from HFD-fed mice in these cells. Herein Rosi treatment was again able to stimulate adipocyte differentiation to a similar extent in WT and Lcn2(-/-) inguinal and epididymal stromal-vascular cells. Thus, combined, our data indicate that Lcn2 has a depot-specific role in HFD-induced adipose tissue remodeling.
C1 [Guo, Hong; Jin, Daozhong; Huang, Merry M.; Chen, Xiaoli] Univ Minnesota Twin Cities, Dept Food Sci & Nutr, St Paul, MN 55108 USA.
[Bazuine, Merlijn; Cushman, Samuel W.] Natl Inst Diabet & Digest & Kidney Dis, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Huang, Merry M.] Cornell Univ, Ithaca, NY 14850 USA.
RP Chen, XL (reprint author), Univ Minnesota Twin Cities, Dept Food Sci & Nutr, 1334 Eckles Ave, St Paul, MN 55108 USA.
EM xlchen@umn.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[R01DK080743]; Minnesota Obesity Center from the NIDDK [2P30DK050456]
FX This research and the manuscript was supported by Grant R01DK080743 (to
X.C.) from the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) and Minnesota Obesity Center (Grant 2P30DK050456 from
the NIDDK).
NR 44
TC 13
Z9 13
U1 1
U2 6
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD OCT
PY 2013
VL 154
IS 10
BP 3525
EP 3538
DI 10.1210/en.2013-1289
PG 14
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222VH
UT WOS:000324759600007
PM 23885013
ER
PT J
AU Li, JH
Jain, S
McMillin, SM
Cui, YH
Gautam, D
Sakamoto, W
Lu, HY
Jou, W
McGuinness, OP
Gavrilova, O
Wess, J
AF Li, Jian Hua
Jain, Shalini
McMillin, Sara M.
Cui, Yinghong
Gautam, Dinesh
Sakamoto, Wataru
Lu, Huiyan
Jou, William
McGuinness, Owen P.
Gavrilova, Oksana
Wess, Juergen
TI A Novel Experimental Strategy to Assess the Metabolic Effects of
Selective Activation of a G(q)-Coupled Receptor in Hepatocytes In Vivo
SO ENDOCRINOLOGY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; HORMONAL-REGULATION; GLUCOSE; LIVER; GLUCAGON;
MICE; HOMEOSTASIS; MECHANISM; CALCIUM; INSULIN
AB Increased hepatic glucose production is a key pathophysiological feature of type 2 diabetes. Like all other cell types, hepatocytes express many G protein-coupled receptors (GPCRs) that are linked to different functional classes of heterotrimeric G proteins. The important physiological functions mediated by G(s)-coupled hepatic glucagon receptors are well-documented. In contrast, little is known about the in vivo physiological roles of hepatocyte GPCRs that are linked to G proteins of the G(q) family. To address this issue, we established a transgenic mouse line (Hep-Rq mice) that expressed a G(q)-linked designer receptor (Rq) in a hepatocyte-selective fashion. Importantly, Rq could no longer bind endogenous ligands but could be selectively activated by a synthetic drug, clozapine-N-oxide. Clozapine-N-oxide treatment of Hep-Rq mice enabled us to determine the metabolic consequences caused by selective activation of a G(q)-coupled GPCR in hepatocytes in vivo. We found that acute Rq activation in vivo led to pronounced increases in blood glucose levels, resulting from increased rates of glycogen breakdown and gluconeogenesis. We also demonstrated that the expression of the V-1b vasopressin receptor, a G(q)-coupled receptor expressed by hepatocytes, was drastically increased in livers of ob/ob mice, a mouse model of diabetes. Strikingly, treatment of ob/ob mice with a selective V-1b receptor antagonist led to reduced glucose excursions in a pyruvate challenge test. Taken together, these findings underscore the importance of G(q)-coupled receptors in regulating hepatic glucose fluxes and suggest novel receptor targets for the treatment of type 2 diabetes.
C1 [Li, Jian Hua; Jain, Shalini; McMillin, Sara M.; Cui, Yinghong; Gautam, Dinesh; Sakamoto, Wataru; Wess, Juergen] Natl Inst Diabet & Digest & Kidney Dis, Mol Signaling Sect, Bethesda, MD 20892 USA.
[Lu, Huiyan] Natl Inst Diabet & Digest & Kidney Dis, Bioorgan Chem Lab, Mouse Transgen Core Facil, Bethesda, MD 20892 USA.
[Jou, William; Gavrilova, Oksana] Natl Inst Diabet & Digest & Kidney Dis, Mouse Metab Core Facil, Bethesda, MD 20892 USA.
[McGuinness, Owen P.] Vanderbilt Univ, Sch Med, Mouse Metab Phenotyping Ctr, Nashville, TN 37232 USA.
RP Wess, J (reprint author), Natl Inst Diabet & Digest & Kidney Dis, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bldg 8A,Room B1A-05,8 Ctr Dr MSC 0810, Bethesda, MD 20892 USA.
EM jianhuali@mail.nih.gov; jurgenw@helix.nih.gov
FU Intramural Research Program of the National Institutes of Health (NIH);
National Institute of Diabetes and Digestive and Kidney Diseases; NIH
[DK059637, DK020593]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (NIH), National Institute of Diabetes and
Digestive and Kidney Diseases, and NIH Grants DK059637 and DK020593.
Metabolic flux studies were performed at the Vanderbilt Mouse Metabolic
Phenotyping Center (U24 DK059637). UDPG and PEP analyses were performed
in the Hormone Assay and Analytical Services Core of the Vanderbilt
Diabetes Research and Training Center (P60 DK020593) and Mouse Metabolic
Phenotyping Center.
NR 38
TC 14
Z9 14
U1 0
U2 1
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD OCT
PY 2013
VL 154
IS 10
BP 3539
EP 3551
DI 10.1210/en.2012-2127
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222VH
UT WOS:000324759600008
PM 23861369
ER
PT J
AU Sokanovic, SJ
Baburski, AZ
Janjic, MM
Stojkov, NJ
Bjelic, MM
Lalosevic, D
Andric, SA
Stojilkovic, SS
Kostic, TS
AF Sokanovic, Srdjan J.
Baburski, Aleksandar Z.
Janjic, Marija M.
Stojkov, Natasa J.
Bjelic, Maja M.
Lalosevic, Dusan
Andric, Silvana A.
Stojilkovic, Stanko S.
Kostic, Tatjana S.
TI The Opposing Roles of Nitric Oxide and cGMP in the Age-Associated
Decline in Rat Testicular Steroidogenesis
SO ENDOCRINOLOGY
LA English
DT Article
ID CELL TESTOSTERONE PRODUCTION; REGULATORY PROTEIN STAR; BROWN-NORWAY RAT;
LEYDIG-CELLS; CAVERNOUS NEUROTOMY; IN-VITRO; EXPRESSION; PATHWAY;
ENZYMES; TESTIS
AB The molecular mechanism of the aging-associated dysfunction of Leydig cells (LCs) is complex and poorly understood. In this study, we analyzed the contribution of nitric oxide (NO) and cGMP signaling to the age-dependent decline in LC function. Significant (>50%) decreases in serum, intratesticular, and LC androgens in aging rats (15-24 months) were accompanied by a proportional increase in NO production, an up-regulation of cGMP levels, and the expression of soluble guanylyl cyclase-1B and protein kinase G1 in LCs. In contrast, LC cAMP levels decreased with age, most likely reflecting the up-regulation of cAMP-specific phosphodiesterase expression. Moreover, the expression of genes encoding enzymes responsible for cholesterol transport and its conversion to T were reduced. Exposing LCs from aged animals to NO further increased cGMP levels and decreased cAMP and androgen production, whereas the addition of cell-permeable 8-bromoguanosine-cGMP alone had the opposite effect. In vivo inhibition of cGMP-specific phosphodiesterase-5 for 3 and 6 months in aged rats led to a partial restoration of androgens, NO, and cyclic nucleotide levels, as well as the expression of steroidogenic and NO/cGMP signaling genes. These results indicate that a progressive increase in NO production contributes to the age-dependent decrease in steroidogenesis in a cGMP-independent manner, whereas the sustained elevation in cGMP levels significantly slows the decline in LC function.
C1 [Sokanovic, Srdjan J.; Baburski, Aleksandar Z.; Janjic, Marija M.; Stojkov, Natasa J.; Bjelic, Maja M.; Andric, Silvana A.; Kostic, Tatjana S.] Univ Novi Sad, Reprod Endocrinol & Signaling Grp, Fac Sci, Dept Biol & Ecol, Novi Sad 21000, Serbia.
[Lalosevic, Dusan] Univ Novi Sad, Fac Med, Novi Sad 21000, Serbia.
[Stojilkovic, Stanko S.] Eunice Kennedy Shiver Natl Inst Child Hlth & Huma, Sect Cellular Signaling, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Kostic, TS (reprint author), Univ Novi Sad, Reprod Endocrinol & Signaling Grp, Novi Sad 21000, Serbia.
EM tatjana.kostic@dbe.uns.ac.rs
FU Serbian Ministry of Science [173057]; Autonomic Province of Vojvodina
Grant [3417]; Eunice Kennedy Shiver National Institute of Child Health
and Human Development intramural grant
FX This work was supported by the Serbian Ministry of Science Grant 173057,
the Autonomic Province of Vojvodina Grant 3417, and a Eunice Kennedy
Shiver National Institute of Child Health and Human Development
intramural grant.
NR 45
TC 4
Z9 5
U1 0
U2 5
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD OCT
PY 2013
VL 154
IS 10
BP 3914
EP 3924
DI 10.1210/en.2013-1307
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 222VH
UT WOS:000324759600043
PM 23885018
ER
PT J
AU Kutty, G
Shroff, R
Kovacs, JA
AF Kutty, Geetha
Shroff, Robert
Kovacs, Joseph A.
TI Characterization of Pneumocystis Major Surface Glycoprotein Gene (msg)
Promoter Activity in Saccharomyces cerevisiae
SO EUKARYOTIC CELL
LA English
DT Article
ID EXPRESSION SITE; DIHYDROPTEROATE SYNTHASE; DIHYDROFOLATE-REDUCTASE;
SP-NOV.; CARINII; IDENTIFICATION; ANTIGENS; HUMANS; RATS
AB Major surface glycoprotein (Msg), the most abundant cell surface protein of Pneumocystis, plays an important role in the interaction of this opportunistic pathogen with host cells, and its potential for antigenic variation may facilitate evasion of host immune responses. In the present study, we have identified and characterized the promoter region of msg in 3 species of Pneumocystis: P. carinii, P. jirovecii, and P. murina. Because Pneumocystis cannot be cultured, promoter activity was measured in Saccharomyces cerevisiae, a related fungus, using a yeast vector modified to utilize the gene coding for Renilla luciferase as a reporter gene. The 5'-flanking sequences of msg from all three Pneumocystis species showed considerable promoter activity, with increases in luciferase activity up to 15- to 44-fold above baseline. Progressive deletions helped define an similar to 13-bp sequence in each Pneumocystis species that appears to be critical for promoter activity. Electrophoretic mobility shift analysis using P. carinii-specific msg promoter sequences demonstrated binding of nuclear proteins of S. cerevisiae. The 144-bp 5'-flanking region of P. murina msg showed 72% identity to that of P. carinii. The 5'-flanking region of P. jirovecii msg showed 58 and 61% identity to those of P. murina and P. carinii, respectively. The msg promoter is a good candidate for inclusion in a construct designed for genetic manipulation of Pneumocystis species.
C1 [Kutty, Geetha; Kovacs, Joseph A.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Shroff, Robert] NCI, Lab Biochem & Mol Biol, NIH, Bethesda, MD 20892 USA.
RP Kovacs, JA (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
EM jkovacs@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health
Clinical Center; National Cancer Institute
FX This research was supported by the Intramural Research Program of the
National Institutes of Health Clinical Center and the National Cancer
Institute.
NR 28
TC 0
Z9 2
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1535-9778
J9 EUKARYOT CELL
JI Eukaryot. Cell
PD OCT
PY 2013
VL 12
IS 10
BP 1349
EP 1355
DI 10.1128/EC.00122-13
PG 7
WC Microbiology; Mycology
SC Microbiology; Mycology
GA 224DE
UT WOS:000324861400004
PM 23893080
ER
PT J
AU Hopman, SMJ
Merks, JHM
de Borgie, CAJM
Aalfs, CM
Biesecker, LG
Cole, T
Eng, C
Legius, E
Maher, ER
van Noesel, MM
Verloes, A
Viskochil, DH
Wagner, A
Weksberg, R
Caron, HN
Hennekam, RCM
AF Hopman, Saskia M. J.
Merks, Johannes H. M.
de Borgie, Corianne A. J. M.
Aalfs, Cora M.
Biesecker, Leslie G.
Cole, Trevor
Eng, Charis
Legius, Eric
Maher, Eamonn R.
van Noesel, Max M.
Verloes, Alain
Viskochil, David H.
Wagner, Anja
Weksberg, Rosanna
Caron, Huib N.
Hennekam, Raoul C. M.
TI The development of a clinical screening instrument for tumour
predisposition syndromes in childhood cancer patients
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Paediatric oncology; Childhood cancer; Screening instrument; Tumour
predisposition syndromes; Delphi process; Questionnaires
ID MORPHOLOGY STANDARD TERMINOLOGY; MALFORMATION SYNDROMES; ELEMENTS;
CHILDREN; ABNORMALITIES; REGION
AB Background: Identification of tumour predisposition syndromes in patients who have cancer in childhood is paramount for optimal care. A screening instrument that can help to identify such patients will facilitate physicians caring for children with cancer. The complete screening instrument should consist of a standardised series of pictures and a screening form for manifestations not visible in the pictures. Here we describe the development of such a screening form based on an international two-stage Delphi process and an initial validation of the complete instrument.
Patients and methods: We identified manifestations that may contribute to the diagnosis of a tumour predisposition syndrome through the Winter-Baraitser Dysmorphology Database and the textbook "Gorlin's Syndromes of the Head and Neck". In a two-round Delphi process, eight international content-experts scored the contribution of each of these manifestations. We performed a clinical validation of the instrument in a selected cohort of 10 paediatric cancer patients from another centre.
Results: In total, 49 manifestations were found to contribute to the diagnosis of a tumour predisposition syndrome and were included in the screening form. The pilot validation study showed that patients suspected of having a tumour predisposition syndrome were recognised. Excellent correlation for indications of patient's referral between the screening instrument and the reference standard (personal evaluation by an experienced clinical geneticist) was found.
Conclusions: The Delphi process performed by international specialists with a function as opinion leaders in their field of expertise, has led to a screening instrument for childhood cancer patients. Patients who may have a tumour predisposition syndrome and thus have an indication to be referred for further genetic analysis, can be identified using the screening instrument. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Hopman, Saskia M. J.; Merks, Johannes H. M.; Caron, Huib N.] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Dept Paediat Oncol, NL-1105 AZ Amsterdam, Netherlands.
[de Borgie, Corianne A. J. M.] Univ Amsterdam, Clin Res Unit, NL-1105 AZ Amsterdam, Netherlands.
[Aalfs, Cora M.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
[Biesecker, Leslie G.] NIH, Intramural Sequencing Ctr NISC, Bethesda, MD 20892 USA.
[Biesecker, Leslie G.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Cole, Trevor] Birmingham Womens Hosp, W Midlands Reg Genet Serv, Birmingham, W Midlands, England.
[Eng, Charis] Cleveland Clin, Genom Med Inst, Cleveland, OH 44106 USA.
[Eng, Charis] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
[Legius, Eric] Catholic Univ Louvain, Ctr Human Genet, B-3000 Louvain, Belgium.
[Maher, Eamonn R.] Univ Birmingham, Sch Clin & Expt Med, Ctr Rare Dis & Personalised Med, Birmingham, W Midlands, England.
[van Noesel, Max M.] Sophia Childrens Univ Hosp, Erasmus Med Ctr, Dept Paediat Oncol, Rotterdam, Netherlands.
[Verloes, Alain] INSERM, U676, Paris, France.
[Verloes, Alain] Univ Paris 07, Fac Med Denis Diderot, Paris, France.
[Verloes, Alain] Hop Robert Debre, AP HP, Serv Genet Clin, F-75019 Paris, France.
[Viskochil, David H.] Univ Utah, Sch Med, Dept Paediat, Div Med Genet, Salt Lake City, UT USA.
[Wagner, Anja] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Weksberg, Rosanna] Hosp Sick Children, Dept Paediat, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada.
[Weksberg, Rosanna] Univ Toronto, Inst Med Sci, Toronto, ON, Canada.
[Hennekam, Raoul C. M.] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Dept Paediat, NL-1105 AZ Amsterdam, Netherlands.
RP Hennekam, RCM (reprint author), Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Dept Paediat, Floor H7,Room 236,Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM r.c.hennekam@amc.uva.nl
RI MAHER, EAMONN/A-9507-2008;
OI MAHER, EAMONN/0000-0002-6226-6918; , Alain/0000-0003-4819-0264; Eng,
Charis/0000-0002-3693-5145
FU Tom Voute Fund; Intramural Research Program of the National Human Genome
Research Institute
FX This study was funded by the 'Tom Voute Fund'. LGB is supported by the
Intramural Research Program of the National Human Genome Research
Institute.
NR 18
TC 5
Z9 5
U1 1
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD OCT
PY 2013
VL 49
IS 15
BP 3247
EP 3254
DI 10.1016/j.ejca.2013.06.015
PG 8
WC Oncology
SC Oncology
GA 226AA
UT WOS:000325005200022
PM 23855994
ER
PT J
AU Kutys, ML
Doyle, AD
Yamada, KM
AF Kutys, Matthew L.
Doyle, Andrew D.
Yamada, Kenneth M.
TI Regulation of cell adhesion and migration by cell-derived matrices
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Review
DE Cell-derived matrix (CDM); Extracellular matrix; 3D cell migration;
Matrix adhesions; Fibrillar topography; Matrix elasticity
ID EXTRACELLULAR-MATRIX; 3-DIMENSIONAL MATRICES; FIBRONECTIN; FIBROBLASTS;
3D; MATURATION; INTEGRINS; SEQUENCE; REVEALS; MANNER
AB Three-dimensional in vitro extracellular matrix models provide a physiological alternative to regular two-dimensional cell culture, though they lack the full diversity of molecular composition and physical properties of whole-animal systems. Cell-derived matrices are extracellular matrices that are the product of matrix secretion and assembly by cells cultured at high density in vitro. After the removal of the cells that produced the matrix, an assembled matrix scaffold is left that closely mimics native stromal fiber organization and Molecular content. Cell-derived matrices have been shown to impart in vivo-like responses to cells cultured in these matrices. In this review, we focus on mechanisms through which the distinct molecular and topographical composition of cell-derived matrices directs cellular behavior, specifically through regulation of cell-matrix adhesions and subsequent contributions to the process of cell migration. Published by Elsevier Inc.
C1 [Kutys, Matthew L.; Doyle, Andrew D.; Yamada, Kenneth M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, Bethesda, MD 20892 USA.
RP Kutys, ML (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Bldg 30,Room 426,30 Convent Dr MSC 4370, Bethesda, MD 20892 USA.
EM kutysml@mail.nih.gov; kyamada@mail.nih.gov
OI Kutys, Matthew /0000-0002-0752-649X
FU Intramural Research Program of the NIDCR, NIH
FX We thank Ryan Petrie and Will Daley for critical reading of the
manuscript. Supported by the Intramural Research Program of the NIDCR,
NIH.
NR 39
TC 21
Z9 22
U1 1
U2 36
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 OCT 1
PY 2013
VL 319
IS 16
SI SI
BP 2434
EP 2439
DI 10.1016/j.yexcr.2013.05.030
PG 6
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 221LG
UT WOS:000324659800006
PM 23751565
ER
PT J
AU Hill, MJ
Heitmann, RJ
Levens, ED
AF Hill, Micah J.
Heitmann, Ryan J.
Levens, Eric D.
TI Trophectoderm morphology grading reflects interactions between embryo
and endometrium REPLY
SO FERTILITY AND STERILITY
LA English
DT Letter
C1 [Hill, Micah J.; Heitmann, Ryan J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Levens, Eric D.] Shady Grove Fertil Reprod Sci Ctr, Rockville, MD USA.
RP Hill, MJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
NR 5
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2013
VL 100
IS 4
BP E24
EP E24
DI 10.1016/j.fertnstert.2013.07.1989
PG 1
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 225WG
UT WOS:000324995200006
PM 23993890
ER
PT J
AU Williams, AR
Zakutansky, SE
Miura, K
Dicks, MDJ
Churcher, TS
Jewell, KE
Vaughan, AM
Turner, AV
Kapulu, MC
Michel, K
Long, CA
Sinden, RE
Hill, AVS
Draper, SJ
Biswas, S
AF Williams, Andrew R.
Zakutansky, Sara E.
Miura, Kazutoyo
Dicks, Matthew D. J.
Churcher, Thomas S.
Jewell, Kerry E.
Vaughan, Aisling M.
Turner, Alison V.
Kapulu, Melissa C.
Michel, Kristin
Long, Carole A.
Sinden, Robert E.
Hill, Adrian V. S.
Draper, Simon J.
Biswas, Sumi
TI Immunisation against a serine protease inhibitor reduces intensity of
Plasmodium berghei infection in mosquitoes
SO INTERNATIONAL JOURNAL FOR PARASITOLOGY
LA English
DT Article
DE Malaria; Vaccine; Mosquito; Antibodies; Serpins
ID MEMBRANE-FEEDING ASSAY; ANOPHELES-GAMBIAE; MALARIA TRANSMISSION;
VACCINE; FALCIPARUM; ANTIBODY; IMMUNITY; ANTIGEN; TITER
AB The mosquito innate immune response is able to clear the majority of Plasmodium parasites. This immune clearance is controlled by a number of regulatory molecules including serine protease inhibitors (serpins). To determine whether such molecules could represent a novel target for a malaria transmission-blocking vaccine, we vaccinated mice with Anopheles gambiae serpin-2. Antibodies against Anopheles gambiae serpin-2 significantly reduced the infection of a heterologous Anopheles species (Anopheles stephensi) by Plasmodium berghei, however this effect was not observed with Plasmodium falciparum. Therefore, this approach of targeting regulatory molecules of the mosquito immune system may represent a novel approach to transmission-blocking malaria vaccines. (C) 2013 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.
C1 [Williams, Andrew R.; Zakutansky, Sara E.; Dicks, Matthew D. J.; Jewell, Kerry E.; Vaughan, Aisling M.; Turner, Alison V.; Kapulu, Melissa C.; Sinden, Robert E.; Hill, Adrian V. S.; Draper, Simon J.; Biswas, Sumi] Univ Oxford, Jenner Inst, Oxford OX3 7DQ, England.
[Miura, Kazutoyo; Long, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Churcher, Thomas S.] Univ London Imperial Coll Sci Technol & Med, Dept Infect Dis Epidemiol, London, England.
[Michel, Kristin] Kansas State Univ, Div Biol, Manhattan, KS 66506 USA.
[Sinden, Robert E.] Univ London Imperial Coll Sci Technol & Med, Div Cell & Mol Biol, London, England.
RP Williams, AR (reprint author), Univ Copenhagen, Fac Hlth & Med Sci, Dept Vet Dis Biol, Groennegaardsvej 15, DK-1870 Frederiksberg C, Denmark.
EM arw@sund.ku.dk
RI Draper, Simon/F-1758-2011;
OI Draper, Simon/0000-0002-9415-1357; Williams, Andrew/0000-0002-8231-282X;
Kapulu, Melissa/0000-0003-0321-7128; Dicks, Matthew/0000-0003-1909-7095;
Churcher, Thomas/0000-0002-8442-0525
FU Gates Foundation Grand Challenges in Global Health (USA); UK MRC
[G1000527]
FX We are grateful to the Jenner Institute Vector Core Facility, UK for
their assistance, and to AlfredoNicosia (Okairos, Italy) for provision
of the ChAd63 vector backbone. This work was supported by a grant from
the Gates Foundation Grand Challenges in Global Health (USA) awarded to
SB. SJD holds a UK MRC Career Development Fellowship (Grant number
G1000527). AVSH and SJD are Jenner Investigators. Conflict of Interest
statement: ARW, AVSH and SJD are named inventors on patent applications
covering malaria vectored vaccines and/or immunisation regimes.
NR 26
TC 7
Z9 7
U1 0
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0020-7519
J9 INT J PARASITOL
JI Int. J. Parasit.
PD OCT
PY 2013
VL 43
IS 11
BP 869
EP 874
DI 10.1016/j.ijpara.2013.06.004
PG 6
WC Parasitology
SC Parasitology
GA 225LY
UT WOS:000324965600001
PM 23872520
ER
PT J
AU Friedman, C
Rindflesch, TC
Corn, M
AF Friedman, Carol
Rindflesch, Thomas C.
Corn, Milton
TI Natural language processing: State of the art and prospects for
significant progress, a workshop sponsored by the National Library of
Medicine
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Article
DE Natural language processing; Biomedical language processing
ID CLINICAL TEXT; INFORMATION EXTRACTION; DE-IDENTIFICATION; BIOMEDICAL
TEXT; SYSTEM; PNEUMONIA; KNOWLEDGE; DATABASE; BIOLOGY; TOOL
AB Natural language processing (NLP) is crucial for advancing healthcare because it is needed to transform relevant information locked in text into structured data that can be used by computer processes aimed at improving patient care and advancing medicine. In light of the importance of NLP to health, the National Library of Medicine (NLM) recently sponsored a workshop to review the state of the art in NLP focusing on text in English, both in biomedicine and in the general language domain. Specific goals of the NLM-sponsored workshop were to identify the current state of the art, grand challenges and specific roadblocks, and to identify effective use and best practices. This paper reports on the main outcomes of the workshop, including an overview of the state of the art, strategies for advancing the field, and obstacles that need to be addressed, resulting in recommendations for a research agenda intended to advance the field. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
C1 [Friedman, Carol] Columbia Univ, Dept Biomed Informat, New York, NY 10027 USA.
[Rindflesch, Thomas C.; Corn, Milton] Natl Lib Med, Div Natl Inst Hlth, Bethesda, MD 20894 USA.
RP Friedman, C (reprint author), Columbia Univ, Dept Biomed Informat, New York, NY 10027 USA.
EM friedman@dbmi.columbia.edu
NR 66
TC 27
Z9 27
U1 2
U2 27
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-0464
EI 1532-0480
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD OCT
PY 2013
VL 46
IS 5
BP 765
EP 773
DI 10.1016/j.jbi.2013.06.004
PG 9
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA 223YO
UT WOS:000324848600001
PM 23810857
ER
PT J
AU Dvorak, CC
Cowan, MJ
Logan, BR
Notarangelo, LD
Griffith, LM
Puck, JM
Kohn, DB
Shearer, WT
O'Reilly, RJ
Fleisher, TA
Pai, SY
Hanson, IC
Pulsipher, MA
Fuleihan, R
Filipovich, A
Goldman, F
Kapoor, N
Small, T
Smith, A
Chan, KW
Cuvelier, G
Heimall, J
Knutsen, A
Loechelt, B
Moore, T
Buckley, RH
AF Dvorak, Christopher C.
Cowan, Morton J.
Logan, Brent R.
Notarangelo, Luigi D.
Griffith, Linda M.
Puck, Jennifer M.
Kohn, Donald B.
Shearer, William T.
O'Reilly, Richard J.
Fleisher, Thomas A.
Pai, Sung-Yun
Hanson, I. Celine
Pulsipher, Michael A.
Fuleihan, Ramsay
Filipovich, Alexandra
Goldman, Frederick
Kapoor, Neena
Small, Trudy
Smith, Angela
Chan, Ka-Wah
Cuvelier, Geoff
Heimall, Jennifer
Knutsen, Alan
Loechelt, Brett
Moore, Theodore
Buckley, Rebecca H.
TI The Natural History of Children with Severe Combined Immunodeficiency:
Baseline Features of the First Fifty Patients of the Primary Immune
Deficiency Treatment Consortium Prospective Study 6901
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE Severe combined immunodeficiency; hematopoietic cell transplantation;
newborn screening
ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION; THYMIC OUTPUT;
SINGLE-CENTER; RECONSTITUTION; SURVIVAL; DISEASE
AB The Primary Immune Deficiency Treatment Consortium (PIDTC) consists of 33 centers in North America. We hypothesized that the analysis of uniform data on patients with severe combined immunodeficiency (SCID) enrolled in a prospective protocol will identify variables that contribute to optimal outcomes following treatment. We report baseline clinical, immunologic, and genetic features of the first 50 patients enrolled, and the initial therapies administered, reflecting current practice in the diagnosis and treatment of both typical (n = 37) and atypical forms (n = 13) of SCID. From August 2010 to May 2012, patients with suspected SCID underwent evaluation and therapy per local center practices. Diagnostic information was reviewed by the PIDTC eligibility review panel, and hematopoietic cell transplantation (HCT) details were obtained from the Center for International Blood and Marrow Transplant Research. Most patients (92 %) had mutations in a known SCID gene. Half of the patients were diagnosed by newborn screening or family history, were younger than those diagnosed by clinical signs (median 15 vs. 181 days; P = < 0.0001), and went to HCT at a median of 67 days vs. 214 days of life (P = < 0.0001). Most patients (92 %) were treated with HCT within 1-2 months of diagnosis. Three patients were treated with gene therapy and 1 with enzyme replacement. The PIDTC plans to enroll over 250 such patients and analyze short and long-term outcomes for factors beneficial or deleterious to survival, clinical outcome, and T- and B-cell reconstitution, and which biomarkers are predictive of these outcomes.
C1 [Dvorak, Christopher C.; Cowan, Morton J.; Puck, Jennifer M.] Univ Calif San Francisco, Div Pediat Allergy Immunol & Bone Marrow Transpla, Benioff Childrens Hosp, San Francisco, CA 94143 USA.
[Logan, Brent R.] Med Coll Wisconsin, Div Biostat, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Notarangelo, Luigi D.] Harvard Univ, Sch Med, Childrens Hosp Boston, Div Immunol, Boston, MA USA.
[Notarangelo, Luigi D.] Harvard Univ, Sch Med, Childrens Hosp Boston, Manton Ctr Orphan Dis Res, Boston, MA USA.
[Griffith, Linda M.] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MA USA.
[Kohn, Donald B.] Univ Calif Los Angeles, Dept Microbiol Mol Genet & Immunol, Los Angeles, CA USA.
[Kohn, Donald B.] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Shearer, William T.; Hanson, I. Celine] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Shearer, William T.; Hanson, I. Celine] Baylor Coll Med, Dept Pathol & Immunol, Houston, TX 77030 USA.
[O'Reilly, Richard J.; Small, Trudy] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Fleisher, Thomas A.] NIH, Dept Lab Med, Bethesda, MA USA.
[Pai, Sung-Yun] Boston Childrens Hosp, Div Hematol & Oncol, Boston, MA USA.
[Pai, Sung-Yun] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Pulsipher, Michael A.] Univ Utah, Sch Med, Div Hematol & Hematol Malignancies, Primary Childrens Med Ctr,Huntsman Canc Inst, Salt Lake City, UT USA.
[Fuleihan, Ramsay] Northwestern Univ, Div Allergy & Immunol, Ann & Robert H Lurie Childrens Hosp Chicago, Feinberg Sch Med, Chicago, IL 60611 USA.
[Filipovich, Alexandra] Cincinnati Childrens Hosp, Div Hematol Oncolog, Cincinnati, OH USA.
[Goldman, Frederick] Univ Alabama, Div Hematol & Oncol, Childrens Hosp Alabama, Tuscaloosa, AL USA.
[Kapoor, Neena] Childrens Hosp Los Angeles, Div Res Immunol & Bone Marrow Transplantat, Los Angeles, CA 90027 USA.
[Smith, Angela] Univ Minnesota, Div Pediat Blood & Marrow Transplantat, Minneapolis, MN USA.
[Chan, Ka-Wah] Texas Transplant Inst, Pediat Stem Cell Transplantat Program, San Antonio, TX USA.
[Cuvelier, Geoff] Univ Manitoba, Dept Pediat & Child Hlth, Manitoba Blood & Marrow Transplant Program, CancerCare Manitoba, Winnipeg, MB R3T 2N2, Canada.
[Heimall, Jennifer] Childrens Hosp Philadelphia, Div Allergy Immunol, Philadelphia, PA 19104 USA.
[Knutsen, Alan] St Louis Univ, Div Pediat Allergy & Immunol, St Louis, MO 63103 USA.
[Loechelt, Brett] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Moore, Theodore] Univ Calif Los Angeles, Div Pediat Hematol Oncol, Los Angeles, CA USA.
[Buckley, Rebecca H.] Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA.
[Buckley, Rebecca H.] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA.
RP Dvorak, CC (reprint author), Univ Calif San Francisco, Div Pediat Allergy Immunol & Bone Marrow Transpla, Benioff Childrens Hosp, 505 Parnassus Ave,M-659, San Francisco, CA 94143 USA.
EM dvorakc@peds.ucsf.edu; mcowan@peds.ucsf.edu; blogan@mcw.edu;
Luigi.Notarangelo@childrens.harvard.edu; LGriffith@niaid.nih.gov;
PuckJ@peds.ucsf.edu; DKohn@mednet.ucla.edu; wtsheare@texaschildrens.org;
oreillyr@mskcc.org; tfleishe@cc.nih.gov;
Sung-Yun.Pai@childrens.harvard.edu; ichanson@texaschildrens.org;
michael.pulsipher@hsc.utah.edu; r-fuleihan@northwestern.edu;
Lisa.Filipovich@cchmc.org; fgoldman@peds.uab.edu; nkapoor@chla.usc.edu;
smallt@mskcc.org; smith719@umn.edu; kawah.chan@mhshealth.com;
Geoff.Cuvelier@cancercare.mb.ca; heimallj@email.chop.edu;
knutsenm@slu.edu; bloechel@childrensnational.org;
tbmoore@mednet.ucla.edu; buckl003@mc.duke.edu
RI Notarangelo, Luigi/F-9718-2016; Kohn, Donald/N-5085-2016
OI Notarangelo, Luigi/0000-0002-8335-0262; Kohn, Donald/0000-0003-1840-6087
FU National Institute of Allergy and Infectious Diseases [1U54AI082973];
NIH Office of Rare Diseases Research; National Center for Advancing
Translational Science
FX This paper is dedicated to the memory of Dr. Trudy Small, a gifted
physician who dedicated her life to improving transplant outcomes for
children with immunodeficiencies. The authors thank Elizabeth Dunn and
Jessica Carlson for their tireless efforts organizing the PIDTC, Yanning
Wang for expert technical assistance from the UCSF core lab, and Mary
Eapen, MD and Qun Xiang from the CIBMTR for assistance with data
analysis. Data collection for this study were in-part facilitated
through the CIBMTR (U24-CA76518; PI Horowitz MM). The PIDTC is a part of
NIH Rare Diseases Clinical Research Network, with the DMCC at the
University of South Florida. Portions of this data were presented as an
oral abstract at the annual meeting of the American Society for Blood
and Marrow Transplant, Salt Lake City, UT, 14 February 2013 (abstract
no. 93). Funding and/or programmatic support for this project has been
provided by Grant #1U54AI082973 from National Institute of Allergy and
Infectious Diseases and the NIH Office of Rare Diseases Research,
National Center for Advancing Translational Science. The views expressed
are those of the authors and do not represent the position of the NIAID,
ORDR/NCATS, NIH, or the US Government.
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PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD OCT
PY 2013
VL 33
IS 7
BP 1156
EP 1164
DI 10.1007/s10875-013-9917-y
PG 9
WC Immunology
SC Immunology
GA 223PM
UT WOS:000324818600004
PM 23818196
ER
PT J
AU Martin, S
Wolters, P
Billings, N
Toledo-Tamula, MA
Hammoud, DA
Welch, P
Darnell, D
Holland, SM
Freeman, AF
AF Martin, Staci
Wolters, Pamela
Billings, Nia
Toledo-Tamula, Mary Anne
Hammoud, Dima A.
Welch, Pamela
Darnell, Dirk
Holland, Steven M.
Freeman, Alexandra F.
TI Neurobehavioral Profiles in Individuals with Hyperimmunoglobulin E
Syndrome (HIES) and Brain White Matter Hyperintensities
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE Hyperimmunoglobulin E Syndrome; Job's Syndrome; cognitive functioning;
psychological functioning; quality of life
ID HYPER-IGE SYNDROME; CONFIRMATORY FACTOR-ANALYSIS; TEST-RETEST
RELIABILITY; NEUROFIBROMATOSIS TYPE-1; FUNCTIONAL ASSESSMENT; EVERYDAY
ATTENTION; COGNITIVE FUNCTION; MRI; ABNORMALITIES; POPULATION
AB Individuals with hyperimmunoglobulin E Syndrome (HIES) have central nervous system abnormalities, including focal white matter hyperintensities (WMH), or unidentified bright objects. This cross-sectional study aimed to describe the cognitive and emotional functioning and quality of life of people with HIES. We also sought to explore the relationship between cognitive functioning and WMHs in this population.
Twenty-nine individuals (13 males) with autosomal-dominant HIES (mean age = 35.1 years, range 16-55) were administered a comprehensive psychological assessment as part of a natural history protocol. The assessment included measures of global cognitive functioning (Wechsler Adult Intelligence Scale-III), memory (California Verbal Learning Test-II, Wechsler Memory Scale-III), executive skills (Delis Kaplan Executive Function System), and attention (Test of Everyday Attention). Emotional symptoms and quality of life also were assessed.
All mean cognitive scores were within normal limits. Mean scores on memory and executive functioning measures were significantly lower than Full Scale IQ scores (ps < .05). Substantial percentages of patients self-reported executive skills to be in the clinical range. Patients with fewer (1-20) versus more (21+) WMHs scored significantly better on measures of global cognitive skills, visual-perceptual skills, and working memory. Mean scores on emotional symptom and quality of life measures were in the average range and unrelated to WMHs.
Global cognitive functioning was average to high average in our sample of individuals with HIES. However, focal brain lesions were associated with lower scores in specific domains. Emotional functioning and quality of life are within normal limits in this sample.
C1 [Martin, Staci; Wolters, Pamela] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Billings, Nia; Toledo-Tamula, Mary Anne; Welch, Pamela] SAIC Frederick Inc, Frederick Natl Lab Canc Res, Clin Res Directorate CMRP, Frederick, MD 21702 USA.
[Hammoud, Dima A.] NIH, Ctr Infect Dis Imaging Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Darnell, Dirk; Holland, Steven M.; Freeman, Alexandra F.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
RP Martin, S (reprint author), 9030 Old Georgetown Rd,107, Bethesda, MD 20892 USA.
EM martins@mail.nih.gov
RI Hammoud, Dima/C-2286-2015
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute; National Institute of Allergy and Infectious
Diseases; Frederick National Laboratory for Cancer Research; National
Cancer Institute, National Institutes of Health [HHSN261200800001E];
[HHSN261200477004C]
FX The authors wish to extend their appreciation to the individuals with
HIES who participated in this research. We also thank Brittany Abel,
M.A. for her assistance. This research was supported by the Intramural
Research Program of the National Institutes of Health, National Cancer
Institute, by the National Institute of Allergy and Infectious Diseases,
and by federal contract HHSN261200477004C. In addition, this project was
funded in whole or in part with federal funds from the Frederick
National Laboratory for Cancer Research and National Cancer Institute,
National Institutes of Health, under Contract No. HHSN261200800001E. 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 47
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PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD OCT
PY 2013
VL 33
IS 7
BP 1175
EP 1184
DI 10.1007/s10875-013-9932-z
PG 10
WC Immunology
SC Immunology
GA 223PM
UT WOS:000324818600006
PM 23963745
ER
PT J
AU Cummings, CM
Caporino, NE
Settipani, CA
Read, KL
Compton, SN
March, J
Sherrill, J
Piacentini, J
McCracken, J
Walkup, JT
Ginsburg, G
Albano, AM
Rynn, M
Birmaher, B
Sakolsky, D
Gosch, E
Keeton, C
Kendall, PC
AF Cummings, Colleen M.
Caporino, Nicole E.
Settipani, Cara A.
Read, Kendra L.
Compton, Scott N.
March, John
Sherrill, Joel
Piacentini, John
McCracken, James
Walkup, John T.
Ginsburg, Golda
Albano, Anne Marie
Rynn, Moira
Birmaher, Boris
Sakolsky, Dara
Gosch, Elizabeth
Keeton, Courtney
Kendall, Philip C.
TI The Therapeutic Relationship in Cognitive-Behavioral Therapy and
Pharmacotherapy for Anxious Youth
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE anxiety; youth; therapeutic relationship; CBT; pharmacotherapy
ID CHILDHOOD ANXIETY DISORDERS; RANDOMIZED CLINICAL-TRIAL; ADOLESCENT
PSYCHOTHERAPY; ALLIANCE; CHILDREN; VARIABLES; OUTCOMES
AB Objective: We examined the therapeutic relationship with cognitive-behavioral therapists and with pharmacotherapists for youth from the Child/Adolescent Anxiety Multimodal Study (Walkup et al., 2008). The therapeutic relationship was examined in relation to treatment outcomes. Method: Participants were 488 youth (ages 7-17 years; 50% male) randomized to cognitive-behavioral therapy (CBT; Coping Cat), pharmacotherapy (sertraline), their combination, or placebo pill. Participants met criteria for generalized anxiety disorder, social phobia, and/or separation anxiety disorder according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994). The therapeutic relationship was assessed by youth report at Weeks 6 and 12 of treatment using the Child's Perception of Therapeutic Relationship scale (Kendall et al., 1997). Outcome measures (Pediatric Anxiety Rating Scale; Research Units on Pediatric Psychopharmacology Anxiety Study Group, 2002; and Clinical Global Impressions Scales; Guy, 1976) were completed by independent evaluators blind to condition. Results: For youth who received CBT only, a stronger therapeutic relationship predicted positive treatment outcome. In contrast, the therapeutic relationship did not predict outcome for youth receiving sertraline, combined treatment, or placebo. Conclusion: A therapeutic relationship may be important for anxious youth who receive CBT alone.
C1 [Cummings, Colleen M.; Caporino, Nicole E.; Settipani, Cara A.; Read, Kendra L.; Kendall, Philip C.] Temple Univ, Dept Psychol, Philadelphia, PA 19122 USA.
[Compton, Scott N.; March, John] Duke Univ, Med Ctr, Dept Psychiat & Behav Serv, Durham, NC 27706 USA.
[Sherrill, Joel] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[Piacentini, John; McCracken, James] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA USA.
[Walkup, John T.] Weill Cornell Med Coll, Div Child & Adolescent Psychiat, New York, NY USA.
[Ginsburg, Golda; Keeton, Courtney] Johns Hopkins Univ, Div Child & Adolescent Psychiat, Sch Med, Baltimore, MD 21218 USA.
[Albano, Anne Marie; Rynn, Moira] Columbia Univ, Med Ctr, Dept Psychiat, New York, NY 10027 USA.
[Birmaher, Boris; Sakolsky, Dara] Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Pittsburgh, PA 15260 USA.
[Gosch, Elizabeth] Philadelphia Coll Osteopath Med, Dept Psychol, Philadelphia, PA USA.
RP Cummings, CM (reprint author), Temple Univ, Dept Psychol, Weiss Hall,1701 North 13th St, Philadelphia, PA 19122 USA.
EM cummings@temple.edu; pkendall@temple.edu
FU NIMH NIH HHS [MH063747, R01 MH063747, U01 MH063747]
NR 44
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U1 3
U2 38
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD OCT
PY 2013
VL 81
IS 5
BP 859
EP 864
DI 10.1037/a0033294
PG 6
WC Psychology, Clinical
SC Psychology
GA 223CE
UT WOS:000324780500012
PM 23750468
ER
PT J
AU Jiraporn, P
Chintrakarn, P
Kim, JC
Liu, YX
AF Jiraporn, Pornsit
Chintrakarn, Pandej
Kim, Jang-Chul
Liu, Yixin
TI Exploring the Agency Cost of Debt: Evidence from the ISS Governance
Standards
SO JOURNAL OF FINANCIAL SERVICES RESEARCH
LA English
DT Article
DE Cost of debt; Agency theory; Bondholders; Bond yields; Corporate
governance; Institutional shareholder services
ID CORPORATE GOVERNANCE; SHAREHOLDER RIGHTS; BOND RATINGS; OWNERSHIP; FIRM;
INFORMATION; INCENTIVES; INVESTMENT; DIRECTORS; PRICES
AB Corporate governance is usually viewed in the context of strengthening shareholder rights and enhancing shareholders' welfare. However, the impact of corporate governance on bondholders is much less understood. We explore how corporate governance influences the cost of debt financing. Using broad governance metrics encompassing fifty governance attributes reported by The Institutional Shareholder Services (ISS), we document that stronger corporate governance is associated with a higher cost of debt. As governance strengthens by one standard deviation, the cost of debt rises by as much as 11 %. The results are robust even after controlling for both firm-specific and issue-specific characteristics. Our results are important because they suggest that corporate governance has a palpable effect on critical corporate outcomes such as credit ratings and bond yields. More importantly, we show that, while corporate governance may mitigate the agency conflict between managers and shareholders, it appears to exacerbate the agency conflict between shareholders and bondholders (the agency cost of debt).
C1 [Jiraporn, Pornsit] Penn State Univ, Great Valley Sch Grad Profess Studies, University Pk, PA 16802 USA.
[Jiraporn, Pornsit] Mahidol Univ, NIDA, Thammasat Business Sch, Bangkok 10700, Thailand.
[Jiraporn, Pornsit] Chiang Mai Univ, Chiang Mai 50000, Thailand.
[Chintrakarn, Pandej] Mahidol Univ, Int Coll, Nakhon Pathom, Thailand.
[Kim, Jang-Chul] No Kentucky Univ, Dept Econ & Finance, Highland Hts, KY 41076 USA.
[Liu, Yixin] Univ New Hampshire, Dept Accounting & Finance, Durham, NH 03824 USA.
RP Chintrakarn, P (reprint author), Mahidol Univ, Int Coll, Nakhon Pathom, Thailand.
EM pxj11@psu.edu; icpandej@mahidol.ac.th
NR 69
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U1 4
U2 20
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0920-8550
J9 J FINANC SERV RES
JI J. Financ. Serv. Res.
PD OCT
PY 2013
VL 44
IS 2
BP 205
EP 227
DI 10.1007/s10693-012-0142-2
PG 23
WC Business, Finance
SC Business & Economics
GA 220CD
UT WOS:000324557400005
ER
PT J
AU Weng, HL
Feng, DC
Radaeva, S
Kong, XN
Wang, L
Liu, Y
Li, Q
Shen, H
Gao, YP
Mullenbach, R
Munker, S
Huang, T
Chen, JL
Zimmer, V
Lammert, F
Mertens, PR
Cai, WM
Dooley, S
Gao, B
AF Weng, Hong-lei
Feng, De-chun
Radaeva, Svetlana
Kong, Xiao-ni
Wang, Lei
Liu, Yan
Li, Qi
Shen, Hong
Gao, Yun-peng
Muellenbach, Roman
Munker, Stefan
Huang, Tong
Chen, Jia-lin
Zimmer, Vincent
Lammert, Frank
Mertens, Peter R.
Cai, Wei-min
Dooley, Steven
Gao, Bin
TI IFN-gamma inhibits liver progenitor cell proliferation in HBV-infected
patients and in 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-fed mice
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Cytokeratin-19; Cytokeratin-7; STAT1; IRF-1; Hepatic stellate cells;
Macrophages
ID INTERFERON-GAMMA; DUCTULAR REACTIONS; STELLATE CELLS; OVAL CELLS;
INJURY; REGENERATION; FIBROSIS; INFLAMMATION; MACROPHAGES; EXPRESSION
AB Background & Aims: Proliferation of liver progenitor cells (LPCs) is associated with inflammation and fibrosis in chronic liver diseases. However, how inflammation and fibrosis affect LPCs remains obscure.
Methods: We examined the role of interferon (IFN)-gamma, an important pro-inflammatory and anti-fibrotic cytokine, in LPC expansion in HBV-infected patients and in mice challenged with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-or cholinedeficient, ethionine-supplemented (CDE) diet as well as in primary LPCs and LPC cell line.
Results: The CK19 staining scores correlated with inflammation and fibrosis grades in the livers from 110 HBV-infected patients. Nine-month IFN-gamma treatment decreased LPC numbers, inflammation, and fibrosis in these HBV-infected patients. Similarly, a two-week IFN-gamma treatment also decreased LPC activation in DDC-treated mice. Disruption of IFN-gamma or its signaling components (e.g., IFNGR, STAT1, and IRF-1) increased LPC proliferation and liver fibrosis in DDC-fed mice. In contrast, deletion of IFN-gamma did not increase, but rather slightly reduced LPC proliferation in CDE-fed mice. In vitro, IFN-gamma attenuated proliferation of the LPC cell line BMOL and of primary LPCs from wild type mice, but not STAT1(-/-) or IRF-1(-/-) mice. Furthermore, co-culture assays suggest that IFN-gamma can indirectly promote LPC proliferation via the activation of macrophages but attenuate it via the inhibition of hepatic stellate cells.
Conclusions: IFN-gamma inhibits LPC expansion via the direct inhibition of LPC proliferation and indirect attenuation of liver fibrosis in the DDC model, but it may also enhance LPC expansion via the promotion of inflammation in the CDE model; thereby playing dual roles in regulating LPC proliferation in vivo. Published by Elsevier B.V. on behalf of the European Association for the Study of the Liver.
C1 [Weng, Hong-lei; Liu, Yan; Li, Qi; Shen, Hong; Muellenbach, Roman; Munker, Stefan; Dooley, Steven] Heidelberg Univ, Med Fac Mannheim, Dept Med 2, Sect Mol Hepatol, Mannheim, Germany.
[Feng, De-chun; Radaeva, Svetlana; Kong, Xiao-ni; Wang, Lei; Gao, Yun-peng; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD 20892 USA.
[Muellenbach, Roman; Zimmer, Vincent; Lammert, Frank] Univ Saarland, Saarland Univ Hosp, Dept Med 2, Homburg, Germany.
[Huang, Tong] Ningbo Univ, Sch Med, Li Hui Li Hosp, Dept Cardiac Vasc Med, Ningbo 315211, Zhejiang, Peoples R China.
[Chen, Jia-lin] First Hosp Jiaxing, Coll Jiaxing, Dept Pathol, Jiaxing, Peoples R China.
[Mertens, Peter R.] Otto Von Guericke Univ, Dept Hypertens & Nephrol, Magdeburg, Germany.
[Cai, Wei-min] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Inst Infect Dis, Hangzhou 310003, Zhejiang, Peoples R China.
RP Dooley, S (reprint author), Heidelberg Univ, Med Fac Mannheim, Dept Med 2, Sect Mol Hepatol, Mannheim, Germany.
EM steven.dooley@medma.uni-heidelberg.de; bgao@mail.nih.gov
RI Feng, Dechun/Q-5962-2016
FU Intramural NIH HHS [Z99 AA999999, ZIA AA000368-11]
NR 30
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Z9 6
U1 1
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD OCT
PY 2013
VL 59
IS 4
BP 738
EP 745
DI 10.1016/j.jhep.2013.05.041
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 218ZY
UT WOS:000324473700015
PM 23747755
ER
PT J
AU Burshtyn, DN
Scharenberg, AM
Wagtmann, N
Rajagopalan, S
Berrada, K
Yi, TL
Kinet, JP
Long, EO
AF Burshtyn, Deborah N.
Scharenberg, Andrew M.
Wagtmann, Nicolai
Rajagopalan, Sumati
Berrada, Karim
Yi, Taolin
Kinet, Jean-Pierre
Long, Eric O.
TI Recruitment of Tyrosine Phosphatase HCP by the Killer Cell Inhibitory
Receptor (Reprinted from The Journal of Immunology, vol 4, pg 77-85,
1996)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Reprint
ID COMPLEX CLASS-I; T-LYMPHOCYTES; ANTIGEN RECEPTOR; SH2 DOMAINS; HLA-C;
HEMATOPOIETIC-CELLS; CYTOPLASMIC DOMAIN; MOLECULAR-CLONING;
TARGET-CELLS; FC-RECEPTORS
AB Cytolysis of target cells by natural killer (NK) cells and by some cytotoxic T cells occurs unless prevented by inhibitory receptors that recognize MHC class I on target cells. Human NK cells express a p58 inhibitory receptor sepecific for HLA-C. We report association of the tyrosine phosphatase HCP with the p58 receptor in NK cells. HCP association was dependent on tyrosine phosphorylation of p58. Phosphotyrosyl peptides corresponding to the p58 tail bound and activated HCP in vitro. Furthermore, introduction of an inactive mutant HCP into an NK cell line prevented the p58-mediated inhibition of target cell lysis. These data imply that the inhibitory function of p58 is dependent on its tyrosine phosphorylation and on recruitment and activation of HCP.
C1 [Burshtyn, Deborah N.; Wagtmann, Nicolai; Rajagopalan, Sumati; Long, Eric O.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Scharenberg, Andrew M.; Kinet, Jean-Pierre] NIAID, Mol Allergy & Immunol Sect, NIH, Rockville, MD 20852 USA.
[Berrada, Karim; Yi, Taolin] Cleveland Clin Fdn, Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA.
RP Burshtyn, DN (reprint author), NIAID, Immunogenet Lab, NIH, 12441 Pk Lawn Dr, Rockville, MD 20852 USA.
RI Long, Eric/G-5475-2011
OI Long, Eric/0000-0002-7793-3728
FU American Cancer Society [DB-74554]; American Heart Association
[NEO-94-074-GIA]
FX We thank S. Rojo for assistance in generating the NK populations, A.
Moretta and C. Bottino for antibodies, J. Gumperz and P. Parham for
transfected cells, H.-G. Klingemann for NK-92, B. Moss for plasmid
pSC65, the National Institutes of Health Blood Bank for human blood
samples, Hoffmann-La Roche for rIL-2, D. Wiest for assitance with
densitometry, and J. O'Shea for helpful discussions. This work was
supported in part by American Cancer Society grant DB-74554 and American
Heart Association grant NEO-94-074-GIA to T. Y.
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PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2013
VL 191
IS 7
BP 3491
EP 3499
PG 9
WC Immunology
SC Immunology
GA 221CH
UT WOS:000324634500003
PM 24058192
ER
PT J
AU Kaminski, JJ
Schattgen, SA
Tzeng, TC
Bode, C
Klinman, DM
Fitzgerald, KA
AF Kaminski, John J.
Schattgen, Stefan A.
Tzeng, Te-Chen
Bode, Christian
Klinman, Dennis M.
Fitzgerald, Katherine A.
TI Synthetic Oligodeoxynucleotides Containing Suppressive TTAGGG Motifs
Inhibit AIM2 Inflammasome Activation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID BLOOD MONONUCLEAR-CELLS; B SURFACE-ANTIGEN; BACTERIAL-DNA; CPG
OLIGODEOXYNUCLEOTIDES; CASPASE-1 ACTIVATION; IMMUNE-RESPONSES;
CYTOPLASMIC DNA; HIN-200 FAMILY; CYTOSOLIC DNA; MICE
AB Synthetic oligodeoxynucleotides (ODNs) comprised of the immunosuppressive motif TTAGGG block TLR9 signaling, prevent STAT1 and STAT4 phosphorylation and attenuate a variety of inflammatory responses in vivo. In this study, we demonstrate that such suppressive ODN abrogate activation of cytosolic nucleic acid-sensing pathways. Pretreatment of dendritic cells and macrophages with the suppressive ODN-A151 abrogated type I IFN, TNF-alpha, and ISG induction in response to cytosolic dsDNA. In addition, A151 abrogated caspase-1-dependent IL-1 beta and IL-18 maturation in dendritic cells stimulated with dsDNA and murine CMV. Inhibition was dependent on A151's phosphorothioate backbone, whereas substitution of the guanosine residues for adenosine negatively affected potency. A151 mediates these effects by binding to AIM2 in a manner that is competitive with immune-stimulatory DNA and as a consequence prevents AIM2 inflammasome complex formation. Collectively, these findings reveal a new route by which suppressive ODNs modulate the immune system and unveil novel applications for suppressive ODNs in the treatment of infectious and autoimmune diseases.
C1 [Kaminski, John J.; Schattgen, Stefan A.; Tzeng, Te-Chen; Fitzgerald, Katherine A.] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol, Worcester, MA 01605 USA.
[Bode, Christian; Klinman, Dennis M.] NCI, Canc & Inflammat Program, NIH, Frederick, MD 21702 USA.
RP Fitzgerald, KA (reprint author), Univ Massachusetts, Sch Med, Lazare Res Bldg,Room 308,364 Plantat St, Worcester, MA 01605 USA.
EM kate.fitzgerald@umassmed.edu
FU National Institutes of Health [AI083215, AI093752]
FX This work was supported by grants from the National Institutes of Health
(AI083215 and AI093752 to K.A.F.).
NR 43
TC 15
Z9 15
U1 0
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 OCT 1
PY 2013
VL 191
IS 7
BP 3876
EP 3883
DI 10.4049/jimmunol.1300530
PG 8
WC Immunology
SC Immunology
GA 221CH
UT WOS:000324634500043
PM 23986531
ER
PT J
AU Gu, L
Ning, H
Qian, XS
Huang, Q
Hou, R
Almourani, R
Fu, MG
Blackshear, PJ
Liu, JG
AF Gu, Ling
Ning, Huan
Qian, Xuesong
Huang, Qi
Hou, Rong
Almourani, Rajaa
Fu, Mingui
Blackshear, Perry J.
Liu, Jianguo
TI Suppression of IL-12 Production by Tristetraprolin through Blocking
NF-kappa B Nuclear Translocation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; INTERFERON REGULATORY FACTOR-8; AU-RICH ELEMENTS;
MESSENGER-RNA; GENE-TRANSCRIPTION; FACTOR-ALPHA; SIGNALING PATHWAYS;
INNATE RESISTANCE; ADAPTIVE IMMUNITY; DENDRITIC CELLS
AB Tristetraprolin (TTP), an mRNA-binding protein, plays a significant role in regulating the expression of adenylate-uridylate-rich elements containing mRNAs. Mice deficient of TTP (TTP-/-) develop a systemic autoimmune inflammatory syndrome characterized by cachexia, conjunctivitis, and dermatitis. IL-12 plays a crucial role in immune defense against infectious and malignant diseases. In this study, we found increased production of IL-12 during endotoxic shock and enhanced Th1 cells in TTP knockout mice. The levels of IL-12 p70 and p40 protein as well as p40 and p35 mRNA were also increased in activated macrophages deficient of TTP. In line with these findings, overexpression of TTP suppressed IL-12 p35 and p40 expression at the mRNA and promoter level, whereas it surprisingly had little effects on their mRNA stability. Our data showed that the inhibitory effects of TTP on p35 gene transcription were completely rescued by overexpression of NF-kappa B p65 and c-Rel but not by the p50 in activated macrophages. Our data further indicated that TTP acquired its inhibition on IL-12 expression through blocking nuclear translocation of NF-kappa B p65 and c-Rel while enhancing p50 upon stimulation. In summary, our study reveals a novel pathway through which TTP suppresses IL-12 production in macrophages, resulting in suppression of Th1 cell differentiation. This study may provide us with therapeutic targets for treatment of inflammatory and autoimmune disorders.
C1 [Gu, Ling; Ning, Huan; Qian, Xuesong; Huang, Qi; Hou, Rong; Almourani, Rajaa; Liu, Jianguo] St Louis Univ, Sch Med, Dept Internal Med, Div Infect Dis Allergy & Immunol, St Louis, MO 63104 USA.
[Huang, Qi] Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing 400016, Peoples R China.
[Fu, Mingui] Univ Missouri, Sch Med, Dept Basic Med Sci, Shock & Trauma Res Ctr, Kansas City, MO 64108 USA.
[Blackshear, Perry J.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Liu, JG (reprint author), St Louis Univ, Sch Med, Dept Internal Med, Div Infect Dis Allergy & Immunol, 1100 South Grand Blvd,DRC Room 811, St Louis, MO 63104 USA.
EM jliu9@slu.edu
FU National Institutes of Health [CA163808, HL098794]
FX This study was supported by National Institutes of Health Grants
CA163808 (to J.L.) and HL098794 (to M.F.).
NR 46
TC 11
Z9 12
U1 1
U2 6
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2013
VL 191
IS 7
BP 3922
EP 3930
DI 10.4049/jimmunol.1300126
PG 9
WC Immunology
SC Immunology
GA 221CH
UT WOS:000324634500048
PM 23997224
ER
PT J
AU Xiao, Y
Woo, WM
Nagao, K
Li, WL
Terunuma, A
Mukouyama, YS
Oro, AE
Vogel, JC
Brownell, I
AF Xiao, Ying
Woo, Wei-Meng
Nagao, Keisuke
Li, Wenling
Terunuma, Atsushi
Mukouyama, Yoh-suke
Oro, Anthony E.
Vogel, Jonathan C.
Brownell, Isaac
TI Perivascular Hair Follicle Stem Cells Associate with a Venule Annulus
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID HEMATOPOIETIC STEM; ENDOTHELIAL-CELLS; PROGENITOR CELLS; VASCULAR NICHE;
DERMAL CELLS; SKIN; ACTIVATION; DIFFERENTIATION; MORPHOGENESIS;
ANGIOGENESIS
AB The perivascular microenvironment helps in maintaining stem cells in many tissues. We sought to determine whether there is a perivascular niche for hair follicle stem cells. The association of vessels and follicle progenitor cells began by embryonic day 14.5, when nascent hair placodes had blood vessels approaching them. By birth, a vascular annulus stereotypically surrounded the keratin 15 negative (K15-) stem cells in the upper bulge and remained associated with the K15- upper bulge throughout the hair cycle. The angiogenic factor Egfl6 was expressed by the K15- bulge and was localized adjacent to the vascular annulus, which comprised post-capillary venules. Although denervation altered the phenotype of upper bulge stem cells, the vascular annulus persisted in surgically denervated mouse skin. The importance of the perivascular niche was further suggested by the fact that vascular annuli formed around the upper bulge of de novo-reconstituted hair follicles before their innervation. Together, these findings demonstrate that the upper bulge is associated with a perivascular niche during the establishment and maintenance of this specialized region of hair follicle stem cells.
C1 [Xiao, Ying; Terunuma, Atsushi; Vogel, Jonathan C.; Brownell, Isaac] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Woo, Wei-Meng; Oro, Anthony E.] Stanford Univ, Sch Med, Program Epithelial Biol, Stanford, CA 94305 USA.
[Nagao, Keisuke] Keio Univ, Ctr Integrated Med Res, Dept Dermatol, Tokyo, Japan.
[Li, Wenling; Mukouyama, Yoh-suke] NHLBI, Lab Stem Cell & Neurovasc Biol, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Brownell, I (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10,Room 12N238,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Isaac.brownell@nih.gov
RI Woo, Wei Meng/H-6594-2015; Nagao, Keisuke/J-5116-2013
OI Nagao, Keisuke/0000-0002-7005-3138
FU NIH Intramural Research Program, Center of Cancer Research, National
Cancer Institute
FX We thank Ms Carole Yee and Mr James Perna for technical assistance; Mark
Udey for discussion and proofreading; and the CCR Confocal Microscopy
Core Facility for assistance in confocal imaging. This research is
supported by the NIH Intramural Research Program, Center of Cancer
Research, National Cancer Institute.
NR 31
TC 7
Z9 8
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
EI 1523-1747
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD OCT
PY 2013
VL 133
IS 10
BP 2324
EP 2331
DI 10.1038/jid.2013.167
PG 8
WC Dermatology
SC Dermatology
GA 224OY
UT WOS:000324899100008
PM 23558405
ER
PT J
AU Adams-Chapman, I
Bann, CM
Das, A
Goldberg, RN
Stoll, BJ
Walsh, MC
Sanchez, PJ
Higgins, RD
Shankaran, S
Watterberg, KL
Duara, S
Miller, NA
Heyne, RJ
Peralta-Carcelen, M
Goldstein, RF
Steichen, JJ
Bauer, CR
Hintz, SR
Evans, PW
Acarregui, MJ
Myers, GJ
Vohr, BR
Wilson-Costello, DE
Pappas, A
Vaucher, YE
Ehrenkranz, RA
McGowan, EC
Dillard, RG
Fuller, J
Benjamin, DK
AF Adams-Chapman, Ira
Bann, Carla M.
Das, Abhik
Goldberg, Ronald N.
Stoll, Barbara J.
Walsh, Michele C.
Sanchez, Pablo J.
Higgins, Rosemary D.
Shankaran, Seetha
Watterberg, Kristi L.
Duara, Shahnaz
Miller, Nancy A.
Heyne, Roy J.
Peralta-Carcelen, Myriam
Goldstein, Ricki F.
Steichen, Jean J.
Bauer, Charles R.
Hintz, Susan R.
Evans, Patricia W.
Acarregui, Michael J.
Myers, Gary J.
Vohr, Betty R.
Wilson-Costello, Deanne E.
Pappas, Athina
Vaucher, Yvonne E.
Ehrenkranz, Richard A.
McGowan, Elisabeth C.
Dillard, Robert G.
Fuller, Janell
Benjamin, Daniel K., Jr.
CA Eunice Kennedy Shriver Natl Inst C
TI Neurodevelopmental Outcome of Extremely Low Birth Weight Infants with
Candida Infection
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID NEONATAL RESEARCH NETWORK; WHITE-MATTER INJURY; NECROTIZING
ENTEROCOLITIS; PRETERM INFANTS; CEREBRAL-PALSY; NERVOUS-SYSTEM;
RISK-FACTORS; INFLAMMATION; FLUCONAZOLE; BACTEREMIA
AB Objective Candida remains an important cause of late-onset infection in preterm infants. Mortality and neurodevelopmental outcome of extremely low birth weight (ELBW) infants enrolled in the Candida study were evaluated based on infection status.
Study design ELBW infants born at Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network (NRN) centers between March 2004 and July 2007 who were screened for suspected sepsis were eligible for inclusion in the Candida study. Primary outcome data for neurodevelopmental impairment (NDI) or death were available for 1317 of the 1515 infants (87%) enrolled in the Candida study. The Bayley Scales of Infant Development-II or -III was administered at 18 months' adjusted age. A secondary comparison was performed with 864 infants enrolled in the NRN Generic Database during the same cohort who were never screened for sepsis and therefore not eligible for the Candida study.
Results Among ELBW infants enrolled in the Candida study, 31% with Candida and 31% with late-onset non-Candida sepsis had NDI at 18 months. Infants with Candida sepsis and/or meningitis had an increased risk of death and were more likely to have the composite outcome of death and/or NDI compared with uninfected infants in adjusted analysis. Compared with infants in the NRN registry never screened for sepsis, overall risk for death were similar but those with Candida infection were more likely to have NDI (OR 1.83, 95% CI 1.01-3.33, P = .047).
Conclusions In this cohort of ELBW infants, those with infection and/or meningitis were at increased risk for death and/or NDI. This risk was highest among those with Candida sepsis and/or meningitis.
C1 [Adams-Chapman, Ira; Stoll, Barbara J.] Emory Univ, Dept Pediat, Atlanta, GA 30303 USA.
[Bann, Carla M.] Social Stat & Environm Sci Unit, Res Triangle Pk, NC USA.
[Das, Abhik] RTI Int, Social Stat & Environm Sci Unit, Rockville, MD USA.
[Goldberg, Ronald N.; Goldstein, Ricki F.; Benjamin, Daniel K., Jr.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[Walsh, Michele C.; Wilson-Costello, Deanne E.] Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA.
[Sanchez, Pablo J.; Miller, Nancy A.; Heyne, Roy J.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Shankaran, Seetha; Pappas, Athina] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Watterberg, Kristi L.; Fuller, Janell] Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
[Duara, Shahnaz; Bauer, Charles R.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Peralta-Carcelen, Myriam] Univ Alabama Birmingham, Div Neonatol, Birmingham, AL USA.
[Steichen, Jean J.] Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA.
[Hintz, Susan R.] Stanford Univ, Sch Med, Dept Pediat, Palo Alto, CA 94304 USA.
[Evans, Patricia W.] Univ Texas Houston, Med Sch Houston, Dept Pediat, Houston, TX USA.
[Acarregui, Michael J.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Myers, Gary J.] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Vohr, Betty R.] Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02908 USA.
[Vaucher, Yvonne E.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Ehrenkranz, Richard A.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
[McGowan, Elisabeth C.] Floating Hosp Children, Tufts Med Ctr, Dept Pediat, Div Newborn Med, Boston, MA USA.
[Dillard, Robert G.] Wake Forest Univ, Winston Salem, NC 27109 USA.
RP Adams-Chapman, I (reprint author), Emory Univ, Sch Med, Dept Pediat, Dev Progress Clin,Div Neonatol, 46 Jesse Hill Jr Dr SE, Atlanta, GA 30303 USA.
EM iadamsc@emory.edu
FU National Institutes of Health; Eunice Kennedy Shriver NICHD; Thrasher
Research Fund; NICHD
FX Supported by grants from the National Institutes of Health and the
Eunice Kennedy Shriver NICHD for the Neonatal Research Network's
Candidiasis Study (Appendix). D.B. received support from the Thrasher
Research Fund and NICHD. The funding agencies provided overall oversight
for study conduct, but all data analyses and interpretation were
independent of the funding agencies. Data collected at participating
sites of the NICHD Neonatal Research Network were transmitted to RTI
International, the data coordinating center for the network, which
stored, managed, and analyzed the data for this study. The authors
declare no conflicts of interest.
NR 29
TC 24
Z9 24
U1 0
U2 8
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD OCT
PY 2013
VL 163
IS 4
BP 961
EP +
DI 10.1016/j.jpeds.2013.04.034
PG 10
WC Pediatrics
SC Pediatrics
GA 224HM
UT WOS:000324873700009
PM 23726546
ER
PT J
AU Sundaram, SS
Alonso, EM
Haber, B
Magee, JC
Fredericks, E
Kamath, B
Kerkar, N
Rosenthal, P
Shepherd, R
Limbers, C
Varni, JW
Robuck, P
Sokol, RJ
AF Sundaram, Shikha S.
Alonso, Estella M.
Haber, Barbara
Magee, John C.
Fredericks, Emily
Kamath, Binita
Kerkar, Nanda
Rosenthal, Philip
Shepherd, Ross
Limbers, Christine
Varni, James W.
Robuck, Patricia
Sokol, Ronald J.
CA Childhood Liver Dis Res Educ
TI Health Related Quality of Life in Patients with Biliary Atresia
Surviving with their Native Liver
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID MINIMAL HEPATIC-ENCEPHALOPATHY; GENERIC CORE SCALES; TRANSPLANT
RECIPIENTS; CHILDREN; PARENTS; DISEASE; PEDSQL(TM)-4.0; RELIABILITY;
VALIDITY
AB Objectives To quantify health related quality of life (HRQOL) of patients with biliary atresia with their native livers and compare them with healthy children and patients with biliary atresia post-liver transplant (LT) and to examine the relationship between HRQOL and medical variables.
Study design A cross-sectional HRQOL study of patients with biliary atresia with their native livers (ages 2-25 years) was conducted and compared with healthy and post-LT biliary atresia samples using Pediatric Quality of Life Inventory 4.0 child self and parent proxy reports, a validated measure of physical/psychosocial functioning.
Results 221 patients with biliary atresia with native livers (54% female, 67% white) were studied. Patient self and parent proxy reports showed significantly poorer HRQOL than healthy children across all domains (P < .001), particularly in emotional and psychosocial functioning. Child self and parent proxy HRQOL scores from patients with biliary atresia with their native livers and post-LT biliary atresia were similar across all domains (P = not significant). Child self and parent proxy reports showed moderate agreement across all scales, except social functioning (poor to fair agreement). On multivariate regression analysis, black race and elevated total bilirubin were associated with lower Total and Psychosocial HRQOL summary scores.
Conclusions HRQOL in patients with biliary atresia with their native livers is significantly poorer than healthy children and similar to children with post-LT biliary atresia. These findings identify significant opportunities to optimize the overall health of patients with biliary atresia.
C1 [Sundaram, Shikha S.; Sokol, Ronald J.] Univ Colorado, Sch Med, Childrens Hosp Colorado, Dept Gastroenterol, Aurora, CO USA.
[Sundaram, Shikha S.; Sokol, Ronald J.] Univ Colorado, Sch Med, Childrens Hosp Colorado, Dept Hepatol, Aurora, CO USA.
[Sundaram, Shikha S.; Sokol, Ronald J.] Univ Colorado, Sch Med, Childrens Hosp Colorado, Dept Nutr, Aurora, CO USA.
[Alonso, Estella M.] Northwestern Univ, Dept Gastroenterol Hepatol & Nutr, Ann & Robert H Lurie Childrens Hosp, Chicago, IL 60611 USA.
[Haber, Barbara] Merck Sharp & Dohme Ltd, Dept Hepatol, Upper Gwyneed, PA USA.
[Haber, Barbara] Childrens Hosp Philadelphia, Dept Pediat, Div Gastroenterol Hepatol & Nutr, Philadelphia, PA 19104 USA.
[Magee, John C.] Univ Michigan, Dept Pediat, Dept Surg, Ann Arbor, MI 48109 USA.
[Fredericks, Emily] Univ Toronto, Hosp Sick Children, Div Gastroenterol Hepatol & Nutr, Toronto, ON M5G 1X8, Canada.
[Kamath, Binita] Univ So Calif, Childrens Hosp, Dept Pediat, Div Gastroenterol & Nutr, Los Angeles, CA 90027 USA.
[Kerkar, Nanda] Univ Calif San Francisco, Benioff Childrens Hosp, Dept Pediat, San Francisco, CA 94143 USA.
[Rosenthal, Philip] Texas Childrens Hopsital Baylor Coll Med, Div Gastroenterol Hepatol & Nutr, Dept Pediat, Houston, TX USA.
[Shepherd, Ross] Baylor Univ, Dept Psychol & Neurosci, Waco, TX 76798 USA.
[Limbers, Christine] Texas A&M Univ, Dept Pediat, College Stn, TX USA.
[Varni, James W.] NIH, Natl Inst Diabet & Digest & Kidney Dis, Bethesda, MD 20892 USA.
RP Sundaram, SS (reprint author), Childrens Hosp Colorado, Digest Hlth Inst, 13123 E 16th Ave,B290, Aurora, CO 80045 USA.
EM shikha.sundaram@childrenscolorado.org
FU National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK)
[U01 DK061693, U54 DK078377, U54DK078377, DK 62530]; National Center for
Research Resources (NCRR) [5M01 RR00069, UL1RR025005, UL1RR025741,
UL1RR026314, UL1RR025780, UL1RR029877, UL1RR024134, UL1RR024153,
UL1RR024131, UL1RR024992]; Eunice Kennedy Shriver National Institute of
Child Health and Human Development [R01 HD045694]; NIDDK DK [62436,
62497, 62453, 62445, 62481, 62466, 62500, 62452, 62470]; NIDD DK [62456]
FX Supported by the National Institute of Diabetes, Digestive, and Kidney
Diseases (NIDDK; U01 DK061693 and U54 DK078377; individual grants
available in the Appendix), National Center for Research Resources
(NCRR; 5M01 RR00069; individual grants available in the Appendix), and
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development (R01 HD045694). The authors declare no conflicts of
interest.; Members of the Childhood Liver Disease Research and Education
Network include:; John Hopkins School of Medicine (supported by NIDDK
U54DK078377 and DK 62530 and NCRR UL1RR025005) Baltimore, MD: Kathy
Schwarz, MD, Robert Anders, MD, PhD, Paul Colombani, MD, Wikrom
Karnsakul, MD, Shalom Anita Osire, Kim Pfeifer, RN, BSN, Laura Wachter;
Ann & Robert H. Lurie Children's Hospital of Chicago (supported by NIDDK
DK 62436 and NCRR UL1RR025741) Chicago, IL: Peter Whitington, MD,
Estella Alonso, MD, Lee Bass, MD, Kelly Dunmars, Denise Jones, Sue
Kelly, RN, BSN, Hector Melin-Aldana, MD, Denise Rizza, PharmD, Ricardo
Superina, MD, Kiley Tkaczyk, Elizabeth Westfall; Cincinnati Children's
Hospital Medical Center (supported by NIDDK DK 62497 and NCRR
UL1RR026314) Cincinnati, OH: Jorge Bezerra, MD, Kevin Bove, MD, Julie
Denlinger, James Heubi, MD, Pinky Jha, Denise LaGory, RPH, Alexander
Miethke, MD, Joseph Palermo, MD, Stacey Reed, Ken Setchell, PhD, Melissa
Stamper, Greg Tiao, MD; Children's Hospital Colorado (supported by NIDDK
DK 62453 and NCRR UL1RR025780) Aurora, CO: Ron Sokol, MD, Megan Dix,
Sheryl Faut, Joan Hines, MPH, Michelle Hite, RN, Jessica Jensen,
Frederick Karrer, MD, Mark Lovell, MD, Cara Mack, MD, Michael Narkewicz,
MD, Timothy Schardt, PharmD, BCPS, Frederick Suchy, MD, Shikha Sundaram,
MD, Johan Van Hove, MD; Mount Sinai School of Medicine (supported by
NIDDK DK 62445 and NCRR UL1RR029877) New York, NY: Ronen Arnon, MD,
Mariel Boyd; Jamie Chu, MD, Ivy Cohen, Kishore Iyer, MD, Margret Magid,
MD; The Children's Hospital of Philadelphia (supported by NIDDK DK 62481
and NCRR UL1RR024134) Philadelphia, PA: Kathleen Loomes, MD, Timothy
Crisci, Jessi Erlichman, MPH, Alan Flake, MD, Josh Friedman, MD, PhD,
Oyinkansola Kusemiju, MPH, Laura Leonard, David Piccoli, MD, Elizabeth
Rand, MD, Pierre Russo, MD, Nancy Spinner, PhD, Eileen Wu; Children's
Hospital of Pittsburgh (supported by NIDDK DK 62466 and NCRR
UL1RR024153) Pittsburgh, PA: Benjamin Shneider, MD, Feras Alissa, MD,
Beverly Bernard, CRNP, A'Delbert Bowen, MD, Kathy Bukauskas, RN, CCRC,
Paul Hoffmann, Ronald Jaffe, MD, Douglas Lindblad, MD, George
Mazariegos, MD, Robert Ortiz-Iguayo, MD, David Perlmutter, MD, Stefan
Scholz, MD, Rakesh Sindhi, MD, Robert Squires, Jr., MD, Veena Venkat,
MD, Jerry Vockley, MD, PhD, Dale Zecca; UCSF Children's Hospital
(supported by NIDDK DK 62500 and NCRR UL1RR024131) San Francisco, CA:
Philip Rosenthal, MD, Laura Bull, PhD, Scott Fields, Shannon Fleck,
Melvin Heyman, MD, Shinjiro Hirose, MD, Vincent Hoang, Grace Kim, MD,
Camille Langlois, John Pech, Claudi Tejeda, John Roberts, MD, Larry
Wang, MD, PhD; Washington University School of Medicine (Site 9
-supported by NIDDK DK 62452 and NCRR UL1RR024992) St. Louis, MO: Yumi
Turmelle, MD, Pat Dillon, MD, Sandra Guelker, BA, Kathleen Harris,
Robert Heuckeroth, MD, Jeffrey Lowell, MD, FACS, Stacy Postma, Jonathan
(Brad) Rider, RPH, David Rudnick, MD, PhD, Janis Stoll, Alexander
Weymann, MD, Frances White, MD; Texas Children's Hospital (supported by
NIDDK DK 62470) Houston, TX: Paula Hertel, MD, Zoe Apted, BA, Mary
Brandt, MD, Jameisha Brown, Beth Carter, MD, Milton Finegold, MD,
Richard Gibbs, PhD, Sanjiv Harpavat, MD, Jennifer Lynds, RPh, PharmD,
Tara McCartney, RPh; St. Louis University School of Medicine, St.;
Louis, MO: Jeffrey Teckman, MD, Vikki Kociela, BSN, CCRC; Riley Hospital
for Children, Indianapolis, IN: Jean Molleston, MD, Molly Bozic, MD,
Beth Byam, RN, Oscar (Bill) Cummings, MD, Vicki Haviland, Ann Klipsch,
RN, Cindy Sawyers, BSRT, Girish Subbarao, MD, Jada Wegere, Karen West;
Seattle Children's Hospital, Seattle, WA: Karen Murray, MD, Kara Cooper,
Laura Finn, MD, Patrick Healey, MD, Simon Horslen, MD, Susan Jacob,
Alexander Miethke, MD, Joseph Palermo, MD, Stacey Reed, Ken Setchell,
PhD, Melissa Stamper, MD; The Hospital for Sick Children, Toronto,
Ontario, CA: Vicky Ng, MD, Allison Chiu, Catherine Chung, MD, Catherine
Day, Maria DeAngelis, Annie Fecteau, MD, Kelsey Hunt, Binita Kamath, MD,
Tanya Kovaleva, Jacob Langer, MD, Constance O'Connor, Claudia Quammie,
Lilatool Shakur, Krista VanRoestel; Children's Hospital Los Angeles, Los
Angeles, CA: Kasper Wang, MD, JoAnna Cavallero, Henri Ford, MD, MHA,
Catherine Goodhue, CPNP, Nanda Kerker, MD, Sonia Michail, MD, Vincent
Hoang, Grace Kim, MD, Camille Langlois, John Pech, John Roberts, MD,
Larry Wang, MD, PhD; Children's Healthcare of Atlanta (Site P [18])
Atlanta, GA: Saul Karpen MD, PhD, Carlos Abramowsky, MD, Liezl de la
Cruz-Tracy, Rose Francois-Marcello, Nitika Gupta, MD, Jim Rhodes,
PharmD, Richard Ricketts, MD, Rene Romero, MD, Katrina Scott, Sundari
Sekar, MBBS, DGO, Bahig Shehata, MD, Taieshia Turner-Green, Miriam Vos,
MD, MSPH; King's College Hospital, London, UK: Richard Thompson National
Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD:
Patricia Robuck, PhD, Edward Doo, MD, Jay Hoofnagle, MD, Averell
Sherker, MD, FRCP, Rebecca Torrance, RN, MSN, Rebekah Van Raaphorst,
MPH, LT; University of Michigan Data Coordinating Center (supported by
NIDD DK 62456) Ann Arbor, MI: John Magee, MD, Karen Jones, Beverley
Marchant, Robert, ScD Parker, Trivellore Raghunathan, PhD, Cathie Spino,
DSc, Wen Ye.
NR 23
TC 14
Z9 15
U1 4
U2 14
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD OCT
PY 2013
VL 163
IS 4
BP 1052
EP +
DI 10.1016/j.jpeds.2013.04.037
PG 8
WC Pediatrics
SC Pediatrics
GA 224HM
UT WOS:000324873700026
PM 23746866
ER
PT J
AU Kumar, P
Shankaran, S
Ambalavanan, N
Kendrick, DE
Pappas, A
Vohr, BR
Poindexter, BB
Das, A
Higgins, RD
AF Kumar, P.
Shankaran, S.
Ambalavanan, N.
Kendrick, D. E.
Pappas, A.
Vohr, B. R.
Poindexter, B. B.
Das, A.
Higgins, R. D.
CA NICHD Neonatal Res Network
TI Characteristics of extremely low-birth-weight infant survivors with
unimpaired outcomes at 30 months of age
SO JOURNAL OF PERINATOLOGY
LA English
DT Article
DE extremely low birth weight; unimpaired outcome; outcome; antenatal
steroids; cerebral palsy
ID EXTREMELY PRETERM INFANTS; NEURODEVELOPMENTAL OUTCOMES; ANTENATAL
CORTICOSTEROIDS; MORTALITY; CHILDREN; RISK; BORN; NETWORK; IMPACT; 1990S
AB OBJECTIVE: To evaluate characteristics of unimpaired outcome in extremely low-birth-weight (ELBW) survivors.
STUDY DESIGN: ELBW infants (n=714) with 30 months' assessments were analyzed. Logistic regression was used to develop a model for the binary outcome of unimpaired versus impaired outcome.
RESULT: Thirty-three percent of infants had an unimpaired outcome. Seventeen percent of ELBW survivors had a Bayley II Mental Developmental Index score of >= 101 and 2% had a score of >= 116. Female gender, use of antenatal steroids (ANS), maternal education >= high school and the absence of major neonatal morbidities were independent predictors of unimpaired outcome. The likelihood of an unimpaired outcome in the presence of major neonatal morbidities was higher in infants exposed to ANS.
CONCLUSION: The majority of unimpaired ELBW survivors had cognitive scores shifted toward the lower end of the normal distribution. Exposure to ANS was associated with higher likelihood of an unimpaired outcome in infants with major neonatal morbidities.
C1 [Kumar, P.] Northwestern Univ, Dept Pediat, Feinberg Sch Med, Chicago, IL 60611 USA.
[Shankaran, S.; Pappas, A.] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Ambalavanan, N.] Univ Alabama Birmingham, Div Neonatol, Birmingham, AL USA.
[Kendrick, D. E.] RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
[Vohr, B. R.] Brown Univ, Dept Pediat, Providence, RI 02912 USA.
[Poindexter, B. B.] Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN 46202 USA.
[Das, A.] RTI Int, Stat & Epidemiol Unit, Rockville, MD USA.
[Higgins, R. D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Kumar, P (reprint author), Univ Mississippi, Med Ctr, Batson Childrens Hosp, Div Newborn Med,Dept Pediat, Jackson, MS 39216 USA.
EM pkumar3@umc.edu
RI Kumar, Prem/B-6691-2009;
OI Ambalavanan, Namasivayam/0000-0003-0731-9092
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD [U10 HD21364, U10 HD21385, U10 HD21397, U10 HD27851,
U10 HD27853, U10 HD27856, U10 HD27871, U10 HD27880, U10 HD27904, U10
HD34216, U10 HD36790, U10 HD40461, U10 HD40689]; National Institutes of
Health (General Clinical Research Center Grants) [M01 RR32, M01 RR39,
M01 RR70, M01 RR80, M01 RR633, M01 RR750, M01 RR6022, M01 RR8084, M01
RR16587]; Neonatal Research Network's Glutamine Study
FX We are indebted to our medical and nursing colleagues and the infants
and their parents who agreed to take part in this study. The following
investigators, in addition to those listed as authors, participated in
this study: NRN Chair; Alan H Jobe, MD, PhD, University of Cincinnati.
Brown University, Women & Infants Hospital of Rhode Island: William Oh,
MD; Betty R Vohr, MD; Angelita Hensman, BSN RNC; Lucy Noel, RN; Barbara
Alksninis, PNP; Martha R Leonard, BA; Rachel A Vogt, MD; Teresa M Leach,
MEd CAES; Victoria E Watson, MS CAS. Case Western Reserve University,
Rainbow Babies & Children's Hospital: Avroy A Fanaroff, MD; Deanne
Wilson-Costello, MD; Nancy S Newman, BA RN; Bonnie S Siner, RN; Harriet
G Friedman, MA. Cincinnati Children's Hospital Medical Center,
University Hospital, and Good Samaritan Hospital: Edward F Donovan, MD;
Jean Steichen, MD; Barb Alexander, RN; Cathy Grisby, BSN CCRC; Marcia
Mersmann, RN; Holly Mincey, RN; Jody Shively, RN; Teresa L Gratton, PA.
Emory University, Children's Healthcare of Atlanta, Grady Memorial
Hospital, and Emory Crawford Long Hospital: Barbara J Stoll, MD; Ira
Adams-Chapman, MD; Ellen Hale, RN BS; Maureen Mulligan LaRossa, RN;
Sheena Carter, PhD. Eunice Kennedy Shriver National Institute of Child
Health and Human Development: Linda L Wright, MD; Elizabeth M McClure,
MEd. Indiana University, University Hospital, Methodist Hospital, Riley
Hospital for Children, and Wishard Health Services: Brenda B Poindexter,
MD MS; James A Lemons, MD; Anna M Dusick, MD; Carolyn Lytle, MD; Darlene
Kardatzke, MD; Marilyn Bull, MD; Greg Eaken, PhD; Lon G Bohnke, MS;
Leslie Richard, RN; Diana D Appel, RN BSN; Dianne Herron, RN; Lucy
Miller, RN BSN CCRC; Leslie Dawn Wilson, RN BSN. RTI International: W
Kenneth Poole, PhD; Betty Hastings; Carolyn Petrie Huitema, MS; Scott E
Schaefer, MS. Stanford University, Lucile Packard Children's Hospital:
David K Stevenson, MD; Susan R Hintz, MD MS; Barry E Fleisher, MD; M
Bethany Ball, BS CCRC; Carol G Kuelper, PhD; Julie C Lee, PhD; Joan M
Baran, PhD; Lori E Bond, PhD; Nicholas St. John, PhD; Renee P Pyle, PhD.
University of Alabama at Birmingham Health System and Children's
Hospital of Alabama: Waldemar A Carlo, MD; Myriam Peralta-Carcelen, MD;
Monica V Collins, RN BSN MaEd; Shirley S Cosby, RN BSN; Vivien A
Phillips, RN BSN; Fred J Biasini, PhD; Kirstin J Bailey, PhD; Richard V
Rector, PhD; Stephanie A Chopko, PhD. University of California -San
Diego Medical Center and Sharp Mary Birch Hospital for Women: Neil N
Finer, MD; Yvonne E Vaucher, MD MPH; Maynard R Rasmussen MD; Kathy
Arnell, RN; Martha G Fuller, RN MSN; Donna Posin, OTR/L MPA. University
of Miami Holtz Children's Hospital: Shahnaz Duara, MD; Charles R Bauer,
MD; Ruth Everett, RN MSN; Alexis N Diaz, BA; Elaine O Mathews, RN; Kasey
Hamlin-Smith, PhD; Lisa Jean-Gilles, BA; Maria Calejo, MS; Silvia M
Frade, BA; Silvia Hiriart-Fajardo, MD; Yamiley Gideon, BA. University of
Texas Southwestern Medical Center at Dallas, Parkland Health & Hospital
System, and Children's Medical Center Dallas: Abbot R Laptook, MD; R Sue
Broyles, MD; Walid A Salhab, MD; Roy J Heyne, MD; Sally Adams, PNP;
Cathy Boatman, MS CIMI; Cristin Dooley, MS; Alicia Guzman; Elizabeth
Heyne, PA; Jackie F Hickman, RN; Linda Madden, PNP; Susie Madison, RN.
Wayne State University, Hutzel Women's Hospital, and Children's Hospital
of Michigan: Seetha Shankaran, MD; Yvette Johnson, MD; Rebecca Bara, RN
BSN; Geraldine Muran, RN BSN; Deborah Kennedy, RN BSN; Laura Goldston,
MA.; Yale University and Yale-New Haven Children's Hospital: Richard A
Ehrenkranz, MD; Patricia Gettner, RN; Monica Konstantino, RN; Elaine
Romano, RN BSN; Nancy Close, PhD; Walter Gilliam, PhD. The Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD; Grants U10 HD21364, U10 HD21385, U10 HD21397, U10 HD27851, U10
HD27853, U10 HD27856, U10 HD27871, U10 HD27880U10 HD27904, U10 HD34216,
U10 HD36790, U10 HD40461, U10 HD40689) and The National Institutes of
Health (General Clinical Research Center Grants M01 RR32, M01 RR39, M01
RR70, M01 RR80, M01 RR633, M01 RR750, M01 RR6022, M01 RR8084 and M01
RR16587) provided grant support for the Neonatal Research Network's
Glutamine Study.
NR 25
TC 3
Z9 3
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0743-8346
J9 J PERINATOL
JI J. Perinatol.
PD OCT
PY 2013
VL 33
IS 10
BP 800
EP 805
DI 10.1038/jp.2013.71
PG 6
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 227DB
UT WOS:000325087700013
PM 23807719
ER
PT J
AU Hiranita, T
Soto, PL
Tanda, G
Kopajtic, TA
Katz, JL
AF Hiranita, Takato
Soto, Paul L.
Tanda, Gianluigi
Kopajtic, Theresa A.
Katz, Jonathan L.
TI Stimulants as Specific Inducers of Dopamine-Independent sigma Agonist
Self-Administration in Rats
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID CONDITIONED PLACE PREFERENCE; RECEPTOR AGONISTS; DISCRIMINATING COCAINE;
PROTEIN EXPRESSION; NUCLEUS-ACCUMBENS; UPTAKE INHIBITORS;
RHESUS-MONKEYS; REINFORCEMENT; ACTIVATION; BRAIN
AB A previous study showed that cocaine self-administration induced dopamine-independent reinforcing effects of sigma agonists mediated by their selective actions at sigma(1) receptors (sigma(1)Rs), which are intracellularly mobile chaperone proteins implicated in abuse-related effects of stimulants. The present study assessed whether the induction was specific to self-administration of cocaine. Rats were trained to self-administer the dopamine releaser, d-methamphetamine (0.01-0.32 mg/kg per injection), the mu-opioid receptor agonist, heroin (0.001-0.032 mg/kg per injection), and the noncompetitive N-methyl-D-aspartate receptor/channel antagonist ketamine (0.032-1.0 mg/kg per injection). As with cocaine, self-administration of d-methamphetamine induced reinforcing effects of the selective sigma R-1 agonists PRE-084 [2-(4-morpholinethyl)1-phenylcyclohexanecarboxylate hydrochloride] and (1)-pentazocine (0.032-1.0 mg/kg per injection, each). In contrast, neither self-administration of heroin nor ketamine induced PRE-084 or (+)-pentazocine (0.032-10 mg/kg per injection, each) self-administration. Although the sigma R-1 agonists did not maintain responding in subjects with histories of heroin or ketamine self-administration, substitution for those drugs was obtained with appropriate agonists (e.g., remifentanil, 0.1-3.2 mu g/kg per injection, for heroin and (5S, 10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine ((+)-MK 801; dizocilpine), 0.32-10.0 mu g/kg per injection, for ketamine). The sigma R antagonist N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(1-pyrrolidinyl)ethylamine dihydrobromide (BD 1008; 1.0-10 mg/kg) dose-dependently blocked PRE-084 self-administration but was inactive against d-methamphetamine, heroin, and ketamine. In contrast, PRE-084 self-administration was affected neither by the dopamine receptor antagonist (+)-butaclamol (10-100 mu g/kg) nor by the opioid antagonist (-)-naltrexone (1.0-10 mg/kg), whereas these antagonists were active against d-methamphetamine and heroin self-administration, respectively. The results indicate that experience specifically with indirect-acting dopamine agonists induces reinforcing effects of previously inactive sigma R-1 agonists. It is further suggested that induced s1R reinforcing mechanisms may play an essential role in treatment-resistant stimulant abuse, suggesting new approaches for the development of effective medications for its treatment.
C1 [Hiranita, Takato; Tanda, Gianluigi; Kopajtic, Theresa A.; Katz, Jonathan L.] NIDA, Psychobiol Sect, Mol Targets & Medicat Discovery Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA.
[Soto, Paul L.] Johns Hopkins Univ, Behav Biol Res Ctr, Sch Med, Baltimore, MD USA.
RP Katz, JL (reprint author), NIDA, Psychobiol Sect, Intramural Res Program, NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM jkatz@intra.nida.nih.gov
RI Hiranita, Takato/G-6567-2011; Tanda, Gianluigi/B-3318-2009
OI Tanda, Gianluigi/0000-0001-9526-9878
FU Intramural Research Program of the National Institutes of Health
[National Institute on Drug Abuse]
FX The research was supported by the Intramural Research Program of the
National Institutes of Health [National Institute on Drug Abuse].
NR 52
TC 5
Z9 5
U1 0
U2 4
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 2013
VL 347
IS 1
BP 20
EP 29
DI 10.1124/jpet.113.207522
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 220KX
UT WOS:000324583600003
PM 23908387
ER
PT J
AU Moreno, P
Mantey, SA
Nuche-Berenguer, B
Reitman, ML
Gonzalez, N
Coy, DH
Jensen, RT
AF Moreno, Paola
Mantey, Samuel A.
Nuche-Berenguer, Bernardo
Reitman, Marc L.
Gonzalez, Nieves
Coy, David H.
Jensen, Robert T.
TI Comparative Pharmacology of Bombesin Receptor Subtype-3, Nonpeptide
Agonist MK-5046, a Universal Peptide Agonist, and Peptide Antagonist
Bantag-1 for Human Bombesin Receptors
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID HUMAN ORPHAN RECEPTOR; ARACHIDONIC-ACID RELEASE; BRADYKININ B-2
RECEPTOR; PANCREATIC ACINI; SUBTYPE-3-DEFICIENT MICE; ANTIMITOTIC
ACTIVITY; SWISS 3T3-CELLS; GENE-EXPRESSION; MOLECULAR-BASIS; CCK1
RECEPTOR
AB Bombesin-receptor-subtype-3 (BRS-3) is an orphan G-protein-coupled receptor of the bombesin (Bn) family whose natural ligand is unknown and which does not bind any natural Bn-peptide with high affinity. It is present in the central nervous system, peripheral tissues, and tumors; however, its role in normal physiology/pathophysiology is largely unknown because of the lack of selective ligands. Recently, MK-5046 [(2S)-1,1,1-trifluoro-2-[4-(1H-pyrazol-1-yl)phenyl]-3-(4-{[1-(trifluoromethyl)cyclopropyl]methyl}-1H-imidazol-2-yl)propan-2-ol] and Bantag-1 [Boc-Phe-His-4-amino-5-cyclohexyl-2,4,5-trideoxypentonyl-Leu-(3-dimethylamino) benzylamide N-methylammonium trifluoroacetate], a nonpeptide agonist and a peptide antagonist, respectively, for BRS-3 have been described, but there have been limited studies on their pharmacology. We studied MK-5046 and Bantag-1 interactions with human Bn-receptors-human bombesin receptor subtype-3 (hBRS-3), gastrin-releasing peptide receptor (GRP-R), and neuromedin B receptor (NMB-R)-and compared them with the nonselective, peptide-agonist [D-Tyr6, beta Ala11, Phe13, Nle14]Bn-(6-14) (peptide #1). Receptor activation was detected by activation of phospholipase C (PLC), mitogen-activated protein kinase (MAPK), focal adhesion kinase (FAK), paxillin, and Akt. In hBRS-3 cells, the relative affinities were Bantag-1 (1.3 nM). peptide #1 (2 nM) > MK-5046 (37-160 nM) > GRP, NMB (>10 mu M), and the binding-dose-inhibition curves were broad (>4 logs), with Hill coefficients differing significantly from unity. Curve-fitting demonstrated high-affinity (MK-5046, K-i = 0.08 nM) and low-affinity (MK-5046, K-i = 11-29 nM) binding sites. For PLC activation in hBRS-3 cells, the relative potencies were MK-5046 (0.02 nM) > peptide #1 (6 nM) > GRP, NMB, Bantag-1 (>10 mu M), and MK-5046 had a biphasic dose response, whereas peptide #1 was monophasic. Bantag-1 was a specific hBRS-3-antagonist. In hBRS-3 cells, MK-5046 was a full agonist for activation of MAPK, FAK, Akt, and paxillin; however, it was a partial agonist for phospholipase A(2) (PLA(2)) activation. The kinetics of activation/duration of action for PLC/MAPK activation of MK-5046 and peptide #1 differed, with peptide #1 causing more rapid stimulation; however, MK-5046 had more prolonged activity. Our study finds that MK-5046 and Bantag-1 have high affinity/selectivity for hBRS-3. The nonpeptide MK-5046 and peptide #1 agonists differ markedly in their receptor coupling, ability to activate different signaling cascades, and kinetics/duration of action. These results show that their hBRS-3 receptor activation is not always concordant and could lead to markedly different cellular responses.
C1 [Moreno, Paola; Mantey, Samuel A.; Nuche-Berenguer, Bernardo; Jensen, Robert T.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
[Reitman, Marc L.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Gonzalez, Nieves] IIS Fdn Jimenez Diaz, Dept Metab Nutr & Hormones, Madrid, Spain.
Ctr Invest Biomed Red Diabet & Enfermedades Metab, Madrid, Spain.
[Coy, David H.] Tulane Hlth Sci Ctr, Dept Med, Peptide Res Labs, New Orleans, LA USA.
RP Jensen, RT (reprint author), NIDDK, Digest Dis Branch, NIH, Bldg 10,Room 9C-103,10 Ctr Dr MSC 1804, Bethesda, MD 20892 USA.
EM robertj@bdg10.niddk.nih.gov
RI Gonzalez, Nieves/N-2199-2014; Reitman, Marc/B-4448-2013
OI Gonzalez, Nieves/0000-0002-1551-2872; Reitman, Marc/0000-0002-0426-9475
FU Intramural Research Program of the National Institutes of Health
[National Institute of Diabetes and Digestive and Kidney Diseases] [ZIA
DK053100-22, ZIA DK053101-22]
FX This work was partially supported by the Intramural Research Program of
the National Institutes of Health [National Institute of Diabetes and
Digestive and Kidney Diseases] [Grants ZIA DK053100-22, ZIA
DK053101-22].
NR 61
TC 9
Z9 9
U1 0
U2 7
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 2013
VL 347
IS 1
BP 100
EP 116
DI 10.1124/jpet.113.206896
PG 17
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 220KX
UT WOS:000324583600011
PM 23892571
ER
PT J
AU Liu, CY
Liu, YC
Wu, C
Armstrong, A
Volpe, GJ
Van der Geest, RJ
Liu, YM
Hundley, WG
Gomes, AS
Liu, S
Nacif, M
Bluemke, DA
Lima, JAC
AF Liu, Chia-Ying
Liu, Yuan-Chang
Wu, Colin
Armstrong, Anderson
Volpe, Gustavo J.
Van der Geest, Rob J.
Liu, Yongmei
Hundley, William G.
Gomes, Antoinette S.
Liu, Songtao
Nacif, Marcelo
Bluemke, David A.
Lima, Joao A. C.
TI Evaluation of Age-Related Interstitial Myocardial Fibrosis With Cardiac
Magnetic Resonance Contrast-Enhanced T-1 Mapping MESA (Multi-Ethnic
Study of Atherosclerosis)
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE aging; magnetic resonance imaging; myocardial fibrosis; T-1 mapping
ID SPONTANEOUSLY HYPERTENSIVE RAT; EXTRACELLULAR VOLUME FRACTION;
HEART-FAILURE; INTRAINDIVIDUAL ASSESSMENT; T1; INFARCTION; DYSFUNCTION;
REPRODUCIBILITY; RESOLUTION; EVOLUTION
AB Objectives This study sought to determine the relationship of cardiovascular magnetic resonance (CMR) measures of tissue composition to age in the Multi-Ethnic Study of Atherosclerosis (MESA).
Background Animal and human studies have demonstrated increased collagen deposition in senescent hearts. New CMR indices of tissue composition by using T-1 mapping are sensitive to the presence of myocardial fibrosis.
Methods A total of 1,231 study participants (51% women; age range 54 to 93 years) of the MESA cohort were evaluated with T-1 mapping by using 1.5-T CMR scanners. None of the participants had focal scar on delayed enhancement CMR. Single-slice T-1 mapping was performed at the midventricular level before and at 12- and 25-min delay after administration of gadolinium contrast by using a modified Look-Locker inversion recovery sequence. The partition coefficient was determined by the slope of the linear relationship of (1/T-1myo vs. 1/T-1blood). The extracellular volume fraction (ECV) was derived accounting for the hematocrit level. Multivariable regression analyses were performed, adjusting for traditional risk factors and left ventricular structure.
Results Women had significantly greater partition coefficient, ECV, and precontrast T-1 than men, as well as lower post-contrast T-1 values (all p < 0.05). In general, linear regression analyses demonstrated that greater partition coefficient, pre-contrast T-1 values, and ECV were associated with older age in men (multivariate regression coefficients = 0.01; 5.9 ms; and 1.04% per 10 years' change; all p < 0.05). ECV was also significantly associated with age in women after multivariable adjustments.
Conclusions CMR parameters that have been associated with myocardial fibrosis were related to older age in the MESA study. Women had higher ECV than men but less ECV change over time. (C) 2013 by the American College of Cardiology Foundation
C1 [Liu, Chia-Ying; Liu, Yuan-Chang; Nacif, Marcelo; Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ Hosp, Dept Radiol, Baltimore, MD 21287 USA.
[Liu, Chia-Ying; Liu, Songtao; Nacif, Marcelo; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Liu, Yuan-Chang] Chang Gung Univ, Coll Med, Chang Gung Mem Hosp Linkou, Dept Med Imaging & Intervent, Taipei, Taiwan.
[Liu, Yuan-Chang; Armstrong, Anderson; Volpe, Gustavo J.; Bluemke, David A.; Lima, Joao A. C.] Johns Hopkins Univ Hosp, Dept Med, Div Cardiol, Baltimore, MD 21287 USA.
[Wu, Colin] NHLBI, Off Biostat, Bethesda, MD 20892 USA.
[Van der Geest, Rob J.] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
[Liu, Yongmei] Wake Forest Univ, Dept Epidemiol & Prevent, Winston Salem, NC USA.
[Hundley, William G.] Wake Forest Univ, Dept Internal Med, Winston Salem, NC USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
RP Lima, JAC (reprint author), Johns Hopkins Univ Hosp, Div Cardiol, Blalock 524D,600 North Wolfe St, Baltimore, MD 21287 USA.
EM jlima@jhmi.edu
RI Ruan, YL/B-9813-2009; Armstrong, Anderson/G-8407-2012; van der Geest,
Rob/J-8193-2015;
OI Armstrong, Anderson/0000-0003-3161-8922; van der Geest,
Rob/0000-0002-9084-5597; Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95160,
N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165,
N01-HC-95166, N01-HC-95167, N01-HC-95168]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95168 from the National Heart, Lung, and Blood Institute. Dr. van
der Geest has served as a consultant for Medis Medical Imaging Systems.
Dr. Lima has a relationship with Bayer HealthCare. All other authors
have reported that they have no relationships relevant to the contents
of this paper to disclose. Deborah Kwon, MD, served as Guest Editor for
this paper.
NR 47
TC 70
Z9 72
U1 1
U2 12
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 OCT 1
PY 2013
VL 62
IS 14
BP 1280
EP 1287
DI 10.1016/j.jacc.2013.05.078
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 221VV
UT WOS:000324689000012
PM 23871886
ER
PT J
AU de Wit, E
Munster, V
AF de Wit, Emmie
Munster, Vincenti
TI MERS-CoV: the intermediate host identified?
SO LANCET INFECTIOUS DISEASES
LA English
DT Editorial Material
ID CORONAVIRUSES
C1 [de Wit, Emmie] NIAID, Dis Modeling & Transmiss Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
[Munster, Vincenti] NIAID, Virus Ecol Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
RP de Wit, E (reprint author), NIAID, Dis Modeling & Transmiss Unit, Virol Lab, Div Intramural Res,NIH,Rocky Mt Labs, Hamilton, MT USA.
EM vincent.munster@nih.gov
OI Munster, Vincent/0000-0002-2288-3196; de Wit, Emmie/0000-0002-9763-7758
FU Intramural NIH HHS [ZIA AI001179-01]
NR 12
TC 3
Z9 3
U1 0
U2 18
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD OCT
PY 2013
VL 13
IS 10
BP 827
EP 828
DI 10.1016/S1473-3099(13)70193-2
PG 2
WC Infectious Diseases
SC Infectious Diseases
GA 224PD
UT WOS:000324899700004
PM 23933068
ER
PT J
AU Modjarrad, K
AF Modjarrad, Kayvon
TI HIV and helminths: time for a new direction
SO LANCET INFECTIOUS DISEASES
LA English
DT Letter
C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Modjarrad, K (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kayvon.modjarrad@nih.gov
NR 5
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
EI 1474-4457
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD OCT
PY 2013
VL 13
IS 10
BP 835
EP 835
DI 10.1016/S1473-3099(13)70239-1
PG 1
WC Infectious Diseases
SC Infectious Diseases
GA 224PD
UT WOS:000324899700013
PM 24070561
ER
PT J
AU Chowell, G
Fuentes, R
Olea, A
Aguilera, X
Nesse, H
Hyman, JM
AF Chowell, G.
Fuentes, R.
Olea, A.
Aguilera, X.
Nesse, H.
Hyman, J. M.
TI THE BASIC REPRODUCTION NUMBER R-0 AND EFFECTIVENESS OF REACTIVE
INTERVENTIONS DURING DENGUE EPIDEMICS: THE 2002 DENGUE OUTBREAK IN
EASTER ISLAND, CHILE
SO MATHEMATICAL BIOSCIENCES AND ENGINEERING
LA English
DT Article
DE Dengue; dengue hemorrhagic fever; epidemic; Easter Island; Chile; 2002
outbreak; mathematical model; reproduction number
ID AEDES-AEGYPTI; FEVER; TRANSMISSION; CLIMATE; MODELS; VIRUS; BRAZIL;
SIMULATION; DYNAMICS; MEXICO
AB We use a stochastic simulation model to explore the effect of reactive intervention strategies during the 2002 dengue outbreak in the small population of Easter Island, Chile. We quantified the effect of interventions on the transmission dynamics and epidemic size as a function of the simulated control intensity levels and the timing of initiation of control interventions. Because no dengue outbreaks had been reported prior to 2002 in Easter Island, the 2002 epidemic provided a unique opportunity to estimate the basic reproduction number R-0 during the initial epidemic phase, prior to the start of control interventions. We estimated R-0 at 27.2 (95%CI: 14.8, 49.3). We found that the final epidemic size is highly sensitive to the timing of start of interventions. However, even when the control interventions start several weeks after the epidemic onset, reactive intervention efforts can have a significant impact on the final epidemic size. Our results indicate that the rapid implementation of control interventions can have a significant effect in reducing the epidemic size of dengue epidemics.
C1 [Chowell, G.] Arizona State Univ, Math & Computat Modeling Sci Ctr, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
[Chowell, G.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Fuentes, R.] Minist Salud, Dept Epidemiol, Santiago, Chile.
[Olea, A.; Aguilera, X.] Univ Desarrollo, Santiago, Chile.
[Nesse, H.] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
[Hyman, J. M.] Tulane Univ, New Orleans, LA 70118 USA.
RP Chowell, G (reprint author), Arizona State Univ, Math & Computat Modeling Sci Ctr, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
EM gchowell@asu.edu; rodrigo.fuentes@minsal.cl; normandin07@gmail.com;
ximenaguilera@gmail.com; hnesse@asu.edu; mhyman@tulane.edu
RI Aguilera, Ximena/D-9861-2014
OI Aguilera, Ximena/0000-0002-8153-6733
FU NIH/NIGMS [1U01GM097661-01]
FX This research (JH) was partially supported by an NIH/NIGMS grant
(1U01GM097661-01) in the Models of Infectious Disease Agent Study
(MIDAS) program.
NR 39
TC 5
Z9 5
U1 4
U2 19
PU AMER INST MATHEMATICAL SCIENCES
PI SPRINGFIELD
PA PO BOX 2604, SPRINGFIELD, MO 65801-2604 USA
SN 1547-1063
J9 MATH BIOSCI ENG
JI Math. Biosci. Eng.
PD OCT-DEC
PY 2013
VL 10
IS 5-6
SI SI
BP 1455
EP 1474
DI 10.3934/mbe.2013.10.1455
PG 20
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 217XV
UT WOS:000324397300013
PM 24245625
ER
PT J
AU Kareva, I
Berezovskaya, F
Karev, G
AF Kareva, Irina
Berezovskaya, Faina
Karev, Georgy
TI MIXED STRATEGIES AND NATURAL SELECTION IN RESOURCE ALLOCATION
SO MATHEMATICAL BIOSCIENCES AND ENGINEERING
LA English
DT Article
DE Natural selection; resource allocation; mathematical model; population
heterogeneity; strategies
ID LIFE-HISTORY EVOLUTION; POPULATION-DYNAMICS; CANCER GENOME; COMPETITION;
DIVERGENCE; DIVERSITY; BACTERIA; BIOFILMS; MODELS
AB An appropriate choice of strategy for resource allocation may frequently determine whether a population will be able to survive under the conditions of severe resource limitations. Here we focus on two classes of strategies allocation of resources towards rapid proliferation, or towards slower proliferation but increased physiological and environmental maintenance. We propose a generalized framework, where individuals within a population can use either strategy in different proportion for utilization of a common dynamical resource in order to maximize their fitness. We use the model to address two major questions, namely, whether either strategy is more likely to be selected for as a result of natural selection, and, if one allows for the possibility of resource over-consumption, whether either strategy is preferable for avoiding population collapse due to resource exhaustion. Analytical and numerical results suggest that the ultimate choice of strategy is determined primarily by the initial distribution of individuals in the population, and that while investment in physiological and environmental maintenance is a preferable strategy in a homogeneous population, no generalized prediction can be made about heterogeneous populations.
C1 [Kareva, Irina] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
[Berezovskaya, Faina] Howard Univ, Dept Math, Washington, DC 20059 USA.
[Karev, Georgy] Natl Inst Biotechnol Informat NCBI, NIH, Bethesda, MD 20894 USA.
RP Kareva, I (reprint author), Arizona State Univ, Sch Human Evolut & Social Change, 900 S Cady Mall, Tempe, AZ 85287 USA.
EM ikareva@asu.edu; fberezovskaya@howard.edu; karev@ncbi.nlm.nih.gov
FU National Science Foundation (NSF) [DMPS-0838705, DMS-1135663]; National
Security Agency (NSA) [H98230-09-1-0104]; Alfred P. Sloan Foundation;
Office of the Provost of Arizona State University; NIH, NCBI
FX This researcht has been supported by grants from the National Science
Foundation (NSF - Grant DMPS-0838705), the National Security Agency (NSA
- Grant H98230-09-1-0104), the Alfred P. Sloan Foundation, the Office of
the Provost of Arizona State University and Intramural Research Program
of the NIH, NCBI. This material is also based upon work partially
supported by the National Science Foundation under Grant No.
DMS-1135663.
NR 33
TC 1
Z9 1
U1 0
U2 13
PU AMER INST MATHEMATICAL SCIENCES
PI SPRINGFIELD
PA PO BOX 2604, SPRINGFIELD, MO 65801-2604 USA
SN 1547-1063
J9 MATH BIOSCI ENG
JI Math. Biosci. Eng.
PD OCT-DEC
PY 2013
VL 10
IS 5-6
SI SI
BP 1561
EP 1586
DI 10.3934/mbe.2013.10.1561
PG 26
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 217XV
UT WOS:000324397300020
PM 24245635
ER
PT J
AU Webb, RC
Bonifas, AP
Behnaz, A
Zhang, YH
Yu, KJ
Cheng, HY
Shi, MX
Bian, ZG
Liu, ZJ
Kim, YS
Yeo, WH
Park, JS
Song, JZ
Li, YH
Huang, YG
Gorbach, AM
Rogers, JA
AF Webb, R. Chad
Bonifas, Andrew P.
Behnaz, Alex
Zhang, Yihui
Yu, Ki Jun
Cheng, Huanyu
Shi, Mingxing
Bian, Zuguang
Liu, Zhuangjian
Kim, Yun-Soung
Yeo, Woon-Hong
Park, Jae Suk
Song, Jizhou
Li, Yuhang
Huang, Yonggang
Gorbach, Alexander M.
Rogers, John A.
TI Ultrathin conformal devices for precise and continuous thermal
characterization of human skin
SO NATURE MATERIALS
LA English
DT Article
ID BLOOD-FLOW; REACTIVE HYPEREMIA; OSCILLATIONS; RESPONSES; DISEASE; RISK
AB Precision thermometry of the skin can, together with other measurements, provide clinically relevant information about cardiovascular health, cognitive state, malignancy and many other important aspects of human physiology. Here, we introduce an ultrathin, compliant skin-like sensor/actuator technology that can pliably laminate onto the epidermis to provide continuous, accurate thermal characterizations that are unavailable with other methods. Examples include non-invasive spatial mapping of skin temperature with millikelvin precision, and simultaneous quantitative assessment of tissue thermal conductivity. Such devices can also be implemented in ways that reveal the time-dynamic influence of blood flow and perfusion on these properties. Experimental and theoretical studies establish the underlying principles of operation, and define engineering guidelines for device design. Evaluation of subtle variations in skin temperature associated with mental activity, physical stimulation and vasoconstriction/dilation along with accurate determination of skin hydration through measurements of thermal conductivity represent some important operational examples.
C1 [Webb, R. Chad; Bonifas, Andrew P.; Kim, Yun-Soung; Yeo, Woon-Hong; Rogers, John A.] Univ Illinois, Dept Mat Sci & Engn, Urbana, IL 61801 USA.
[Behnaz, Alex; Gorbach, Alexander M.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
[Zhang, Yihui] Tsinghua Univ, Ctr Mech & Mat, Beijing 100084, Peoples R China.
[Zhang, Yihui; Cheng, Huanyu; Bian, Zuguang; Li, Yuhang; Huang, Yonggang] Northwestern Univ, Dept Civil & Environm Engn, Evanston, IL 60208 USA.
[Zhang, Yihui; Cheng, Huanyu; Bian, Zuguang; Li, Yuhang; Huang, Yonggang] Northwestern Univ, Dept Mech Engn, Evanston, IL 60208 USA.
[Zhang, Yihui; Cheng, Huanyu; Bian, Zuguang; Li, Yuhang; Huang, Yonggang] Northwestern Univ, Ctr Engn & Hlth, Evanston, IL 60208 USA.
[Zhang, Yihui; Cheng, Huanyu; Bian, Zuguang; Li, Yuhang; Huang, Yonggang] Northwestern Univ, Skin Dis Res Ctr, Evanston, IL 60208 USA.
[Yu, Ki Jun; Park, Jae Suk] Univ Illinois, Dept Elect & Comp Engn, Urbana, IL 61801 USA.
[Shi, Mingxing] Southwest Jiaotong Univ, Sch Mech & Engn, Chengdu 610031, Peoples R China.
[Bian, Zuguang] Zhejiang Univ, Ningbo Inst Technol, Ningbo 315100, Zhejiang, Peoples R China.
[Liu, Zhuangjian] Inst High Performance Comp, Singapore 138632, Singapore.
[Song, Jizhou] Univ Miami, Dept Mech & Aerosp Engn, Coral Gables, FL 33146 USA.
RP Rogers, JA (reprint author), Univ Illinois, Dept Mat Sci & Engn, Urbana, IL 61801 USA.
EM jrogers@illinois.edu
RI Song, Jizhou/B-1935-2008; Huang, Yonggang/B-6998-2009; Cheng,
Huanyu/J-7379-2015; Rogers, John /L-2798-2016;
OI Cheng, Huanyu/0000-0001-6075-4208; Webb, Richard/0000-0002-4252-8239;
Yeo, Woon-Hong/0000-0002-5526-3882
FU National Science Foundation [DGE-1144245, ECCS-0824129]; Materials
Research Laboratory and Center for Microanalysis of Materials at the
University of Illinois at Urbana-Champaign; National Security Science
and Engineering Faculty Fellowship; Air Force Office of Scientific
Research; Intramural Research Program of NIBIB, NIH
FX This material is based on work supported by the National Science
Foundation under Grant No. DGE-1144245,Grant No. ECCS-0824129 and
through the Materials Research Laboratory and Center for Microanalysis
of Materials at the University of Illinois at Urbana-Champaign. J.A.R.
acknowledges financial support through a National Security Science and
Engineering Faculty Fellowship.The work on silicon nanomembranes was
financially supported by a MURI grant from the Air Force Office of
Scientific Research. This research was supported in part by the
Intramural Research Program of NIBIB,NIH. The authors would like to
thank H. Eden for his invaluable critique and insight ful comments
during preparation of this manuscript
NR 24
TC 189
Z9 193
U1 24
U2 178
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1476-1122
J9 NAT MATER
JI Nat. Mater.
PD OCT
PY 2013
VL 12
IS 10
BP 938
EP 944
DI 10.1038/NMAT3755
PG 7
WC Chemistry, Physical; Materials Science, Multidisciplinary; Physics,
Applied; Physics, Condensed Matter
SC Chemistry; Materials Science; Physics
GA 222MU
UT WOS:000324736000021
PM 24037122
ER
PT J
AU Lee, Y
Karuppagounder, SS
Shin, JH
Lee, YI
Ko, HS
Swing, D
Jiang, HS
Kang, SU
Lee, BD
Kang, HC
Kim, D
Tessarollo, L
Dawson, VL
Dawson, TM
AF Lee, Yunjong
Karuppagounder, Senthilkumar S.
Shin, Joo-Ho
Lee, Yun-Il
Ko, Han Seok
Swing, Debbie
Jiang, Haisong
Kang, Sung-Ung
Lee, Byoung Dae
Kang, Ho Chul
Kim, Donghoon
Tessarollo, Lino
Dawson, Valina L.
Dawson, Ted M.
TI Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal
loss
SO NATURE NEUROSCIENCE
LA English
DT Article
ID APOPTOSIS-INDUCING FACTOR; RNA SYNTHETASE COMPLEX;
POLYMERASE-1-DEPENDENT CELL-DEATH; PARKINS PROTECTIVE FUNCTION; MUTANT
ALPHA-SYNUCLEIN; UBIQUITIN LIGASE; S-NITROSYLATION; DISEASE; STRESS;
NEURODEGENERATION
AB The defining pathogenic feature of Parkinson's disease is the age-dependent loss of dopaminergic neurons. Mutations and inactivation of parkin, an ubiquitin E3 ligase, induce Parkinson's disease through accumulation of pathogenic substrates. We found that transgenic overexpression of a parkin substrate, aminoacyl-tRNA synthetase complex interacting multifunctional protein-2 (AIMP2), led to a selective, age-dependent, progressive loss of dopaminergic neurons via activation of poly(ADP-ribose) polymerase-1 (PARP1). AIMP2 accumulation in vitro and in vivo resulted in PARP1 overactivation and dopaminergic cell toxicity via direct association of these proteins in the nucleus, providing a path to PARP1 activation other than DNA damage. Inhibition of PARP1 through gene deletion or drug inhibition reversed behavioral deficits and protected against dopamine neuron death in AIMP2 transgenic mice. These data indicate that brain-permeable PARP inhibitors could effectively delay or prevent disease progression in Parkinson's disease.
C1 [Lee, Yunjong; Karuppagounder, Senthilkumar S.; Shin, Joo-Ho; Lee, Yun-Il; Ko, Han Seok; Jiang, Haisong; Kang, Sung-Ung; Lee, Byoung Dae; Kang, Ho Chul; Kim, Donghoon; Dawson, Valina L.; Dawson, Ted M.] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Neuroregenerat & Stem Cell Programs, Baltimore, MD 21218 USA.
[Lee, Yunjong] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA.
[Lee, Yunjong; Karuppagounder, Senthilkumar S.; Shin, Joo-Ho; Lee, Yun-Il; Ko, Han Seok; Jiang, Haisong; Kang, Sung-Ung; Lee, Byoung Dae; Kang, Ho Chul; Kim, Donghoon; Dawson, Valina L.; Dawson, Ted M.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Lee, Yunjong; Karuppagounder, Senthilkumar S.; Shin, Joo-Ho; Jiang, Haisong; Kang, Sung-Ung; Dawson, Valina L.; Dawson, Ted M.] Adrienne Helis Malvin Med Res Fdn, New Orleans, LA USA.
[Shin, Joo-Ho] Sungkyunkwan Univ, Sch Med, Samsung Biomed Res Inst, Div Pharmacol,Dept Mol Cell Biol, Suwon, South Korea.
[Ko, Han Seok; Kim, Donghoon] Diana Helis Henry Med Res Fdn, New Orleans, LA USA.
[Swing, Debbie; Tessarollo, Lino] NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Lee, Byoung Dae] Kyung Hee Univ, Dept Neurosci, Age Related & Brain Dis Res Ctr, Seoul, South Korea.
[Kang, Ho Chul] Ajou Univ, Sch Med, Dept Biomed Sci, Suwon 441749, South Korea.
[Kang, Ho Chul] Ajou Univ, Sch Med, Dept Physiol, Suwon 441749, South Korea.
[Dawson, Valina L.; Dawson, Ted M.] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD USA.
RP Dawson, VL (reprint author), Johns Hopkins Univ, Sch Med, Inst Cell Engn, Neuroregenerat & Stem Cell Programs, Baltimore, MD 21218 USA.
EM vdawson@jhmi.edu; tdawson@jhmi.edu
RI Karuppagounder, Senthilkumar/I-6752-2013;
OI Karuppagounder, Senthilkumar/0000-0002-3281-9913; Lee,
Yunjong/0000-0003-0182-2279; Dawson, Valina/0000-0002-2915-3970
FU US National Institutes of Health [NS38377]; JPB Foundation; Samsung
Scholarship Foundation; Adrienne Helis Malvin Medical Research
Foundation; Diana Helis Henry Medical Research Foundation; Intramural
Research Program of the National Cancer Institute, Center for Cancer
Research
FX This work was supported by grants from the US National Institutes of
Health (NS38377) and the JPB Foundation. Y.-I.L. was supported by the
Samsung Scholarship Foundation. T.M.D. is the Leonard and Madlyn
Abramson Professor in Neurodegenerative Diseases. The authors
acknowledge the joint participation and support by the Adrienne Helis
Malvin Medical Research Foundation and the Diana Helis Henry Medical
Research Foundation through its direct engagement in the continuous
active conduct of medical research in conjunction with the Johns Hopkins
Hospital and the Johns Hopkins University School of Medicine and the
Foundation's Parkinson's Disease Programs. D.S. and L.T. were supported
by the Intramural Research Program of the National Cancer Institute,
Center for Cancer Research, US National Institutes of Health.
NR 52
TC 40
Z9 41
U1 1
U2 11
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 OCT
PY 2013
VL 16
IS 10
BP 1392
EP +
DI 10.1038/nn.3500
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 223HM
UT WOS:000324795300011
PM 23974709
ER
PT J
AU Peschel, A
Otto, M
AF Peschel, Andreas
Otto, Michael
TI Phenol-soluble modulins and staphylococcal infection
SO NATURE REVIEWS MICROBIOLOGY
LA English
DT Article
ID QUORUM-SENSING SYSTEM; AMINO-ACID-SEQUENCE; PEPTIDE RECEPTOR 2; AUREUS
INFECTIONS; HUMAN NEUTROPHILS; VIRULENCE DETERMINANTS; REGULATOR AGR;
EPIDERMIDIS; BIOFILMS; IDENTIFICATION
AB Staphylococcus aureus is an important human pathogen and a leading cause of death worldwide. Phenol-soluble modulins (PSMs) have recently emerged as a novel toxin family defining the virulence potential of highly aggressive S. aureus isolates. PSMs have multiple roles in staphylococcal pathogenesis, causing lysis of red and white blood cells, stimulating inflammatory responses and contributing to biofilm development and the dissemination of biofilm-associated infections. Moreover, the pronounced capacity of PSMs to kill human neutrophils after phagocytosis might explain failures in the development of anti-staphylococcal vaccines. Here, we discuss recent progress made in our understanding of the biochemical and genetic properties of PSMs and their role in S. aureus pathogenesis, and suggest potential avenues to target PSMs for the development of anti-staphylococcal drugs.
C1 [Peschel, Andreas] Univ Tubingen, Cellular & Mol Microbiol Div, Interfac Inst Microbiol & Infect Med, D-72076 Tubingen, Germany.
[Otto, Michael] NIAID, Pathogen Mol Genet Sect, Lab Human Bacterial Pathogenesis, NIH, Bethesda, MD 20892 USA.
RP Otto, M (reprint author), NIAID, Pathogen Mol Genet Sect, Lab Human Bacterial Pathogenesis, NIH, 9000 Rockville Pike Bldg 33 1W10, Bethesda, MD 20892 USA.
EM motto@niaid.nih.gov
OI Otto, Michael/0000-0002-2222-4115
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, US National Institutes of Health; German Research
Council [SFB685, TRR34]
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, US National
Institutes of Health (to M.O.) and by the German Research Council
(grants SFB685 and TRR34 to A.P).
NR 65
TC 71
Z9 71
U1 2
U2 39
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1740-1526
EI 1740-1534
J9 NAT REV MICROBIOL
JI Nat. Rev. Microbiol.
PD OCT
PY 2013
VL 11
IS 10
BP 667
EP 673
DI 10.1038/nrmicro3110
PG 7
WC Microbiology
SC Microbiology
GA 221HP
UT WOS:000324649000013
PM 24018382
ER
PT J
AU Doyle, SM
Genest, O
Wickner, S
AF Doyle, Shannon M.
Genest, Olivier
Wickner, Sue
TI Protein rescue from aggregates by powerful molecular chaperone machines
SO NATURE REVIEWS MOLECULAR CELL BIOLOGY
LA English
DT Review
ID NUCLEOTIDE EXCHANGE FACTOR; AAA PLUS DISAGGREGASE; YEAST PRION
PROPAGATION; N-TERMINAL DOMAIN; HSP70 CHAPERONES; ESCHERICHIA-COLI;
HSP100 CHAPERONES; SUBSTRATE-BINDING; STRUCTURAL BASIS; CLPA CHAPERONE
AB Protein quality control within the cell requires the interplay of many molecular chaperones and proteases. When this quality control system is disrupted, polypeptides follow pathways leading to misfolding, inactivity and aggregation. Among the repertoire of molecular chaperones are remarkable proteins that forcibly untangle protein aggregates, called disaggregases. Structural and biochemical studies have led to new insights into how these proteins collaborate with co-chaperones and utilize ATP to power protein disaggregation. Understanding how energy-dependent protein disaggregating machines function is universally important and clinically relevant, as protein aggregation is linked to medical conditions such as Alzheimer's disease, Parkinson's disease, amyloidosis and prion diseases.
C1 [Doyle, Shannon M.; Genest, Olivier; Wickner, Sue] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Wickner, S (reprint author), NCI, Mol Biol Lab, NIH, 37 Convent Dr,Bldg 37,Room 5144, Bethesda, MD 20892 USA.
EM doyles@mail.nih.gov; wickners@mail.nih.gov
FU Intramural Research Program of the US National institutes of Health
(NIH); National Cancer Institute; Center for Cancer Research
FX The authors thank J. Hoskins and M. Markovski for critical reading of
the manuscript and helpful discussions. The research in the authors'
laboratory was supported by the Intramural Research Program of the US
National institutes of Health (NIH), the National Cancer Institute and
the Center for Cancer Research.
NR 157
TC 67
Z9 68
U1 9
U2 56
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-0072
J9 NAT REV MOL CELL BIO
JI Nat. Rev. Mol. Cell Biol.
PD OCT
PY 2013
VL 14
IS 10
BP 617
EP 629
DI 10.1038/nrm3660
PG 13
WC Cell Biology
SC Cell Biology
GA 223MU
UT WOS:000324810500011
PM 24061228
ER
PT J
AU Vitucci, M
Karpinich, NO
Bash, RE
Werneke, AM
Schmid, RS
White, KK
McNeill, RS
Huff, B
Wang, S
Van Dyke, T
Miller, CR
AF Vitucci, Mark
Karpinich, Natalie O.
Bash, Ryan E.
Werneke, Andrea M.
Schmid, Ralf S.
White, Kristen K.
McNeill, Robert S.
Huff, Byron
Wang, Sophie
Van Dyke, Terry
Miller, C. Ryan
TI Cooperativity between MAPK and PI3K signaling activation is required for
glioblastoma pathogenesis
SO NEURO-ONCOLOGY
LA English
DT Article
DE astrocytes; genetically engineered mouse; glioblastoma; invasion; Pten
ID NEURAL STEM/PROGENITOR CELLS; INTEGRATED GENOMIC ANALYSIS; IN-VIVO;
MALIGNANT ASTROCYTOMAS; CANCER SUSCEPTIBILITY; DISEASE PROGRESSION;
TUMOR SUPPRESSION; MOUSE MODELS; PTEN LOSS; GLIOMA
AB Background. Glioblastoma (GBM) genomes feature recurrent genetic alterations that dysregulate core intracellular signaling pathways, including the G1/S cell cycle checkpoint and the MAPK and PI3K effector arms of receptor tyrosine kinase (RTK) signaling. Elucidation of the phenotypic consequences of activated RTK effectors is required for the design of effective therapeutic and diagnostic strategies.
Methods. Geneticallydefined, G1/S checkpoint-defective cortical murine astrocytes with constitutively active Kras and/or Pten deletion mutations were used to systematically investigate the individual and combined roles of these 2 RTK signaling effectors in phenotypic hallmarks of glioblastoma pathogenesis, including growth, migration, and invasion in vitro. A novel syngeneic orthotopic allograft model system was used to examine in vivo tumorigenesis.
Results. Constitutively active Kras and/or Pten deletion mutations activated both MAPK and PI3K signaling. Their combination led to maximal growth, migration, and invasion of G1/S-defective astrocytes in vitro and produced progenitor-like transcriptomal profiles that mimic human proneural GBM. Activation of both RTK effector arms was required for in vivo tumorigenesis and produced highly invasive, proneural-like GBM.
Conclusions. These results suggest that cortical astrocytes can be transformed into GBM and that combined dysregulation of MAPK and PI3K signaling revert G1/S-defective astrocytes to a primitive gene expression state. This genetically-defined, immunocompetent model of proneural GBM will be useful for preclinical development of MAPK/PI3K-targeted, subtype-specific therapies.
C1 [Vitucci, Mark] Univ N Carolina, Sch Med, Curriculum Genet & Mol Biol, Chapel Hill, NC 27599 USA.
[Karpinich, Natalie O.] Univ N Carolina, Sch Med, Dept Cellular & Mol Physiol, Chapel Hill, NC 27599 USA.
[Bash, Ryan E.; Werneke, Andrea M.; Schmid, Ralf S.; Huff, Byron; Miller, C. Ryan] Univ N Carolina, Sch Med, Div Neuropathol, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
[Schmid, Ralf S.; Miller, C. Ryan] Univ N Carolina, Sch Med, Program Mol Biol & Biotechnol, Chapel Hill, NC 27599 USA.
[Schmid, Ralf S.; White, Kristen K.; Miller, C. Ryan] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Miller, C. Ryan] Univ N Carolina, Sch Med, Dept Neurol, Chapel Hill, NC 27599 USA.
[Miller, C. Ryan] Univ N Carolina, Sch Med, Neurosci Ctr, Chapel Hill, NC 27599 USA.
[Wang, Sophie; Van Dyke, Terry] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
[Van Dyke, Terry] NCI, Ctr Adv Preclin Res, Frederick, MD 21701 USA.
RP Miller, CR (reprint author), Univ N Carolina, Sch Med, 6109B Neurosci Res Bldg,Campus Box 7250, Chapel Hill, NC 27599 USA.
EM rmiller@med.unc.edu
RI Miller, Ryan/B-9365-2008;
OI Miller, Ryan/0000-0002-0096-8762; Schmid, Ralf/0000-0002-1721-5775
FU American Cancer Society [PF-06-283-01-MGO]; Damon Runyon Cancer Research
Foundation [CI-45-09]; UNC University Cancer Research Fund (UCRF);
Department of Defense [W81XWH-09-2-0042]; National Cancer Institute
[3P30CA016086]; National Institute of Environmental Health Sciences
[3P30ES010126]; UCRF
FX NOK was supported by a postdoctoral fellowship from the American Cancer
Society (PF-06-283-01-MGO). CRM is a Damon Runyon-Genentech Clinical
Investigator supported in part by a Clinical Investigator Award from the
Damon Runyon Cancer Research Foundation (CI-45-09). This work was
supported in part by grants to CRM from the UNC University Cancer
Research Fund (UCRF) and the Department of Defense (W81XWH-09-2-0042).
The UNC TPL is supported, in part, by grants from the National Cancer
Institute (3P30CA016086), National Institute of Environmental Health
Sciences (3P30ES010126), Department of Defense (W81XWH-09-2-0042), and
UCRF.
NR 49
TC 17
Z9 17
U1 0
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2013
VL 15
IS 10
BP 1317
EP 1329
DI 10.1093/neuonc/not084
PG 13
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 223UT
UT WOS:000324837500005
PM 23814263
ER
PT J
AU Hicks, D
Farsani, GT
Laval, S
Collins, J
Martoni, E
Shah, A
Zou, Y
Koch, M
Bonnemann, C
Lochmuller, H
Bushby, K
Roberts, M
Straub, V
AF Hicks, D.
Farsani, G. Torabi
Laval, S.
Collins, J.
Martoni, E.
Shah, A.
Zou, Y.
Koch, M.
Bonnemann, C.
Lochmuller, H.
Bushby, K.
Roberts, M.
Straub, V.
TI Collagen XII as a new disease gene for Bethlem-like myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Hicks, D.; Farsani, G. Torabi; Laval, S.; Shah, A.; Lochmuller, H.; Bushby, K.; Straub, V.] MRC Ctr Neuromuscular Dis Newcastle, Inst Med Genet, Newcastle Upon Tyne, Tyne & Wear, England.
[Collins, J.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Martoni, E.] Univ Ferrara, Dept Expt & Diagnost Med, I-44100 Ferrara, Italy.
[Zou, Y.; Bonnemann, C.] NINDS, NIH, Bethesda, MD 20892 USA.
[Koch, M.] Univ Cologne, Ctr Biochem, D-50931 Cologne, Germany.
[Roberts, M.] Hope Hosp, Dept Neurol, Salford M6 8HD, Lancs, England.
[Roberts, M.] Hope Hosp, Dept Neuropathol, Salford M6 8HD, Lancs, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 739
EP 739
DI 10.1016/j.nmd.2013.06.379
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500006
ER
PT J
AU Zou, Y
Zwolanek, D
Hu, Y
Schreiber, G
Brockmann, K
Izu, Y
Tian, Z
Devoto, M
Gandhy, S
Meier, M
Stetefeld, J
Hicks, D
Straub, V
Voermans, N
Birk, DE
Barton, ER
Koch, M
Bonnemann, CG
AF Zou, Y.
Zwolanek, D.
Hu, Y.
Schreiber, G.
Brockmann, K.
Izu, Y.
Tian, Z.
Devoto, M.
Gandhy, S.
Meier, M.
Stetefeld, J.
Hicks, D.
Straub, V.
Voermans, N.
Birk, D. E.
Barton, E. R.
Koch, M.
Boennemann, C. G.
TI Collagen type XII: A new congenital matrix and muscle disease
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Zou, Y.; Hu, Y.; Gandhy, S.; Boennemann, C. G.] NINDS, NIH, Neuromuscular & Neurogenet Disorders Childhood Se, Bethesda, MD 20892 USA.
[Zwolanek, D.; Koch, M.] Univ Cologne, Ctr Biochem, D-50931 Cologne, Germany.
[Schreiber, G.] Clin Ctr Pediat Neurol, Kassel, Germany.
[Brockmann, K.] Univ Gottingen, Dept Pediat & Pediat Neurol, D-37073 Gottingen, Germany.
[Izu, Y.; Birk, D. E.] Univ S Florida, Dept Mol Pharmacol & Physiol, Tampa, FL USA.
[Tian, Z.; Barton, E. R.] Univ Penn, Sch Dent Med, Dept Anat & Cell Biol, Philadelphia, PA 19104 USA.
[Devoto, M.] Childrens Hosp Philadelphia, Div Human Genet, Philadelphia, PA 19104 USA.
[Meier, M.; Stetefeld, J.] Univ Manitoba, Dept Chem, Winnipeg, MB R3T 2N2, Canada.
[Hicks, D.; Straub, V.] Newcastle Univ, Inst Med Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Voermans, N.] Radbouts Univ Nijmegen Med Ctr, Dept Neurol, Nijmegen, Netherlands.
RI Voermans, N.C./L-4724-2015
NR 0
TC 0
Z9 0
U1 0
U2 4
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 OCT
PY 2013
VL 23
IS 9-10
BP 739
EP 740
DI 10.1016/j.nmd.2013.06.380
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500007
ER
PT J
AU Foley, AR
Quijano-Roy, S
Collins, J
Straub, V
McCallum, M
Deconinck, N
Mercuri, E
Pane, M
D'Amico, A
Bertini, E
North, K
Ryan, MM
Auh, S
Muntoni, F
Bonnemann, CG
AF Foley, A. R.
Quijano-Roy, S.
Collins, J.
Straub, V.
McCallum, M.
Deconinck, N.
Mercuri, E.
Pane, M.
D'Amico, A.
Bertini, E.
North, K.
Ryan, M. M.
Auh, S.
Muntoni, F.
Boennemann, C. G.
TI Natural history of pulmonary function in collagen VI-related myopathies:
An international study
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Foley, A. R.; Muntoni, F.] UCL Inst Child Hlth, Dubowitz Neuromuscular Ctr, London, England.
[Foley, A. R.; Muntoni, F.] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Quijano-Roy, S.] Raymond Poincare Univ Hosp UVSQ, Garches Neuromuscular Ctr GNMH, Garches, France.
[Collins, J.] Cincinnati Childrens Hosp Med Ctr, Div Neurol, Cincinnati, OH 45229 USA.
[Straub, V.; McCallum, M.] Newcastle Univ, Int Ctr Life, Inst Human Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Deconinck, N.] Hop Univ Enfants Reine Fabiola, Dept Neurol, Brussels, Belgium.
[Mercuri, E.; Pane, M.] Univ Cattolica Sacro Cuore, Dept Paediat Neurol, I-00168 Rome, Italy.
[D'Amico, A.; Bertini, E.] Bambino Gesu Pediat Hosp, Mol Med Lab, Rome, Italy.
[North, K.] Univ Sydney, Childrens Hosp Westmead, Inst Neurosci & Muscle Res, Sydney, NSW 2006, Australia.
[Ryan, M. M.] Univ Melbourne, Royal Childrens Hosp, Murdoch Childrens Res Inst, Dept Neurol, Melbourne, Vic, Australia.
[Auh, S.] NINDS, NIH, Biostat Unit, Bethesda, MD 20892 USA.
[Boennemann, C. G.] NINDS, NIH, Neuromuscular & Neurogenet Disorders Childhood Se, Neurogenet Branch, Bethesda, MD 20892 USA.
RI d'amico, adele/J-9203-2016
OI d'amico, adele/0000-0003-2438-2624
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 741
EP 742
DI 10.1016/j.nmd.2013.06.386
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500013
ER
PT J
AU Meilleur, KG
Linton, MM
Rutkowski, A
Leach, ME
Jain, M
Jolley, C
Barton, M
McGraw, P
Collins, J
Donkervoort, S
Dastgir, J
Fontana, JR
Sawnani, H
Bonnemann, CG
AF Meilleur, K. G.
Linton, M. M.
Rutkowski, A.
Leach, M. E.
Jain, M.
Jolley, C.
Barton, M.
McGraw, P.
Collins, J.
Donkervoort, S.
Dastgir, J.
Fontana, J. R.
Sawnani, H.
Bonnemann, C. G.
TI Postural changes in forced vital capacity characterize congenital
muscular dystrophy subtypes
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Meilleur, K. G.] NINR, NIH, Bethesda, MD 20892 USA.
[Linton, M. M.; Rutkowski, A.] Kaiser Permanente, Los Angeles, CA USA.
[Leach, M. E.; Donkervoort, S.; Dastgir, J.; Bonnemann, C. G.] NINDS, NIH, Bethesda, MD 20892 USA.
[Jain, M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Jolley, C.; Barton, M.; McGraw, P.; Fontana, J. R.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Collins, J.; Sawnani, H.] Cincinatti Childrens Hosp Med Ctr, Cincinnati, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 742
EP 742
DI 10.1016/j.nmd.2013.06.387
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500014
ER
PT J
AU Bolduc, V
Zou, Y
Bonnemann, CG
AF Bolduc, V.
Zou, Y.
Bonnemann, C. G.
TI siRNA -mediated allele-specific silencing of a dominant negative COL6A3
mutation causing Ullrich Congenital muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Bolduc, V.; Zou, Y.; Bonnemann, C. G.] NINDS, NIH, Porter Neurosci Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 744
EP 744
DI 10.1016/j.nmd.2013.06.394
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500021
ER
PT J
AU Jain, M
Hall, D
Waite, M
Collins, J
Meilleur, K
Rutkowski, A
Dastgir, J
Donkervoort, S
Leach, M
Bonnemann, C
AF Jain, M.
Hall, D.
Waite, M.
Collins, J.
Meilleur, K.
Rutkowski, A.
Dastgir, J.
Donkervoort, S.
Leach, M.
Bonnemann, C.
TI Knee extensor muscle force correlates with and may predict sit to stand
ability in congenital muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Jain, M.; Waite, M.; Collins, J.] NIH, Clin Res Ctr, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Hall, D.] Idaho State Univ, Dept Phys Therapy, Pocatello, ID 83209 USA.
[Meilleur, K.] NINR, NIH, Bethesda, MD 20892 USA.
[Rutkowski, A.] Kaiser SCPMG, Los Angeles, CA USA.
[Rutkowski, A.] Cure CMD, Los Angeles, CA USA.
[Dastgir, J.; Donkervoort, S.; Leach, M.; Bonnemann, C.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 745
EP 746
DI 10.1016/j.nmd.2013.06.398
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500025
ER
PT J
AU Cho, A
Malicdan, MC
Nonaka, I
Hayashi, YK
Nishino, I
Noguchi, S
AF Cho, A.
Malicdan, M. C.
Nonaka, I.
Hayashi, Y. K.
Nishino, I.
Noguchi, S.
TI Antioxidant capacity is impaired in hyposialylated myotubes of GNE
myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Cho, A.; Nonaka, I.; Hayashi, Y. K.; Nishino, I.; Noguchi, S.] Natl Ctr Neurol & Psychiat, Dept Neuromuscular Res, Tokyo, Japan.
[Malicdan, M. C.] NHGRI, NIH, Med Genet Branch, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
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 OCT
PY 2013
VL 23
IS 9-10
BP 757
EP 757
DI 10.1016/j.nmd.2013.06.431
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500058
ER
PT J
AU Santi, M
Medne, L
Bharucha-Goebel, D
Bonnemann, C
Dastgir, J
Zukosky, K
Shieh, P
Winder, T
Tennekoon, G
Finkel, R
Dowling, J
Monnier, N
AF Santi, M.
Medne, L.
Bharucha-Goebel, D.
Bonnemann, C.
Dastgir, J.
Zukosky, K.
Shieh, P.
Winder, T.
Tennekoon, G.
Finkel, R.
Dowling, J.
Monnier, N.
TI Variable clinical and histological features in severe congenital RYR1
associated myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Santi, M.; Medne, L.; Bharucha-Goebel, D.; Zukosky, K.; Shieh, P.; Winder, T.; Tennekoon, G.; Finkel, R.; Dowling, J.; Monnier, N.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Bonnemann, C.; Dastgir, J.] NINDS Neurosci, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 762
EP 762
DI 10.1016/j.nmd.2013.06.447
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500074
ER
PT J
AU Vuillerot, C
Rippert, P
Berard, C
Bonnemann, C
Meilleur, K
Jain, M
Waite, M
Payan, CAM
Hamroun, D
Poirot, I
Ecochard, R
AF Vuillerot, C.
Rippert, P.
Berard, C.
Bonnemann, C.
Meilleur, K.
Jain, M.
Waite, M.
Payan, C. A. M.
Hamroun, D.
Poirot, I.
Ecochard, R.
TI A cross sectional validation study of the English version of the
NM-Score in patients with neuromuscular diseases
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Vuillerot, C.; Bonnemann, C.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Rippert, P.; Ecochard, R.] Hosp Civils Lyon, Lyon, France.
[Berard, C.; Poirot, I.] Hop Femme Mere Enfant, Hosp Civils Lyon, Bron, France.
[Meilleur, K.] NINR, NIH, Bethesda, MD 20892 USA.
[Jain, M.; Waite, M.] NIH, Bethesda, MD 20892 USA.
[Payan, C. A. M.] Hop La Pitie Salpetriere, AP HP, Paris, France.
[Hamroun, D.] Hop Arnaud de Villeneuve, Ctr Hosp Univ Montpellier, Montpellier, France.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 791
EP 791
DI 10.1016/j.nmd.2013.06.539
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500166
ER
PT J
AU Vuillerot, C
Rippert, P
Jain, M
Waite, M
Glanzman, A
Kinet, V
Auh, S
Berard, C
Payan, CAM
Hamroun, D
Poirot, I
Ecochard, R
Bonnemann, C
AF Vuillerot, C.
Rippert, P.
Jain, M.
Waite, M.
Glanzman, A.
Kinet, V.
Auh, S.
Berard, C.
Payan, C. A. M.
Hamroun, D.
Poirot, I.
Ecochard, R.
Bonnemann, C.
TI The Rasch-scaled motor function measure for patients with congenital
disorders of muscle
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Vuillerot, C.; Bonnemann, C.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Rippert, P.] Hosp Civils Lyon, Pole Informat Med Evaluat Rech, Lyon, France.
[Jain, M.; Waite, M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Glanzman, A.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Kinet, V.] Clin Univ St Luc Univ Catholique Louvain, Ctr Reference Malad Neuromusculaires, Brussels, Belgium.
[Auh, S.] NINDS, NIH, Bethesda, MD 20892 USA.
[Berard, C.; Poirot, I.] Hop Femme Mere Enfant, Hosp Civils Lyon, Serv Med Phys & Readaptat Pediat, Bron, France.
[Payan, C. A. M.] Hop La Pitie Salpetriere, AP HP, Paris, France.
[Hamroun, D.] Hop Arnaud de Villeneuve, Ctr Hosp Univ Montpellier, Montpellier, France.
[Ecochard, R.] Hosp Civils Lyon, Serv Biostat, Lyon, France.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2013
VL 23
IS 9-10
BP 791
EP 792
DI 10.1016/j.nmd.2013.06.540
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500167
ER
PT J
AU Jain, M
Logaraj, R
Waite, M
Shieh, CY
Dastgir, J
Donkervoort, S
Leach, M
Bonnemann, C
AF Jain, M.
Logaraj, R.
Waite, M.
Shieh, C. Y.
Dastgir, J.
Donkervoort, S.
Leach, M.
Bonnemann, C.
TI Validity of the 2 min walk test as an outcome measure in individuals
with CMD and other neuromuscular diseases
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Jain, M.; Logaraj, R.; Waite, M.] NIH, Clin Res Ctr, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Shieh, C. Y.] NIH, Bethesda, MD 20892 USA.
[Dastgir, J.; Donkervoort, S.; Leach, M.; Bonnemann, C.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 792
EP 792
DI 10.1016/j.nmd.2013.06.541
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500168
ER
PT J
AU Dastgir, J
Rutkowski, A
Alvarez, R
Cossette, S
Yan, K
Hoffmann, R
Sewry, C
Hayashi, Y
Moore, SA
Goebel, H
Bonnemann, C
Lawlor, MW
AF Dastgir, J.
Rutkowski, A.
Alvarez, R.
Cossette, S.
Yan, K.
Hoffmann, R.
Sewry, C.
Hayashi, Y.
Moore, S. A.
Goebel, H.
Bonnemann, C.
Lawlor, M. W.
TI Common data elements for muscle biopsy reporting
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Dastgir, J.; Bonnemann, C.] NINDS, NIH, Neurogenet Branch, Neurogenet & Neuromuscular Disorders Childhood Se, Bethesda, MD 20892 USA.
[Rutkowski, A.; Alvarez, R.; Cossette, S.] Cure Congenital Muscular Dystrophy, Olathe, KS USA.
[Yan, K.; Hoffmann, R.] Med Coll Wisconsin, Quantitat Hlth Sci Sect, Milwaukee, WI 53226 USA.
[Sewry, C.] Dubowitz Neuromuscular Ctr, Inst Child Hlth, London, England.
[Sewry, C.] Great Ormond St Hosp Sick Children, London, England.
[Hayashi, Y.] NCNP, Natl Inst Neurosci, Tokyo, Japan.
[Moore, S. A.] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA.
[Goebel, H.] Johannes Gutenberg Univ Mainz, Dept Neuropathol, D-55122 Mainz, Germany.
[Lawlor, M. W.] Med Coll Wisconsin, Dept Pathol & Lab Med, Milwaukee, WI 53226 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 794
EP 794
DI 10.1016/j.nmd.2013.06.548
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500175
ER
PT J
AU Kesari, A
Punetha, J
Uapinyoying, P
Clarke, N
Waddell, L
North, K
Plotz, P
Tesi-Rocha, C
Bonnemann, C
Grosmann, C
Bertorini, T
Hoffman, E
AF Kesari, A.
Punetha, J.
Uapinyoying, P.
Clarke, N.
Waddell, L.
North, K.
Plotz, P.
Tesi-Rocha, C.
Bonnemann, C.
Grosmann, C.
Bertorini, T.
Hoffman, E.
TI Next-generation sequencing meets genetic diagnostics: Development of a
comprehensive workflow for neuromuscular disorders
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Clarke, N.] Childrens Hosp Westmead, Neurogenet Res Unit, Westmead, NSW, Australia.
[Waddell, L.; North, K.] Childrens Hosp Westmead, Inst Neurosci & Muscle Res, Westmead, NSW, Australia.
[Plotz, P.] NIAMS, Bethseda, MD USA.
[Bonnemann, C.] NINDS, Bethseda, MD USA.
[Grosmann, C.] Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA.
[Bertorini, T.] Univ Tennessee, Memphis, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 795
EP 795
DI 10.1016/j.nmd.2013.06.551
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500178
ER
PT J
AU Dastgir, J
Vuillerot, C
Harrison, K
Poon, A
Donkervoort, S
Leach, M
Jain, M
Meilleur, K
Rutkowski, A
Mankodi, A
Bonnemann, C
AF Dastgir, J.
Vuillerot, C.
Harrison, K.
Poon, A.
Donkervoort, S.
Leach, M.
Jain, M.
Meilleur, K.
Rutkowski, A.
Mankodi, A.
Bonnemann, C.
TI Acoustic radiation force impulse imaging for the differentiation of
muscle tissue stiffness in neuromuscular disorders
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Dastgir, J.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, Bethesda, MD 20892 USA.
[Vuillerot, C.; Harrison, K.; Poon, A.; Donkervoort, S.; Leach, M.; Meilleur, K.; Bonnemann, C.] NINDS, NIH, Neurogenet Branch, Neurogenet & Neuromuscular Disorders Childhood Se, Bethesda, MD 20892 USA.
[Jain, M.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Mankodi, A.] NINDS, NIH, Neurogenet Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2013
VL 23
IS 9-10
BP 811
EP 811
DI 10.1016/j.nmd.2013.06.603
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500230
ER
PT J
AU Lin, X
Brubaker, L
Bajraktari, I
Ohman, R
Griggs, R
Fischbeck, K
Mankodi, A
AF Lin, X.
Brubaker, L.
Bajraktari, I.
Ohman, R.
Griggs, R.
Fischbeck, K.
Mankodi, A.
TI Effects of ZASP mutations on Z-disc proteins associated with
myofibrillar myopathy in skeletal muscle
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Lin, X.; Brubaker, L.; Bajraktari, I.; Ohman, R.; Fischbeck, K.; Mankodi, A.] NINDS, NIH, Bethesda, MD 20892 USA.
[Griggs, R.] Univ Rochester, Med Ctr, Dept Neurol, Rochester, NY 14627 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 819
EP 819
DI 10.1016/j.nmd.2013.06.628
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500255
ER
PT J
AU Lin, X
Ruiz, J
Bajraktari, I
Banerjee, S
Gribble, K
Griggs, R
Fischbeck, K
Mankodi, A
AF Lin, X.
Ruiz, J.
Bajraktari, I.
Banerjee, S.
Gribble, K.
Griggs, R.
Fischbeck, K.
Mankodi, A.
TI ZASP -sZM mutations in myofibrillar myopathy cause skeletal muscle
Z-disc disruption by disassembling alpha-actinin cross-linked skeletal
actin filaments
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Lin, X.; Ruiz, J.; Bajraktari, I.; Banerjee, S.; Gribble, K.; Fischbeck, K.; Mankodi, A.] NINDS, NIH, Neurogenet Branch, Bethesda, MD 20892 USA.
[Griggs, R.] Univ Rochester, Med Ctr, Rochester, NY 14627 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 819
EP 819
DI 10.1016/j.nmd.2013.06.629
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500256
ER
PT J
AU Minetti, GC
Feige, JN
Bombard, F
Birnbaumer, L
Glass, DJ
Fornaro, M
AF Minetti, G. C.
Feige, J. N.
Bombard, F.
Birnbaumer, L.
Glass, D. J.
Fornaro, M.
TI G alpha i2 signaling is required for skeletal muscle regeneration and
for satellite cell differentiation
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Minetti, G. C.; Feige, J. N.; Bombard, F.] Novartis, Basel, Switzerland.
[Birnbaumer, L.] NIH, Bethesda, MD 20892 USA.
[Glass, D. J.] Novartis, Cambridge, MA USA.
[Fornaro, M.] Novartis, Msd, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2013
VL 23
IS 9-10
BP 838
EP 838
DI 10.1016/j.nmd.2013.06.690
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500317
ER
PT J
AU Lundberg, IE
Tjarnlund, A
Bottai, M
Rider, LG
Werth, VP
Pilkington, C
de Visser, M
Alfredsson, L
Amato, AA
Barohn, RJ
Liang, MH
Singh, JA
Miller, FW
AF Lundberg, I. E.
Tjarnlund, A.
Bottai, M.
Rider, L. G.
Werth, V. P.
Pilkington, C.
de Visser, M.
Alfredsson, L.
Amato, A. A.
Barohn, R. J.
Liang, M. H.
Singh, J. A.
Miller, F. W.
TI Progress report on the development of new classification criteria for
adult and juvenile idiopathic inflammatory myopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 18th International Congress of the World-Muscle-Society (WMS)
CY OCT 01-05, 2013
CL CA
SP World Muscle Soc
C1 [Lundberg, I. E.; Tjarnlund, A.] Karolinska Inst, Karolinska Univ Hosp, Dept Med, Rheumat Unit, SE-17176 Solna, Sweden.
[Bottai, M.; Alfredsson, L.] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[Rider, L. G.; Miller, F. W.] NIEHS, NIH, US Dept HHS, Environm Autoimmun Grp,Program Clin Res, Bethesda, MD USA.
[Werth, V. P.] Philadelphia VAMC, Philadelphia, PA USA.
[Werth, V. P.] Hosp Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
[Pilkington, C.] Great Ormond St Hosp Sick Children, Dept Rheumatol, London WC1N 3JH, England.
[de Visser, M.] Univ Amsterdam, Acad Med Ctr, Dept Neurol, NL-1105 AZ Amsterdam, Netherlands.
[Amato, A. A.] Harvard Univ, Sch Med, Dept Neurol, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Barohn, R. J.] Univ Kansas, Med Ctr, Dept Neurol, Kansas City, KS USA.
[Liang, M. H.] Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA.
[Singh, J. A.] Univ Alabama Birmingham, Birmingham, AL USA.
[Singh, J. A.] VA Med Ctr, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2013
VL 23
IS 9-10
BP 844
EP 845
DI 10.1016/j.nmd.2013.06.710
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 225OP
UT WOS:000324972500337
ER
PT J
AU Kim, SW
Hooker, JM
Otto, N
Win, K
Muench, L
Shea, C
Carter, P
King, P
Reid, AE
Volkow, ND
Fowler, JS
AF Kim, Sung Won
Hooker, Jacob M.
Otto, Nicola
Win, Khaing
Muench, Lisa
Shea, Colleen
Carter, Pauline
King, Payton
Reid, Alicia E.
Volkow, Nora D.
Fowler, Joanna S.
TI Whole-body pharmacokinetics of HDAC inhibitor drugs, butyric acid,
valproic acid and 4-phenylbutyric acid measured with carbon-11 labeled
analogs by PET
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE C-11]valproic acid; [C-11]butyric acid; [C-11]4-phenylbutyric acid;
Pharmacokinetics; Positron emission tomography; Histone deacetylase
(HDAC)
ID HISTONE DEACETYLASE INHIBITORS; INCREASED FETAL-HEMOGLOBIN; BETA-GLOBIN
DISORDERS; DISEASE MOUSE MODEL; SODIUM-BUTYRATE; ULCERATIVE-COLITIS;
COLONIC-MUCOSA; IN-VIVO; PHENYLBUTYRATE; MEMORY
AB The fatty acids, n-butyric acid (BA), 4-phenylbutyric acid (PBA) and valproic acid (VPA, 2-propylpentanoic acid) have been used for many years in the treatment of a variety of CNS and peripheral organ diseases including cancer. New information that these drugs alter epigenetic processes through their inhibition of histone deacetylases (HDACs) has renewed interest in their biodistribution and pharmacokinetics and the relationship of these properties to their therapeutic and side effect profiles. In order to determine the pharmacokinetics and biodistribution of these drugs in primates, we synthesized their carbon-11 labeled analogues and performed dynamic positron emission tomography (PET) in six female baboons over 90 min. The carbon-11 labeled carboxylic acids were prepared by using (CO2)-C-11 and the appropriate Grignard reagents. [C-11]BA was metabolized rapidly (only 20% of the total carbon-11 in plasma was parent compound at 5 min post injection) whereas for VPA and PBA 98% and 85% of the radioactivity were the unmetabolized compound at 30 min after their administration respectively. The brain uptake of all three carboxylic acids was very low (<0.006%ID/cc, BA > VPA > PBA), which is consistent with the need for very high doses for therapeutic efficacy. Most of the radioactivity was excreted through the kidneys and accumulated in the bladder. However, the organ biodistribution between the drugs differed. [C-11]BA showed relatively high uptake in spleen and pancreas whereas [C-11]PBA showed high uptake in liver and heart. Notably, [C-11]VPA showed exceptionally high heart uptake possibly due to its involvement in lipid metabolism. The unique biodistribution of each of these drugs may be of releVance in understanding their therapeutic and side effect profile including their teratogenic effects. Published by Elsevier Inc.
C1 [Kim, Sung Won; Muench, Lisa; Volkow, Nora D.] NIAAA, Lab Neuroimaging, Upton, NY 11973 USA.
[Hooker, Jacob M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Nucl Med & Mol Imaging, Boston, MA USA.
[Otto, Nicola] Johannes Gutenberg Univ Mainz, Inst Organ Chem, D-55122 Mainz, Germany.
[Win, Khaing] St Josephs Coll, Dept Biol & Chem, Brooklyn, NY USA.
[Shea, Colleen; Carter, Pauline; King, Payton; Fowler, Joanna S.] Brookhaven Natl Lab, Upton, NY 11973 USA.
[Reid, Alicia E.] CUNY Medgar Evers Coll, Brooklyn, NY 11225 USA.
[Volkow, Nora D.] Natl Inst Drug Abuse, Bethesda, MD USA.
RP Kim, SW (reprint author), NIAAA, Lab Neuroimaging, Upton, NY 11973 USA.
EM sunny.kim@nih.gov; hooker@nmr.mgh.harvard.edu
OI Hooker, Jacob/0000-0002-9394-7708
FU U.S. Department of Energy, Office of Biological and Environmental
Research [DE-AC02-98CH10886]; NIH Intramural Program of the National
Institute on Alcohol Abuse and Alcoholism; BNL Science Undergraduate
Laboratory Internship Program; Deutscher Akademischer Austauschdienst
(DAAD), Bonn, Germany; [1R01DA030321]
FX This work was performed at Brookhaven National Laboratory (BNL) with
infrastructure support from the U.S. Department of Energy, Office of
Biological and Environmental Research under contract DE-AC02-98CH10886.
The NIH Intramural Program of the National Institute on Alcohol Abuse
and Alcoholism (SWK, LM, NDV) and grant 1R01DA030321 (JMH, SWK) provided
research support. Additional support was provided by the BNL Science
Undergraduate Laboratory Internship Program (KW) and the Deutscher
Akademischer Austauschdienst (DAAD), Bonn, Germany (NO). We thank
Michael Schueller for cyclotron operations and Donald Warner for PET
operations.
NR 48
TC 12
Z9 12
U1 5
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD OCT
PY 2013
VL 40
IS 7
BP 912
EP 918
DI 10.1016/j.nucmedbio.2013.06.007
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 221JW
UT WOS:000324656100008
PM 23906667
ER
PT J
AU Ananias, HJK
Yu, ZL
Hoving, HD
Rosati, S
Dierckx, RA
Wang, F
Yan, YJ
Chen, XY
Pruim, J
Lub-de Hooge, MN
Helfrich, W
Elsinga, PH
de Jong, IJ
AF Ananias, Hildo J. K.
Yu, Zilin
Hoving, Hilde D.
Rosati, Stefano
Dierckx, Ruth A.
Wang, Fan
Yan, Yongjun
Chen, Xiaoyuan
Pruim, Jan
Lub-de Hooge, Marjolijn N.
Helfrich, Wijnand
Elsinga, Philip H.
de Jong, Igle J.
TI Application of (99m)Technetium-HYNIC(tricine/TPPTS)-Aca-Bombesin(7-14)
SPECT/CT in prostate cancer patients A first-in-man study
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE Prostate cancer; SPECT/CT; Bombesin; GRPR; First-in-man
ID GASTRIN-RELEASING-PEPTIDE; RADIOLABELED BOMBESIN ANALOGS; RECEPTOR;
IMMUNOREACTIVITY; BIOPSIES
AB Rationale: The peptide bombesin (BBN) and its derivatives exhibit high binding affinity for the gastrin-releasing peptide receptor (GRPR), which is highly expressed in prostate cancer. We used the BBN-based radiopharmaceutical (99m)Technetium-HYNIC(tricine/TPPTS)-Aca-Bombesin(7-14) (Tc-99m-HABBN) to perform a first-in-man clinical pilot study to evaluate the feasibility of Tc-99m-HABBN SPECT/CT for detection of prostate cancer in patients.
Methods: Eight patients with biopsy-proven prostate cancer who were scheduled for either radical prostatectomy or external beam radiotherapy underwent Tc-99m-HABBN scintigraphy and SPECT/CT prior to treatment. Serial blood samples were taken to assess blood radioactivity and to determine in vivo metabolic stability. Clinical parameters were measured and reported side effects, if present, were recorded. Prostate cancer specimens of all patients were immunohistochemically stained for GRPR.
Results: Tc-99m-HABBN was synthesized with high radiochemical yield, purity and specific activity. There were no significant changes in clinical parameters, and there were no adverse or subjective side effects. Low metabolic stability was observed, as less than 20% of Tc-99m-HABBN was intact after 30 min. Immunohistochemical staining for GRPR was observed in the prostate cancer specimens in all patients. Tc-99m-HABBN scintigraphy and SPECT/CT did not detect prostate cancer in patients with proven disease.
Conclusions: Tc-99m-HABBN SPECT/CT for visualization of prostate cancer is safe but hampered by an unexpected low in vivo metabolic stability in man. The difference between the excellent in vitro stability of Tc-99m-HABBN in human serum samples determined in our previous study regarding Tc-99m-HABBN and the low in vivo metabolic stability determined in this study, is striking. This issue warrants further study of peptide-based radiopharmaceuticals. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Ananias, Hildo J. K.; Hoving, Hilde D.; de Jong, Igle J.] Univ Groningen, Univ Med Ctr Groningen, Dept Urol, Groningen, Netherlands.
[Yu, Zilin; Dierckx, Ruth A.; Pruim, Jan; Lub-de Hooge, Marjolijn N.; Elsinga, Philip H.] Univ Groningen, Univ Med Ctr Groningen, Dept Nucl Med & Mol Imaging, Groningen, Netherlands.
[Rosati, Stefano] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol, Groningen, Netherlands.
[Wang, Fan] Peking Univ, Med Isotopes Res Ctr, Beijing, Peoples R China.
[Yan, Yongjun; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD USA.
[Lub-de Hooge, Marjolijn N.] Univ Groningen, Univ Med Ctr Groningen, NL-9712 RB Groningen, Netherlands.
[Helfrich, Wijnand] Univ Groningen, Univ Med Ctr Groningen, Dept Surg, Lab Translat Surg Oncol, Groningen, Netherlands.
[Pruim, Jan] Univ Stellenbosch, Tygerberg Hosp, Dept Nucl Med, ZA-7600 Stellenbosch, South Africa.
RP Ananias, HJK (reprint author), Univ Med Ctr Groningen, Dept Urol, Hanzepl 1, NL-9712 RB Groningen, Netherlands.
EM h.j.k.ananias@umcg.nl
FU Dutch Cancer Society [KWF 2008-4243]; Dutch Urology Foundation
(Stichting Urologie); Jan Komelis de Cock Stichting (J.K. de Cock
Stichting) [08-02]; Center for Translational Molecular Medicine (project
Prostate Cancer Molecular Medicine) [030-203]
FX This work was supported by grants from the Dutch Cancer Society (KWF
2008-4243), the Dutch Urology Foundation 1973 (Stichting Urologie 1973),
the Jan Komelis de Cock Stichting (J.K. de Cock Stichting 08-02) and the
Center for Translational Molecular Medicine (project Prostate Cancer
Molecular Medicine 030-203).
NR 26
TC 10
Z9 10
U1 0
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD OCT
PY 2013
VL 40
IS 7
BP 933
EP 938
DI 10.1016/j.nucmedbio.2013.05.009
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 221JW
UT WOS:000324656100011
PM 23891351
ER
PT J
AU Clayton, JA
Eydelman, M
Vitale, S
Manukyan, Z
Kramm, R
Datiles, M
Temple, A
Murphy, E
Kim, J
Hilmantel, G
Rorer, E
Hammel, K
Ferris, F
AF Clayton, Janine Austin
Eydelman, Malvina
Vitale, Susan
Manukyan, Zorayr
Kramm, Robert
Datiles, Manuel, III
Temple, Alana
Murphy, Elizabeth
Kim, Jonghyeon
Hilmantel, Gene
Rorer, Eva
Hammel, Keri
Ferris, Frederick, III
TI Web-based versus Paper Administration of Common Ophthalmic
Questionnaires Comparison of Subscale Scores
SO OPHTHALMOLOGY
LA English
DT Article
ID DRY EYE DISEASE; VISUAL FUNCTION QUESTIONNAIRE; PSYCHOMETRIC PROPERTIES;
OUTCOME MEASURES; LIFE; EQUIVALENCE; RELIABILITY; AGREEMENT; IMPACT;
TRIAL
AB Objective: To compare participants' responses to Web-based and paper-and-pencil versions of an ophthalmic, patient-reported outcome (PRO) questionnaire.
Design: Questionnaire development.
Participants: Matched subjects with ocular surface disease (OSD) (n = 68) and without OSD (controls, n = 50).
Methods: Subjects completed a standard, paper-and-pencil and a Web-based version of the same questionnaire in randomized order. The administered questionnaire included several ophthalmic PRO subscales: the National Eye Institute's (NEI's) Refractive Error Quality of Life Instrument's Clarity of Vision, Near Vision, Far Vision, Glare, Symptoms, Worry, and Satisfaction with Correction subscales; the Ocular Surface Disease Index's (OSDI's) Symptoms subscale; and the NEI's Visual Function Questionnaire's Driving subscale. Possible scores for each subscale ranged from 0 (no difficulty) to 100 (most difficulty). Agreement of subscale scores between modes of administration was assessed using the Bland-Altman approach and multivariable logistic regression.
Main Outcome Measures: Subscale scores and an unweighted average total score for each mode of administration.
Results: Mean differences in scores between modes of administration ranged from -2.1 to +2.3 units. Although no differences were found to be statistically significant, the Worry and Satisfaction with Correction subscales approached statistical significance (P = 0.07 and 0.08, respectively). Although most subscale mean differences in score did not differ significantly by gender, age (>= 40 vs. <40 years), disease status (OSD vs. control), order of administration, or time between completion of the questionnaires, women had slightly greater score differences than men for the Driving (P = 0.04) and Clarity of Vision (P = 0.03) subscales; those with OSD had greater score differences for Clarity of Vision than did controls (P = 0.0006); and those aged >= 40 years had slightly greater differences in OSDI Symptoms subscale than those aged <40 years (P = 0.04).
Conclusions: To our knowledge, this Food and Drug Administration and NEI collaboration is the first study to evaluate the equivalence of Web-based and paper versions of ophthalmic PRO questionnaires. We found no evidence of clinically significant differences between scores obtained by the 2 modes for any of the examined subscales. A Web-based instrument should yield scores equivalent to those obtained by standard methods, providing a useful tool that may facilitate ophthalmic innovation. (C) 2013 by the American Academy of Ophthalmology.
C1 [Clayton, Janine Austin] NIH, Off Res Womens Hlth, Off Director, Bethesda, MD 20892 USA.
[Clayton, Janine Austin; Vitale, Susan; Datiles, Manuel, III; Temple, Alana; Murphy, Elizabeth; Ferris, Frederick, III] NEI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Eydelman, Malvina; Kramm, Robert; Hilmantel, Gene; Rorer, Eva] US FDA, Div Ophthalm & Ear Nose & Throat Devices, Off Device Evaluat, Ctr Devices & Radiol Hlth, Silver Spring, MD USA.
[Manukyan, Zorayr; Kim, Jonghyeon; Hammel, Keri] Emmes Corp, Rockville, MD USA.
RP Eydelman, M (reprint author), 10903 New Hampshire Ave,Bldg 66,2410, Silver Spring, MD 20993 USA.
EM Malvina.eydelman@fda.hhs.gov
OI Datiles, Manuel III B./0000-0003-4660-1664
FU National Eye Institute Intramural Research Program/National Institutes
of Health/Department of Health and Human Services; FDA Office of Women's
Health
FX National Eye Institute Intramural Research Program/National Institutes
of Health/Department of Health and Human Services, and FDA Office of
Women's Health. The mention of commercial products, their sources, or
their use in connection with material reported is not to be construed as
an actual or implied endorsement of such products by the Department of
Health and Human Services.
NR 20
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
J9 OPHTHALMOLOGY
JI Ophthalmology
PD OCT
PY 2013
VL 120
IS 10
BP 2151
EP 2159
DI 10.1016/j.ophtha.2013.03.019
PG 9
WC Ophthalmology
SC Ophthalmology
GA 227CQ
UT WOS:000325086400035
PM 23714321
ER
PT J
AU Labus, JS
Gupta, A
Coveleskie, K
Tillisch, K
Kilpatrick, L
Jarcho, J
Feier, N
Bueller, J
Stains, J
Smith, S
Suyenobu, B
Naliboff, B
Mayer, EA
AF Labus, Jennifer S.
Gupta, Arpana
Coveleskie, Kristen
Tillisch, Kirsten
Kilpatrick, Lisa
Jarcho, Johanna
Feier, Natasha
Bueller, Joshua
Stains, Jean
Smith, Suzanne
Suyenobu, Brandall
Naliboff, Bruce
Mayer, Emeran A.
TI Sex differences in emotion-related cognitive processes in irritable
bowel syndrome and healthy control subjects
SO PAIN
LA English
DT Article
DE Emotion recognition; Irritable bowel syndrome; Sex differences
ID NOXIOUS VISCERAL STIMULATION; REGIONAL BRAIN RESPONSE; FACIAL
EXPRESSIONS; NEURAL RESPONSES; FEARFUL FACES; IBS PATIENTS; FUNCTIONAL
CONNECTIVITY; GENDER-DIFFERENCES; AMYGDALA ACTIVITY; ABDOMINAL-PAIN
AB Greater responsiveness of emotional arousal circuits in relation to delivered visceral pain has been implicated as underlying central pain amplification in irritable bowel syndrome (IBS), with female subjects showing greater responses than male subjects. Functional magnetic resonance imaging was used to measure neural responses to an emotion recognition paradigm, using faces expressing negative emotions (fear and anger). Sex and disease differences in the connectivity of affective and modulatory cortical circuits were studied in 47 IBS (27 premenopausal female subjects) and 67 healthy control subjects (HCs; 38 premenopausal female subjects). Male subjects (IBS + HC) showed greater overall brain responses to stimuli than female subjects in prefrontal cortex, insula, and amygdala. Effective connectivity analyses identified major sex- and disease-related differences in the functioning of brain networks related to prefrontal regions, cingulate, insula, and amygdala. Male subjects had stronger connectivity between anterior cingulate subregions, amygdala, and insula, whereas female subjects had stronger connectivity to and from the prefrontal modulatory regions (medial/dorsolateral cortex). Male IBS subjects demonstrate greater engagement of cortical and affect-related brain circuitry compared to male control subjects and female subjects, when viewing faces depicting emotions previously shown to elicit greater behavioral and brain responses in male subjects. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
C1 [Labus, Jennifer S.; Gupta, Arpana; Coveleskie, Kristen; Tillisch, Kirsten; Kilpatrick, Lisa; Feier, Natasha; Bueller, Joshua; Stains, Jean; Smith, Suzanne; Suyenobu, Brandall; Naliboff, Bruce; Mayer, Emeran A.] Oppenheimer Family Ctr Neurobiol Stress & Pain &, Los Angeles, CA USA.
[Labus, Jennifer S.; Tillisch, Kirsten; Bueller, Joshua; Suyenobu, Brandall; Naliboff, Bruce; Mayer, Emeran A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90024 USA.
[Jarcho, Johanna] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Naliboff, Bruce; Mayer, Emeran A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90024 USA.
[Mayer, Emeran A.] Univ Calif Los Angeles, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90024 USA.
RP Mayer, EA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Digest Dis, Gail & Gerald Oppenheimer Family Ctr Neurobiol St, CHS 42-210 MC737818,10833 Le Conte Ave, Los Angeles, CA 90024 USA.
EM emayer@ucla.edu
RI Kilpatrick, Lisa/E-6995-2015;
OI Jarcho, Johanna/0000-0001-9075-6968
FU National Institute of Digestive Diabetes and Kidney Diseases (NIDDK)
[DK48351, R24 AT002681]; US Department of Veterans Affairs VA Merit
Review
FX This research was supported in part by grants from the National
Institute of Digestive Diabetes and Kidney Diseases (NIDDK) DK48351
(E.A.M.), R24 AT002681 (E.A.M.), and the US Department of Veterans
Affairs VA Merit Review (B.N.).
NR 81
TC 34
Z9 34
U1 2
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD OCT
PY 2013
VL 154
IS 10
BP 2088
EP 2099
DI 10.1016/j.pain.2013.06.024
PG 12
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 219AK
UT WOS:000324475500027
PM 23791896
ER
PT J
AU Iannotti, RJ
Wang, J
AF Iannotti, Ronald J.
Wang, Jing
TI Trends in Physical Activity, Sedentary Behavior, Diet, and BMI Among US
Adolescents, 2001-2009
SO PEDIATRICS
LA English
DT Article
DE trends; obesity; physical activity; diet; adolescent; gender
ID SCHOOL-AGED CHILDREN; HEALTH BEHAVIOR; EATING PATTERNS; RISK-FACTORS;
OBESITY; ASSOCIATIONS; TELEVISION; VALIDITY; DETERMINANTS; RELIABILITY
AB OBJECTIVE: The high prevalence of adolescent obesity in the United States has been attributed to population changes in physical activity (PA), sedentary behaviors, and dietary behaviors. This study examines 8-year trends in these behaviors in US adolescents ages 11 to 16.
METHODS: Nationally representative samples of US students in grades 6 to 10 were recruited during the 2001-2002 (N = 14 607), 2005-2006 (N = 9150), and 2009-2010 (N = 10 848) school years by using multistage stratified designs, with census regions and grades as strata, and school districts as the primary sampling units. African-American and Hispanic students were oversampled to obtain better estimates for those groups. Using the Health Behavior in School-aged Children quadrennial surveys, identical questions assessed BMI, PA, and sedentary and dietary behaviors at each school year. Logistic and linear regression analyses were conducted taking into account the sampling design and controlling for age, gender, race/ethnicity, and family affluence.
RESULTS: Across the quadrennial surveys, significant increases were identified in number of days with at least 60 minutes of PA, daily consumption of fruits and vegetables, eating breakfast on weekdays and weekends, and BMI. Television viewing and consumption of sweets and sweetened beverages decreased across this same period. These same patterns were seen in all racial/ethnic groups.
CONCLUSIONS: These patterns suggest that public health efforts to improve the obesity-related behaviors of US adolescents may be having some success. However, alternative explanations for the increase in BMI over the same period need to be considered.
C1 [Iannotti, Ronald J.; Wang, Jing] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Bethesda, MD 20892 USA.
RP Iannotti, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, 6100 Execut Blvd,7B05, Bethesda, MD 20892 USA.
EM iannottr@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [N01-HD-5-3401]; Maternal and Child Health Bureau of the
Health Resources and Services Administration; National Institutes of
Health (NIH)
FX This research was supported in part by the intramural research program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development (Contract N01-HD-5-3401) and by the Maternal and Child
Health Bureau of the Health Resources and Services Administration with
the first author (Dr Iannotti) as principal investigator. Funded by the
National Institutes of Health (NIH).
NR 40
TC 40
Z9 41
U1 3
U2 36
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2013
VL 132
IS 4
BP 606
EP 614
DI 10.1542/peds.2013-1488
PG 9
WC Pediatrics
SC Pediatrics
GA 227FI
UT WOS:000325095400038
PM 24043281
ER
PT J
AU Vohr, BR
Stephens, BE
McDonald, SA
Ehrenkranz, RA
Laptook, AR
Pappas, A
Hintz, SR
Shankaran, S
Higgins, RD
Das, A
AF Vohr, Betty R.
Stephens, Bonnie E.
McDonald, Scott A.
Ehrenkranz, Richard A.
Laptook, Abbot R.
Pappas, Athina
Hintz, Susan R.
Shankaran, Seetha
Higgins, Rosemary D.
Das, Abhik
CA NICHD Neonatal Res Network
TI Cerebral Palsy and Growth Failure at 6 to 7 Years
SO PEDIATRICS
LA English
DT Article
DE encephalopathy; hypoxia-ischemia; hypothermia; cerebral palsy; growth
ID HYPOXIC-ISCHEMIC ENCEPHALOPATHY; GASTROESOPHAGEAL REFLUX; NEONATAL
ENCEPHALOPATHY; PERINATAL ASPHYXIA; YOUNG-CHILDREN; LINEAR GROWTH;
HEALTH-STATUS; DISABILITIES; ADOLESCENTS; DYSFUNCTION
AB OBJECTIVE: To evaluate the association between severity of cerebral palsy (CP) and growth to 6 to 7 years of age among children with moderate to severe (Mod/Sev) hypoxic ischemic encephalopathy (HIE). It was hypothesized that children with Mod/Sev CP would have poorer growth, lower cognitive scores, and increased rehospitalization rates compared with children with no CP (No CP).
METHODS: Among 115 of 122 surviving children followed in the hypothermia trial for neonatal HIE, growth parameters and neurodevelopmental status at 18 to 22 months and 6 to 7 years were available. Group comparisons (Mod/Sev CP and No CP) with unadjusted and adjusted analyses for growth <10th percentile and z scores by using Fisher's exact tests and regression modeling were conducted.
RESULTS: Children with Mod/Sev CP had high rates of slow growth and cognitive and motor impairment and rehospitalizations at 18 to 22 months and 6 to 7 years. At 6 to 7 years of age, children with Mod/Sev CP had increased rates of growth parameters <10th percentile compared with those with No CP (weight, 57% vs 3%; height, 70% vs 2%; and head circumference, 82% vs 13%; P < .0001). Increasing severity of slow growth was associated with increasing age (P < .04 for weight, P < .001 for length, and P < .0001 for head circumference). Gastrostomy feeds were associated with better growth.
CONCLUSIONS: Term children with HIE who develop Mod/Sev CP have high and increasing rates of growth <10th percentile by 6 to 7 years of age. These findings support the need for close medical and nutrition management of children with HIE who develop CP.
C1 [Vohr, Betty R.; Stephens, Bonnie E.; Laptook, Abbot R.] Brown Univ, Alpert Med Sch, Providence, RI 02912 USA.
[Vohr, Betty R.; Laptook, Abbot R.] Women & Infants Hosp Rhode Isl, Providence, RI 02905 USA.
[McDonald, Scott A.] RTI Int, Res Triangle Pk, NC USA.
[Ehrenkranz, Richard A.] Yale Univ, Sch Med, Dept Pediat, Yale New Haven Hosp, New Haven, CT 06510 USA.
[Pappas, Athina; Shankaran, Seetha] Wayne State Univ, Dept Pediat, Childrens Hosp Michigan, Detroit, MI 48202 USA.
[Pappas, Athina; Shankaran, Seetha] Hutzel Womens Hosp, Detroit, MI USA.
[Hintz, Susan R.] Stanford Univ, Sch Med, Dept Pediat, Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA.
[Higgins, Rosemary D.] NICHHD, NIH, Bethesda, MD 20892 USA.
[Das, Abhik] RTI Int, Rockville, MD USA.
RP Vohr, BR (reprint author), Women & Infants Hosp Rhode Isl, 101 Dudley St, Providence, RI 02905 USA.
EM bvohr@wihri.org
FU National Institutes of Health, the Eunice Kennedy Shriver National
Institute of Child Health and Human Development; National Institutes of
Health
FX The National Institutes of Health, the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, provided grant support
for the Neonatal Research Network's Whole-Body Hypothermia Trial and its
6-7 Year School-age Follow-up (recruitment July 2000 through May 2003;
follow-up July 2006 through May 2010). Funded by the National Institutes
of Health.
NR 40
TC 9
Z9 9
U1 0
U2 6
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2013
VL 132
IS 4
BP E905
EP E914
DI 10.1542/peds.2012-3915
PG 10
WC Pediatrics
SC Pediatrics
GA 227FI
UT WOS:000325095400012
PM 24019415
ER
PT J
AU Bharmal, N
Kaplan, RM
Shapiro, MF
Kagawa-Singer, M
Wong, MD
Mangione, CM
Divan, H
McCarthy, WJ
AF Bharmal, Nazleen
Kaplan, Robert M.
Shapiro, Martin F.
Kagawa-Singer, Marjorie
Wong, Mitchell D.
Mangione, Carol M.
Divan, Hozefa
McCarthy, William J.
TI The association of religiosity with overweight/obese body mass index
among Asian Indian immigrants in California
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Asian Indian; Religiosity; Obesity
ID CARDIOVASCULAR-DISEASE RISK; NUTRITION EXAMINATION SURVEY;
UNITED-STATES; SOUTH ASIANS; HISPANIC IMMIGRANTS; NATIONAL-HEALTH;
LIFE-STYLE; ACCULTURATION SCALE; PHYSICAL-ACTIVITY; FOOD-CONSUMPTION
AB Objective. The aim of this study was to examine the association between religiosity and overweight or obese body mass index among a multi-religious group of Asian Indian immigrants residing in California.
Methods. We examined cross-sectional survey data obtained from in-language telephone interviews with 3228 mostly immigrant Asian Indians in the 2004 California Asian Indian Tobacco Survey using multivariate logistic regression.
Results. High self-identified religiosity was significantly associated with higher BMI after adjusting for socio-demographic and acculturation measures. Highly religious Asian Indians had 1.53 greater odds (95% CI: 1.18, 2.00) of being overweight or obese than low religiosity immigrants, though this varied by religious affiliation. Religiosity was associated with greater odds of being overweight/obese for Hindus (OR 1.54; 95% CI: 1.08, 2.22) and Sikhs (OR 1.88; 95% CI: 1.07, 3.30), but not for Muslims (OR 0.69; 95% CI: 0.28, 1.70).
Conclusions. Religiosity in Hindus and Sikhs, but not immigrant Muslims, appears to be independently associated with greater body mass index among Asian Indians. If this finding is confirmed, future research should identify potentially mutable mechanisms by which religion-specific religiosity affects overweight/ obesity risk. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Bharmal, Nazleen; Shapiro, Martin F.; Wong, Mitchell D.; Mangione, Carol M.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Kaplan, Robert M.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Kagawa-Singer, Marjorie] Univ Calif Los Angeles, Dept Community Hlth Sci, Fielding Sch Publ Hlth, Los Angeles, CA USA.
[Divan, Hozefa] HealthCore Inc, Andover, MA USA.
[McCarthy, William J.] Univ Calif Los Angeles, Dept Hlth Policy & Management, Fielding Sch Publ Hlth, Los Angeles, CA USA.
RP Bharmal, N (reprint author), Univ Calif Los Angeles, Dept Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90024 USA.
EM nbharmal@mednet.ucla.edu
OI Wong, Mitchell/0000-0002-4800-8410
NR 87
TC 3
Z9 3
U1 3
U2 20
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 OCT
PY 2013
VL 57
IS 4
BP 315
EP 321
DI 10.1016/j.ypmed.2013.06.003
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 223FC
UT WOS:000324789100009
PM 23769898
ER
PT J
AU Cotugna, N
Fanelli-Kuczmarksi, M
Clymer, J
Hotchkiss, L
Zonderman, AB
Evans, MK
AF Cotugna, Nancy
Fanelli-Kuczmarksi, Marie
Clymer, Julie
Hotchkiss, Lawrence
Zonderman, Alan B.
Evans, Michele K.
TI Sodium intake of special populations in the Healthy Aging in
Neighborhoods of Diversity Across the Life Span (HANDLS) study
SO PREVENTIVE MEDICINE
LA English
DT Article
DE Nutrition/diet; Hypertension; Health promotion; Public health;
Prevention; Lifestyle modification/health behavior
ID AMERICAN-HEART-ASSOCIATION; BLOOD-PRESSURE; HYPERTENSION; REDUCTION;
DISEASE; ENERGY
AB Objective: The sodium intake of participants of the Healthy Aging in Neighborhoods of Diversity across the Life Span study who were in three of the special population groups identified by the Dietary Guidelines for Americans, 2010 (those with hypertension, African Americans, and those >= 51 years) was analyzed to determine if they met sodium recommendations.
Methods: The sample included 2152 African American and White subjects, aged 30-64 years. Major dietary sources of sodium for each group were determined from two 24-hour dietary recalls, and dietary intakes were compared with sodium recommendations. Dietary potassium was also evaluated.
Results: The intakes of the groups studied exceeded 1500 mg of sodium while their potassium intakes were lower than the Adequate Intake of 4700 mg. The major contributors of sodium included "cold cuts, sausage, and franks," "protein foods," and yeast breads.
Conclusions: Excessive sodium intake characterized the diet of an urban, socioeconomically diverse population who are hypertensive or at risk for having hypertension. These findings have implications for health professionals and the food industry. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Cotugna, Nancy; Fanelli-Kuczmarksi, Marie; Hotchkiss, Lawrence] Univ Delaware, Dept Behav Hlth & Nutr, Newark, DE 19701 USA.
[Clymer, Julie] Wilmington VA Med Hosp, Wilmington, DE USA.
[Zonderman, Alan B.] NIA, Res Resources Branch, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
[Evans, Michele K.] NIA, Intramural Res Program, Lab Epidemiol & Populat Sci, NIH, Baltimore, MD 21224 USA.
RP Cotugna, N (reprint author), Univ Delaware, Dept Behav Hlth & Nutr, 26 N Coll Ave, Newark, DE 19701 USA.
EM ncotugna@udel.edu
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 28
TC 2
Z9 2
U1 1
U2 14
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 OCT
PY 2013
VL 57
IS 4
BP 334
EP 338
DI 10.1016/j.ypmed.2013.06.006
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 223FC
UT WOS:000324789100012
PM 23769900
ER
PT J
AU Stavru, F
Palmer, AE
Wang, CX
Youle, RJ
Cossart, P
AF Stavru, Fabrizia
Palmer, Amy E.
Wang, Chunxin
Youle, Richard J.
Cossart, Pascale
TI Atypical mitochondrial fission upon bacterial infection
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE mitochondrial dynamics; live cell imaging; actin
ID MAMMALIAN-CELLS; LISTERIA-MONOCYTOGENES; ENDOPLASMIC-RETICULUM;
PROTEOLYTIC CLEAVAGE; OUTER-MEMBRANE; PROTEIN HFIS1; MORPHOLOGY; FUSION;
DRP1; APOPTOSIS
AB We recently showed that infection by Listeria monocytogenes causes mitochondrial network fragmentation through the secreted pore-forming toxin listeriolysin O (LLO). Here, we examine factors involved in canonical fusion and fission. Strikingly, LLOinduced mitochondrial fragmentation does not require the traditional fission machinery, as Drp1 oligomers are absent from fragmented mitochondria following Listeria infection or LLO treatment, as the dynamin-like protein 1 (Drp1) receptor Mff is rapidly degraded, and as fragmentation proceeds efficiently in cells with impaired Drp1 function. LLO does not cause processing of the fusion protein optic atrophy protein 1 (Opa1), despite inducing a decrease in the mitochondrial membrane potential, suggesting a unique Drp1-and Opa1-independent fission mechanism distinct from that triggered by uncouplers or the apoptosis inducer staurosporine. We show that the ER marks LLO-induced mitochondrial fragmentation sites even in the absence of functional Drp1, demonstrating that the ER activity in regulating mitochondrial fission can be induced by exogenous agents and that the ER appears to regulate fission by a mechanism independent of the canonical mitochondrial fission machinery.
C1 [Stavru, Fabrizia; Palmer, Amy E.; Cossart, Pascale] Inst Pasteur, Unite Interact Bacteries Cellules, F-75015 Paris, France.
[Stavru, Fabrizia; Palmer, Amy E.; Cossart, Pascale] Inst Natl Sante & Rech Med, U604, F-75015 Paris, France.
[Stavru, Fabrizia; Palmer, Amy E.; Cossart, Pascale] INRA, Unite Contrat 2020, F-75015 Paris, France.
[Wang, Chunxin; Youle, Richard J.] Natl Inst Neurol Disorders & Stroke, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Palmer, Amy E.] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA.
[Palmer, Amy E.] Univ Colorado, BioFrontiers Inst, Boulder, CO 80309 USA.
RP Stavru, F (reprint author), Inst Pasteur, Unite Interact Bacteries Cellules, F-75015 Paris, France.
EM fabrizia.stavru@pasteur.fr; pcossart@pasteur.fr
RI Wang, Chunxin/B-9312-2016
OI Wang, Chunxin/0000-0001-6015-6806
FU Institut Pasteur Institut National de la Sant [604]; Institut National
de la Recherche Agronomique Unit; Nationale pour la Recherche;
postdoctoral fellowships from European Molecular Biology Organization;
Fondation pour la Recherche Medicale; Intramural Research Program of the
National Institutes of Neurological Disorders and Stroke; National
Institutes of Health
FX We thank Dr. K. Mihara for Drp1 knockout MEFs, Drs. Yoko Shibata and Tom
Rapoport for U2OS-Sec61 beta GFP cells, and Drs. Gia Voeltz and A. van
der Bliek for constructs; Dr. Tham Tho-Nam for excellent technical
support and the Plate-Forme Imagerie Dynamique staff at Institut Pasteur
for support; Dr. Ascel Samba-Louaka for critical reading of the
manuscript; and Drs. Janet Shaw and Aurelien Roux for insightful
discussions. This work received financial support from the Institut
Pasteur Institut National de la Sante et de la Recherche Medicale Unite
604, Institut National de la Recherche Agronomique Unite Sous Contrat
2020, Fondation Louis Jeantet, European Research Council Advanced Grant
233348 MODELIST, and Agence Nationale pour la Recherche (ERANET
Pathogenomics Grant LISTRESS and Grant Blanc MITOPATHO). F.S. was
supported by postdoctoral fellowships from European Molecular Biology
Organization and the Fondation pour la Recherche Medicale. C.W. and R.Y.
are supported in part by the Intramural Research Program of the National
Institutes of Neurological Disorders and Stroke, National Institutes of
Health. P.C. is a Howard Hughes Medical Institute Senior International
Research Scholar.
NR 40
TC 27
Z9 28
U1 0
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 OCT 1
PY 2013
VL 110
IS 40
BP 16003
EP 16008
DI 10.1073/pnas.1315784110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 227II
UT WOS:000325105500047
PM 24043775
ER
PT J
AU Kundu, P
Brenowitz, ND
Voon, V
Worbe, Y
Vertes, PE
Inati, SJ
Saad, ZS
Bandettini, PA
Bullmore, ET
AF Kundu, Prantik
Brenowitz, Noah D.
Voon, Valerie
Worbe, Yulia
Vertes, Petra E.
Inati, Souheil J.
Saad, Ziad S.
Bandettini, Peter A.
Bullmore, Edward T.
TI Integrated strategy for improving functional connectivity mapping using
multiecho fMRI
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE resting state fMRI; human neuroimaging; time series
ID INDEPENDENT COMPONENT ANALYSIS; BRAIN ACTIVITY; HEAD MOTION; MRI;
ALGORITHMS; REGRESSION; ARTIFACT; IMPACT; BOLD; EPI
AB Functional connectivity analysis of resting state blood oxygen level-dependent (BOLD) functional MRI is widely used for noninvasively studying brain functional networks. Recent findings have indicated, however, that even small (<= 1 mm) amounts of head movement during scanning can disproportionately bias connectivity estimates, despite various preprocessing efforts. Further complications for interregional connectivity estimation from time domain signals include the unaccounted reduction in BOLD degrees of freedom related to sensitivity losses from high subject motion. To address these issues, we describe an integrated strategy for data acquisition, denoising, and connectivity estimation. This strategy builds on our previously published technique combining data acquisition with multiecho (ME) echo planar imaging and analysis with spatial independent component analysis (ICA), called ME-ICA, which distinguishes BOLD (neuronal) and non-BOLD (artifactual) components based on linear echo-time dependence of signals-a characteristic property of BOLD T-2* signal changes. Here we show for 32 control subjects that this method provides a physically principled and nearly operator-independent way of removing complex artifacts such as motion from resting state data. We then describe a robust estimator of functional connectivity based on interregional correlation of BOLD-independent component coefficients. This estimator, called independent components regression, considerably simplifies statistical inference for functional connectivity because degrees of freedom equals the number of independent coefficients. Compared with traditional connectivity estimation methods, the proposed strategy results in fourfold improvements in signal-to-noise ratio, functional connectivity analysis with improved specificity, and valid statistical inference with nominal control of type 1 error in contrasts of connectivity between groups with different levels of subject motion.
C1 [Kundu, Prantik; Brenowitz, Noah D.; Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Bethesda, MD 20814 USA.
[Inati, Souheil J.; Bandettini, Peter A.] NIMH, Funct MRI Core Facil, Bethesda, MD 20814 USA.
[Saad, Ziad S.] NIMH, Stat & Sci Comp Core, Bethesda, MD 20814 USA.
[Kundu, Prantik; Voon, Valerie; Worbe, Yulia; Vertes, Petra E.; Bullmore, Edward T.] Univ Cambridge, Behav & Clin Neurosci Inst, Cambridge CB2 1QP, England.
[Bullmore, Edward T.] Cambridgeshire Peterborough Natl Hlth Syst Fdn Tr, Natl Inst Hlth Res, Cambridge Biomed Res Ctr, Cambridge SW1A 2NS, England.
[Bullmore, Edward T.] GlaxoSmithKline, Clin Unit Cambridge, Cambridge CB2 0QQ, England.
RP Kundu, P (reprint author), NIMH, Sect Funct Imaging Methods, Bethesda, MD 20814 USA.
EM kundup@mail.nih.gov
OI Kundu, Prantik/0000-0001-9367-3068; Vertes, Petra
E./0000-0002-0992-3210; Bullmore, Edward/0000-0002-8955-8283
FU National Institutes of Health-Cambridge Scholars Program
FX P.K. is supported by the National Institutes of Health-Cambridge
Scholars Program. V. V. is a Wellcome Trust Clinical Fellow. fMRI data
collection was supported by the National Institute of Health Research
Cambridge Biomedical Research Centre.
NR 22
TC 40
Z9 40
U1 1
U2 13
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 OCT 1
PY 2013
VL 110
IS 40
BP 16187
EP 16192
DI 10.1073/pnas.1301725110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 227II
UT WOS:000325105500078
PM 24038744
ER
PT J
AU Graber, TE
Hebert-Seropian, S
Khoutorsky, A
David, A
Yewdell, JW
Lacaille, JC
Sossin, WS
AF Graber, Tyson E.
Hebert-Seropian, Sarah
Khoutorsky, Arkady
David, Alexandre
Yewdell, Jonathan W.
Lacaille, Jean-Claude
Sossin, Wayne S.
TI Reactivation of stalled polyribosomes in synaptic plasticity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE RNA granule; mGluR-LTD; translation elongation; microtubule-associated
protein 1b
ID LONG-TERM DEPRESSION; MENTAL-RETARDATION PROTEIN; FRAGILE-X;
HIPPOCAMPAL-NEURONS; RNA GRANULES; TRANSLATION INITIATION; DEPENDENT
TRANSLATION; AUTISM; PATHOPHYSIOLOGY; TRANSLOCATION
AB Some forms of synaptic plasticity require rapid, local activation of protein synthesis. Although this is thought to reflect recruitment of mRNAs to free ribosomes, this would limit the speed and magnitude of translational activation. Here we provide compelling in situ evidence supporting an alternative model in which synaptic mRNAs are transported as stably paused polyribosomes. Remarkably, we show that metabotropic glutamate receptor activation allows the synthesis of proteins that lead to a functional long-term depression phenotype even when translation initiation has been greatly reduced. Thus, neurons evolved a unique mechanism to swiftly translate synaptic mRNAs into functional protein upon synaptic signaling using stalled polyribosomes to bypass the rate-limiting step of translation initiation. Because dysregulated plasticity is implicated in neurodevelopmental and psychiatric disorders such as fragile X syndrome, this work uncovers a unique translational target for therapies.
C1 [Graber, Tyson E.; Sossin, Wayne S.] McGill Univ, Montreal Neurol Inst, Dept Neurol & Neurosurg, Montreal, PQ H3A 2B4, Canada.
[Hebert-Seropian, Sarah; Lacaille, Jean-Claude] Univ Montreal, Grp Rech Syst Nerveux Cent, Dept Neurosci, Montreal, PQ H3T 1J4, Canada.
[Khoutorsky, Arkady] McGill Univ, Dept Biochem, Montreal, PQ H3A 1A3, Canada.
[Khoutorsky, Arkady] McGill Univ, Goodman Canc Res Ctr, Montreal, PQ H3A 1A3, Canada.
[David, Alexandre; Yewdell, Jonathan W.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Sossin, WS (reprint author), McGill Univ, Montreal Neurol Inst, Dept Neurol & Neurosurg, Montreal, PQ H3A 2B4, Canada.
EM wayne.sossin@mcgill.ca
FU Montreal Neurological Institute; Fonds de recherche du Quebec-Sante;
Universite de Montreal; Canadian Institutes of Health Research
FX Pateamine A was a generous gift of Dr. Jerry Pelletier. The GFP-FMRP
expression plasmid was a kind gift of Dr. Keith Murai. T. E. G. is
supported by a Jeanne Timmins-Costello Fellowship from the Montreal
Neurological Institute and a Postdoctoral Fellowship from the Fonds de
recherche du Quebec-Sante. S.H.-S. is supported by a Graduate
Studentship from Universite de Montreal. This work was funded by the
Canadian Institutes of Health Research (J.-C.L. and W. S. S.) and Fonds
de recherche du Quebec-Sante (J.-C.L. and W. S. S.). J.-C.L. is the
recipient of the Canada Research Chair in Cellular and Molecular
Neurophysiology.
NR 35
TC 38
Z9 38
U1 1
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 OCT 1
PY 2013
VL 110
IS 40
BP 16205
EP 16210
DI 10.1073/pnas.1307747110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 227II
UT WOS:000325105500081
PM 24043809
ER
PT J
AU Schaefer, J
Giangrande, E
Weinberger, DR
Dickinson, D
AF Schaefer, Jonathan
Giangrande, Evan
Weinberger, Daniel R.
Dickinson, Dwight
TI The global cognitive impairment in schizophrenia: Consistent over
decades and around the world
SO SCHIZOPHRENIA RESEARCH
LA English
DT Review
DE Schizophrenia; Cognition; Neuropsychology; Meta-analysis; Processing
speed; Memory
ID BIPOLAR AFFECTIVE-DISORDER; RECENT-ONSET SCHIZOPHRENIA; EVENT-RELATED
POTENTIALS; WORKING-MEMORY; 1ST-EPISODE SCHIZOPHRENIA; NEUROCOGNITIVE
DEFICITS; NEUROPSYCHOLOGICAL PERFORMANCE; EXECUTIVE FUNCTIONS; SPECTRUM
DISORDERS; HEALTHY CONTROLS
AB Objective: Schizophrenia results in cognitive impairments as well as positive, negative, and disorganized symptomatology. The present study examines the extent to which these cognitive deficits are generalized across domains, potential moderator variables, and whether the pattern of cognitive findings reported in schizophrenia has remained consistent over time and across cultural and geographic variation.
Method: Relevant publications from 2006 to 2011 were identified through keyword searches in PubMed and an examination of reference lists. Studies were included if they (1) compared the cognitive performance of adult schizophrenia patients and healthy controls, (2) based schizophrenia diagnoses on contemporary diagnostic criteria, (3) reported information sufficient to permit effect size calculation, (4) were reported in English, and (5) reported data for neuropsychological tests falling into at least 3 distinct cognitive domains. A set of 100 non-overlapping studies was identified, and effect sizes (Hedge's g) were calculated for each cognitive variable.
Results: Consistent with earlier analyses, patients with schizophrenia scored significantly lower than controls across all cognitive tests and domains (grand mean effect size, g = -1.03). Patients showed somewhat larger impairments in the domains of processing speed (g = -1.25) and episodic memory (g = -1.23). Our results also showed few inconsistencies when grouped by geographic region.
Conclusions: The present study extends findings from 1980 to 2006 of a substantial, generalized cognitive impairment in schizophrenia, demonstrating that this finding has remained robust over time despite changes in assessment instruments and alterations in diagnostic criteria, and that it manifests similarly in different regions of the world despite linguistic and cultural differences. Published by Elsevier B.V.
C1 [Schaefer, Jonathan; Giangrande, Evan; Weinberger, Daniel R.; Dickinson, Dwight] NIMH, Genes Cognit & Psychosis Program, IRP, NIH, Bethesda, MD 20892 USA.
[Schaefer, Jonathan; Giangrande, Evan; Weinberger, Daniel R.; Dickinson, Dwight] NIMH, Clin Brain Disorders Branch, IRP, NIH, Bethesda, MD 20892 USA.
[Weinberger, Daniel R.] Johns Hopkins Univ, Med Ctr, Lieber Inst Brain Dev, Baltimore, MD 21205 USA.
RP Dickinson, D (reprint author), NIMH, Genes Cognit & Psychosis Program, IRP, NIH, 10 Ctr Dr,MSC 1379, Bethesda, MD 20892 USA.
EM Dwight.Dickinson@nih.gov
OI Schaefer, Jonathan/0000-0003-4112-9268
FU National Institute of Mental Health Intramural Research Program
FX Support for this research was provided by the National Institute of
Mental Health Intramural Research Program via direct funding to the
Weinberger Lab. The authors of this manuscript report no competing
interests.
NR 132
TC 87
Z9 91
U1 4
U2 58
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD OCT
PY 2013
VL 150
IS 1
BP 42
EP 50
DI 10.1016/j.schres.2013.07.009
PG 9
WC Psychiatry
SC Psychiatry
GA 216OZ
UT WOS:000324294700011
PM 23911259
ER
PT J
AU Mao, SH
Goodrich, RJ
Hauser, R
Schrader, SM
Chen, Z
Krawetz, SA
AF Mao, Shihong
Goodrich, Robert J.
Hauser, Russ
Schrader, Steven M.
Chen, Zhen
Krawetz, Stephen A.
TI Evaluation of the effectiveness of semen storage and sperm purification
methods for spermatozoa transcript profiling
SO SYSTEMS BIOLOGY IN REPRODUCTIVE MEDICINE
LA English
DT Article
DE mitochondrial RNA; preferentially isolated transcripts; stable
transcript pairs
ID RNAS; IDENTIFICATION; FERTILIZATION; FERTILE; FRESH
AB Different semen storage and sperm purification methods may affect the integrity of isolated spermatozoa! RNA. RNA-Seq was applied to determine whether semen storage methods (pelleted vs. liquefied) and somatic cell lysis buffer (SCLB) vs. PureSperm (PS) purification methods affect the quantity and quality of sperm RNA. The results indicate that the method of semen storage does not markedly impact RNA profiling whereas the choice of purification can yield significant differences. RNA-Seq showed that the majority of mitochondrial and mid-piece associated transcripts were lost after SCLB purification, which indicated that the mid-piece of spermatozoa may have been compromised. In addition, the number of stable transcript pairs from SCLB-samples was less than that from the PS samples. This study supports the view that PS purification better maintains the integrity of spermatozoal RNAs.
C1 [Mao, Shihong; Goodrich, Robert J.; Krawetz, Stephen A.] Wayne State Univ, Dept Obstet & Gynecol, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Hauser, Russ] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Vincent Mem Obstet & Gynecol Serv, Boston, MA USA.
[Hauser, Russ] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Schrader, Steven M.] NIOSH, Cincinnati, OH 45226 USA.
[Schrader, Steven M.; Chen, Zhen] NIH, LIFE Study Team, Bethesda, MD 20892 USA.
[Chen, Zhen] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Krawetz, SA (reprint author), Wayne State Univ, Dept Obstet & Gynecol, 271 CS Mott Ctr,275 E Hancock Ave, Detroit, MI 48201 USA.
EM steve@compbio.med.wayne.edu
FU Charlotte B. Failing Professorship; Harvard School of Public Health;
National Institute of Environmental Health Sciences [ES017285]; Eunice
Kennedy Shriver National Institute of Child Health and Human Development
[25PM6]; LIFE Study Working Group, Division of Epidemiology, Statistics,
and Prevention Research
FX The authors declare no conflicts of interest. This work was supported in
part by the Charlotte B. Failing Professorship to SAK, a GENI pilot
grant to SAK and RH from Harvard School of Public Health; National
Institute of Environmental Health Sciences (Grant Number ES017285) to RH
and SAK and in part by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
Contract 25PM6 in collaboration with the LIFE Study Working Group,
Division of Epidemiology, Statistics, and Prevention Research who
provided semen samples for analysis.
NR 27
TC 7
Z9 7
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1939-6368
J9 SYST BIOL REPROD MED
JI Syst. Biol. Reprod. Med.
PD OCT
PY 2013
VL 59
IS 5
BP 287
EP 295
DI 10.3109/19396368.2013.817626
PG 9
WC Andrology; Reproductive Biology
SC Endocrinology & Metabolism; Reproductive Biology
GA 221OQ
UT WOS:000324668600009
PM 23869956
ER
PT J
AU Clemente, JG
Lindell, SG
Higley, JD
Suomi, SJ
Barr, CS
AF Clemente, J. G.
Lindell, S. G.
Higley, J. D.
Suomi, S. J.
Barr, C. S.
TI DOPAMINE D4 RECEPTOR GENE (DRD4) VARIATION PREDICTS INCREASED AGGRESSION
IN RHESUS MACAQUES
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Clemente, J. G.; Lindell, S. G.; Barr, C. S.] NIAAA, NIH, LNG, SCBG, Rockville, MD 20852 USA.
[Suomi, S. J.] NICHD, NIH, LCE, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 77
BP 54
EP 54
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700078
ER
PT J
AU Lindell, SG
Clemente, JG
Barr, CS
AF Lindell, S. G.
Clemente, J. G.
Barr, C. S.
TI POLYMORPHISM IN THE OPRM1 GENE AMONG OLD WORLD MONKEYS
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Lindell, S. G.; Clemente, J. G.; Barr, C. S.] NIAAA, NIH, LNG, SCBG, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 78
BP 54
EP 54
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700079
ER
PT J
AU Sorenson, AN
Garcia, DJ
Gartman, PJ
Schwandt, ML
Barr, CS
Suomi, SJ
Higley, JD
AF Sorenson, A. N.
Garcia, D. J.
Gartman, P. J.
Schwandt, M. L.
Barr, C. S.
Suomi, S. J.
Higley, J. D.
TI EARLY REARING CONDITIONS AFFECT MONOAMINE METABOLITE LEVELS DURING
PERIODS OF SOCIAL SEPARATION STRESS: A NONHUMAN PRIMATE MODEL USING
SOCIAL SEPARATION (MACACA MULATTA)
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Sorenson, A. N.; Garcia, D. J.; Gartman, P. J.; Higley, J. D.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
[Schwandt, M. L.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
[Barr, C. S.] NIAAA, Sect Comparat Behav Genom, LNG, NIH, Bethesda, MD 20892 USA.
[Suomi, S. J.] NICHHD, NIH, Anim Ctr, LCE, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 82
BP 56
EP 56
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700083
ER
PT J
AU Jackson, J
Page, HE
Sorenson, AN
Schwandt, M
Barr, C
Suomi, S
Higley, JD
AF Jackson, J.
Page, H. E.
Sorenson, A. N.
Schwandt, M.
Barr, C.
Suomi, S.
Higley, J. D.
TI EFFECT OF THE SEROTONIN TRANSPORTER GENOTYPE AND ENVIRONMENT (GXE) ON
INFANT-MOTHER RELATIONSHIPS DURING REUNIONS IN RHESUS MACAQUES (MACACA
MULATTA)
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Jackson, J.; Page, H. E.; Sorenson, A. N.; Higley, J. D.] Brigham Young Univ, Dept Psychol, Provo, UT 84121 USA.
[Schwandt, M.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
[Barr, C.] NIAAA, Sect Comparat Behav Genom, LNG, NIH, Bethesda, MD 20892 USA.
[Suomi, S.] NICHHD, NIH, Anim Ctr, LCE, Poolesville, MD 20837 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 105
BP 63
EP 63
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700105
ER
PT J
AU O'Connell, PH
Bennett, MT
Sorenson, AN
Schwandt, ML
Barr, CS
Suomi, SJ
Higley, JD
AF O'Connell, P. H.
Bennett, M. T.
Sorenson, A. N.
Schwandt, M. L.
Barr, C. S.
Suomi, S. J.
Higley, J. D.
TI MOTHER'S 5-HTTLPR GENOTYPE X INFANT'S GENOTYPE AFFECT MOTHER-INFANT
INTERACTIONS AND OUTCOMES: AGGRESSION, ANXIETY, AND SOCIAL BEHAVIOR
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [O'Connell, P. H.; Bennett, M. T.; Sorenson, A. N.; Higley, J. D.] Brigham Young Univ, Dept Psychol, Provo, UT 84606 USA.
[Schwandt, M. L.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
[Barr, C. S.] NIAAA, Sect Comparat Behav Genom, LNG, NIH, Bethesda, MD 20892 USA.
[Suomi, S. J.] NICHHD, NIH, Anim Ctr, LCE, Poolesville, MD 20837 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 108
BP 64
EP 64
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700108
ER
PT J
AU Paukner, A
Simpson, EA
Ferrari, PF
Suomi, SJ
AF Paukner, A.
Simpson, E. A.
Ferrari, P. F.
Suomi, S. J.
TI VISUAL ATTENTION TO FACIAL GESTURES IN INFANT MACAQUES: SELECTIVE
ATTENTION TO THE EYE REGION IN NEONATAL IMITATORS
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Paukner, A.; Simpson, E. A.; Ferrari, P. F.; Suomi, S. J.] NIH, Comparat Ethol Lab, Anim Ctr, Poolesville, MD 20837 USA.
[Simpson, E. A.; Ferrari, P. F.] Univ Parma, I-43100 Parma, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 109
BP 64
EP 64
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700109
ER
PT J
AU Dettmer, AM
Woodward, RA
Novak, MA
Meyer, JS
Suomi, SJ
AF Dettmer, A. M.
Woodward, R. A.
Novak, M. A.
Meyer, J. S.
Suomi, S. J.
TI CAUSES AND CONSEQUENCES OF THE "PALACE COUP": WHAT HAIR CORTISOL TELLS
US ABOUT THE MATRILINEAL OVERTHROW AT THE LCE FIELD STATION
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Dettmer, A. M.; Woodward, R. A.; Suomi, S. J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, NIH, Poolesville, MD 20837 USA.
[Novak, M. A.; Meyer, J. S.] Univ Massachusetts, Dept Psychol, Amherst, MA 01003 USA.
NR 0
TC 0
Z9 0
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 132
BP 71
EP 71
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700130
ER
PT J
AU Schwandt, ML
Suomi, SJ
Higley, JD
Barr, CS
AF Schwandt, M. L.
Suomi, S. J.
Higley, J. D.
Barr, C. S.
TI EXTREME AND MINIMAL RESPONSE TO EARLY SOCIAL STRESS IN RHESUS MACAQUES
(MACACA MULATTA) PREDICTS THE RESPONSE TO SOCIAL CHALLENGE LATER IN LIFE
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Schwandt, M. L.] NIAAA, LCTS, NIH, Bethesda, MD 20892 USA.
[Suomi, S. J.] NICHD, LCE, NIH, Bethesda, MD USA.
[Higley, J. D.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
[Barr, C. S.] NIAAA, LNG, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 153
BP 78
EP 78
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700151
ER
PT J
AU Riddle, A
Paukner, A
AF Riddle, A.
Paukner, A.
TI FUR RUBBING BEHAVIOR AFFECTS SOCIAL COHESION AMONG CAPUCHIN MONKEYS
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Riddle, A.; Paukner, A.] NIH, Anim Ctr, Dickerson, MD 20842 USA.
NR 0
TC 0
Z9 0
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 154
BP 79
EP 79
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700152
ER
PT J
AU Driscoll, CA
Blackistone, K
Clemente, J
Lindell, SG
Suomi, SJ
Barr, CS
AF Driscoll, C. A.
Blackistone, K.
Clemente, J.
Lindell, S. G.
Suomi, S. J.
Barr, C. S.
TI EXOME SEQUENCE COMPARISONS FOR FUNCTIONAL VARIATION IN AN INDIAN AND A
CHINESE MACAQUE (MACACA MULATTA)
SO AMERICAN JOURNAL OF PRIMATOLOGY
LA English
DT Meeting Abstract
CT 36th Annual Meeting of the American-Society-of-Primatologists
CY JUN 19-22, 2013
CL San Juan, PR
SP Amer Soc Primatologists
C1 [Driscoll, C. A.; Blackistone, K.; Clemente, J.; Lindell, S. G.; Barr, C. S.] NIAAA, Sect Comparat Behav Genom, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Suomi, S. J.] NICHHD, Lab Comparat Ethol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0275-2565
J9 AM J PRIMATOL
JI Am. J. Primatol.
PD OCT
PY 2013
VL 75
SU 1
MA 176
BP 86
EP 86
PG 1
WC Zoology
SC Zoology
GA 205BF
UT WOS:000323414700173
ER
PT J
AU Homan, R
Esmaeil, N
Mendelsohn, L
Kato, GJ
AF Homan, Reynold
Esmaeil, Nadia
Mendelsohn, Laurel
Kato, Gregory J.
TI A fluorescence method to detect and quantitate sterol esterification by
lecithin: cholesterol acyltransferase
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Dehydroergosterol; Dehydroergosteryl ester; Cholesterol oxidase;
Apolipoprotein A-I mimetic; Amphipathic peptide; Sickle cell disease
ID HIGH-DENSITY-LIPOPROTEIN; I MIMETIC PEPTIDES; HUMAN-PLASMA; INITIAL
RATE; MEMBRANES; DISEASE; DEHYDROERGOSTEROL; HYDROPHOBICITY; SEPARATION;
SUBSTRATE
AB We describe a simple but sensitive fluorescence method to accurately detect the esterification activity of lecithin:cholesterol acyltransferase (LCAT). The new assay protocol employs a convenient mix, incubate, and measure scheme. This is possible by using the fluorescent sterol dehydroergosterol (DHE) in place of cholesterol as the LCAT substrate. The assay method is further enhanced by incorporation of an amphiphilic peptide in place of apolipoprotein A-I as the lipid emulsifier and LCAT activator. Specific fluorescence detection of DHE ester synthesis is achieved by employing cholesterol oxidase to selectively render unesterified DHE nonfluorescent. The assay accurately detects LCAT activity in buffer and in plasma that is depleted of apolipoprotein B lipoproteins by selective precipitation. Analysis of LCAT activity in plasmas from control subjects and sickle cell disease (SCD) patients confirms previous reports of reduced LCAT activity in SCD and demonstrates a strong correlation between plasma LCAT activity and LCAT content. The fluorescent assay combines the sensitivity of radiochemical assays with the simplicity of nonradiochemical assays to obtain accurate and robust measurement of LCAT esterification activity. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Homan, Reynold; Esmaeil, Nadia] AlphaCore Pharma, Ann Arbor, MI 48103 USA.
[Mendelsohn, Laurel; Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Homan, R (reprint author), AlphaCore Pharma, Ann Arbor, MI 48103 USA.
EM reynh@comcast.net
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU Small Business Innovation Research (SBIR) from the National Heart, Lung,
and Blood Institute, National Institutes of Health [1 R43
HL092656-01A1]; National Institutes of Health Division of Intramural
Research [1 ZIA HL006013-04]
FX Portions of this work were funded by a Small Business Innovation
Research (SBIR) grant to AlphaCore Pharma from the National Heart, Lung,
and Blood Institute, National Institutes of Health (1 R43
HL092656-01A1). G.J.K. and L.M. are supported by the National Institutes
of Health Division of Intramural Research (1 ZIA HL006013-04). The
authors thank Bruce Auerbach and Brian Krause for helpful discussions
and ideas and for facilitating the production of rhLCAT. The authors
also thank research nurse Marlene Peters-Lawrence for recruiting
subjects and thank all of the patients who provided blood samples.
NR 41
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U1 1
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
EI 1096-0309
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD OCT 1
PY 2013
VL 441
IS 1
BP 80
EP 86
DI 10.1016/j.ab.2013.06.018
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 209ZW
UT WOS:000323800100014
PM 23851343
ER
PT J
AU Sutherland, MT
Carroll, AJ
Salmeron, BJ
Ross, TJ
Hong, LE
Stein, EA
AF Sutherland, Matthew T.
Carroll, Allison J.
Salmeron, Betty Jo
Ross, Thomas J.
Hong, L. Elliot
Stein, Elliot A.
TI Down-Regulation of Amygdala and Insula Functional Circuits by
Varenicline and Nicotine in Abstinent Cigarette Smokers
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Amygdala; insula; nicotine; resting-state functional connectivity;
varenicline; withdrawal
ID RECEPTOR PARTIAL AGONIST; SUSTAINED-RELEASE BUPROPION; RANDOMIZED
CONTROLLED-TRIAL; DEFAULT-MODE; SMOKING-CESSATION; BRAIN NETWORKS;
STRUCTURAL CONNECTIVITY; HEAD MOTION; ADDICTION; STATE
AB Background: Although the amygdala and insula are regarded as critical neural substrates perpetuating cigarette smoking, little is known about their circuit-level interactions with interconnected regions during nicotine withdrawal or following pharmacotherapy administration. To elucidate neurocircuitry associated with early smoking abstinence, we examined the impact of varenicline and nicotine, two modestly efficacious pharmacologic cessation aids, on amygdala-and insula-centered circuits using resting-state functional connectivity (rsFC).
Methods: In a functional magnetic resonance imaging study employing a two-drug, placebo-controlled design, 24 overnight-abstinent smokers and 20 nonsmokers underwent similar to 17 days of varenicline and placebo pill administration and were scanned, on different days under each condition, wearing a transdermal nicotine or placebo patch. We examined the impact of varenicline and nicotine (both alone and in combination) on amygdala-and insula-centered rsFC using seed-based assessments.
Results: Beginning with a functionally defined amygdala seed, we observed that rsFC strength in an amygdala-insula circuit was down-regulated by varenicline and nicotine in abstinent smokers. Using this identified insula region as a new seed, both drugs similarly decreased rsFC between the insula and constituents of the canonical default-mode network (posterior cingulate cortex, ventromedial/dorsomedial prefrontal cortex, parahippocampus). Drug-induced rsFC modulations were critically linked with nicotine withdrawal, as similar effects were not detected in nonsmokers.
Conclusions: These results suggest that nicotine withdrawal is associated with elevated amygdala-insula and insula-default-mode network interactions. As these potentiated interactions were down-regulated by two pharmacotherapies, this effect may be a characteristic shared by pharmacologic agents promoting smoking cessation. Decreased rsFC in these circuits may contribute to amelioration of subjective withdrawal symptoms.
C1 [Sutherland, Matthew T.] Florida Int Univ, Dept Psychol, Miami, FL 33199 USA.
[Sutherland, Matthew T.; Carroll, Allison J.; Salmeron, Betty Jo; Ross, Thomas J.; Stein, Elliot A.] Natl Inst Drug Abuse, Neuroimaging Res Branch, Intramural Res Program, NIH,US Dept Hlth & Human Serv, Baltimore, MD USA.
[Hong, L. Elliot] Univ Maryland, Sch Med, Dept Psychiat, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA.
RP Sutherland, MT (reprint author), Florida Int Univ, Dept Psychol, Room 295,11299 SW 8th St, Miami, FL 33199 USA.
EM sutherlm@nida.nih.gov
RI Salmeron, Betty Jo/M-1793-2016;
OI Salmeron, Betty Jo/0000-0003-1699-9333; Ross, Thomas/0000-0002-7745-3572
FU National Institute on Drug Abuse, Intramural Research Program, National
Institutes of Health, US Department of Health and Human Services
FX This work was sponsored by the National Institute on Drug Abuse,
Intramural Research Program, National Institutes of Health, US
Department of Health and Human Services.
NR 66
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Z9 33
U1 4
U2 31
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 OCT 1
PY 2013
VL 74
IS 7
BP 538
EP 546
DI 10.1016/j.biopsych.2013.01.035
PG 9
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 216UJ
UT WOS:000324310000011
PM 23506999
ER
PT J
AU de Zwart, JA
van Gelderen, P
Liu, ZM
Duyn, JH
AF de Zwart, Jacco A.
van Gelderen, Peter
Liu, Zhongming
Duyn, Jeff H.
TI Independent Sources of Spontaneous BOLD Fluctuation Along the Visual
Pathway
SO BRAIN TOPOGRAPHY
LA English
DT Article
DE Resting state fMRI; Human visual system; Brain connectivity; Correlation
analysis; Callosal pathway; Thalamic pathway
ID STATE FUNCTIONAL CONNECTIVITY; CORPUS-CALLOSUM; HUMAN BRAIN; STRUCTURAL
CONNECTIVITY; FMRI; CORTEX; THALAMUS; AREAS; MRI; ACTIVATION
AB In resting-state functional magnetic resonance imaging (fMRI) experiments, correlation analysis can be used to identify clusters of cortical regions that may be functionally connected. Although such functional connectivity is often assumed to reflect cortico-cortical connections, a potential confound is the contribution of subcortical brain regions, many of which have strong anatomical connectivity to cortical regions and may also enable cortico-cortical interactions through trans-thalamic pathways. To investigate this, we performed resting state fMRI of the human visual system, including cortical regions and subcortical nuclei of the pulvinar and lateral geniculate. Regression analysis was used to investigate the dependence of the measured inter-regional correlations upon afferents from specific retinal, thalamic and cortical regions as well as systemic global signal fluctuation. A high level of inter-hemispheric correlation (cc = 0.95) was found in the visual cortex that could not be explained by activity in the subcortical nuclei investigated; in addition a relatively low level of inter-hemispheric correlation (cc = 0.39-0.42) was found in vision-related thalamic nuclei that could not be explained by direct anatomical connections or their cortical inputs. These findings suggest that spontaneous fMRI signal correlations within the human visual system originate from a mixture of independent signal sources that may be transmitted through thalamo-cortical, cortico-thalamic, and cortico-cortical connections either trans-callosal or trans-thalamic in origin. Our findings thus call for more cautious interpretation of resting state functional connectivity in terms of any single type of anatomical connectivity.
C1 [de Zwart, Jacco A.; van Gelderen, Peter; Liu, Zhongming; Duyn, Jeff H.] NINDS, Adv MRI Sect, LFMI, NIH, Bethesda, MD 20892 USA.
RP de Zwart, JA (reprint author), NINDS, Adv MRI Sect, LFMI, NIH, Bldg 10,Rm B1D-728,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jacco.dezwart@nih.gov
FU National Institute of Neurological Disorders and Stroke, NIH
FX This work was sponsored by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, NIH.
NR 42
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U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0896-0267
J9 BRAIN TOPOGR
JI Brain Topogr.
PD OCT
PY 2013
VL 26
IS 4
BP 525
EP 537
DI 10.1007/s10548-013-0290-1
PG 13
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 217AM
UT WOS:000324328700001
PM 23660870
ER
PT J
AU Liu, W
Park, Y
Purdue, MP
Giovannucci, E
Cho, E
AF Liu, Wei
Park, Yikyung
Purdue, Mark P.
Giovannucci, Edward
Cho, Eunyoung
TI A large cohort study of nonsteroidal anti-inflammatory drugs and renal
cell carcinoma incidence in the National Institutes of Health-AARP Diet
and Health Study
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Anti-inflammatory agents/nonsteroidal; Carcinoma/renal cell; NIH-AARP;
Cohort studies
ID LOW-DOSE ASPIRIN; CANCER INCIDENCE; PRIMARY PREVENTION; ANALGESIC USE;
RISK; ACETAMINOPHEN; METAANALYSIS; HYPERTENSION; TRIALS; USERS
AB Existing epidemiologic evidence for the association between nonsteroidal anti-inflammatory drugs (NSAIDs) and renal cell carcinoma (RCC) risk is inconsistent.
We investigated the association between the use of aspirin and nonaspirin NSAIDs and RCC risk in the National Institutes of Health-American Association of Retired Persons (AARP) Diet and Health Study, for which 298,468 AARP members free of cancer, aged 50-71 years, completed a survey on use of NSAIDs (1996-1997). Multivariate Cox proportional hazards models were used to estimate the hazard ratio (HR).
The state cancer registry and mortality index linkage identified 1,084 incident RCC cases through 31 December 2006. No statistically significant associations between the use of aspirin or nonaspirin NSAIDs and RCC risk were found. Compared to nonuse of any NSAIDs, the multivariate-adjusted HRs were 0.95 (95 % CI 0.75-1.21) and 0.93 (95 % CI 0.68-1.26) for monthly use of aspirin and nonaspirin NSAIDs, respectively, 0.92 (95 % CI: 0.69-1.23) and 1.11 (95 % CI: 0.76-1.62) for weekly use, 0.87 (95 % CI: 0.69-1.11) and 1.06 (95 % CI: 0.75-1.48) for daily use; and 0.95 (95 % CI 0.78-1.14) for the use of both aspirin and nonaspirin NSAIDs. We found some suggestions of an increased risk of RCC associated with frequent NSAID use among participants who were < 63 years and a reduced risk associated with aspirin use among those a parts per thousand yen63 years. No significant associations were found in other stratified analyses by gender, BMI, smoking, history of diabetes, or history of hypertension.
RCC risk was not significantly associated with NSAID use overall. The difference in association by age needs to be explored further.
C1 [Liu, Wei; Giovannucci, Edward; Cho, Eunyoung] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med,Dept Med, Boston, MA 02115 USA.
[Park, Yikyung; Purdue, Mark P.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Cho, Eunyoung] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Cho, E (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med,Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.
EM enyoung.cho@channing.harvard.edu
RI Purdue, Mark/C-9228-2016;
OI Purdue, Mark/0000-0003-1177-3108; Park, Yikyung/0000-0002-6281-489X
FU Intramural Research Program of the NIH, National Cancer Institute
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute. 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 by 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 (FCDC) under contract with the Florida Department of
Health (FDOH). The views expressed herein are solely those of the
authors and do not necessarily reflect those of the FCDC or FDOH. 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 Epidemiology 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. Cancer incidence data from Arizona were collected by the
Arizona Cancer Registry, Division of Public Health Services, Arizona
Department of Health Services. Cancer incidence data from Texas were
collected by the Texas Cancer Registry, Cancer Epidemiology and
Surveillance Branch, Texas Department of State Health Services. Cancer
incidence data from Nevada were collected by the Nevada Central Cancer
Registry, Center for Health Data and Research, Bureau of Health Planning
and Statistics, State Health Division, State of Nevada Department of
Health and Human Services. We are indebted to the participants in the
NIH-AARP Diet and Health Study for their out-standing cooperation. We
also thank Sigurd Hermansen and Kerry Grace Morrissey from Westat for
study outcomes ascertainment and management and Leslie Carroll
NR 28
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U1 0
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2013
VL 24
IS 10
BP 1865
EP 1873
DI 10.1007/s10552-013-0263-4
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 216AF
UT WOS:000324252500010
PM 23868221
ER
PT J
AU Li, Q
Lan, Q
Zhang, YW
Bassig, BA
Holford, TR
Leaderer, B
Boyle, P
Zhu, Y
Qin, Q
Chanock, S
Rothman, N
Zheng, TZ
AF Li, Qian
Lan, Qing
Zhang, Yawei
Bassig, Bryan A.
Holford, Theodore R.
Leaderer, Brian
Boyle, Peter
Zhu, Yong
Qin, Qin
Chanock, Stephen
Rothman, Nathaniel
Zheng, Tongzhang
TI Role of one-carbon metabolizing pathway genes and gene-nutrient
interaction in the risk of non-Hodgkin lymphoma
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Dietary nutrients; Folate; One-carbon metabolizing genes; Non-Hodgkin
lymphoma; Cancer
ID METHYLENETETRAHYDROFOLATE REDUCTASE GENE; SERINE
HYDROXYMETHYLTRANSFERASE GENES; MALIGNANT-LYMPHOMA; ENVIRONMENT
INTERACTIONS; ALTERS SUSCEPTIBILITY; LYMPHOCYTIC-LEUKEMIA; THYMIDYLATE
SYNTHASE; COMMON MUTATION; POLYMORPHISMS; FOLATE
AB Genetic polymorphisms in one-carbon metabolizing pathway genes have been associated with risk of malignant lymphoma. However, the results have been inconsistent. The objectives of this study were to examine the potential relationship between gene-nutrient interactions and the risk of non-Hodgkin lymphoma (NHL).
We examined 25 polymorphisms in 16 one-carbon metabolism genes for their main effect and gene-nutrient interactions in relation to NHL risk among 518 incident cases and 597 population-based controls of Connecticut women enrolled between 1996 and 2000.
A significantly reduced risk of NHL was associated with the homozygous TT genotype in CBS (rs234706, Ex9+33C > T) (OR = 0.51, 95 % CI 0.31-0.84), the homozygous CC genotype in MBD2 (rs603097, -2176C > T) (OR = 0.37, 95 % CI 0.17-0.79), the heterozygote AG genotype in FTHFD (rs1127717, Ex21+31A > G) (OR = 0.73, 95 % CI 0.55-0.98), and a borderline significantly reduced risk of NHL was observed for the homozygous CC genotype in MTRR (rs161870, Ex5+136T > C) (OR = 0.23, 95 % CI 0.05-1.04). The reduced risk of NHL associated with these genotypes was predominately in those with higher dietary vitamin B6 and methionine intakes, as well as with higher dietary folate intake although results were less stable. A borderline significantly increased risk of NHL was also observed for CBS (rs1801181, Ex13+41C > T), FTHFD (rs2305230, Ex10-40G > T), SHMT1 (rs1979277, Ex12+138C > T), and SHMT1 (rs1979276, Ex12+236T > C), and these associations appeared to be contingent on dietary nutrient intakes.
Our results suggest that variation in several one-carbon metabolizing pathway genes may influence the risk of NHL through gene-nutrient interactions involving dietary nutrient intakes.
C1 [Li, Qian; Zhang, Yawei; Bassig, Bryan A.; Holford, Theodore R.; Leaderer, Brian; Zhu, Yong; Zheng, Tongzhang] Yale Univ, Sch Publ Hlth, Dept Environm Hlth Sci, New Haven, CT 06510 USA.
[Li, Qian] Icahn Sch Med Mt Sinai, Dept Prevent Med, New York, NY USA.
[Lan, Qing; Chanock, Stephen; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Boyle, Peter] IPRI, Lyon, France.
[Qin, Qin] Univ So Maine, Wise Lab Environm & Genet Toxicol, Portland, ME 04103 USA.
RP Zheng, TZ (reprint author), Yale Univ, Sch Publ Hlth, Dept Environm Hlth Sci, New Haven, CT 06510 USA.
EM tongzhang.zheng@yale.edu
RI Boyle, Peter/A-4380-2014
OI Boyle, Peter/0000-0001-6251-0610
FU National Institutes of Health [CA62006]; National Institutes of Health,
National Cancer Institute; National Institutes of Health Fogarty
[D43TW008323-01, D43TW007864-01]
FX This work was supported by the National Institutes of Health (Grant
CA62006), the Intramural Research Program of the National Institutes of
Health, National Cancer Institute, and the National Institutes of Health
Fogarty (training Grants D43TW008323-01 and D43TW007864-01).
NR 43
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U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2013
VL 24
IS 10
BP 1875
EP 1884
DI 10.1007/s10552-013-0264-3
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 216AF
UT WOS:000324252500011
PM 23913011
ER
PT J
AU Safaeian, M
Rajaraman, P
Hartge, P
Yeager, M
Linet, M
Butler, MA
Ruder, AM
Purdue, MP
Hsing, A
Beane-Freeman, L
Hoppin, JA
Albanes, D
Weinstein, SJ
Inskip, PD
Brenner, A
Rothman, N
Chatterjee, N
Gillanders, EM
Chanock, SJ
Wang, SS
AF Safaeian, Mahboobeh
Rajaraman, Preetha
Hartge, Patricia
Yeager, Meredith
Linet, Martha
Butler, Mary Ann
Ruder, Avima M.
Purdue, Mark P.
Hsing, Ann
Beane-Freeman, Laura
Hoppin, Jane A.
Albanes, Demetrius
Weinstein, Stephanie J.
Inskip, Peter D.
Brenner, Alina
Rothman, Nathaniel
Chatterjee, Nilanjan
Gillanders, Elizabeth M.
Chanock, Stephen J.
Wang, Sophia S.
TI Joint effects between five identified risk variants, allergy, and
autoimmune conditions on glioma risk
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Single-nucleotide polymorphisms; Glioma; Allergies; Autoimmune
conditions; Gene-environment interaction
ID GENOME-WIDE ASSOCIATION; HIGH-GRADE GLIOMA; BRAIN-TUMORS; 1ST-DEGREE
RELATIVES; AGRICULTURAL HEALTH; SUSCEPTIBILITY LOCI; NERVOUS-SYSTEM;
CANCER; HISTORY; ADULTS
AB Common variants in two of the five genetic regions recently identified from genome-wide association studies (GWAS) of risk of glioma were reported to interact with a history of allergic symptoms. In a pooled analysis of five epidemiologic studies, we evaluated the association between the five GWAS implicated gene variants and allergies and autoimmune conditions (AIC) on glioma risk (851 adult glioma cases and 3,977 controls). We further evaluated the joint effects between allergies and AIC and these gene variants on glioma risk. Risk estimates were calculated as odds ratios (OR) and 95 % confidence intervals (95 % CI), adjusted for age, gender, and study. Joint effects were evaluated by conducting stratified analyses whereby the risk associations (OR and 95 % CI) with the allergy or autoimmune conditions for glioma were evaluated by the presence or absence of the 'at-risk' variant, and estimated p interaction by fitting models with the main effects of allergy or autoimmune conditions and genotype and an interaction (product) term between them. Four of the five SNPs previously reported by others were statistically significantly associated with increased risk of glioma in our study (rs2736100, rs4295627, rs4977756, and rs6010620); rs498872 was not associated with glioma in our study. Reporting any allergies or AIC was associated with reduced risks of glioma (allergy: adjusted OR = 0.71, 95 % CI 0.55-0.91; AIC: adjusted OR = 0.65, 95 % CI 0.47-0.90). We did not observe differential association between allergic or autoimmune conditions and glioma by genotype, and there were no statistically significant p interactions. Stratified analysis by glioma grade (low and high grade) did not suggest risk differences by disease grade. Our results do not provide evidence that allergies or AIC modulate the association between the four GWAS-identified SNPs examined and risk of glioma.
C1 [Safaeian, Mahboobeh; Rajaraman, Preetha; Hartge, Patricia; Linet, Martha; Purdue, Mark P.; Hsing, Ann; Beane-Freeman, Laura; Albanes, Demetrius; Weinstein, Stephanie J.; Inskip, Peter D.; Brenner, Alina; Rothman, Nathaniel; Chatterjee, Nilanjan] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Safaeian, Mahboobeh] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Yeager, Meredith; Weinstein, Stephanie J.] NCI, Core Genom Res, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Butler, Mary Ann; Ruder, Avima M.] NIOSH, Ctr Dis Control & Prevent, Atlanta, GA USA.
[Hoppin, Jane A.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC USA.
[Gillanders, Elizabeth M.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Wang, Sophia S.] City Hope Natl Med Ctr, Div Etiol, Dept Populat Sci, Duarte, CA USA.
RP Safaeian, M (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
EM safaeianm@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015; Purdue, Mark/C-9228-2016; Beane Freeman,
Laura/C-4468-2015
OI Purdue, Mark/0000-0003-1177-3108; Beane Freeman,
Laura/0000-0003-1294-4124
FU National Cancer Institute; National Institute for Occupational Safety
and Health; National Cancer Institute [N01-CO-12400]; NIEHS
FX The study was funded by Intramural Research Program of the National
Cancer Institute and the National Institute for Occupational Safety and
Health. It was been funded in whole or in part with federal funds from
the National Cancer Institute under contract N01-CO-12400. The funding
source for AHS is from the Intramural Program of NIEHS. AHS Data release
P1REL0506_02. We are indebted to the scientific and field efforts of Tim
Sheehy, Laurie Burdette, Aurelie Vogt, Annelie Landgren, Zhaoming Wang,
Arti Aranasi, Michelle Brotzman, Lisa Newman, and Peter Hui.
NR 27
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U1 0
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2013
VL 24
IS 10
BP 1885
EP 1891
DI 10.1007/s10552-013-0244-7
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 216AF
UT WOS:000324252500012
PM 23903690
ER
PT J
AU Hong, CW
Abi-Jaoudeh, N
Wood, BJ
AF Hong, Cheng William
Abi-Jaoudeh, Nadine
Wood, Bradford J.
TI Needle Slippage From Needle Hub Hardware During Ablation
SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Letter
ID DEVICE
C1 [Hong, Cheng William; Abi-Jaoudeh, Nadine; Wood, Bradford J.] NIH, Ctr Intervent Oncol, Ctr Clin, Bethesda, MD 20892 USA.
[Hong, Cheng William] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44195 USA.
RP Hong, CW (reprint author), NIH, Ctr Intervent Oncol, Ctr Clin, 10 Ctr Dr MSC 1182, Bethesda, MD 20892 USA.
EM william.hong@nih.gov; abijaoudehn@cc.nih.gov; bwood@nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 3
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0174-1551
J9 CARDIOVASC INTER RAD
JI Cardiovasc. Interv. Radiol.
PD OCT
PY 2013
VL 36
IS 5
BP 1436
EP 1437
DI 10.1007/s00270-013-0575-5
PG 2
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 216AG
UT WOS:000324252600034
PM 23417683
ER
PT J
AU Allen, HF
Wade, PA
Kutateladze, TG
AF Allen, Hillary F.
Wade, Paul A.
Kutateladze, Tatiana G.
TI The NuRD architecture
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE NuRD complex; Chromatin
ID HISTONE DEACETYLASE COMPLEX; CHROMATIN-REMODELING COMPLEX; ALPHA
TRANSACTIVATION FUNCTIONS; EMBRYONIC STEM-CELLS; MI-2/NURD COMPLEX;
TRANSCRIPTIONAL REPRESSION; ESTROGEN-RECEPTOR; DNA-DAMAGE; STRUCTURAL
BASIS; BINDING-PROTEIN
AB The nucleosome remodeling and deacetylase (NuRD) complex regulates chromatin organization, gene transcription, genomic stability and developmental signaling. NuRD has a unique dual enzymatic activity, containing an ATPase and a histone deacetylase among its six core subunits. Recent studies indicate that NuRD composition and the interplay between subunits may dictate the diverse functions of the complex. In this review, we examine the structures and biological roles of the NuRD subunits and discuss new avenues of research to advance our understanding of the NuRD-mediated signaling network.
C1 [Allen, Hillary F.; Kutateladze, Tatiana G.] Univ Colorado, Sch Med, Dept Pharmacol, Aurora, CO 80045 USA.
[Allen, Hillary F.; Kutateladze, Tatiana G.] Univ Colorado, Sch Med, Neurosci Program, Aurora, CO 80045 USA.
[Wade, Paul A.] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
RP Kutateladze, TG (reprint author), Univ Colorado, Sch Med, Dept Pharmacol, Aurora, CO 80045 USA.
EM Tatiana.Kutateladze@ucdenver.edu
FU NIH [GM096863]; Intramural Research Program of the US National Institute
of Environmental Health Sciences, NIH [Z01ES101965]; Neuroscience
Graduate training grant [T32HD041697]
FX The authors apologize to our many colleagues whose work could not be
cited here due to space constraints. This work was supported by the NIH
grant, GM096863 to T. G. K. This work was supported, in part, by the
Intramural Research Program of the US National Institute of
Environmental Health Sciences, NIH (Project Number Z01ES101965 to P. A.
W.). H. F. A. is supported by the Neuroscience Graduate training grant,
T32HD041697.
NR 103
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U1 1
U2 23
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD OCT
PY 2013
VL 70
IS 19
BP 3513
EP 3524
DI 10.1007/s00018-012-1256-2
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 216FF
UT WOS:000324266700003
PM 23340908
ER
PT J
AU Lee, NC
Kononenko, AV
Lee, HS
Tolkunova, EN
Liskovykh, MA
Masumoto, H
Earnshaw, WC
Tomilin, AN
Larionov, V
Kouprina, N
AF Lee, Nicholas Co
Kononenko, Artem V.
Lee, Hee-Sheung
Tolkunova, Elena N.
Liskovykh, Mikhail A.
Masumoto, Hiroshi
Earnshaw, William C.
Tomilin, Alexey N.
Larionov, Vladimir
Kouprina, Natalay
TI Protecting a transgene expression from the HAC-based vector by different
chromatin insulators
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article
DE Insulator; tDNA-gamma-satellite; cHS4; Human artificial chromosome-HAC
ID HUMAN ARTIFICIAL CHROMOSOME; TRANSFORMATION-ASSOCIATED RECOMBINATION;
TRANSFER-RNA GENES; CONDITIONAL CENTROMERE; NEW-GENERATION; STEM-CELLS;
DNA; DELIVERY; CLONING; HETEROCHROMATIN
AB Human artificial chromosomes (HACs) are vectors that offer advantages of capacity and stability for gene delivery and expression. Several studies have even demonstrated their use for gene complementation in gene-deficient recipient cell lines and animal transgenesis. Recently, we constructed an advance HAC-based vector, alphoid(tetO)-HAC, with a conditional centromere. In this HAC, a gene-loading site was inserted into a centrochromatin domain critical for kinetochore assembly and maintenance. While by definition this domain is permissive for transcription, there have been no long-term studies on transgene expression within centrochromatin. In this study, we compared the effects of three chromatin insulators, cHS4, gamma-satellite DNA, and tDNA, on the expression of an EGFP transgene inserted into the alphoid(tetO)-HAC vector. Insulator function was essential for stable expression of the transgene in centrochromatin. In two analyzed host cell lines, a tDNA insulator composed of two functional copies of tRNA genes showed the highest barrier activity. We infer that proximity to centrochromatin does not protect genes lacking chromatin insulators from epigenetic silencing. Barrier elements that prevent gene silencing in centrochromatin would thus help to optimize transgenesis using HAC vectors.
C1 [Lee, Nicholas Co; Kononenko, Artem V.; Lee, Hee-Sheung; Larionov, Vladimir; Kouprina, Natalay] NCI, Labs Mol Pharmacol, Bethesda, MD 20892 USA.
[Tolkunova, Elena N.; Liskovykh, Mikhail A.; Tomilin, Alexey N.] Russian Acad Sci, Inst Cytol, St Petersburg 194064, Russia.
[Masumoto, Hiroshi] Kazusa DNA Res Inst, Dept Human Genome Res, Lab Cell Engn, Kisarazu, Chiba 2920818, Japan.
[Earnshaw, William C.] Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Edinburgh EH9 3JR, Midlothian, Scotland.
RP Larionov, V (reprint author), NCI, Labs Mol Pharmacol, Bethesda, MD 20892 USA.
EM larionov@mail.nih.gov; kouprinn@mail.nih.gov
RI Tomilin, Alexey/C-3361-2014; Lee, Nicholas/F-3668-2015;
OI Tomilin, Alexey/0000-0002-1137-7167; lee, nicholas/0000-0003-2628-6599
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, USA; Wellcome Trust [073915]; Ministry of
Education, Culture, Sports, Science and Technology of Japan; Kazusa DNA
Research Institute Foundation; Goskontrakt [02.512.11.2085]; Russian
Academy of Sciences "Molecular and Cellular Biology"; Program of the
Presidium of the Russian Academy of Sciences "Molecular and Cellular
Biology"
FX This work was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research, USA (V. L. and
N.K.), the Wellcome Trust of which W. C. E. is a Principal Research
Fellow (grant number 073915), the Grand-in-Aid for Scientific Research
from Ministry of Education, Culture, Sports, Science and Technology of
Japan (H. M.), the Kazusa DNA Research Institute Foundation (H. M.), by
Goskontrakt 02.512.11.2085 (A. V. T.) and by the programme of the
Russian Academy of Sciences "Molecular and Cellular Biology" (A. V. T).
A. V. T., E. T., and M. L. were also supported by the Program of the
Presidium of the Russian Academy of Sciences "Molecular and Cellular
Biology". The authors would like to thank the CRC, LRBGE
NR 43
TC 9
Z9 9
U1 0
U2 6
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD OCT
PY 2013
VL 70
IS 19
BP 3723
EP 3737
DI 10.1007/s00018-013-1362-9
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 216FF
UT WOS:000324266700015
PM 23677492
ER
PT J
AU Price, JD
Linder, G
Li, WP
Zimmermann, B
Rother, KI
Malek, R
Alattar, M
Tarbell, KV
AF Price, J. D.
Linder, G.
Li, W. P.
Zimmermann, B.
Rother, K. I.
Malek, R.
Alattar, M.
Tarbell, K. V.
TI Effects of short-term sitagliptin treatment on immune parameters in
healthy individuals, a randomized placebo-controlled study
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article
DE cytokine; dipeptidyl-peptidase 4; GLP-1; immune function
ID DIPEPTIDYL-PEPTIDASE-IV; T-CELLS; RHEUMATOID-ARTHRITIS; MICE; CD26;
INHIBITION; ENZYME; PROLIFERATION; INFLAMMATION; CHEMOTAXIS
AB Sitagliptin, a dipeptidyl-peptidase 4 (DPP-4) inhibitor, improves blood glucose control in patients with type 2 diabetes by blocking cleavage of glucagon-like peptide 1 (GLP-1). In type 2 diabetes patients sitagliptin use is associated with an increase in minor infections, and in new-onset type 1 diabetes patients the ability of sitagliptin to dampen autoimmunity is currently being tested. DPP-4, also known as CD26, is expressed on leucocytes and can inactivate many chemokines important for leucocyte migration, as well as act as a co-stimulatory molecule on T cells. Therefore, this study was conducted to test whether sitagliptin is immunomodulatory. In this randomized, placebo-controlled trial, healthy volunteers were given sitagliptin or placebo daily for 28 days, and blood was drawn for immune assays. No significant differences were observed in the percentage of leucocyte subsets within peripheral blood mononuclear cells (PBMCs), plasma chemokine/cytokine levels or cytokines released by stimulation of PBMCs with either lipopolysaccharide (LPS) or anti-CD3. Individuals taking sitagliptin displayed increases in the percentage of cells expressing higher levels of CD26 at early time-points compared to placebo controls, but these differences resolved by day 28 of treatment. Therefore, in healthy volunteers, treatment with sitagliptin daily for 28 days does not overtly alter systemic immune function.
C1 [Price, J. D.; Linder, G.; Li, W. P.; Zimmermann, B.; Rother, K. I.; Malek, R.; Alattar, M.; Tarbell, K. V.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
RP Tarbell, KV (reprint author), NIDDK, Immune Tolerance Sect, Diabet Endocrinol & Obes Branch, NIH,CRC,West Labs, Bldg 10,5-5940, Bethesda, MD 20892 USA.
EM tarbellk@niddk.nih.gov
OI Tarbell, Kristin/0000-0003-3738-379X
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK)
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK). We would like to thank Michelle Ashmus for coordinating patient
recruitment, Dr Monica Skarulis for serving as the medically responsible
investigator, Drs Xiongce Zhao and Elizabeth Wright for help with
statistical analysis, the NIH Center for Human Immunology, specifically
Phil McCoy and Angelique Biancotto for flow cytometry and multiplex
support, and Dr Francesco Marincola, Ena Wang and Hui Liu for help with
gene expression analysis. In addition, Mary Walter and the NIDDK Central
Laboratory helped with GLP-1 assays, DPP-4 activity assays, sample
storage and database maintenance. NIH pharmacy, including Judith
Starling provided the drug with matching placebo and performed
randomization.
NR 28
TC 13
Z9 13
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD OCT
PY 2013
VL 174
IS 1
BP 120
EP 128
DI 10.1111/cei.12144
PG 9
WC Immunology
SC Immunology
GA 213HH
UT WOS:000324045900013
PM 23711188
ER
PT J
AU Pamporaki, C
Darr, R
Bursztyn, M
Glockner, S
Bornstein, SR
Lenders, JWM
Pacak, K
Krinner, A
Eisenhofer, G
AF Pamporaki, Christina
Daerr, Roland
Bursztyn, Michael
Gloeckner, Stephan
Bornstein, Stefan R.
Lenders, Jacques W. M.
Pacak, Karel
Krinner, Axel
Eisenhofer, Graeme
TI Plasma-free vs deconjugated metanephrines for diagnosis of
phaeochromocytoma
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID FRACTIONATED METANEPHRINES; URINARY METANEPHRINES; CATECHOLAMINES;
METABOLISM; EFFICACY; CURVES
AB Background The diagnosis of phaeochromocytoma is commonly performed by the measurements of plasma-free normetanephrine and metanephrine. Plasma-deconjugated normetanephrine and metanephrine have been proposed as alternative, equivalent, but easier to measure biomarkers.
Objective The aim of this study was to compare the diagnostic performance of plasma-free vs deconjugated normetanephrine and metanephrine in patients tested for phaeochromocytoma.
Methods The study population included a reference group of 262 normotensive and hypertensive volunteers, 198 patients with phaeochromocytoma and 528 patients initially suspected of having the tumour, but with negative investigations after at least 2years of follow-up. Measurements were performed using liquid chromatography with electrochemical detection.
Results Plasma concentrations of free normetanephrine were 17-fold higher in patients with phaeochromocytoma than in the reference population, a 72% larger (P < 0.001) difference than that for the 10-fold higher levels of plasma-deconjugated normetanephrine. In contrast, relative increases in plasma concentrations of free and deconjugated metanephrine were similar. Using upper cut-offs established in the reference population, measurements of plasma-free metabolites provided superior diagnostic performance than deconjugated metabolites according to measures of both sensitivity (97% vs 92%, P = 0.002) and specificity (93% vs 89%, P = 0.012). The area under the receiver operating characteristic curve for the free metabolites was larger than that for the deconjugated metabolites (0.986 vs 0.965, P < 0.001).
Conclusion Measurements of plasma-free normetanephrine and metanephrine are superior to the deconjugated metabolites for diagnosis of phaeochromocytoma.
C1 [Pamporaki, Christina; Eisenhofer, Graeme] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Inst Clin Chem & Lab Med, D-01307 Dresden, Germany.
[Pamporaki, Christina; Daerr, Roland; Bursztyn, Michael; Gloeckner, Stephan; Bornstein, Stefan R.; Lenders, Jacques W. M.; Eisenhofer, Graeme] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Med 3, D-01307 Dresden, Germany.
[Lenders, Jacques W. M.] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, NL-6525 ED Nijmegen, Netherlands.
[Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Krinner, Axel] Tech Univ Dresden, Inst Med Informat & Biometry, Fac Med, Dresden, Germany.
RP Pamporaki, C (reprint author), Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Inst Clin Chem & Lab Med, Fetscherstr 74, D-01307 Dresden, Germany.
EM Christina.Pamporaki@uniklinikum-dresden.de
RI Lenders, J.W.M./L-4487-2015
FU Erasmus fellowship; Deutsche Forschungsgesellschaft [EI855/1-1]
FX C.P. is supported under an Erasmus fellowship. This work was supported
by the Deutsche Forschungsgesellschaft (EI855/1-1).
NR 28
TC 5
Z9 5
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD OCT
PY 2013
VL 79
IS 4
BP 476
EP 483
DI 10.1111/cen.12191
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 211SY
UT WOS:000323932200005
PM 23461656
ER
PT J
AU Kruth, HS
AF Kruth, Howard S.
TI Fluid-Phase Pinocytosis of LDL by Macrophages: A Novel Target to Reduce
Macrophage Cholesterol Accumulation in Atherosclerotic Lesions
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Article
DE Atherosclerosis; macrophages; LDL; cholesterol; fluid-phase pinocytosis;
macropinocytosis; LXR; phosphoinositide 3-kinase; M-CSF; GM-CSF
ID LOW-DENSITY-LIPOPROTEIN; FOAM CELL-FORMATION; COLONY-STIMULATING FACTOR;
MONOCYTE-DERIVED MACROPHAGES; RECEPTOR-MEDIATED ENDOCYTOSIS; MOUSE
PERITONEAL-MACROPHAGES; LIVER-X RECEPTORS; SCAVENGER RECEPTOR;
HYPERLIPIDEMIC MICE; LIPID-METABOLISM
AB Circulating low-density lipoprotein (LDL) that enters the blood vessel wall is the main source of cholesterol that accumulates within atherosclerotic plaques. Much of the deposited cholesterol accumulates within plaque macrophages converting these macrophages into cholesterol-rich foamy looking cells. Cholesterol accumulation in macrophages contributes to cholesterol retention within the vessel wall, and promotes vessel wall inflammation and thrombogenicity. Thus, how macrophages accumulate cholesterol and become foam cells has been the subject of intense investigation. It is generally believed that macrophages accumulate cholesterol only through scavenger receptor-mediated uptake of modified LDL. However, an alternative mechanism for macrophage foam cell formation that does not depend on LDL modification or macrophage receptors has been elucidated. By this alternative mechanism, macrophages show receptor-independent uptake of unmodified native LDL that is mediated by fluid-phase pinocytosis. In receptor-independent, fluid-phase pinocytosis, macrophages take up LDL as part of the fluid that they ingest during micropinocytosis within small vesicles called micropinosomes, and by macropinocytosis within larger vacuoles called macropinosomes. This produces cholesterol accumulation in macrophages to levels characteristic of macrophage foam cells in atherosclerotic plaques. Fluid-phase pinocytosis of LDL is a plausible mechanism that can explain how macrophages accumulate cholesterol and become disease-causing foam cells. Fluid-phase pinocytosis of LDL is a relevant pathway to target for modulating macrophage cholesterol accumulation in atherosclerosis. Recent studies show that phosphoinositide 3-kinase (PI3K), liver X receptors (LXRs), the macrophage colony-stimulating factor (M-CSF) receptor, and protein kinase C (PKC) mediate macrophage macropinocytosis of LDL, and thus, these may be relevant targets to inhibit macrophage cholesterol accumulation in atherosclerosis.
C1 NHLBI, Sect Expt Atherosclerosis, NIH, Bethesda, MD 20892 USA.
RP Kruth, HS (reprint author), NHLBI, Sect Expt Atherosclerosis, NIH, Bldg 10,Room 5N-113,10 Ctr Dr MSC 1422, Bethesda, MD 20892 USA.
EM kruthh@nhlbi.nih.gov
FU Intramural Research Program, National Heart, Lung, and Blood Institute,
National Institutes of Health
FX This work was supported by the Intramural Research Program, National
Heart, Lung, and Blood Institute, National Institutes of Health.
NR 69
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Z9 10
U1 0
U2 10
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD OCT
PY 2013
VL 19
IS 33
BP 5865
EP 5872
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 214MA
UT WOS:000324136300005
PM 23438954
ER
PT J
AU Bakhsheshian, J
Hall, MD
Robey, RW
Herrmann, MA
Chen, JQ
Bates, SE
Gottesman, MM
AF Bakhsheshian, Joshua
Hall, Matthew D.
Robey, Robert W.
Herrmann, Michelle A.
Chen, Jin-Qiu
Bates, Susan E.
Gottesman, Michael M.
TI Overlapping Substrate and Inhibitor Specificity of Human and Murine
ABCG2
SO DRUG METABOLISM AND DISPOSITION
LA English
DT Article
ID BREAST-CANCER RESISTANCE; COLON-CARCINOMA CELLS; P-GLYCOPROTEIN;
MULTIDRUG-RESISTANCE; IN-VIVO; PHOTODYNAMIC THERAPY; HALF-TRANSPORTER;
DRUG-RESISTANCE; FUMITREMORGIN-C; CYCLOSPORINE-A
AB ABCG2 (also known as breast cancer resistance protein) is an ATP-binding cassette (ABC) transporter localized to the plasma membrane where it mediates the efflux of xenobiotics, including potential therapeutics. Studies investigating Abcg2 function at the blood-brain barrier in mouse models are often compared with human ABCG2 function. It is critical to understand the nature of species differences between mouse and human ABCG2, since extrapolations are made from murine data to humans. Two independent drug-selected cell line pairs expressing human or mouse ABCG2 were compared for efflux of fluorescent substrates using flow cytometry. To this end, we developed and characterized a new mouse Abcg2-expressing subline that demonstrated efflux of known fluorescent ABCG2 substrates and increased resistance to mitoxantrone, which is reduced in the presence of the ABCG2 inhibitor Ko143. Our results indicate that the substrate specificity of human and mouse ABCG2 is very similar. We identified a new human and mouse ABCG2 substrate, a porphyrin analog, purpurin18 (Pp-18), which is not a substrate for P-glycoprotein or multidrug resistance protein 1. The ability of inhibitors to block efflux activity of ABCG2 was assessed using Pp-18. Inhibitors also demonstrated similar effects on human and mouse ABCG2. Chrysin, benzoflavone, and cyclosporin A inhibited Pp-18 efflux in both human and mouse ABCG2. The similarity of the substrate and inhibitor specificity of human and mouse ABCG2 supports interpretation of mouse models in understanding the clinical, pharmacological, and physiologic roles of ABCG2.
C1 [Bakhsheshian, Joshua; Hall, Matthew D.; Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Robey, Robert W.; Bates, Susan E.] NCI, Canc Therapeut Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Herrmann, Michelle A.; Chen, Jin-Qiu] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, NIH, 37 Convent Dr,Rm 2108, Bethesda, MD 20892 USA.
EM mgottesman@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health
[National Cancer Institute]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health [National Cancer Institute]. J.B. is a
National Institutes of Health Medical Research Scholar. The authors
declare no conflicts of interest.
NR 53
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U1 1
U2 9
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0090-9556
J9 DRUG METAB DISPOS
JI Drug Metab. Dispos.
PD OCT
PY 2013
VL 41
IS 10
BP 1805
EP 1812
DI 10.1124/dmd.113.053140
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 219QK
UT WOS:000324523100013
PM 23868912
ER
PT J
AU Jenewein, J
Moergeli, H
Sprott, H
Honegger, D
Brunner, L
Ettlin, D
Grillon, C
Bloch, K
Brugger, M
Schwegler, K
Schumacher, S
Hasler, G
AF Jenewein, J.
Moergeli, H.
Sprott, H.
Honegger, D.
Brunner, L.
Ettlin, D.
Grillon, C.
Bloch, K.
Bruegger, M.
Schwegler, K.
Schumacher, S.
Hasler, G.
TI Fear-learning deficits in subjects with fibromyalgia syndrome?
SO EUROPEAN JOURNAL OF PAIN
LA English
DT Article
ID RHEUMATOID-ARTHRITIS; MUSCULOSKELETAL PAIN; ANXIETY; HUMANS; AVOIDANCE;
PREVALENCE; MECHANISMS; RESPONSES; DISORDER; AMYGDALA
AB Background Fibromyalgia syndrome (FMS) is frequently associated with psychiatric conditions, particularly anxiety. Deficits in contingency learning during fear conditioning have been hypothesized to increase anxiety and, consequently, pain sensation in susceptible individuals. The goal of this study was to examine the relationship between contingency learning and pain experience in subjects with FMS and rheumatoid arthritis (RA).
Methods Fourteen female FMS subjects, 14 age-matched female RA subjects and 14 age-matched female healthy controls (HCs) were included in a fear-conditioning experiment. The conditioned stimulus (CS) consisted of visual signs, the unconditioned stimulus (US) of thermal stimuli. CS- predicted low-temperature exposure (US), while CS+ was followed by low or high temperature.
Results In the FMS group, only 50% of the subjects were aware of the US-CS contingency, whereas 86% of the RA subjects and all of the HCs were aware of the contingency. CS+ induced more anxiety than CS- in RA subjects and HCs. As expected, low-temperature exposure was experienced as less painful after CS- than after CS+ in these subjects. FMS subjects did not show such adaptive conditioning. The effects of the type of CS on heart rate changes were significant in the HCs and the aware FMS subjects, but not in the unaware FMS subjects.
Conclusions Contingency learning deficits represent a potentially promising and specific, but largely unstudied, psychopathological factor in FMS. Deficits in contingency learning may increase anxiety and, consequently, pain sensation. These findings have the potential to contribute to the development of novel therapeutic approaches for FMS.
C1 [Jenewein, J.; Moergeli, H.; Honegger, D.; Schumacher, S.; Hasler, G.] Univ Zurich Hosp, Dept Psychiat & Psychotherapy, CH-8091 Zurich, Switzerland.
[Jenewein, J.; Sprott, H.; Brunner, L.] Univ Zurich Hosp, Dept Rheumatol, CH-8091 Zurich, Switzerland.
[Jenewein, J.; Sprott, H.; Brunner, L.] Univ Zurich Hosp, Inst Med Phys, CH-8091 Zurich, Switzerland.
[Ettlin, D.] Univ Zurich, Clin Dent, Zurich, Switzerland.
[Grillon, C.] NIMH, Mood & Anxiety Disorders Program, Intramural Res Program, Bethesda, MD 20892 USA.
[Bloch, K.] Univ Zurich Hosp, Dept Pneumol, CH-8091 Zurich, Switzerland.
[Bruegger, M.] Univ Zurich, Inst Neuropsychol, Zurich, Switzerland.
[Schwegler, K.] Univ Basel, Div Cognit Neurosci, Basel, Switzerland.
[Hasler, G.] Univ Bern, Psychiat Univ Hosp, Bern, Switzerland.
RP Jenewein, J (reprint author), Univ Zurich Hosp, Dept Psychiat & Psychotherapy, CH-8091 Zurich, Switzerland.
EM josef.jenewein@usz.ch
RI Hasler, Gregor/E-4845-2012; Ettlin, Dominik/D-2808-2016;
OI Hasler, Gregor/0000-0002-8311-0138; /0000-0001-7353-073X; Jenewein,
Josef/0000-0003-4271-918X
FU Hermann Klaus Foundation, Zurich, Switzerland; Werner Alfred Selo
Foundation, Zurich, Switzerland; Kurt and Senta Herrmann Foundation,
Zurich, Switzerland
FX This work was supported by the Hermann Klaus Foundation, Zurich,
Switzerland; Werner Alfred Selo Foundation, Zurich, Switzerland; and the
Kurt and Senta Herrmann Foundation, Zurich, Switzerland.
NR 50
TC 9
Z9 9
U1 3
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1090-3801
J9 EUR J PAIN
JI Eur. J. Pain
PD OCT
PY 2013
VL 17
IS 9
BP 1374
EP 1384
DI 10.1002/j.1532-2149.2013.00300.x
PG 11
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 211SM
UT WOS:000323930700014
PM 23468076
ER
PT J
AU Costa-Guda, J
Soong, CP
Parekh, VI
Agarwal, SK
Arnold, A
AF Costa-Guda, Jessica
Soong, Chen-Pang
Parekh, Vaishali I.
Agarwal, Sunita K.
Arnold, Andrew
TI Germline and Somatic Mutations in Cyclin-Dependent Kinase Inhibitor
Genes CDKN1A, CDKN2B, and CDKN2C in Sporadic Parathyroid Adenomas
SO HORMONES & CANCER
LA English
DT Article
ID MULTIPLE ENDOCRINE NEOPLASIA; TUMOR-SUPPRESSOR; LINE MUTATIONS; GROWTH;
HYPERPARATHYROIDISM; CANDIDATE; CANCER; P21
AB The molecular pathogenesis of sporadic parathyroid adenomas is incompletely understood. The possible role of cyclin-dependent kinase inhibitor (CDKI) genes was raised by recognition of cyclin D1 as a parathyroid oncogene, identification of rare germline mutations in CDKI genes in patients with multiple endocrine neoplasia type 1; that in rodents, mutation in Cdkn1b caused parathyroid tumors; and subsequently through identification of rare predisposing germline sequence variants and somatic mutation of CDKN1B, encoding p27(kip1), in sporadic human parathyroid adenoma. We therefore sought to determine whether mutations/variants in the other six CDKI genes CDKN1A, CDKN1C, CDKN2A, CDKN2B, CDKN2C, and CDKN2D, encoding p21, p57, p14(ARF)/p16, p15, p18, and p19, respectively, contribute to the development of typical parathyroid adenomas. In a series of 85 sporadic parathyroid adenomas, direct DNA sequencing identified alterations in five adenomas (6 %): Two contained distinct heterozygous changes in CDKN1A, one germline and one of undetermined germline status; one had a CDKN2B germline alteration, accompanied by loss of the normal allele in the tumor (LOH); two had variants of CDKN2C, one somatic and one germline with LOH. Abnormalities of three of the mutant proteins were readily demonstrable in vitro. Thus, germline mutations/rare variants in CDKN1A, CDKN2B, and CDKN2C likely contribute to the development of a significant subgroup of common sporadic parathyroid adenomas, and somatic mutation in CDKN2C further suggests a direct role for CDKI alteration in conferring a selective growth advantage to parathyroid cells, providing novel support for the concept that multiple CDKIs can play primary roles in human neoplasia.
C1 [Costa-Guda, Jessica; Soong, Chen-Pang; Arnold, Andrew] Univ Connecticut, Sch Med, Ctr Mol Med, Farmington, CT 06030 USA.
[Costa-Guda, Jessica; Soong, Chen-Pang; Arnold, Andrew] Univ Connecticut, Sch Med, Div Endocrinol & Metab, Farmington, CT 06030 USA.
[Parekh, Vaishali I.; Agarwal, Sunita K.] NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Arnold, A (reprint author), Univ Connecticut, Sch Med, Ctr Mol Med, 263 Farmington Ave, Farmington, CT 06030 USA.
EM molecularmedicine@uchc.edu
RI Agarwal, Sunita/D-1428-2016
OI Agarwal, Sunita/0000-0002-7557-3191
FU National Institutes of Health [DHHS/NIDCR 5 T32-DE07302, 1
F32-DE021307]; Intramural Research Program of the National Institutes of
Health, National Institute of Diabetes and Digestive and Kidney Diseases
[1ZIADK075035-03]; Murray-Heilig Fund in Molecular Medicine
FX We wish to thank Ms. Kristin Corrado for expert technical assistance.
This work was supported in part by grants DHHS/NIDCR 5 T32-DE07302 and 1
F32-DE021307 (to J.C.G.) from the National Institutes of Health; the
Intramural Research Program of the National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases (SKA;
Project number: 1ZIADK075035-03); and by the Murray-Heilig Fund in
Molecular Medicine.
NR 28
TC 13
Z9 15
U1 2
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1868-8497
J9 HORM CANCER-US
JI Horm. Cancer
PD OCT
PY 2013
VL 4
IS 5
BP 301
EP 307
DI 10.1007/s12672-013-0147-9
PG 7
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA 213OF
UT WOS:000324066400005
PM 23715670
ER
PT J
AU Boland, JF
Chung, CC
Roberson, D
Mitchell, J
Zhang, XJ
Im, KM
He, J
Chanock, SJ
Yeager, M
Dean, M
AF Boland, Joseph F.
Chung, Charles C.
Roberson, David
Mitchell, Jason
Zhang, Xijun
Im, Kate M.
He, Ji
Chanock, Stephen J.
Yeager, Meredith
Dean, Michael
TI The new sequencer on the block: comparison of Life Technology's Proton
sequencer to an Illumina HiSeq for whole-exome sequencing
SO HUMAN GENETICS
LA English
DT Article
ID HUMAN GENOME; FREQUENT MUTATIONS; CELL CARCINOMA; ION TORRENT; DNA;
DISEASE; IDENTIFICATION; STRATEGIES; PLATFORMS; FRAMEWORK
AB We assessed the performance of the new Life Technologies Proton sequencer by comparing whole-exome sequence data in a Centre d'Etude du Polymorphisme Humain trio (family 1463) to the Illumina HiSeq instrument. To simulate a typical user's results, we utilized the standard capture, alignment and variant calling methods specific to each platform. We restricted data analysis to include the capture region common to both methods. The Proton produced high quality data at a comparable average depth and read length, and the Ion Reporter variant caller identified 96 % of single nucleotide polymorphisms (SNPs) detected by the HiSeq and GATK pipeline. However, only 40 % of small insertion and deletion variants (indels) were identified by both methods. Usage of the trio structure and segregation of platform-specific alleles supported this result. Further comparison of the trio data with Complete Genomics sequence data and Illumina SNP microarray genotypes documented high concordance and accurate SNP genotyping of both Proton and Illumina platforms. However, our study underscored the problem of accurate detection of indels for both the Proton and HiSeq platforms.
C1 [Boland, Joseph F.; Chung, Charles C.; Roberson, David; Mitchell, Jason; Zhang, Xijun; He, Ji; Chanock, Stephen J.; Yeager, Meredith] NCI, Canc Genom Res Lab, Div Canc Epidemiol & Genet, NIH,DHHS, Gaithersburg, MD 20877 USA.
[Boland, Joseph F.; Chung, Charles C.; Roberson, David; Mitchell, Jason; Zhang, Xijun; He, Ji; Yeager, Meredith] SAIC Frederick Inc, Frederick Natl Lab Canc Res, Gaithersburg, MD USA.
[Im, Kate M.; Dean, Michael] NCI, Expt Immunol Lab, Ctr Canc Res, NIH,DHHS, Frederick, MD 21702 USA.
RP Dean, M (reprint author), NCI, Expt Immunol Lab, Ctr Canc Res, NIH,DHHS, Frederick, MD 21702 USA.
EM bolandj2@mail.nih.gov; deanm@mail.nih.gov
RI Dean, Michael/G-8172-2012
OI Dean, Michael/0000-0003-2234-0631
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Intramural Research Program of the Division of
Cancer Epidemiology and Genetics; Center for Cancer Research, National
Cancer Institute, NIH, DHHS, Bethesda, MD, USA
FX This research has been funded in whole or in part with federal funds
from the National Cancer Institute, National Institutes of Health, under
Contract No. HHSN261200800001E and supported in part by the Intramural
Research Program of the Division of Cancer Epidemiology and Genetics and
the Center for Cancer Research, National Cancer Institute, NIH, DHHS,
Bethesda, MD, USA. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services or does mention of trade names, commercial products, or
organizations imply endorsement by the U.S. Government.
NR 30
TC 39
Z9 42
U1 1
U2 55
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 2013
VL 132
IS 10
BP 1153
EP 1163
DI 10.1007/s00439-013-1321-4
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 216ZA
UT WOS:000324324500004
PM 23757002
ER
PT J
AU Gertz, EM
Schaffer, AA
Agarwala, R
Bonnet-Garnier, A
Rogel-Gaillard, C
Hayes, H
Mage, RG
AF Gertz, E. Michael
Schaeffer, Alejandro A.
Agarwala, Richa
Bonnet-Garnier, Amelie
Rogel-Gaillard, Claire
Hayes, Helene
Mage, Rose G.
TI Accuracy and coverage assessment of Oryctolagus cuniculus (rabbit) genes
encoding immunoglobulins in the whole genome sequence assembly
(OryCun2.0) and localization of the IGH locus to chromosome 20
SO IMMUNOGENETICS
LA English
DT Article
DE Rabbit; Immunoglobulin genes; Heavy chains; Fluorescence in situ
hybridization; Chromosome 20; Light chains
ID HEAVY-CHAIN LOCUS; SPLENIC GERMINAL-CENTERS; ZEALAND WHITE-RABBITS;
ANTIBODY REPERTOIRE; V-H; CYTOGENETIC MAP; BASILEA RABBITS;
MESSENGER-RNA; B-CELLS; REGION
AB We report on the analyses of genes encoding immunoglobulin heavy and light chains in the rabbit 6.51x whole genome assembly. This OryCun2.0 assembly confirms previous mapping of the duplicated IGK1 and IGK2 loci to chromosome 2 and the IGL lambda light chain locus to chromosome 21. The most frequently rearranged and expressed IGHV1 that is closest to IG DH and IGHJ genes encodes rabbit VHa allotypes. The partially inbred Thorbecke strain rabbit used for whole-genome sequencing was homozygous at the IGK but heterozygous with the IGHV1a1 allele in one of 79 IGHV-containing unplaced scaffolds and IGHV1a2, IGHM, IGHG, and IGHE sequences in another. Some IGKV, IGLV, and IGHA genes are also in other unplaced scaffolds. By fluorescence in situ hybridization, we assigned the previously unmapped IGH locus to the q-telomeric region of rabbit chromosome 20. An approximately 3-Mb segment of human chromosome 14 including IGH genes predicted to map to this telomeric region based on synteny analysis could not be located on assembled chromosome 20. Unplaced scaffold chrUn0053 contains some of the genes that comparative mapping predicts to be missing. We identified discrepancies between previous targeted studies and the OryCun2.0 assembly and some new BAC clones with IGH sequences that can guide other studies to further sequence and improve the OryCun2.0 assembly. Complete knowledge of gene sequences encoding variable regions of rabbit heavy, kappa, and lambda chains will lead to better understanding of how and why rabbits produce antibodies of high specificity and affinity through gene conversion and somatic hypermutation.
C1 [Gertz, E. Michael; Schaeffer, Alejandro A.; Agarwala, Richa] NIH, Natl Ctr Biotechnol Informat, NLM, Bethesda, MD 20894 USA.
[Bonnet-Garnier, Amelie] INRA, Biol Dev & Reprod UMR1198, F-78352 Jouy En Josas, France.
[Bonnet-Garnier, Amelie] ENVA, F-94704 Maisons Alfort, France.
[Rogel-Gaillard, Claire; Hayes, Helene] INRA, UMR Genet Anim & Biol Integrat 1313, F-78352 Jouy En Josas, France.
[Mage, Rose G.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Mage, RG (reprint author), NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
EM rm3z@nih.gov
OI Gertz, E. Michael/0000-0001-8390-4387; Bonnet-Garnier,
Amelie/0000-0002-2095-3365
FU NIH; NIAID; NLM; Animal Genetics and Animal Physiology Divisions of INRA
FX This research was supported by the Intramural Research Programs of the
NIH, NIAID, and NLM and by the Animal Genetics and Animal Physiology
Divisions of INRA. We thank Dr. Josef Platzer, Roche Diagnostics,
Penzberg, Germany for the gift of the 27 N5 BAC; Dr. Jessica Alfoldi of
the Broad Institute for rabbit RNASeq data; Drs. Christoph Rader, Nancy
McCartney-Francis, and Michael Mage for suggestions to improve the
manuscript; and Daniel Schaffer for assistance with the figures.
NR 64
TC 6
Z9 6
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0093-7711
J9 IMMUNOGENETICS
JI Immunogenetics
PD OCT
PY 2013
VL 65
IS 10
BP 749
EP 762
DI 10.1007/s00251-013-0722-9
PG 14
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 217UC
UT WOS:000324386100005
PM 23925440
ER
PT J
AU Zafrani, L
Ince, C
Yuen, PST
AF Zafrani, Lara
Ince, Can
Yuen, Peter S. T.
TI Microparticles during sepsis: target, canary or cure?
SO INTENSIVE CARE MEDICINE
LA English
DT Editorial Material
ID ENDOTHELIAL MICROPARTICLES; ACTIVATION
C1 [Zafrani, Lara] St Louis Univ Hosp, Med Intens Care Unit, F-75010 Paris, France.
[Ince, Can] Univ Amsterdam, Acad Med Ctr, Dept Translat Physiol, NL-1105 AZ Amsterdam, Netherlands.
[Yuen, Peter S. T.] NIDDK, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD USA.
RP Zafrani, L (reprint author), St Louis Univ Hosp, Med Intens Care Unit, 1 Ave Claude Vellefaux, F-75010 Paris, France.
EM lara.zafrani@sls.aphp.fr
RI Yuen, Peter/B-1954-2008
OI Yuen, Peter/0000-0001-9557-3909
FU Intramural NIH HHS
NR 13
TC 2
Z9 2
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0342-4642
J9 INTENS CARE MED
JI Intensive Care Med.
PD OCT
PY 2013
VL 39
IS 10
BP 1854
EP 1856
DI 10.1007/s00134-013-3047-0
PG 3
WC Critical Care Medicine
SC General & Internal Medicine
GA 215TK
UT WOS:000324233200027
PM 23925546
ER
PT J
AU Kohut, SJ
Fivel, PA
Blough, BE
Rothman, RB
Mello, NK
AF Kohut, Stephen J.
Fivel, Peter A.
Blough, Bruce E.
Rothman, Richard B.
Mello, Nancy K.
TI Effects of methcathinone and 3-Cl-methcathinone (PAL-434) in cocaine
discrimination or self-administration in rhesus monkeys
SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Cocaine; discrimination; dopamine; self-administration; serotonin
ID CHRONIC D-AMPHETAMINE; DOPAMINE TRANSPORTER OCCUPANCY; CHRONIC BUSPIRONE
TREATMENT; MONOAMINE RELEASERS; REINFORCING STRENGTH; VARYING
SELECTIVITY; UPTAKE INHIBITORS; DRUG-THERAPY; ABUSE; SEROTONIN
AB Monoamine releasers with varying selectivity for dopamine (DA)/norepinephrine and serotonin (5-HT) release are potential treatment medications for cocaine abuse. Although DA-selective monoamine releasers effectively reduce cocaine abuse, their clinical usefulness is limited by abuse liability. It is hypothesized that increasing 5-HT neurotransmission may reduce the abuse-related effects of DA releasers, but the optimal DA: 5-HT release ratio remains to be determined. This study in rhesus monkeys compared the effects of two compounds with differing potency for 5-HT release. Methcathinone and 3-Cl-methcathinone (PAL-434) have equal potency for DA release, but PAL-434 has 10-fold higher potency for 5-HT release. In drug discrimination studies, monkeys were trained to discriminate cocaine (0.4 mg/kg i.m.) from saline in a two-key, food-reinforced procedure. In drug self-administration studies, a separate group of monkeys was trained to respond for cocaine [0.01 mg/kg/injection (inj)] and food (1 g pellets) under a second order schedule of reinforcement [FR2(VR16:S)]. When responding was stable, methcathinone (0.1-0.56 mg/kg. h i.v.) or PAL-434 (0.32-1.8 mg/kg. h i.v.) was administered chronically (one injection every 20 min for 23 h/d) for 7-10 d. In discrimination studies, both compounds dose-dependently increased cocaine-like responding but with different potencies (cocaine=methcathinone>PAL-434). Chronic treatment with methcathinone or PAL-434 dose-dependently and selectively reduced cocaine self-administration. PAL-434 was about 4-fold and methcathinone about 1.6-fold more potent at decreasing cocaine-over food-maintained responding. These data suggest that compounds with moderate selectivity for DA vs. 5-HT release (8-15-fold) may be effective for the treatment of cocaine dependence.
C1 [Kohut, Stephen J.; Fivel, Peter A.; Mello, Nancy K.] Harvard Univ, Sch Med, McLean Hosp, Alcohol & Drug Abuse Res Ctr, Belmont, MA 02478 USA.
[Blough, Bruce E.] Res Triangle Inst, Res Triangle Pk, NC 27709 USA.
[Rothman, Richard B.] NIDA, IRP, OD, NIH, Baltimore, MD USA.
RP Kohut, SJ (reprint author), Harvard Univ, Sch Med, McLean Hosp, Alcohol & Drug Abuse Res Ctr, 115 Mill St, Belmont, MA 02478 USA.
EM skohut@mclean.harvard.edu
FU National Institute on Drug Abuse, National Institute of Health
[R01-DA002519, R01-DA012970]; Intramural Research Program of the
National Institute of Health, National Institute on Drug Abuse
FX N.K.M. was supported by grant number R01-DA002519 and B. E. B.
R01-DA012970 from the National Institute on Drug Abuse, National
Institute of Health. This research was supported in part by the
Intramural Research Program of the National Institute of Health,
National Institute on Drug Abuse. We thank Sherilyn Pappal, George
Anderson, Meredith Mahnke and Olga Smirnova for excellent technical
assistance.
NR 57
TC 6
Z9 6
U1 1
U2 5
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1461-1457
J9 INT J NEUROPSYCHOPH
JI Int. J. Neuropsychopharmacol.
PD OCT
PY 2013
VL 16
IS 9
BP 1985
EP 1998
DI 10.1017/S146114571300059X
PG 14
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 213AT
UT WOS:000324026000007
PM 23768644
ER
PT J
AU Savitz, J
Hodgkinson, CA
Martin-Soelch, C
Shen, PH
Szczepanik, J
Nugent, AC
Herscovitch, P
Grace, AA
Goldman, D
Drevets, WC
AF Savitz, Jonathan '
Hodgkinson, Colin A.
Martin-Soelch, Chantal
Shen, Pei-Hong
Szczepanik, Joanna
Nugent, Allison C.
Herscovitch, Peter
Grace, Anthony A.
Goldman, David
Drevets, Wayne C.
TI DRD2/ANKK1 Taq1A polymorphism (rs1800497) has opposing effects on D-2/3
receptor binding in healthy controls and patients with major depressive
disorder
SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Depression; dopamine 2 receptor; positron emission tomography; reward;
Taq1A
ID AVAILABILITY IN-VIVO; A1 ALLELE; C957T POLYMORPHISM; DRD2 GENE;
DOPAMINE; VOLUNTEERS; STRIATUM; STRESS; SYSTEM; BRAIN
AB The A1 allele of the DRD2/ANKK1 Taq1A polymorphism (rs1800497) is associated with reduced striatal D-2/3 receptor binding in healthy individuals (Con) as well as depression and addiction. However, the effect of rs1800497 on D-2/3 receptor binding in depressed patients as well as the SNP's effect on D-2/3 binding during reward-associated dopamine release is unknown. Twelve unmedicated patients with major depressive disorder (MDD) and 24 Con completed PET scans with [C-11]raclopride, once without receiving monetary rewards (baseline) and once while winning money. In Con, the A1 allele was associated with reduced baseline binding potential (BPND) in the middle caudate and ventral striatum. However, in MDD patients the A1 allele was associated with increased baseline BPND in these regions. There were no significant associations between rs1800497 and change in BPND during reward-associated dopamine release. Conceivably, the A1 allele predisposes to depression and addiction via its effect on the post-synaptic D-2 receptor.
C1 [Savitz, Jonathan '; Drevets, Wayne C.] Laureate Inst Brain Res, Tulsa, OK 74136 USA.
[Savitz, Jonathan '] Univ Tulsa, Fac Community Med, Tulsa, OK 74104 USA.
[Savitz, Jonathan '; Szczepanik, Joanna; Drevets, Wayne C.] NIMH, Sect Neuroimaging Mood & Anxiety Disorders, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA.
[Hodgkinson, Colin A.; Shen, Pei-Hong; Goldman, David] NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA.
[Martin-Soelch, Chantal] Univ Zurich Hosp, Dept Psychiat & Psychotherapy, Zurich, Switzerland.
[Nugent, Allison C.] NIMH, NIH, Bethesda, MD 20892 USA.
[Herscovitch, Peter] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Grace, Anthony A.] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA.
[Grace, Anthony A.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Grace, Anthony A.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
[Drevets, Wayne C.] Johnson & Johnson Pharmaceut Res & Dev, Titusville, NJ USA.
RP Savitz, J (reprint author), Laureate Inst Brain Res, 6655 S Yale Ave, Tulsa, OK 74136 USA.
EM jonathansavitz@hotmail.com
RI Savitz, Jonathan/C-3088-2009; Goldman, David/F-9772-2010;
OI Savitz, Jonathan/0000-0001-8143-182X; Goldman,
David/0000-0002-1724-5405; Grace, Anthony/0000-0003-1864-5504
FU NIH/Division of Intramural Research Program for the NIMH; NIH/Division
of Intramural Research Program for the NIAAA; William K. Warren
Foundation
FX This study was funded by the NIH/Division of Intramural Research
Programs for the NIMH and the NIAAA. Drs Savitz and Drevets also
received support from The William K. Warren Foundation. The Foundation
played no role in the writing of the manuscript or in the decision to
publish. We thank Jerry Jacobs and staff at the NIH Clinical Center PET
Department for their support. We also thank Michele Drevets and Joan
Collins, as well as the staff at 5SW for their clinical support.
Finally, we acknowledge all those individuals who volunteered to take
part in our studies.
NR 40
TC 12
Z9 12
U1 1
U2 13
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1461-1457
J9 INT J NEUROPSYCHOPH
JI Int. J. Neuropsychopharmacol.
PD OCT
PY 2013
VL 16
IS 9
BP 2095
EP 2101
DI 10.1017/S146114571300045X
PG 7
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 213AT
UT WOS:000324026000015
PM 23683269
ER
PT J
AU Diaz-Padilla, I
Hirte, H
Oza, AM
Clarke, BA
Cohen, B
Reedjik, M
Zhang, T
Kamel-Reid, S
Ivy, SP
Hotte, SJ
Razak, AAR
Chen, EX
Brana, I
Wizemann, M
Wang, LS
Siu, LL
Bedard, PL
AF Diaz-Padilla, Ivan
Hirte, Hal
Oza, Amit M.
Clarke, Blaise A.
Cohen, Brenda
Reedjik, Michael
Zhang, Tong
Kamel-Reid, Suzanne
Ivy, S. Percy
Hotte, Sebastien J.
Razak, Albiruni A. R.
Chen, Eric X.
Brana, Irene
Wizemann, Monika
Wang, Lisa
Siu, Lillian L.
Bedard, Philippe L.
TI A phase Ib combination study of RO4929097, a gamma-secretase inhibitor,
and temsirolimus in patients with advanced solid tumors
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE RO4929097; Temsirolimus; Clinical trial; Notch; Gamma-secretase
inhibitor
ID BREAST-CANCER; NOTCH1; POOR; JAG1
AB Background To determine the recommended phase II dose (RP2D) and assess the safety, pharmacokinetics (PKs) and pharmacodynamics of RO4929097in combination with temsirolimus. Methods Escalating doses of RO4929097 and temsirolimus were administered at three dose levels. Patients received once daily oral RO4929097 on a 3 days on/4 days off schedule every week, and weekly intravenous temsirolimus. Blood samples were collected for PK analysis. Archival tissue specimens were collected for Notch pathway biomarker analysis and genotyping of frequent oncogenic mutations. Results Seventeen patients with refractory advanced solid tumors were enrolled in three dose levels (DLs): DL1 (RO4929097 10 mg; Temsirolimus 25 mg), DL2 (RO4929097 20 mg; Temsirolimus 25 mg), and DL3 (RO4929097 20 mg; Temsirolimus 37.5 mg). The most common toxicities related to the study drug combination included: fatigue (82 %; grade 3 6 %), mucositis, (71 %; grade 3 6 %), neutropenia (59 %; grade 3 12 %), anemia (59 %; grade 3 0 %), and hypertriglyceridemia (59 %; grade 3 0 %). Two dose-limiting toxicities, grade 3 rash and grade 3 mucositis, were observed in the same patient in the first dose level prompting dose expansion. Eleven patients (73 %) had stable disease as their best response. Co-administration of RO4929097 was associated with increased clearance and reduced exposure to temsirolimus, suggestive of drug-drug interaction via CYP3A4 induction. No correlation between the expression of Notch pathway biomarkers or genotype and time to progression was noted. Conclusions RO4929097 can be safely combined with temsirolimus in patients with advanced solid tumors. The RP2D was established at 20 mg of RO4929097 combined with 37.5 mg of temsirolimus.
C1 [Diaz-Padilla, Ivan; Oza, Amit M.; Razak, Albiruni A. R.; Chen, Eric X.; Brana, Irene; Wizemann, Monika; Wang, Lisa; Siu, Lillian L.; Bedard, Philippe L.] Univ Toronto, Dept Med, Princess Margaret Canc Ctr, Div Med Oncol & Hematol, Toronto, ON M5G 2M9, Canada.
[Hirte, Hal; Hotte, Sebastien J.] JuravinskiCanc Ctr, Hamilton, ON, Canada.
[Clarke, Blaise A.] Univ Toronto, Dept Lab Med, Toronto, ON M5G 2M9, Canada.
[Cohen, Brenda; Reedjik, Michael] Univ Hlth Network, Princess Margaret Canc Ctr, Dept Surg Oncol, Toronto, ON, Canada.
[Zhang, Tong; Kamel-Reid, Suzanne] Univ Hlth Network, Ontario Canc Inst, Dept Cellular & Mol Biol, Toronto, ON, Canada.
[Ivy, S. Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Bedard, PL (reprint author), Univ Toronto, Dept Med, Princess Margaret Canc Ctr, Div Med Oncol & Hematol, 610 Univ Ave,5-125, Toronto, ON M5G 2M9, Canada.
EM philippe.bedard@uhn.ca
FU US National Cancer Institute [PJC-005/NCI-8500, U01-CA132123]
FX This study (PJC-005/NCI-8500) is conducted by the Princess Margaret
Hospital Phase I Consortium with support from the US National Cancer
Institute U01 Cooperative Agreement Award (U01-CA132123).
NR 18
TC 22
Z9 22
U1 0
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD OCT
PY 2013
VL 31
IS 5
BP 1182
EP 1191
DI 10.1007/s10637-013-0001-5
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 216HF
UT WOS:000324272100010
PM 23860641
ER
PT J
AU Hallett, V
Lecavalier, L
Sukhodolsky, DG
Cipriano, N
Aman, MG
McCracken, JT
McDougle, CJ
Tierney, E
King, BH
Hollander, E
Sikich, L
Bregman, J
Anagnostou, E
Donnelly, C
Katsovich, L
Dukes, K
Vitiello, B
Gadow, K
Scahill, L
AF Hallett, Victoria
Lecavalier, Luc
Sukhodolsky, Denis G.
Cipriano, Noreen
Aman, Michael G.
McCracken, James T.
McDougle, Christopher J.
Tierney, Elaine
King, Bryan H.
Hollander, Eric
Sikich, Linmarie
Bregman, Joel
Anagnostou, Evdokia
Donnelly, Craig
Katsovich, Lily
Dukes, Kimberly
Vitiello, Benedetto
Gadow, Kenneth
Scahill, Lawrence
TI Exploring the Manifestations of Anxiety in Children with Autism Spectrum
Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorders; Anxiety; Measurement; Clinical Trials
ID PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST;
OBSESSIVE-COMPULSIVE SCALE; YOUNG-PEOPLE; SYMPTOMS; VALIDITY;
RELIABILITY; RISPERIDONE; ADOLESCENTS; COMMUNITY
AB This study explores the manifestation and measurement of anxiety symptoms in 415 children with ASDs on a 20-item, parent-rated, DSM-IV referenced anxiety scale. In both high and low-functioning children (IQ above vs. below 70), commonly endorsed items assessed restlessness, tension and sleep difficulties. Items requiring verbal expression of worry by the child were rarely endorsed. Higher anxiety was associated with functional language, IQ above 70 and higher scores on several other behavioral measures. Four underlying factors emerged: Generalized Anxiety, Separation Anxiety, Social Anxiety and Over-arousal. Our findings extend our understanding of anxiety across IQ in ASD and provide guidance for improving anxiety outcome measurement.
C1 [Hallett, Victoria; Sukhodolsky, Denis G.; Cipriano, Noreen; Katsovich, Lily; Scahill, Lawrence] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[Hallett, Victoria; Sukhodolsky, Denis G.; Cipriano, Noreen; Katsovich, Lily; Scahill, Lawrence] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
[Lecavalier, Luc; Aman, Michael G.] Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA.
[McCracken, James T.] Univ Calif Los Angeles, Sch Med, Div Child & Adolescent Psychiat, Semel Inst Neurosci, Los Angeles, CA USA.
[McDougle, Christopher J.] Massachusetts Gen Hosp Children, Lurie Ctr Autism, Boston, MA USA.
[McDougle, Christopher J.] Harvard Univ, Sch Med, Boston, MA USA.
[Tierney, Elaine] Kennedy Krieger Inst, Dept Psychiat, Baltimore, MD USA.
[King, Bryan H.] Univ Washington, Dept Psychiat, Seattle Childrens Hosp, Seattle, WA 98195 USA.
[Hollander, Eric] Albert Einstein Coll Med, Montefiore Med Ctr, New York, NY USA.
[Sikich, Linmarie] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
[Bregman, Joel] Ctr Autism, Philadelphia, PA USA.
[Anagnostou, Evdokia] Univ Toronto, Dept Pediat, Bloorview Res Inst, Toronto, ON, Canada.
[Donnelly, Craig] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Psychiat, Hanover, NH 03756 USA.
[Dukes, Kimberly] DM STAT Inc, Malden, MA USA.
[Dukes, Kimberly] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
[Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
[Gadow, Kenneth] SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
RP Scahill, L (reprint author), Emory Univ, Marcus Autism Ctr, 1920 Briarcliff Rd, Atlanta, GA 30329 USA.
EM lawrence.scahill@emory.edu
OI Scahill, Lawrence/0000-0001-5073-1707; Sukhodolsky,
Denis/0000-0002-5401-792X
FU NCATS NIH HHS [UL1 TR001108]; NCRR NIH HHS [UL1 RR024139, UL1 RR025755,
UL1 RR025761, UL1RR024139]; NICHD NIH HHS [U01 HD045023, U01-HD045023];
NIDA NIH HHS [N01MH80011]; NIMH NIH HHS [U54-MH066398, N01MH70001,
N01MH70009, N01MH70010, N01MH80011, U01 MH070009, U01 MH070010, U10
MH066764, U10 MH066766, U10 MH066768, U10MH66764, U10MH66766,
U10MH66768, U54 MH066398, U54 MH066418, U54 MH066494, U54 MH066673, U54
MH068172, U54-MH066418, U54-MH066494, U54-MH066673, U54-MH068172]
NR 41
TC 31
Z9 31
U1 1
U2 45
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2013
VL 43
IS 10
BP 2341
EP 2352
DI 10.1007/s10803-013-1775-1
PG 12
WC Psychology, Developmental
SC Psychology
GA 217FD
UT WOS:000324341500010
PM 23400347
ER
PT J
AU Orom, H
Kiviniemi, MT
Shavers, VL
Ross, L
Underwood, W
AF Orom, Heather
Kiviniemi, Marc T.
Shavers, Vickie L.
Ross, Levi
Underwood, Willie, III
TI Perceived risk for breast cancer and its relationship to mammography in
Blacks, Hispanics, and Whites
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Race; Hispanic; African American; Mammography; Breast neoplasms;
Perceived risk
ID HEALTH BELIEF MODEL; AFRICAN-AMERICAN WOMEN; ETHNIC-DIFFERENCES;
SUSCEPTIBILITY; PERCEPTIONS; GUIDELINES; BEHAVIORS; KNOWLEDGE; CONTEXT;
INCOME
AB A challenge for health behavior science is to develop theory and best practices that take cultural diversity into account. Using data from Black, Hispanic, and White respondents to the 2003 Health Information National Trends Survey, we examined racial/ethnic differences in: (1) breast cancer risk perceptions/worry; (2) the associations between perceived risk/worry and ever having received a mammogram; and (3) perceived risk/worry and having had at least 2 mammograms over a 4-year period (consecutive mammography). Compared to White race/ethnicity, Black race/ethnicity was associated with lower perceived absolute risk and comparative risk for developing cancer. For the sample as a whole, higher perceived risk (both absolute risk and comparative risk) and worry predicted greater odds of mammography use; however, this was not true for Hispanics. In stratified analyses, perceived risk and worry were not associated with mammography use for either Hispanics or Blacks whereas they were for Whites; however, this interaction effect was significant only for Hispanics vs. Whites. Results support the need for formative research to identify determinants of health behavior prior to cancer prevention message planning for diverse audiences in order to accommodate racial/ethnic differences not only in the level of perceived risk, but also the association between risk perception to behavior change in that community.
C1 [Orom, Heather; Kiviniemi, Marc T.] SUNY Buffalo, Dept Community Hlth & Hlth Behav, Buffalo, NY 14214 USA.
[Shavers, Vickie L.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Ross, Levi] Roswell Pk Canc Inst, Dept Hlth Dispar, Buffalo, NY 14263 USA.
[Underwood, Willie, III] Roswell Pk Canc Inst, Dept Urol, Buffalo, NY 14263 USA.
RP Orom, H (reprint author), SUNY Buffalo, Dept Community Hlth & Hlth Behav, 304 Kimball Tower,3435 Main St, Buffalo, NY 14214 USA.
EM horom@buffalo.edu
OI Ross, Levi/0000-0002-3833-0836
FU NCI NIH HHS [K01 CA148889, K07CA106225, K07 CA106225]
NR 49
TC 12
Z9 12
U1 1
U2 14
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
J9 J BEHAV MED
JI J. Behav. Med.
PD OCT
PY 2013
VL 36
IS 5
BP 466
EP 476
DI 10.1007/s10865-012-9443-z
PG 11
WC Psychology, Clinical
SC Psychology
GA 215YT
UT WOS:000324248000003
PM 22772713
ER
PT J
AU Stipelman, BA
Augustson, E
McNeel, T
AF Stipelman, Brooke A.
Augustson, Erik
McNeel, Timothy
TI The relationship among smoking, sleep, and chronic rheumatic conditions
commonly associated with pain in the national health interview survey
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Cigarette; Smoking; Sleep; Chronic pain; Population; Rheumatology
ID QUALITY-OF-LIFE; LOW-BACK-PAIN; CIGARETTE-SMOKING; MUSCULOSKELETAL PAIN;
GENERAL-POPULATION; FIBROMYALGIA SYNDROME; RISK-FACTOR; TOBACCO USE;
NICOTINE; ADOLESCENTS
AB Chronic rheumatic conditions are typically characterized by chronic pain and are uniquely associated with increased rates of cigarette smoking and poor sleep quality. However, no study has examined the possible additive or interactive effects of these two health behaviors in individuals diagnosed with a chronic rheumatic condition. The goal of this study is to examine the relationship between cigarette smoking and sleep in a population sample of individuals diagnosed with a chronic rheumatic condition and related functional impairment. Cross sectional survey data was obtained from the 2007 National Health Interview Survey. Individuals diagnosed with a chronic rheumatic condition were more likely to be a former or current smoker compared to non-diagnosed individuals. Individuals with a chronic rheumatic condition were more likely to report < 6 h of sleep per night and endorsed significantly more insomnia and daytime sleepiness. There was no interaction between diagnosis of a chronic rheumatic condition and smoking status on any of the sleep outcomes assessed. Finally, an interaction was observed suggesting individuals with a chronic rheumatic condition who currently smoke are more likely to report averaging < 6 h of sleep per night and frequent insomnia compared to individuals with a chronic rheumatic condition who never smoked. These results suggest both a unique and additive relationship between smoking and sleep in individuals with a chronic rheumatic condition. Findings can likely be generalized to other conditions commonly associated with chronic pain.
C1 [Stipelman, Brooke A.] NCI, Sci Res & Technol Branch, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Augustson, Erik] NCI, Tobacco Control Res Branch, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[McNeel, Timothy] Informat Management Serv Inc, Silver Spring, MD USA.
RP Stipelman, BA (reprint author), NCI, Sci Res & Technol Branch, Behav Res Program, Div Canc Control & Populat Sci, 6130 Execut Blvd,MSC 7326,Execut Plaza North,Room, Rockville, MD 20892 USA.
EM stipelmanba@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 63
TC 3
Z9 3
U1 2
U2 16
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
J9 J BEHAV MED
JI J. Behav. Med.
PD OCT
PY 2013
VL 36
IS 5
BP 539
EP 548
DI 10.1007/s10865-012-9447-8
PG 10
WC Psychology, Clinical
SC Psychology
GA 215YT
UT WOS:000324248000010
PM 22864597
ER
PT J
AU Singh, GK
Siahpush, M
Altekruse, SF
AF Singh, Gopal K.
Siahpush, Mohammad
Altekruse, Sean F.
TI Time Trends in Liver Cancer Mortality, Incidence, and Risk Factors by
Unemployment Level and Race/Ethnicity, United States, 1969-2011
SO JOURNAL OF COMMUNITY HEALTH
LA English
DT Article
DE Liver cancer; Mortality; Incidence; Unemployment; Race/ethnicity;
Inequality
ID SOCIOECONOMIC DIFFERENTIALS; LIFE EXPECTANCY; MEN; POPULATIONS;
INEQUALITIES; IMMIGRANT; PATTERNS; HEALTH
AB This study examined unemployment and racial/ethnic disparities in liver cancer mortality, incidence, survival, and risk factors in the United States between 1969 and 2011. Census-based unemployment rates were linked to 1969-2009 county-level mortality and incidence data, whereas 2006-2011 National Health Interview Surveys were used to examine variations in hepatitis infection and alcohol consumption. Age-adjusted mortality rates, risk-ratios, and rate-differences were calculated by year, sex, race, and county-unemployment level. Log-linear, Poisson, and logistic regression and disparity indices were used to model trends and differentials. Although liver-cancer mortality rose markedly for all groups during 1969-2011, higher unemployment levels were associated with increased mortality and incidence rates in each time period. Both absolute and relative inequalities in liver cancer mortality according to unemployment level increased over time for both males and females and for those aged 25-64 years. Compared to the lowest-unemployment group, those aged 25-64 in the highest-unemployment group had 56 and 115 % higher liver-cancer mortality in 1969-1971 and 2005-2009, respectively. Regardless of unemployment levels, Asian/Pacific Islanders and Hispanics had the highest mortality and incidence rates. The adjusted odds of hepatitis infection and heavy drinking were 38-39 % higher among the unemployed than employed. Liver-cancer mortality and incidence have risen steadily among all racial/ethnic, sex, and socioeconomic groups. Faster increases in mortality among the highest-unemployment group have led to a widening gap in mortality over time. Disparities in mortality and incidence are consistent with similar inequalities in hepatitis infection and alcohol consumption.
C1 [Singh, Gopal K.] US Dept HHS, Hlth Resources & Serv Adm, Maternal & Child Hlth Bur, Rockville, MD 20857 USA.
[Siahpush, Mohammad] Univ Nebraska, Med Ctr, Dept Hlth Promot Social & Behav Hlth, Omaha, NE 68198 USA.
[Altekruse, Sean F.] NCI, NIH, Surveillance Res Program, Rockville, MD 20852 USA.
RP Singh, GK (reprint author), US Dept HHS, Hlth Resources & Serv Adm, Maternal & Child Hlth Bur, 5600 Fishers Lane,Room 18-41, Rockville, MD 20857 USA.
EM gsingh@hrsa.gov; msiahpush@unmc.edu; sean.altekruse@nih.gov
NR 46
TC 10
Z9 11
U1 0
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0094-5145
EI 1573-3610
J9 J COMMUN HEALTH
JI J. Community Health
PD OCT
PY 2013
VL 38
IS 5
BP 926
EP 940
DI 10.1007/s10900-013-9703-z
PG 15
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 214FU
UT WOS:000324118300021
PM 23689953
ER
PT J
AU Ramirez, AS
AF Ramirez, A. Susana
TI Effects of Ethnic Targeting on the Perceived Effectiveness of Cancer
Prevention Messages Among Latinas and Non-Latina White Women
SO JOURNAL OF HEALTH COMMUNICATION
LA English
DT Article
ID HEALTH; CAMPAIGNS; BEHAVIOR; ACCULTURATION; COMMUNICATION; SEGMENTATION;
DISPARITIES; TELEVISION; QUESTIONS; HISPANICS
AB In general, efforts to target Latinos are made through Spanish-language messages, yet 75% of U.S. Latinos are bilingual or English dominant. Acculturation (adapting mainstream traits) is associated with increased lifestyle-related risk behaviors. Latinos maintain cultural traits and ethnic identification even as they appear to acculturate (e.g., through language). This raises questions about how to communicate health information to more-acculturated Latinos who are not reached by traditional Spanish outreach yet may not identify with general-market messages. This study tested the relative efficacy of English-language messages targeted to Latinas, compared with general-market messages, among highly acculturated Latina women and non-Latina White women. In this pair of online experiments, Latinas (n=715) and non-Latina White women (n=704) rated the perceived effectiveness of general-market versus Latina-targeted Pap smear and mammogram public service announcements. In 1 of 2 experiments ethnically targeted messages were rated relatively more effective for the intended audience and equally effective for the general audience. The author discusses implications for how campaigns reach U.S. Latinos across the acculturation spectrum.
C1 [Ramirez, A. Susana] NCI, Canc Prevent Fellowship Program, NIH, Bethesda, MD 20892 USA.
RP Ramirez, AS (reprint author), NCI, Canc Prevent Fellowship Program, 6120 Execut Blvd,Room 150E,MSC 7105, Bethesda, MD 20892 USA.
EM ramirezas@mail.nih.gov
FU NCI NIH HHS [P20-CA095856-06, P20 CA095856]
NR 44
TC 3
Z9 3
U1 3
U2 10
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1081-0730
EI 1087-0415
J9 J HEALTH COMMUN
JI J. Health Commun.
PD OCT 1
PY 2013
VL 18
IS 10
BP 1256
EP 1273
DI 10.1080/10810730.2013.778362
PG 18
WC Communication; Information Science & Library Science
SC Communication; Information Science & Library Science
GA 212QZ
UT WOS:000323999200008
PM 23829690
ER
PT J
AU Li, B
Chow, TWS
Huang, D
AF Li, Bing
Chow, Tommy W. S.
Huang, Di
TI A novel feature selection method and its application
SO JOURNAL OF INTELLIGENT INFORMATION SYSTEMS
LA English
DT Article
DE Alzheimer's disease; Class-based distance metric; Feature selection;
Mutual information; Rough sets
ID SUPERVISED FEATURE-SELECTION; INPUT FEATURE-SELECTION; MUTUAL
INFORMATION; ROUGH SETS; ATTRIBUTE REDUCTION; CLASSIFICATION;
ALGORITHMS; SYSTEMS; TABLES; RULES
AB In this paper, a novel feature selection method based on rough sets and mutual information is proposed. The dependency of each feature guides the selection, and mutual information is employed to reduce the features which do not favor addition of dependency significantly. So the dependency of the subset found by our method reaches maximum with small number of features. Since our method evaluates both definitive relevance and uncertain relevance by a combined selection criterion of dependency and class-based distance metric, the feature subset is more relevant than other rough sets based methods. As a result, the subset is near optimal solution. In order to verify the contribution, eight different classification applications are employed. Our method is also employed on a real Alzheimer's disease dataset, and finds a feature subset where classification accuracy arrives at 81.3 %. Those present results verify the contribution of our method.
C1 [Li, Bing; Chow, Tommy W. S.] City Univ Hong Kong, Dept Elect Engn, Kowloon, Hong Kong, Peoples R China.
[Huang, Di] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Li, B (reprint author), City Univ Hong Kong, Dept Elect Engn, 83 Tat Chu Ave, Kowloon, Hong Kong, Peoples R China.
EM bingli5@student.cityu.edu.hk
FU National Institute on Aging [UO1 AG016976]
FX National Alzheimer's Coordinating Center, funded by the National
Institute on Aging (UO1 AG016976), provides the uniform Alzheimer's
disease data set (2005-2011).
NR 68
TC 1
Z9 2
U1 2
U2 25
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0925-9902
EI 1573-7675
J9 J INTELL INF SYST
JI J. Intell. Inf. Syst.
PD OCT
PY 2013
VL 41
IS 2
BP 235
EP 268
DI 10.1007/s10844-013-0243-x
PG 34
WC Computer Science, Artificial Intelligence; Computer Science, Information
Systems
SC Computer Science
GA 214FR
UT WOS:000324118000005
PM 25530672
ER
PT J
AU Miller, JC
Volz, EM
AF Miller, Joel C.
Volz, Erik M.
TI Model hierarchies in edge-based compartmental modeling for infectious
disease spread
SO JOURNAL OF MATHEMATICAL BIOLOGY
LA English
DT Article
ID CONTACT NETWORK; RANDOM GRAPHS; TRANSMISSION; EPIDEMICS; DYNAMICS
AB We consider the family of edge-based compartmental models for epidemic spread developed in Miller et al. (J R Soc Interface 9(70):890-906, 2012). These models allow for a range of complex behaviors, and in particular allow us to explicitly incorporate duration of a contact into our mathematical models. Our focus here is to identify conditions under which simpler models may be substituted for more detailed models, and in so doing we define a hierarchy of epidemic models. In particular we provide conditions under which it is appropriate to use the standard mass action SIR model, and we show what happens when these conditions fail. Using our hierarchy, we provide a procedure leading to the choice of the appropriate model for a given population. Our result about the convergence of models to the mass action model gives clear, rigorous conditions under which the mass action model is accurate.
C1 [Miller, Joel C.] Penn State Univ, Dept Math, University Pk, PA 16802 USA.
[Miller, Joel C.] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
[Miller, Joel C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Miller, Joel C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Ctr Communicable Dis Dynam, Boston, MA 02115 USA.
[Volz, Erik M.] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
RP Miller, JC (reprint author), Penn State Univ, Dept Math, University Pk, PA 16802 USA.
EM joel.c.miller.research@gmail.com
RI Miller, Joel/C-4229-2015;
OI Miller, Joel/0000-0003-4426-0405; Volz, Erik/0000-0001-6268-8937
FU RAPIDD program of the Science and Technology Directorate; Department of
Homeland Security; Fogarty International Center, National Institutes of
Health; Center for Communicable Disease Dynamics; Department of
Epidemiology; Harvard School of Public Health from the National
Institute Of General Medical Sciences [U54GM088558]; NIH [K01 AI091440]
FX JCM was supported by (1) the RAPIDD program of the Science and
Technology Directorate, Department of Homeland Security and the Fogarty
International Center, National Institutes of Health and (2) the Center
for Communicable Disease Dynamics, Department of Epidemiology, Harvard
School of Public Health under Award Number U54GM088558 from the National
Institute Of General Medical Sciences. EMV was supported by NIH K01
AI091440. The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National
Institute Of General Medical Sciences or the National Institutes of
Health.
NR 24
TC 6
Z9 7
U1 0
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0303-6812
J9 J MATH BIOL
JI J. Math. Biol.
PD OCT
PY 2013
VL 67
IS 4
BP 869
EP 899
DI 10.1007/s00285-012-0572-3
PG 31
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA 215ZH
UT WOS:000324249600005
PM 22911242
ER
PT J
AU Lee, SY
Chen, SL
Chang, YH
Chen, PS
Huang, SY
Tzeng, NS
Wang, YS
Wang, LJ
Lee, IH
Yeh, TL
Yang, YK
Lu, RB
Hong, JS
AF Lee, Sheng-Yu
Chen, Shiou-Lan
Chang, Yun-Hsuan
Chen, Po See
Huang, San-Yuan
Tzeng, Nian-Sheng
Wang, Yu-Shan
Wang, Liang-Jen
Lee, I. Hui
Yeh, Tzung Lieh
Yang, Yen Kuang
Lu, Ru-Band
Hong, Jau-Shyong
TI Add-on memantine to valproate treatment increased HDL-C in bipolar II
disorder
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Bipolar II disorder; Memantine; Treatment; HDL-C
ID HIGH-DENSITY-LIPOPROTEIN; MAJOR DEPRESSIVE DISORDER; MOOD DISORDERS;
CHOLESTEROL LEVELS; RATING-SCALE; OPEN-LABEL; LATE-LIFE; STROKE;
MECHANISMS; HYPOMANIA
AB Memantine is a noncompetitive NMDA receptor antagonist. As an augmenting agent, it has an antidepressant-like and mood-stabilizing effect. Memantine also reduces binge eating episodes and weight. We investigated whether memantine added on to valproate (VPA) is more effective than VPA alone for treating BP-II depression and improving the patient's metabolic profile. This was a randomized, double-blind, controlled study. BP-II patients undergoing regular VPA treatments were randomly assigned to one of two groups: VPA plus either add-on [1] memantine (5 mg/day) (n = 62) or [2] placebo (n = 73) for 12 weeks. The Young Mania Rating Scale (YMRS) and Hamilton Depression Rating Scale (HDRS) were used to evaluate clinical response. Height, weight, fasting serum glucose, fasting total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides were followed regularly. Multiple linear regressions with generalized estimating equation methods were used to analyze the effects of memantine on clinical performance. There were no significant differences in pre- and post-treatment YMRS and HDRS scores between the VPA + memantine and VPA + placebo groups. Although there were no significant differences in the pre- and post-treatment values of most metabolic indices between the two groups, there was a significant increase of HDL-C (p = 0.009) in the VPA + memantine group compared with the VPA + placebo group. This increase remained significant even after controlling for body mass index (BMI) (p = 0.020). We conclude that add-on memantine plus VPA treatment of BP-II depression increases the blood level of HDL-C even in the absence of change in affective symptoms.
Trial registration: NCT01188148 (https://register.clinicaltrials.gov/), Trial date was from 1st August, 2008 to 31st July, 2012 in National Cheng Kung University and Tr-Service General Hospital. (C) 2013 Elsevier Ltd.. All rights reserved.
C1 [Lee, Sheng-Yu; Chen, Shiou-Lan; Chen, Po See; Lee, I. Hui; Yeh, Tzung Lieh; Yang, Yen Kuang; Lu, Ru-Band] Natl Cheng Kung Univ, Dept Psychiat, Tainan 70428, Taiwan.
[Chen, Shiou-Lan; Wang, Yu-Shan; Lu, Ru-Band] Natl Cheng Kung Univ, Inst Behav Med, Tainan 70428, Taiwan.
[Chang, Yun-Hsuan; Lu, Ru-Band] Natl Cheng Kung Univ, Coll Med & Hosp, Inst Allied Hlth Sci, Tainan 70428, Taiwan.
[Huang, San-Yuan; Tzeng, Nian-Sheng] Natl Def Med Ctr, Triserv Gen Hosp, Dept Psychiat, Taipei, Taiwan.
[Wang, Liang-Jen] Kaohsiung Chang Gung Mem Hosp, Dept Child & Adolescent Psychiat, Kaohsiung, Taiwan.
[Wang, Liang-Jen] Chang Gung Univ, Coll Med, Kaohsiung, Taiwan.
[Lu, Ru-Band] Natl Cheng Kung Univ, Addict Res Ctr, Tainan 70428, Taiwan.
[Hong, Jau-Shyong] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
RP Lu, RB (reprint author), Natl Cheng Kung Univ, Inst Behav Med, Dept Psychiat, Coll Med & Hosp,Addict Ctr, 138 Sheng Li Rd, Tainan 70428, Taiwan.
EM rblu@mail.ncku.edu.tw
RI Ruan, YL/B-9813-2009
FU Taiwan National Science Council [NSC98-2314-B-006-022-MY3]; Taiwan
Department of Health [DOH 95-TD-M-113-055]; Taiwan National Health
Research Institute [NHRI-EX-97-9738N1]; National Cheng Kung University
Project for Promoting Academic Excellence and Developing World Class
Research Centers
FX This work was supported in part by grant NSC98-2314-B-006-022-MY3 (to
RBL) from the Taiwan National Science Council, grant DOH 95-TD-M-113-055
(to RBL) from the Taiwan Department of Health, grant NHRI-EX-97-9738N1
(to RBL) from the Taiwan National Health Research Institute, and the
National Cheng Kung University Project for Promoting Academic Excellence
and Developing World Class Research Centers.
NR 67
TC 7
Z9 7
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
EI 1879-1379
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD OCT
PY 2013
VL 47
IS 10
BP 1343
EP 1348
DI 10.1016/j.jpsychires.2013.06.017
PG 6
WC Psychiatry
SC Psychiatry
GA 212TC
UT WOS:000324004700009
PM 23870798
ER
PT J
AU Rosemblat, G
Resnick, MP
Auston, I
Shin, D
Sneiderman, C
Fizsman, M
Rindflesch, TC
AF Rosemblat, Graciela
Resnick, Melissa P.
Auston, Ione
Shin, Dongwook
Sneiderman, Charles
Fizsman, Marcelo
Rindflesch, Thomas C.
TI Extending SemRep to the public health domain
SO JOURNAL OF THE AMERICAN SOCIETY FOR INFORMATION SCIENCE AND TECHNOLOGY
LA English
DT Article
DE natural language processing; knowledge representation; semantic analysis
ID INFORMATION; SYSTEM; MANAGEMENT; ONTOLOGY; QUALITY; DESIGN
AB We describe the use of a domain-independent method to extend a natural language processing (NLP) application, SemRep (Rindflesch, Fiszman, & Libbus, 2005), based on the knowledge sources afforded by the Unified Medical Language System (UMLS (R); Humphreys, Lindberg, Schoolman, & Barnett, 1998) to support the area of health promotion within the public health domain. Public health professionals require good information about successful health promotion policies and programs that might be considered for application within their own communities. Our effort seeks to improve access to relevant information for the public health profession, to help those in the field remain an information-savvy workforce. Natural language processing and semantic techniques hold promise to help public health professionals navigate the growing ocean of information by organizing and structuring this knowledge into a focused public health framework paired with a user-friendly visualization application as a way to summarize results of PubMed (R) searches in this field of knowledge.
C1 [Rosemblat, Graciela; Resnick, Melissa P.; Auston, Ione; Shin, Dongwook; Sneiderman, Charles; Fizsman, Marcelo; Rindflesch, Thomas C.] Natl Lib Med, Lister Hill Ctr, Bethesda, MD 20894 USA.
RP Rosemblat, G (reprint author), Natl Lib Med, Lister Hill Ctr, Bldg 38A,07S713B,8600 Rockville Pike, Bethesda, MD 20894 USA.
EM grosemblat@mail.nih.gov; Melissa.P.Resnick@uth.tmc.edu;
ione_auston@nlm.nih.gov; shindongwoo@mail.nih.gov;
csneiderman@mail.nih.gov; fiszman@mail.nih.gov; trindflesch@mail.nih.gov
OI Resnick, Melissa/0000-0001-9699-852X
FU National Library of Medicine; Intramural Research Program of the
National Institutes of Health, National Library of Medicine
FX This research was supported in part by an appointment to the NLM
Associate Fellowship Program sponsored by the National Library of
Medicine and administered by the Oak Ridge Institute for Science and
Education. This study was also supported by the Intramural Research
Program of the National Institutes of Health, National Library of
Medicine.
NR 41
TC 2
Z9 2
U1 0
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1532-2882
J9 J AM SOC INF SCI TEC
JI J. Am. Soc. Inf. Sci. Technol.
PD OCT
PY 2013
VL 64
IS 10
BP 1963
EP 1974
DI 10.1002/asi.22899
PG 12
WC Computer Science, Information Systems; Information Science & Library
Science
SC Computer Science; Information Science & Library Science
GA 213ZS
UT WOS:000324100000001
PM 24729747
ER
PT J
AU Satheshkumar, PS
Weisberg, AS
Moss, B
AF Satheshkumar, P. S.
Weisberg, Andrea S.
Moss, Bernard
TI Vaccinia Virus A19 Protein Participates in the Transformation of
Spherical Immature Particles to Barrel-Shaped Infectious Virions
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID EXTERNAL SCAFFOLD; MATURE VIRION; MORPHOGENESIS; MEMBRANE; REPLICATION;
GENOME; GENE; BIOGENESIS; REPRESSION; EXPRESSION
AB The A19L open reading frame of vaccinia virus encodes a 9-kDa protein that is conserved in all sequenced chordopoxviruses, yet until now it has not been specifically characterized in any species. We appended an epitope tag after the start codon of the A19L open reading frame without compromising infectivity. The protein was synthesized after viral DNA replication and was phosphorylated independently of the vaccinia virus F10 kinase. The A19 protein was present in purified virions and was largely resistant to nonionic detergent extraction, suggesting a location within the core. A conditional lethal mutant virus was constructed by placing the A19 open reading frame under the control of the Escherichia coli lac repressor system. A19 synthesis and infectious virus formation were dependent on inducer. In the absence of inducer, virion morphogenesis was interrupted, and spherical dense particles that had greatly reduced amounts of the D13 scaffold accumulated in place of barrel-shaped mature virions. The infectivity of purified A19-deficient particles was more than 2 log units less than that of A19-containing virions. Nevertheless, the A19-deficient particles contained DNA, and except for the absence of A19 and decreased core protein processing, they appeared to have a similar protein composition as A19-containing virions. Thus, the A19 protein participates in the maturation of immature vaccinia virus virions to infectious particles.
C1 [Satheshkumar, P. S.; Weisberg, Andrea S.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This research was supported by intramural funds of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 45
TC 4
Z9 5
U1 0
U2 8
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 OCT
PY 2013
VL 87
IS 19
BP 10700
EP 10709
DI 10.1128/JVI.01258-13
PG 10
WC Virology
SC Virology
GA 214WV
UT WOS:000324169200025
PM 23885081
ER
PT J
AU Satheshkumar, PS
Olano, LR
Hammer, CH
Zhao, M
Moss, B
AF Satheshkumar, P. S.
Olano, L. Renee
Hammer, Carl H.
Zhao, Ming
Moss, Bernard
TI Interactions of the Vaccinia Virus A19 Protein
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NUCLEAR-LOCALIZATION SIGNALS; INTRACELLULAR MATURE VIRIONS; DISULFIDE
BOND FORMATION; RNA-POLYMERASE; MONOCLONAL-ANTIBODIES; MEMBRANE-PROTEIN;
TRANSCRIPTION; GENE; MORPHOGENESIS; SUBUNIT
AB The A19 protein of vaccinia virus (VACV) is conserved among chordopoxviruses, expressed late in infection, packaged in the virus core, and required for a late step in morphogenesis. Multiple-sequence alignments of A19 homologs indicated conservation of a series of lysines and arginines, which could represent a nuclear localization or nucleic acid binding motif, and a pair of CXXC motifs that suggested a zinc finger or redox active sites. The importance of the CXXC motif was confirmed by cysteine-to-serine substitutions, which rendered the altered protein unable to trans-complement infectivity of a null mutant. Nevertheless, the cysteines were not required for function of the poxvirus-specific redox pathway. Epitope-tagged A19 proteins were detected in the nucleus and cytoplasm in both infected and uninfected cells, but this distribution was unaffected by alanine substitutions of the arginine residues, which only partially reduced the ability of the mutated protein to trans-complement infectivity. Viral proteins specifically associated with affinity-purified A19 were identified by mass spectrometry as components of the transcription complex, including RNA polymerase subunits, RAP94 (RNA polymerase-associated protein 94), early transcription factors, capping enzyme, and nucleoside triphosphate phosphohydrolase I, and two core proteins required for morphogenesis. Further studies suggested that the interaction of A19 with the RNA polymerase did not require RAP94 or other intermediate or late viral proteins but was reduced by mutation of cysteines in the putative zinc finger domain. Although A19 was not required for incorporation of the transcription complex in virus particles, the transcriptional activity of A19-deficient virus particles was severely reduced.
C1 [Satheshkumar, P. S.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Olano, L. Renee; Hammer, Carl H.; Zhao, Ming] NIAID, Res Technol Sect, Res Technol Branch, NIH, Rockville, MD USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This research was supported by intramural funds of the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 44
TC 4
Z9 4
U1 2
U2 9
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 OCT
PY 2013
VL 87
IS 19
BP 10710
EP 10720
DI 10.1128/JVI.01261-13
PG 11
WC Virology
SC Virology
GA 214WV
UT WOS:000324169200026
PM 23885084
ER
EF